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Biomedical subjects

H Ginsberg

Publications and source records attributed to H Ginsberg.

At least 19 recordsLinked to original sources
PubMed1992

Protection of iodine-125 brachytherapy brain injury in the rat with the 21-aminosteroid U-74389F.

Radiation protection was studied in a rat brachytherapy brain injury model. Radiation lesions were produced by stereotactic placement of high-activity iodine-125 seeds on the frontal lobe of F-344 rats. A minimum dose of 80 Gy was delivered to a 5.5-mm-radius volume. Radiation damage was evaluated 24 h after removal of the seeds by T1-weighted gadolinium-enhanced magnetic resonance imaging on a 1.5-T unit. Computerized three-dimensional reconstruction of the lesions seen on magnetic resonance imaging was performed to calculate the volume of radiation injury. Two experiments were performed with rats of different weights (mean, 300 g; mean, 180 g). All animals underwent surgical placement of an indwelling internal jugular catheter before brachytherapy. Treated animals received the 21-aminosteroid U-74389F 5 mg/kg intravenously every 6 hours during the implant and for 24 hours after the removal of the iodine-125 seed. Control animals were administered vehicle only. In both experiments, a statistically significant reduction in volume of radiation damage was observed in the U-74389F-treated group compared with the control group.

Animals↗
PubMed1990

Serum IgG and IgA antibodies specific to Epstein-Barr virus capsid antigen in a longitudinal study of human immunodeficiency virus infection and disease progression in homosexual men.

A longitudinal study of serum IgG and IgA antibody titers to Epstein-Barr virus (EBV) viral capsid antigen (VCA) was carried out in 218 homosexual men at various stages of human immunodeficiency virus (HIV) infection. The serum samples tested were obtained from the following groups: 24 HIV seroconverters, 41 persistently HIV-seropositive asymptomatic individuals, 22 seropositives who developed AIDS-related complex (ARC), 29 HIV seropositives who developed lymphadenopathy syndrome (LAS), 35 HIV seronegatives with LAS, 36 asymptomatic HIV seronegatives, and 31 AIDS patients. Blind-tested samples were titrated for IgG and IgA EBV-VCA antibodies by immunoperoxidase assay (IPA). Cross-sectional analysis indicated that all HIV-seropositive subjects exhibited significantly elevated EBV IgG and IgA antibody titers compared with HIV-seronegative subjects. The proportions with EBV-VCA IgA antibodies at a titer of greater than or equal to 128 rose during the course of HIV infection and progression of the disease: 8% in HIV seronegatives, 11% in HIV seronegatives with LAS, 25% in HIV seronegatives prior to HIV seroconversion, 44% in asymptomatic HIV seropositives, 34% in LAS, 50% in ARC, and 58% in AIDS patients. An increase in EBV-VCA IgG and IgA titers was detected following HIV seroconversion and in samples obtained 6 months before disease progression to LAS. These data suggest the possible involvement of EBV in the natural history of HIV infection and disease progression. The possibility that EBV-VCA IgA antibody levels would be of value in prediction of progression of HIV-related illness is discussed.

AIDS-Related Complex↗
PubMed1989

High-density lipoprotein cholesterol is reduced in patients with sarcoidosis.

PURPOSE: Sarcoidosis is a disease in which the proliferation of monocyte-macrophage-derived cells is observed. In other diseases characterized by expansion of the monocyte-macrophage system, such as Gaucher's disease and myeloid metaplasia, abnormalities of lipoprotein metabolism have been demonstrated. To determine whether similar abnormalities in lipoprotein cholesterol concentrations could be identified in patients with sarcoidosis, we studied total cholesterol, low-density lipoprotein (LDL) cholesterol, and high-density lipoprotein (HDL) cholesterol as well as triglyceride levels in 52 patients with biopsy-proven sarcoidosis. PATIENTS AND METHODS: Patients had no other medical disorders and were not being treated with corticosteroids or antimalarial agents. Blood samples were collected by venipuncture after an overnight fast. Plasma total cholesterol and triglyceride levels were measured using enzymatic techniques. Lipoprotein cholesterol was quantified by lipoprotein fractionation. HDL cholesterol was measured as cholesterol remaining in the supernatant after precipitation of LDL and very-low-density lipoprotein from whole plasma by the heparin-maganese chloride method. Computation was used to determine the level of LDL cholesterol. RESULTS: We found significantly reduced levels of total cholesterol (183.9 +/- 27.6 versus 194.3 +/- 16.5 mg/dl, mean +/- SD, p = 0.021) and HDL cholesterol (41.2 +/- 13.0 versus 51.9 +/- 6.1 mg/dl, p = 0.0001) in sarcoid patients versus an age-, sex-, and race-matched reference group. Differences were not observed in triglyceride or LDL cholesterol levels (p greater than 0.05). CONCLUSION: These findings are similar to those observed in the myeloproliferative diseases, Gaucher's disease, and rheumatoid arthritis and suggest a functional role for monocytes-macrophages in the regulation of serum lipoprotein cholesterol levels.

Adult↗
PubMed1989

Effects of sleep deprivation on cognitive ability and skills of pediatrics residents.

The stress and long working hours of medical residency have become the basis for controversy over whether current training structures and processes adversely affect residents' skills and well-being and the quality of patient care. The authors measured cognitive and skills performances of 45 sleep-deprived pediatrics residents by using questions like those on the pediatrics board certification examination and using patient-care tasks that required coordination and dexterity. The residents were randomly divided into two groups--one stayed awake for 24 hours, the other for 34 hours--and were tested on cognitive and skills performances before and after sleep deprivation. Sleep deprivation did not have a significant effect on cognitive performance. Of the three skills tested, the residents overall needed more time to perform umbilical artery catheterization, but the group deprived of sleep for 34 hours performed vein cannulation more quickly than the group deprived for 24 hours. Implications for these findings are discussed in the context of the ongoing controversy over the structure and process of medical education.

Animals↗
PubMed1989

Chenodeoxycholic acid normalizes elevated lipoprotein secretion and catabolism in cerebrotendinous xanthomatosis.

Cerebrotendinous xanthomatosis (CTX) is a rare inherited lipid storage disease caused by a defect in bile acid synthesis in which cholesterol and its product cholestanol are deposited in neurological and vascular tissue. Therapy with chenodeoxycholic acid but not with the 7 beta-epimeric ursodeoxycholic acid is usually successful. In an untreated patient, total and low density lipoprotein (LDL) cholesterol were found to be low (134 +/- 11 and 78 +/- 8 mg/dl, respectively). The production rate (PR) and fractional catabolic rate (FCR) of very low density (VLDL) apolipoprotein B (apoB) were, however, both markedly increased (34.7 mg/kg per day and 13.7 pools/day, respectively vs. 15.1 +/- 5.0 mg/kg per day and 6.2 +/- 3.8 pools/day in controls) while the PR and FCR of LDL apoB were moderately elevated (16.3 mg/kg per day and 0.65 pools/day, respectively vs. 12.9 +/- 1.2 mg/kg per day and 0.52 +/- 0.10 pools/day in controls). After 1 month of 750 mg/day of chenodeoxycholic acid, the FCR and PR of both VLDL and LDL apoB became normal while total plasma cholesterol increased significantly to 145 +/- 18 mg/dl. In a second patient who had been receiving 750 mg/day of chenodeoxycholic acid for 6 months lipoprotein kinetics were normal. These parameters did not change when the subject was switched to 750 mg/day ursodeoxycholic acid. We postulate that cholesterol biosynthesis in CTX is derepressed by a diminished hepatic pool of chenodeoxycholic acid and that the elevated secretion of apoB is a response to the increased rate of cholesterol production.

Adult↗
PubMed1986

Hypocholesterolemia and acute myelogenous leukemia. Association between disease activity and plasma low-density lipoprotein cholesterol concentrations.

Plasma total, low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol concentrations were determined in 32 patients admitted with either acute nonlymphocytic leukemia or chronic myelogenous leukemia in blast crisis. Measurements were repeated in 15 of these individuals during a leukopenic period induced by chemotherapy and in 6 of the latter group when they had achieved remission. Initial plasma total, LDL, and HDL cholesterol levels in 15 male (111.9 +/- 27.9; 53.7 +/- 10.4; 23.7 +/- 22.5 mg/dl) and 17 female (124.0 +/- 42.0; 68.6 +/- 32.0; 29.4 +/- 13.9 mg/dl) patients were markedly reduced compared with age and sex-matched control values (all P less than 0.01). Remission in six subjects was associated with significant increases in total cholesterol (162.0 +/- 61.0 vs. 111.5 +/- 47.9 mg/dl; P less than 0.02) and LDL cholesterol (106.8 +/- 51.2 vs. 43.5 +/- 31.3 mg/dl; P less than 0.05) compared with their baseline values. Chemotherapy-induced leukopenia was associated with inconsistant changes in plasma cholesterol levels although LDL cholesterol increased in all patients who subsequently achieved remission. LDL cholesterol levels fell dramatically in two patients who relapsed. These results indicate that LDL cholesterol concentrations may be of value in assessing disease activity in individuals with acute myelogenous leukemia.

Adult↗
PubMed1984

Diet and the decrease of coronary heart disease.

Total plasma cholesterol is a powerful predictor of death related to coronary heart disease (CHD). Strong evidence indicates that reducing the plasma cholesterol level results in in a decrease in the expected incidence of CHD. The decline in the death rate from CHD in the U.S. population over the past 2 decades has occurred simultaneously with a reduction in the consumption of cholesterol and saturated fat and a dramatic increase in the use of unsaturated vegetable oils. Over the same period, the mean cholesterol level has decreased at least 5%. This finding explains up to one-third of the decline in CHD mortality observed since 1968.

Adult↗
PubMed1984

Very low-density lipoprotein metabolism in an unusual case of lipoatrophic diabetes.

Complete acquired lipoatrophic diabetes (LD) is characterized by nonketotic insulin-resistant diabetes, elevated very low-density lipoprotein (VLDL) triglyceride (TG) levels, and absent subcutaneous fat. We studied a young child in whom LD atypically developed after the onset of type 1 diabetes mellitus. On uncontrolled home diet the patient had triglyceride levels over 1,000 mg/dL on multiple occasions. In order to demonstrate the effects of caloric and dietary-fat restriction on VLDL metabolism, 3H-glycerol and autologous 125I-VLDL were used to quantitate the turnover of VLDL-TG and VLDL-apolipoprotein B (apo B) during two periods of caloric restriction. Consumption of a 900-kcal 40-g fat diet resulted in a plasma triglyceride level of 1383 mg/dL (ten-fold elevation). This hypertriglyceridemia was associated with markedly increased production rates of both VLDL-TG (73.7 mg/kg/h) and VLDL-apo B (126.9 mg/kg/d). Consumption of a 900-kcal 25-g fat diet resulted in a plasma TG level of 663 mg/dL. This reduction in plasma TG was associated with a 40% decrease in VLDL-TG production rate (PR) (45.1 mg/kg/h). There was no change in the production rate (PR) of VLDL-apo B. The hypertriglyceridemia in this patient was due to marked over production of VLDL. Furthermore, the studies demonstrate: (1) the independent benefits of caloric and dietary-fat restriction in the treatment of LD, and (2) that fat restriction lowered plasma triglyceride by its effect on the VLDL-TG production rate.

Apolipoproteins↗
PubMed1984

The effect of chronic hypocholesterolemia in myeloproliferative disease on the distribution of plasma and erythrocyte tocopherol.

The presence of hypocholesterolemia and increased erythrocyte lipid peroxidation susceptibility in myeloproliferative disorders raised the possibility of coexistent tocopherol deficiency. Plasma and red blood cell (RBC) alpha-tocopherol, beta- + gamma-tocopherol, and free cholesterol were determined simultaneously by high performance liquid chromatography in 22 patients and 26 controls. Plasma alpha-tocopherol was correlated most highly with plasma free cholesterol and secondarily with RBC alpha-tocopherol in both groups. Plasma-free cholesterol and alpha-tocopherol were significantly reduced in myeloproliferative disease, although the ratio between the two remained normal. Erythrocyte tocopherol and free cholesterol concentrations were normal in myeloproliferative disease. High relative retention of tocopherol by erythrocytes was most pronounced in patients with the lowest plasma alpha-tocopherol and free cholesterol levels. The normal RBC tocopherol levels in these patients with chronic hypocholesterolemia indicate that the observed increase in RBC peroxidation susceptibility is not explainable by a deficiency of RBC vitamin E.

Cholesterol↗
PubMed1984

Reduced plasma concentrations of total, low density lipoprotein and high density lipoprotein cholesterol in patients with Gaucher type I disease.

Plasma lipid and serum apoprotein concentrations were determined in twenty-nine individuals with Gaucher type I disease. Plasma total cholesterol, low density lipoprotein (LDL) cholesterol and high density lipoprotein (HDL) cholesterol were all significantly reduced in the patients with Gaucher disease compared to a group of matched control subjects. Total, LDL and HDL cholesterol were lower in males than in females with Gaucher disease. These sex differences appeared to be inversely correlated with the severity of disease manifestations which were greater in the males. Serum levels of apoprotein-B and apoprotein-AI, the major structural apoproteins of LDL and HDL, respectively, were decreased in the subjects with Gaucher disease. Thus, the reductions in LDL and HDL cholesterol were associated with reduced numbers of lipoprotein particles in plasma. In contrast, apoprotein-E, a protein which is secreted by several tissues, including activated macrophages and which may mediate hepatic catabolism of lipoproteins, was elevated in the patients. Since macrophages may also catabolize lipoproteins, Gaucher disease may serve as a model for the effect of activated macrophages upon human lipoprotein metabolism.

Adolescent↗
PubMed1984

Evidence that the penton base of adenovirus is involved in potentiation of toxicity of Pseudomonas exotoxin conjugated to epidermal growth factor.

When KB cells are incubated for 1 h with human adenovirus type 2 or type 5 (1 microgram/ml) and a conjugate of epidermal growth factor and Pseudomonas exotoxin (EGF-PE), protein synthesis is inhibited by 80 to 90%. Under these conditions, neither adenovirus nor EGF-PE alone has any effect on host protein synthesis. Thus, adenovirus enhances the toxicity of EGF-PE. A number of antibodies to intact virus and capsid components were tested for their ability to block the enhancing activity and virus uptake. At appropriate dilutions, antibodies prepared against intact virus and penton base blocked the enhancing activity without affecting virus uptake. Antibodies against hexon and fiber blocked virus uptake and enhancing activity in parallel. These studies suggest that the penton base is important in lysis of the vesicles which contain adenovirus and EGF-PE, and this base allows virus and toxin to enter the cytoplasm.

Adenoviruses, Human↗
PubMed1984

Increased erythrocyte susceptibility to lipid peroxidation in myeloproliferative disorders.

The recognition of abnormal lipoprotein metabolism that produces chronic hypocholesterolemia in myeloproliferative disorders and the known influence of altered plasma lipid levels on erythrocyte membranes prompted a study of erythrocyte susceptibility to lipid peroxidation in myeloproliferative disease. Malonyldialdehyde generation during an oxidant challenge of erythrocyte suspensions of standardized hemoglobin concentration with H2O2 was significantly greater in 32 patients with myeloproliferative disease than in 47 hematologically normal subjects. The myeloproliferative disease group had significantly lower plasma total, HDL-, and LDL-cholesterol, erythrocyte indices, and erythrocyte deformability, and higher reticulocyte counts and serum lactic dehydrogenase. In the myeloproliferative disease group, mean corpuscular hemoglobin concentration, reticulocyte count, and erythrocyte count were significant variables in accounting for the observed variation in peroxidation susceptibility. Erythrocytes of patients with myeloproliferative disease had elevated concentrations of reduced glutathione, normal glutathione stability, and normal alpha-tocopherol content. These studies demonstrate increased susceptibility to oxidative damage in myeloproliferative disease despite normal or increased concentrations of the major antioxidant compounds of the erythrocyte. The presence of reticulocytosis, elevated serum lactic dehydrogenase, and decreased erythrocyte deformability suggests that lipid peroxidation susceptibility is associated with in vivo hemolysis and may contribute to the anemia that complicates myeloproliferative disease.

Cholesterol↗
PubMed1983

Hypocholesterolemia as a manifestation of disease activity in chronic myelocytic leukemia.

A patient with chronic myelocytic leukemia and hypocholesterolemia displayed marked fluctuations in plasma cholesterol in response to several therapeutic maneuvers. During chemotherapy there was a reciprocal relation between low density lipoprotein (LDL) cholesterol levels and the degree of leukocytosis and splenomegaly. LDL cholesterol increased after splenectomy, but continued to cycle inversely with the leukocyte count. Receptor-mediated degradation of 125I-labeled LDL (125I-LDL) by mononuclear cells in vitro also showed cyclical changes which were unrelated to the number of immature myeloid cells in the population or the level of plasma cholesterol. 125I-LDL degradation rate was normal or slightly increased during relapse and after remission was achieved, but was greatly increased when tested during periods of remission induction. This patient illustrates that significant changes in plasma total and LDL cholesterol occur in chronic myelocytic leukemia in association with alterations in proliferative state. Tumor load, the presence of an enlarged spleen, and changes in lipid metabolism of circulating cells all appear to contribute to the reduction in LDL cholesterol levels.

Adult↗