title
stringlengths 2
512
| issue
stringlengths 0
29
| pages
stringlengths 1
35
| abstract
stringlengths 0
6.04k
| journal
stringlengths 2
239
| authors
listlengths 0
77
| pubdate
stringlengths 4
10
| pmid
stringlengths 1
7
| mesh_terms
stringlengths 0
2.39k
| publication_types
stringlengths 12
284
| chemical_list
stringlengths 0
920
| keywords
stringlengths 0
1.52k
| doi
stringlengths 0
69
| references
listlengths 0
1.3k
| delete
bool 1
class | languages
stringclasses 95
values | vernacular_title
stringlengths 0
491
| pmc
stringclasses 2
values | other_id
stringlengths 0
44
| medline_ta
stringlengths 2
96
| nlm_unique_id
stringlengths 7
9
| issn_linking
stringlengths 0
9
| country
stringclasses 90
values | grant_ids
listlengths 0
23
| _inserted_at
unknown | _read_from
stringclasses 109
values |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
Incontinentia pigmenti. | 5(3) | 361-77 | Incontinentia pigmenti (IP) is an unusual genodermatosis occurring almost exclusively in female patients. IP is characterized by swirling hyperpigmented skin lesions and associated with a high incidence of systemic defects. Nearly one third of patients present with neurologic complications. Consequently, neurologists and other clinicians involved in the care of these patients must be able to identify the cutaneous markers and systemic findings of IP. This article discusses the clinical presentations, laboratory findings, and pathogenesis of IP. A systematic approach to the evaluation and management of patients with IP is presented. | Neurologic clinics | [
{
"affiliation": "",
"forename": "B A",
"identifier": "",
"initials": "BA",
"lastname": "Cohen"
}
] | 1987-08 | 3306331 | D006801:Humans; D007184:Incontinentia Pigmenti / Q000175:diagnosis* / Q000235:genetics; D010375:Pedigree; D010859:Pigmentation Disorders / Q000175:diagnosis*; D012306:Risk | D016428:Journal Article; D016454:Review | [] | false | eng | Neurol Clin | 8219232 | 0733-8619 | United States | [] | "2024-08-13T08:46:10.611381Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||||
Dermatomyositis. | 5(3) | 379-403 | Dermatomyositis is a condition that combines an inflammatory myopathy with characteristic cutaneous disease. This disorder is closely related to polymyositis, which has all the muscular features of dermatomyositits without the presence of skin disease. Both dermatomyositits and polymyositis may occur in the presence of other collagen vascular diseases such as lupus erythematosus, scleroderma, Sjögren's syndrome, rheumatoid arthritis, and various vasculitides. Dermatomyositis seems to be characterized by an increased frequency of internal malignancy and both dermatomyositis and polymyositis are associated with morbidity and mortality. Therefore, prompt and aggressive therapy is necessary. | Neurologic clinics | [
{
"affiliation": "",
"forename": "J P",
"identifier": "",
"initials": "JP",
"lastname": "Callen"
}
] | 1987-08 | 3306332 | D003882:Dermatomyositis / Q000175:diagnosis*; D006801:Humans; D009369:Neoplasms / Q000175:diagnosis | D016428:Journal Article; D016454:Review | [] | false | eng | Neurol Clin | 8219232 | 0733-8619 | United States | [] | "2024-08-13T08:46:10.613232Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||||
Sjögren's syndrome. Cutaneous, immunologic, and nervous system manifestations. | 5(3) | 405-26 | The studies recounted in this review have demonstrated that cutaneous vasculitis is a frequent extraglandular manifestation of primary Sjögren's syndrome. Two histopathologic types of vasculitis have been detected. One type, a leukocytoclastic angiitis, is found in association with high-titer anti-Ro(SS-A) antibodies, rheumatoid factor, hypergammaglobulinemia, and hypocomplementemia. The second type, a mononuclear inflammatory vasculopathy, in sharp contrast, is found in association with low-titer Ro(SS-A) antibodies, normocomplementemia, and absence of hypergammaglobulinemia and rheumatoid factor. Both types of vasculitis are found in association with peripheral nervous system and CNS disease. The peripheral nervous system and CNS disease involves the entire neuroaxis and preliminary data indicate that a vasculopathy is the cause of the peripheral nervous system and CNS disease. Evoked sensory response testing, CSF analysis, and MRI have proved to be very valuable techniques in investigating these patients with Sjögren's syndrome. Preliminary data suggest that high doses of prednisone or immunosuppressive agents are effective in treating these patients. | Neurologic clinics | [
{
"affiliation": "",
"forename": "T T",
"identifier": "",
"initials": "TT",
"lastname": "Provost"
},
{
"affiliation": "",
"forename": "D",
"identifier": "",
"initials": "D",
"lastname": "Vasily"
},
{
"affiliation": "",
"forename": "E",
"identifier": "",
"initials": "E",
"lastname": "Alexander"
}
] | 1987-08 | 3306333 | D001323:Autoantibodies / Q000032:analysis*; D006801:Humans; D009422:Nervous System Diseases / Q000175:diagnosis*; D012859:Sjogren's Syndrome / Q000175:diagnosis* / Q000276:immunology; D014657:Vasculitis / Q000175:diagnosis* | D016428:Journal Article; D013485:Research Support, Non-U.S. Gov't; D013487:Research Support, U.S. Gov't, P.H.S.; D016454:Review | D001323:Autoantibodies | [] | false | eng | Neurol Clin | 8219232 | 0733-8619 | United States | [
{
"agency": "NHLBI NIH HHS",
"country": "United States",
"grant_acronym": "HL",
"grant_id": "HL34723"
},
{
"agency": "NIADDK NIH HHS",
"country": "United States",
"grant_acronym": "AM",
"grant_id": "R01 AM25650"
}
] | "2024-08-13T08:46:10.614005Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||
Behçet's disease. | 5(3) | 427-40 | Behçet's disease is a complex, multisystem disease that was first described in 1937 by the Turkish dermatologist, Hulusi Behçet, but may have been recognized since ancient times. In his original description, Behçet referred to a symptom complex of recurrent oral aphthous ulcers, genital aphthae, and iritis that could lead to blindness. Additional clinical manifestations include the pathergy phenomenon (the induction of a cutaneous pustular neutrophilic vascular reaction after intradermal trauma), arthritis, thrombophlebitis, erythema nodosum-like cutaneous lesions, and neurologic signs and symptoms ranging from benign intracranial hypertension to a condition resembling multiple sclerosis. The author discusses epidemiology, diagnosis, clinical aspects, pathology, clinical course of the disease, and therapy. | Neurologic clinics | [
{
"affiliation": "",
"forename": "J L",
"identifier": "",
"initials": "JL",
"lastname": "Jorizzo"
}
] | 1987-08 | 3306334 | D001528:Behcet Syndrome / Q000175:diagnosis*; D003937:Diagnosis, Differential; D006801:Humans; D012871:Skin Diseases / Q000175:diagnosis* | D016428:Journal Article; D016454:Review | [] | false | eng | Neurol Clin | 8219232 | 0733-8619 | United States | [] | "2024-08-13T08:46:10.614725Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||||
Ataxia-telangiectasia. | 5(3) | 447-9 | Ataxia-telangiectasia is an autosomal recessive disorder characterized by early ataxia, oculocutaneous telangiectasias, sinopulmonary infections, selective immunodeficiency, and a high risk of malignancy. The appearance of the telangiectasias often allows the diagnosis to be made in a child with ataxia. | Neurologic clinics | [
{
"affiliation": "",
"forename": "A S",
"identifier": "",
"initials": "AS",
"lastname": "Paller"
}
] | 1987-08 | 3306335 | D001260:Ataxia Telangiectasia / Q000175:diagnosis* / Q000235:genetics; D002648:Child; D006801:Humans; D012306:Risk | D016428:Journal Article; D016454:Review | [] | false | eng | Neurol Clin | 8219232 | 0733-8619 | United States | [] | "2024-08-13T08:46:10.615601Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||||
Cutaneous manifestations of neurologic infections in children. | 5(3) | 459-82 | Neurologic infections in children are frequently accompanied by cutaneous findings that may direct the physician toward the correct diagnosis. In some instances, the appearance of an eruption (such as erythema chronicum migrans and Lyme disease) is specific or a rapid bedside diagnostic test (Tzanck preparation for herpes simplex) is extremely helpful in sorting out the differential diagnosis of a child's illness. In this article, cutaneous clues to some of the more important childhood infections will be reviewed. | Neurologic clinics | [
{
"affiliation": "",
"forename": "R A",
"identifier": "",
"initials": "RA",
"lastname": "Silverman"
}
] | 1987-08 | 3306337 | D002648:Child; D006801:Humans; D009422:Nervous System Diseases / Q000175:diagnosis*; D012874:Skin Diseases, Infectious / Q000175:diagnosis* | D016428:Journal Article; D016454:Review | [] | false | eng | Neurol Clin | 8219232 | 0733-8619 | United States | [] | "2024-08-13T08:46:10.616218Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||||
Epidermal nevus syndrome. | 5(3) | 451-7 | Epidermal nevi are linear hamartomas of epidermal structures that usually appear at birth or during infancy. Patients with the epidermal nevus syndrome have epidermal nevi with abnormalities of the central nervous system, eyes, and bones, and other cutaneous alterations. | Neurologic clinics | [
{
"affiliation": "",
"forename": "A S",
"identifier": "",
"initials": "AS",
"lastname": "Paller"
}
] | 1987-08 | 3306336 | D002493:Central Nervous System Diseases / Q000175:diagnosis*; D006801:Humans; D009378:Neoplasms, Multiple Primary / Q000175:diagnosis*; D009506:Nevus / Q000175:diagnosis*; D012878:Skin Neoplasms / Q000175:diagnosis*; D013577:Syndrome | D016428:Journal Article; D016454:Review | [] | false | eng | Neurol Clin | 8219232 | 0733-8619 | United States | [] | "2024-08-13T08:46:10.616957Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||||
The psyche and the skin. | 5(3) | 483-97 | The concept of psychosomatic disorders has been undergoing great evolutionary changes during the past 20 to 30 years. There is no longer any significant or reasonable disagreement that the brain and body mutually interact, and the pathways of those interactions are being explored and explained. Enormous amounts of work are being done to unravel the workings of the brain, which is more complex than any other organ because of neural connections and networking of astronomic proportions. | Neurologic clinics | [
{
"affiliation": "",
"forename": "R",
"identifier": "",
"initials": "R",
"lastname": "Masters"
}
] | 1987-08 | 3306338 | D005162:Factitious Disorders / Q000175:diagnosis; D006801:Humans; D011602:Psychophysiologic Disorders / Q000175:diagnosis*; D012871:Skin Diseases / Q000175:diagnosis*; D013315:Stress, Psychological / Q000150:complications | D016428:Journal Article; D016454:Review | [] | false | eng | Neurol Clin | 8219232 | 0733-8619 | United States | [] | "2024-08-13T08:46:10.617695Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||||
[People who supported progress of cardiovascular surgery]. | 88(6) | 657-62 | Nihon Geka Gakkai zasshi | [
{
"affiliation": "",
"forename": "T",
"identifier": "",
"initials": "T",
"lastname": "Horiuchi"
}
] | 1987-06 | 3306339 | D000818:Animals; D006348:Cardiac Surgical Procedures / Q000266:history*; D049673:History, 20th Century; D006801:Humans; D014656:Vascular Surgical Procedures / Q000266:history* | D016456:Historical Article; D016428:Journal Article; D016454:Review | [] | false | jpn | Nihon Geka Gakkai Zasshi | 0405405 | 0301-4894 | Japan | [] | "2024-08-13T08:46:10.619295Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||||
[Clinicohistopathological and immunohistochemical studies on intrapancreatic spread of pancreatic carcinoma]. | 88(6) | 735-42 | Clinicohistopathological and immunohistochemical studies on intrapancreatic spread of pancreatic carcinoma were performed on 30 cases with total pancreatectomy accompanied by portal vein resection. In the observation of HE stained tissue sections of 25 cases of carcinoma of head of the pancreas, the intrapancreatic spread from the head to body or tail was observed in 9 out of 25 cases (36%). However, by the immunostaining of CEA, CA19-9 and Dupan 2, small cancer nests surrounded by fibrous tissues could be easily detected and intrapancreatic continuous spread from the head to body or tail was observed in 15 out of 25 cases (60%). The intrapancreatic spread of the carcinoma correlated with portal invasion of carcinoma, hardness of the body and tail, obstruction of main pancreatic duct and irregular pancreaticogram. The intraoperative quick immunostaining on the cryostat sections of the pancreatic tissue, together with the HE staining, is useful to determine the intrapancreatic spread of the carcinoma. The indication of total pancreatectomy for pancreatic carcinoma can be determined by these results. | Nihon Geka Gakkai zasshi | [
{
"affiliation": "",
"forename": "A",
"identifier": "",
"initials": "A",
"lastname": "Nakao"
},
{
"affiliation": "",
"forename": "T",
"identifier": "",
"initials": "T",
"lastname": "Ichihara"
},
{
"affiliation": "",
"forename": "T",
"identifier": "",
"initials": "T",
"lastname": "Nonami"
},
{
"affiliation": "",
"forename": "A",
"identifier": "",
"initials": "A",
"lastname": "Harada"
},
{
"affiliation": "",
"forename": "H",
"identifier": "",
"initials": "H",
"lastname": "Takagi"
},
{
"affiliation": "",
"forename": "T",
"identifier": "",
"initials": "T",
"lastname": "Koshikawa"
},
{
"affiliation": "",
"forename": "H",
"identifier": "",
"initials": "H",
"lastname": "Nagura"
}
] | 1987-06 | 3306340 | D000951:Antigens, Neoplasm / Q000032:analysis*; D015295:Antigens, Tumor-Associated, Carbohydrate; D002272:Carcinoembryonic Antigen / Q000032:analysis*; D006651:Histocytochemistry; D006801:Humans; D007124:Immunoenzyme Techniques; D009361:Neoplasm Invasiveness; D010179:Pancreas / Q000473:pathology*; D010190:Pancreatic Neoplasms / Q000175:diagnosis / Q000473:pathology* | D004740:English Abstract; D016428:Journal Article | D000951:Antigens, Neoplasm; D015295:Antigens, Tumor-Associated, Carbohydrate; D002272:Carcinoembryonic Antigen | [] | false | jpn | Nihon Geka Gakkai Zasshi | 0405405 | 0301-4894 | Japan | [] | "2024-08-13T08:46:10.620163Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||
[Long-term follow-up study of renal autotransplantation in reno-vascular hypertension]. | 88(6) | 761-7 | Therapeutic effects of heterotopic renal transplantation for renovascular hypertension were evaluated in ten patients with a follow-up period of more than three years. These ten patients consisted of 4 males and 6 females with the range of age from 21 to 55. The causes of renovascular hypertension were fibromuscular dysplasia in five patients, atherosclerosis in 3 and aortitis syndrome in 2. All the ten patients had a unilateral stenosis of the renal artery. At 3 years after operation, the blood pressure fell to normal range without any medication in 9 patients (90%) and it could be controlled with antihypertensive drugs in the remaining one patient. Operative mortality or deterioration of graft function was not experienced in any of them. One of the female patients had three deliveries after operation. The heterotopic renal autotransplantation is a therapeutic method to be selected for renovascular hypertension, since excellent and stable long-term results can be achieved. | Nihon Geka Gakkai zasshi | [
{
"affiliation": "",
"forename": "M",
"identifier": "",
"initials": "M",
"lastname": "Fukuda"
},
{
"affiliation": "",
"forename": "I",
"identifier": "",
"initials": "I",
"lastname": "Aikawa"
},
{
"affiliation": "",
"forename": "Y",
"identifier": "",
"initials": "Y",
"lastname": "Omori"
},
{
"affiliation": "",
"forename": "N",
"identifier": "",
"initials": "N",
"lastname": "Yoshimura"
},
{
"affiliation": "",
"forename": "S",
"identifier": "",
"initials": "S",
"lastname": "Suzuki"
},
{
"affiliation": "",
"forename": "T",
"identifier": "",
"initials": "T",
"lastname": "Yasumura"
},
{
"affiliation": "",
"forename": "T",
"identifier": "",
"initials": "T",
"lastname": "Oka"
}
] | 1987-06 | 3306341 | D000328:Adult; D000368:Aged; D001015:Aortic Arch Syndromes / Q000150:complications; D001161:Arteriosclerosis / Q000150:complications; D001794:Blood Pressure; D005260:Female; D005352:Fibromuscular Dysplasia / Q000150:complications; D005500:Follow-Up Studies; D006801:Humans; D006978:Hypertension, Renovascular / Q000209:etiology / Q000503:physiopathology / Q000601:surgery*; D016030:Kidney Transplantation; D008297:Male; D008875:Middle Aged | D004740:English Abstract; D016428:Journal Article | [] | false | jpn | Nihon Geka Gakkai Zasshi | 0405405 | 0301-4894 | Japan | [] | "2024-08-13T08:46:10.621157Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||||
[The procurement technic from the same donor in heart and liver transplantation]. | 88(6) | 792 | Nihon Geka Gakkai zasshi | [
{
"affiliation": "",
"forename": "Y",
"identifier": "",
"initials": "Y",
"lastname": "Morishita"
},
{
"affiliation": "",
"forename": "T",
"identifier": "",
"initials": "T",
"lastname": "Harada"
},
{
"affiliation": "",
"forename": "Y",
"identifier": "",
"initials": "Y",
"lastname": "Moriyama"
},
{
"affiliation": "",
"forename": "A",
"identifier": "",
"initials": "A",
"lastname": "Ikoma"
},
{
"affiliation": "",
"forename": "H",
"identifier": "",
"initials": "H",
"lastname": "Koyanagi"
},
{
"affiliation": "",
"forename": "R",
"identifier": "",
"initials": "R",
"lastname": "Kamimura"
},
{
"affiliation": "",
"forename": "M",
"identifier": "",
"initials": "M",
"lastname": "Hashiguchi"
},
{
"affiliation": "",
"forename": "T",
"identifier": "",
"initials": "T",
"lastname": "Kumagae"
},
{
"affiliation": "",
"forename": "A",
"identifier": "",
"initials": "A",
"lastname": "Taira"
}
] | 1987-06 | 3306342 | D000818:Animals; D003080:Cold Temperature; D004285:Dogs; D016027:Heart Transplantation; D016031:Liver Transplantation; D009926:Organ Preservation / Q000379:methods*; D014019:Tissue Donors | D016428:Journal Article | [] | false | jpn | Nihon Geka Gakkai Zasshi | 0405405 | 0301-4894 | Japan | [] | "2024-08-13T08:46:10.622299Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||||
[Study on optimal size of tricuspid valve annular area in annuloplasty]. | 88(6) | 793 | Nihon Geka Gakkai zasshi | [
{
"affiliation": "",
"forename": "M",
"identifier": "",
"initials": "M",
"lastname": "Higashidate"
},
{
"affiliation": "",
"forename": "K",
"identifier": "",
"initials": "K",
"lastname": "Tamiya"
},
{
"affiliation": "",
"forename": "K",
"identifier": "",
"initials": "K",
"lastname": "Akiyama"
},
{
"affiliation": "",
"forename": "Y",
"identifier": "",
"initials": "Y",
"lastname": "Harada"
},
{
"affiliation": "",
"forename": "Y",
"identifier": "",
"initials": "Y",
"lastname": "Takanashi"
},
{
"affiliation": "",
"forename": "Y",
"identifier": "",
"initials": "Y",
"lastname": "Imai"
}
] | 1987-06 | 3306343 | D000818:Animals; D004285:Dogs; D006439:Hemodynamics; D008991:Monitoring, Physiologic; D013536:Suture Techniques; D014261:Tricuspid Valve / Q000033:anatomy & histology / Q000503:physiopathology / Q000601:surgery* | D016428:Journal Article | [] | false | jpn | Nihon Geka Gakkai Zasshi | 0405405 | 0301-4894 | Japan | [] | "2024-08-13T08:46:10.623150Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||||
Synthesis of hybrid bisnucleoside 5',5"'-P1,P4-tetraphosphates by aminoacyl-tRNA synthetases. | 75(1) | 15-21 | Aminoacyl tRNA synthetases, by means of a back reaction, are able to synthesize certain 5', 5"'-P1, P4-bisnucleoside tetraphosphates of biological importance, such as Ap4A. Here it is shown that HisRS and TrpRS (Bacillus stearothermophilus) and AlaRS (E. coli) also synthesize the hybrid compounds Ap4G, Ap4C, and Ap4U. GlnRS (E. coli) is unable to synthesize any of the above compounds. AlaRS synthesizes Ap4U very poorly, and Ap4C and Ap4G almost as effectively as Ap4A. HisRS and TrpRS synthesize Ap4G, Ap4U and Ap3U quite effectively, and Ap4C very poorly. The fact that hybrid bisnucleoside tetraphosphates can be made by the same enzymes, and at rates comparable to Ap4A, suggests that these compounds may also occur in vivo. | Molecular and cellular biochemistry | [
{
"affiliation": "",
"forename": "T W",
"identifier": "",
"initials": "TW",
"lastname": "Traut"
}
] | 1987-05 | 3306344 | D000227:Adenine Nucleotides / Q000096:biosynthesis*; D000604:Amino Acyl-tRNA Synthetases / Q000378:metabolism*; D003562:Cytidine / Q000031:analogs & derivatives / Q000096:biosynthesis; D015226:Dinucleoside Phosphates; D004926:Escherichia coli / Q000201:enzymology; D001411:Geobacillus stearothermophilus / Q000201:enzymology; D006151:Guanosine / Q000031:analogs & derivatives / Q000096:biosynthesis; D009843:Oligoribonucleotides / Q000096:biosynthesis*; D014529:Uridine / Q000031:analogs & derivatives / Q000096:biosynthesis | D016428:Journal Article; D013486:Research Support, U.S. Gov't, Non-P.H.S. | D000227:Adenine Nucleotides; D015226:Dinucleoside Phosphates; D009843:Oligoribonucleotides; C040818:adenosine 5'-P(1)-tetraphosphate-P(4)-5'''-guanosine; C049629:adenosine(5')tetraphosphate uridine; D006151:Guanosine; C053243:adenosine 5'-P(1)-triphosphate-P(3)-5'''-uridine; C020733:diadenosine tetraphosphate; D003562:Cytidine; C053244:adenosine 5' P(1)-tetraphosphate-P(4)-5'''-cytidine; D000604:Amino Acyl-tRNA Synthetases; D014529:Uridine | 10.1007/BF00231604 | [
{
"citation": "Biochem Biophys Res Commun. 1966 Jul 6;24(1):91-7",
"pmid": "5338216"
},
{
"citation": "Biochemistry. 1982 Oct 12;21(21):5273-9",
"pmid": "6756470"
},
{
"citation": "Biochem Biophys Res Commun. 1966 Jul 6;24(1):98-105",
"pmid": "4290754"
},
{
"citation": "J Biol Chem. 1981 Jan 10;256(1):198-204",
"pmid": "7005211"
},
{
"citation": "J Biol Chem. 1982 Dec 25;257(24):14613-5",
"pmid": "7174656"
},
{
"citation": "Anal Biochem. 1983 Oct 1;134(1):1-10",
"pmid": "6318593"
},
{
"citation": "Proc Natl Acad Sci U S A. 1983 Dec;80(24):7496-500",
"pmid": "6369319"
},
{
"citation": "Mol Cell Biochem. 1983;52(1):3-11",
"pmid": "6346051"
},
{
"citation": "Anal Biochem. 1982 Aug;124(2):327-32",
"pmid": "7149233"
},
{
"citation": "J Biol Chem. 1978 Jul 25;253(14):4960-5",
"pmid": "670172"
},
{
"citation": "Biochemistry. 1984 Jan 17;23(2):182-90",
"pmid": "6365159"
},
{
"citation": "Proc Natl Acad Sci U S A. 1976 Nov;73(11):3984-8",
"pmid": "1069282"
},
{
"citation": "Eur J Biochem. 1982 Aug;126(1):135-42",
"pmid": "7128581"
},
{
"citation": "Biochemistry. 1983 Sep 13;22(19):4353-7",
"pmid": "6626505"
},
{
"citation": "Eur J Biochem. 1975 Aug 15;56(2):335-41",
"pmid": "1175627"
},
{
"citation": "Mol Pharmacol. 1986 Aug;30(2):159-63",
"pmid": "3016499"
},
{
"citation": "J Biol Chem. 1983 Jun 10;258(11):6827-34",
"pmid": "6304059"
},
{
"citation": "J Biol Chem. 1982 Oct 10;257(19):11644-50",
"pmid": "6749844"
},
{
"citation": "Biochimie. 1981 Nov-Dec;63(11-12):827-30",
"pmid": "6277395"
}
] | false | eng | Mol Cell Biochem | 0364456 | 0300-8177 | Netherlands | [] | "2024-08-13T08:46:10.625269Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Cell type-specific expressions of c-ras gene products in the normal rat. | 75(1) | 23-32 | Expression of proteins encoded by the ras proto-oncogenes was examined immunohistochemically in formalin-fixed, paraffin-embedded tissues of the normal rat using anti-ras p21 antibodies generated against synthetic peptides. Cell type specific expressions of ras gene products were detected in distal tubules of kidney, megakaryocytes in spleen, neural cells in cerebrum, Purkinje cells in cerebellum, cells lining the pulmonary alveoli and cells in the epithelium of intestinal villi. Region specific expressions of the ras proteins were observed in spleen and thymus, where the ras proteins were detected in splenic nodules including germinal centers and thymic medulla, respectively. These findings suggest that the c-ras gene products in normal rat organs are expressed in specific cell-types within a tissue and may be associated with degree of cellular differentiation. | Molecular and cellular biochemistry | [
{
"affiliation": "",
"forename": "T",
"identifier": "",
"initials": "T",
"lastname": "Tanaka"
},
{
"affiliation": "",
"forename": "N",
"identifier": "",
"initials": "N",
"lastname": "Ida"
},
{
"affiliation": "",
"forename": "C",
"identifier": "",
"initials": "C",
"lastname": "Waki"
},
{
"affiliation": "",
"forename": "H",
"identifier": "",
"initials": "H",
"lastname": "Shimoda"
},
{
"affiliation": "",
"forename": "D J",
"identifier": "",
"initials": "DJ",
"lastname": "Slamon"
},
{
"affiliation": "",
"forename": "M J",
"identifier": "",
"initials": "MJ",
"lastname": "Cline"
}
] | 1987-05 | 3306345 | D000818:Animals; D005786:Gene Expression Regulation; D006651:Histocytochemistry; D007124:Immunoenzyme Techniques; D011518:Proto-Oncogene Proteins / Q000235:genetics / Q000378:metabolism*; D016283:Proto-Oncogene Proteins p21(ras); D051381:Rats; D011919:Rats, Inbred Strains; D014018:Tissue Distribution | D016428:Journal Article; D013485:Research Support, Non-U.S. Gov't; D013487:Research Support, U.S. Gov't, P.H.S. | D011518:Proto-Oncogene Proteins; D016283:Proto-Oncogene Proteins p21(ras) | 10.1007/BF00231605 | [
{
"citation": "Nature. 1985 May 16-22;315 (6016):242-5",
"pmid": "3923359"
},
{
"citation": "Nature. 1982 Oct 14;299(5884):593-6",
"pmid": "6181415"
},
{
"citation": "Proc Natl Acad Sci U S A. 1979 Oct;76(10):5355-9",
"pmid": "228288"
},
{
"citation": "Cell. 1984 Jul;37(3):1027-33",
"pmid": "6430564"
},
{
"citation": "Cell. 1985 Dec;43(3 Pt 2):615-21",
"pmid": "2416466"
},
{
"citation": "Cell. 1984 Nov;39(1):141-8",
"pmid": "6091907"
},
{
"citation": "Proc Natl Acad Sci U S A. 1984 Aug;81(16):5227-31",
"pmid": "6382261"
},
{
"citation": "Science. 1984 Apr 20;224(4646):256-62",
"pmid": "6538699"
},
{
"citation": "Nature. 1984 Aug 9-15;310(5977):508-11",
"pmid": "6611509"
},
{
"citation": "Nature. 1984 Sep 20-26;311(5983):273-5",
"pmid": "6148703"
},
{
"citation": "Cell. 1984 Mar;36(3):607-12",
"pmid": "6365329"
},
{
"citation": "Nature. 1984 Oct 11-17;311(5986):562-5",
"pmid": "6482968"
},
{
"citation": "Nature. 1981 Aug 6;292(5823):506-11",
"pmid": "6265801"
},
{
"citation": "Mol Cell Biochem. 1986 Apr;70(1):97-104",
"pmid": "3520294"
},
{
"citation": "Proc Natl Acad Sci U S A. 1984 Nov;81(22):6953-7",
"pmid": "6438627"
},
{
"citation": "Nature. 1982 Nov 11;300(5888):149-52",
"pmid": "7133135"
},
{
"citation": "Science. 1985 Apr 5;228(4695):96-9",
"pmid": "3856323"
},
{
"citation": "Nature. 1982 Oct 14;299(5884):640-4",
"pmid": "6289129"
},
{
"citation": "Proc Natl Acad Sci U S A. 1985 May;82(10):3400-4",
"pmid": "3858828"
},
{
"citation": "N Engl J Med. 1986 Jan 16;314(3):133-7",
"pmid": "2417118"
},
{
"citation": "Cell. 1980 Apr;19(4):1005-14",
"pmid": "6247068"
},
{
"citation": "Proc Natl Acad Sci U S A. 1984 Jan;81(1):71-5",
"pmid": "6320174"
},
{
"citation": "Cell. 1985 Jan;40(1):27-36",
"pmid": "2981630"
},
{
"citation": "Proc Natl Acad Sci U S A. 1984 Jun;81(12):3670-4",
"pmid": "6587382"
},
{
"citation": "Proc Natl Acad Sci U S A. 1984 Nov;81(22):7141-5",
"pmid": "6594688"
},
{
"citation": "Nature. 1984 Jul 12-18;310(5973):147-50",
"pmid": "6610834"
},
{
"citation": "Cell. 1985 Oct;42(3):841-8",
"pmid": "2996779"
},
{
"citation": "Nature. 1985 Jan 17-23;313(5999):241-3",
"pmid": "3918269"
},
{
"citation": "Science. 1984 Nov 16;226(4676):860-2",
"pmid": "6436980"
},
{
"citation": "Cell. 1986 Jan 31;44(2):329-36",
"pmid": "3002633"
},
{
"citation": "Cancer Res. 1986 Mar;46(3):1465-70",
"pmid": "3510727"
},
{
"citation": "Proc Natl Acad Sci U S A. 1984 Sep;81(18):5704-8",
"pmid": "6148751"
}
] | false | eng | Mol Cell Biochem | 0364456 | 0300-8177 | Netherlands | [
{
"agency": "NCI NIH HHS",
"country": "United States",
"grant_acronym": "CA",
"grant_id": "CA15619"
},
{
"agency": "NCI NIH HHS",
"country": "United States",
"grant_acronym": "CA",
"grant_id": "CA36827"
}
] | "2024-08-13T08:46:10.627029Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Glycolysis--new concepts in an old pathway. | 76(1) | 3-14 | A survey of the existing data on the interactions of glycolytic enzymes with the cellular structure in mammalian tissues has substantiated the occurrence of an extensive degree of such associations in all tissues and during all stages of development. Furthermore, a considerable specificity was evident between the individual multiple forms of the enzymes in relation to these associations. In reviewing these data, a model has been developed which proposes that the glycolytic sequence is best described as consisting of a number of segments in vivo, each segment formed by a cluster of isozymes, many of which can interact with the actin containing filaments of the cytomatrix. The novel features of this segmentation and compartmentation have been described, and evidence has been provided that these phenomena collectively play a key role in meeting the different types of energy requirement in the cytoplasm of divergent cell types, with the wide selection of isozymes in this system offering the potential for increased flexibility and control in this important area of metabolism. | Molecular and cellular biochemistry | [
{
"affiliation": "",
"forename": "C J",
"identifier": "",
"initials": "CJ",
"lastname": "Masters"
},
{
"affiliation": "",
"forename": "S",
"identifier": "",
"initials": "S",
"lastname": "Reid"
},
{
"affiliation": "",
"forename": "M",
"identifier": "",
"initials": "M",
"lastname": "Don"
}
] | 1987-07 | 3306346 | D000818:Animals; D005075:Biological Evolution; D002451:Cell Compartmentation; D004798:Enzymes / Q000378:metabolism; D006019:Glycolysis; D006128:Growth; D008322:Mammals / Q000378:metabolism | D016428:Journal Article; D016454:Review | D004798:Enzymes | 10.1007/BF00219393 | [
{
"citation": "Adv Enzyme Regul. 1986;25:297-305",
"pmid": "3544705"
},
{
"citation": "J Biol Chem. 1980 Jul 10;255(13):6314-21",
"pmid": "7391020"
},
{
"citation": "Enzyme. 1973;15(1):224-38",
"pmid": "4593960"
},
{
"citation": "Int J Biochem. 1986;18(1):7-13",
"pmid": "3080348"
},
{
"citation": "Biochem Int. 1986 Jul;13(1):71-7",
"pmid": "3753511"
},
{
"citation": "Mech Ageing Dev. 1985 Jun;31(1):69-87",
"pmid": "4033234"
},
{
"citation": "Cell. 1983 Apr;32(4):1093-103",
"pmid": "6340835"
},
{
"citation": "J Cell Biol. 1984 Jul;99(1 Pt 2):222s-225s",
"pmid": "6746730"
},
{
"citation": "Am J Physiol. 1984 Feb;246(2 Pt 2):R133-51",
"pmid": "6364846"
},
{
"citation": "Biochem J. 1977 Jul 1;165(1):165-7",
"pmid": "889571"
},
{
"citation": "Arch Biochem Biophys. 1983 Oct 1;226(1):285-91",
"pmid": "6639054"
},
{
"citation": "Eur J Biochem. 1970 Aug;15(2):360-6",
"pmid": "5502667"
},
{
"citation": "J Biol Chem. 1977 Nov 10;252(21):7418-20",
"pmid": "144126"
},
{
"citation": "J Histochem Cytochem. 1969 Apr;17(4):225-37",
"pmid": "4240499"
},
{
"citation": "J Supramol Struct. 1979;12(2):165-75",
"pmid": "397369"
},
{
"citation": "Arch Biochem Biophys. 1983 Aug;225(1):384-9",
"pmid": "6614929"
},
{
"citation": "Mech Ageing Dev. 1985 May 31;30(3):299-317",
"pmid": "4021561"
},
{
"citation": "Mech Ageing Dev. 1985 Jul-Aug;31(2):197-212",
"pmid": "4058069"
},
{
"citation": "Int J Biochem. 1986;18(5):445-51",
"pmid": "2940130"
},
{
"citation": "Biochim Biophys Acta. 1986 Sep 5;873(1):127-35",
"pmid": "3741878"
},
{
"citation": "Arch Biochem Biophys. 1972 Nov;153(1):258-65",
"pmid": "4650612"
},
{
"citation": "Curr Top Cell Regul. 1980;16:1-54",
"pmid": "6995028"
},
{
"citation": "Mech Ageing Dev. 1978 Jun;7(6):455-64",
"pmid": "353393"
},
{
"citation": "CRC Crit Rev Biochem. 1981;11(2):105-43",
"pmid": "7030618"
}
] | false | eng | Mol Cell Biochem | 0364456 | 0300-8177 | Netherlands | [] | "2024-08-13T08:46:10.628438Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
[Pictures from the world of the child]. | 135(7) | 355-62 | Monatsschrift Kinderheilkunde : Organ der Deutschen Gesellschaft fur Kinderheilkunde | [
{
"affiliation": "",
"forename": "G",
"identifier": "",
"initials": "G",
"lastname": "Kauffmann"
}
] | 1987-07 | 3306348 | D001154:Art / Q000266:history*; D002648:Child; D002657:Child Development; D005060:Europe; D049669:History, 16th Century; D049670:History, 17th Century; D049671:History, 18th Century; D006801:Humans | D016456:Historical Article; D016428:Journal Article | [] | false | ger | Bilder aus der Welt des Kindes. | Monatsschr Kinderheilkd | 8206462 | 0026-9298 | Germany | [] | "2024-08-13T08:46:10.629672Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||||
Reassessment of LAK phenomenology: a review. | 6(3) | 109-15 | Natural immunity and cell growth regulation | [
{
"affiliation": "",
"forename": "E",
"identifier": "",
"initials": "E",
"lastname": "Lotzová"
},
{
"affiliation": "",
"forename": "R B",
"identifier": "",
"initials": "RB",
"lastname": "Herberman"
}
] | 1987 | 3306350 | D000818:Animals; D000954:Antigens, Surface / Q000032:analysis; D003602:Cytotoxicity, Immunologic; D006801:Humans; D007111:Immunity, Cellular; D007376:Interleukin-2 / Q000502:physiology*; D007694:Killer Cells, Natural / Q000276:immunology*; D051379:Mice; D051381:Rats | D016428:Journal Article; D013487:Research Support, U.S. Gov't, P.H.S.; D016454:Review | D000954:Antigens, Surface; D007376:Interleukin-2 | [] | false | eng | Nat Immun Cell Growth Regul | 8407979 | 0254-7600 | Switzerland | [
{
"agency": "NCI NIH HHS",
"country": "United States",
"grant_acronym": "CA",
"grant_id": "CA 39632"
}
] | "2024-08-13T08:46:10.631424Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||||
[Diagnosis of gynecologic diseases in childhood and adolescence]. | 135(7) | 369-73 | Monatsschrift Kinderheilkunde : Organ der Deutschen Gesellschaft fur Kinderheilkunde | [
{
"affiliation": "",
"forename": "V",
"identifier": "",
"initials": "V",
"lastname": "Terruhn"
}
] | 1987-07 | 3306349 | D000293:Adolescent; D002648:Child; D020681:Colposcopes; D005260:Female; D005831:Genital Diseases, Female / Q000175:diagnosis*; D006801:Humans; D014621:Vagina / Q000002:abnormalities | D016428:Journal Article; D016454:Review | [] | false | ger | Diagnostik gynäkologischer Erkrankungen im Kindes- und Jugendalter. | Monatsschr Kinderheilkd | 8206462 | 0026-9298 | Germany | [] | "2024-08-13T08:46:10.632109Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||||
[The "side-effects" of plasmids (R-plasmids and virulence)]. | 3-9 | Many plasmids affect the host cells. Their effects cannot be explained only by the expression of the well-known genes coding for antibioticresistance, bacteriocinogeny and hemolysis or the analogous genes (side-effects). The side effects are not characteristic of all plasmids operating under similar conditions. Forecasting of the side-effects inducikility by any definite plasmid is impossible now. Sometimes the same functions exert the contrary effects on the bacterial cell. The connection between the presence of plasmids, especially R-plasmids and the complex cellular property, virulence, is of great interest. Often, bacteria become less virulent obtaining the plasmids. Two possible reasons causing such an effect are discussed. The first one is a direct effect of plasmids on cellular physiology. The second reason is connected with population shifts caused by the fact that the cells with initial low virulence possess the recipient ability predominantly. The decreased virulence of bacteria harbouring R-plasmids, in authors opinion, is quite a natural phenomenon based on plasmid host cells adaptation to the existence in "the realm of antimicrobial agents". | Molekuliarnaia genetika, mikrobiologiia i virusologiia | [
{
"affiliation": "",
"forename": "I V",
"identifier": "",
"initials": "IV",
"lastname": "Domaradskiĭ"
}
] | 1987-06 | 3306351 | D001419:Bacteria / Q000235:genetics* / Q000472:pathogenicity; D011815:R Factors / Q000235:genetics*; D014774:Virulence | D004740:English Abstract; D016428:Journal Article; D016454:Review | [] | false | rus | O "pobochnykh" éffektakh plazmid (R-plazmidy i virulentnost'). | Mol Gen Mikrobiol Virusol | 9315607 | 0208-0613 | Russia (Federation) | [] | "2024-08-13T08:46:10.632706Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||||
Chemical and biological characterization of hazardous industrial waste. II. Eukaryotic bioassay of a wood-preserving bottom sediment. | 180(1) | 43-53 | The eukaryotic haploid and diploid forms of Aspergillus nidulans were used to detect gene mutations and various types of chromosome damage, respectively, in the acid, base and neutral fractions of a wood-preserving bottom sediment. The corresponding response to prokaryotic mutagenicity assays and major chemical constituents of the 3 waste fractions were described by Donnelly et al. (1987). The haploid methionine system detected genotoxic compounds in all 3 primary waste fractions without metabolic activation. With metabolic activation, the maximum response observed in the gene mutation assay was induced by the base fraction. In the diploid assay without metabolic activation, the acid fraction induced the maximum number of major chromosome abnormalities, while the base fraction induced the maximum number of minor deletions or insertions. These results appear to reflect the different composition of the waste fractions since each fraction induced a different type of genetic damage in the two bioassays employed. Alternately, because exposure in the diploid assay was during a growth stage, the results may reflect a varying response at different points of the cell division cycle. The results obtained using eukaryotic bioassays indicate that the wood preserving waste contains compound(s) capable of inducing point mutations, chromosome damage, recombination, and compound(s) acting as spindle poisons. | Mutation research | [
{
"affiliation": "",
"forename": "K C",
"identifier": "",
"initials": "KC",
"lastname": "Donnelly"
},
{
"affiliation": "",
"forename": "K W",
"identifier": "",
"initials": "KW",
"lastname": "Brown"
},
{
"affiliation": "",
"forename": "B R",
"identifier": "",
"initials": "BR",
"lastname": "Scott"
}
] | 1987-09 | 3306353 | D001233:Aspergillus nidulans / Q000187:drug effects*; D001681:Biological Assay; D004305:Dose-Response Relationship, Drug; D006238:Haploidy; D006863:Hydrogen-Ion Concentration; D007220:Industrial Waste / Q000032:analysis; D009152:Mutagenicity Tests; D009153:Mutagens / Q000032:analysis*; D014934:Wood | D016428:Journal Article; D013486:Research Support, U.S. Gov't, Non-P.H.S. | D007220:Industrial Waste; D009153:Mutagens | 10.1016/0027-5107(87)90065-0 | [] | false | eng | Mutat Res | 0400763 | 0027-5107 | Netherlands | [] | "2024-08-13T08:46:10.633732Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Effects of UV repair, error-prone repair and critical site of mutation on mutagenesis induced by N-nitrosamines. | 180(1) | 11-20 | Many N-nitrosamines have been assayed for mutagenic activity in bacteria but few have been systematically compared in a series of strains. In this study through the use of several Salmonella tester strains, we have examined the effects of Uvr repair, error-prone repair, and the critical site for mutation (GC or AT base pair) on the mutagenic activities of a diverse group of N-nitrosamines. We have employed the histidine autotrophs, TA1975 (uvrB+), TA1535 (uvrB-) and TA100 (uvrB-/pKM101) which are hisG46 strains, sensitive mainly to G-C base damage, and TA104 (uvrB-/pKM101), a hisG428 strain, which can be reverted at the hisG428 locus by damage to A-T base-pairs, or by suppression at G-C base pairs. The N-nitrosamines studied were, N-nitroso: dimethylamine, diethylamine, dipropylamine, dibutylamine, pyrrolidine, piperidine, morpholine, methylbenzylamine, bis-(2-hydroxypropyl)amine, bis-(2-oxopropyl)amine and 3,4-dichloropyrrolidine. For all of the nitrosamines larger than diethylnitrosamine (except for methylbenzylnitrosamine) mutagenesis was greatly enhanced (3-20 X) by the lack of uvrB activity, indicating that the DNA adducts produced by these nitrosamines can be classified as "bulky adducts". For most nitrosamines the plasmid, pKM101, enhanced mutagenesis in hisG46 strains, several fold, suggesting that error-prone DNA repair plays a role in mutagenesis by these compounds. All of the compounds tested were more mutagenic in TA100 than TA104 except diethylnitrosamine and methylbenzylnitrosamine which were more potent in TA104. Revertants induced by all of the nitrosamines in TA100 were due predominantly to damage at G-C base pairs. Revertants induced by all the nitrosamines except diethylnitrosamine and dibutylnitrosamine resulted mainly from damage to G-C base pairs in TA104. | Mutation research | [
{
"affiliation": "",
"forename": "M",
"identifier": "",
"initials": "M",
"lastname": "Zielenska"
},
{
"affiliation": "",
"forename": "J B",
"identifier": "",
"initials": "JB",
"lastname": "Guttenplan"
}
] | 1987-09 | 3306352 | D001483:Base Sequence; D004247:DNA / Q000187:drug effects*; D004249:DNA Damage; D004260:DNA Repair; D004305:Dose-Response Relationship, Drug; D006639:Histidine; D009154:Mutation / Q000187:drug effects*; D009602:Nitrosamines / Q000494:pharmacology*; D012486:Salmonella typhimurium / Q000187:drug effects / Q000235:genetics*; D013329:Structure-Activity Relationship; D013489:Suppression, Genetic | D016428:Journal Article; D013487:Research Support, U.S. Gov't, P.H.S. | D009602:Nitrosamines; D006639:Histidine; D004247:DNA | 10.1016/0027-5107(87)90062-5 | [] | false | eng | Mutat Res | 0400763 | 0027-5107 | Netherlands | [
{
"agency": "NIEHS NIH HHS",
"country": "United States",
"grant_acronym": "ES",
"grant_id": "ES03332"
}
] | "2024-08-13T08:46:10.634791Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Evidence for the presence of mutagenic compounds other than chromium in particles from mild steel welding. | 180(1) | 55-65 | A modified Salmonella/microsome liquid culture assay was used to investigate the mutagenicity of the particulate fraction from mild steel welding. Previous reports have implicated compounds of chromium VI as the mutagenic and toxic agents in welding fumes, since only the particles from welding on stainless steel, which contains 15-25% chromium, were mutagenic, whereas particles from welding on mild steel, which contain less than 0.1% chromium, were not mutagenic or toxic. In this investigation, mild steel particles were shown to contain direct-acting and promutagenic compounds that induced frameshift mutations. The mutagenic agents, which were insoluble in sodium phosphate buffer, did not include chromium VI or organic compounds. Further, the expression of mutation appears to require a cell-particle interaction for the release of the mutagenic species from the particles. | Mutation research | [
{
"affiliation": "",
"forename": "N W",
"identifier": "",
"initials": "NW",
"lastname": "Biggart"
},
{
"affiliation": "",
"forename": "R R",
"identifier": "",
"initials": "RR",
"lastname": "Rinehart"
},
{
"affiliation": "",
"forename": "J",
"identifier": "",
"initials": "J",
"lastname": "Verfaillie"
}
] | 1987-09 | 3306354 | D000332:Aerobiosis; D000336:Aerosols; D000497:Alloys; D000693:Anaerobiosis; D001711:Biotransformation; D003102:Colloids; D008670:Metals / Q000032:analysis; D008862:Microsomes, Liver / Q000378:metabolism; D009152:Mutagenicity Tests; D009153:Mutagens / Q000032:analysis; D012486:Salmonella typhimurium / Q000187:drug effects; D013232:Steel; D014896:Welding | D016428:Journal Article | D000336:Aerosols; D000497:Alloys; D003102:Colloids; D008670:Metals; D009153:Mutagens; D013232:Steel | 10.1016/0027-5107(87)90066-2 | [] | false | eng | Mutat Res | 0400763 | 0027-5107 | Netherlands | [] | "2024-08-13T08:46:10.636966Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Inhibitory effects of thiols on a mutagenic contaminant from the synthesis of N-nitrosothiazolidine. | 180(1) | 75-9 | The effect of S9 and various thiols were studied for potential modifying effects on a mutagenic trace artifact ('NTHZ') formed during the synthesis of N-nitrosothiazolidine (NTHZ) from cysteamine, formaldehyde and nitrite. Induced and uninduced S9 prepared from Syrian hamster livers reduced mutagenic activity in Salmonella TA100. Incorporation of boiled S9 into the preincubation medium produced similar effects, indicating a non-enzymatic mechanism for the detoxification reaction. Thiols alone also lowered revertant yields, and inhibitory efficacy was, in general, related to the pKa of the compound. At equimolar concentrations mutagenic activity was reduced in the following order (pKa values in parentheses): Thioglycolate (10.7) greater than mercaptoethanol (9.6) greater than reduced glutathione (8.8) greater than cysteine (8.35) greater than cystine (8.2). N-Acetylcysteine (9.52) and cysteamine (8.35), however, did not fit this pattern. The results of this study suggest that normal hepatic mechanisms may minimize 'NTHZ' genotoxicity thereby reducing potential health risks associated with its exposure. | Mutation research | [
{
"affiliation": "",
"forename": "A J",
"identifier": "",
"initials": "AJ",
"lastname": "Miller"
},
{
"affiliation": "",
"forename": "W",
"identifier": "",
"initials": "W",
"lastname": "Fiddler"
}
] | 1987-09 | 3306355 | D000818:Animals; D006224:Cricetinae; D066298:In Vitro Techniques; D008658:Inactivation, Metabolic; D008862:Microsomes, Liver / Q000378:metabolism; D009153:Mutagens / Q000037:antagonists & inhibitors*; D009603:Nitroso Compounds / Q000138:chemical synthesis / Q000633:toxicity*; D012486:Salmonella typhimurium / Q000187:drug effects; D013438:Sulfhydryl Compounds / Q000494:pharmacology*; D013844:Thiazoles / Q000138:chemical synthesis / Q000633:toxicity* | D016428:Journal Article | D009153:Mutagens; D009603:Nitroso Compounds; D013438:Sulfhydryl Compounds; D013844:Thiazoles; C042199:N-nitrosothiazolidine | 10.1016/0027-5107(87)90068-6 | [] | false | eng | Mutat Res | 0400763 | 0027-5107 | Netherlands | [] | "2024-08-13T08:46:10.637800Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
[Identification in utero of malformations of the 1st brachial arch]. | 12(2) | 9-16 | Mondo ortodontico | [
{
"affiliation": "",
"forename": "G P",
"identifier": "",
"initials": "GP",
"lastname": "Farronato"
},
{
"affiliation": "",
"forename": "R",
"identifier": "",
"initials": "R",
"lastname": "Giudici"
},
{
"affiliation": "",
"forename": "F",
"identifier": "",
"initials": "F",
"lastname": "Lalatta"
},
{
"affiliation": "",
"forename": "L",
"identifier": "",
"initials": "L",
"lastname": "Stripparo"
}
] | 1987 | 3306347 | D001934:Branchial Region; D000013:Congenital Abnormalities / Q000175:diagnosis; D005260:Female; D006801:Humans; D008342:Mandibulofacial Dysostosis / Q000175:diagnosis; D010855:Pierre Robin Syndrome / Q000175:diagnosis; D011247:Pregnancy; D011296:Prenatal Diagnosis; D013577:Syndrome; D014463:Ultrasonography | D004740:English Abstract; D016428:Journal Article | [] | false | ita | Riconoscimento in utero di malformazioni del primo arco brachiale. | Mondo Ortod | 7703267 | 0391-2000 | Italy | [] | "2024-08-13T08:46:10.638589Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||||
Mutants of Saccharomyces cerevisiae deficient in adenine phosphoribosyltransferase. | 180(1) | 81-7 | Spontaneous and ethyl methanesulfate induced mutants of Saccharomyces cerevisiae, with partial and complete deficiency of adenine phosphoribosyltransferase (APRT, EC 2.4.2.7), were isolated by selection for resistance to 8-azaadenine. Matings between totally deficient mutants and tester strain resulted in diploid heterozygotes that were sensitive to azaadenine. Upon sporulation and tetrad analysis, azaadenine resistance (and APRT deficiency) segregated as expected for a single Mendelian gene. Hypoxanthine-guanine phosphoribosyltransferase (EC 2.4.2.8) activity in the mutants was similar to that in the wild-type cells. There was no detectable activity of adenine aminohydrolase (EC 3.5.4.2) in the wild-type or mutant cells. | Mutation research | [
{
"affiliation": "",
"forename": "A",
"identifier": "",
"initials": "A",
"lastname": "Sahota"
},
{
"affiliation": "",
"forename": "P K",
"identifier": "",
"initials": "PK",
"lastname": "Ranjekar"
},
{
"affiliation": "",
"forename": "J",
"identifier": "",
"initials": "J",
"lastname": "Alfonzo"
},
{
"affiliation": "",
"forename": "A S",
"identifier": "",
"initials": "AS",
"lastname": "Lewin"
},
{
"affiliation": "",
"forename": "M W",
"identifier": "",
"initials": "MW",
"lastname": "Taylor"
}
] | 1987-09 | 3306356 | D000225:Adenine / Q000031:analogs & derivatives / Q000494:pharmacology; D000228:Adenine Phosphoribosyltransferase / Q000172:deficiency / Q000235:genetics*; D004352:Drug Resistance, Microbial; D005020:Ethyl Methanesulfonate; D005800:Genes, Fungal; D007041:Hypoxanthine Phosphoribosyltransferase / Q000378:metabolism; D009154:Mutation; D010430:Pentosyltransferases / Q000235:genetics*; D012441:Saccharomyces cerevisiae / Q000235:genetics* | D016428:Journal Article; D013487:Research Support, U.S. Gov't, P.H.S. | D005020:Ethyl Methanesulfonate; D010430:Pentosyltransferases; D000228:Adenine Phosphoribosyltransferase; D007041:Hypoxanthine Phosphoribosyltransferase; D000225:Adenine; C006654:8-azaadenine | 10.1016/0027-5107(87)90069-8 | [] | false | eng | Mutat Res | 0400763 | 0027-5107 | Netherlands | [
{
"agency": "NIADDK NIH HHS",
"country": "United States",
"grant_acronym": "AM",
"grant_id": "AM25498"
},
{
"agency": "NIEHS NIH HHS",
"country": "United States",
"grant_acronym": "ES",
"grant_id": "ES CA 03501"
}
] | "2024-08-13T08:46:10.639798Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Molecular aspects of DNA repair. | 184(2) | 67-86 | Mutation research | [
{
"affiliation": "",
"forename": "E C",
"identifier": "",
"initials": "EC",
"lastname": "Friedberg"
},
{
"affiliation": "",
"forename": "C",
"identifier": "",
"initials": "C",
"lastname": "Backendorf"
},
{
"affiliation": "",
"forename": "J",
"identifier": "",
"initials": "J",
"lastname": "Burke"
},
{
"affiliation": "",
"forename": "A",
"identifier": "",
"initials": "A",
"lastname": "Collins"
},
{
"affiliation": "",
"forename": "L",
"identifier": "",
"initials": "L",
"lastname": "Grossman"
},
{
"affiliation": "",
"forename": "J H",
"identifier": "",
"initials": "JH",
"lastname": "Hoeijmakers"
},
{
"affiliation": "",
"forename": "A R",
"identifier": "",
"initials": "AR",
"lastname": "Lehmann"
},
{
"affiliation": "",
"forename": "E",
"identifier": "",
"initials": "E",
"lastname": "Seeberg"
},
{
"affiliation": "",
"forename": "G P",
"identifier": "",
"initials": "GP",
"lastname": "van der Schans"
},
{
"affiliation": "",
"forename": "A A",
"identifier": "",
"initials": "AA",
"lastname": "van Zeeland"
}
] | 1987-09 | 3306357 | D000818:Animals; D003001:Cloning, Molecular; D004260:DNA Repair; D005057:Eukaryotic Cells / Q000502:physiology; D005796:Genes; D005822:Genetic Vectors; D006801:Humans; D008745:Methylation; D009154:Mutation; D011387:Prokaryotic Cells / Q000502:physiology | D016428:Journal Article; D013485:Research Support, Non-U.S. Gov't; D016454:Review | 10.1016/0167-8817(87)90063-0 | [] | false | eng | Mutat Res | 0400763 | 0027-5107 | Netherlands | [] | "2024-08-13T08:46:10.641010Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||||
Sodium arsenite inhibits spontaneous and induced mutations in Escherichia coli. | 184(2) | 99-105 | Sodium arsenite at a non-toxic concentration was found to inhibit strongly mutagenesis induced by ultraviolet light (UV), 4-nitroquinoline-1-oxide (4NQO), furylfuramide (AF-2) and methyl methane-sulfonate (MMS) as well as spontaneous mutation in the reversion assay of E. coli WP2uvrA/pKM101. The effect was not, however, seen in the case of the mutagenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). In order to elucidate the mechanism of the mutation-inhibitory effect of sodium arsenite, its action on umuC gene expression and DNA-repair systems was investigated. It was found that sodium arsenite depressed beta-galactosidase induction, corresponding to the umuC gene expression. For UV-irradiated E. coli strains possessing different DNA-repair capacities, sodium arsenite decreased the UV survival rates of WP2, WP2uvrA[uvrA] and WP67[uvrA polA], increased those of SOS-uninducible strains having either the recA+ or uvrA+ such as CM571 [recA], CM561 [lexA(Ind-)] and CM611[uvrA lexA (Ind-)], and did not affect that of the uvrA recA double mutant, WP100. From these results, we assume that sodium arsenite may have at least two roles in its antimutagenesis: as an inhibitor of umuC gene expression, and as an enhancer of the error-free repairs depending on the uvrA and recA genes. | Mutation research | [
{
"affiliation": "",
"forename": "T",
"identifier": "",
"initials": "T",
"lastname": "Nunoshiba"
},
{
"affiliation": "",
"forename": "H",
"identifier": "",
"initials": "H",
"lastname": "Nishioka"
}
] | 1987-09 | 3306358 | D001151:Arsenic / Q000494:pharmacology*; D018053:Arsenites; D004260:DNA Repair / Q000187:drug effects*; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics*; D005786:Gene Expression Regulation / Q000528:radiation effects; D005798:Genes, Bacterial; D009153:Mutagens / Q000037:antagonists & inhibitors*; D009154:Mutation / Q000187:drug effects* / Q000528:radiation effects; D013014:SOS Response, Genetics / Q000187:drug effects*; D017670:Sodium Compounds; D014466:Ultraviolet Rays | D016428:Journal Article | D018053:Arsenites; D009153:Mutagens; D017670:Sodium Compounds; C017947:sodium arsenite; D001151:Arsenic | 10.1016/0167-8817(87)90065-4 | [] | false | eng | Mutat Res | 0400763 | 0027-5107 | Netherlands | [] | "2024-08-13T08:46:10.643054Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Are mitochondrial DNA mutations involved in the carcinogenic process? | 186(2) | 149-60 | Mutation research | [
{
"affiliation": "",
"forename": "J W",
"identifier": "",
"initials": "JW",
"lastname": "Shay"
},
{
"affiliation": "",
"forename": "H",
"identifier": "",
"initials": "H",
"lastname": "Werbin"
}
] | 1987-09 | 3306359 | D000818:Animals; D002273:Carcinogens / Q000494:pharmacology / Q000633:toxicity; D002471:Cell Transformation, Neoplastic / Q000235:genetics; D003043:Cocarcinogenesis; D004249:DNA Damage; D004258:DNA Polymerase III / Q000378:metabolism; D004272:DNA, Mitochondrial / Q000187:drug effects / Q000235:genetics*; D008322:Mammals; D008928:Mitochondria / Q000502:physiology* / Q000648:ultrastructure; D008954:Models, Biological; D009154:Mutation; D009369:Neoplasms / Q000235:genetics* / Q000648:ultrastructure; D009374:Neoplasms, Experimental / Q000139:chemically induced / Q000235:genetics; D009857:Oncogenes | D016428:Journal Article; D013485:Research Support, Non-U.S. Gov't; D013487:Research Support, U.S. Gov't, P.H.S.; D016454:Review | D002273:Carcinogens; D004272:DNA, Mitochondrial; D004258:DNA Polymerase III | 10.1016/0165-1110(87)90028-5 | [] | false | eng | Mutat Res | 0400763 | 0027-5107 | Netherlands | [
{
"agency": "NCI NIH HHS",
"country": "United States",
"grant_acronym": "CA",
"grant_id": "CA40065"
}
] | "2024-08-13T08:46:10.643992Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||
N-nitrosamines: bacterial mutagenesis and in vitro metabolism. | 186(2) | 81-134 | Many nitrosamines are potent mutagens. The rate-limiting step in their in vitro metabolism to mutagens is usually a single enzymatic reaction catalyzed by one or more of the many cytochrome P-450-dependent mixed-function oxidases present in the microsomal cell fraction. Current evidence indicates that this reaction activates nitrosamines to alpha-hydroxynitrosamines, which have half-lives on the order of seconds. This product decomposes to an aldehyde and a much shorter-lived ultimate metabolite which is probably an alkyl diazonium ion or an alkyl carbocation. This may react with DNA leading to premutagenic adducts. Such adducts represent a very small fraction of the ultimate mutagen, with the rest reacting with water to yield the corresponding alcohol. Evidence for this pathway includes (1) the observation of deuterium isotope effects in metabolism and mutagenesis, (2) products (aldehydes, alcohols, and N2) consistent with this pathway, (3) studies on metabolism of nitrosamines using purified cytochrome P-450, (4) formation of DNA adducts such as O6-alkylguanines which are consistent with those expected from the ultimate mutagen, (5) expected products and genotoxic effects of other sources of activated nitrosamines, e.g., alpha-acetoxynitrosamines, alkanediazotates and related compounds. Hydroxylation of nitrosamines at other positions also occurs in vitro (usually to a lesser extent), but these products are generally stable and must be further metabolized to exert mutagenic effects (with the exception of N-nitrosoalkyl(formylmethyl)amines, which are direct-acting mutagens). Because only low percentages of nitrosamines are metabolized in vitro, the contribution to mutagenesis by secondary metabolism is small. In this respect, in vitro metabolism can differ significantly from in vivo metabolism. Bacterial mutagenesis by nitrosamines has most often been studied in Salmonella typhimurium and to a lesser extent E. coli. Mutagenesis by nitrosamines generally requires a source of microsomes (a 9000 X g supernatant fraction is often used), and NADPH. Liver fractions from Aroclor-1254- or PB-induced rodents have been most frequently employed but liver fractions from untreated animals, and homogenates of other organs (lung, kidney, nasal mucosa, and pancreas) have also been utilized. Liver homogenates from humans are generally similar to those from untreated rats in metabolizing nitrosamines to mutagens but large interindividual variations are observed. Mutagenesis is often most effective using a liquid preincubation, a slightly acidic incubation mixture and hamster liver fractions.(ABSTRACT TRUNCATED AT 400 WORDS) | Mutation research | [
{
"affiliation": "",
"forename": "J B",
"identifier": "",
"initials": "JB",
"lastname": "Guttenplan"
}
] | 1987-09 | 3306361 | D000478:Alkylation; D000818:Animals; D001419:Bacteria / Q000187:drug effects* / Q000235:genetics; D001711:Biotransformation; D003577:Cytochrome P-450 Enzyme System / Q000378:metabolism; D004249:DNA Damage; D004260:DNA Repair; D004269:DNA, Bacterial / Q000187:drug effects; D008862:Microsomes, Liver / Q000201:enzymology; D009152:Mutagenicity Tests; D009153:Mutagens / Q000096:biosynthesis; D009374:Neoplasms, Experimental / Q000139:chemically induced; D009602:Nitrosamines / Q000378:metabolism / Q000494:pharmacology* / Q000633:toxicity; D010084:Oxidation-Reduction; D012377:Rodentia; D013329:Structure-Activity Relationship | D003160:Comparative Study; D016428:Journal Article; D013487:Research Support, U.S. Gov't, P.H.S.; D016454:Review | D004269:DNA, Bacterial; D009153:Mutagens; D009602:Nitrosamines; D003577:Cytochrome P-450 Enzyme System | 10.1016/0165-1110(87)90026-1 | [] | false | eng | Mutat Res | 0400763 | 0027-5107 | Netherlands | [
{
"agency": "NIEHS NIH HHS",
"country": "United States",
"grant_acronym": "ES",
"grant_id": "ES03332"
}
] | "2024-08-13T08:46:10.644874Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Oncogene activation by chromosomal rearrangement in chronic myelocytic leukemia. | 186(2) | 161-72 | A considerable number of human tumors, especially leukemias and lymphomas is associated with a consistent specific chromosome translocation. At a number of the breakpoint regions of these specific aberrations are c-oncogenes (c-onc) located. The structure and/or expression of some of these c-onc is altered as a result of the specific translocation. In the CML-specific (9;22) translocation the transposition of the c-abl oncogene to the chromosome 22 bcr sequences results in the production of a chimeric bcr/c-abl fusion protein. This result strongly suggests that tumor-specific chromosomal aberrations can lead to the activation of cellular oncogenes. | Mutation research | [
{
"affiliation": "",
"forename": "A",
"identifier": "",
"initials": "A",
"lastname": "De Klein"
}
] | 1987-09 | 3306360 | D001483:Base Sequence; D002892:Chromosomes, Human, Pair 22 / Q000648:ultrastructure; D002899:Chromosomes, Human, Pair 9 / Q000648:ultrastructure*; D004273:DNA, Neoplasm / Q000235:genetics; D005786:Gene Expression Regulation; D006801:Humans; D007951:Leukemia, Myeloid / Q000235:genetics*; D008954:Models, Biological; D009857:Oncogenes; D010677:Philadelphia Chromosome; D011518:Proto-Oncogene Proteins / Q000096:biosynthesis / Q000235:genetics*; D016315:Proto-Oncogene Proteins c-abl; D011519:Proto-Oncogenes; D014178:Translocation, Genetic | D016428:Journal Article; D016454:Review | D004273:DNA, Neoplasm; D011518:Proto-Oncogene Proteins; D016315:Proto-Oncogene Proteins c-abl | 10.1016/0165-1110(87)90029-7 | [] | false | eng | Mutat Res | 0400763 | 0027-5107 | Netherlands | [] | "2024-08-13T08:46:10.646088Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Base-substitution and frameshift mutagenesis by sodium chloride and potassium chloride in Saccharomyces cerevisiae. | 189(1) | 11-4 | Sodium chloride (NaCl) and potassium chloride (KCl) are both capable of inducing lethality and mutations when each is administered at a molarity of two for different lengths of time to logarithmic phase cells of the yeast Saccharomyces cerevisiae. Analysis of the revertants indicates that the reversions can be base substitutions, of both the transition and the transversion type, as well as frameshift mutations. At equal molarity, with the frequency of mutations as the criterion, KCl and NaCl are equally efficient in inducing all types of mutations. | Mutation research | [
{
"affiliation": "",
"forename": "K R",
"identifier": "",
"initials": "KR",
"lastname": "Parker"
},
{
"affiliation": "",
"forename": "R C",
"identifier": "",
"initials": "RC",
"lastname": "von Borstel"
}
] | 1987-09 | 3306362 | D002470:Cell Survival / Q000187:drug effects; D009152:Mutagenicity Tests; D009154:Mutation / Q000187:drug effects*; D009994:Osmolar Concentration; D011189:Potassium Chloride / Q000494:pharmacology*; D012441:Saccharomyces cerevisiae / Q000235:genetics; D012965:Sodium Chloride / Q000494:pharmacology* | D016428:Journal Article; D013485:Research Support, Non-U.S. Gov't | D012965:Sodium Chloride; D011189:Potassium Chloride | 10.1016/0165-1218(87)90028-0 | [] | false | eng | Mutat Res | 0400763 | 0027-5107 | Netherlands | [] | "2024-08-13T08:46:10.647023Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
In vitro testing as a step in the evaluation of in vivo genotoxicity. | 189(1) | 7-10 | Mutation research | [
{
"affiliation": "",
"forename": "F H",
"identifier": "",
"initials": "FH",
"lastname": "Sobels"
}
] | 1987-09 | 3306364 | D001853:Bone Marrow / Q000187:drug effects; D002273:Carcinogens; D002869:Chromosome Aberrations; D005854:Germ Cells / Q000187:drug effects; D009152:Mutagenicity Tests / Q000379:methods*; D009153:Mutagens; D012486:Salmonella typhimurium / Q000187:drug effects; D014018:Tissue Distribution | D016428:Journal Article | D002273:Carcinogens; D009153:Mutagens | 10.1016/0165-1218(87)90027-9 | [] | false | eng | Mutat Res | 0400763 | 0027-5107 | Netherlands | [] | "2024-08-13T08:46:10.648911Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||
N-chloropiperidine and calcium hypochlorite: possible examples of toxicity-dependent clastogenicity in vitro. | 189(1) | 59-68 | N-Chloropiperidine (NCP) has been reported to be both toxic and mutagenic in a wide range of in vitro and in vivo genotoxicity assays, however, few experimental details or numerical data have been presented to support these claims. The latter facts, together with the lack of any clear structural precedent for the mutagenicity of this agent, led us to re-evaluate it using the Salmonella mutation assay and the mouse bone marrow micronucleus test. The absence of mutagenic activity observed in both of these systems indicates that the genotoxicity of NCP and related chloramines remains to be unequivocally established. In particular, the potent clastogenicity to CHO cells reported for NCP may be related solely to oxidative denaturation of cellular proteins induced by hypochlorous acid, a hydrolysis product of NCP. Separate reports indicate that calcium hypochlorite (bleaching powder) is also clastogenic in vitro but not in vivo. We therefore suggest that N-chloropiperidine may prove of value as a model compound for studies designed to distinguish genotoxic clastogenicity (specifically DNA-reactive) from general toxicity-mediated clastogenicity. | Mutation research | [
{
"affiliation": "",
"forename": "J",
"identifier": "",
"initials": "J",
"lastname": "Ashby"
},
{
"affiliation": "",
"forename": "R",
"identifier": "",
"initials": "R",
"lastname": "Mohammed"
},
{
"affiliation": "",
"forename": "R D",
"identifier": "",
"initials": "RD",
"lastname": "Callander"
}
] | 1987-09 | 3306363 | D000818:Animals; D001853:Bone Marrow / Q000648:ultrastructure; D002118:Calcium / Q000633:toxicity*; D017610:Calcium Compounds; D002470:Cell Survival / Q000187:drug effects*; D002869:Chromosome Aberrations; D003520:Cyclophosphamide / Q000633:toxicity; D051379:Mice; D009154:Mutation / Q000187:drug effects*; D010880:Piperidines / Q000633:toxicity*; D012486:Salmonella typhimurium / Q000187:drug effects; D008941:Spindle Apparatus / Q000187:drug effects | D016428:Journal Article; D013485:Research Support, Non-U.S. Gov't | D017610:Calcium Compounds; D010880:Piperidines; C004488:calcium hypochlorite; C028563:N-chloropiperidine; D003520:Cyclophosphamide; D002118:Calcium | 10.1016/0165-1218(87)90033-4 | [] | false | eng | Mutat Res | 0400763 | 0027-5107 | Netherlands | [] | "2024-08-13T08:46:10.649939Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Candida albicans and Candida tropicalis antigens studied by SDS polyacrylamide gel electrophoresis and Western blot. | 30(6) | 271-80 | Mykosen | [
{
"affiliation": "",
"forename": "S M",
"identifier": "",
"initials": "SM",
"lastname": "Bruneau"
},
{
"affiliation": "",
"forename": "R M",
"identifier": "",
"initials": "RM",
"lastname": "Guinet"
}
] | 1987-06 | 3306369 | D000946:Antigens, Fungal / Q000032:analysis*; D002175:Candida / Q000276:immunology*; D002176:Candida albicans / Q000276:immunology*; D004591:Electrophoresis, Polyacrylamide Gel; D007118:Immunoassay; D007124:Immunoenzyme Techniques | D016428:Journal Article | D000946:Antigens, Fungal | 10.1111/j.1439-0507.1987.tb03979.x | [] | false | eng | Mykosen | 0400765 | 0027-5557 | Germany | [] | "2024-08-13T08:46:10.650701Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||
Peroxidative activation of 3,3'-dichlorobenzidine to mutagenic products in the Salmonella typhimurium test. | 191(3-4) | 139-43 | The direct and H2O2-dependent mutagenicity of 3,3'-dichlorobenzidine (DCB) were compared in Salmonella tester strains TA98, TA98/1,8-DNP6, TA100 and TA102 using the Ames test. DCB exhibited both direct and H2O2-dependent mutagenicity to both tester strains TA98 and TA98/1,8-DNP6. This H2O2-dependent mutagenicity of DCB was prevented by horseradish peroxidase. DCB, in contrast to its effects in tester strains TA98, was not mutagenic to TA100 and TA102 either directly or in the presence of H2O2. These results suggest that mechanisms, perhaps enzymes endogenous to tester strains TA98, may play a role in the activation of DCB. | Mutation research | [
{
"affiliation": "",
"forename": "B",
"identifier": "",
"initials": "B",
"lastname": "Lang"
},
{
"affiliation": "",
"forename": "M M",
"identifier": "",
"initials": "MM",
"lastname": "Iba"
}
] | 1987 | 3306365 | D015101:3,3'-Dichlorobenzidine / Q000378:metabolism* / Q000633:toxicity; D001560:Benzidines / Q000378:metabolism* / Q000633:toxicity; D001711:Biotransformation; D006735:Horseradish Peroxidase / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000633:toxicity*; D009152:Mutagenicity Tests; D009153:Mutagens / Q000378:metabolism*; D012486:Salmonella typhimurium / Q000187:drug effects | D016428:Journal Article; D013486:Research Support, U.S. Gov't, Non-P.H.S. | D001560:Benzidines; D009153:Mutagens; D015101:3,3'-Dichlorobenzidine; C029876:benzidine; D006861:Hydrogen Peroxide; D006735:Horseradish Peroxidase | 10.1016/0165-7992(87)90144-8 | [] | false | eng | Mutat Res | 0400763 | 0027-5107 | Netherlands | [] | "2024-08-13T08:46:10.651613Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Plant cells at different stages in their growth curve differentially activate promutagens. | 191(3-4) | 151-5 | Mutagenic activity of the promutagens 2-aminofluorene (2AF) and a contaminant of 4-nitro-o-phenylenediamine (NOP-X) was followed in Ames Salmonella strain TA98 following metabolism by cotton and carrot cell suspension cultures using the plant cell/microbe coincubation assay. Both cell lines were capable of activating each chemical. However, activation capacities of the cell lines differed relative to their respective stage of growth when used. For 2AF activation early-log phase cotton cells and mid-log phase carrot cells proved superior while mid-log phase cotton cells and stationary phase carrot cells proved superior for NOP-X activation. These data indicate that the phase of the growth cycle at which plant cells are harvested can significantly affect their promutagen activation potential. | Mutation research | [
{
"affiliation": "",
"forename": "J M",
"identifier": "",
"initials": "JM",
"lastname": "Gentile"
},
{
"affiliation": "",
"forename": "D",
"identifier": "",
"initials": "D",
"lastname": "Heydenburg"
},
{
"affiliation": "",
"forename": "L",
"identifier": "",
"initials": "L",
"lastname": "Hertel"
},
{
"affiliation": "",
"forename": "M J",
"identifier": "",
"initials": "MJ",
"lastname": "Plewa"
}
] | 1987 | 3306366 | D001711:Biotransformation; D005449:Fluorenes / Q000494:pharmacology; D009152:Mutagenicity Tests; D009153:Mutagens / Q000378:metabolism*; D010655:Phenylenediamines / Q000494:pharmacology; D018521:Plant Physiological Phenomena; D012486:Salmonella typhimurium / Q000187:drug effects | D016428:Journal Article; D013487:Research Support, U.S. Gov't, P.H.S. | D005449:Fluorenes; D009153:Mutagens; D010655:Phenylenediamines; C012177:2-aminofluorene; C012277:1,2-diamino-4-nitrobenzene | 10.1016/0165-7992(87)90146-1 | [] | false | eng | Mutat Res | 0400763 | 0027-5107 | Netherlands | [
{
"agency": "NIEHS NIH HHS",
"country": "United States",
"grant_acronym": "ES",
"grant_id": "ES-02384"
}
] | "2024-08-13T08:46:10.652668Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Inhibitory effect of antifungal agents on germ tube formation in Candida albicans. | 30(6) | 281-7 | Mykosen | [
{
"affiliation": "",
"forename": "M",
"identifier": "",
"initials": "M",
"lastname": "Schaude"
},
{
"affiliation": "",
"forename": "H",
"identifier": "",
"initials": "H",
"lastname": "Ackerbauer"
},
{
"affiliation": "",
"forename": "H",
"identifier": "",
"initials": "H",
"lastname": "Mieth"
}
] | 1987-06 | 3306370 | D000499:Allylamine / Q000031:analogs & derivatives / Q000494:pharmacology*; D000588:Amines / Q000494:pharmacology*; D000935:Antifungal Agents / Q000494:pharmacology*; D002176:Candida albicans / Q000187:drug effects* / Q000254:growth & development; D009281:Naphthalenes / Q000494:pharmacology*; D000077291:Terbinafine | D003160:Comparative Study; D016428:Journal Article | D000588:Amines; D000935:Antifungal Agents; D009281:Naphthalenes; D000499:Allylamine; C029178:naftifine; D000077291:Terbinafine | 10.1111/j.1439-0507.1987.tb03980.x | [] | false | eng | Mykosen | 0400765 | 0027-5557 | Germany | [] | "2024-08-13T08:46:10.653547Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||
Recent views on amyotrophic lateral sclerosis with emphasis on electrophysiological studies. | 10(6) | 490-502 | Peripheral electrophysiological studies are of particular value of elucidating the anatomy and pathophysiology of neuromuscular diseases, but they can also help in providing clues to the etiology of the disease. Recent studies of the motor units in chronic denervating conditions including amyotrophic lateral sclerosis (ALS) are reviewed. These indicate that reinnervation is a relatively active process which compensates for the progressive loss of motoneurons in ALS until more than 50% of the motoneurons have died. There seems to be no predilection for death of motoneurons of any particular size in ALS. Fasciculations may arise both proximally and distally. The dying-back change is not a major feature of ALS. These and other data cast doubt on the etiological theories that ALS arises from premature aging of motoneurons, deficiency of motoneuron trophic factors, or an inhibitor of a motoneuronal sprouting factor, and point to the need to study metabolic changes intrinsic to the motoneuron in ALS. | Muscle & nerve | [
{
"affiliation": "",
"forename": "W G",
"identifier": "",
"initials": "WG",
"lastname": "Bradley"
}
] | 1987 | 3306367 | D000690:Amyotrophic Lateral Sclerosis / Q000503:physiopathology*; D000870:Anterior Horn Cells / Q000502:physiology*; D004594:Electrophysiology; D006801:Humans; D009046:Motor Neurons / Q000502:physiology*; D009132:Muscles / Q000503:physiopathology*; D009468:Neuromuscular Diseases / Q000503:physiopathology; D011051:Poliomyelitis / Q000150:complications | D016428:Journal Article; D016454:Review | 10.1002/mus.880100603 | [] | false | eng | Muscle Nerve | 7803146 | 0148-639X | United States | [] | "2024-08-13T08:46:10.655232Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||
The interaction of a Trypanosoma cruzi surface protein with Vero cells and its relationship with parasite adhesion. | 24(2) | 175-84 | Previous studies have shown that adhesion to fibroblastic cells of cell culture-derived trypomastigotes of Trypanosoma cruzi probably occurs through a ligand-receptor interaction. The results now obtained indicate that solubilization with a mild detergent ('Chaps', 0.8%) of 125I-surface proteins of trypomastigotes, followed by detergent removal and interaction of the solubilized proteins with a monolayer of intact Vero cells, brings about binding to the cells of a parasite surface protein, which exhibits a molecular weight of 83,000 and isoelectric point of 8.1-8.6 upon two-dimensional polyacrylamide gel electrophoresis. This polypeptide was detected in extracts of highly adherent, extracellularly incubated parasites, but not in extracts of poorly adhesive, recently released trypomastigotes. The detergent-free extracts of incubated trypomastigotes inhibit attachment of live parasites to Vero cells, while extracts of fresh trypomastigotes are nearly ineffective. Binding of the parasite polypeptide to the cells is stimulated by parasite trypsinization or activation in the presence of tunicamycin, and it is inhibited by the presence of mannan or by Vero cell trypsinization, thus showing a similar behaviour to that observed for parasite attachment to Vero cells under these conditions. These results suggest that the surface membranes of activated, highly adherent T. cruzi trypomastigotes contain an 83 kDa polypeptide which acts as a lectin-like protein that can interact with the surface of Vero fibroblasts, probably through mannose residues of a glycoprotein receptor of the host cell. | Molecular and biochemical parasitology | [
{
"affiliation": "",
"forename": "M A",
"identifier": "",
"initials": "MA",
"lastname": "Boschetti"
},
{
"affiliation": "",
"forename": "M M",
"identifier": "",
"initials": "MM",
"lastname": "Piras"
},
{
"affiliation": "",
"forename": "D",
"identifier": "",
"initials": "D",
"lastname": "Henríquez"
},
{
"affiliation": "",
"forename": "R",
"identifier": "",
"initials": "R",
"lastname": "Piras"
}
] | 1987-06 | 3306372 | D000268:Adhesiveness; D000818:Animals; D001345:Autoradiography; D002462:Cell Membrane / Q000378:metabolism / Q000502:physiology*; D004591:Electrophoresis, Polyacrylamide Gel; D006790:Host-Parasite Interactions; D008565:Membrane Proteins / Q000378:metabolism*; D010455:Peptides / Q000378:metabolism; D014349:Trypanosoma cruzi / Q000378:metabolism*; D014709:Vero Cells | D016428:Journal Article; D013485:Research Support, Non-U.S. Gov't | D008565:Membrane Proteins; D010455:Peptides | 10.1016/0166-6851(87)90104-6 | [] | false | eng | Mol Biochem Parasitol | 8006324 | 0166-6851 | Netherlands | [] | "2024-08-13T08:46:10.656119Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Resistance of nematode secretory products to cleavage by mast cell proteinases. | 24(2) | 137-45 | Mast cell proteinases are known to be released in response to helminth infection, and are, in particular, characteristic of the immune rejection of intestinal nematode parasites. In intestinal mucosal tissue the relevant enzyme is rat mast cell proteinase II (RMCP II) and that of other tissues, including the lung, is rat mast cell proteinase I (RMCP I). The function of these enzymes is unknown, and we have examined the possibility that they directly attack the parasites. This was done by examining the cleavage patterns produced by both proteinases on 125I-labelled excretory/secretory (ES) products of two intestinal nematodes (the infective larva of Ascaris suum, and adult Nippostrongylus brasiliensis) and one which has a pulmonary migration route (the third/fourth stage larva of A. suum). It was first established that all the labelled molecules were proteinaceous, by their susceptibility to broad spectrum proteinases, and that none were host components carried over into culture, by their antigenicity to infected hosts. All the nematode ES products were found to be remarkably resistant to RMCP I and II, only one major component of the infective larva of A. suum being cleaved by both enzymes. This was not found to reflect a resistance to serine proteinases in general, since selected ES components were cleaved by chymotrypsin and trypsin. This would, therefore, argue that, if the enzymes play any direct role in the immune expulsion of nematodes, it is unlikely to be successfully directed at their secretions. | Molecular and biochemical parasitology | [
{
"affiliation": "",
"forename": "F",
"identifier": "",
"initials": "F",
"lastname": "Qureshi"
},
{
"affiliation": "",
"forename": "M W",
"identifier": "",
"initials": "MW",
"lastname": "Kennedy"
},
{
"affiliation": "",
"forename": "S",
"identifier": "",
"initials": "S",
"lastname": "Gibson"
},
{
"affiliation": "",
"forename": "P Z",
"identifier": "",
"initials": "PZ",
"lastname": "Ye"
},
{
"affiliation": "",
"forename": "H R",
"identifier": "",
"initials": "HR",
"lastname": "Miller"
}
] | 1987-06 | 3306371 | D000818:Animals; D000947:Antigens, Helminth / Q000276:immunology; D001200:Ascaris / Q000276:immunology / Q000378:metabolism*; D053818:Chymases; D004591:Electrophoresis, Polyacrylamide Gel; D010450:Endopeptidases / Q000378:metabolism*; D009559:Nippostrongylus / Q000276:immunology / Q000378:metabolism*; D011506:Proteins / Q000276:immunology / Q000378:metabolism*; D051381:Rats; D012697:Serine Endopeptidases | D016428:Journal Article; D013485:Research Support, Non-U.S. Gov't | D000947:Antigens, Helminth; D011506:Proteins; D010450:Endopeptidases; D012697:Serine Endopeptidases; D053818:Chymases | 10.1016/0166-6851(87)90100-9 | [] | false | eng | Mol Biochem Parasitol | 8006324 | 0166-6851 | Netherlands | [] | "2024-08-13T08:46:10.657250Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Circumsporozoite gene of a Plasmodium falciparum strain from Thailand. | 24(3) | 289-94 | The nucleotide and deduced amino acid sequences of the CS gene of a Plasmodium falciparum strain from Thailand (T4) are presented. Comparison with the nucleotide sequences of two other P. falciparum CS genes, 7G8 from Brazil and Wellcome from West Africa, shows that: the coding regions outside the repeats of T4 and 7G8 are co-extensive and lack 30 nucleotides present in the Wellcome strain 5' to the repeats; in this region, T4 also differs at 3 nucleotide positions from the 7G8 and the Wellcome strains; in the region 3' to the repeats, T4 differs at two positions from 7G8 and at two other positions from the Wellcome strain--remarkably, all of these differences result in amino acid substitutions; the structure of the tandem repeats in the CS gene of T4 is, 5' to 3', [NANP-NVDP] X 3, [NANP] X 38, which is different from that of the two other strains. Due to the use of synonymous codons, the repetition of the sequence is more precise at the amino acid level than at the nucleotide level. These features contrast with those observed in the CS genes of other plasmodial species. | Molecular and biochemical parasitology | [
{
"affiliation": "",
"forename": "H A",
"identifier": "",
"initials": "HA",
"lastname": "del Portillo"
},
{
"affiliation": "",
"forename": "R S",
"identifier": "",
"initials": "RS",
"lastname": "Nussenzweig"
},
{
"affiliation": "",
"forename": "V",
"identifier": "",
"initials": "V",
"lastname": "Enea"
}
] | 1987-07 | 3306373 | D000595:Amino Acid Sequence; D000818:Animals; D000953:Antigens, Protozoan / Q000235:genetics*; D000954:Antigens, Surface / Q000235:genetics*; D001483:Base Sequence; D003001:Cloning, Molecular; D004247:DNA / Q000032:analysis*; D005796:Genes; D010963:Plasmodium falciparum / Q000235:genetics* / Q000276:immunology; D015800:Protozoan Proteins; D012091:Repetitive Sequences, Nucleic Acid; D012689:Sequence Homology, Nucleic Acid; D013785:Thailand | D003160:Comparative Study; D016428:Journal Article; D013485:Research Support, Non-U.S. Gov't; D013486:Research Support, U.S. Gov't, Non-P.H.S. | D000953:Antigens, Protozoan; D000954:Antigens, Surface; D015800:Protozoan Proteins; C041595:circumsporozoite protein, Protozoan; D004247:DNA | 10.1016/0166-6851(87)90161-7 | [] | false | eng | Mol Biochem Parasitol | 8006324 | 0166-6851 | Netherlands | [] | "2024-08-13T08:46:10.658386Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Trial of a cysteine proteinase inhibitor, EST, in experimental chloroquine myopathy in rats. | 10(6) | 516-23 | The administration of 50 mg/kg/day of chloroquine to rats for 8 weeks produced the chloroquine myopathy characterized by autophagic vacuole formation and increases in lysosomal enzymes, especially cathepsins B & L. Coadministration of 10 mg/kg/day of a potent cysteine proteinase inhibitor, EST, and chloroquine prevented the induction of the chloroquine myopathy. Rats already suffering from the chloroquine myopathy were treated with 10 mg/kg/day of EST together with chloroquine injections for 5 weeks and also recovered remarkably from the myopathy. Thus, EST may be beneficial for myopathies associated with autophagic vacuoles. | Muscle & nerve | [
{
"affiliation": "",
"forename": "H",
"identifier": "",
"initials": "H",
"lastname": "Sugita"
},
{
"affiliation": "",
"forename": "I",
"identifier": "",
"initials": "I",
"lastname": "Higuchi"
},
{
"affiliation": "",
"forename": "M",
"identifier": "",
"initials": "M",
"lastname": "Sano"
},
{
"affiliation": "",
"forename": "S",
"identifier": "",
"initials": "S",
"lastname": "Ishiura"
}
] | 1987 | 3306368 | D000818:Animals; D002738:Chloroquine / Q000037:antagonists & inhibitors; D003546:Cysteine Endopeptidases; D010450:Endopeptidases; D007930:Leucine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D008247:Lysosomes / Q000201:enzymology; D008297:Male; D009132:Muscles / Q000201:enzymology / Q000473:pathology; D009135:Muscular Diseases / Q000139:chemically induced* / Q000188:drug therapy / Q000473:pathology; D009929:Organ Size; D011480:Protease Inhibitors; D051381:Rats; D011919:Rats, Inbred Strains | D016428:Journal Article; D013485:Research Support, Non-U.S. Gov't | D011480:Protease Inhibitors; D002738:Chloroquine; D010450:Endopeptidases; D003546:Cysteine Endopeptidases; D007930:Leucine; C108192:aloxistatin | 10.1002/mus.880100605 | [] | false | eng | Muscle Nerve | 7803146 | 0148-639X | United States | [] | "2024-08-13T08:46:10.660438Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
A controlled clinical trial of high-dose methylprednisolone in the treatment of severe sepsis and septic shock. | 317(11) | 653-8 | The use of high-dose corticosteroids in the treatment of severe sepsis and septic shock remains controversial. Our study was designed as a prospective, randomized, double-blind, placebo-controlled trial of high-dose methylprednisolone sodium succinate for severe sepsis and septic shock. Diagnosis was based on the clinical suspicion of infection plus the presence of fever or hypothermia (rectal temperature greater than 38.3 degrees C [101 degrees F] or less than 35.6 degrees C [96 degrees F]), tachypnea (greater than 20 breaths per minute), tachycardia (greater than 90 beats per minute), and the presence of one of the following indications of organ dysfunction: a change in mental status, hypoxemia, elevated lactate levels, or oliguria. Three hundred eighty-two patients were enrolled. Treatment--either methylprednisolone sodium succinate (30 mg per kilogram of body weight) or placebo--was given in four infusions, starting within two hours of diagnosis. No significant differences were found in the prevention of shock, the reversal of shock, or overall mortality. In the subgroup of patients with elevated serum creatinine levels (greater than 2 mg per deciliter) at enrollment, mortality at 14 days was significantly increased among those receiving methylprednisolone (46 of 78 [59 percent] vs. 17 of 58 [29 percent] among those receiving placebo; P less than 0.01). Among patients treated with methylprednisolone, significantly more deaths were related to secondary infection. We conclude that the use of high-dose corticosteroids provides no benefit in the treatment of severe sepsis and septic shock. | The New England journal of medicine | [
{
"affiliation": "",
"forename": "R C",
"identifier": "",
"initials": "RC",
"lastname": "Bone"
},
{
"affiliation": "",
"forename": "C J",
"identifier": "",
"initials": "CJ",
"lastname": "Fisher"
},
{
"affiliation": "",
"forename": "T P",
"identifier": "",
"initials": "TP",
"lastname": "Clemmer"
},
{
"affiliation": "",
"forename": "G J",
"identifier": "",
"initials": "GJ",
"lastname": "Slotman"
},
{
"affiliation": "",
"forename": "C A",
"identifier": "",
"initials": "CA",
"lastname": "Metz"
},
{
"affiliation": "",
"forename": "R A",
"identifier": "",
"initials": "RA",
"lastname": "Balk"
}
] | 1987-09-10 | 3306374 | D000328:Adult; D000368:Aged; D001424:Bacterial Infections / Q000188:drug therapy* / Q000401:mortality; D002986:Clinical Trials as Topic; D006801:Humans; D008775:Methylprednisolone / Q000008:administration & dosage*; D008875:Middle Aged; D011446:Prospective Studies; D011897:Random Allocation; D012772:Shock, Septic / Q000188:drug therapy* / Q000401:mortality | D016430:Clinical Trial; D016428:Journal Article; D016449:Randomized Controlled Trial; D013485:Research Support, Non-U.S. Gov't | D008775:Methylprednisolone | 10.1056/NEJM198709103171101 | [] | false | eng | N Engl J Med | 0255562 | 0028-4793 | United States | [] | "2024-08-13T08:46:10.661848Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
A prospective study of ultrasonography in the diagnosis of appendicitis. | 317(11) | 666-9 | The diagnosis of appendicitis is frequently difficult. We studied prospectively the diagnostic accuracy and clinical impact of abdominal ultrasonography in 111 consecutive patients thought to have appendicitis. Ultrasonography was performed with small high-resolution, linear-array transducers, with the abdomen compressed to displace or compress bowel and fat. Among 52 patients later shown in surgery to have appendicitis, ultrasonography was unequivocally positive in 39 (sensitivity, 75 percent). Of 31 patients in whom appendicitis was definitely excluded, none had a positive ultrasound examination (specificity, 100 percent). The sensitivity in those with a perforated appendix (28.5 percent) was much lower than in those with acute nonperforating appendicitis (80.5 percent) or appendiceal mass (89 percent), but the low sensitivity did not influence clinical management, since the need for surgery in patients with a perforated appendix was clinically obvious. Ultrasonography resulted in changes in the proposed management in 29 of the 111 patients (26 percent). It also led to the correct diagnosis in the 16 patients who were found to have a disease other than appendicitis. We conclude that ultrasonography is a useful aid in the diagnosis of appendicitis. | The New England journal of medicine | [
{
"affiliation": "",
"forename": "J B",
"identifier": "",
"initials": "JB",
"lastname": "Puylaert"
},
{
"affiliation": "",
"forename": "P H",
"identifier": "",
"initials": "PH",
"lastname": "Rutgers"
},
{
"affiliation": "",
"forename": "R I",
"identifier": "",
"initials": "RI",
"lastname": "Lalisang"
},
{
"affiliation": "",
"forename": "B C",
"identifier": "",
"initials": "BC",
"lastname": "de Vries"
},
{
"affiliation": "",
"forename": "S D",
"identifier": "",
"initials": "SD",
"lastname": "van der Werf"
},
{
"affiliation": "",
"forename": "J P",
"identifier": "",
"initials": "JP",
"lastname": "Dörr"
},
{
"affiliation": "",
"forename": "R A",
"identifier": "",
"initials": "RA",
"lastname": "Blok"
}
] | 1987-09-10 | 3306375 | D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001062:Appendectomy; D001064:Appendicitis / Q000175:diagnosis* / Q000601:surgery; D002648:Child; D003937:Diagnosis, Differential; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D014463:Ultrasonography / Q000379:methods* | D016428:Journal Article | 10.1056/NEJM198709103171103 | [] | false | eng | N Engl J Med | 0255562 | 0028-4793 | United States | [] | "2024-08-13T08:46:10.662995Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||
Dynamic alteration in splenic function during acute falciparum malaria. | 317(11) | 675-9 | Plasmodium-infected erythrocytes lose their normal deformability and become susceptible to splenic filtration. In animal models, this is one mechanism of antimalarial defense. To assess the effect of acute falciparum malaria on splenic filtration, we measured the clearance of heated 51Cr-labeled autologous erythrocytes in 25 patients with acute falciparum malaria and in 10 uninfected controls. Two groups of patients could be distinguished. Sixteen patients had splenomegaly, markedly accelerated clearance of the labeled erythrocytes (clearance half-time, 8.4 +/- 4.4 minutes [mean +/- SD] vs. 62.5 +/- 36.5 minutes in controls; P less than 0.001), and a lower mean hematocrit than did the patients without splenomegaly (P less than 0.001). In the nine patients without splenomegaly, clearance was normal. After institution of antimalarial chemotherapy, however, the clearance in this group accelerated to supernormal rates similar to those in the patients with splenomegaly, but without the development of detectable splenomegaly. Clearance was not significantly altered by treatment in the group with splenomegaly. Six weeks later, normal clearance rates were reestablished in most patients in both groups. We conclude that splenic clearance of labeled erythrocytes is enhanced in patients with malaria if splenomegaly is present and is enhanced only after treatment if splenomegaly is absent. Whether this enhanced splenic function applies to parasite-infected erythrocytes in patients with malaria and has any clinical benefit will require further studies. | The New England journal of medicine | [
{
"affiliation": "",
"forename": "S",
"identifier": "",
"initials": "S",
"lastname": "Looareesuwan"
},
{
"affiliation": "",
"forename": "M",
"identifier": "",
"initials": "M",
"lastname": "Ho"
},
{
"affiliation": "",
"forename": "Y",
"identifier": "",
"initials": "Y",
"lastname": "Wattanagoon"
},
{
"affiliation": "",
"forename": "N J",
"identifier": "",
"initials": "NJ",
"lastname": "White"
},
{
"affiliation": "",
"forename": "D A",
"identifier": "",
"initials": "DA",
"lastname": "Warrell"
},
{
"affiliation": "",
"forename": "D",
"identifier": "",
"initials": "D",
"lastname": "Bunnag"
},
{
"affiliation": "",
"forename": "T",
"identifier": "",
"initials": "T",
"lastname": "Harinasuta"
},
{
"affiliation": "",
"forename": "D J",
"identifier": "",
"initials": "DJ",
"lastname": "Wyler"
}
] | 1987-09-10 | 3306376 | D000328:Adult; D002860:Chromium Radioisotopes; D004912:Erythrocytes / Q000502:physiology; D005260:Female; D006801:Humans; D008288:Malaria / Q000503:physiopathology*; D008297:Male; D010963:Plasmodium falciparum; D013154:Spleen / Q000503:physiopathology*; D013163:Splenomegaly / Q000503:physiopathology | D016428:Journal Article; D013485:Research Support, Non-U.S. Gov't | D002860:Chromium Radioisotopes | 10.1056/NEJM198709103171105 | [] | false | eng | N Engl J Med | 0255562 | 0028-4793 | United States | [] | "2024-08-13T08:46:10.664304Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 37-1987. A 50-year-old man with bilateral pneumonia and respiratory failure. | 317(11) | 694-702 | The New England journal of medicine | [] | 1987-09-10 | 3306377 | D003937:Diagnosis, Differential; D004917:Erythromycin / Q000627:therapeutic use; D005455:Fluorescent Antibody Technique; D006801:Humans; D007875:Legionella / Q000302:isolation & purification; D007877:Legionnaires' Disease / Q000175:diagnosis* / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D011014:Pneumonia / Q000175:diagnosis* / Q000188:drug therapy | D002363:Case Reports; D016428:Journal Article | D004917:Erythromycin | 10.1056/NEJM198709103171108 | [] | false | eng | N Engl J Med | 0255562 | 0028-4793 | United States | [] | "2024-08-13T08:46:10.665284Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||
Tempering the technological diagnosis of appendicitis. | 317(11) | 703-4 | The New England journal of medicine | [
{
"affiliation": "",
"forename": "S I",
"identifier": "",
"initials": "SI",
"lastname": "Schwartz"
}
] | 1987-09-10 | 3306378 | D001064:Appendicitis / Q000175:diagnosis*; D003936:Diagnosis, Computer-Assisted; D006801:Humans; D014463:Ultrasonography | D016421:Editorial | 10.1056/NEJM198709103171109 | [] | false | eng | N Engl J Med | 0255562 | 0028-4793 | United States | [] | "2024-08-13T08:46:10.666002Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||||
Lack of effect of ABO blood-group antigens on survival after cardiac transplantation. | 317(12) | 772-3 | The New England journal of medicine | [
{
"affiliation": "",
"forename": "S J",
"identifier": "",
"initials": "SJ",
"lastname": "Shumway"
},
{
"affiliation": "",
"forename": "W A",
"identifier": "",
"initials": "WA",
"lastname": "Baumgartner"
},
{
"affiliation": "",
"forename": "L M",
"identifier": "",
"initials": "LM",
"lastname": "Soule"
},
{
"affiliation": "",
"forename": "T J",
"identifier": "",
"initials": "TJ",
"lastname": "Gardner"
},
{
"affiliation": "",
"forename": "B A",
"identifier": "",
"initials": "BA",
"lastname": "Reitz"
}
] | 1987-09-17 | 3306382 | D000017:ABO Blood-Group System; D016027:Heart Transplantation; D006801:Humans; D014184:Transplantation, Homologous / Q000401:mortality | D016422:Letter | D000017:ABO Blood-Group System | 10.1056/NEJM198709173171219 | [] | false | eng | N Engl J Med | 0255562 | 0028-4793 | United States | [] | "2024-08-13T08:46:10.667971Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||
Efficacy of Haemophilus influenzae type b polysaccharide-diphtheria toxoid conjugate vaccine in infancy. | 317(12) | 717-22 | Haemophilus influenzae type b capsular polysaccharide-diphtheria toxoid conjugate vaccine has recently been shown to be capable of inducing antibodies to H. influenzae in infants. In an evaluation of its clinical efficacy, 60,000 children were enrolled in an open trial in Finland. Children born on odd-numbered days between October 1, 1985, and September 30, 1986, received the vaccine at 3, 4, 6, and 14 months; those born on even-numbered days served as controls. The geometric mean antibody titer measured in a cohort of 99 children rose from a prevaccination level of 0.08 microgram per milliliter at three months of age to 0.42 microgram per milliliter at seven months. Only minor adverse reactions were reported. Up to February 1987, two cases of invasive H. influenzae infection had occurred among the children who had received three doses of vaccine, whereas 12 cases had occurred among the controls (P = 0.0005 by Poisson one-tailed test). The rate of short-term (average follow-up time, five months) protection provided by this conjugate vaccine in infancy was thus 83 percent. | The New England journal of medicine | [
{
"affiliation": "",
"forename": "J",
"identifier": "",
"initials": "J",
"lastname": "Eskola"
},
{
"affiliation": "",
"forename": "H",
"identifier": "",
"initials": "H",
"lastname": "Peltola"
},
{
"affiliation": "",
"forename": "A K",
"identifier": "",
"initials": "AK",
"lastname": "Takala"
},
{
"affiliation": "",
"forename": "H",
"identifier": "",
"initials": "H",
"lastname": "Käyhty"
},
{
"affiliation": "",
"forename": "M",
"identifier": "",
"initials": "M",
"lastname": "Hakulinen"
},
{
"affiliation": "",
"forename": "V",
"identifier": "",
"initials": "V",
"lastname": "Karanko"
},
{
"affiliation": "",
"forename": "E",
"identifier": "",
"initials": "E",
"lastname": "Kela"
},
{
"affiliation": "",
"forename": "P",
"identifier": "",
"initials": "P",
"lastname": "Rekola"
},
{
"affiliation": "",
"forename": "P R",
"identifier": "",
"initials": "PR",
"lastname": "Rönnberg"
},
{
"affiliation": "",
"forename": "J S",
"identifier": "",
"initials": "JS",
"lastname": "Samuelson"
}
] | 1987-09-17 | 3306379 | D000907:Antibodies, Bacterial / Q000032:analysis; D016667:Bacterial Capsules; D001428:Bacterial Vaccines / Q000008:administration & dosage / Q000009:adverse effects / Q000276:immunology*; D002986:Clinical Trials as Topic; D004168:Diphtheria Toxoid / Q000008:administration & dosage / Q000009:adverse effects / Q000276:immunology*; D005260:Female; D006192:Haemophilus Infections / Q000517:prevention & control*; D018073:Haemophilus Vaccines; D006193:Haemophilus influenzae / Q000276:immunology*; D006801:Humans; D007223:Infant; D008297:Male; D011135:Polysaccharides, Bacterial | D016430:Clinical Trial; D018848:Controlled Clinical Trial; D016428:Journal Article; D013485:Research Support, Non-U.S. Gov't | D000907:Antibodies, Bacterial; D001428:Bacterial Vaccines; D004168:Diphtheria Toxoid; D018073:Haemophilus Vaccines; C044237:Haemophilus influenzae type b polysaccharide vaccine; D011135:Polysaccharides, Bacterial | 10.1056/NEJM198709173171201 | [] | false | eng | N Engl J Med | 0255562 | 0028-4793 | United States | [] | "2024-08-13T08:46:10.669095Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Allogeneic bone marrow transplantation in a patient with chemotherapy-resistant progressive histiocytosis X. | 317(12) | 773-4 | The New England journal of medicine | [
{
"affiliation": "",
"forename": "L P",
"identifier": "",
"initials": "LP",
"lastname": "Dehner"
}
] | 1987-09-17 | 3306383 | D016026:Bone Marrow Transplantation; D004351:Drug Resistance; D006646:Histiocytosis, Langerhans-Cell / Q000628:therapy*; D006801:Humans; D014184:Transplantation, Homologous | D016422:Letter | 10.1056/NEJM198709173171221 | [] | false | eng | N Engl J Med | 0255562 | 0028-4793 | United States | [] | "2024-08-13T08:46:10.670125Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||||
Effect of gradual withdrawal on the rebound sleep disorder after discontinuation of triazolam. | 317(12) | 722-8 | Sixty volunteers with insomnia participated in a randomized, double-blind, controlled clinical trial. After an initial six nights of placebo, 30 subjects (the abrupt-withdrawal group) received 0.5 mg of triazolam nightly for 7 to 10 nights, after which they received placebo. The other 30 subjects (the tapered-dosage group) received the same initial placebo treatment, then triazolam at 0.5 mg for seven nights, at 0.25 mg for two nights, and at 0.125 mg for two nights, and then placebo. As compared with the initial placebo period, the triazolam period significantly reduced the interval before the onset of sleep (sleep latency), and it prolonged sleep duration, reduced the number of awakenings, and improved the self-rated soundness of sleep in all cohorts. In the abrupt-withdrawal group, plasma levels of triazolam were undetectable the morning after the first night of placebo substitution, and subjects reported prolongation of sleep latency (57 minutes longer than base line), reduction in sleep duration (1.4 hours less than base line), and increased awakenings (1.2 per night above base line). The symptoms of rebound sleep disorder lasted one or possibly two nights, and there was a reversion toward base line on subsequent placebo nights. In the tapered-dosage group, however, plasma triazolam levels fell gradually to zero, and rebound symptoms were decreased or eliminated. Thus, rebound sleep disorder following abrupt discontinuation of triazolam can be attenuated by a regimen of tapering. | The New England journal of medicine | [
{
"affiliation": "",
"forename": "D J",
"identifier": "",
"initials": "DJ",
"lastname": "Greenblatt"
},
{
"affiliation": "",
"forename": "J S",
"identifier": "",
"initials": "JS",
"lastname": "Harmatz"
},
{
"affiliation": "",
"forename": "M A",
"identifier": "",
"initials": "MA",
"lastname": "Zinny"
},
{
"affiliation": "",
"forename": "R I",
"identifier": "",
"initials": "RI",
"lastname": "Shader"
}
] | 1987-09-17 | 3306380 | D000328:Adult; D002986:Clinical Trials as Topic; D004311:Double-Blind Method; D004334:Drug Administration Schedule; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D011897:Random Allocation; D007319:Sleep Initiation and Maintenance Disorders / Q000139:chemically induced / Q000517:prevention & control*; D013375:Substance Withdrawal Syndrome / Q000209:etiology / Q000517:prevention & control*; D014229:Triazolam / Q000008:administration & dosage* / Q000009:adverse effects / Q000097:blood | D016430:Clinical Trial; D016428:Journal Article; D016449:Randomized Controlled Trial; D013485:Research Support, Non-U.S. Gov't; D013487:Research Support, U.S. Gov't, P.H.S. | D014229:Triazolam | 10.1056/NEJM198709173171202 | [] | false | eng | N Engl J Med | 0255562 | 0028-4793 | United States | [
{
"agency": "NIA NIH HHS",
"country": "United States",
"grant_acronym": "AG",
"grant_id": "AG-00106"
},
{
"agency": "NIMH NIH HHS",
"country": "United States",
"grant_acronym": "MH",
"grant_id": "MH-34223"
}
] | "2024-08-13T08:46:10.671297Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Cyclosporine for myasthenia gravis. | 317(12) | 770 | The New England journal of medicine | [
{
"affiliation": "",
"forename": "D",
"identifier": "",
"initials": "D",
"lastname": "Elkharrat"
},
{
"affiliation": "",
"forename": "M",
"identifier": "",
"initials": "M",
"lastname": "Goulon"
},
{
"affiliation": "",
"forename": "P",
"identifier": "",
"initials": "P",
"lastname": "Gajdos"
}
] | 1987-09-17 | 3306381 | D002986:Clinical Trials as Topic; D003524:Cyclosporins / Q000627:therapeutic use*; D004311:Double-Blind Method; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D009157:Myasthenia Gravis / Q000188:drug therapy* | D016430:Clinical Trial; D003160:Comparative Study; D016422:Letter | D003524:Cyclosporins; D007166:Immunosuppressive Agents | 10.1056/NEJM198709173171215 | [] | false | eng | N Engl J Med | 0255562 | 0028-4793 | United States | [] | "2024-08-13T08:46:10.672305Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||
The use of ketoconazole as an inhibitor of steroid production. | 317(13) | 812-8 | The New England journal of medicine | [
{
"affiliation": "",
"forename": "N",
"identifier": "",
"initials": "N",
"lastname": "Sonino"
}
] | 1987-09-24 | 3306384 | D000305:Adrenal Cortex Hormones / Q000096:biosynthesis*; D000728:Androgens / Q000096:biosynthesis; D003864:Depression, Chemical; D006801:Humans; D006854:Hydrocortisone / Q000096:biosynthesis; D007654:Ketoconazole / Q000494:pharmacology / Q000627:therapeutic use*; D008297:Male | D016428:Journal Article; D016454:Review | D000305:Adrenal Cortex Hormones; D000728:Androgens; D007654:Ketoconazole; D006854:Hydrocortisone | 10.1056/NEJM198709243171307 | [] | false | eng | N Engl J Med | 0255562 | 0028-4793 | United States | [] | "2024-08-13T08:46:10.673128Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||
Propranolol in the prevention of first upper gastrointestinal tract hemorrhage in patients with cirrhosis of the liver and esophageal varices. | 317(14) | 856-61 | We conducted a prospective, randomized, multicenter, single-blind trial of propranolol as compared with placebo in the prevention of first upper gastrointestinal tract bleeding in patients with cirrhosis of the liver. A total of 230 patients (90 percent with alcoholism and 46 percent with a Child-Pugh grade C classification) with large esophageal varices without previous bleeding were randomly assigned to receive either propranolol (n = 118) or placebo (n = 112), after they had been divided into two groups according to the severity of their liver disease. The end points of the study were bleeding and death. The dose of propranolol was progressively increased to decrease the heart rate by 20 to 25 percent. The final doses were 40 mg of conventional propranolol and 160 and 320 mg of long-acting propranolol daily in 22 percent, 60 percent, and 18 percent of patients, respectively. The mean (+/- SD) follow-up time among survivors without bleeding was 436 +/- 172 days. The cumulative percentages of patients free of bleeding two years after inclusion in the study were 74 percent (95 percent confidence limits, 61 and 83) in the propranolol group and 39 percent (95 percent confidence limits, 15 and 69) in the placebo group (P less than 0.05). Cumulative two-year survival was 72 percent (95 percent confidence limits, 60 and 81) in the propranolol group and 51 percent (95 percent confidence limits, 37 and 64) in the placebo group (P less than 0.05). The advantage of propranolol over placebo was maintained when potentially confounding variables were adjusted with use of the Cox model. Side effects occurred in 17 percent of the patients who received propranolol and led to the stopping of treatment in 11 percent. We conclude that propranolol can decrease the incidence of first bleeding and death during a period of two years in patients with cirrhosis and large varices. | The New England journal of medicine | [
{
"affiliation": "",
"forename": "J P",
"identifier": "",
"initials": "JP",
"lastname": "Pascal"
},
{
"affiliation": "",
"forename": "P",
"identifier": "",
"initials": "P",
"lastname": "Cales"
}
] | 1987-10-01 | 3306385 | D002986:Clinical Trials as Topic; D004932:Esophageal and Gastric Varices / Q000150:complications*; D005260:Female; D005500:Follow-Up Studies; D006471:Gastrointestinal Hemorrhage / Q000401:mortality / Q000517:prevention & control*; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D008103:Liver Cirrhosis / Q000150:complications*; D008104:Liver Cirrhosis, Alcoholic / Q000150:complications; D008297:Male; D008875:Middle Aged; D011433:Propranolol / Q000008:administration & dosage / Q000627:therapeutic use*; D011446:Prospective Studies; D011897:Random Allocation | D016430:Clinical Trial; D016428:Journal Article; D016449:Randomized Controlled Trial | D011433:Propranolol | 10.1056/NEJM198710013171403 | [] | false | eng | N Engl J Med | 0255562 | 0028-4793 | United States | [] | "2024-08-13T08:46:10.675103Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Central nervous system toxicity after liver transplantation. The role of cyclosporine and cholesterol. | 317(14) | 861-6 | We describe severe central nervous system (CNS) toxicity, manifested by confusion, cortical blindness, quadriplegia, seizures, and coma, associated with cyclosporine treatment in three patients undergoing liver transplantation. CT and magnetic resonance studies disclosed a severe, diffuse disorder of the white matter. All side effects and radiographic findings were reversed with discontinuation or a reduction in the dose of cyclosporine. We also observed an inverse association between CNS side effects and total serum cholesterol levels after transplantation. A retrospective analysis of 54 liver transplantations performed in 48 patients revealed that 13 patients had symptoms of CNS toxicity associated with the use of cyclosporine. These patients' total serum cholesterol levels in the first week after transplantation were reduced as compared with those in patients without symptoms (mean +/- SE, 94 +/- 4 mg per deciliter vs. 132 +/- 6, or 2.44 +/- 0.10 mmol per liter vs. 3.43 +/- 0.16). We conclude that cyclosporine therapy for immunosuppression in liver transplantation may cause a syndrome of encephalopathy, seizures, and white-matter changes and that this is most likely to occur in patients with low total serum cholesterol levels after transplantation. | The New England journal of medicine | [
{
"affiliation": "",
"forename": "P C",
"identifier": "",
"initials": "PC",
"lastname": "de Groen"
},
{
"affiliation": "",
"forename": "A J",
"identifier": "",
"initials": "AJ",
"lastname": "Aksamit"
},
{
"affiliation": "",
"forename": "J",
"identifier": "",
"initials": "J",
"lastname": "Rakela"
},
{
"affiliation": "",
"forename": "G S",
"identifier": "",
"initials": "GS",
"lastname": "Forbes"
},
{
"affiliation": "",
"forename": "R A",
"identifier": "",
"initials": "RA",
"lastname": "Krom"
}
] | 1987-10-01 | 3306386 | D001766:Blindness / Q000139:chemically induced; D001921:Brain / Q000187:drug effects*; D001927:Brain Diseases / Q000097:blood / Q000139:chemically induced; D002784:Cholesterol / Q000097:blood*; D003128:Coma / Q000139:chemically induced; D003221:Confusion / Q000139:chemically induced; D003524:Cyclosporins / Q000009:adverse effects*; D005260:Female; D006801:Humans; D016031:Liver Transplantation; D008875:Middle Aged; D011183:Postoperative Complications; D011782:Quadriplegia / Q000139:chemically induced; D012189:Retrospective Studies; D012640:Seizures / Q000139:chemically induced | D002363:Case Reports; D016428:Journal Article | D003524:Cyclosporins; D002784:Cholesterol | 10.1056/NEJM198710013171404 | [] | false | eng | N Engl J Med | 0255562 | 0028-4793 | United States | [] | "2024-08-13T08:46:10.676211Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
How did Medicare's prospective payment system affect hospitals? | 317(14) | 867-73 | Using data from 1982 and 1984, we examined how Medicare's prospective payment system affected hospitals. The study showed that hospitals paid through the prospective payment system had significantly lower increases in Medicare costs and greater declines in Medicare use than did other hospitals. Unlike these other hospitals, for which Medicare costs approximately equaled Medicare revenues, hospitals receiving prospective payment kept Medicare costs from rising as fast as Medicare revenues, earning the profit that the prospective payment system allowed. The opportunity to earn a profit led hospitals to slow increases in Medicare costs, regardless of the level of revenue constraint. However, the more the prospective payment system constrained hospitals' revenues, the more hospitals slowed increases in Medicare costs. In the most constrained hospitals, slower increases in Medicare costs were accompanied by slower increases in total hospital spending. The least constrained hospitals slowed Medicare cost increases the least and did not show their overall spending. These hospitals nevertheless increased their profit margins the most, since the prospective payment system's federal rate paid them the highest rates relative to base-year costs. Since federal rates produced extra profits, not extra cost containment, their appropriateness is questionable. The prospective payment system should be modified to eliminate windfalls while continuing to promote cost containment. | The New England journal of medicine | [
{
"affiliation": "",
"forename": "J",
"identifier": "",
"initials": "J",
"lastname": "Feder"
},
{
"affiliation": "",
"forename": "J",
"identifier": "",
"initials": "J",
"lastname": "Hadley"
},
{
"affiliation": "",
"forename": "S",
"identifier": "",
"initials": "S",
"lastname": "Zuckerman"
}
] | 1987-10-01 | 3306387 | D003363:Cost Control; D003625:Data Collection; D005376:Financial Management / Q000639:trends*; D005377:Financial Management, Hospital / Q000639:trends*; D006761:Hospitals / Q000706:statistics & numerical data; D007182:Income; D006278:Medicare / Q000191:economics*; D011445:Prospective Payment System / Q000191:economics*; D011907:Rate Setting and Review / Q000379:methods; D013659:Tax Equity and Fiscal Responsibility Act; D013660:Taxes; D014481:United States | D003160:Comparative Study; D016428:Journal Article; D013486:Research Support, U.S. Gov't, Non-P.H.S. | 10.1056/NEJM198710013171405 | [] | false | eng | N Engl J Med | 0255562 | 0028-4793 | United States | [] | "2024-08-13T08:46:10.677338Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||
Serologic studies in the diagnosis and management of meningitis due to Sporothrix schenckii. | 317(15) | 935-40 | Eight patients have previously been reported to have central nervous system infections caused by Sporothrix schenckii. In those patients the fungus proved quite difficult to culture, delaying correct diagnosis and treatment. We describe seven additional patients with sporotrichosis meningitis, all of whom had antibody to this fungus in cerebrospinal fluid and serum. The antibody in the cerebrospinal fluid was most likely produced locally, as evidenced by its oligoclonality and the relatively high ratio of immunoglobulin to albumin in the cerebrospinal fluid as compared with the serum. Only one of these seven patients, who had active sporotrichosis of the knee joint, had obvious extrameningeal infection. None of 130 patients with meningitis known to be caused by other agents and none of 170 patients with other neurologic disorders had antibody to S. schenckii in their cerebrospinal fluid. We suggest that cerebrospinal fluid should be tested for S. schenckii antibody (in addition to other fungal agents) in any patient with chronic meningitis for which no cause is discovered by the usual diagnostic tests. | The New England journal of medicine | [
{
"affiliation": "",
"forename": "E N",
"identifier": "",
"initials": "EN",
"lastname": "Scott"
},
{
"affiliation": "",
"forename": "L",
"identifier": "",
"initials": "L",
"lastname": "Kaufman"
},
{
"affiliation": "",
"forename": "A C",
"identifier": "",
"initials": "AC",
"lastname": "Brown"
},
{
"affiliation": "",
"forename": "H G",
"identifier": "",
"initials": "HG",
"lastname": "Muchmore"
}
] | 1987-10-08 | 3306388 | D000328:Adult; D000908:Antibodies, Fungal / Q000032:analysis* / Q000134:cerebrospinal fluid; D002908:Chronic Disease; D005260:Female; D006801:Humans; D007124:Immunoenzyme Techniques; D007074:Immunoglobulin G / Q000032:analysis; D007841:Latex Fixation Tests; D008297:Male; D008581:Meningitis / Q000175:diagnosis*; D008875:Middle Aged; D012709:Serum Albumin / Q000032:analysis; D013175:Sporothrix / Q000276:immunology*; D013174:Sporotrichosis / Q000175:diagnosis* | D016428:Journal Article; D013486:Research Support, U.S. Gov't, Non-P.H.S. | D000908:Antibodies, Fungal; D007074:Immunoglobulin G; D012709:Serum Albumin | 10.1056/NEJM198710083171505 | [] | false | eng | N Engl J Med | 0255562 | 0028-4793 | United States | [] | "2024-08-13T08:46:10.678473Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Kidney transplantation from anencephalic donors. | 317(15) | 960-1 | The New England journal of medicine | [
{
"affiliation": "",
"forename": "K",
"identifier": "",
"initials": "K",
"lastname": "O'Rourke"
}
] | 1987-10-08 | 3306389 | D000757:Anencephaly; D001926:Brain Death; D004992:Ethics, Medical; D006801:Humans; D007231:Infant, Newborn; D016030:Kidney Transplantation; D014019:Tissue Donors | D016422:Letter | 10.1056/NEJM198710083171513 | [] | false | eng | N Engl J Med | 0255562 | 0028-4793 | United States | [] | "2024-08-13T08:46:10.679441Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||||
Bone marrow transplantation for thalassemia. | 317(15) | 964 | The New England journal of medicine | [
{
"affiliation": "",
"forename": "S",
"identifier": "",
"initials": "S",
"lastname": "Piomelli"
},
{
"affiliation": "",
"forename": "N",
"identifier": "",
"initials": "N",
"lastname": "Lerner"
},
{
"affiliation": "",
"forename": "A",
"identifier": "",
"initials": "A",
"lastname": "Cohen"
},
{
"affiliation": "",
"forename": "E",
"identifier": "",
"initials": "E",
"lastname": "Schwartz"
},
{
"affiliation": "",
"forename": "D",
"identifier": "",
"initials": "D",
"lastname": "Nathan"
},
{
"affiliation": "",
"forename": "L",
"identifier": "",
"initials": "L",
"lastname": "Wolfe"
},
{
"affiliation": "",
"forename": "D",
"identifier": "",
"initials": "D",
"lastname": "Weatherall"
},
{
"affiliation": "",
"forename": "A",
"identifier": "",
"initials": "A",
"lastname": "Nienhuis"
}
] | 1987-10-08 | 3306390 | D000293:Adolescent; D016026:Bone Marrow Transplantation; D002648:Child; D006801:Humans; D013789:Thalassemia / Q000628:therapy* | D016422:Letter | 10.1056/nejm198710083171516 | [] | false | eng | N Engl J Med | 0255562 | 0028-4793 | United States | [] | "2024-08-13T08:46:10.681423Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||||
Medicare-designated centers for cardiac transplantation. | 317(15) | 966-7 | The New England journal of medicine | [
{
"affiliation": "",
"forename": "R W",
"identifier": "",
"initials": "RW",
"lastname": "Evans"
}
] | 1987-10-08 | 3306391 | D014487:Centers for Medicare and Medicaid Services, U.S.; D016027:Heart Transplantation; D006752:Hospital Planning / Q000592:standards*; D006801:Humans; D006278:Medicare; D014481:United States | D016422:Letter | 10.1056/NEJM198710083171518 | [] | false | eng | N Engl J Med | 0255562 | 0028-4793 | United States | [] | "2024-08-13T08:46:10.682112Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||||
Interaction between Candida agglutinins and antifungal agents. | 99(1) | 21-4 | Antifungal agents alter the function and morphology of Candida cell membranes and cell walls. We observed that brief (30 minute) exposure to either amphotericin B or clotrimazole inhibited the agglutination of Candida blastoconidia by murine bronchoalveolar lavage fluid. This inhibition required continuous drug presence. Neither amphotericin nor clotrimazole inhibited Candida agglutination by concanavalin A or pooled human serum. These results demonstrate that antifungal drugs can produce rapid changes in the surface characteristics of some fungi. | Mycopathologia | [
{
"affiliation": "",
"forename": "J C",
"identifier": "",
"initials": "JC",
"lastname": "Lutz"
},
{
"affiliation": "",
"forename": "K M",
"identifier": "",
"initials": "KM",
"lastname": "Nugent"
}
] | 1987-07 | 3306393 | D000371:Agglutination / Q000187:drug effects; D000373:Agglutinins / Q000378:metabolism*; D000666:Amphotericin B / Q000378:metabolism / Q000494:pharmacology*; D000818:Animals; D002176:Candida albicans / Q000187:drug effects* / Q000276:immunology / Q000648:ultrastructure; D002462:Cell Membrane / Q000187:drug effects; D002473:Cell Wall / Q000187:drug effects; D003022:Clotrimazole / Q000378:metabolism / Q000494:pharmacology*; D003208:Concanavalin A / Q000378:metabolism; D007093:Imidazoles / Q000494:pharmacology*; D051379:Mice | D016428:Journal Article; D013487:Research Support, U.S. Gov't, P.H.S. | D000373:Agglutinins; D007093:Imidazoles; D003208:Concanavalin A; D000666:Amphotericin B; D003022:Clotrimazole | 10.1007/BF00436676 | [
{
"citation": "J Antimicrob Chemother. 1986 Mar;17(3):269-79",
"pmid": "3516967"
},
{
"citation": "Sabouraudia. 1980 Sep;18(3):211-28",
"pmid": "7001652"
},
{
"citation": "Antimicrob Agents Chemother. 1985 May;27(5):692-4",
"pmid": "4015066"
},
{
"citation": "Antimicrob Agents Chemother. 1980 Oct;18(4):593-7",
"pmid": "7004343"
},
{
"citation": "J Infect Dis. 1985 Nov;152(5):1037-43",
"pmid": "4045244"
},
{
"citation": "J Infect Dis. 1986 Oct;154(4):665-9",
"pmid": "3528319"
},
{
"citation": "Infect Immun. 1985 Nov;50(2):598-600",
"pmid": "2932390"
},
{
"citation": "Rev Infect Dis. 1985 Jan-Feb;7(1):51-65",
"pmid": "3920746"
},
{
"citation": "J Med Vet Mycol. 1986 Feb;24(1):5-22",
"pmid": "3517278"
},
{
"citation": "Can J Microbiol. 1982 Oct;28(10):1119-26",
"pmid": "6295583"
},
{
"citation": "Antimicrob Agents Chemother. 1979 May;15(5):716-22",
"pmid": "393163"
},
{
"citation": "J Gen Microbiol. 1978 Apr;105(2):263-73",
"pmid": "347030"
},
{
"citation": "Biochim Biophys Acta. 1976 Dec 2;455(2):452-65",
"pmid": "793632"
},
{
"citation": "Annu Rev Pharmacol Toxicol. 1983;23:303-30",
"pmid": "6307124"
}
] | false | eng | Mycopathologia | 7505689 | 0301-486X | Netherlands | [
{
"agency": "NIAID NIH HHS",
"country": "United States",
"grant_acronym": "AI",
"grant_id": "AI(22356)"
}
] | "2024-08-13T08:46:10.683340Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Natural occurrence of Nocardia in soil of Tucumán: physiological characteristics. | 99(1) | 15-9 | This is the first study initiated in Argentina to establish the presence of species of Nocardia from soil samples. These samples were gathered in different areas of Tucumán. Thirty three pathogenic strains of Nocardia were isolated by the paraffin bait method. Out of them, 28 were N. brasiliensis, 3 N. asteroides and 2 N. caviae. N. brasiliensis was widely distributed in the soil of the areas tested. It is proved that N. caviae, so rarely found in other regions of the world, occurs in Tucumán. A detailed study of the morphological and physiological characteristics for identification is discussed. | Mycopathologia | [
{
"affiliation": "",
"forename": "A",
"identifier": "",
"initials": "A",
"lastname": "van Gelderen de Komaid"
},
{
"affiliation": "",
"forename": "R",
"identifier": "",
"initials": "R",
"lastname": "Runco de Laborda"
},
{
"affiliation": "",
"forename": "R",
"identifier": "",
"initials": "R",
"lastname": "Salim"
}
] | 1987-07 | 3306392 | D001118:Argentina; D009615:Nocardia / Q000166:cytology / Q000302:isolation & purification* / Q000502:physiology; D009616:Nocardia asteroides / Q000166:cytology / Q000302:isolation & purification* / Q000502:physiology; D012988:Soil Microbiology; D013696:Temperature | D016428:Journal Article; D013485:Research Support, Non-U.S. Gov't | 10.1007/BF00436675 | [
{
"citation": "Sabouraudia. 1968 Jun;6(3):260-6",
"pmid": "5679672"
},
{
"citation": "J Bacteriol. 1959 Dec;78:852-7",
"pmid": "13802253"
},
{
"citation": "Ann Inst Pasteur (Paris). 1963 Oct;105:795-7",
"pmid": "14093801"
},
{
"citation": "Am Rev Respir Dis. 1961 Sep;84:337-47",
"pmid": "13704444"
},
{
"citation": "J Bacteriol. 1957 Jan;73(1):15-27",
"pmid": "13405855"
},
{
"citation": "J Bacteriol. 1965 Sep;90(3):822-3",
"pmid": "16562088"
},
{
"citation": "J Gen Microbiol. 1962 Jan;27:1-10",
"pmid": "13900489"
},
{
"citation": "J Bacteriol. 1955 Feb;69(2):147-50",
"pmid": "14353819"
},
{
"citation": "Indian J Med Res. 1964 Oct;52:1057-61",
"pmid": "14252233"
},
{
"citation": "Rev Inst Salubr Enferm Trop. 1960 Sep;20:147-51",
"pmid": "13900235"
}
] | false | eng | Mycopathologia | 7505689 | 0301-486X | Netherlands | [] | "2024-08-13T08:46:10.684459Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||
International Commission on the Taxonomy of Fungi (ICTF). Code of practice for systematic mycologists. | 99(1) | 3-7 | Fourteen points which mycologists dealing with the systematics of fungi (including yeasts) are encouraged to adhere to in their work are presented as a Code of Practice for Systematic Mycologists. Adoption of these will encourage both stability in nomenclature and uniformity in approaches to the descriptions of fungi. | Mycopathologia | [
{
"affiliation": "",
"forename": "L",
"identifier": "",
"initials": "L",
"lastname": "Sigler"
},
{
"affiliation": "",
"forename": "D L",
"identifier": "",
"initials": "DL",
"lastname": "Hawksworth"
}
] | 1987-07 | 3306394 | D005658:Fungi / Q000145:classification*; D009172:Mycology / Q000379:methods*; D009626:Terminology as Topic | D016428:Journal Article; D016454:Review | 10.1007/BF00436673 | [
{
"citation": "Microbiol Sci. 1986 Jun;3(6):168-71",
"pmid": "3153158"
},
{
"citation": "Microbiol Sci. 1984 Apr;1(1):18-21",
"pmid": "6444089"
}
] | false | eng | Mycopathologia | 7505689 | 0301-486X | Netherlands | [] | "2024-08-13T08:46:10.685341Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||
Selective inactivation of heterokaryons of Candida albicans by anaerobiosis. | 99(1) | 31-9 | Heterokaryons (hets), but not monokaryons of Candida albicans die when grown anaerobically on minimal medium. Their rates of inactivation increase with decreases in growth temperatures from 37 degrees C to 25 degrees C. At 10 degrees C, however, anaerobiosis is not lethal and suppresses the inactivation which normally occurs among hets cultured aerobically at that temperature. Killing of hets by anaerobiosis can be altered significantly by certain exogenously provided amino acids or intermediates of oxidative respiration. Aspartic acid alone promotes inactivation whereas alanine, glutamic acid or lysine individually have no effects. However, glutamate and lysine combined afford slight protection against inactivation while aspartate and glutamate combined, with or without lysine, are highly protective: the activity of the aspartate-glutamate combination is completely negated by the addition of alanine. Other common amino acids have no effects on het responses to anaerobiosis other than the ability, when combined, to relieve the antagonism of alanine for the aspartate-glutamate combination. Anaerobic survivals are also enhanced by oxalacetic acid or alpha-ketoglutaric acid, and even more so by a combination of these two intermediates. The resistances to inactivation elicited by the oxalacetate alpha-ketoglutarate or aspartate-glutamate combinations are not additive. These relationships are interpreted to signify that inactivation of hets by anaerobic growth is largely, if not exclusively, due to depletion of their oxalacetic acid and alpha-ketoglutaric acid contents for amino acid biosyntheses, and the unique inability of het cells to replenish those keto acids upon subsequent return to aerobic conditions. The observations are consistent with previous indications that mitochondria formed by hets are functionally abnormal. | Mycopathologia | [
{
"affiliation": "",
"forename": "A",
"identifier": "",
"initials": "A",
"lastname": "Sarachek"
}
] | 1987-07 | 3306395 | D000596:Amino Acids / Q000378:metabolism*; D000693:Anaerobiosis; D002176:Candida albicans / Q000254:growth & development* / Q000378:metabolism; D003470:Culture Media; D007656:Ketoglutaric Acids / Q000378:metabolism; D010071:Oxaloacetates / Q000378:metabolism; D010101:Oxygen Consumption; D011523:Protoplasts; D013696:Temperature | D016428:Journal Article | D000596:Amino Acids; D003470:Culture Media; D007656:Ketoglutaric Acids; D010071:Oxaloacetates | 10.1007/BF00436678 | [
{
"citation": "J Cell Comp Physiol. 1953 Feb;41(1):23-36",
"pmid": "13034889"
},
{
"citation": "J Gen Microbiol. 1974 May;82(1):77-95",
"pmid": "4153146"
},
{
"citation": "Antonie Van Leeuwenhoek. 1963;29:112-20",
"pmid": "13991450"
},
{
"citation": "Curr Genet. 1986;10(9):685-93",
"pmid": "3329044"
},
{
"citation": "Biochim Biophys Acta. 1984 Jan 27;779(1):65-87",
"pmid": "6318829"
},
{
"citation": "Mol Gen Genet. 1974;128(1):73-85",
"pmid": "4150855"
},
{
"citation": "Antonie Van Leeuwenhoek. 1976;42(1-2):33-48",
"pmid": "821392"
},
{
"citation": "J Clin Microbiol. 1980 Mar;11(3):226-33",
"pmid": "6769944"
},
{
"citation": "Mycopathologia. 1983 Nov 21;83(2):87-95",
"pmid": "6366568"
},
{
"citation": "Antonie Van Leeuwenhoek. 1975;41(3):229-38",
"pmid": "1108784"
},
{
"citation": "J Bacteriol. 1972 Jan;109(1):25-33",
"pmid": "4400414"
},
{
"citation": "Curr Genet. 1984 Apr;8(3):181-7",
"pmid": "24177737"
},
{
"citation": "Biochem Soc Trans. 1982 Oct;10(5):328-9",
"pmid": "6128277"
},
{
"citation": "Mycopathologia. 1985 Nov;92(2):121-3",
"pmid": "3908936"
},
{
"citation": "J Cell Comp Physiol. 1954 Jun;43(3):271-81",
"pmid": "13192151"
},
{
"citation": "Mutat Res. 1985 Oct;152(1):15-23",
"pmid": "3900712"
},
{
"citation": "J Cell Sci. 1985 Feb;73:207-20",
"pmid": "3894384"
},
{
"citation": "Sabouraudia. 1982 Sep;20(3):251-60",
"pmid": "6753192"
},
{
"citation": "Arch Mikrobiol. 1972;82(1):38-54",
"pmid": "4554417"
},
{
"citation": "J Biol Chem. 1985 May 25;260(10 ):6069-79",
"pmid": "3997814"
},
{
"citation": "Antonie Van Leeuwenhoek. 1978;44(2):193-201",
"pmid": "375832"
},
{
"citation": "Cell. 1983 Apr;32(4):1279-86",
"pmid": "6301690"
},
{
"citation": "Antonie Van Leeuwenhoek. 1974;40(1):153-60",
"pmid": "4363483"
},
{
"citation": "J Biol Chem. 1984 Jan 25;259(2):1288-93",
"pmid": "6319381"
},
{
"citation": "Arch Microbiol. 1981 Mar;129(1):1-8",
"pmid": "7013727"
}
] | false | eng | Mycopathologia | 7505689 | 0301-486X | Netherlands | [] | "2024-08-13T08:46:10.687633Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Cancer nursing in South Africa: a general overview. | 2(6) | 29-31, 33 | Nursing RSA = Verpleging RSA | [
{
"affiliation": "",
"forename": "H",
"identifier": "",
"initials": "H",
"lastname": "Brink"
}
] | 1987-06 | 3306396 | D049673:History, 20th Century; D006801:Humans; D009369:Neoplasms / Q000401:mortality; D009859:Oncology Nursing / Q000266:history*; D013019:South Africa | D016456:Historical Article; D016428:Journal Article | [] | false | eng | Nurs RSA | 8703817 | 0258-1647 | South Africa | [] | "2024-08-13T08:46:10.688505Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||||
Blood transfusion and autotransfusion during liver transplantation. | 24(6) | 15-6 | NATNews | [
{
"affiliation": "",
"forename": "E",
"identifier": "",
"initials": "E",
"lastname": "Lovell"
},
{
"affiliation": "",
"forename": "M",
"identifier": "",
"initials": "M",
"lastname": "Smith"
}
] | 1987-06 | 3306397 | D001803:Blood Transfusion; D001804:Blood Transfusion, Autologous / Q000295:instrumentation / Q000379:methods; D006801:Humans; D016031:Liver Transplantation | D016428:Journal Article | [] | false | eng | NATNEWS | 1251427 | 0027-6049 | England | [] | "2024-08-13T08:46:10.689124Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||||
Trials of vaccine against AIDS to begin in humans. | 328(6133) | 747 | Nature | [
{
"affiliation": "",
"forename": "C",
"identifier": "",
"initials": "C",
"lastname": "Ezzell"
}
] | 1987 | 3306398 | D000163:Acquired Immunodeficiency Syndrome / Q000517:prevention & control*; D002986:Clinical Trials as Topic; D006801:Humans; D014481:United States; D014612:Vaccines | D016430:Clinical Trial; D016433:News | D014612:Vaccines | 10.1038/328747a0 | [] | false | eng | Nature | 0410462 | 0028-0836 | England | [] | "2024-08-13T08:46:10.690085Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||
Prokaryotic and eukaryotic cell-cycle proteins. | 328(6133) | 766 | Nature | [
{
"affiliation": "",
"forename": "A C",
"identifier": "",
"initials": "AC",
"lastname": "Robinson"
},
{
"affiliation": "",
"forename": "J F",
"identifier": "",
"initials": "JF",
"lastname": "Collins"
},
{
"affiliation": "",
"forename": "W D",
"identifier": "",
"initials": "WD",
"lastname": "Donachie"
}
] | 1987 | 3306399 | D000595:Amino Acid Sequence; D001426:Bacterial Proteins; D004926:Escherichia coli / Q000378:metabolism*; D005656:Fungal Proteins; D015003:Yeasts / Q000378:metabolism* | D003160:Comparative Study; D016422:Letter | D001426:Bacterial Proteins; D005656:Fungal Proteins | 10.1038/328766a0 | [] | false | eng | Nature | 0410462 | 0028-0836 | England | [] | "2024-08-13T08:46:10.690694Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||
Kidney problems. | 329(6134) | 7 | Nature | [] | 1987 | 3306401 | D004992:Ethics, Medical; D006801:Humans; D007194:India; D016030:Kidney Transplantation; D014019:Tissue Donors | D016433:News | 10.1038/329007d0 | [] | false | eng | Nature | 0410462 | 0028-0836 | England | [] | "2024-08-13T08:46:10.691299Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||||
The yeast DNA repair gene RAD6 encodes a ubiquitin-conjugating enzyme. | 329(6135) | 131-4 | The RAD6 gene of the yeast Saccharomyces cerevisiae is required for a variety of cellular functions including DNA repair. The discovery that the RAD6 gene product can catalyse the covalent attachment of ubiquitin to other proteins suggests that the multiple functions of the RAD6 protein are mediated by its ubiquitin-conjugating activity. | Nature | [
{
"affiliation": "",
"forename": "S",
"identifier": "",
"initials": "S",
"lastname": "Jentsch"
},
{
"affiliation": "",
"forename": "J P",
"identifier": "",
"initials": "JP",
"lastname": "McGrath"
},
{
"affiliation": "",
"forename": "A",
"identifier": "",
"initials": "A",
"lastname": "Varshavsky"
}
] | 1987 | 3306404 | D000595:Amino Acid Sequence; D001483:Base Sequence; D003001:Cloning, Molecular; D004260:DNA Repair; D005796:Genes; D005800:Genes, Fungal; D008025:Ligases / Q000235:genetics*; D012441:Saccharomyces cerevisiae / Q000201:enzymology / Q000235:genetics*; D044767:Ubiquitin-Protein Ligases | D016428:Journal Article | D044767:Ubiquitin-Protein Ligases; D008025:Ligases | 10.1038/329131a0 | [] | false | eng | Nature | 0410462 | 0028-0836 | England | [] | "2024-08-13T08:46:10.692040Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Heat shock factor is regulated differently in yeast and HeLa cells. | 329(6134) | 81-4 | When cells are exposed to elevated temperatures, transcription of a small set of genes, the heat-shock genes, is activated. This response is mediated by a short DNA sequence, the heat-shock element (HSE), which is thought to be the binding site for a specific transcription factor. Studies with Drosophila show that this protein binds to HSEs only in heat-shocked cells, suggesting that changes in factor binding are responsible for gene activation. We have investigated the properties of HSE-binding proteins from yeast and HeLa cells. In HeLa cells, binding activity is present only after heat shock. In contrast, control and heat-shocked yeast cells yield the same amount of HSE-binding activity; however, the mobility of protein-HSE complexes on polyacrylamide gels is altered following heat shock. This mobility difference can be significantly reduced by treatment of crude extracts with phosphatase. We propose that the yeast heat-shock factor binds constitutively to DNA but only activates transcription after heat-induced phosphorylation. | Nature | [
{
"affiliation": "",
"forename": "P K",
"identifier": "",
"initials": "PK",
"lastname": "Sorger"
},
{
"affiliation": "",
"forename": "M J",
"identifier": "",
"initials": "MJ",
"lastname": "Lewis"
},
{
"affiliation": "",
"forename": "H R",
"identifier": "",
"initials": "HR",
"lastname": "Pelham"
}
] | 1987 | 3306402 | D005786:Gene Expression Regulation; D005796:Genes; D006367:HeLa Cells / Q000378:metabolism; D006360:Heat-Shock Proteins / Q000235:genetics*; D006358:Hot Temperature; D006801:Humans; D007700:Kinetics; D046911:Macromolecular Substances; D012441:Saccharomyces cerevisiae / Q000235:genetics* / Q000378:metabolism; D015533:Transcriptional Activation | D003160:Comparative Study; D016428:Journal Article; D013485:Research Support, Non-U.S. Gov't | D006360:Heat-Shock Proteins; D046911:Macromolecular Substances | 10.1038/329081a0 | [] | false | eng | Nature | 0410462 | 0028-0836 | England | [] | "2024-08-13T08:46:10.693887Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
History of optics: John Elliot MD (1747-1787). | 329(6134) | 19-20 | Nature | [
{
"affiliation": "",
"forename": "J D",
"identifier": "",
"initials": "JD",
"lastname": "Mollon"
}
] | 1987 | 3306400 | D049671:History, 18th Century; D006801:Humans; D055095:Optics and Photonics / Q000266:history*; D014785:Vision, Ocular; D014796:Visual Perception | D019215:Biography; D016456:Historical Article; D016428:Journal Article | 10.1038/329019a0 | [] | false | eng | Nature | 0410462 | 0028-0836 | England | [] | "2024-08-13T08:46:10.694526Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||||
Cell biology. Ubiquitous cycles of repair. | 329(6135) | 109 | Nature | [
{
"affiliation": "",
"forename": "S",
"identifier": "",
"initials": "S",
"lastname": "Sedgwick"
},
{
"affiliation": "",
"forename": "L",
"identifier": "",
"initials": "L",
"lastname": "Johnston"
}
] | 1987 | 3306403 | D002453:Cell Cycle; D004249:DNA Damage; D004260:DNA Repair; D005800:Genes, Fungal; D012441:Saccharomyces cerevisiae / Q000235:genetics* | D016433:News | 10.1038/329109a0 | [] | false | eng | Nature | 0410462 | 0028-0836 | England | [] | "2024-08-13T08:46:10.695094Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||||
Failure of familial Alzheimer's disease to segregate with the A4-amyloid gene in several European families. | 329(6135) | 153-5 | The gene coding for the amyloid protein, a component of neuritic plaques found in brain tissue from patients with Alzheimer's disease, has been localized to chromosome 21, and neighbouring polymorphic DNA markers segregate with Alzheimer's disease in several large families. These data, and the association of Alzheimer's disease with Down's syndrome, suggest that overproduction of the amyloid protein, or production of an abnormal variant of the protein, may be the underlying pathological change causing Alzheimer's disease. We have identified a restriction fragment length polymorphism of the A4-amyloid gene, and find recombinants in two Alzheimer's disease families between Alzheimer's disease and the A4-amyloid locus. This demonstrates that the gene for plaque core A4-amyloid cannot be the locus of a defect causing Alzheimer's disease in these families. These data indicate that alterations in the plaque core amyloid gene cannot explain the molecular pathology for all cases of Alzheimer's disease. | Nature | [
{
"affiliation": "",
"forename": "C",
"identifier": "",
"initials": "C",
"lastname": "Van Broeckhoven"
},
{
"affiliation": "",
"forename": "A M",
"identifier": "",
"initials": "AM",
"lastname": "Genthe"
},
{
"affiliation": "",
"forename": "A",
"identifier": "",
"initials": "A",
"lastname": "Vandenberghe"
},
{
"affiliation": "",
"forename": "B",
"identifier": "",
"initials": "B",
"lastname": "Horsthemke"
},
{
"affiliation": "",
"forename": "H",
"identifier": "",
"initials": "H",
"lastname": "Backhovens"
},
{
"affiliation": "",
"forename": "P",
"identifier": "",
"initials": "P",
"lastname": "Raeymaekers"
},
{
"affiliation": "",
"forename": "W",
"identifier": "",
"initials": "W",
"lastname": "Van Hul"
},
{
"affiliation": "",
"forename": "A",
"identifier": "",
"initials": "A",
"lastname": "Wehnert"
},
{
"affiliation": "",
"forename": "J",
"identifier": "",
"initials": "J",
"lastname": "Gheuens"
},
{
"affiliation": "",
"forename": "P",
"identifier": "",
"initials": "P",
"lastname": "Cras"
}
] | 1987 | 3306405 | D000328:Adult; D000544:Alzheimer Disease / Q000235:genetics*; D000682:Amyloid / Q000235:genetics*; D016229:Amyloid beta-Peptides; D002874:Chromosome Mapping; D002891:Chromosomes, Human, Pair 21; D005260:Female; D005796:Genes; D008040:Genetic Linkage; D006801:Humans; D008297:Male; D010375:Pedigree; D011110:Polymorphism, Genetic; D011498:Protein Precursors / Q000235:genetics | D002363:Case Reports; D016428:Journal Article; D013485:Research Support, Non-U.S. Gov't | D000682:Amyloid; D016229:Amyloid beta-Peptides; D011498:Protein Precursors | 10.1038/329153a0 | [] | false | eng | Nature | 0410462 | 0028-0836 | England | [] | "2024-08-13T08:46:10.696289Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
A liver-stage-specific antigen of Plasmodium falciparum characterized by gene cloning. | 329(6135) | 164-7 | The liver phase of development of malaria parasites has been studied only recently and remains poorly understood compared to the other stages such as sporozoïtes, merozoïtes and gametes. Access to liver forms of Plasmodium falciparum has been improved by the development of in vivo and in vitro propagation methods, but the yield of mature schizonts remains limited and does not allow a detailed antigenic analysis. To date, only immunofluorescence assays (IFA) have permitted a description of a species and liver-stage-specific antigen(s) (LSA; ref. 3). Monospecific antibodies to these antigens have not been obtained due either to difficulty in immunizing mice (against LSA), or to poor stability of human monoclonal antibodies. Therefore, as a means of characterizing the LSA, we used an alternative immunological approach to identify clones of the corresponding LSA genes. We describe here the isolation of a DNA sequence coding for a P. falciparum liver-stage-specific antigen composed of repeats of 17 amino-acids, which is immunogenic in man. | Nature | [
{
"affiliation": "",
"forename": "C",
"identifier": "",
"initials": "C",
"lastname": "Guerin-Marchand"
},
{
"affiliation": "",
"forename": "P",
"identifier": "",
"initials": "P",
"lastname": "Druilhe"
},
{
"affiliation": "",
"forename": "B",
"identifier": "",
"initials": "B",
"lastname": "Galey"
},
{
"affiliation": "",
"forename": "A",
"identifier": "",
"initials": "A",
"lastname": "Londono"
},
{
"affiliation": "",
"forename": "J",
"identifier": "",
"initials": "J",
"lastname": "Patarapotikul"
},
{
"affiliation": "",
"forename": "R L",
"identifier": "",
"initials": "RL",
"lastname": "Beaudoin"
},
{
"affiliation": "",
"forename": "C",
"identifier": "",
"initials": "C",
"lastname": "Dubeaux"
},
{
"affiliation": "",
"forename": "A",
"identifier": "",
"initials": "A",
"lastname": "Tartar"
},
{
"affiliation": "",
"forename": "O",
"identifier": "",
"initials": "O",
"lastname": "Mercereau-Puijalon"
},
{
"affiliation": "",
"forename": "G",
"identifier": "",
"initials": "G",
"lastname": "Langsley"
}
] | 1987 | 3306406 | D000328:Adult; D000595:Amino Acid Sequence; D000818:Animals; D000953:Antigens, Protozoan / Q000032:analysis / Q000235:genetics*; D001483:Base Sequence; D002427:Cebidae; D003001:Cloning, Molecular; D005260:Female; D005455:Fluorescent Antibody Technique; D005796:Genes; D006801:Humans; D008099:Liver / Q000469:parasitology* / Q000473:pathology; D008288:Malaria / Q000473:pathology; D010963:Plasmodium falciparum / Q000235:genetics* / Q000276:immunology | D016428:Journal Article; D013485:Research Support, Non-U.S. Gov't | D000953:Antigens, Protozoan | 10.1038/329164a0 | [] | false | eng | Nature | 0410462 | 0028-0836 | England | [] | "2024-08-13T08:46:10.697553Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Catalysis of protein folding by prolyl isomerase. | 329(6136) | 268-70 | Rates of protein folding reactions vary considerably. Some denatured proteins regain the native conformation within milliseconds or seconds, whereas others refold very slowly in the time range of minutes or hours. Varying folding rates are observed not only for different proteins, but can also be detected for single polypeptide species. This originates from the co-existence of fast- and slow-folding forms of the unfolded protein, which regain the native state with different rates. The proline hypothesis provides a plausible explanation for this heterogeneity. It assumes that the slow-folding molecules possess non-native isomers of peptide bonds between proline and another residue, and that crucial steps in the refolding of the slow-folding molecules are limited in rate by the slow reisomerization of such incorrect proline peptide bonds. Recently the enzyme peptidyl-prolyl cis-trans isomerase (PPIase) was discovered and purified from pig kidney. It catalyses efficiently the cis in equilibrium trans isomerization of proline imidic peptide bonds in oligopeptides. Here we show that it also catalyses slow steps in the refolding of a number of proteins of which fast- and slow-folding species have been observed and where it was suggested that proline isomerization was involved in slow refolding. The efficiency of catalysis depends on the accessibility for the isomerase of the particular proline peptide bonds in the refolding protein chain. | Nature | [
{
"affiliation": "",
"forename": "K",
"identifier": "",
"initials": "K",
"lastname": "Lang"
},
{
"affiliation": "",
"forename": "F X",
"identifier": "",
"initials": "FX",
"lastname": "Schmid"
},
{
"affiliation": "",
"forename": "G",
"identifier": "",
"initials": "G",
"lastname": "Fischer"
}
] | 1987 | 3306408 | D000591:Amino Acid Isomerases / Q000378:metabolism*; D000818:Animals; D002384:Catalysis; D007668:Kidney / Q000201:enzymology; D007700:Kinetics; D010446:Peptide Fragments; D019696:Peptidylprolyl Isomerase; D011392:Proline / Q000378:metabolism; D011487:Protein Conformation; D012259:Ribonuclease, Pancreatic; D013552:Swine | D016428:Journal Article | D010446:Peptide Fragments; D011392:Proline; D012259:Ribonuclease, Pancreatic; D000591:Amino Acid Isomerases; D019696:Peptidylprolyl Isomerase | 10.1038/329268a0 | [] | false | eng | Nature | 0410462 | 0028-0836 | England | [] | "2024-08-13T08:46:10.699654Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
What progress has been made in creating a national system for organ procurement and transplantation? | 1(7) | 21-30, 34 | Nephrology news & issues | [] | 1987-08 | 3306412 | D006801:Humans; D016030:Kidney Transplantation; D009927:Tissue and Organ Procurement / Q000191:economics / Q000331:legislation & jurisprudence* | D016428:Journal Article | [] | false | eng | Nephrol News Issues | 8709753 | 0896-1263 | United States | [] | "2024-08-13T08:46:10.700336Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||||
Production of recombinant insulin begins. | 329(6136) | 193 | Nature | [
{
"affiliation": "",
"forename": "S",
"identifier": "",
"initials": "S",
"lastname": "Dickman"
}
] | 1987 | 3306407 | D005860:Germany, West; D007328:Insulin / Q000096:biosynthesis*; D011994:Recombinant Proteins / Q000096:biosynthesis* | D016433:News | D007328:Insulin; D011994:Recombinant Proteins | 10.1038/329193b0 | [] | false | eng | Nature | 0410462 | 0028-0836 | England | [] | "2024-08-13T08:46:10.700854Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||
A structural model for the retroviral proteases. | 329(6137) | 351-4 | In many retroviruses the 5' end of the pol gene codes for a protease vital for the processing of the gag polyprotein into the separate core proteins. In some viruses this protease is encoded at the 3' end of the gag gene, or between the gag and pol genes in a different reading frame to either. A sequence, Asp-Thr-Gly, which is conserved in retroviral proteases is also conserved in the active sites of aspartic proteases, an observation which has led to the suggestion that the retroviral proteases could belong to this family. We have examined the sequences of the aspartic and retroviral protease families, using pattern-recognition, structure prediction and molecular modelling techniques, and conclude that the viral protease sequences probably correspond to a single domain of an aspartic protease and may function in a dimeric form. We have constructed a model of the pol-protease of human immunodeficiency virus 1 (HIV-1) to test this hypothesis. | Nature | [
{
"affiliation": "",
"forename": "L H",
"identifier": "",
"initials": "LH",
"lastname": "Pearl"
},
{
"affiliation": "",
"forename": "W R",
"identifier": "",
"initials": "WR",
"lastname": "Taylor"
}
] | 1987 | 3306411 | D000595:Amino Acid Sequence; D016282:Aspartic Acid Endopeptidases; D001665:Binding Sites; D010450:Endopeptidases; D006678:HIV / Q000201:enzymology; D016333:HIV Protease; D046911:Macromolecular Substances; D010447:Peptide Hydrolases; D011487:Protein Conformation; D012190:Retroviridae / Q000201:enzymology* | D003160:Comparative Study; D016428:Journal Article | D046911:Macromolecular Substances; D010450:Endopeptidases; D010447:Peptide Hydrolases; D016282:Aspartic Acid Endopeptidases; D016333:HIV Protease | 10.1038/329351a0 | [] | false | eng | Nature | 0410462 | 0028-0836 | England | [] | "2024-08-13T08:46:10.701533Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Is dose adjustment of non-steroidal anti-inflammatory drugs necessary in the elderly? A review of the pharmacokinetics of NSAID in the aged. | 30(5-6) | 248-58 | The Netherlands journal of medicine | [
{
"affiliation": "",
"forename": "P A",
"identifier": "",
"initials": "PA",
"lastname": "Jansen"
},
{
"affiliation": "",
"forename": "C A",
"identifier": "",
"initials": "CA",
"lastname": "van Ginneken"
},
{
"affiliation": "",
"forename": "F W",
"identifier": "",
"initials": "FW",
"lastname": "Gribnau"
}
] | 1987-06 | 3306414 | D000368:Aged; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage / Q000378:metabolism*; D005260:Female; D006801:Humans; D007700:Kinetics; D008297:Male | D016428:Journal Article; D016454:Review | D000894:Anti-Inflammatory Agents, Non-Steroidal | [] | false | eng | Neth J Med | 0356133 | 0300-2977 | Netherlands | [] | "2024-08-13T08:46:10.702558Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||||
A case of reactive arthritis following Yersinia pseudotuberculosis enteritis. | 30(5-6) | 278-80 | The Netherlands journal of medicine | [
{
"affiliation": "",
"forename": "R J",
"identifier": "",
"initials": "RJ",
"lastname": "Lionarons"
},
{
"affiliation": "",
"forename": "M",
"identifier": "",
"initials": "M",
"lastname": "van Zoeren"
},
{
"affiliation": "",
"forename": "J N",
"identifier": "",
"initials": "JN",
"lastname": "Verhagen"
},
{
"affiliation": "",
"forename": "H A",
"identifier": "",
"initials": "HA",
"lastname": "Lammers"
}
] | 1987-06 | 3306415 | D000328:Adult; D001168:Arthritis / Q000209:etiology*; D004751:Enteritis / Q000150:complications*; D006801:Humans; D008297:Male; D015009:Yersinia Infections / Q000150:complications*; D015012:Yersinia pseudotuberculosis Infections / Q000150:complications* | D002363:Case Reports; D016428:Journal Article | [] | false | eng | Neth J Med | 0356133 | 0300-2977 | Netherlands | [] | "2024-08-13T08:46:10.703384Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||||
The heat shock response of E. coli is regulated by changes in the concentration of sigma 32. | 329(6137) | 348-51 | Cells subjected to a heat shock, or a variety of other stresses increase the synthesis of a set of proteins, known as heat shock proteins. This response is apparently universal, occurring in the entire range from bacterial to mammalian cells. In Escherichia coli heat shock protein synthesis transiently increases following a shift from 30 degrees C to 42 degrees C as a result of changes in transcription initiation at heat shock promoters. Heat shock promoters are recognized by RNA polymerase containing a sigma factor of relative molecular mass (Mr) 32,000 (32K) E sigma 32 and not E sigma 70, the major form of RNA polymerase holoenzyme. To determine whether changes in the concentration of sigma 32 regulate this response, we measured the amount of sigma 32 before and after shift to high temperature and found that it increased transiently during heat shock as a result of changes in sigma 32 synthesis and stability. Our results indicate that sigma 32 is directly responsible for regulation of the heat shock response. | Nature | [
{
"affiliation": "",
"forename": "D B",
"identifier": "",
"initials": "DB",
"lastname": "Straus"
},
{
"affiliation": "",
"forename": "W A",
"identifier": "",
"initials": "WA",
"lastname": "Walter"
},
{
"affiliation": "",
"forename": "C A",
"identifier": "",
"initials": "CA",
"lastname": "Gross"
}
] | 1987 | 3306410 | D001426:Bacterial Proteins / Q000096:biosynthesis / Q000235:genetics; D012321:DNA-Directed RNA Polymerases / Q000378:metabolism; D004591:Electrophoresis, Polyacrylamide Gel; D004926:Escherichia coli / Q000378:metabolism*; D005786:Gene Expression Regulation; D006360:Heat-Shock Proteins / Q000096:biosynthesis* / Q000235:genetics; D006358:Hot Temperature; D007118:Immunoassay; D007700:Kinetics; D007763:Lac Operon; D009876:Operon; D011401:Promoter Regions, Genetic; D012333:RNA, Messenger / Q000096:biosynthesis; D012808:Sigma Factor / Q000096:biosynthesis* / Q000235:genetics; D014157:Transcription Factors / Q000096:biosynthesis* | D016428:Journal Article; D013487:Research Support, U.S. Gov't, P.H.S. | D001426:Bacterial Proteins; D006360:Heat-Shock Proteins; D012333:RNA, Messenger; D012808:Sigma Factor; D014157:Transcription Factors; D012321:DNA-Directed RNA Polymerases | 10.1038/329348a0 | [] | false | eng | Nature | 0410462 | 0028-0836 | England | [] | "2024-08-13T08:46:10.704276Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
An evaluation of the dialysate solutions for continuous ambulatory peritoneal dialysis. | 30(5-6) | 301-7 | The Netherlands journal of medicine | [
{
"affiliation": "",
"forename": "N",
"identifier": "",
"initials": "N",
"lastname": "Lameire"
}
] | 1987-06 | 3306416 | D004573:Electrolytes; D006801:Humans; D009995:Osmosis; D010531:Peritoneal Dialysis, Continuous Ambulatory; D012996:Solutions / Q000592:standards* | D016428:Journal Article; D016454:Review | D004573:Electrolytes; D012996:Solutions | [] | false | eng | Neth J Med | 0356133 | 0300-2977 | Netherlands | [] | "2024-08-13T08:46:10.706221Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||||
A novel HLA class II molecule (DR alpha-DQ beta) created by mismatched isotype pairing. | 329(6137) | 339-41 | Human major histocompatibility complex (MHC) class II molecules are heterodimeric glycoproteins composed of non-covalently associated alpha and beta chains. Only isotype-matched alpha-beta associations have been described in man; these can occur either by cis- or trans-complementation (HLA-DR, DQ, DP). Here evidence is provided for the existence of a new type of hybrid molecule (DR alpha-DQ beta) arising by mixed-isotype pairing in human B-cell lines. Class II isotype-mismatched heterodimers have been recently reported in the mouse after transfection of class II genes, and our data demonstrate that such interisotypic pairing can occur in untransfected cells. This crosspairing greatly enhances the repertoire of the class II antigens that regulate immune responses and leads us to reconsider the HLA-disease association. | Nature | [
{
"affiliation": "",
"forename": "V",
"identifier": "",
"initials": "V",
"lastname": "Lotteau"
},
{
"affiliation": "",
"forename": "L",
"identifier": "",
"initials": "L",
"lastname": "Teyton"
},
{
"affiliation": "",
"forename": "D",
"identifier": "",
"initials": "D",
"lastname": "Burroughs"
},
{
"affiliation": "",
"forename": "D",
"identifier": "",
"initials": "D",
"lastname": "Charron"
}
] | 1987 | 3306409 | D000911:Antibodies, Monoclonal; D001402:B-Lymphocytes / Q000276:immunology*; D002460:Cell Line; D004591:Electrophoresis, Polyacrylamide Gel; D006681:HLA-D Antigens; D006683:HLA-DQ Antigens; D006684:HLA-DR Antigens; D006801:Humans; D007163:Immunosorbent Techniques; D007525:Isoelectric Focusing; D046911:Macromolecular Substances; D055503:Protein Multimerization | D016428:Journal Article; D013485:Research Support, Non-U.S. Gov't | D000911:Antibodies, Monoclonal; D006681:HLA-D Antigens; D006683:HLA-DQ Antigens; D006684:HLA-DR Antigens; D046911:Macromolecular Substances | 10.1038/329339a0 | [] | false | eng | Nature | 0410462 | 0028-0836 | England | [] | "2024-08-13T08:46:10.707104Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Oxalate dynamics in chronic renal failure. Comparison with normal subjects and patients with primary hyperoxaluria. | 46(3) | 253-7 | In order to separate the effect of oxalate retention in primary hyperoxaluria with renal failure from that of excessive oxalate synthesis and to determine the optimum time for renal transplantation in primary hyperoxaluria, we have studied a series of patients with different degrees of renal failure due to other causes. The results were compared with those obtained in studies on 8 patients with primary hyperoxaluria at different levels of residual overall renal function. In the patients with renal failure unrelated to primary hyperoxaluria, oxalate retention increases rapidly when the glomerular filtration rate (GFR) decreases below about 20 ml X min-1. These results suggest that the reduced renal excretory contribution to oxalate accumulation in primary hyperoxaluria would be expected to be particularly important in this range of GFR. In primary hyperoxaluria, oxalate retention occurs when GFR is only a little below the reference range and measures to remove oxalate from the body should be considered when the GFR falls below 40 ml X min-1 X 1.73 m-2, with a view to their introduction when the GFR is in the range 20-25 ml X min-1 X 1.73 m-2. | Nephron | [
{
"affiliation": "",
"forename": "S H",
"identifier": "",
"initials": "SH",
"lastname": "Morgan"
},
{
"affiliation": "",
"forename": "P",
"identifier": "",
"initials": "P",
"lastname": "Purkiss"
},
{
"affiliation": "",
"forename": "R W",
"identifier": "",
"initials": "RW",
"lastname": "Watts"
},
{
"affiliation": "",
"forename": "M A",
"identifier": "",
"initials": "MA",
"lastname": "Mansell"
}
] | 1987 | 3306417 | D002250:Carbon Radioisotopes; D005919:Glomerular Filtration Rate; D006801:Humans; D006959:Hyperoxaluria / Q000378:metabolism*; D006960:Hyperoxaluria, Primary / Q000378:metabolism* / Q000628:therapy; D007676:Kidney Failure, Chronic / Q000378:metabolism* / Q000628:therapy; D016030:Kidney Transplantation; D009942:Organometallic Compounds; D010070:Oxalates / Q000378:metabolism*; D004369:Pentetic Acid; D006435:Renal Dialysis; D016284:Technetium Tc 99m Pentetate | D003160:Comparative Study; D016428:Journal Article | D002250:Carbon Radioisotopes; D009942:Organometallic Compounds; D010070:Oxalates; D004369:Pentetic Acid; D016284:Technetium Tc 99m Pentetate | 10.1159/000184364 | [] | false | eng | Nephron | 0331777 | 1660-8151 | Switzerland | [] | "2024-08-13T08:46:10.707971Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Anti-HTLV-III antibodies in dialyzed or transplanted patients in Spain. | 46(3) | 325-6 | Nephron | [
{
"affiliation": "",
"forename": "J",
"identifier": "",
"initials": "J",
"lastname": "Teixidó"
},
{
"affiliation": "",
"forename": "E",
"identifier": "",
"initials": "E",
"lastname": "Argelagués"
},
{
"affiliation": "",
"forename": "A",
"identifier": "",
"initials": "A",
"lastname": "Caralps"
},
{
"affiliation": "",
"forename": "R",
"identifier": "",
"initials": "R",
"lastname": "Romero"
},
{
"affiliation": "",
"forename": "F",
"identifier": "",
"initials": "F",
"lastname": "Oppenheimer"
},
{
"affiliation": "",
"forename": "M J",
"identifier": "",
"initials": "MJ",
"lastname": "Ricart"
},
{
"affiliation": "",
"forename": "J",
"identifier": "",
"initials": "J",
"lastname": "Martorell"
},
{
"affiliation": "",
"forename": "J M",
"identifier": "",
"initials": "JM",
"lastname": "Griñó"
},
{
"affiliation": "",
"forename": "R",
"identifier": "",
"initials": "R",
"lastname": "Solá"
}
] | 1987 | 3306418 | D000914:Antibodies, Viral / Q000032:analysis*; D006678:HIV / Q000276:immunology*; D006801:Humans; D016030:Kidney Transplantation; D006435:Renal Dialysis; D013030:Spain; D065227:Transfusion Reaction | D016422:Letter | D000914:Antibodies, Viral | 10.1159/000184378 | [] | false | eng | Nephron | 0331777 | 1660-8151 | Switzerland | [] | "2024-08-13T08:46:10.709094Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||
Captopril therapy in preeclampsia. | 46(3) | 329-30 | Nephron | [
{
"affiliation": "",
"forename": "B H",
"identifier": "",
"initials": "BH",
"lastname": "Hurault de Ligny"
},
{
"affiliation": "",
"forename": "J P",
"identifier": "",
"initials": "JP",
"lastname": "Ryckelynck"
},
{
"affiliation": "",
"forename": "P",
"identifier": "",
"initials": "P",
"lastname": "Mintz"
},
{
"affiliation": "",
"forename": "G",
"identifier": "",
"initials": "G",
"lastname": "Levy"
},
{
"affiliation": "",
"forename": "G",
"identifier": "",
"initials": "G",
"lastname": "Muller"
}
] | 1987 | 3306419 | D000328:Adult; D002216:Captopril / Q000097:blood / Q000627:therapeutic use*; D005260:Female; D006801:Humans; D011225:Pre-Eclampsia / Q000188:drug therapy*; D011247:Pregnancy; D011263:Pregnancy Trimester, Third | D002363:Case Reports; D016422:Letter | D002216:Captopril | 10.1159/000184380 | [] | false | eng | Nephron | 0331777 | 1660-8151 | Switzerland | [] | "2024-08-13T08:46:10.710138Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||
H.R. 2470, the Medicare Catastrophic Protection Act of 1987. | 5(4) | 155-6 | Nursing economic$ | [] | 1987 | 3306413 | D002388:Catastrophic Illness / Q000191:economics*; D006801:Humans; D006278:Medicare / Q000331:legislation & jurisprudence*; D014481:United States | D016428:Journal Article | [] | false | eng | Nurs Econ | 8404213 | 0746-1739 | United States | [] | "2024-08-13T08:46:10.710739Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||||
Immunosuppression and renal transplantation. | 46 Suppl 1() | 1-4 | Nephron | [
{
"affiliation": "",
"forename": "A P",
"identifier": "",
"initials": "AP",
"lastname": "Monaco"
}
] | 1987 | 3306420 | D006084:Graft Rejection; D006801:Humans; D007165:Immunosuppression Therapy; D016030:Kidney Transplantation; D008991:Monitoring, Physiologic | D016428:Journal Article; D016454:Review | 10.1159/000184427 | [] | false | eng | Nephron | 0331777 | 1660-8151 | Switzerland | [] | "2024-08-13T08:46:10.712308Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||||
OKT3: First-dose safety and success. | 46 Suppl 1() | 12-8 | Orthoclone OKT3 is a murine monoclonal antibody that has been shown to be effective in reversing acute rejection episodes. In a randomized, multicenter trial, Orthoclone OKT3 reversed 94% of acute rejection episodes; conventional treatments reversed only 75%. However, early trials also disclosed some limitations of OKT3 therapy, such as a severe febrile or bronchospastic response following the initial injection, recurrent rejection episodes after discontinuation of OKT3 administration, or the host's production of antibodies to the murine immunoglobulin. In later experiments modifications and precautions applied to the therapeutic helped to control first-dose reactions and decrease antibody production from 86 to 39%. Furthermore, recurrent rejection episodes occurring after discontinuation of OKT3 therapy in azathioprine-prednisone-treated patients have been shown to be reversible in most cases: a 75% rate of long-term (14- to 26-month) allograft survival has been achieved in these patients. More recently, OKT3 treatment administered to allograft recipients receiving cyclosporin has been shown to benefit 15-20% of patients when administered at the time of rejection. This combination approach not only reverses the rejection, but also seems to significantly reduce the incidence of subsequent rejection episodes. OKT3 has raised clinical immunosuppressive specificity to a higher level than previous therapies such as steroids or cytotoxic agents. OKT3 appears to be safe and effective therapy for patients receiving cyclosporin or azathioprine-prednisone therapy. Despite certain unresolved limitations, it may be a successful prototype for future, even more highly specific, immunosuppressive protocols. | Nephron | [
{
"affiliation": "",
"forename": "A B",
"identifier": "",
"initials": "AB",
"lastname": "Cosimi"
}
] | 1987 | 3306421 | D000911:Antibodies, Monoclonal / Q000008:administration & dosage / Q000009:adverse effects / Q000627:therapeutic use*; D002986:Clinical Trials as Topic; D006084:Graft Rejection; D006801:Humans; D016030:Kidney Transplantation; D011654:Pulmonary Edema / Q000209:etiology; D011897:Random Allocation | D016430:Clinical Trial; D016428:Journal Article | D000911:Antibodies, Monoclonal | 10.1159/000184430 | [] | false | eng | Nephron | 0331777 | 1660-8151 | Switzerland | [] | "2024-08-13T08:46:10.712902Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Use of OKT3 with cyclosporin and steroids for reversal of acute kidney and liver allograft rejection. | 46 Suppl 1() | 19-33 | OKT3 monoclonal antibody therapy was added to preexisting baseline immunosuppressive treatment with ciclosporin and steroids to treat rejection in 52 recipients of cadaveric livers and 10 recipients of cadaveric kidneys. Rejection was controlled in 75% of patients treated, often after high-dose steroid therapy had failed. Rejection recurred during the 17-month follow-up period, after completion of OKT3, in only 25% of the patients who had responded. The safety and effectiveness of this monoclonal therapy, added to ciclosporin and steroids, has been established in this study. | Nephron | [
{
"affiliation": "",
"forename": "J J",
"identifier": "",
"initials": "JJ",
"lastname": "Fung"
},
{
"affiliation": "",
"forename": "A J",
"identifier": "",
"initials": "AJ",
"lastname": "Demetris"
},
{
"affiliation": "",
"forename": "K A",
"identifier": "",
"initials": "KA",
"lastname": "Porter"
},
{
"affiliation": "",
"forename": "S",
"identifier": "",
"initials": "S",
"lastname": "Iwatsuki"
},
{
"affiliation": "",
"forename": "R D",
"identifier": "",
"initials": "RD",
"lastname": "Gordon"
},
{
"affiliation": "",
"forename": "C O",
"identifier": "",
"initials": "CO",
"lastname": "Esquivel"
},
{
"affiliation": "",
"forename": "R",
"identifier": "",
"initials": "R",
"lastname": "Jaffe"
},
{
"affiliation": "",
"forename": "A",
"identifier": "",
"initials": "A",
"lastname": "Tzakis"
},
{
"affiliation": "",
"forename": "B W",
"identifier": "",
"initials": "BW",
"lastname": "Shaw"
},
{
"affiliation": "",
"forename": "T E",
"identifier": "",
"initials": "TE",
"lastname": "Starzl"
}
] | 1987 | 3306422 | D000293:Adolescent; D000328:Adult; D000911:Antibodies, Monoclonal / Q000008:administration & dosage*; D002648:Child; D002675:Child, Preschool; D002986:Clinical Trials as Topic; D003524:Cyclosporins / Q000008:administration & dosage*; D004359:Drug Therapy, Combination; D006084:Graft Rejection; D006801:Humans; D007223:Infant; D016030:Kidney Transplantation; D008099:Liver / Q000473:pathology; D016031:Liver Transplantation; D008875:Middle Aged; D013256:Steroids / Q000008:administration & dosage* | D016430:Clinical Trial; D016428:Journal Article; D013485:Research Support, Non-U.S. Gov't; D013486:Research Support, U.S. Gov't, Non-P.H.S.; D013487:Research Support, U.S. Gov't, P.H.S. | D000911:Antibodies, Monoclonal; D003524:Cyclosporins; D013256:Steroids | 10.1159/000184431 | [
{
"citation": "Immunol Rev. 1982;63:73-110",
"pmid": "6804370"
},
{
"citation": "Transplantation. 1981 Dec;32(6):535-9",
"pmid": "7041358"
},
{
"citation": "Transplantation. 1981 Feb;31(2):143-5",
"pmid": "6266084"
},
{
"citation": "Surg Gynecol Obstet. 1982 Jun;154(6):819-25",
"pmid": "7043758"
},
{
"citation": "J Immunol. 1983 Nov;131(5):2356-61",
"pmid": "6605385"
},
{
"citation": "Ann Surg. 1976 Sep;184(3):352-68",
"pmid": "786192"
},
{
"citation": "Lancet. 1968 Jun 1;1(7553):1174-6",
"pmid": "4172292"
},
{
"citation": "Surgery. 1969 Sep;66(3):546-9",
"pmid": "4896070"
},
{
"citation": "Transplant Proc. 1981 Mar;13(1 Pt 1):499-503",
"pmid": "7022882"
},
{
"citation": "J Nucl Med. 1972 Nov;13(11):795-800",
"pmid": "4562617"
},
{
"citation": "Surg Gynecol Obstet. 1963 Oct;117:385-95",
"pmid": "14065716"
},
{
"citation": "Transplantation. 1984 Nov;38(5):469-74",
"pmid": "6388068"
},
{
"citation": "J Immunol. 1984 Jul;133(1):129-32",
"pmid": "6327822"
},
{
"citation": "J Pediatr. 1986 Mar;108(3):393-8",
"pmid": "3512808"
},
{
"citation": "Proc Natl Acad Sci U S A. 1981 Mar;78(3):1805-8",
"pmid": "6165018"
},
{
"citation": "Nature. 1975 Aug 7;256(5517):495-7",
"pmid": "1172191"
},
{
"citation": "Gastroenterology. 1979 Aug;77(2):375-88",
"pmid": "376395"
},
{
"citation": "N Engl J Med. 1981 Aug 6;305(6):308-14",
"pmid": "6454075"
},
{
"citation": "Transplantation. 1984 Dec;38(6):695-701",
"pmid": "6390834"
},
{
"citation": "J Immunol. 1980 Jun;124(6):2708-13",
"pmid": "6966296"
},
{
"citation": "Transplantation. 1983 Nov;36(5):587-9",
"pmid": "6356523"
},
{
"citation": "Surg Gynecol Obstet. 1980 Jul;151(1):17-26",
"pmid": "6992310"
},
{
"citation": "Surg Gynecol Obstet. 1967 Feb;124(2):301-8",
"pmid": "4163340"
},
{
"citation": "Am J Med. 1965 Aug;39:184-98",
"pmid": "14320684"
},
{
"citation": "Int J Immunopharmacol. 1981;3(3):183-6",
"pmid": "6457003"
},
{
"citation": "Semin Liver Dis. 1985 Nov;5(4):357-68",
"pmid": "3909430"
},
{
"citation": "Ann Surg. 1968 Sep;168(3):392-415",
"pmid": "4877589"
},
{
"citation": "J Immunol. 1984 Jul;133(1):123-8",
"pmid": "6327821"
},
{
"citation": "Cell. 1982 Oct;30(3):735-43",
"pmid": "6982759"
},
{
"citation": "Science. 1979 Oct 19;206(4416):347-9",
"pmid": "314668"
},
{
"citation": "Lancet. 1978 Dec 23-30;2(8104-5):1323-7",
"pmid": "82836"
},
{
"citation": "Circulation. 1972 May;45(5 Suppl 1):I147-53",
"pmid": "4554349"
},
{
"citation": "Transplantation. 1979 Dec;28(6):461-4",
"pmid": "390784"
},
{
"citation": "N Engl J Med. 1985 Aug 8;313(6):337-42",
"pmid": "2861567"
},
{
"citation": "Transplant Proc. 1985 Feb;17(1):259-263",
"pmid": "21151802"
},
{
"citation": "Nature. 1983 Jun 16-22;303(5918):625-7",
"pmid": "6343888"
},
{
"citation": "J Exp Med. 1984 Nov 1;160(5):1284-99",
"pmid": "6208306"
},
{
"citation": "Transplant Proc. 1981 Mar;13(1 Pt 1):286-8",
"pmid": "7022840"
},
{
"citation": "Transplantation. 1984 Dec;38(6):720-6",
"pmid": "6239416"
}
] | false | eng | Nephron | 0331777 | 1660-8151 | Switzerland | [
{
"agency": "NIDDK NIH HHS",
"country": "United States",
"grant_acronym": "DK",
"grant_id": "R01 DK029961-19"
},
{
"agency": "NIADDK NIH HHS",
"country": "United States",
"grant_acronym": "AM",
"grant_id": "AM-29961"
}
] | "2024-08-13T08:46:10.714714Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
OKT3 rescue in refractory renal rejection. | 46 Suppl 1() | 34-40 | A community hospital-based transplant program participated in the study of Orthoclone OKT3 as a treatment for refractory renal rejection. A total of 16 patients receiving varied oral immunosuppressive regimens, and developing steroid-resistant acute rejection, were treated with OKT3. Thirteen of the 16 patients completed a 10-day course of therapy with reversal of rejection in all 13. Rerejection occurred in 1 of the 13 patients; the remaining 12 have normal renal function. Fever, chills, and diarrhea were the most common side effects, lasting an average of 72 h. Based on this experience, OKT3 was found to be an effective drug in refractory rejection with minimal complications or risks of administration. | Nephron | [
{
"affiliation": "",
"forename": "L",
"identifier": "",
"initials": "L",
"lastname": "Kahana"
},
{
"affiliation": "",
"forename": "J",
"identifier": "",
"initials": "J",
"lastname": "Baxter"
}
] | 1987 | 3306423 | D000328:Adult; D000911:Antibodies, Monoclonal / Q000008:administration & dosage / Q000627:therapeutic use*; D002986:Clinical Trials as Topic; D005260:Female; D006084:Graft Rejection; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D016030:Kidney Transplantation; D008297:Male; D008875:Middle Aged; D012078:Renal Artery Obstruction / Q000209:etiology; D013927:Thrombosis / Q000209:etiology | D002363:Case Reports; D016430:Clinical Trial; D016428:Journal Article | D000911:Antibodies, Monoclonal; D007166:Immunosuppressive Agents | 10.1159/000184432 | [] | false | eng | Nephron | 0331777 | 1660-8151 | Switzerland | [] | "2024-08-13T08:46:10.715947Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Therapeutic use of OKT3 monoclonal antibody for acute renal allograft rejection. | 46 Suppl 1() | 41-7 | OKT3, a murine monoclonal anti-T-cell antibody, was used to treat acute renal allograft rejection crises in 140 patients. When used for primary treatment of initial rejections, it was effective in all 20 recipients of related-donor (RD) grafts and in 70 of 74 recipients of cadaver-donor (CD) grafts. OKT3 was also used for resistant rejection unresponsive to conventional antirejection drugs and was effective in 11 of 13 RD and in 26 of 33 CD recipients. Rerejection occurred in 58% of patients in the OKT3 primary treatment group and in 35% of patients in the OKT3 rescue group. Fifty-nine percent of the patients produced anti-OKT3 antibodies. Nearly all recipients experienced a flu-like syndrome following the first and second daily doses of OKT3. Two-year actuarial patient survivals were 100 and 96% for RD and CD recipients, respectively. In the OKT3 primary treatment group, two-year actuarial RD and CD graft survivals were 91 and 76%, respectively. In the OKT3 rescue group, the two-year actuarial RD and CD graft survivals were 85 and 55%, respectively. A proposed immunosuppressive effect of OKT3 is T-cell inactivation by blocking antigen receptors linked to OKT3-reactive molecules. Reuse of OKT3 for recurrent rejection or subsequent organs may be hampered by anti-OKT3 antibody production. OKT3 is an effective steroid-sparing treatment for renal allograft rejection. | Nephron | [
{
"affiliation": "",
"forename": "D J",
"identifier": "",
"initials": "DJ",
"lastname": "Norman"
},
{
"affiliation": "",
"forename": "C F",
"identifier": "",
"initials": "CF",
"lastname": "Shield"
},
{
"affiliation": "",
"forename": "J M",
"identifier": "",
"initials": "JM",
"lastname": "Barry"
},
{
"affiliation": "",
"forename": "K",
"identifier": "",
"initials": "K",
"lastname": "Henell"
},
{
"affiliation": "",
"forename": "M B",
"identifier": "",
"initials": "MB",
"lastname": "Funnell"
},
{
"affiliation": "",
"forename": "J",
"identifier": "",
"initials": "J",
"lastname": "Lemon"
}
] | 1987 | 3306424 | D000888:Antibodies, Anti-Idiotypic / Q000096:biosynthesis; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D002986:Clinical Trials as Topic; D005260:Female; D006084:Graft Rejection; D006801:Humans; D016030:Kidney Transplantation; D007958:Leukocyte Count; D008297:Male; D013601:T-Lymphocytes / Q000276:immunology | D016430:Clinical Trial; D016428:Journal Article | D000888:Antibodies, Anti-Idiotypic; D000911:Antibodies, Monoclonal | 10.1159/000184433 | [] | false | eng | Nephron | 0331777 | 1660-8151 | Switzerland | [] | "2024-08-13T08:46:10.717900Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Comparison of antimouse and antihorse antibody production during the treatment of allograft rejection with OKT3 or antithymocyte globulin. | 46 Suppl 1() | 48-51 | Antimouse antibody is produced from 40 to 68% of the time after administration of Orthoclone OKT3. In patients treated with OKT3, however, if the concomitant immunosuppression is not decreased, the incidence of the antibody production is reduced to 40%. Similarly, 33% of patients developed antihorse antibody after the initial antithymocyte globulin (ATG) administration. Most of the time, the antibody production is low-titered for both OKT3 and ATG. | Nephron | [
{
"affiliation": "",
"forename": "C F",
"identifier": "",
"initials": "CF",
"lastname": "Shield"
},
{
"affiliation": "",
"forename": "D J",
"identifier": "",
"initials": "DJ",
"lastname": "Norman"
},
{
"affiliation": "",
"forename": "P",
"identifier": "",
"initials": "P",
"lastname": "Marlett"
},
{
"affiliation": "",
"forename": "A J",
"identifier": "",
"initials": "AJ",
"lastname": "Fucello"
},
{
"affiliation": "",
"forename": "G",
"identifier": "",
"initials": "G",
"lastname": "Goldstein"
}
] | 1987 | 3306425 | D000818:Animals; D000888:Antibodies, Anti-Idiotypic / Q000096:biosynthesis*; D000911:Antibodies, Monoclonal / Q000009:adverse effects / Q000276:immunology / Q000627:therapeutic use*; D000961:Antilymphocyte Serum / Q000009:adverse effects / Q000276:immunology / Q000627:therapeutic use*; D001379:Azathioprine / Q000627:therapeutic use; D002986:Clinical Trials as Topic; D006084:Graft Rejection; D006736:Horses; D006801:Humans; D051379:Mice; D013045:Species Specificity; D013601:T-Lymphocytes / Q000276:immunology | D016430:Clinical Trial; D003160:Comparative Study; D016428:Journal Article | D000888:Antibodies, Anti-Idiotypic; D000911:Antibodies, Monoclonal; D000961:Antilymphocyte Serum; D001379:Azathioprine | 10.1159/000184434 | [] | false | eng | Nephron | 0331777 | 1660-8151 | Switzerland | [] | "2024-08-13T08:46:10.718822Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Monoclonal antibody therapy with ciclosporin and steroids in nonmatched cadaveric renal transplants. | 46 Suppl 1() | 56-9 | Thirty-six ciclosporin-prednisone-treated recipients of nonmatched cadaver renal allografts were given a course of Orthoclone OKT3 monoclonal antibody for steroid-resistant cell-mediated rejection. Although side effects were common, only 2 patients had to be withdrawn from therapy and there were no deaths related to therapy. Twenty-three (63.9%) allografts were rescued with OKT3 therapy and 21 (58.3%) of the grafts have continued to function well. We conclude that OKT3 is an effective agent for the treatment of steroid-resistant cell-mediated rejection and that rebound rejection can be prevented in most patients if adequate therapy with ciclosporin-prednisone is maintained. | Nephron | [
{
"affiliation": "",
"forename": "R D",
"identifier": "",
"initials": "RD",
"lastname": "Gordon"
},
{
"affiliation": "",
"forename": "T E",
"identifier": "",
"initials": "TE",
"lastname": "Starzl"
},
{
"affiliation": "",
"forename": "J J",
"identifier": "",
"initials": "JJ",
"lastname": "Fung"
},
{
"affiliation": "",
"forename": "S",
"identifier": "",
"initials": "S",
"lastname": "Iwatsuki"
},
{
"affiliation": "",
"forename": "C O",
"identifier": "",
"initials": "CO",
"lastname": "Esquivel"
},
{
"affiliation": "",
"forename": "A",
"identifier": "",
"initials": "A",
"lastname": "Tzakis"
},
{
"affiliation": "",
"forename": "S",
"identifier": "",
"initials": "S",
"lastname": "Todo"
}
] | 1987 | 3306426 | D000293:Adolescent; D000328:Adult; D000911:Antibodies, Monoclonal / Q000008:administration & dosage* / Q000009:adverse effects; D002648:Child; D002986:Clinical Trials as Topic; D003524:Cyclosporins / Q000008:administration & dosage*; D004064:Digestive System / Q000187:drug effects; D004359:Drug Therapy, Combination; D005260:Female; D006084:Graft Rejection; D006801:Humans; D016030:Kidney Transplantation; D008297:Male; D008875:Middle Aged; D011241:Prednisone / Q000008:administration & dosage* | D016430:Clinical Trial; D016428:Journal Article; D013485:Research Support, Non-U.S. Gov't; D013486:Research Support, U.S. Gov't, Non-P.H.S.; D013487:Research Support, U.S. Gov't, P.H.S. | D000911:Antibodies, Monoclonal; D003524:Cyclosporins; D011241:Prednisone | 10.1159/000184436 | [
{
"citation": "J Exp Med. 1984 Nov 1;160(5):1284-99",
"pmid": "6208306"
},
{
"citation": "Surg Gynecol Obstet. 1967 Feb;124(2):301-8",
"pmid": "4163340"
},
{
"citation": "Ann Surg. 1984 Oct;200(4):535-42",
"pmid": "6385877"
},
{
"citation": "Cell. 1982 Oct;30(3):735-43",
"pmid": "6982759"
},
{
"citation": "Surg Gynecol Obstet. 1982 Jun;154(6):819-25",
"pmid": "7043758"
},
{
"citation": "Transplantation. 1981 Dec;32(6):535-9",
"pmid": "7041358"
},
{
"citation": "N Engl J Med. 1981 Aug 6;305(6):308-14",
"pmid": "6454075"
},
{
"citation": "Nephron. 1987;46 Suppl 1:19-33",
"pmid": "3306422"
}
] | false | eng | Nephron | 0331777 | 1660-8151 | Switzerland | [
{
"agency": "NIDDK NIH HHS",
"country": "United States",
"grant_acronym": "DK",
"grant_id": "R01 DK029961-19"
},
{
"agency": "NIADDK NIH HHS",
"country": "United States",
"grant_acronym": "AM",
"grant_id": "AM-29961"
}
] | "2024-08-13T08:46:10.720107Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Lipoprotein lipid abnormalities in healthy renal transplant recipients: persistence of low HDL2 cholesterol. | 47(1) | 17-21 | There is disagreement about the prevalence and character of lipoprotein lipid abnormalities in renal transplant patients. To test the hypothesis that these abnormalities may be related to the coexistence of medical conditions and medications which affect lipoprotein metabolism in these patients, triglyceride (TG), cholesterol (C), high-density lipoprotein (HDL) and HDL-C subfractions were measured in 26 transplanted patients (10 F/16 M), control subjects matched for age, sex, weight and race and uremic patients being treated with hemodialysis. Female transplant recipients had higher TG (181 +/- 47 vs. 68 +/- 6 mg/dl; p less than 0.001), C (242 +/- 19 vs. 165 +/- 9 mg/dl; p less than 0.01), and low-density lipoprotein (LDL)-C (155 +/- 15 vs. 93 +/- 8 mg/dl; p less than 0.01) than controls. Levels of HDL-C were similar, but HDL2 was significantly lower in the transplanted patients (9 +/- 2 vs. 19 +/- 2 mg/dl; p less than 0.01). Compared to the uremic patients, female transplanted patients had higher C (242 +/- 19 vs. 178 +/- 22 mg/dl; p less than 0.01), LDL-C (155 +/- 15 vs. 94 +/- 18 mg/dl; p less than 0.01), HDL-C (51 +/- 5 vs. 32 +/- 4 mg/dl; p less than 0.001) and HDL3-C (42 +/- 4 vs. 26 +/- 2 mg/dl; p less than 0.001); however, HDL2-C levels were not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS) | Nephron | [
{
"affiliation": "",
"forename": "W H",
"identifier": "",
"initials": "WH",
"lastname": "Ettinger"
},
{
"affiliation": "",
"forename": "W L",
"identifier": "",
"initials": "WL",
"lastname": "Bender"
},
{
"affiliation": "",
"forename": "A P",
"identifier": "",
"initials": "AP",
"lastname": "Goldberg"
},
{
"affiliation": "",
"forename": "W R",
"identifier": "",
"initials": "WR",
"lastname": "Hazzard"
}
] | 1987 | 3306427 | D000328:Adult; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D005260:Female; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood / Q000628:therapy; D016030:Kidney Transplantation; D008075:Lipoproteins, HDL / Q000097:blood*; D008077:Lipoproteins, LDL / Q000097:blood*; D008297:Male; D008875:Middle Aged; D006435:Renal Dialysis; D012727:Sex Characteristics; D014280:Triglycerides / Q000097:blood* | D016428:Journal Article; D013485:Research Support, Non-U.S. Gov't; D013487:Research Support, U.S. Gov't, P.H.S. | D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D014280:Triglycerides | 10.1159/000184450 | [] | false | eng | Nephron | 0331777 | 1660-8151 | Switzerland | [
{
"agency": "NCRR NIH HHS",
"country": "United States",
"grant_acronym": "RR",
"grant_id": "RR 02719"
}
] | "2024-08-13T08:46:10.721126Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Membranous nephropathy accompanied by angiolymphoid hyperplasia of the skin. | 47(1) | 32-5 | A 24-year-old female developed a painless swelling adjacent to the left ear. This was shown to be eosinophilic angiolymphoid hyperplasia (ALH). Three months later she developed a nephrotic syndrome. Renal biopsy revealed membranous nephropathy. This is the first non-Japanese case of dermal eosinophilic ALH and nephrotic syndrome; steroid treatment followed by surgical removal of the tumour resulted in complete remission in the renal lesion. | Nephron | [
{
"affiliation": "",
"forename": "S",
"identifier": "",
"initials": "S",
"lastname": "Sonkodi"
},
{
"affiliation": "",
"forename": "K",
"identifier": "",
"initials": "K",
"lastname": "Jarmay"
},
{
"affiliation": "",
"forename": "I",
"identifier": "",
"initials": "I",
"lastname": "Korom"
},
{
"affiliation": "",
"forename": "E",
"identifier": "",
"initials": "E",
"lastname": "Kemeny"
},
{
"affiliation": "",
"forename": "E",
"identifier": "",
"initials": "E",
"lastname": "Szabo"
},
{
"affiliation": "",
"forename": "G",
"identifier": "",
"initials": "G",
"lastname": "Abraham"
},
{
"affiliation": "",
"forename": "I",
"identifier": "",
"initials": "I",
"lastname": "Sonkodi"
},
{
"affiliation": "",
"forename": "O",
"identifier": "",
"initials": "O",
"lastname": "Ribari"
},
{
"affiliation": "",
"forename": "G",
"identifier": "",
"initials": "G",
"lastname": "Mohacsi"
}
] | 1987 | 3306428 | D000328:Adult; D000796:Angiolymphoid Hyperplasia with Eosinophilia / Q000150:complications* / Q000473:pathology; D005260:Female; D005455:Fluorescent Antibody Technique; D006801:Humans; D008854:Microscopy, Electron; D009404:Nephrotic Syndrome / Q000150:complications* / Q000473:pathology; D012867:Skin / Q000473:pathology* | D002363:Case Reports; D016428:Journal Article | 10.1159/000184453 | [] | false | eng | Nephron | 0331777 | 1660-8151 | Switzerland | [] | "2024-08-13T08:46:10.723354Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
|||||
Correlation between blood prostaglandins and blood pressure in chronic renal failure. | 47(1) | 49-55 | Plasma prostaglandins (PGs; PGE2, PGF2 alpha, 6-keto-PGF 1 alpha and TXB2) and plasma renin activity (PRA) were measured in 94 end-stage renal disease (ESRD) patients including 15 undialyzed, 74 maintenance-hemodialyzed and 5 anephric patients, and in 27 healthy controls. In the healthy controls, 6-keto-PGF 1 alpha inversely correlated with age, while TXB2 and the TXB2/6-keto-PGF 1 alpha ratio correlated with age. In the ESRD patients, 6-keto-PGF 1 alpha showed a tendency to decrease with age, and the TXB2/6-keto-PGF 1 alpha ratio significantly correlated with age. The undialyzed group showed significantly higher blood pressure and TXB2 but significantly lower 6-keto-PGF1 alpha compared to the other groups. In the dialyzed group, PGE2 and 6-keto-PGF1 alpha tended to be lower and TXB2 higher compared to the healthy control group. In the dialyzed group, 6-keto-PGF1 alpha correlated inversely with blood pressure independently from PRA. As for PGF2 alpha, it was higher in the undialyzed, dialyzed and anephric groups than in the healthy control group. These results suggested that PGs were involved in blood pressure abnormalities, and that PGI2 played an important role in controlling blood pressure in ESRD patients as one of the depressor factors. | Nephron | [
{
"affiliation": "",
"forename": "T",
"identifier": "",
"initials": "T",
"lastname": "Kishimoto"
},
{
"affiliation": "",
"forename": "T",
"identifier": "",
"initials": "T",
"lastname": "Terada"
},
{
"affiliation": "",
"forename": "T",
"identifier": "",
"initials": "T",
"lastname": "Okahara"
},
{
"affiliation": "",
"forename": "Y",
"identifier": "",
"initials": "Y",
"lastname": "Abe"
},
{
"affiliation": "",
"forename": "S",
"identifier": "",
"initials": "S",
"lastname": "Yamagami"
},
{
"affiliation": "",
"forename": "M",
"identifier": "",
"initials": "M",
"lastname": "Maekawa"
}
] | 1987 | 3306429 | D000328:Adult; D000375:Aging / Q000097:blood; D001794:Blood Pressure; D005260:Female; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000201:enzymology / Q000628:therapy; D008297:Male; D008875:Middle Aged; D011453:Prostaglandins / Q000097:blood*; D006435:Renal Dialysis; D012083:Renin / Q000097:blood* | D003160:Comparative Study; D016428:Journal Article | D011453:Prostaglandins; D012083:Renin | 10.1159/000184456 | [] | false | eng | Nephron | 0331777 | 1660-8151 | Switzerland | [] | "2024-08-13T08:46:10.724231Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
||||
Alpha interferon clinical trial for multiple sclerosis: design considerations. | 6(1-2) | 85-92 | The design and course of a placebo-controlled alpha-2 interferon trial in MS patients are described. No beneficial effect of the interferon on the course of MS could be shown. | Neuroepidemiology | [
{
"affiliation": "",
"forename": "M",
"identifier": "",
"initials": "M",
"lastname": "Alter"
},
{
"affiliation": "",
"forename": "J",
"identifier": "",
"initials": "J",
"lastname": "Greenstein"
},
{
"affiliation": "",
"forename": "D",
"identifier": "",
"initials": "D",
"lastname": "Camenga"
},
{
"affiliation": "",
"forename": "L",
"identifier": "",
"initials": "L",
"lastname": "LaRue"
}
] | 1987 | 3306431 | D000328:Adult; D002986:Clinical Trials as Topic / Q000379:methods; D005260:Female; D006801:Humans; D007370:Interferon Type I / Q000009:adverse effects / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D009103:Multiple Sclerosis / Q000188:drug therapy* / Q000503:physiopathology | D016430:Clinical Trial; D018848:Controlled Clinical Trial; D016428:Journal Article; D016449:Randomized Controlled Trial | D007370:Interferon Type I | 10.1159/000110102 | [] | false | eng | Neuroepidemiology | 8218700 | 0251-5350 | Switzerland | [] | "2024-08-13T08:46:10.725014Z" | https://ftp.ncbi.nlm.nih.gov/pubmed/baseline/pubmed24n0110.xml.gz |
Subsets and Splits