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Biomedical subjects

S Banerjee

Publications and source records attributed to S Banerjee.

At least 235 records · Page 13Linked to original sources
PubMed2000

Transient pathological Q waves in suspected acute myocardial infarction: 'electrical stunning'.

In acute coronary syndromes the development of pathological Q waves is usually taken as evidence of established myocardial infarction (MI). We describe two patients with suspected acute MI who developed transient pathological Q waves. Cardiac enzymes were normal and cardiac catheterisation showed severe proximal coronary disease. Recognition of 'non-infarction' Q waves is important and may influence management of these patients.

Aged↗
PubMed2000

An epidemiological survey of carcinoma cervix in north Bengal zone.

Correlation between various epidemiological factors and carcinoma cervix patients in North Bengal zone has been studied for the first time. Significant correlation between elderly women (41-50 years age group), low socio-economic status (SES), first coitus before 17 years of age, low literacy rate and this illness has been established. Suggestion has been made for improvement of the picture. Oncology and radiotherapy department of North Bengal Medical College and Hospital should be utilised as the centre for National Cancer Registration Project in North Bengal zone.

Adolescent↗
PubMed2000

Stromal sarcoma of breast: a case report.

A 34 years unmarried female was admitted with an ulcerated foul smelling growth in her right breast. On examination the fungating mass measured 17.5 cm x 15 cm in central and lower part of right breast involving the nipple and areola. The ulcer was covered with slough and rest part of the breast appeared bosselated. Her Hb was 4 g/dl and incision biopsy from the margin of the tumour showed histology of sarcoma. The patient was infused 6 units of blood and right sided total mastectomy was done. Histopathological examination confirmed it was a case of stromal sarcoma of breast. Chemotherapy was started with vincristine, adriamycin and cylophosphamide. The patient was doing well in next follow-up.

Adult↗
PubMed2000

Diverse manifestation of arrhythmogenic right ventricular dysplasia in a family.

Arrhythmogenic right ventricular dysplasia (ARVD) is a cardiomyopathy of unknown cause associated with life-threatening arrhythmias. The purpose of this case report is two-fold: (i) To highlight the utility of a definite set of diagnostic criteria encompassing structural, histologic, electrocardiographic, arrhythmic and genetic factors in establishing diagnosis of ARVD in institutions like ours which are handicapped by lack of magnetic resonance imaging (MRI) and endomyocardial biopsy facilities, (ii) to present diverse arrhythmic manifestations in a single family.

Adolescent↗
PubMed1999

The Tourette syndrome diagnostic confidence index: development and clinical associations.

BACKGROUND: The clinical characteristics of Tourette syndrome (TS) present challenges for the systematic determination of whether individuals are affected and severity. Vocal and motor tics wax and wane, decrease over time, and may be voluntarily suppressible, and therefore may be absent at interview. Current instruments measure symptoms at interview or rate symptom severity only. METHOD: To minimize error in case ascertainment and produce an instrument measuring lifetime likelihood of having had TS, clinical members of the American Tourette Syndrome Association International Genetic Collaboration developed the Diagnostic Confidence Index (DCI). The expert group worked collaboratively with progressive revision in consensus workshops using existing diagnostic criteria as guidelines. The DCI produces a score from 0 to 100 that is a measure of the likelihood of having or ever having had TS. RESULTS: The DCI was administered to 280 consecutive patients with TS attending a TS clinic; 264 (94%) completed it, indicating high feasibility and acceptability. Its correlation with other instruments and associations with psychopathology provide support for its being a lifetime measure of TS. CONCLUSIONS: The DCI is a useful, practicable instrument in the clinic or research practice allowing an assessment of lifetime likelihood of TS. Further work is needed to test the DCI's psychometric properties, such as its validity and reliability in populations of interest.

Adolescent↗
PubMed1999

Lipid-Drug Interaction and Colligative Properties in Phospholipid Vesicles.

Imipramine penetration into the lipid core of a membrane was demonstrated through measurements on lipid monolayers (surface pressure and surface potential). The surface pressure measurements allow us to calculate the intrinsic binding constant (partition coefficient) for the lipid-Imipramine interaction. This latter value is in correct agreement with the results obtained by electrophoretic mobility measurements on liposomes. In addition, it was observed that the same mole fraction of "lipid-soluble drug" (Chlorpromazine or Imipramine) incorporated in a given lipidic phase (DPPC) induced the same shift in the transition temperature. Copyright 1999 Academic Press.

Journal Article↗
PubMed1999

Alteration of hMSH2 and DNA polymerase beta genes in breast carcinomas and fibroadenomas.

Genomic stability is preserved by error-free DNA replication, post-replicative proofreading, DNA repair, and recombinational events. In essence, DNA repair genes are recognized to play key roles in such stability. We report evidence for expression of the wild-type and a truncated form of DNA polymerase beta (polbeta) proteins, a base-excision repair gene, in breast carcinomas and fibroadenomas, a benign breast disease. An 87-bp deleted variant of polbeta was identified to be prevalent in microsatellite unstable breast tumors and fibroadenomas. A large deletion of 1476 bp, as well as point mutations in human MutS homolog 2 (hMSH2) cDNA, was revealed in breast carcinomas. The protein truncation assay confirmed the 1476-bp deletion as a premature protein. This is the first evidence for variant forms of hMSH2 that are associated with breast cancer. Genomic instability in the hMSH2 and polbeta genes may facilitate the occurrence of mutator phenotype in breast cancer.

Breast Neoplasms↗
PubMed1999

Nuclear factor-kappaB plays an essential role in the late phase of ischemic preconditioning in conscious rabbits.

Although it is recognized that late preconditioning (PC) results from upregulation of cardioprotective genes, the specific transcription factor(s) that govern this genetic adaptation remains unknown. The aim of this study was to test the hypothesis that the development of late PC is mediated by nuclear factor-kappaB (NF-kappaB) and to elucidate the mechanisms that control the activation of NF-kappaB after an ischemic stimulus in vivo. A total of 152 chronically instrumented, conscious rabbits were used. A sequence of six 4-minute coronary occlusion/4-minute reperfusion cycles, which elicits late PC, induced rapid activation of NF-kappaB, as evidenced by a marked increase in p65 content (+164%; Western immunoblotting) and NF-kappaB DNA binding activity (+306%; electrophoretic mobility shift assay) in nuclear extracts isolated 30 minutes after the last reperfusion. These changes were attenuated 2 hours after ischemic PC and resolved by 4 hours. Competition and supershift assays confirmed the specificity of the NF-kappaB DNA complex signals. The mobility of the NF-kappaB DNA complex was shifted by anti-p65 and anti-p50 antibodies but not by anti-c-Rel antibodies, indicating that the subunits of NF-kappaB involved in gene activation after ischemic PC consist of p65-p50 heterodimers. Pretreatment with the NF-kappaB inhibitor diethyldithiocarbamate (DDTC; 150 mg/kg IP 15 minutes before ischemic PC) completely blocked the nuclear translocation and increased DNA binding activity of NF-kappaB. The same dose of DDTC completely blocked the cardioprotective effects of late PC against both myocardial stunning and myocardial infarction, indicating that NF-kappaB activation is essential for the development of this phenomenon in vivo. The ischemic PC-induced activation of NF-kappaB was also blocked by pretreatment with Nomega-nitro-L-arginine (L-NA), a nitric oxide synthase (NOS) inhibitor, N-2-mercaptopropionyl glycine (MPG), a reactive oxygen species (ROS) scavenger, chelerythrine, a protein kinase C (PKC) inhibitor, and lavendustin A, a tyrosine kinase inhibitor (all given at doses previously shown to block late PC), indicating that ischemic PC activates NF-kappaB via formation of NO and ROS and activation of PKC- and tyrosine kinase-dependent signaling pathways. A subcellular redistribution and increased DNA binding activity of NF-kappaB quantitatively similar to those induced by ischemic PC could be reproduced pharmacologically by giving the NO donor diethylenetriamine/NO (DETA/NO) (at a dose previously shown to elicit late PC), demonstrating that NO in itself can activate NF-kappaB in the heart. Taken together, these results provide direct evidence that activation of NF-kappaB is a critical step in the signal transduction pathway that underlies the development of the late phase of ischemic PC in conscious rabbits. The finding that four different pharmacological manipulations (L-NA, MPG, chelerythrine, and lavendustin A) produced similar inhibition of NF-kappaB suggests that this transcription factor is a common downstream pathway through which multiple signals elicited by ischemic stress (NO, ROS, PKC, tyrosine kinases) act to induce gene expression. To our knowledge, this is the first demonstration that NO can promote NF-kappaB activation in the heart, a finding that identifies a new biological function of NO and may have important implications for various pathophysiological conditions in which NO is involved and for nitrate therapy.

Alkaloids↗
PubMed1999

Isoform-selective activation of protein kinase C by nitric oxide in the heart of conscious rabbits: a signaling mechanism for both nitric oxide-induced and ischemia-induced preconditioning.

Although isoform-selective translocation of protein kinase C (PKC) epsilon appears to play an important role in the late phase of ischemic preconditioning (PC), the mechanism(s) responsible for such translocation remains unclear. Furthermore, the signaling pathway that leads to the development of late PC after exogenous administration of NO in the absence of ischemia (NO donor-induced late PC) is unknown. In the present study we tested the hypothesis that NO activates PKC and that this is the mechanism for the development of both ischemia-induced and NO donor-induced late PC. A total of 95 chronically instrumented, conscious rabbits were used. In rabbits subjected to ischemic PC (six 4-minute occlusion/4-minute reperfusion cycles), administration of the NO synthase inhibitor Nomega-nitro-L-arginine (group III), at doses previously shown to block the development of late PC, completely blocked the ischemic PC-induced translocation of PKCepsilon but not of PKCeta, indicating that increased formation of NO is an essential mechanism whereby brief ischemia activates the epsilon isoform of PKC. Conversely, a translocation of PKCepsilon and -eta quantitatively similar to that induced by ischemic PC could be reproduced pharmacologically with the administration of 2 structurally unrelated NO donors, diethylenetriamine/NO (DETA/NO) and S-nitroso-N-acetylpenicillamine (SNAP), at doses previously shown to elicit a late PC effect. The particulate fraction of PKCepsilon increased from 35+/-2% of total in the control group (group I) to 60+/-1% after ischemic PC (group II) (P<0.05), to 54+/-2% after SNAP (group IV) (P<0.05) and to 52+/-2% after DETA/NO (group V) (P<0.05). The particulate fraction of PKCeta rose from 66+/-5% in the control group to 86+/-3% after ischemic PC (P<0.05), to 88+/-2% after SNAP (P<0.05) and to 85+/-1% after DETA/NO (P<0.05). Neither ischemic PC nor NO donors had any appreciable effect on the subcellular distribution of PKCalpha, -beta1, -beta2, -gamma, -delta, - micro, or -iota/lambda; on total PKC activity; or on the subcellular distribution of total PKC activity. Thus, the effects of SNAP and DETA/NO on PKC closely resembled those of ischemic PC. The DETA/NO-induced translocation of PKCepsilon (but not that of PKCeta) was completely prevented by the administration of the PKC inhibitor chelerythrine at a dose of 5 mg/kg (group VI) (particulate fraction of PKCepsilon, 38+/-4% of total, P<0.05 versus group V; particulate fraction of PKCeta, 79+/-2% of total). The same dose of chelerythrine completely prevented the DETA/NO-induced late PC effect against both myocardial stunning (groups VII through X) and myocardial infarction (groups XI through XV), indicating that NO donors induce late PC by activating PKC and that among the 10 isozymes of PKC expressed in the rabbit heart, the epsilon isotype is specifically involved in the development of this form of pharmacological PC. In all groups examined (groups I through VI), the changes in the subcellular distribution of PKCepsilon protein were associated with parallel changes in PKCepsilon isoform-selective activity, whereas total PKC activity was not significantly altered. Taken together, the results provide direct evidence that isoform-selective activation of PKCepsilon is a critical step in the signaling pathway whereby NO initiates the development of a late PC effect both after an ischemic stimulus (endogenous NO) and after treatment with NO-releasing agents (exogenous NO). To our knowledge, this is also the first report that NO can activate PKC in the heart. The finding that NO can promote isoform-specific activation of PKC identifies a new biological function of this radical and a new mechanism in the signaling cascade of ischemic PC and may also have important implications for other pathophysiological conditions in which NO is involved and for nitrate therapy.

Alkaloids↗
PubMed1999

Probing Static Structure of Colloid-Polymer Suspensions with Multiply Scattered Light.

Time-dependent measurements of light propagation were conducted in aqueous dispersions of 523 nm diameter polystyrene at concentrations between 0.1 and 0.4 solids volume fraction in order to assess how particle correlation is influenced by depletion interactions arising from the addition of soluble polyethyleneoxide (PEO). In the absence of polymer, the transport scattering length can be predicted from Mie scattering theory and the Percus-Yevick (P-Y) model for static structure of a dense hard-sphere colloidal solution. Depletion forces arising from the addition of PEO of varying molecular weights influenced the spatial ordering of the dispersion and caused a further increase in the transport scattering length beyond that predicted by hard-sphere static structure factor but similar to that predicted by the mean sphere approximation (MSA) to the P-Y model described by Ye et al. (1996). Onset of flocculation occurred with increased PEO addition and correlated with PEO molecular weight. Phase separation was noted by no further change in the transport scattering length, except when flocculation was induced by the highest molecular weight PEO. The use of time-dependent measurements of light propagation in dense systems provides an alternative to small-angle light, neutron, and X-ray scattering characterization of interaction potentials in dense, multiply scattering samples and promises further fruitful investigation of colloidal particle interactions in suspensions. Copyright 1999 Academic Press.

Journal Article↗
PubMed1999

EUROCARE: a cross-national study of co-resident spouse carers for people with Alzheimer's disease: II--A qualitative analysis of the experience of caregiving.

BACKGROUND: Spouses caring for a partner with dementia are subject to physical, psychological and social stresses. In view of the part played by spouse carers in preventing admission to institutional care, a fuller understanding of the subjective experience of caring is an important area of enquiry. Qualitative analysis of their accounts of the difficulties and rewards in looking after their partners may indicate strategies to support them and to alleviate the stresses that they experience. METHOD: Twenty co-resident spouses of people with NINCDS-ADRDA probable dementia of the Alzheimer's type, who had been diagnosed as such within the past 12-36 months, were recruited from service contacts in each of 14 out of the 15 countries of the EU. All completed a semi-structured interview that included open-ended questions about the experience of caring. RESULTS: Overall, the most commonly expressed difficulties reflected: loss of companionship through diminished quality of communication; loss of reciprocity as carers experienced their partners' growing dependency; and deterioration in their partners' social behaviour. Satisfaction from caring stemmed from: a feeling of job satisfaction; continued reciprocity and mutual affection; companionship; and the fulfillment of a sense of duty. CONCLUSION: Spouse carers in the 14 countries described the difficulties and rewards of caring in similar terms. This suggests commonality of experience, in spite of diversity in informal and statutory provision of care for older people between different countries.

Aged↗
PubMed1999

Review: Somatization in the elderly.

Somatization is a common medical problem encountered at all levels of medical care. It is strongly associated with use of services and may be difficult to treat. Somatization in the elderly has been traditionally seen as a masked presentation of depression. Population studies have shown no consistent increase in somatization among the elderly, and the elderly may down-play physical symptoms. Among the elderly depressed, somatization is common and may be commoner if physical illness is also present. Psychological distress is usually acknowledged, not masked, in the elderly depressed. Neuroticism, as well as psychiatric illness, may be an important aetiological factor for somatization in the elderly. Treatment strategies must attend to underlying psychiatric disorders, but there is a need for studies of treatment of the phenomenon in the elderly.

Adult↗
PubMed1999

Modulatory potential of Spirulina fusiformis on carcinogen metabolizing enzymes in Swiss albino mice.

The modulatory potential of Spirulina fusiformis was observed on the hepatic and extrahepatic carcinogen metabolizing enzymes in Swiss albino mice at a dose of 800 mg/kg b.w. given orally. A significant reduction in the hepatic cytochrome P-450 content was observed in the group treated with Spirulina in comparison with the control group. The hepatic glutathione S-transferase activity was induced significantly by Spirulina treatment. There was no change in the extrahepatic glutathione S-transferase activity after the animals were fed with Spirulina.

Animals↗
PubMed1999

Ischemic preconditioning increases iNOS transcript levels in conscious rabbits via a nitric oxide-dependent mechanism.

Recent studies implicate iNOS as the mediator of the late phase of ischemic preconditioning (PC). However, it is unknown whether induction of iNOS activity is mediated by transcriptional, post-transcriptional, translational, or post-translational mechanisms. To address this issue, we isolated and sequenced a partial iNOS cDNA expressed in preconditioned rabbit myocardium. Using a rabbit-specific probe generated from this sequence, we measured the steady state levels of the iNOS transcript after ischemic PC [six cycles of 4-min occlusion/4-min reperfusion (O/R)]. Three hours after ischemic PC, the iNOS mRNA levels in the ischemic/reperfused region were increased approximately three-fold relative to samples from the non-ischemic region and from control rabbits. This increase in mRNA levels was completely abolished by pretreatment with the NOS inhibitor Nomega -nitro- L-arginine. Conversely, administration of the NO donor nitroglycerin induced an increase in iNOS mRNA levels similar to that induced by ischemic PC. We conclude that in the conscious rabbit, ischemic PC induces an increase in iNOS mRNA levels, and that this induction is triggered by increased generation of NO during the PC stimulus. These results provide direct evidence that upregulation of iNOS is a natural response of the heart to a brief ischemic stress and that NO itself, in the absence of ischemia, upregulates myocardial iNOS transcript levels, a finding that may have implications for nitrate therapy. This previously unrecognized NO-dependent upregulation of iNOS mRNA is likely to play an important role in the development of late PC as well as in many other pathophysiological conditions in which NO is implicated.

Amino Acid Sequence↗
PubMed1999

Evaluation of hepatoprotective activity of Cassia fistula leaf extract.

Hepatoprotective activity of the n-heptane extract of Cassia fistula leaves was investigated in rats by inducing hepatotoxicity with carbon tetrachloride:liquid paraffin (1:1). The extract has been shown to possess significant protective effect by lowering the serum levels of transminases (SGOT and SGPT), bilirubin and alkaline phosphatase (ALP). The extract of C. fistula at a dose of 400 mg/kg showed significant hepatoprotective activity which was comparable to that of a standard hepatoprotective agent.

Alanine Transaminase↗
PubMed1999

Technetium-99m complexes of polydentate amine-pyrrole and amine-thiophene ligands.

Novel polydentate amine-pyrrole and amine-thiophene ligands were synthesized and characterized by 1H and 13C NMR spectroscopy. Radiochemical studies with 99mTc were carried out at 0.1-100 microM of technetium. Complexation yields were estimated from thin layer chromatography (TLC), paper electrophoresis, and solvent extraction studies. The 99mTc complexes formed were found to be neutral and lipophilic. Complexes with the corresponding imine-ligands were formed in lower yields. Biodistribution studies of the 99mTc complexes of these ligands showed no significant uptake in brain or heart, and the clearance was mainly through the hepatobiliary system.

Animals↗