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Biomedical subjects

H Friedman

Publications and source records attributed to H Friedman.

At least 397 records · Page 22Linked to original sources
PubMed1979

B and T lymphocyte activation by murine leukemia virus infection.

FLV is suppressive both in vivo and in vitro in terms of the specific sheep RBC induced antibody response. FLV-containing extracts from infected spleens were found to be markedly immunosuppressive. However, these extracts stimulated the background PFC response to SRBC in vitro, whereas similar background responses were depressed in infected animals. Furthermore the virus-containing extracts were mitogenic for normal spleen cells in vitro. Thus, FLV infection may cause immunocyte division (i.e., transformation) as an early event followed later by marked impairment of the function of the cells as evinced by their failure to respond normally to challenge immunization.

Animals↗
PubMed1979

Herpes simplex esophagitis: a cause of upper-gastrointestinal bleeding.

Two patients with hemorrhagic esophagitis secondary to esophageal invasion with herpes simplex virus, type 1, are reported. Microscopic examination of the esophageal mucosa revealed multinucleated cells and intranuclear inclusions which are typical of herpes simplex infection. Herpes virus was cultured from each patient. Thus, hemorrhagic esophagitis due to esophageal invasion by herpes simplex virus may be a more frequent cause of upper-gastrointestinal bleeding than previously recognized.

Aged↗
PubMed1979

Lip biopsy in connective tissue diseases. A review and study of seventy cases.

The labial salivary glands from seventy patients with systemic lupus erythematosus (twenty cases), systemic progressive sclerosis (twenty-two cases), rheumatoid arthritis (twenty-three cases), and Sjögren's syndrome (five cases) and from fifty subjects without connective tissue diseases were studied by means of light and fluorescence microscopy. The availability of the lip biopsy as a diagnostic tool is stressed, but a differential diagnosis between the different connective tissue diseases was not achieved. Yet some of the latter disclosed peculiar lesions. The role of the inflammatory and degenerative components, as well as the pathogenesis of the lesions, is discussed.

Amyloid↗
PubMed1979

Stimulation by a hydroxythiazolobenzimidazole of enhanced formation of antibodies to sheep erythrocytes in vitro and in vivo.

A hydroxythiazolobenzimidazole, a low molecular weight compound, was found to have an immunoenhancing effect on both the in vivo and in vitro antibody response of mouse spleen cells to an optimum immunizing dose of sheep red blood cells. At noncytotoxic concentrations the optimum range of 25 to 50 micrograms per 5 x 19(6) spleen cells was most effective in vitro. Concentrations greater than 100 micrograms per culture were toxic in vitro and reduced cell viability as well as antibody responsiveness. The compound enhanced to an even greater degree the antibody response of spleen cell cultures immunized with suboptimum doses of SRBC. The background PFC response, in the absence of SRBC, also was stimulated by the benzimidazole. These immunoenhancing responses were not related to mitogenic effects, since increased thymidine uptake did not occur when normal mouse spleen cells were incubated with graded doses of the compound. Therefore, the immunostimulatory properties of the compound, both in vivo and in vitro, were not due to mitogenic stimulation of lymphoid cells.

Animals↗
PubMed1979

Factors from lymphoid cell tumor affecting immune responses.

Friend leukemia virus induces erythroblastic leukemia in genetically susceptible BALB/c mice. FLV-containing leukemic cells markedly depressed the humoral immune response to SRBC in the appropriate mouse strain. Both immunosuppression and leukemogenesis were readily transmitted by cell-free virus-containing homogenates of the FLV leukemic splenocytes into normal BALB/c mice. In the present study it was found that both Friend leukemic splenocytes as well as virus containing extracts from the leukemic cells were neutralized by heating and by specific antisera. Suppressive activity passed through a 0.45 mu filter but not a 300,000 MW filter and could be pelleted at 100,000 x g. They were also highly resistant to inactivation by irradiation. Mice given leukemic splenocytes after irradiation with up to 32.000 rads still developed leukemia. Addition of either normal or irradiated FLV-leukemic cells to normal spleen cell cultures in vitro markedly suppressed antibody formation. At least 32,000 rads were required to significantly impair the immuno-suppressive activity of the FLV-leukemic cells. Thus, virus per se appears to be directly responsible for suppression of antibody formation to FLV.

Animals↗
PubMed1979

Macrophage factors that enhance the antibody response.

The immunological mechanism of the primary in vitro antibody responses to sheep erythrocyte antigens involves soluble immunomodulatory factors. These studies have demonstrated that the stimulation of immunocytes with lipopolysaccharide (LPS) induced the release of a helper factor which appeared to be a monokine. This helper factor was released by stimulated adherent splenocyte cultures but not by nonadherent cell populations. The P388D-transformed macrophage cell line also produced the factor in response to LPS. LPS-induced helper factors were absorbed from solution by bone marrow cells but not by thymocytes, thereby indicating that the factor may selectively bind to B-cells or to undifferentiated stem cells. Mature T-cells did not appear to be involved in the immunostimulatory effects of this macrophage-derived factor as evidenced by the results of several studies. These included observations that splenocytes from athymic BALB/c nu nu mice both produced the factor and responded to it.

Animals↗
PubMed1979

Suppression of in vitro antibody response by spleen cells of mice infected with Friend-associated lymphatic leukemia virus.

The ability of spleen cells of mice infected with oncornaviruses to depress the in vitro antibody responsiveness of normal lymphoid cells was exploited in an attempt to clarify the role played by the lymphatic leukemia virus (LLV) component in the immunodepressive properties of the Friend leukemia complex. Spleen cells of mice infected with LLV or, for comparison, with the entire complex were added to cultures of sheep erythrocyte-primed uninfected spleen cells, and the antibody-forming cells produced by the latter, after antigen restimulation, were assayed. The addition within 2 days from culture initiation of low numbers of cells infected with either virus preparation suppressed all stages of the response affecting the production of both immunoglobulin M and immunoglobulin G antibody. The activity of infected cells resisted doses of ultraviolet radiation which inhibit cell multiplication but was abolished by disrupting the cells and was prevented by the presence of anti-LLV antibodies. The LLV-infected spleen cells responsible for suppression were not removed by treatments which selectively remove or kill macrophages and exhibited surface properties of B lymphocytes. These results were interpreted as indicating that the effect is due to virus (or viral products) released by B cells. The suppressing cells in the spleens of mice in the early days of Friend leukemia complex infection presented superimposable properties, supporting the concept that their activity is also due to the LLV they release in large quantities. However, in later stages of infection, the spleens of Friend leukemia complex-infected mice also contained non-B-suppressing cells possibly derived from the proliferation of nonlymphoid LLV-producing cells caused by the neoplastic process.

Animals↗
PubMed1979

Morphologic effects following massive exchange transfusions with a stroma-free hemoglobin solution. II. Kidney.

The effects on renal morphology of exchange transfusion with stroma-free hemoglobin solutions (SFHS) were compared in rats to the results obtained using an asanguineous resuscitative fluid containing albumin. Animals underwent 75 per cent blood volume replacement, and tissue collected at intervals after the exchange transfusion was examined by light and electron microscopy. Urine volumes, osmolarity, and pH also were determined, and serum creatinine and blood urea nitrogen were measured both before and after exchange transfusion. Hemoglobin was filtered through the renal glomerular basement membrane, and a portion was reabsorbed into the proximal tubular cells in the form of absorption droplets. Unabsorbed hemoglobin was excreted in the urine. Despite a distention of proximal and distal tubules 5 hours after exchange transfusion with SFHS, there was no ultrastructural evidence of renal parenchymal damage. Proximal tubular cells of albumin-exchanged animals contained fewer protein absorption droplets and no intraluminal material. The apparent higher rate of glomerular filtration of hemoglobin over albumin probably reflected the dissociation of hemoglobin into dimers, resulting in a diuresis. Urine volumes were 3 times greater in SFHS-exchanged animals than in albumin-treated rats, and the urine was relatively hypoosmolar in the former. The greater urine volumes in SFHS-treated animals also were associated with a large reduction in intravascular fluid volume. There was no alteration of serum creatinine or blood urea nitrogen after exchange transfusion with albumin and only a mild elevation in blood urea nitrogen in SFHS-treated rats. The latter most likely was a result of prerenal hypovolemia. SFHS, even when exchange-transfused in massive quantities, does not appear to affect renal function or ultrastructural morphology adversely. However, the rapid disappearance of hemoglobin from the intravascular space, the consequent loss of intravascular fluid volume, and the diuresis induced by its administration are complications which must be overcome before the product can be a useful adjunct in the treatment of hemorrhagic shock.

Animals↗
PubMed1978

Murine lymphoma-induced immunosuppression: requirement for direct tumour cell contact.

The FBL-3 lymphoma cell line caused impaired antibody formation in vivo when injected into mice intraperitoneally, and in vitro when added to normal syngeneic spleen cells immunized in vitro with sheep erythrocytes. Immunosuppression occurred only when intact viable tumor cells were cocultivated with the normal spleen cells. As few as 10(5) FBL-3 cells, when added to 5 X 10(6) normal cells, impaired antibody formation. However, cell-free extracts of filtrates from even much larger numbers of tumor cells did not affect antibody formation, either in vitro or in vivo. Heating the tumor cells at 56 degrees C or irradiation with as little as 1000 rads completely abolished immunosuppressive activity, both in vitro and in vivo. Separation of viable tumor cells from target antibody-forming cells by cell-impermeable membranes prevented immunosuppression, showing that direct cell-to-cell contact is required for immunosuppression.

Antibody Formation↗