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Biomedical subjects

A Ganesh

Publications and source records attributed to A Ganesh.

At least 37 records · Page 2Linked to original sources
PubMed1999

Acinetobacter meningitis following head trauma.

A case of acinetobacter meningitis following head injury in a patient who developed cerebrospinal fluid otorrhea, and did not have any neurosurgical procedure, is presented. Previously reported cases are cited, with a review of the literature. Pefloxacin monotherapy is associated with a poor clinical response.

Acinetobacter Infections↗
PubMed1999

Mycobacterium fortuitum endocarditis and meningitis after balloon mitral valvotomy.

Mycobacteria rarely cause endocardial infections. We describe the clinical course of a patient who developed endocarditis, and meningitis with Mycobacterium fortuitum following balloon mitral valvotomy. The patient was treated with amikacin and clarithromycin but did not respond. She developed haemolytic anaemia as the terminal event.

Adult↗
PubMed1997

Mutator phenotype in Msh2-deficient murine embryonic fibroblasts.

Embryonic fibroblast cell lines were established from mice deficient, heterozygous, or proficient for Msh2, one of the three known DNA mismatch repair genes involved in hereditary nonpolyposis colon cancer (HNPCC). Cell lines were established by transfection of primary mouse embryo fibroblasts with E7 and Ras oncogenes or mutant p53. Spontaneously immortalized cells derived from the primary cultures were also studied. To determine whether these cells developed a mutator phenotype similar to that found in colon cancer cells deficient in mismatch repair, we measured mutation rates, microsatellite instability, and sensitivities to a range of DNA-damaging agents. The mutator phenotype detected in the E7 and Ras or mutant p53-immortalized Msh2-/- mouse cells was similar to that found in human mismatch repair-deficient colorectal carcinoma cell lines. Mutation rates to ouabain resistance were increased 8-12-fold relative to lines from Msh2+/+ mice, and microsatellite instability was detectable in 12-18% of subclones derived from the Msh2-/- line but was undetectable in subclones developed from the Msh2+/+ line. Furthermore, E7 and Ras or spontaneously immortalized Msh2-/- cells were significantly more resistant to the cytotoxic effects of 6-thioguanine relative to Msh2+/+ cells. In contrast, these lines showed various responses to UV light and cis-platinum, suggesting that mismatch repair deficiency was not the sole determinant for sensitivity to these DNA-damaging agents. Particular attention was paid to the properties of cells heterozygous for the Msh2 mutant gene, which would mimic the situation of an HNPCC carrier. However, our studies failed to reveal any properties of these cells that might provide a growth advantage or predispose them for the acquisition of further mutations. This observation is consistent with the model that inactivation of the wild-type Msh2 allele is a critical step for tumorigenesis in HNPCC patients.

Animals↗
PubMed1997

Epidemiological features of acquired immunodeficiency syndrome in southern India.

AIDS was diagnosed in 187 men and 24 women (M:F = 8:1) from April 1987 till December 1994 at the Christian Medical College Hospital, Vellore. The doubling time of the occurrence of AIDS cases was 14 months; during 1987-90 there were an average of 5.7 cases per year; in 1991-93 there were 28 per year; in 1994 there were 104 cases. The mean age of patients was 33 yr for men and 31 for women. Among men, the primary mode of infection was heterosexual contact with female commercial sex workers. Among women, the most common source of infection was their husbands. There were 4 bisexuals and one homosexual subject who might have acquired infection by having sex with other men. There were 135 subjects from urban and 76 from rural communities. Most subjects belonged to the lower socio-economic classes. These data show that HIV infection had been very widespread in this region, both urban and rural.

Acquired Immunodeficiency Syndrome↗
PubMed1996

Evaluation of an ELISA for the diagnosis of brucellosis.

Brucela serology using ELISA and standard agglutination test was performed on 23 patients with prolonged fever where the test was requested, on 26 randomly chosen patients with prolonged fever where it was not requested and on 17 controls. ELISA was positive in 39.1, 26.9 and 0 per cent respectively in these groups. Brucellosis may often be unsuspected because of its varied clinical manifestations and may be a more important cause of fever than previously considered. Our data reaffirm that ELISA is superior to the standard agglutination test for the diagnosis of brucellosis.

Agglutination Tests↗
PubMed1996

Melioidosis In India: the tip of the iceberg?

Diagnosis of melioidosis by the isolation of Burkholderia pseudomallei from one or more body fluid/tissue specimens of 6 Indian subjects, 5 of whom had not travelled outside India, is reported. The places of residence of these 6 and one patient previously reported, namely Tripura (2), Kerala (2), Orissa (1), Tamil Nadu (1) and Maharashtra (1) are therefore potentially endemic for melioidosis. B.pseudomallei closely resembles common contaminant Pseudomonas sp. and are easily mis-identified in microbiology laboratories. We surmise that melioidosis is underdiagnosed and underreported in India and we alert clinicians, microbiologists and public health professionals to the possibility of melioidosis being far more common than previously recognised.

Adolescent↗
PubMed1995

Molecular analysis of mutations in mutator colorectal carcinoma cell lines.

The nature of mutations occurring in two colorectal carcinoma cell lines deficient in mismatch repair and displaying mutator phenotypes was determined. One of the lines (HCT116) exhibited a higher level of microsatellite instability than the second (DLD-1), although the rate of mutation at the selectable locus encoding the purine salvage enzyme hypoxanthine guanine phosphoribosyl transferase (HPRT) was equally elevated (about 350-450-fold relative to mismatch repair proficient cell lines). Transitions were the major class of mutations in the two mutator lines. In DLD-1 these mutations recurred at several sites that appeared to be hotspots. Frameshifts at a run of six guanine residues in the coding sequence for HPRT constituted 35% of mutations in HCT116. These frameshifts were highly unstable and reverted to wild type at high frequency. Larger deletions were also detected in HCT116. Although these deletions constituted a small proportion of mutations compared with the other types, our data suggest that the rate of deletion is elevated relative to mismatch repair proficient (hMLH1+) cell lines. These observations suggest that the gene(s) altered in DLD-1 may preferentially affect the repair of base mismatches while the alteration(s) in HCT116 may affect the repair of both mismatches and frameshifts.

Base Sequence↗
PubMed1994

Mutator phenotypes in human colorectal carcinoma cell lines.

Recent studies have revealed that tumors in patients with hereditary nonpolyposis colon cancer are associated with high-frequency alterations of microsatellite sequences. To investigate the mechanisms and consequences of this form of genetic instability, we identified three colorectal carcinoma cell lines that express dinucleotide-repeat instability like that found in hereditary nonpolyposis colon cancer tumors and show increased rates of spontaneous mutation at selectable loci. However, the pattern of hypermutation in these cell lines differed significantly. In one line (HCT116), microsatellite mutations occurred at a remarkably high rate (approximately 10(-2) mutations per cell per generation), whereas this rate was considerably lower in the two other lines (DLD-1 and HCT15). The rate of mutation at the locus encoding hypoxanthine guanine phosphoribosyltransferase was substantially elevated (200- to 600-fold) in all three tumor cell lines, yet the types of mutations arising differed. A specific frame-shift hotspot accounted for 24% of hypoxanthine guanine phosphoribosyltransferase mutations in HCT116. The frequency of mutations at this site was reduced significantly in DLD-1 and HCT15 lines. These data suggest that the mutatw phenotypes in the colorectal carcinoma cell lines could be the consequence of mutator genes affecting different repair or error-avoidance pathways.

Cell Line↗
PubMed1993

Repair and misrepair of site-specific DNA double-strand breaks by human cell extracts.

The rejoining by human cell extracts of a double-strand break induced by endonuclease treatment at one of several sites within a small DNA molecule was studied. Rejoining was found at each of 8 sites tested, but the rejoin efficiency varied with the nature of the break (e.g., breaks with cohesive ends were rejoined more efficiently than blunt-ended breaks). Extracts from primary and immortalized cell lines, as well as those from individuals with ataxia telangiectasia (A-T), showed the same pattern of relative rejoin efficiencies. However, mis-rejoining varied with the cell extract used, and was particularly elevated with two immortalized A-T cell lines. Mixing experiments showed that the mis-rejoining property of extracts could act in a semi-dominant fashion, depending on the individual efficiencies of the component extracts. The mis-rejoin mechanism involved deletion at sites of short direct repeats at various distances from the initial break site. A model of deletion formation (the strand-exposure and repair model) is restated to explain the sequence repeat dependence found, and is compared to models of homologous DNA recombination.

Ataxia Telangiectasia↗
PubMed1992

A mechanism for deletion formation in DNA by human cell extracts: the involvement of short sequence repeats.

DNA molecules carrying a site-specific double-strand break were exposed to nuclear extracts from human cell lines. It was shown previously that breaks could be rejoined correctly by human extracts, but that a proportion of the rejoined molecules had suffered deletions and insertions. The 'mis-rejoined' proportion was higher with cell extracts from an individual with the disorder ataxia-telangiectasia than with normal cell extracts. We now show by sequence analysis that deletions in extract-treated molecules occur exclusively between short direct repeats (2-6 base pairs). A mis-rejoined molecule containing an insertion of 300 bp also had a repeat-based deletion at the same site. A number of different direct repeats are involved; however, some clustering of these occurs especially on the upstream side of the initial breakpoint. These data are most simply interpreted in terms of a model of deletion formation involving single-strand exposure and repair, perhaps with the action of other DNA-metabolising enzymes influencing the frequency with which some repeats are involved.

Ataxia Telangiectasia↗
PubMed1992

Clinical and laboratory profile of AIDS in India.

The clinical features and results of laboratory investigations of the first 19 Indian patients with AIDS seen in our hospital are presented. Weight loss, fever, and diarrhea were the most common symptoms. Tuberculosis (TB) was the most common secondary infectious disease; among 13 patients, seven had only pulmonary TB, five had pulmonary and extrapulmonary TB, and one had only extrapulmonary TB. Oropharyngeal candidiasis was found in 11 patients. Other secondary infections were predominantly by virulent bacteria. Opportunistic infections other than candidiasis were infrequent; one patient had cryptococcosis, two had symptomatic cryptosporidiosis, one had noncoagulase-positive staphylococcus septicemia, and one had cytomegalovirus retinitis. Reduced lymphocyte counts (particularly of the CD4 subset), anemia, hypoalbuminemia, hyperglobulinemia, and elevated liver enzyme levels were frequent laboratory findings. Six patients are under follow-up, two are lost to follow-up, and 11 have died. Lymphocyte counts less than 500/mm3 were only seen in those patients who subsequently died. Response to antituberculosis therapy was good in several patients. Thus, the clinical profile of Indian patients with AIDS is not different from the common picture of patients of low socioeconomic and poor hygienic standards; patients presented with TB, undernutrition, and multiple infections. Therefore, a large population of patients with AIDS in India will not be recognized unless they are tested for evidence of HIV infection.

Acquired Immunodeficiency Syndrome↗