Biomedical subjects
J Westall
Publications and source records attributed to J Westall.
Tuberculosis levelling off worldwide.
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Poor education linked with teen pregnancies.
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Shackling of prisoners denounced.
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Sickle cell disease is poorly managed.
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Diminished interferon-gamma and lymphocyte proliferation in neonatal and postpartum primary herpes simplex virus infection.
Interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha production and lymphocyte proliferation in response to herpes simplex virus (HSV) antigen were assessed in 13 neonates and 3 parturient women with primary HSV infection. In comparison with 9 nonparturient adults, the neonates and parturient women showed significantly (P less than .01) diminished HSV antigen-stimulated lymphocyte proliferation and IFN-gamma production in the first 3-6 weeks after onset of infection. TNF alpha production did not differ significantly among HSV-infected groups. The impairment in neonatal cellular immunity was due, at least in part, to a specific deficit in response to HSV antigen. Lymphocyte proliferation and TNF alpha production in response to the mitogen concanavalin A (ConA) were comparable in adults and infants, but ConA-stimulated IFN-gamma production in infants was diminished throughout the study period. In contrast, HSV antigen-stimulated IFN-gamma production was comparable in infants and adults after 6 weeks. Not all patients with diminished cellular immune responses to HSV antigen manifested severe clinical disease. Nevertheless, patients with significant clinical morbidity had diminished cellular immune responses to HSV antigen. These results suggest that delayed acquisition of antigen-specific cellular immunity in primary HSV infection predisposes to more severe clinical disease.
Community care for the seriously mentally ill.
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Decreased production of interferon-gamma by human neonatal cells. Intrinsic and regulatory deficiencies.
Human neonatal lymphocytes produced little macrophage activation factor in response to mitogens. This correlated with decreased production of interferon-gamma (IFN gamma): adult lymphokines contained 894.2 +/- 177.1 U/ml, whereas neonatal cord and peripheral lymphokines contained 66.9 +/- 17.0 and 116.7 +/- 29.6 U/ml by bioassay. Results by radioimmunoassay (RIA) for IFN gamma were similar. In contrast, the interleukin 2 content of cord lymphokines was greater (P less than 0.01) and that of neonatal peripheral blood lymphokines similar to that of adults. Interleukin 1 production and interleukin 2 receptor expression and affinity were similar for adult and neonatal cells. Interleukins 1 and 2 in amounts comparable to those in adult lymphokines did not increase production of macrophage activation factor or IFN gamma by neonatal cells. Neonatal cells did not contain intracellular IFN or degrade exogenous IFN. Excess suppressor activity was not found in neonatal cultures. Addition of IFN alpha, 10,000-50,000 U/ml of interleukin 2 or phorbol myristate acetate (PMA) to cord mononuclear cells or of adult monocytes or PMA to cord T cells increased IFN gamma production compared to cells stimulated with concanavalin A (ConA) alone. Nevertheless, under optimal conditions (T cells + PMA + Con A), adult cells produced much more IFN gamma (1,360 +/- 261 U/ml by RIA) than cord cells (122 +/- 37 U/ml). Staphylococcal enterotoxin A (SEA) stimulated cord cell IFN gamma production at low cell densities; nevertheless, adult cells produced more IFN in response to SEA 1,341 +/- 350 U/ml) than cord cells (350 +/- 33 U/ml). Decreased production of IFN gamma by neonatal cells appears to be due both to differences in their intrinsic capacity to produce IFN gamma and to differences in regulatory mechanisms.
Activation of neonatal and adult human macrophages by alpha, beta, and gamma interferons.
Increasing evidence suggests that gamma interferon (IFN-gamma) is the major or sole factor in human lymphokines which activates blood monocyte-derived macrophages (M phi) to inhibit or kill Toxoplasma gondii and certain other intracellular pathogens. In the current studies, we found that IFN-gamma effectively activated tissue M phi from adults (peritoneal M phi) and from newborns (placental M phi) as well as blood-derived M phi from adults and from newborns to kill or to inhibit the replication of T. gondii. Results with purified and recombinant IFN-gamma and with adult and newborn M phi were similar. IFN-gamma-treated M phi were equally or more active against T. gondii than were freshly isolated monocytes and M phi. Recombinant IFN-alpha A and IFN-beta were less effective than IFN-gamma. IFN-gamma also inhibited survival and replication of T. gondii in WISH cells more effectively than did IFN-alpha and IFN-beta. These findings are consistent with an important role for IFN-gamma in the control of Toxoplasma infection and indicate that the anti-Toxoplasma activity of resting and IFN-gamma-activated adult and neonatal M phi is similar. The increased susceptibility of neonates to T. gondii is not due to a defect in M phi effector function.