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Biomedical subjects

D Weil

Publications and source records attributed to D Weil.

At least 109 records · Page 6Linked to original sources
PubMed1985

Isolation and characterization of the human fibrillar collagen genes.

In order to elucidate some of the mechanisms leading to the pathological expression of the human fibrillar collagens, as well as to understand the evolution of these loci, specific cDNA and genomic clones have been isolated. The primary structure of the COOH-terminal propeptide of the four collagen chains and either part or the entire exon/intron arrangement of the genes have been determined. Interspecies and pairwise comparison revealed that the four loci have evolved at slightly different rates, maintaining, however, remarkably similar exon/intron arrangement. The fibrillar genes, albeit sharing the same elaborate structure, exhibit different sizes that correlate with the average length of their intron sequences, possibly because of their different chromosomal origin.

Animals↗
PubMed1985

Assignment to chromosome 12 of the gene coding for the human cell surface antigen CD9(p24) using the monoclonal antibody ALB6.

An analysis of 20 independent man-mouse and man-hamster hybrids has shown that the gene coding for the cell-surface protein CD9(p24), a differentiation antigen recognized by the monoclonal antibody ALB6, is located on chromosome 12. A positive correlation was shown between CD9(p24) and chromosome 12 and all other chromosomes were excluded. In addition a synteny was observed between CD9(p24) and LDH-B, a well known marker of chromosome 12 (out of 27 hybrids, 15 were LDH-B+ ALB6+ and 12 were LDH-B-ALB6-). Expression of the antigen in hybrid CH-35K issued from parental fibroblasts possessing a balanced reciprocal translocation 46,X,Y,t(X,12)(q23,q12) indicated that the gene for CD9(p24) is probably localized on 12q12----pter. Monoclonal antibodies ALB6, Ba2 and 602/29 recognize the same protein of molecular weight 21 to 24 KD controlled by a gene located on chromosome 12. It is known that Ba2 and 602/29 recognize two different epitopes but the existence of a third epitope recognized by ALB6 remains to be shown.

Animals↗
PubMed1984

The beta chorionic gonadotropin-beta luteinizing gene cluster maps to human chromosome 19.

We used a cloned human cDNA probe homologous to the placenta chorionic gonadotropin beta subunit (CGB) and to the pituitary luteinizing hormone beta subunit (LHB) and Southern blotting techniques to analyse DNA from a series of rodent X human somatic cell hybrids for the presence of specific gonadotropin beta subunit related sequences. Our results provide evidence for the assignment and linkage of the eight genes (or pseudogenes) coding for the beta subunit of these glycoprotein hormones to chromosome 19. Moreover, we observed a strict concordance between the permissivity of mouse X man hybrid cells to enteroviruses (which is linked to the presence of specific cell receptors encoded by human chromosome 19) and the presence of CGB and LHB related sequences, thus confirming the localization of the structural genes for the beta subunits on chromosome 19.

Animals↗
PubMed1984

Gene for apolipoprotein CII is on human chromosome 19.

We have used a cloned cDNA probe for human apolipoprotein CII (apo CII) and Southern blotting techniques to identify the human apo CII gene in DNA from a series of rodent X human somatic cell hybrids. Our results provide evidence for the assignment of this gene to human chromosome 19.

Apolipoproteins C↗
PubMed1984

A study of chromosomal changes associated with amplified dihydrofolate reductase genes in rat hepatoma cells and their dedifferentiated variants.

We have examined the karyological consequences of dihydrofolate reductase gene amplification in a series of six rat hepatoma cell lines, all derived from the same clone. Cells of three of these lines express a series of liver-specific functions whereas those of three others fail to express these functions. Cells of each line have been subjected to stepwise selection for methotrexate resistance and, in most cases, resistance is associated with a 40-50-fold amplification of sequences hybridizing to a dihydrofolate reductase cDNA probe. In one line no modified chromosome is observed, whereas in two others the amplified genes are associated with an expanded chromosomal region. R-banding analysis of these karyotypes showed that few changes have occurred. These observations apply to two of the well-differentiated lines, and to a variant able to revert to the differentiated state. In contrast, in the two stably dedifferentiated hepatoma cell lines, amplified dihydrofolate reductase genes are found on large chromosomes of variable size, on ring chromosomes, and on chromosomes containing terminal, median, or multiple centromeres. We conclude that the nature of the chromosomal changes associated with dihydrofolate reductase gene amplification are the result of differences in cell lines rather than in the protocols employed for selection.

Animals↗
PubMed1984

Spread of a toxic-shock syndrome-associated strain of Staphylococcus aureus and measurement of antibodies to staphylococcal enterotoxin F.

A gentamicin-resistant isolate of Staphylococcus aureus producing staphylococcal enterotoxin F (SEF) was isolated from a burn unit nurse during three episodes of toxic-shock syndrome (TSS). The nurse's reciprocal titer of antibodies to SEF was less than or equal to 5 during the three episodes, and when the titer rose to 1,000 no further relapses occurred despite continued colonization. The unusual antibiotic susceptibility pattern of the organism enabled demonstration of its spread. During four months, 12 (41%) of 29 burn unit patients, three other burn unit nurses, and a household contact of the nurse with TSS became colonized. None, including two patients whose initial reciprocal titers were less than or equal to 5, developed TSS. This experience illustrates significant cross-transmission of a TSS-associated strain and a temporal association of antibodies to SEF with cessation of recurrences of TSS. Additional factors must explain why other individuals lacking antibodies to SEF did not develop TSS.

Adult↗
PubMed1984

Assignment of the human gene for delta aminolevulinate dehydrase to chromosome 9 by somatic cell hybridization and specific enzyme immunoassay.

A non-competitive enzyme immunoassay specific for delta aminolevulinate dehydrase has been devised and applied to rodent-human hybrid cell lines. Two different conditions have been used, one specific for the human enzyme and the other indicative of both rodent and human enzymes. The ratio of the values obtained under the two conditions was used to discriminate between positive and negative clones. By this method the gene for ALA dehydrase has been assigned to chromosome 9.

Animals↗
PubMed1984

Outbreak of JK diphtheroid infections associated with environmental contamination.

The group JK diphtheroid organism is a multiply resistant opportunistic pathogen which infects immunocompromised patients sporadically. We describe the first reported outbreak of JK diphtheroid infections, in which four cases of bacteremia and one Hickman catheter site infection occurred during 4 weeks on a hematology ward. On this ward, JK diphtheroid was recovered from 17 of 39 patients, 10 of 17 30-ft3 (0.840-m3) air samples, surfaces in 9 of 13 patient rooms, and hands of 4 of 22 personnel. Previously identified risk factors for JK diphtheroid sepsis (male gender, broad-spectrum antibiotic therapy, granulocytopenia, and prolonged hospital stay) were present in infected patients but did not distinguish them from patients who were only colonized. Emphasis on aseptic practices was associated with termination of the outbreak and negative hand cultures from personnel, despite continued patient colonization and environmental contamination.

Air Microbiology↗
PubMed1984

Aspirin inhibits vascular plasminogen activator activity in vivo. Studies utilizing a new assay to quantify plasminogen activator activity.

Vascular or tissue-type plasminogen activator (TPA) is a key enzyme in physiologic fibrinolysis. To study the role of prostaglandins in modulating the synthesis and release of TPA in vivo, we prospectively studied the effect of aspirin (650 mg/d X 2) on TPA activity in 13 human subjects before and after 10 min of forearm venous occlusion. TPA activity was quantified by a newly developed enzyme-linked immunosorbent assay that both measures and differentiates between TPA and urokinase (UK)-like plasminogen activator activity. This assay is based on the observation that the concentration of alpha 2-plasmin inhibitor-plasmin complexes in Reptilase-clotted plasma increases linearly in proportion to the amount of activator added. Resting TPA activity was higher in women than in men (0.56 +/- 0.59 vs. 0.15 +/- 0.11 U/ml, P = 0.049). Venous occlusion induced an eightfold rise in TPA activity in women (to 4.5 U/ml, P = 0.006) and a 15-fold rise in men (to 2.28 U/ml, P = 0.004), whereas UK activity was not detected. Aspirin inhibited the rise in TPA activity after venous occlusion by 69% in men (P = 0.004) and 70% in women (P = 0.014). In contrast, aspirin had no effect on pre- or post-occlusion hematocrits or Factor VIII-related antigen levels. There was no correlation between plasma salicylate level and percentage inhibition of TPA. Neither exogenous aspirin (0-1 microgram/ml) nor salicylate (0-70 micrograms/ml) inhibited the generation of alpha 2-plasmin inhibitor-plasmin complexes by exogenous TPA or interfered with the assay system. We conclude that aspirin may have an antifibrinolytic effect in man that has not been previously described.

Aspirin↗
PubMed1984

The genes coding for A alpha-, B beta-, and gamma-chains of fibrinogen map to 4q2.

We used cloned cDNA probes for the A alpha-, B beta-, and gamma-chains of human fibrinogen and Southern blotting techniques to analyze DNA from a series of rodent X human somatic cell hybrids for the presence of specific fibrinogen-related sequences. Our results provide evidence for the assignment of the three genes for fibrinogen to chromosome 4. Moreover, by direct gene-dosage determination in two patients with chromosome 4 unbalanced rearrangements, we refined the regional chromosomal assignment to 4q2, thus suggesting that these three genes whose expression is coordinately regulated are closely linked.

Animals↗
PubMed1984

The structural gene for transferrin (TF) maps to 3q21----3qter.

A cloned human cDNA for transferrin (TF) was used as hybridization probe in analysing a series of rodent x human somatic cell hybrids for the presence of human TF sequences. The assignment to chromosome 3 was further refined to region 3q21----3qter using hybrids that carried a translocated chromosome 3 and fibroblasts from a patient trisomic for this region. The gene for TF therefore maps to the same region as the gene for transferrin receptor (TFR) thereby defining an iron transport region on 3q2 to which the transferrin-related tumor associated antigen p97 may also belong. It follows that the genes for pseudocholinesterase (CHE1), ceruleoplasmin (CP) and alpha-2HS-glycoprotein (A2HS) which belong to the, as yet unassigned, linkage group of TF, now also map to chromosome 3 in man.

Animals↗
PubMed1983

[Localization of the LDHA-GST3-ESA4 synthetic group on human chromosome 11. Analyses of the classic man-rodent hybrids and of a new type (not adhering to the wall)].

Analysis of different human tissues showed that glutathione S-transferase (GST) of fibroblasts and leucocytes is GST3, an enzyme found in liver extracts by Board (1981). Consequently, the GST localized on human chromosome 11 by Silberstein and Shows (1981, 1982) is GST3. Analysis of tissue extracts showed a new GST band, very intense in muscle extracts and very weak or absent in other tissues, and called GSTM. Analysis of man-rodent hydrids showed synteny between LDHA, GST3, ESA4 and localization of this synteny group on chromosome 11. Analysis of discordant percentages and discordant types between markers favored the following assignments: LDHA on 11p12, GST3 on 11q13 leads to 11qter, ESA on 11q13 leads to 11q22. The present study suggests assignment of GST3 to 11q13 leads to 11q22. Different types of man-rodent hybrids are useful for human gene mapping. A new type hybrid, as used here (nonadhering to glass or plastic surfaces), appears useful because of rapid proliferation and growth in suspension, the latter feature facilitating culture and harvesting.

Animals↗
PubMed1982

Human type I procollagen genes are located on different chromosomes.

A recombinant plasmid containing sequences complementary to human pro-alpha l(I) collagen mRNA was used for the chromosomal assignment of the pro-alpha l(I) collagen gene. Restriction endonuclease analysis of DNA from mouse-human and Chinese hamster-human somatic cell hybrids revealed cosegregation with human chromosome 17. Hybrids containing derivative chromosomes with a t(2;17)(q14;q21) translocation showed cosegregation of the pro-alpha l(I) gene with the segment 17q21 leads to qter. In situ hybridization on human metaphasic chromosomes confirmed this conclusion.

Amino Acid Sequence↗
PubMed1982

Nosocomial Legionnaires' disease caused by aerosolized tap water from respiratory devices.

Five cases of nosocomial Legionnaires' disease which occurred over a five-month period were retrospectively investigated. Chart review showed that during the two- to 10-day incubation period before the onset of illness, all of the patients inhaled aerosolized tap water from jet nebulizers (four patients) or from a portable room humidifier (one patient), and all received high dosages of corticosteroids or adrenocorticotropic hormone. Exposure to both factors was highly significant (P less than 0.000001) when compared with the rate of exposure in 69 control patients. Environmental cultures yielded Legionella pneumophila from tap water and from reservoirs of tap water-filled respiratory devices. The yield was highest from hot tap water, in which the free chlorine level was less than 0.05 parts per million. Thus, Legionnaires' disease may be caused by contaminated aerosols from respiratory devices, and the use of contaminated tap water in such devices represents a previously unrecognized hazard to which corticosteroid-treated patients should not be exposed.

Adrenal Cortex Hormones↗
PubMed1982

Assignment of the human pro alpha 2(I) collagen structural gene (COLIA2) to chromosome 7 by molecular hybridization.

A cDNA for the pro alpha 2 chain of human type I collagen has been recently cloned and amplified. We have used this specific probe to identify the human chromosome carrying the pro alpha 2(I) collagen gene. The DNA from 17 independent human/hamster and human/mouse somatic cell hybrids was digested by Eco RI and the restriction pattern analyzed in Southern blot experiments, using the 32P-labeled cDNA as a hybridization probe. The gene coding for the pro alpha 2 collagen subunit could be unambiguously assigned to human chromosome 7. All the other chromosomes, including chromosome 17, were excluded.

Animals↗