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Biomedical subjects

J F Balavoine

Publications and source records attributed to J F Balavoine.

18 recordsLinked to original sources
PubMed2003

Severe thrombocytopenic purpura due to rubella infection in a patient with systemic lupus erythematosus.

We report the case of a woman suffering from systemic lupus erythematosus who developed a severe thrombocytopenic purpura (platelet count < 1 x 10(9)/l) secondary to rubella infection. The search for antiplatelet antibodies revealed transient circulating anti-GPIIb-IIIa and anti-GPIb-IX platelet antibodies. After a few weeks, bound anti-GPIIb-IIIa antiplatelet antibodies were still detectable and they persisted several months after recovery, probably in relation to a mild autoimmune thrombocytopenia related to systemic lupus erythematosus. To our knowledge, this is the first case report of severe thrombocytopenic purpura due to rubella in an adult with systemic lupus erythematosus.

Adult↗
PubMed1987

A urine inhibitor of interleukin 1 activity affects both interleukin 1 alpha and 1 beta but not tumor necrosis factor alpha.

Urine from monocytic leukemia and other febrile patients contains an inhibitor of interleukin 1 (IL-1), as measured by prostaglandin E2 and collagenase production by human fibroblasts and synovial cells. With the use of recombinant IL-1, the IL-1 inhibitor was partially purified by using ammonium sulfate precipitation, anion-exchange, and gel filtration chromatographies. IL-1 inhibitory activity elutes with an 18,000 to 25,000 apparent molecular size. The same fractions also inhibit IL-1 assayed by the proliferation of murine thymocytes and human fibroblasts. Both forms of human recombinant IL-1, IL-1 alpha and IL-1 beta, which show only 26% homology, but nevertheless bind to the same receptor, are affected by this natural inhibitor to the same extent. In contrast, human recombinant tumor necrosis factor, which shares some of the biologic activities of IL-1, is not inhibited by the urinary IL-1 inhibitor. This study shows that the various biologic activities of both forms of human recombinant IL-1 are inhibited by a partially purified natural urine-derived factor.

Cell Division↗
PubMed1986

[Persistent generalized lymphadenopathies in homosexuals and drug addicts: changes in humoral and cellular immunity].

In two groups of subjects at risk for acquired immune deficiency syndrome (AIDS), homosexual males and intravenous drug users with persistent generalized lymphadenopathy, humoral and cell-mediated immunity were compared. A small group of patients with definite AIDS were also studied. It was found that levels of immunoglobulins, serological markers for virus and other infections, cell-mediated immunity and histology of lymph nodes were similar in homosexuals and drug users, whereas the lymphocyte sub-populations differed completely. The number of T4+ lymphocytes was markedly decreased in homosexuals but normal in drug users; the number of T8+ lymphocytes was much higher in drug users than in homosexuals. This discrepancy may explain the extremely low prevalence of AIDS cases observed among Swiss drug users as compared with the high frequency noted among homosexuals.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Altered functions of peripheral blood monocytes in homosexual males and intravenous drug users with persistent generalized lymphadenopathy.

Persistent generalized lymphadenopathy (PGL) is observed predominantly in subjects at risk of developing AIDS. Twenty-seven individuals belonging to such groups: twelve homosexual males and fifteen intravenous drug users, were investigated for immunological abnormalities with particular attention to monocyte functions. They were compared with five AIDS patients. Twenty out of twenty-two individuals had anti-LAV/HTLV-III antibodies and most had abnormalities characteristic of AIDS: polyclonal hypergammaglobulinemia, decreased cell-mediated immunity, inverted T-cell helper/suppressor ratio and histological alterations of lymph nodes. As for peripheral blood monocyte functions, phagocytic capacity and production of O2- were normal and bactericidal capacity was decreased. Monocytes cultured in the presence of concanavalin A produced less PGE2 and more IL-1/MCF than normal monocytes. Similar abnormalities were found using monocytes from AIDS patients. These data suggest that monocytes from patients with PGL have functional alterations that may be either intrinsic or secondary to lymphocyte dysfunction(s); these alterations do not account for the decreased capacity of lymphocytes to respond to mitogens but may explain the uncontrolled activation of B cells.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Prostaglandin E2 and collagenase production by fibroblasts and synovial cells is regulated by urine-derived human interleukin 1 and inhibitor(s).

Interleukin 1 (IL-1) possesses multiple biological activities that may be blocked selectively by different inhibitors. Some known inhibitors block the lymphocyte activating factor (LAF/IL-1) but not the mononuclear cell factor (MCF/IL-1) measured by its capacity to stimulate prostaglandin E2 (PGE2) and collagenase production. The presence of IL-1 in vivo may be difficult to detect due to the presence of inhibitor(s) and the level of the inhibitor(s) may vary depending upon pathological conditions. We have found that urine from three patients with monocytic leukemia (M5) contained high levels of inhibitor(s) of MCF/IL-1, whereas urine of normal subjects did not contain significant amounts. Urine from two patients with other blood neoplasic diseases also contained little inhibitory activity. The MCF/IL-1 inhibitor(s), which also acts on human recombinant IL-1 beta, is approximately 25-35 kD, is not retained on concanavalin A-Sepharose column and can be partially destroyed with urea and boiling. At this stage of the purification the fraction containing the MCF/IL-1 inhibitor(s) also inhibits the LAF/IL-1 assay. However, this inhibitor(s) is probably distinct from other inhibitors already described.

Adult↗
PubMed1984

Interleukin 1 can replace monocytes for the specific human B-cell response to a particulate antigen.

It is shown that the anti-trinitrophenyl (TNP) response of human B cells to trinitrophenyl polyacrylamide beads (TNP-PAA) is monocyte dependent. This response is abolished by extensive adherent cell depletion and restored by the addition of monocytes. The optimal response is obtained with 3% monocytes, higher numbers being suppressive. Supernatants from muramyl dipeptide (MDP)-activated monocytes can restore the response of monocyte-depleted preparations even when cells are cultured at suboptimal concentration. A partially purified preparation of interleukin (IL-1) has a comparable restorative ability. The following arguments suggest that monocytes do not function as antigen-presenting cells for this particulate antigen: (i) antigen-pulsed monocytes induce neither an anti-TNP response nor a specific T-cell proliferative response; (ii) allogeneic monocytes function as well as autologous monocytes to restore the response of nonadherent cells; (iii) HLA-DR-negative cells from the human leukemia cell line K562 can replace monocytes for this response. Monocyte supernatants do not replace T cells for the response of B-enriched lymphocytes, showing that T cells are directly involved in B-cell activation.

Acrylic Resins↗
PubMed1984

Captopril and immune regulation.

We examined the in vitro effect of captopril (2.5 to 5 micrograms/ml) on the primary antibody response of human B cells. Captopril suppresses (by 50%) the specific anti-trinitrophenyl (TNP) response of unfractionated peripheral blood mononuclear cells (PBM) but not that of nonadherent PBM. The susceptibility to captopril suppression can be restored in the latter cell cultures by 10% adherent radioresistant cells. This suppression is independent of prostaglandins. In transfer experiments, cells preincubated with 5 micrograms/ml captopril suppress the antibody response of autologous nonadherent PBM. The inductive phase of this suppression requires both adherent cells and radiosensitive T cells. Once induced, the suppression can be transferred by isolated T effector cells. In vivo after a unique oral intake of captopril a moderate suppressor activity can be demonstrated in adherent cells from normal individuals. We conclude that captopril interferes with the immune regulation by inducing a suppressor circuit involving monocytes and a T8 suppressor effector lymphocyte.

Antibody Formation↗
PubMed1983

[Acute kidney failure: age is not a factor in the prognosis].

The mortality of acute renal failure (ARF) remains distressingly high despite intensive dialysis and remarkable advances in critical care medicine. This lack of survival improvement may be due to an increased frequency of septic ARF and/or the association with multiple organ dysfunction. The role of age, as a factor indicative of a poor prognosis is a matter of controversy. To evaluate this role we have analysed the final outcome of 103 patients with ARF treated between october 1978 and february 1982 by one or more hemodialysis. The average age was 65.1 +/- 14.9 years (mean +/- standard deviation): 64 patients were over 65 years of age (74.7 +/- 10.2), 39 were under this age (47.5 +/- 14.4). Septic causes were found in 64 cases. Sixty eight patients (66%) died during the period of ARF. Mortality was 67% in patients under 65 years of age and 66% in patients over this age (p greater than 0.90). The outcome of septic ARF was independent of age (mortality rate: 79% for patients less than 65 years, 81% for patients greater than 65 years (p greater than 0.90)). The poor prognosis is probably related to multiple organ dysfunction and specially to acute respiratory distress (89% mortality). It can be concluded that patient's age does not worsen the prognosis of ARF.

Acute Kidney Injury↗