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Biomedical subjects

S Mukherjee

Publications and source records attributed to S Mukherjee.

At least 289 records · Page 16Linked to original sources
PubMed1991

Abnormal growth of skin fibroblasts from schizophrenic patients.

Fibroblast cultures were established from skin biopsies of 18 schizophrenic patients (14 on drug and 4 off drug) and 13 normal subjects, and growth parameters (initial growth and rate of growth) and morphology were studied. Fibroblasts from patients took significantly longer to grow than did normal fibroblasts. Cell lines were established within 2 weeks for all normal controls, but for only 6 (33%) of 18 schizophrenic patients. The rate of growth (doubling time) was also significantly longer for fibroblasts from patients than from normals. Neither time to establishment of initial growth nor doubling time was related to age, sex, age at onset, duration of illness, or medication status in the patients. Fibroblasts from normals showed uniform, long (slender), characteristic spindle-like, bipolar appearance, with unidirectional orientation, both while growing from explant as well as after subculturing. By contrast, fibroblasts from patients generally showed random size (shorter and flatter), mostly spiny, multipolar cells with short stubby projections, and an irregular orientation resulting in a criss-cross pattern, and often exhibited poor attachment. Fibroblasts from skin biopsies of patients who were drug free at the time of biopsy showed similar initial growth, doubling time, and morphology to those from patients who were receiving neuroleptic treatment. In vitro challenge of skin biopsies of normal subjects with haloperidol in culture resulted in slight delay in initial growth and marginal increase in doubling time. However, the morphology remained normal. Possible molecular mechanisms that may be associated with abnormal growth of fibroblasts in schizophrenia are discussed.

Adolescent↗
PubMed1991

Specificity of smooth pursuit eye movement and visual fixation abnormalities in schizophrenia. Comparison to mania and normal controls.

Smooth pursuit eye movements (SPEM) were assessed in 30 schizophrenic patients, 12 lithium-free manic patients, and 20 normal controls. Compared to schizophrenic patients, manic patients evidenced less SPEM impairment in an attention enhancing, sinusoidal target motion condition and had superior performance during a visual fixation condition. SPEM and visual fixation dysfunctions may be more common in schizophrenic than in acutely manic patients, even when the latter are characterized by marked attentional dysfunction, poor interepisode psychosocial functioning, and psychosis.

Adult↗
PubMed1991

The prevalence of tardive dyskinesia.

A total of 2250 subjects from psychiatric and geriatric settings was examined for abnormal involuntary movements by the same team of trained raters employing a standard examination technique and rating scale. "Spontaneous" dyskinesia rates were 1.3% among 400 healthy elderly people surveyed at senior citizens centers, 4.8% among medical geriatric inpatients and ranged from 0 to 2% among psychiatric patients never exposed to neuroleptics. For samples of neuroleptic-treated patients, prevalence rates ranged from 13.3% among patients at a voluntary psychiatric hospital to 36.1% among state hospital patients. Logistic regression analyses revealed a large effect of age on tardive dyskinesia prevalence and an interaction of age with sex. Among younger subjects, men had higher rates; among subjects over age 40, rates were higher for women. Edentulousness and presence of other neurological disorders were possible contributors to high rates for the elderly. Even with control for age, sex and duration of neuroleptic exposure, prevalence differed markedly across study site.

Adult↗
PubMed1991

Observation on serum prolactin in hepatic cirrhosis.

Serum prolactin assays in patients of hepatic cirrhosis were analysed. Patients with cirrhosis had higher values of serum prolactin (27.2 +/- 5.1 ng/ml in males and 38.4 +/- 4.1 ng/ml in females) as compared to control subjects (p less than 0.05). Majority of patients of cirrhosis with suspected portal-systemic encephalopathy had significantly higher serum prolactin than those without encephalopathy (p less than 0.05). Significantly higher values of serum prolactin on admission had positive correlation with mortality (p less than 0.01). Clinico-biochemical severity of hepatic dysfunction was directly correlated with level of serum prolactin. The present study reveals the possibility of diagnostic and prognostic values of serum prolactin in cirrhosis, specially in clinical/sub-clinical subsets of portal-systemic encephalopathy.

Biomarkers↗
PubMed1991

Myositis ossificans progressiva.

Myositis ossificans progressiva is a rare, incurable disease causing progressive ossification of skeletal muscles leading to total immobility. We report one such case.

Adult↗
PubMed1991

Some prospective observations on recent outbreak of typhoid fever in West Bengal.

The present study was designed to study the clinical behaviour of a recent epidemic of typhoid fever in West Bengal. Of 46 cases studied, 67% (31) had chloramphenicol resistant typhoid fever. The chloramphenicol-resistant cases were comparatively severe in nature with higher complication and mortality rates. Salmonella typhi resistant to chloramphenicol were also resistant to ampicillin, cloxaxillin and cotrimoxazole. Strains of Salmonella typhi sensitive to chloramphenicol retained their sensitivity to these other antimicrobials.

Adult↗
PubMed1990

Effects of dimethylbenz[a]anthracene-induced malignancy on the subcellular distribution of peripheral benzodiazepine receptors in submandibular glands of rats.

The binding of [3H]Ro 5-4864 to peripheral benzodiazepine receptors (PBRs) was studied in normal and malignant submandibular glands of rats. The carcinoma was induced by implantation of 7,12-dimethylbenz[a]anthracene (DMBA) into the glands. [3H]Ro 5-4864 binding to normal and malignant submandibular glands indicated one population of binding sites with high affinity (KD of 3.4 and 4.4 nM for normal and malignant respectively) and saturability (Bmax) of 487 and 321 pmol/g tissue for normal and malignant respectively). Subcellular localization of PBRs indicates that mitochondria was the primary locale of the receptor in both cases and the decrease in Bmax was due primarily to a decrease in the binding capacity of PBRs in mitochondria.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1990

Cigarette smoking and neuroleptic-induced parkinsonism.

Several studies have reported an apparent protective effect of cigarette smoking for the risk of idiopathic Parkinson's disease (IPD). These observations are supported by neurochemical studies demonstrating enhancement of central dopaminergic neurotransmission by nicotine. We studied the prevalence and severity of neuroleptic-induced parkinsonism (NIP) in relation to cigarette smoking in a homogeneous sample of 130 psychiatric inpatients receiving long-term neuroleptic treatment. Despite the fact that smokers had significantly higher dosage of neuroleptics during the month prior to evaluation and longer exposure to medication, they presented with significantly less prevalence and severity of NIP than nonsmokers. These findings suggest that the inverse association between smoking and IPD may apply to NIP.

Antipsychotic Agents↗
PubMed1990

The chlorpromazine inhibition of transport ATPase and acetylcholinesterase activities in the microsomal membranes of rat in vitro and in vivo.

Chlorpromazine, an antipsychotic drug, is found to inhibit Na+,K(+)-ATPase activity in rat brain microsomal membranes in vitro in concentration and time dependent manner but some inconsistency is observed when the effect was studied with respect to different temperatures. Various ligands and/or substrate affect the inhibition by chlorpromazine in different ways. The in vivo study with this drug shows that the activities of Na+,K(+)-ATPase, Ca2(+)-ATPase and acetylcholinesterase in the microsomal membranes of different organs are inhibit with increases in concentration or lengths of time of treatment and then levels off.

Acetylcholinesterase↗
PubMed1990

Quantitative analyses of plasma cholinesterase isozymes in haloperidol-treated rats.

We describe a quantitative slab gel electrophoresis procedure that allows quantitative determination of plasma levels of discrete cholinesterase isozymes. Using this method, the effects of haloperidol treatment on plasma cholinesterase isozyme levels were examined in normal rats. Eight isozymes were detected by enzymatic reaction with either of two substrates (alpha-naphthyl acetate, NA; acetylthiocholine iodide, AcTCh), and then quantified using densitometric scanning. With AcTCh substrate, the activities of two major isozymes (1 and 2) were found to be linear with increasing quantities of applied plasma. With NA as substrate, Iso-OMPA (a pseudocholinesterase inhibitor) inhibited activities of all isozymes, except isozymes 2 and 8. With either substrate, BW284C51 (acetylcholinesterase inhibitor) inhibited 100% and 13% of activity of isozymes 2 and 8, respectively, and with AcTCh substrate, 37% of isozyme 1. Based on the differential patterns of substrate specificity and action of inhibitors, and the reproducibility of patterns, we propose that these isozymes represent distinct molecular species. Short-term (14 days) and long-term (45 days) haloperidol treatment both resulted in altered levels of specific cholinesterase (ChE) isozymes. On the average, with AcTCh substrate, haloperidol treatment increased levels of isozymes 1 and 2 by 30% and 8%, respectively, after 14 days, and by 50% and 30%, respectively, after 45 days. Isozymes 3 through 8 showed minor changes. Plasma levels of isozymes 1 and 2 returned to baseline pretreatment values after a 40-day drug-free period. No significant change was observed after either short- or long-term treatment with clozapine, imipramine, or saline, or after an acute (less than 5 days) haloperidol treatment. No change was noted in RBC-ChE levels as function of treatment. These findings indicate that, in the rat, chronic haloperidol treatment results in differential changes in the plasma levels of discrete ChE isozymes. We have suggested that these changes reflect an alteration of central dopaminergic-cholinergic balance.

Acetylcholinesterase↗