Bhuniya S.,Midnapore Medical College and Hospital |
Sabyasachi C.,Calcutta Medical College and Hospital |
Indranil S.,Burdwan Medical College and Hospital |
Sumit R.T.,Rg Kar Medical College And Hospital |
Mita S.,Rg Kar Medical College And Hospital
Annals of Thoracic Medicine | Year: 2012
Context: Prevalence of tuberculous pleural effusion is very high in the Asian subcontinent but very few studies have come up from this part of the world about the course of recovery of pulmonary functions after institution of anti-tubercular therapy (ATT) and thoracentesis. Aims: To study initial lung function impairment, changes over time after institution of ATT and thoracentesis and residual abnormalities left at the end of six months of treatment. Settings and Design: Randomized open level interventional study over two years in 52 patients at a tertiary level teaching hospital. Methods: The study population was divided into two equal groups, A (therapeutic thoracentesis) and B (diagnostic thoracentesis). Spirometry, chest radiograph and ultrasonography of thorax were done initially and at each follow-up visit up to six months. Statistical analysis was done (P value < 0.05 considered significant). Results: Both groups were comparable initially. After six months none in group A and five patients in group B had minimal pleural effusion. During follow up, mean percentage predicted of FEV1 and FVC increased more in A than in B and the differences were statistically significant (P < 0.05). Pleural thickening, initially absent in both groups, was found to be more in B as compared to A at subsequent follow-up visits and this was statistically significant (P < 0.05). Conclusions: Thoracentesis should be considered in addition to anti-TB treatment, especially in large effusions, in order to relieve dyspnea, avoid possibility of residual pleural thickening and risk of developing restrictive functional impairment.
Sanyal J.,Anthropological Survey of India |
Sarkar B.,Anthropological Survey of India |
Banerjee T.K.,National Neurosciences Center |
Mukherjee S.C.,Calcutta Medical College and Hospital |
And 2 more authors.
Neurological Research | Year: 2011
Objectives: Mutations in the DJ-1 gene have been described in autosomal recessive Parkinson's disease (PD) of European ancestry, Ashkenazi Jews, and Afro-Caribbean patients. Up to date, there is a lack of information about the prevalence of DJ-1 mutations among Indian PD patients. Materials and methods: In this study, we examined for DJ-1 mutations in Eastern Indian PD patients. Exons (no. 2-7) and intron boundaries of the DJ-1 gene were screened in 300 individuals (PD, 150; controls, 150) by direct sequencing. Results: A total of six intronic variants (IVS4-30T>G, IVS4+45G>A, IVS4+46G>A, IVS4-98G>A, IVS5+31G>A and IVS5+69G>C) were detected including one novel intronic change (IVS5+69G>C). Clinical features of the two patients exhibiting IVS5+69G>C (novel change) were compared and both were found to have early onset PD. IVS4+30T>G, IVS4+45G>A, and IVS4+46G>A were found to be present equally both in the patient and control cohorts. We did not find any DJ-1 mutations in our study. Conclusion: Our results suggest that, unlike Parkin, pathogenic DJ-1 mutations seem to be restricted in certain populations and are unlikely to be of clinical importance in the eastern part of India. © W. S. Maney & Son Ltd 2011.
Sanyal J.,Anthropological Survey of India |
Chakraborty D.P.,Bankura Medical College and Hospital |
Sarkar B.,Anthropological Survey of India |
Banerjee T.K.,National Neuroscience Center |
And 3 more authors.
Canadian Journal of Neurological Sciences | Year: 2010
Background: While the cause of Parkinson's disease (PD) remains unknown, evidence suggests certain environmental factors, such as well water drinking, herbicides, pesticides exposure and neurotoxins, may trigger the chain of oxidative reactions culminating in the death of dopaminergic neurons in substantia nigra to cause Parkinsonism. To investigate the possible impact of environmental risk factors for idiopathic PD, a case-control study was performed in the Eastern India. Methods: During the period from January 1st, 2006 and December 10th, 2009, 175 PD patients (140 men, 35 women) and 350 non-Parkinson age-sex matched controls were included in the study. Subjects were given a structured neurological examination and completed an administered questionnaire which elicited detailed information on demographic data, pesticides, herbicides family history, occupation, dietary and smoking habits. Results: The multivariate analysis revealed that family history of PD, pesticide exposure, exposure to toxins other than pesticides and herbicides, rural living and previous history of depression were associated with increased risk of PD, whereas, smoking appeared to be a protective factor. Well water drinking for at least five years, though a significant risk factor on univariate analysis (OR=4.5, 95% CI=2.1-9.9), could not be proved significant in multivariate analysis. Head trauma, vegetarian dietary habit, occupation involving physical exertion and exposure to domestic pets were not as significant risk factors. Conclusion: Results of our study support the hypothesis of multifactorial etiology of PD with environmental factors acting on a genetically susceptible host.
Mitra S.,Chittaranjan National Cancer Institute |
Indra D.M.,Chittaranjan National Cancer Institute |
Bhattacharya N.,Chittaranjan National Cancer Institute |
Singh R.K.,Chittaranjan National Cancer Institute |
And 7 more authors.
Genes Chromosomes and Cancer | Year: 2010
To understand the importance of frequent deletion of 3p22.3 in cervical carcinogenesis, alterations (deletion/methylation/expression) of the candidate genes STAC, MLH1, ITGA9, and RBSP3, located in the region, were analyzed in 24 cervical intraepithelial neoplasia (CIN) and 137 uterine cervical carcinoma (CACX) samples. In CIN, RBSP3 deletion (48%) and methylation (26%) were high compared with the other genes (4-9%). In CACX, alterations of these genes were as follows: deletion: STAC (54%) > MLH1 (46%) > RBSP3 (45%) > ITGA9 (41%), methylation: RBSP3 (25%) > ITGA9 (24%) > STAC (19%) > MLH1 (13%). Overall, alterations of RBSP3 showed association with CIN, whereas for STAC and MLH1, this frequency increased significantly from CIN → Stage I/II and for ITGA9 from CIN → Stage I/II and also from Stage I/II → Stage III/IV. Quantitative mRNA expression analysis showed differential reduced expression of these genes in CACX concordant to their molecular alterations. The more active RBSP3B splice variant was underexpressed in CACX. RB1 was infrequently deleted in CACX. Concordance was seen between (i) inactivation of RBSP3 and intense p-RB1 nuclear immunostaining and (ii) low/absence of MLH1 expression and its molecular alterations in CACX. In normal cervical epithelium, p-RB1 immunostaining was low in differentiated cells, whereas MLH1 staining was seen in both nucleus and cytoplasm irrespective of differentiation stage. Alterations of the genes were significantly associated with poor prognosis. High parity (≥5)/early sexual debut (≤19 years) coupled with RBSP3 alterations/RB1 deletion predicted worst prognosis. Thus, inactivation of RBSP3 might be one of the early events in cervical carcinogenesis. © 2009 Wiley-Liss, Inc.
Ghosh A.,Chittaranjan National Cancer Institute |
Ghosh S.,Chittaranjan National Cancer Institute |
Maiti G.P.,Chittaranjan National Cancer Institute |
Sabbir M.G.,Chittaranjan National Cancer Institute |
And 4 more authors.
Cancer Science | Year: 2010
To understand the association between candidate tumor suppressor genes (TSGs) human mismatch repair protein homologue 1 (hMLH1), AP20 region gene 1 (APRG1), integrin α RLC (ITGA9), RB1 serine phosphates from human chromosome 3 (RBSP3) at chromosomal 3p22.3 region and development of head and neck squamous cell carcinoma (HNSCC), alterations (deletion/promoter methylation/expression) of these genes were analyzed in 65 dysplastic lesions and 84 HNSCC samples. Clinicopathological correlations were made with alterations of the genes. In HNSCC, deletion frequencies of hMLH1, ITGA9, and RBSP3 were comparatively higher than APRG1. Overall alterations (deletion/methylation) of hMLH1, ITGA9, and RBSP3 were high (45-55%) in mild dysplasia and comparable in subsequent stages of tumor progression. Quantitative RT-PCR analysis showed reduced expression of these genes in tumors concordant to their molecular alterations. An in vitro demethylation experiment by 5-aza-2′-deoxycytidine confirmed the promoter hypermethylation of RBSP3 in Hep2 and UPCI:SCC084 cell lines. Functionally less-active RBSP3A isoform was predominant in tumor tissues contrary to the adjacent normal tissue of tumors where more active RBSP3B isoform was prevalent. In immunohistochemical analysis, intense nuclear staining of hMLH1 and pRB (phosphorylated RB, the substrate of RBSP3) proteins were seen in the basal layer of normal epithelium. In tumors, concordance was seen between (i) low/intermediate level of hMLH1 expression and its molecular alterations; and (ii) intense nuclear staining of pRB and RBSP3 alterations. Poor patient outcome was seen with hMLH1 and RBSP3 alterations. Moreover, in absence of human papilloma virus (HPV) infection, tobacco-addicted patients with hMLH1, RBSP3 alterations, and nodal invasions showed poor prognosis. Thus our data suggests that dysregulation of hMLH1, ITGA9, and RBSP3 associated multiple cellular pathways are needed for the development of early dysplastic lesions of the head and neck. (Cancer Sci 2010). © 2010 Japanese Cancer Association.