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Biomedical subjects

D Segre

Publications and source records attributed to D Segre.

At least 37 records · Page 2Linked to original sources
PubMed1989

[Current approach to the treatment of acute pancreatitis with reference to the use of somatostatin].

A series of 172 cases of acute pancreatitis encountered between 1-1-79 and 30-4-88, including 57 treated with somatostatin is presented. A comparison between the latter and the other cases treated with a variety of drugs (aprotinin, cimetidine, ranitidine) led to the following conclusions: 1) somatostatin significantly improves the clinical course of acute oedematous pancreatitis with circumscribed necrosis; 2) it makes no difference to the development of cases with diffuse necrosis and haemorrhage.

Acute Disease↗
PubMed1989

Age-related changes in the degeneracy of the mouse T-cell repertoire.

Aging is associated with a decline in T-cell-dependent immune responses. As the number of T-cells remains relatively constant throughout life, the observed decline in T-cell function may reflect qualitative changes in the T-cells themselves or in the composition of the T-cell population. In this investigation, the quality of the T-cell response was studied in young-adult and aged B6C3F1 mice by assessing the degeneracy of the hapten-specific proliferative response to the antigen-MHC complex. Degeneracy was defined as the ability of lymph node cells from mice contact-sensitized to the hapten TNP to proliferate in response to in vitro stimulation with haptenated allogeneic antigen-presenting cells, thus escaping strict MHC restriction. It was found that, although degeneracy occurred in both age groups, it was more prevalent and of a greater magnitude in the young than in the old lymphocytes. These results suggest that there are qualitative differences in T-cell populations derived from young-adult and aged mice.

Aging↗
PubMed1988

Impairment of T-helper function by a Plasmodium berghei-derived immunosuppressive factor.

Mice injected with an immunosuppressive factor (ISF) extracted from Plasmodium berghei-infected rat erythrocytes have a reduced antibody response to unrelated antigens. T-cells from ISF-treated mice failed to provide adequate help to naive, syngeneic B-cells in the primary IgM response in vitro to sheep red blood cells and to dinitrophenylated keyhole limpet hemocyanin. The same T-cells, however, were able to cooperate with memory B-cells in the secondary IgG response. No other cellular deficit was detected in ISF-treated mice; B-cells and macrophages behaved normally, and there was no detectable excess of suppressor cells. The T-cell impairment was not reflected in decreased production of interleukin 2, but was also shown by the diminished delayed type hypersensitivity reaction to sheep red blood cells of ISF-treated mice.

Animals↗
PubMed1985

Cyclophosphamide-induced suppressor cells in mice: suppression of the antibody response in vitro and characterization of the effector cells.

It was found earlier that nonspecific suppressor cells obtained from the spleen of mice injected with cyclophosphamide (Cy) at a dose of 200 mg/kg body wt are nonadherent, surface Ig negative, and Thy-1 negative. It is now reported that Cy-induced suppressor (Cy-S) cells suppress the in vitro primary and secondary humoral responses in a dose-dependent manner. Suppressor activity is a property of a low density cell that is found in the spleen from 5 to 11 days after Cy administration. Cy-S cells are negative for a number of T-cell markers and are nonadherent to plastic. They are not agglutinated by peanut agglutinin and do not acquire the Thy-1 antigen after treatment with thymosin, suggesting that they are not T-cell precursors. While NK activity was detected in the Cy-S cell preparations, this activity was removed by treatment with antibodies specific for the Qa-5 antigen and complement without affecting the suppressor activity. Cy-S cells are, therefore, distinct from B cells, T cells, NK cells, and macrophages.

Animals↗
PubMed1985

Modulation of autoimmunity in NZB mice by cyclophosphamide-induced, nonspecific suppressor cells.

A group of NZB mice received six biweekly injections of cyclophosphamide-induced nonspecific suppressor cells, with treatment commencing at 2 mo of age. Mice were evaluated for Coombs and natural thymocytotoxic antibody at 6-wk intervals thereafter, and for anti-DNA autoantibodies, total IgM and IgG levels, and renal histology at selected time points. The administration of suppressor cells resulted in marked and prolonged suppression of both Coombs and natural thymocytotoxic antibody reactivity in the majority of animals while not measurably affecting the levels of anti-DNA autoantibodies, the total IgM and IgG levels, or the life span of the mice.

Animals↗
PubMed1985

[Multidisciplinary radiological diagnosis of hepatic angioma in cancer patients].

72 cases of hepatic angioma were examined. These were occasionally found during control investigations of patients treated for extrahepatic primary cancer, or revealed by ultrasound studies of patients not supposed to be affected by cancer. Prospective comparison in 18 cases was made between echotomographic, tomodensitometric and angiographic findings with purpose of pointing out possible correlations between the X-ray images and the anatomopathological pictures. Finally, the best diagnostic procedure was established for suspected hepatic angioma, in both a cancerous and a non cancerous patients.

Angiography↗
PubMed1984

Effects of long-term treatment of mice with anti-I-J monoclonal antibody and dialyzable leukocyte extract on immune function and lifespan.

In 1969 Walford hypothesized that age-related dysfunctions of the immune system may be involved in the pathogenesis of the lesions and disease of aging. Studies were initiated to test whether immunologic interventions intended to maintain the integrity of the immune system would delay the onset of diseases of aging and prolong lifespan. Adult BC3F1 mice were treated with anti-I-J monoclonal antibody, with human dialyzable leukocyte extract, or with saline once a week for one year. Spleen cells from the mice were then assayed for suppressor, T-helper and B-cell activity. Treatment with dialyzable leukocyte extract decreased the elevated nonspecific suppressor activity. Mice treated with anti-I-J antibody had elevated T-helper cell activity. In another experiment, mice were treated weekly with anti-I-J antibody, dialyzable leukocyte extract, or saline from 18 months of age until natural death. The mice were immunized with avian gammaglobulin at 27 and again at 29 months of age. Both types of immunologic intervention resulted in a greater secondary antibody response than that of the saline-treated control mice. Mice treated with anti-I-J antibody survived longer than did mice of the other two groups. There was a correlation between the magnitude of the secondary response of individual mice and their lifespan. The results provide support for the immunologic theory of aging.

Aging↗
PubMed1982

Characterization of cyclophosphamide-induced suppressor cells.

Spleen cells from mice injected with cyclophosphamide (200 mg/kg body weight) suppress the secondary immunoglobulin (IgG antibody response of memory cells to a T-dependent antigen, dinitrolphenylated (DNP) human gamma globulin, in Millipore diffusion chambers. Characterization of the suppressor cell revealed that it was nylon wool nonadherent, insensitive to treatment with anti-Thy 1.2 or anti-Ig serum plus C, found in spleen but not thymus or lymph nodes, generated in thymectomized mice and nude mice, and heat-sensitive. Because of these unique characteristics, it was concluded that the suppressor cell was not a typical B cell, T cell, or macrophage. The suppressor cell was found to be regulated, i.e., inhibited, by a T cell found in the thymus and possibly the lymph nodes of normal mice. The suppressor cells may have biological significance in relation to development of self-tolerance.

Animals↗
PubMed1982

Diagnosis of histoplasmosis and blastomycosis by an antiglobulin hemagglutination test.

An antiglobulin hemagglutination test was developed for detection of antibody directed to Histoplasma capsulatum and Blastomyces dermatitidis. The substances responsible for spontaneous agglutination of erythrocytes were removed from histoplasmin and blastomycin by vacuum dialysis, and partial purification of the antigens by gel filtration chromatography on Sephadex G-150 allowed removal of additional nonantigenic material which competed with the antigens for binding on the erythrocyte surface. The test was sensitive enough to detect antibodies in sera which were negative by complement fixation, immunodiffusion, or both, but it failed to discriminate reliably between antibody directed to H capsulatum and antibody directed to B dermatitidis. Erythrocytes sensitized with partially purified blastomycin produced some false-positive reactions with normal canine sera; this was corrected by diluting the antigen before sensitization of the erythrocytes.

Animals↗
PubMed1981

Immunosuppression in murine malaria: a soluble immunosuppressive factor derived from Plasmodium berghei-infected blood.

Mice infected with Plasmodium berghei have a depressed immune response to a variety of antigens. We report the extraction, purification, and characterization of a soluble immunosuppressive substance derived from P. berghei-infected mouse blood. A crude extract, prepared by solubilization of infected erythrocytes in a Parr cell disruption bomb, reduced the anti-DNP PFC response of mice injected with the extract 1 day before immunization. Purification of the immunosuppressant was accomplished by precipitation with 50% saturated ammonium sulfate followed by chromatography on Sephadex G-150 in the presence of 6 M guanidine hydrochloride. The immunosuppressive activity was recovered in the last fraction eluted from the Sephadex G-150 column that contained low m.w. components. The activity was abrogated by trypsin digestion, but not by periodate oxidation. Volume for volume, the purified immunosuppressant had a 100-fold greater activity than the crude extract from which it was derived. It suppressed the response to the T-dependent antigens DNP-KLH and SRBC, but not to the T-independent antigen DNP-Ficoll.

Animals↗
PubMed1980

[Protective effect of citicoline on renal ischemia].

The protective role of cyticholine was investigated on rabbit and dog kidneys subjected to temporary ischaemia. Following right nephrectomy, the right kidneys of 13 rabbits were subjected to warm ischaemia for 60'. Death occurred for various reasons within 48 hr. Histological examination suggested that tubular epithelium damage was less in the animals treated with cyticholine. In a similar experiment on 6 dogs after local and general infusion of cyticholine, warm ischaemia for 90' was followed by death in 33%, compared with 87.5% of the controls. Blood creatinine and BUN returned to normal between the 6th and the 8th days in the four surviving animals. The data suggest that cyticholine assists the functional recovery of kidneys subjected to warm ischaemia for more than 30' and limits tubular damage.

Animals↗
PubMed1980

Generation of suppressor T cells during the primary response of murine spleen cells in diffusion chambers.

A vigorous secondary response to DNP is elicited by dinitrophenylated keyhole limpet hemocyanin (DNP-KLH) in spleen cells from primed mice cultured in Millipore diffusion chambers. However, the same antigen under the same conditions does not elicit a primary response in normal spleen cells. In contract, foreign erythrocytes elicit a primary response and function as an effective carrier for the primary response to a hapten. We found that the failure of haptenated protein to induce a primary response in diffusion chambers can be attributed to the generation of suppressor T cells by the protein. Cultures of T depleted normal spleen cells, supplemented with carrier-specific helper T cells, developed a DNP-specific primary response upon stimulation with DNP-KLH.

Animals↗
PubMed1979

Inhibition of the humoral response by spleen cells from cyclophosphamide-treated mice.

Spleen cells obtained from mice injected with cyclophosphamide (200 mg/kg body weight) suppressed the secondary IgG antibody response of memory cells to a T-dependent antigen, DNP-HGG, in Millipore diffusion chambers. Significant suppression (greater than 50%) was found from 5 to 14 days following cyclophosphamide treatment, with peak suppression (86%) on day 7. The primary IgM antibody response to DNP-Ficoll, a T-independent antigen, was not suppressed by these cells. In contrast, suppression was observed in the primary IgM response to sheep red blood cells, a T-dependent antigen. In addition, treatment of the suppressor cell population with anti-Thy-1 serum and complement did not inhibit suppressor activity. We concluded that the suppressor activity was not attributable to a typical T cell, and that the target of suppression was not a B cell. Preliminary evidence suggests that the suppressor activity is regulated, directly or indirectly, by a T cell.

Animals↗