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Biomedical subjects

R Rubin

Publications and source records attributed to R Rubin.

At least 163 records · Page 9Linked to original sources
PubMed1985

[Paracoccidioidomycosis, an imported tropical disease].

Tropical mycoses are very rare diseases in this country. To date there have only been two published observations of paracoccidioidomycosis in the Federal Republic of Germany. In these rare cases the diagnosis is often delayed because paracoccidioidomycosis imitates frequently appearing and well-known diseases like tuberculosis or sarcoidosis. The diagnostic and therapeutic aspects are illustrated in a recently observed patient from Peru. Therapy consisted of ketoconazole 400 mg/day orally administered with good results and only transient side effects.

Adult↗
PubMed1984

Mechanisms of the killing of cultured hepatocytes by hydrogen peroxide.

Mechanisms of H2O2-induced cell injury were explored in primary cultures of rat hepatocytes. Cells prepared from male rats and cultured for 1 day prior to treatment were killed by H2O2 either added directly to the medium at 0.25-2 mM or generated in situ by glucose oxidase (0.25-2 U/ml) or xanthine oxidase (20-120 mM/ml) and 2 mM xanthine. Catalase protected the cells in each case. Lipid peroxidation as measured by the accumulation of malondialdehyde (MDA) preceded the cell death due to H2O2 added directly to the cultures or generated in the medium. The antioxidants N,N'-diphenyl-p-phenylenediamine (DPPD) and promethazine prevented the accumulation of MDA in both cases and protected the cells treated with H2O2 directly. DPPD and promethazine did not react directly with H2O2. Other antioxidants including butylated hydroxytoluene, vitamin E, and N-propylgallate had varied protective activity against the addition of H2O2 in proportion to their ability to reduce MDA accumulation. In glucose oxidase-treated cultures, DPPD and promethazine prevented the cell killing during the first hour but failed to protect between 1 and 3 h despite prevention of lipid peroxidation. The cell killing between 1 and 3 h in the presence of DPPD was prevented by catalase indicating its dependence upon continued generation of H2O2. Further addition of H2O2 in the presence of DPPD also increased the number of dead cells without lipid peroxidation. The data are consistent with at least two mechanisms of hepatocyte killing by H2O2. The first pathway is prevented by the antioxidants DPPD and promethazine and is very likely related to the peroxidation of membrane phospholipids. The second is independent of lipid peroxidation yet dependent upon the continued presence of H2O2.

Animals↗
PubMed1984

Electrophoretic patterns of proteins in cystic fibrosis sweat.

The abnormal gene product in cystic fibrosis has not been identified. We report that two-dimensional polyacrylamide gel electrophoresis of 125I-labeled sweat proteins coupled with fluorography and rare earth screen radioautography reveals an absence of an acidic protein of molecular weight 60,000 in sweat collected from 9 patients with cystic fibrosis. The protein spot was present in sweat from heterozygotes and from controls.

Child↗
PubMed1983

Brain-derived fibroblast growth factor: a study of its inactivation.

Brain fibroblast growth factor has been identified as a component of myelin basic protein. Its activity is destroyed when treated with a variety of solvents including dilute acid, organic solvents and solutions of guanidine hydrochloride. These conditions do not alter the encephalitogenic properties of myelin basic protein.

Animals↗
PubMed1983

Association studies between Type 1 (insulin-dependent) diabetes and 27 genetic markers: lack of association between Type 1 diabetes and Kidd blood group.

One hundred and three unrelated patients with Type 1 (insulin-dependent) diabetes were typed for HLA, properdin factor B (BF), glyoxalase 1 (GLO), Kidd blood group, and 24 other genetic markers. Observed distributions of marker phenotypes among these patients were compared with those expected according to population frequencies, in an attempt to detect associations between Type 1 diabetes and the markers. Strong associations between Type 1 diabetes and both HLA and properdin factor B were confirmed, as was a lack of association between Type 1 diabetes and glyoxalase (GLO). There was an apparent deviation from Hardy-Weinberg equilibrium at the GLO locus, and statistically significant distortions in the distributions of pancreatic amylase (AMY2), galactose-1-phosphate uridyl transferase (GALT), and group-specific component (GC) among Type 1 diabetes patients, but these results are not significant when corrected for performance of multiple tests. An increase in the Lewis-negative phenotype reported elsewhere was observed here but was not statistically significant. A distortion in the distribution of Kidd types reported elsewhere was not confirmed.

Blood Group Antigens↗
PubMed1983

A search for heterogeneity in insulin dependent diabetes mellitus (IDDM): HLA and autoimmune studies in simplex, multiplex and multigenerational families.

HLA antigens (A, B, C and DR loci), serum islet cell antibodies, thyrogastric antibodies, and insulin antibodies were studied in 77 families (25 simplex, 42 multiplex, and 10 multigenerational). In order to test for intrafamilial constancy and intergroup variation, we compared simplex with multiplex families, HLA identical and non identical siblings within families, as well as groups of families characterized by different DR alleles (DR3, DR4, and DR3/DR4) for various immunologic and clinical characteristics. These comparisons did not reveal all the distinct subgroups suggested by different cross-sectional population studies, but did provide evidence for a compound form having an aggregation of different high risk alleles. This study suggests that in many cases (and possibly especially in families with multiple affected individuals), there are several different genetic influences leading to IDDM.

Antibodies↗
PubMed1983

HLA genotypic study of insulin-dependent diabetes the excess of DR3/DR4 heterozygotes allows rejection of the recessive hypothesis.

The genetics of insulin-dependent diabetes mellitus (IDDM) is currently an area of controversy, with some investigators proposing heterogeneity within the HLA region and even the existence of non-HLA-linked susceptibility genes, and others maintaining that a simple autosomal recessive gene linked to HLA with reduced penetrance is an adequate explanation. To resolve this latter question, we report here a simple method of testing whether a single HLA-linked susceptibility gene is inherited in a recessive fashion when it is associated with two different HLA alleles, as is the case for IDDM. It is shown that if the number of DR3/DR4 heterozygotes in a diabetic population exceeds the combined sum of DR3/3 and DR4/4 homozygotes in that same diabetic population, then a recessive mode of inheritance can be rejected. The advantages of the method are that it does not depend on ratios, as do relative risk calculations, nor does it depend on control data, but is based only on studies of the diabetics themselves. With data on 193 genotyped IDDM patients, we can clearly reject the recessive mode of inheritance, since the number of heterozygotes is 68 compared with a maximum of 22 homozygotes (P less than 10(-4)). Eight other published studies are in concordance with these results. Therefore, a nonparametric test, independent of the significance of any individual study, rejects equality of heterozygotes and homozygotes (P less than 0.002) and rejects the simple recessive mode of inheritance as a direct consequence. We conclude that more complex modes of inheritance of HLA-linked IDDM susceptibility, such as two different diabetogenic alleles or multiple loci, must be entertained. DIABETES 32:169-174, February 1983.

Alleles↗
PubMed1982

Ambulatory serial excision of giant nevi.

Nevi over the size of a dime at the time of birth should probably be removed. Nevi this size often cannot be differentiated histologically from the true giant nevus that may cover over 50% of the body. Giant nevi have a 2%-30% malignant potential. In order to avoid the morbidity of split-thickness skin grafts when removing the larger nevi, we have been successful in serially excising many nevi as ambulatory procedures. Most moderately large nevi, regardless of their location, can be managed with this method.

Ambulatory Surgical Procedures↗
PubMed1982

BK papovavirus infections in renal transplant recipients: contribution of donor kidneys.

Infections due to BK papovavirus frequently occur in renal transplant recipients [2] and may be involved in a variety of syndromes, including ureteral obstruction, deterioration of graft function, and pancreatic disease. The source of the BK papovavirus in these cases is not clear. Because the renal allograft has been implicated as a source of primary cytomegalovirus infections in renal transplant recipients [3], we investigated the possibility that donor kidneys may also contribute to the transmission of BK papovavirus. A fourfold or greater increase in titers of HAI antibodies to BK papovavirus was observed in 55 (24%) of 230 renal transplant recipients. Seronegative recipients who received kidneys from seropositive donors were 3.5 times more likely to develop an infection due to BK papovavirus than were seronegative recipients of kidneys from seronegative donors. The antibody status of the donor did not affect the likelihood of an increase in titers of antibody to BK papovavirus in seropositive recipients. These results suggest that BK papovavirus may be transmitted with transplanted kidneys and that transplant recipients who are at risk for primary infection by this route are more than twice as likely to have increased titers of antibody to BK papovavirus as those who are at risk for the reactivation of an infection. Further studies should be performed to define the relative role of cadaver vs. living, related kidney donors in the transmission of BK papovavirus and the clinical syndromes that are related to primary and reactivated infections.

Humans↗