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J J Stern

Publications and source records attributed to J J Stern.

At least 37 records · Page 2Linked to original sources
PubMed1993

Early diagnosis of ectopic pregnancy using receiver-operator characteristic curves of serum progesterone concentrations.

The objective was to assess the usefulness of serum progesterone concentrations in the differentiation of intra-uterine (viable and non-viable) and extra-uterine pregnancies. Progesterone concentrations were prospectively measured at 4, 5 and 6 weeks gestation in 338 pregnancies which resulted in 242 viable births, 81 abortions and 15 ectopic pregnancies. Progesterone threshold analysis was performed using receiver-operator characteristic curves. The progesterone threshold value for ectopic pregnancy at 4 weeks was 5 ng/ml, at 5 weeks 10 ng/ml and at 6 weeks 20 ng/ml. A significant difference was observed between all intra-uterine versus ectopic pregnancies (P = 0.0005), but not between viable versus non-viable intra-uterine pregnancies (P = 0.37). The differences were most clearly defined at 4 weeks and decreased with increasing gestation. We conclude that serum progesterone and gestational age taken together can differentiate intra-uterine from extra-uterine pregnancies with a very high sensitivity and specificity at 4 weeks gestation, a time when ectopic pregnancies are not evident on ultrasound examination.

Abortion, Spontaneous↗
PubMed1993

Current status of immunologic recurrent pregnancy loss.

Normal mammalian pregnancy is confronted with a great number of self (autoimmune) and foreign (alloimmune) antigens that modulate the immune system of the mother. When maternal immune response is affected, recurrent pregnancy loss can result. Recurrent pregnancy loss affects 2% to 5% of reproducing couples. Half of these failures can be explained by genetic, hormonal, infectious, and anatomic factors. Eighty percent of the unexplained failures are proposed to have an immunologic cause. HLA typing, mixed lymphocytotoxic antibody tests, mixed lymphocyte culture reactions, lupus anticoagulant tests, and antiphospholipid antibody determination are methods used to study and differentiate between auto- and alloimmune response. Experimental therapies, including leukocyte immunization, seminal plasma suppositories, intravenous immunoglobulin, aspirin and prednisone, and heparin, have been tried to manage this condition. Results of randomized placebo-controlled clinical trials will aid in the choice of treatment for recurrent pregnancy loss. New assays to diagnose auto- and alloimmune factors in recurrent pregnancy loss are being investigated.

Abortion, Habitual↗
PubMed1992

Mechanism of recurrent spontaneous abortion. I. Ultrasonographic findings.

OBJECTIVES: Our objective was to study the mechanisms of early pregnancy loss with ultrasonographic findings in pregnancies that terminated in repeat abortion in women with recurrent spontaneous abortion compared with patients with spontaneous abortion with no previous spontaneous abortion and with women with recurrent spontaneous abortion who had viable pregnancies. STUDY DESIGN: A prospective, unselected study of 83 pregnancies followed from 4 to 12 weeks of gestation. Weekly transvaginal ultrasonography.among 43 pregnancies terminating in abortion were compared with 40 pregnancies ending in live birth with the Fisher exact test with a p value of significance assigned at less than 0.05. RESULT: A significant difference in the presence of fetal heart activity was observed at 6 weeks +/- 5 days among women who subsequently aborted when recurrent spontaneous abortions were compared with no history of abortion (55% and 14%, p less than 0.02). Fetal pole size was small in 86% of pregnancies lost after fetal heart activity. CONCLUSION: Ultrasonographic examination at 6 weeks can diagnose impending abortion with a sensitivity of 85%, specificity of 93%, positive predictive value of 92%, and negative predictive value of 87% among women with recurrent spontaneous abortion.

Abortion, Habitual↗
PubMed1991

Immunology of ovarian failure.

Ovarian failure is the result of depletion of ovarian follicles. Naturally occurring ovarian failure usually takes place around 50 years of age in the human. Premature ovarian failure occurs in 1% of women and is the result of acceleration of rate of ovarian follicular depletion in the majority of cases. Cytokines are involved in the mechanisms of ovarian follicular atresia, whether it occurs at a normal or accelerated rate. It is the balance between the actions of TGF alpha and TGF beta upon the granulosa cell that determines the fate of a nonluteinized follicle and between LH and INF gamma that determines destiny of a luteinized follicle. When granulosa cells express MHC antigens in response to IFN gamma or genetic stimulus, an autoimmune reaction ensures resulting in follicular atresia. If the immune processes proceed continuously rather than cyclically, premature ovarian failure occurs. Thus, not only do the immunologic and endocrinologic systems need to communicate to allow normal ovarian function, evidence exists to support the concept that they interact in the pathophysiology of ovarian failure.

Adult↗
PubMed1988

Role of L3T4+ and LyT-2+ cells in experimental visceral leishmaniasis.

In contrast to euthymic (nu/+) BALB/c mice, athymic nude (nu/nu) BALB/c mice fail to control the visceral intracellular replication of Leishmania donovani, do not generate the macrophage-activating lymphokine IFN-gamma, and show little or no granulomatous tissue response. To characterize the T cell requirement for successful defense against L. donovani, nude mice were first reconstituted with unfractionated nu/+ immune spleen cells, which readily conferred the capacity to control and eliminate visceral (hepatic) L. donovani. In reconstituted mice, acquired resistance was paralleled by the ability of spleen cells to generate high levels of leishmanial Ag-stimulated IFN-gamma and the development of well formed liver granulomas. In contrast, nude mice reconstituted with either L3T4+- or Lyt-2+-enriched immune spleen cells alone failed to control visceral parasite replication and did not develop effective granulomas despite the finding that transfer of L3T4+ cells largely and Lyt-2+ cells partially restored the capacity to secrete IFN-gamma. To determine whether both T cell subsets were also required in a normal host, nu/+ BALB/c mice were treated with cell-depleting anti-L3T4 and anti-Lyt-2 mAb. Depletion of either T cell subset inhibited the acquisition of resistance to L. donovani and impaired the tissue granulomatous response. Thus, successful T cell-dependent host defense towards intracellular L. donovani and the tissue expression (granulomas) of this mechanism appear to require both L3T4+ and Lyt-2+ cells. A primary role for the L3T4+ cell may be IFN-gamma production; the role of the Lyt-2+ cell and the precise interaction of the two T cell subsets remain to be identified.

Animals↗
PubMed1988

Oral fluconazole therapy for patients with acquired immunodeficiency syndrome and cryptococcosis: experience with 22 patients.

PURPOSE: Cryptococcus neoformans causes infections in up to 10 percent of patients with the acquired immunodeficiency syndrome (AIDS). Nearly 50 percent of AIDS patients with previously treated cryptococcal meningitis will experience a relapse within six months. To reduce the likelihood of relapse, a maintenance regimen of amphotericin B is often administered weekly. However, the drug's intravenous route of administration and considerable toxicity have led to a search for alternative antifungal agents. In this report, we document our experience with fluconazole, a new oral triazole antifungal agent. PATIENTS AND METHODS: Twenty-two patients with AIDS and various forms of cryptococcosis were treated in an open-label study with 50 to 400 mg/day of fluconazole. The following laboratory studies were done on a monthly basis: complete blood cell count, liver function tests, serum creatinine level, serum cryptococcal antigen level, and serum fluconazole level. Lumbar puncture was performed in patients with meningitis every four to eight weeks to evaluate cerebrospinal fluid cryptococcal antigen, India ink preparation findings, fungal culture, fluconazole level, and protein, glucose, and cell count. RESULTS: Of seven patients with active culture-positive infections, four showed clinical and microbiologic responses (three of four with meningitis, one of three with extraneural cryptococcosis). Fifteen patients who had already undergone successful amphotericin B therapy for either meningitis (n = 14) or pneumonia (n = 1) received fluconazole as prophylaxis against relapse. Fourteen patients remained free of infection during 11 to 64 weeks of suppressive therapy; one patient with meningitis experienced relapse after 26 weeks of treatment. Reverse reactions were limited to increases in hepatic enzyme levels in four patients. CONCLUSION: These results appear sufficiently encouraging to warrant further trials of this oral agent in the suppression of chronic cryptococcosis and perhaps in the treatment of acute infection.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Experimental visceral leishmaniasis: production of interleukin 2 and interferon-gamma, tissue immune reaction, and response to treatment with interleukin 2 and interferon-gamma.

During the first 2 to 4 weeks of progressive visceral infection with the intracellular protozoan, Leishmania donovani, spleen cells from BALB/c mice failed in response to leishmanial antigen to produce either of the activating T cell-derived lymphokines, interleukin 2 (IL 2) or gamma-interferon (IFN-gamma). Four weeks after infection, however, antigen-induced IL 2 and IFN-gamma secretion emerged and coincided with the onset of control over parasite replication and the subsequent killing of greater than 80% of intrahepatic L. donovani. The development of this immunosecretory activity correlated with the hepatic tissue response at the site of parasitized Kupffer cells. This response progressed from Kupffer cell fusion (week 1) to fusion plus a mononuclear cell infiltrate (week 2) to well-organized granuloma formation (weeks 4 to 8). In contrast, T cell-deficient nude BALB/c mice exerted no control over L. donovani, their spleen cells failed to generate antigen-induced IFN-gamma, and at 4 weeks, their livers were devoid of any tissue reaction. Since spleen cells from 2-week infected normal mice did not produce antigen-stimulated IL 2 or IFN-gamma, these mice were treated with recombinant (r) lymphokines. Various protocols using both high and low dose human rIL 2 had no antileishmanial effect. Hepatic parasite replication was completely halted, however, by macrophage-activating doses of murine rIFN-gamma. These results reemphasize that an intact T cell-dependent response is required for successful defense against L. donovani, indicate that this immune response can be measured at both the cellular (secretory) and tissue levels, and confirm that IFN-gamma can exert an antileishmanial effect in vivo.

Animals↗
PubMed1984

Murine amebiasis: the role of the macrophage in host defense.

The congenitally athymic nude (nu/nu) mouse was studied as a model for amebic liver disease, using Entamoeba histolytica. Despite intrahepatic inoculation of massive numbers of amebae, we could not produce sustained infections in nu/nu mice. We also failed to induce hepatic amebiasis in thymus-intact nu/+ and +/+ littermates, or in nu/+ mice pretreated with rabbit antimouse thymocyte globulin. Humoral response was measured in both the nu/nu and nu/+ mice. Nu/+ but not nu/nu animals developed a specific IgG response after challenge with E. histolytica. There were no significant IgM responses. Pretreatment with silica increased susceptibility of both nu/nu and nu/+ mice to development of liver abscesses. These studies suggest that host resistance in murine amebiasis is critically dependent upon the macrophage, but not upon T cell-mediated defenses.

Animals↗
PubMed1976

Ventromedial hypothalamus and short-term feeding suppression by caerulein in male rats.

A series of six experiments examined the neural loci responsible for caerulein's suppression of eating. Caerulein is a decapeptide chemically and physiologically similar to cholecystokinin, a naturally occurring gut hormone in rats. Rats with lesions in the ventromedial hypothalamus (VMH) showed reduced sensitivity to caerulein (1 mug/kg); rats with lateral hypothalamic (LH) destruction showed heightened sensitivity. Microinjections of caerulein into the VMH, but not into the LH, limited feeding. Finally, tritiated caerulein was selectively bound to tissue in the VMH. The results are discussed in terms of the hypothesis that the VMH manages postprandial inhibition in the rat.

Animals↗