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Biomedical subjects

R L Hirsch

Publications and source records attributed to R L Hirsch.

At least 73 records · Page 4Linked to original sources
PubMed1980

Lymphocyte responsiveness to acetylcholine receptor in rats with experimental autoimmune myasthenia gravis.

We examined the time course of lymphocyte responsiveness to acetylcholine receptor (AChR) in rats with experimental autoimmune myasthenia gravis (EAMG). Rats were immunized with purified torpedo AChR. At intervals of one to eight weeks later, lymphocytes from the lymph nodes and spleen were cultured with purified torpedo AChR and rat muscle extract containing AChR. Lymphocyte responsiveness (stimulation index) was determined from uptake of 3H-labeled thymidine by the cultured cells. The response of lymphocytes to torpedo antigen began earlier and rose more rapidly than that to the homologous (rat) antigen. Lymph node cells responded more promptly than spleen lymphocytes. The stimulation indexes peaked at four to six weeks while antibodies to both antigen continued to rise. Delineation of this pattern of lymphocyte responsiveness sheds further light on the pathogenesis of the autoimmune response in EAMG and will be useful in the future design of immunotherapeutic strategies.

Acetylcholine↗
PubMed1980

The role of complement in viral infections. II. the clearance of Sindbis virus from the bloodstream and central nervous system of mice depleted of complement.

The following studies were performed to investigate the mechanism(s) by which the complement system limits Sindbis virus infection in the central nervous system of mice. After the intracerebral inoculation of Sindbis virus, no differences in mortality or viral growth in the central nervous system were observed between normal mice and mice depleted of complement by treatment with cobra venom factor. In addition, animals that had been inoculated subcutaneously with Sindbis virus and depleted of complement after the viremic phase had ended did not show any differences in mortality or viral growth in the central nervous system. In contrast, it was found that after the intracardiac inoculation of virus, complement-depleted mice demonstrated a defect in the clearance of infectious virus from the blood. These studies suggest that the increased growth of virus in the brains of complement-depleted mice after the subcutaneous inoculation of Sindbis virus is due to a defect in clearance of infectious virus from the bloodstream rather than to a primary defect within the central nervous system.

Animals↗
PubMed1980

An evaluation of the CODABAR symbol in blood-banking automation.

The CODABAR system has been used in blood banking automation since 1976 when it was introduced by 16 blood centers and transfusion services throughout the United States in a test program coordinated by the American Blood Commission Committee for Commonality in Blood Banking Automation. Since then CODABAR has been used in sample identification on Groupamatic and Technicon automated blood-typing equipment, in the labeling of blood products and in their distribution. It is widely used by a number of blood centers in the United States and has been adopted by the 14 regional blood centers in the United Kingdom, as well as blood centers in Switzerland, the Netherlands and Japan. Some properties of the CODABAR symbol that are relevant to the high accuracy requirements of blood banking are described and preliminary test data are presented.

Autoanalysis↗
PubMed1979

Interactions between immune cells and antibody in protection from fatal Sindbis virus encephalitis.

Transfer of anti-Sindbis virus serum, obtained from peripherally inoculated donors, protected mice from an otherwise fatal intracerebral infection with neuroadapted Sindbis virus (NSV). F(ab)'2 preparations of serum were not protective, indicating that the Fc piece of immunoglobulin G was important. Complement-depleted animals were protected with anti-NSV serum, ruling out as essential the complement-fixing function of the Fc piece. The presence of protective antibody correlated with the ability of serum to inhibit T-cell cytotoxicity. However, experiments using athymic nude mice showed that T cells played no role in killing the mice since the 50% lethal dose was the same as that in normal BALB/c mice, and that T cells were not required for protection since athymic nude mice were protected with antibody alone. Cyclophosphamide treatment of NSV-infected mice ablated the protective capacity of anti-NSV serum. Therefore, a non-T cell, cyclophosphamide-sensitive cell was required for antibody-mediated protection.

Animals↗
PubMed1978

The effect of complement depletion on the course of Sindbis virus infection in mice.

The course of Sindbis virus infection in 12-day-old BALB/c mice was altered significantly in animals depleted of the third component of complement (C3) by treatment with purified cobra venom factor (CoVF). Although the same percentage of C3-depleted and normal animals died (30%) after the subcutaneous inoculation of 1000 PFU Sindbis virus, the mean day of death was later in C3-depleted mice (8.4 days) than in controls (6.5 days). In addition, morbidity was prolonged in C3-depleted mice. Growth of virus at the inoculation site in the foot was not different; however, viremia was prolonged and the amount of virus in the brain was 1000-fold greater 6 days after infection in C3-depleted animals. These studies demonstrated that complement plays an important role in the host's response to Sindbis virus infection by participating in both beneficial and immunopathologic responses to the infection.

Aging↗
PubMed1977

Temperature effects on lymphocyte transformation invitro.

Phytohemagglutinin (PHA)-induced transformation of normal rat peripheral lymphocytes has been studied at a wide range of culture temperatures (4 degrees C to 42 degrees C). Lymphocyte transformation was maximum at 37 degrees C while insignificant stimulation was observed between 4 degrees C and 30 degrees C. Temperatures above 37 degrees C produced sub=optimal transformation as measured by synthesis of DNA and protein, and appearance of lymphoblasts. Binding studies using 125I-PHA indicate that the low temperature inhibition of lymphocyte transformation could be a result of excess lectin (being available as a result of low temperature) bound to the cell surface, preventing the initiation of the molecular events associated with transformation.

Cell Membrane↗
PubMed1975

Hepatitis B surface antigen in blood donors: further observations.

A survey of 128,000 volunteer blood donors from the Greater New York metropolitan area revealed that first-time male donors were positive for hepatitis B surface antigen (HBsAg) 2.5 times more frequently than were first-time female donors; Negroes and Mongols were positive four to 20 times more frequently than Caucasians. The ratio of ad to ay seemed to be higher in non-Caucasian antigen carriers than in Caucasian carriers. Among both Caucasians and non-Caucasians the rate of positivity declined after the age of 50. An excess prevalence of HBsAg was observed in donors with the lowest level of education and in those with the highest level. HBsAg was detectable nine times less frequently among repeat donors than among first-time donors (0.2 vs.1.90 per 1,000). Detection of HBsAg was unrelated to ABO-Rh blood groups. Several mechanisms for these wide variations of antigen detection are possible.

ABO Blood-Group System↗