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B Chattopadhyay

Publications and source records attributed to B Chattopadhyay.

At least 19 recordsLinked to original sources
PubMed2006

Interaction of HIPPI with putative promoter sequence of caspase-1 in vitro and in vivo.

To investigate the mechanism of increased expression of caspase-1 in Hippi expressing HeLa and Neuro 2A cells, reported earlier, we report here that HIPPI directly interacted with upstream sequence of caspase-1 gene (-700 to +17, 717 bp). Deletion of this 717 bp sequence and further analysis by electrophoretic mobility shift assay and fluorescence quenching revealed that HIPPI interacted with 60 bp (-151 to -92) upstream sequence of caspase-1. We also observed by chromatin immunoprecipitation assay that HIPPI interacted with the 717 bp sequence in vivo. In luciferase assay, when expression of the reporter gene was driven by either 717 bp or 60 bp caspase-1 upstream sequences, luciferase activity was increased in GFP-Hippi expressing HeLa cells in comparison to that obtained with parental HeLa cells with the same constructs. Similar result was obtained in Neuro2A cells with 717 bp caspase-1 upstream sequence. In summary, we showed that HIPPI could interact with the putative promoter sequence of caspase-1 and increased the expression of the downstream gene suggesting that HIPPI could act as transcription regulator.

Adaptor Proteins, Signal Transducing↗
PubMed2005

High prevalence of spinocerebellar ataxia type 1 in an ethnic Tamil community in India.

OBJECTIVE: To study the prevalence, clinical and molecular genetic characteristics of cerebellar ataxia in an ethnic Tamil community in India. METHODS: An epidemiological study of cerebellar ataxia was done in two villages in the Indian state of Tamilnadu where its prevalence was observed to be high. All the people were screened and the clinical characteristics of those with ataxia were recorded. Genetic analysis was done in those with ataxia and in two asymptomatic control groups - group I belonging to the affected community and group II belonging to the unaffected community. The clinical and genetic results are correlated. Measures to help the community are suggested. RESULTS: The total population of the two villages was 378. Among them 345 belonged to Vanniyakula Kshatriyar community and 33 to another. Cerebellar ataxia was found in 25 individuals belonging only to the former community (7.2%). The mean age of onset was 39.8 years and the salient features were ataxic gait (100%), dysarthria (100%), pyramidal signs (72%), slow saccades (48%) and bleeding diathesis (12%). Genetic studies were done in 17 of the study group. All showed pathological expansion of CAG repeats above 40, in chromosome 6p, diagnostic of SCA1. 7 of the 18 in the control group (I) and none in control group (II) had CAG repeats above 40. CONCLUSION: The prevalence of SCA1 is high (7.2%) in this ethnic Tamil community with a large asymptomatic group waiting to manifest. The symptomatic individuals need social support and rehabilitation. Appropriate counseling, prenatal evaluation and therapy will prevent the spread of disease to the next generation.

Adolescent↗
PubMed2004

Molecular analysis of GAA repeats and four linked bi-allelic markers in and around the frataxin gene in patients and normal populations from India.

Friedreich ataxia (FRDA), the most common type of ataxia worldwide, is an autosomal recessive disease. Homozygous expansion of GAA repeats in the first intron of the frataxin gene constitute the major type of mutation that causes the disease. The prevalence of FRDA in diverse ethnic populations of India has not been widely studied. We have studied the distribution of polymorphic GAA repeats in the frataxin gene among 6 clinically diagnosed patients and 160 ethnically matched normal individuals, to gather information on the prevalence of FRDA in the eastern part of India. Homozygous expansion in the range of 250-730 GAA repeats was detected among the patients. Among normal individuals, we observed a unimodal distribution of GAA repeats, consisting of 10 different alleles ranging from 7 to 16 GAA repeats, where the 9 repeat allele had maximal frequency. Only 5.9% of all chromosomes were found to harbour >12 GAA repeats. Haplotype analysis using closely linked four bi-allelic markers in and around the frataxin gene indicated that 66.7% of the expanded alleles harbour the ATCC haplotype that has been reported worldwide. This haplotype was present in 53.3% of the chromosomes with >12 GAA repeats, and accounted for only 3.8% of chromosomes with 7 to 12 GAA repeats. We found one novel haplotype, ACCT, among the expanded alleles as well as among normal individuals, though at low frequency; this haplotype may be characteristic of Indian populations.

Adolescent↗
PubMed2003

Variation of CAG repeats and two intragenic polymorphisms at SCA3 locus among Machado-Joseph disease/SCA3 patients and diverse normal populations from eastern India.

OBJECTIVES: MJD1/SCA3 is the most common type of spinocerebellar ataxia (SCA) worldwide. To explain the low prevalence of the disease among SCA patients from eastern India, we analysed CAG repeats and two bi-allelic intragenic markers at SCA3 locus among 412 normal individuals and 10 patients. MATERIALS AND METHODS: For CAG repeat analysis, PCR amplified fragments were run on polyacrylamide gel, transferred to a membrane, probed with (CAG)10 and detected on an autoradiograph. Bi-allelic markers were analysed using allele specific PCR amplification. RESULTS: Large normal alleles (>33 CAG repeats) were 0.015 in pooled populations. All the patients had the common haplotype C-A as observed worldwide. Frequency of C-A haplotype among large normal alleles was 0.75. CONCLUSIONS: Observed low prevalence of SCA3 could be because of the low prevalence of large normal alleles that might act as the reservoir for the expanded alleles. SCA3 mutation in Indian populations had the same origin as found worldwide.

Ataxin-3↗
PubMed2001

Control of infection wards--are they worthwhile?

Prevention and control of hospital-acquired infections is a major issue challenging the Infection Control Team in the United Kingdom. Confronted with this problem, a control of infection ward was opened to segregate as many patients as possible from the rest of the hospital in order to prevent transmission of infection to other vulnerable patients. The author, as the Control of Infection Doctor, discusses in detail the strengths and weaknesses of such an arrangement and expresses his personal views as to whether it is a worthwhile and cost-effective method to combat hospital-acquired infection.

Attitude of Health Personnel↗
PubMed2000

Analysis of CAG repeats in SCA1, SCA2, SCA3, SCA6, SCA7 and DRPLA loci in spinocerebellar ataxia patients and distribution of CAG repeats at the SCA1, SCA2 and SCA6 loci in nine ethnic populations of eastern India.

To identify various subtypes of spinocerebellar ataxias (SCAs) among 57 unrelated individuals clinically diagnosed as ataxia patients we analysed the SCA1, SCA2, SCA3, SCA6, SCA7 and DRPLA loci for expansion of CAG repeats. We detected CAG repeat expansion in 6 patients (10.5%) at the SCA1 locus. Ten of the 57 patients (17.5%) had CAG repeat expansion at the SCA2 locus, while four had CAG expansion at the SCA3/MJD locus (7%). At the SCA6 locus there was a single patient (1.8%) with 21 CAG repeats. We have not detected any patient with expansion in the SCA7 and DRPLA loci. To test whether the frequencies of the large normal alleles in SCA1, SCA2 and SCA6 loci can reflect some light on prevalence of the subtypes of SCAs we studied the CAG repeat variation in these loci in nine ethnic sub-populations of eastern India from which the patients originated. We report here that the frequency of large normal alleles (>31 CAG repeats) in SCA1 locus to be 0.211 of 394 chromosomes studied. We also report that the frequency of large normal alleles (>22 CAG repeats) at the SCA2 locus is 0.038 while at the SCA6 locus frequency of large normal alleles (>13 repeats) is 0.032. We discussed our data in light of the distribution of normal alleles and prevalence of SCAs in the Japanese and white populations.

Adolescent↗
PubMed2000

Control of MRSA.

Explore the source record for details and available documents.

Humans↗
PubMed1998

Trying to control MRSA causes more problems than it solves.

Despite occasional reports of local success, the steadily increasing prevalence of strains of Staphylococcus aureus resistant to methicillin (MRSA) shows that attempts to limit their spread do not work. In this commentary we suggest that efforts to control the spread of methicillin-resistance are counterproductive, and that energies should instead be directed towards the control of outbreaks of disease and preventing the emergence of antibiotic resistance.

Cross Infection↗
PubMed1994

Outbreak of gentamicin, ciprofloxacin-resistant Pseudomonas aeruginosa in an intensive care unit, traced to contaminated quivers.

An outbreak of gentamicin, ciprofloxacin-resistant Pseudomonas aeruginosa in an intensive care unit, was investigated. The majority of isolates were from sputum and the organism was not isolated from any other patient in the hospital, except those admitted to the unit. A prospective study was set up, and the organism was found to be associated with contaminated quivers, used to store suction tubing between use on ventilated patients. Once the quivers were disinfected and changed between patients daily, the outbreak stopped. Suction of ventilated patients may be an important source of contamination of the respiratory tract with nosocomial pathogens. It is important that infection control teams regularly review procedures to ensure the correct practices are being followed, so that nosocomial outbreaks of infection may be prevented.

Ciprofloxacin↗
PubMed1994

Pseudobacteraemia.

Pseudobacteraemia occurs when bacteria isolated from blood cultures have originated from outside the patient's bloodstream. Failure to recognize that pseudobacteraemia is taking place and is not true infection may result in patient morbidity, unnecessary therapy and a significant waste of health care resources. Pseudobacteraemia may occur as a result of contamination introduced at any stage of blood culturing, from taking the blood to processing it in the laboratory. In most reported cases, contamination has occurred as a result of faulty aseptic technique, and thus pseudobacteraemia is usually preventable. Episodes of pseudobacteraemia require prompt investigation, but their recognition may be extremely difficult. Here we review pseudobacteraemia and recommend guidelines for its recognition, investigation and prevention.

Bacteremia↗