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Biomedical subjects

B S Rabin

Publications and source records attributed to B S Rabin.

At least 19 recordsLinked to original sources

Induction of c-Fos immunoreactivity in the rat forebrain by conditioned and unconditioned aversive stimuli.

The protein product of the c-fos proto-oncogene was immunocytochemically localized in forebrain regions of adult male Lewis rats subjected to a physically aversive footshock stimulus or a Pavlovian-conditioned, non-aversive, auditory stimulus. Animals receiving the conditioned stimulus were first conditioned by repeatedly pairing electric footshock, the unconditioned stimulus (US), with an auditory cue, the conditioned stimulus (CS). These animals were later tested with the CS in the absence of the US, a procedure which, like footshock itself, suppresses immune function. In animals exposed to the conditioned or unconditioned stressor, c-Fos was strongly expressed in cells of the paraventricular nuclei (PVN) of the hypothalamus, some of which contain corticotropin-releasing hormone (CRH), and other forebrain areas directly associated with autonomic function, the ventral lateral septal nuclei (LSV), the medial amygdaloid nuclei (AME), the sensorimotor cortex, the basal ganglia and thalamic nuclei. Control animals exhibited very little or no c-Fos in the above areas. The identified forebrain nuclei can now be targeted for further study aimed at elucidating their role in stress-induced immune alteration.

Animals

The prevalence of autoantibodies among right and left handed schizophrenic patients and control subjects.

Sera from schizophrenic patients (n = 186) and healthy control subjects (n = 346) were tested for the presence of seven common autoantibodies by standard immunological methods. The association between handedness and autoantibodies was tested in a multi-way contingency table using a log-linear model. For men, but not women, nondextrals (patients and controls) were twice as likely to test positive for autoantibodies than dextrals (p = 0.0002). Although more women (33%) than men (24%) tested positive for autoantibodies, handedness was not a distinguishing factor among women. These data suggest that sinistrality and gender are associated with autoantibodies in a subgroup of schizophrenic patients and healthy control subjects.

Adult

Altered interleukin-2 production in schizophrenia: association between clinical state and autoantibody production.

Mitogen-stimulated interleukin-2 (IL-2) production was measured in 122 patients who met Research Diagnostic Criteria for schizophrenia and 98 normal control subjects. The presence of autoantibodies against seven common antigens was also determined. There was no relationship between the presence of circulating autoantibodies and IL-2 production in control subjects. In patients, however, autoantibody-positive, acutely ill patients had significantly lower IL-2 production as compared with other patients and control subjects. Never-medicated patients showed the same trends for decreased IL-2 production in association with autoantibodies. These data suggest that decreased IL-2 production is associated with acute illness in schizophrenic patients who produce autoantibodies, a trait known to be associated with increased vulnerability to autoimmune disease.

Adult

Stress-induced alterations in interferon production and class II histocompatibility antigen expression.

Mild electric foot-shock has been shown to be a stressor that can alter immune responses. Male Lewis rats were exposed to one session of 16 5.0-s 1.6-mA foot-shocks. Production of interferon-gamma by splenocytes in response to concanavalin-A was decreased in spleens from the shocked rats compared to control spleens. Spleen cells from rats treated with nadolol, a peripherally acting beta-adrenergic receptor antagonist, and then shocked, showed dose-dependent attenuation of the suppression of interferon-gamma production. This suggests that catecholamines mediate shock-induced suppression of interferon-gamma production. The percentage of splenic mononuclear cells expressing class II histocompatibility (Ia) antigens on their surfaces from spleens of shocked rats was determined by flow cytometry. Significantly decreased class II positive mononuclear cells were present in the spleens of shocked rats in comparison to the spleens of control rats. This may reflect an alteration of cell trafficking or decreased production of class II antigens.

Animals

Corticosterone-independent alteration of lymphocyte mitogenic function by amphetamine.

Amphetamine, a neural stimulatory agent with acute effects mimicking those of stress, is shown here to elevate plasma corticosterone levels and suppress spleen and peripheral blood lymphocyte (PBL) mitogenic responses to concanavalin A (Con A) and phytohemagglutinin (PHA) when administered to rats. Pretreatment of the rats with propranolol, a nonselective beta-adrenergic receptor antagonist, totally prevented the amphetamine-induced suppression of lymphocyte mitogenic reactivity to Con A and PHA in the spleen and to PHA in the peripheral blood; however, the PBL mitogenic response to Con A was only partially restored. Although the amphetamine-induced alterations in immune function were prevented by propranolol pretreatment, the elevated plasma corticosterone response was not. This suggests that corticosterone is not modulating the mitogenic activity of splenic lymphocytes or PHA-reactive PBLs. On the other hand, Con A-reactive PBLs may be affected by corticosterone and/or other mechanisms, which may include the catecholamines.

Amphetamine

Left-handed first-episode, neuroleptic-naive schizophrenic patients have a higher prevalence of autoantibodies.

Using standard immunological techniques, sera from first-episode, neuroleptic-naive schizophrenic patients (n = 51) and age, race and sex matched healthy controls (n = 51) were screened for seven common autoantibodies. Significantly more left-handed (67%) than right-handed (23%) schizophrenic patients had autoantibodies (p = 0.011). Left-handed schizophrenic patients were six times more likely than right-handed patients or controls and four times more likely than left-handed controls to test positive for autoantibodies (p = 0.012). These data suggest that disease and sinistrality contribute to the excess of autoantibodies in schizophrenia.

Adult

Elevated IgG anti-histone antibodies in a subgroup of medicated schizophrenic patients.

A total of 57 schizophrenic patients (of which 17 were first-episode, neuroleptic naive) and 76 healthy controls were screened for anti-histone IgG antibodies using an enzyme immunoassay (ELISA). All patients had significantly higher anti-histone antibody titers than controls (t = 3.1, p less than 0.003). Previously medicated patients had significantly higher titers than neuroleptic-naive first episode patients (t = 2.87, p less than 0.006). This study suggests that neuroleptic medications are associated with anti-histone antibodies.

Adult

Serum autoantibodies in patients with Alzheimer's disease and vascular dementia and in nondemented control subjects.

BACKGROUND AND PURPOSE: In this study we sought to evaluate the clinical significance of serum autoantibodies to dementing processes. METHODS: We assessed 40 age-matched subjects: 10 patients with probable Alzheimer's disease, 10 with possible Alzheimer's disease with cerebrovascular disease, 10 with vascular dementia, and 10 nondemented control subjects. Serum from each subject was tested for the presence of antithyroglobulin antibody, thyroid antimicrosomal antibody, gastric anti-parietal cell antibody, anti-smooth muscle antibody, antinuclear antibody, rheumatoid factor, antineuronal antibody, and anticardiolipin antibody. In addition, we investigated the sera of these patients for the presence of an antivascular antibody directed against the vascular basement membrane proteoglycan antigen and for circulating immune complexes. RESULTS: Autoantibodies were present in 100% of the patients with possible Alzheimer's disease with cerebrovascular disease, 80% of those with vascular dementia, 40% of those with probable Alzheimer's disease, and 30% of the nondemented control subjects. The highest number of autoantibodies was observed in patients with vascular dementia and possible Alzheimer's disease with cerebrovascular disease. Antinuclear antibody was present in 60% of vascular dementia patients and antineuronal antibody in 50% of these patients. However, no individual autoantibody could differentiate Alzheimer's disease from cerebrovascular disorders. Immune complexes were detected in the serum of 20-30% of each patient group. Neither the patient nor the control sera was found to contain antiendothelial antibody. CONCLUSIONS: Despite the relatively small number of individuals examined in each category, the elevated number of autoantibodies associated with possible Alzheimer's disease with cerebrovascular disease and vascular dementia indicates a possible link between the presence of autoantibodies and cerebrovascular disorders in dementia.

Aged

Serum immunoglobulin changes in relation to tonsil and adenoid surgery.

In the course of clinical trials of tonsillectomy, adenoidectomy, and adenotonsillectomy, we measured serum levels of immunoglobulins G, A, and M by rate nephelometry in 268 subjects at baseline and at intervals after receipt or nonreceipt of surgery. Up to 30 months after baseline we observed a consistent pattern of change only in levels of immunoglobulin G, decreases in which tended to occur more commonly and be of greater magnitude in subjects who received tonsillectomy or adenotonsillectomy than in corresponding control subjects. However, in both surgical and control subjects the subsequent incidence of throat infection showed no relationship to either contemporaneous immunoglobulin levels or changes from baseline levels. A decline in serum immunoglobulins following tonsillectomy appears not to be a risk factor for developing throat infection, and may reflect a reduction in antigenic stimulation.

Adenoidectomy

Stressor-induced changes in mitogenic activity are not associated with decreased interleukin 2 production or changes in lymphocyte subsets.

Splenic lymphocytes from Lewis rats that received presentations of physically aversive electric shock demonstrated a marked reduction in responsiveness to T-cell mitogens such as concanavalin A. This study examined cellular mechanisms which may be responsible for this functional alteration. There was no difference in distribution of T-cell subsets from shocked and nonshocked rats. There was no difference in the production of interleukin 2 (IL-2) nor was there a difference in the percentage of IL-2 receptor positive T cells or T-cell subsets after culture for 24 hr. However, there was a marked lack of mitogenic stimulation in splenocytes from shocked rats when stimulated with the calcium ionophore A23187. This indicates a defect in the biochemical pathways necessary to activate T-cell mitogenesis.

Animals

Familial and sporadic insulin-dependent diabetes: evidence for heterogeneous etiologies?

Heterogeneity within insulin-dependent diabetes mellitus (IDDM) has been hypothesized, but few studies have focused on differences which may exist between familial and sporadic IDDM cases. Presenting characteristics for 330 white, newly diagnosed IDDM cases were evaluated. Familial cases were older (10.2 +/- 5.1 years vs 7.9 +/- 4.2 years, P = 0.010) and had, on average, less severe metabolic disturbances at presentation, as demonstrated by lower mean hemoglobin A1 (12.6 +/- 2.4% vs 14.4 +/- 2.6%, P = 0.001) and mean insulin dose at discharge (0.62 +/- 0.35 U/kg/day vs 0.85 +/- 0.29 U/kg/day, P less than 0.001), and higher mean plasma bicarbonate concentrations (19.3 +/- 3.9 mmol/l vs 15.8 +/- 5.9 mmol/l, P = 0.023) and mean plasma C-peptide levels (0.35 +/- 0.36 pmol/ml vs 0.14 +/- 0.15 pmol/ml, P less than 0.001). Further analyses on a subset of IDDM cases (n = 100) indicated that initial differences in metabolic indices observed at diagnosis were no longer apparent at one-year post-diagnosis. These results suggest that the etiology of familial and sporadic IDDM is similar and that the less severe presentation observed at diagnosis in the familial cases may be due to earlier identification of the disease, reflecting increased parental knowledge of diabetic symptoms and/or frequent testing for diabetes.

Age Factors

Alterations in specific antibody production due to rank and social instability.

Separate studies examined the influence of the social environment of male cynomolgus macaques on primary and secondary antibody responses to immunization with tetanus toxoid. All animals showed evidence of both primary and secondary anti-tetanus antibody response. In the first study, subordinate animals had a greater primary antibody response to tetanus toxoid, while a single social reorganization (acute stressor) did not influence the response. In the second study, social rank was not associated with the secondary antibody response but repeated social reorganizations (chronic stressor) resulted in a greater level of specific antibody production in comparison to nonreorganized controls. These effects could not be accounted for on the basis of nonspecific differences in total serum IgG or serum albumin.

Animals

Serum auto-antibodies in Alzheimer's disease.

The prevalence and clinical significance of non-CNS auto-antibodies in the serum of patients with probable and possible Alzheimer's disease (AD) was determined. Serum was obtained from 88 patients and 55 normal controls. Serum from each subject was tested for the presence of seven different auto-antibodies. Auto-antibodies were detected in 44% of the subjects with probable AD, 70% with possible AD with cerebrovascular disease (CVD), 45% with possible AD and other disease and 42% of normal controls. Although a subpopulation of AD patients with CVD showed a trend to an increased predisposition to develop autoimmune disease, these results do not support the relationship of AD and serum auto-antibodies or autoimmune disease.

Aged

Long-term follow-up of children born to women immunized with tetanus toxoid during pregnancy.

Ten years after transplacental immunization with tetanus toxoid, the antibody responses of the immunized children to a booster immunization with 5 Lf tetanus toxoid did not differ from those of the control children. The tetanus toxoid-stimulated lymphocyte proliferative responses showed that there was no tolerance to tetanus toxoid induced by transplacental immunization, and the stimulation indices suggested that there may be some long-term memory for tetanus toxoid among the T lymphocytes in children who had been transplacentally immunized by maternal immunization with a standard dose of tetanus toxoid.

Antibodies, Bacterial