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Biomedical subjects

J Goudsmit

Publications and source records attributed to J Goudsmit.

At least 397 records · Page 22Linked to original sources
PubMed1982

The role of BK virus in acute respiratory tract disease and the presence of BKV DNA in tonsils.

The significance of BKV infections relative to infections by generally tested respiratory agents was investigated in children with acute respiratory disease. Paired sera from 177 children admitted to a hospital for acute respiratory disease were tested for significant rises in antibodies. Sera from seven patients showed a seroconversion to BKV and clinical signs of acute upper respiratory tract infection were exhibited by each of these patients. BKV infections were present in 8% of the patients with upper respiratory tract disease while seroconversions to adenovirus (2%), influenza A virus (1%), parainfluenza virus (5%), RS virus (6%) and mycoplasma pneumoniae (1%) were observed in 15% of the patients with upper respiratory tract disease. BKV was isolated from the urine of one child with tonsillitis with a concomitant seroconversion to BKV. Tonsils from children with recurrent attacks of acute respiratory disease were tested for the presence of BKV DNA by hybridization with a cloned genomic 32P-labeled DNA of prototype BKV. Five of twelve tonsil DNAs showed hybridization with BKV DNA. Each tonsil showing hybridization with BKV DNA contained multiple nonintegrated copies of the BKV genome per diploid amount of host cell DNA. Attempts to recover infective BKV by transfection of primary human embryonic cells with tonsil DNAs or by co-cultivation of tonsillar cells with primary human embryonic cells were unsuccessful.

Acute Disease↗
PubMed1981

Hypersensitivity to central serotonin receptor activation in scrapie-infected hamsters and the effect of serotonergic drugs on scrapie symptoms.

Low doses of the serotonin agonist, quipazine, and the serotonin precursor, L-5-hydroxytryptophan methyl ester, produce small but significant reductions in scrapie-induced ataxia and action jerks in hamsters. Higher doses of both drugs elicit a behavioral syndrome specific for central serotonin receptor activation. Scrapie-infected hamsters show a dramatic hypersensitivity to both drugs compared to control animals. This suggests that scrapie infection in hamsters causes a disturbance in the serotonergic pathway of the brain stem.

5-Hydroxytryptophan↗
PubMed1981

Cytogenetic studies of familial and sporadic Alzheimer disease.

We present cytogenetic findings in 7 familial and 5 sporadic Alzheimer disease (AD) patients and 34 unaffected relatives, spouses, and normal controls. Our study was prompted by reports of increased chromosome abnormalities in patients and family members at risk for AD. Coded peripheral blood chromosome preparations were evaluated for aneuploidy, aberration rates, and banding patterns. Statistical analyses of our results showed no increase in aneuploidy or aberrations in AD patients, their relatives, or normals. Chromosome loss or gain in aneuploid cells was not specific except in two individuals. These two older persons studied, one with AD and one unaffected, were observed to have increased sex chromosome aneuploidy. This finding was attributed to aging and was not considered to be an effect of AD.

Adult↗
PubMed1981

Familial Alzheimer's disease in two kindreds of the same geographic and ethnic origin. A clinical and genetic study.

Alzheimer's disease (AD) occurred in 37 individuals from two kindreds of Jewish ancestry with a mode of transmission suggesting an autosomal dominant genetic trait. Both kindreds originated from Byelorussia and spoke the Lithuanian dialect of Yiddish. In one of the two families one case of pathologically confirmed AD occurred with clinical and neuropathological signs of Parkinson's disease. In the other family one case of amyotrophic lateral sclerosis and one case of Down's syndrome occurred, both without clinical or pathological signs of AD. In the single kindred tested, a study of the chromosome 6 markers HLA, Bf and GLO failed to reveal a correlation between the transmission of AD and the segregation of these markers. The association of increased aneuploidy of peripheral blood chromosomes with AD was not confirmed in either of these families. Genetic differences between the familial and the sporadic form of AD are discussed.

Adult↗
PubMed1981

Biologic distinction between sporadic and familial Alzheimer disease by an in vitro cell fusion test.

In vitro cell-fusing activity of brain suspensions prepared from patients with Alzheimer disease occurred in 10 of 17 familial cases (59%), a level similar to that seen in transmissible Creutzfeldt-Jakob disease (CJD), but in only 3 of 17 sporadic cases (17%), a level not statistically different from that in nonneurologic control patients. This biologic distinction between the familial and sporadic forms of Alzheimer disease may be related to the previously reported transmission to primates of a CJD-like disease from two familial cases of Alzheimer disease.

Adult↗
PubMed1980

Evidence for and against the transmissibility of Alzheimer disease.

Nonhuman primates were inoculated intracerebrally with brain tissue from 52 patients with confirmed Alzheimer disease (AD) in order to investigate the possibility of an infectious etiology. Animals inoculated with brain tissue from two patients with familial AD developed a spongiform encephalopathy that was indistinguishable from Creutzfeldt-Jakob disease (CJD). Seventeen other cases of AD on test for more than 50 months failed to produce similar changes, and 33 cases have not been incubating for a sufficient period of time to ascertain the presence of a transmissible agent. The initial transmission of spongiform encephalopathy with brain tissue from the two familial cases of AD has not been reproduced and the association between AD and an infectious agent has not yet been demonstrated with any reasonable degree of certainty. The frequent overlap of clinical symptoms of AD and CJD, and the occurrence of cases of CJD and AD in the same families indicate the need for continuing research on the relationship between the two diseases.

Alzheimer Disease↗
PubMedDate not supplied

Low levels of specific T cell activation marker CD27 accompanied by elevated levels of markers for non-specific immune activation in the cerebrospinal fluid of patients with AIDS dementia complex.

Concentrations of soluble receptors for tumor necrosis factor (sTNFR-p55 and sTNFR-p75) and soluble T cell antigens CD25 and CD27 (sCD25 and sCD27) were measured in paired serum/cerebrospinal fluid (CSF) samples of 15 patients with AIDS dementia complex (ADC) and 15 HIV-infected control subjects (11 with other central nervous system (CNS) infections and four without CNS infection). In this study levels of sTNFR-p55, sTNFR-p75 and sCD25 were elevated in the CSF of ADC patients and of the 11 patients with other CNS infections, whereas CSF-levels of the specific T cell marker sCD27 were lower in patients with ADC as compared to the control subjects with and without other CNS infections. This pattern suggests a relative failure of eliciting a T cell-mediated immune response intrathecally in patients with ADC.

AIDS Dementia Complex↗
PubMedDate not supplied

Immunodominant B-cell clones responsive to an HIV-1 neutralization and cell fusion inhibition epitope in chimpanzee-to-chimpanzee passages of HTLV-IIIB and LAV-1.

Chimpanzees infected with the HIV-1 strains HTLV-IIIB or LAV-1 in primary, secondary or tertiary passages developed neutralizing antibodies binding to variable domain V3 in the carboxyl terminal half of the external envelope (amino acids 309-317). Nonapeptide antigens reflecting either the HTLV-IIIB/LAV-1 neutralization epitope (IQRGPGRAF, designated 3B) or peptide analogues (ITKGPGRVI, designated RF; IQRGPGRVI, designated 3B/RF; ITKGPGRAF, designated RF/3B) were previously shown to be able to distinguish antibody populations in a polyclonal response of rabbits to these peptides. Sera from chimpanzees infected with the HIV-1 strains HTLV-IIIB and LAV-1 were tested for the presence of antibodies reactive to these nonapeptides. Sera from 3 chimpanzees infected with a primary LAV-1 or HTLV-IIIB passage, 2 chimpanzees infected with blood from the primary infected chimpanzees and from 1 chimpanzee infected with blood from a secondary passage animal, all bound peptides 3B and 3B/RF, sharing the sequence IQRGPGR, in equally high tires. In 2 primary passage animals and in 1 secondary passage animal, the capacity to bind to peptides 3B and 3B/RF was equally high, indicating clonality of these B-cell responses. Contrasting results were obtained with the sera from 1 primary, 1 secondary and 1 tertiary passage animal, showing stronger binding to the 3B/RF peptide than to the 3B peptide. The animals with antibodies binding strongly to the 3B peptide had an early HTLV-IIIB-induced cell-fusion-inhibiting (CFI) antibody response, while the animals with antibodies binding strongly to the 3B/RF peptide had a late HTLV-IIIB-induced CFI antibody response. This difference in binding to the 3B peptide might result from antigenic variation in the neutralization domain of the inoculum virus(es). The conservation of the antibody specificity for the neutralization epitope of the inoculum strain might open the way to type circulating virus strains by antibody specificity for a panel of peptide analogues derived from the V3 domain of the external envelope of distinct HIV-1 strains.

Amino Acid Sequence↗