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R Ganguli

Publications and source records attributed to R Ganguli.

70 records · Page 4Linked to original sources
PubMed1989

Bidirectional interaction between the central nervous system and the immune system.

We believe that any questions regarding whether the CNS can alter immune system functions no longer remain. It can conclusively be stated that the immune system is susceptible to influences of the CNS. It remains to be determined whether all classes of lymphocytes, NK cells, macrophages, polymorphonuclear leukocytes, and other antigen-processing cells are all susceptible to CNS influences. We have presented evidence that peripheral blood lymphocytes may not reflect the immunological activity of lymphocytes within lymphatic tissue after being influenced by a stressor. Thus, all types of immunological cells must be evaluated in different organs. Whether the immune system of young and old animals respond in the same way must also be determined. The sex of the animal needs to be taken into consideration. What immune responses are important to measure? Do in vitro responses reflect the ability of an animal to resist infectious disease or susceptibility to autoimmune and malignant diseases? Certainly, absence of an immune response is detrimental to health. It must be determined whether moderately suppressed immune function in multiple compartments is as detrimental as total absence of an immune response in a single immunological compartment. The data that we have presented with respect to adjuvant arthritis indicate that an immune response in the peripheral of the animal can be modified by a stressor and influence an immunopathological process. This may indicate that the most important immune compartment to evaluate with respect to altering disease susceptibility is the peripheral blood and that lymphoid tissue may be interesting, but not clinically relevant. The reasons why the peripheral blood and lymphoid tissue differ in their immunological function following exposure to a stressor must be determined. We have reviewed information indicating that lymphoid tissue is innervated and that such innervation can modify immune function. In addition, hormones released by the CNS may alter immune function. Yet, much of this data are contradictory and whether immune enhancement or suppression occurs is not clearly defined with respect to any experimental manipulation involving denervation or the addition of hormones to in vitro cultures. Whether this reflects the age of the experimental animal, the type of immune response being measured, the adequacy of the experimental procedure, background rearing conditions of the animals, the amount of noise in the animal room, the diet of the animals, or the number of animals housed per cage all remain to be determined. Our purpose has not been to provide a comprehensive review of all of the data relating to the immune system/CNS interaction.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

The central nervous system--immune system relationship.

Research investigating the pathogenesis of schizophrenia has demonstrated that cellular immune reactions, such as those that occur in known autoimmune diseases, may participate in producing alterations of the central nervous system. Furthermore, epidemiologic studies of immune-mediated diseases have suggested that activation of the central nervous system by stressful stimuli may be capable of influencing the function of the immune system. In support of that interaction, research using animal models of stress has provided valuable information as to the effect of stress on basic immune function and susceptibility to infectious disease. Possible hormonal and direct mechanisms of the central nervous system-immune system interaction have been proposed.

Autoimmune Diseases↗
PubMed1987

Electroencephalographic sleep in young, never-medicated schizophrenics. A comparison with delusional and nondelusional depressives and with healthy controls.

Electroencephalographic (EEG) sleep characteristics of young, never-medicated, nonschizoaffective schizophrenics were compared with the EEG sleep of patients with major depressive disorders (delusional and nondelusional) and with that of healthy controls. Schizophrenics had decreased sleep continuity comparable to delusional depressives. Slow-wave sleep percent was similar to that seen in healthy controls, as was the intranight temporal distribution of EEG delta activity. However, schizophrenics showed diminished delta counts per minute of non-rapid eye movement (NREM) sleep and a decreased total delta wave count. In contrast, depressives showed diminished slow-wave sleep percent compared with controls, greatly decreased delta activity (more so than did the schizophrenics), and an altered temporal distribution of delta activity, as evidenced by a shift of delta activity from the first to the second NREM period. Minutes of slow-wave sleep in the schizophrenics was inversely correlated with the severity of negative symptoms independent of the effects of age and the presence of depression. The schizophrenics showed normal REM latency and first REM period duration, in contrast to the depressives. These findings, reviewed in the historical context of sleep physiologic studies of schizophrenia over the past 30 years, suggest that young, never-medicated schizophrenics do not show the characteristic constellation of abnormalities in the first NREM-REM cycle seen in patients with major depression. However, decreased slow-wave sleep should be investigated as a possible marker for negative symptoms in schizophrenia.

Adult↗
PubMed1987

Clinical and laboratory evidence of autoimmunity in acute schizophrenia.

A number of assays were performed to assess immunologic function in 28 patients with clinically well-defined schizophrenia. Our data provide laboratory evidence that patients with schizophrenia have characteristics consistent with an autoimmune process, directed to components of the brain, which may participate in either the pathogenesis or etiology of schizophrenia. One-third of our patients had a clinically evident autoimmune syndrome unrelated to their psychiatric illness. Of the nine patients with an autoimmune disease, two had one autoantibody in their serum and five had more than one autoantibodies. Twelve of eighteen patients without clinical evidence of autoimmune disease had no detectable autoantibodies. Mitogenic responses to PHA and PWM were significantly reduced in the patient population when compared to controls. Fifty percent of the patients had an increased percentage (greater than 5%) of blood-borne HLA-DR (+) OKT4 (+) T-helper lymphocytes. Immune reactivity toward brain antigens was sought by measuring lymphocyte transformation to a saline extract of frontal lobe, and by immunoblotting of antigens extracted from frontal lobe, cingulate gyrus, interventricular septum, and hippocampus. Lymphocyte transformation did not reveal differences between patient and control groups. Normal sera were found to contain antibody to some of these brain antigens. However, patients with schizophrenia had antibody to antigens of the hippocampus, septal region and cingulate gyrus which were not encountered during analysis of normal sera.

Acute Disease↗
PubMed1985

Tardive dyskinesia, impaired recall, and informed consent.

Schizophrenics (N = 9) were examined for signs of tardive dyskinesia and given detailed information about the disorder. Recall of this information was assessed after 2 weeks, and further instruction was given to those with defective recall. Retesting after a further 2 weeks revealed that all patients without tardive dyskinesia had some recall, but 5 of 9 patients with tardive dyskinesia could not remember any discussion having taken place (p = .29). The presence of memory problems in patients with tardive dyskinesia would have implications for the pathogenesis and management of the disorder.

Adult↗
PubMed1983

Interaction of nogalamycin with chromatin.

Number of available nogalamycin binding sites in Sarcoma-180 chromatin is less than that present in Sarcoma-180 DNA. Gradual removal of proteins from chromatin by salt leads to increase in available drug binding sites, without appreciable alteration in binding affinity. Histones restrict the accessibility of nogalamycin to chromosomal DNA, whereas high mobility group (HMG) proteins have no effect. Association of histone H1 with chromosomal DNA has a more marked inhibitory effect on nogalamycin binding than other types of histones. Chromosomal protein induced conformational change in DNA appears to be the main factor in determining the availability of strong binding sites.

Chromatin↗
PubMedDate not supplied

Slow-wave sleep and symptomatology in schizophrenia and related psychotic disorders.

Deficits in slow-wave sleep (SWS), or delta sleep, are frequently seen in schizophrenia, but their relationship with schizophrenic symptomatology remains unclear. We examined the association between visually scored and automated measures of SWS and positive and negative symptoms in a series of unmedicated patients with schizophrenia and related psychotic disorders. Total and average automated delta wave counts were significantly inversely associated with negative symptoms overall, and the psychomotor poverty syndrome in particular. Total delta counts were also inversely related to the disorganization syndrome. No relation was seen between reality distortion or the Brief Psychiatric Rating Scale (BPRS) positive symptoms and SWS. These findings support the view that SWS deficits may be related to negative symptoms of schizophrenia and may perhaps be mediated by impaired functioning of frontothalamic neural circuits.

Adult↗
PubMedDate not supplied

Immune abnormalities in schizophrenia: evidence for the autoimmune hypothesis.

The autoimmune basis for schizophrenia has been investigated for the last 60 years. Although numerous immune abnormalities have been reported, the current literature is viewed with much skepticism because most of the studies have failed to control for extraneous factors that may have influenced the findings. Principally, antipsychotic medication, duration of illness, and current clinical state (acutely psychotic or remitted) may considerably alter immune response, as may other factors such as nutritional status, substance abuse, and concurrent medical illness. We review recent studies that employed current diagnostic criteria and modern immunologic techniques. (These studies were located by use of a Medline search on the terms schizophrenia and psychosis, cross-referenced with immune abnormalities, lymphokines, antibodies, lymphocytes, HLA, and medication, and by perusing the reference lists in the articles found through this search.) Immune abnormalities that have been replicated in studies of schizophrenic patients include increased prevalence of antinuclear antibodies, decreased production of interleukin-2, and increased serum concentrations of interleukin-2 receptor and interleukin-6. Given the current importance of autoimmunity as an etiologic mechanism in several branches of medicine, further studies are needed, especially those having a longitudinal design and including drug-naive patients.

Antibodies, Antinuclear↗