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Featured researches published by Gandhi Bm.


Transactions of The Royal Society of Tropical Medicine and Hygiene | 1987

Enzyme linked protein-A: An ELISA for detection of amoebic antibody

Gandhi Bm; M. Irshad; T.C. Chawla; Tandon Bn

Enzyme linked protein-A was used to develop an enzyme linked immunosorbent assay (ELISA) system for the detection of circulating antibodies to amoebic antigen. The specificity of protein-A to bind IgG only through Fc receptors, makes the test more specific for the detection of IgG antibodies to amoebic antigen. The ELISA system was used to detect amoebic antibody in control subjects (56), patients with amoebic liver abscess (79) and Entamoeba histolytica cyst-passers (10) and the results compared with those of indirect haemagglutination assay (IHA). The ELISA was more sensitive and detected 74.7% of cases with amoebic antibody in amoebic liver abscess compared with 66.7% detected by IHA. The test was more specific, sensitive and easy to perform and is recommended as a test of choice for the serological diagnosis of amoebic liver abscess.


Journal of Clinical Gastroenterology | 1989

Fibronectin in acute and subacute hepatic failure

Anand Ac; M. Irshad; Subrat K. Acharya; Gandhi Bm; Y. K. Joshi; Tandon Bn

The mean plasma fibronectin (FN) concentrations in 30 patients with fulminant hepatic failure (FHF) and in 10 patients with subacute hepatic failure (SAHF) were 111.2 ± 70 and 123.5 ± 46.5 μg/ml, respectively, significantly lower than that of normal controls (362.0 ± 69.2 μg/ml) and patients with uncomplicated viral hepatitis (320 ± 58.5 μg/ml) (p < 0.001). Plasma FN levels showed significant negative correlation with serum glutamic pyruvate transaminase values in the FHF group (p < 0.02) and with prothrombin time in the SAHF group (p < 0.02). Serial estimation of plasma FN showed that failure of FN levels to rise despite fresh plasma infusions indicates poor prognosis in these patients. The reduced availability of FN may be responsible for the impaired Kupffer cell function and consequent increased susceptibility to endotoxemia and the bacterial infections seen in these patients.


The Lancet | 1987

Prevalence of amoebic antibody in population affected by epidemic non-A, non-B hepatitis

Tandon Bn; Gandhi Bm; M. Irshad; Subrat K. Acharya; Y. K. Joshi

blood OH-CQ was 114 ng/ml. She was given 1-2 g CQ base and seven doses of quinine sulphate 650 mg over 3 days, followed by three tablets of pyrimethamine 25 mg/sulphadoxine 500 mg, and was cured clinically and parasitologically by March 28. On April 15, during the 39th week of pregnancy, she was delivered of a healthy 2950 g girl. Mother and child have remained well and aparasitaemic. In a Rieckmann microtesf with parasites and red blood cells collected on March 26, mature schizonts were present in the well containing 5’7 pmol CQ but not in the well containing 8-0 pmol; thus the infection was classified as resistant to CQ. In the 48-hour test,8 however, done with the original parasite isolate and with parasites adapted to continuous culture, a sensitive response pattern


Gastroenterologia Japonica | 1990

Hepatitis B virus replication in patients with chronic liver diseases

Gandhi Bm; M. Irshad; Subrat K. Acharya; Y. K. Joshi; Tandon Bn

SummaryOne hundred and seventy five subjects with chronic liver diseases which included patients with chronic active hepatitis (90), liver cirrhosis (31) and asymptomatic hepatitis B carriers (54), were included in the study. Hepatitis B virus (HBV) specific DNA-polymerase activity and HBe-markers were tested as markers of HBV-multiplicaiton. In HBsAg positive samples, DNA-P activity was positive in 44.4% of the HBV carriers, 52.9% of the patients with chronic active hepatitis and 81.8% of the patients with liver cirrhosis. The corresponding figures for the presence of HBeAg in these groups were 18.5, 26.5 and 45.5% respectively. Virus multiplication was also observed in 41.1 and 44.4% patients with chronic active hepatitis and liver cirrhosis respectively, in the absence of HBsAg. The results of the present study show that hepatitis B virus is the most important etiological factor of chronic liver diseases in India. Most of our patients of chronic liver diseases seems to have contacted HBV infection as young adults and the mode of transmission is likely to be horizontal rather than vertical. The virus replicating markers correlate well with the severity of the liver injury and decreased with the age. DNA-P activity is a more sensitive marker of viral multiplication than HBeAg. Viral multiplication was also found to occur in the absence of the usual HBV markers. Continued viral multiplication in patients with chronic active hepatitis and liver cirrhosis is implicated in continued liver injury and progressive liver disease.


Gastroenterologia Japonica | 1990

Significance of anti-pre-S antibodies in patients with fulminant hepatic failure

M. Irshad; Gandhi Bm; Subrat K. Acharya; Y. K. Joshi; Tandon Bn

SummaryAnti-pre-S antibody was tested in 38 sera from patients with fulminant hepatitis (positive for HBsAg and/or IgM anti-HBc) using a specific solid phase enzyme linked immunosorbent assay (ELISA). Anti-pre-S activity was detected in 50 percent sera samples positive for HBsAg but negative for IgM antiHBc. There were 12.5% sera positive for both HBsAg as well as IgM anti-HBc and 75% sera negative for HBsAg but positive for IgM anti-HBc. The prevalence of HBV-specific DNA-polymerase activity was high in all the three groups whereas anti-HBs positivity was low. Anti-pre-S activity was observed both in the presence as well as in the absence of DNA-polymerase activity. High-anti-pre-S level in fulminant hepatitis B patients was assumed to be implicated in the fast clearance of HBsAg from circulation.


The Lancet | 1988

OUTBREAK OF DENGUE FEVER IN DELHI

Subrat K. Acharya; P. Buch; M. Irshad; Gandhi Bm; Y. K. Joshi; Tandon Bn


Indian Journal of Medical Research | 1986

Post transfusion hepatitis--a prospective study.

Patwari Si; M. Irshad; Gandhi Bm; Y. K. Joshi; Nundy S; Tandon Bn


Indian Journal of Medical Research | 1986

Increasing HBV reservoir by post-transfusion HBV infection in India.

Patwari Si; M. Irshad; Gandhi Bm; Y. K. Joshi; Nundy S; Tandon Bn


Indian Journal of Medical Research | 1985

Hepatitis A epidemic in Kerala state (India) in 1980.

Y. K. Joshi; Tandon Bn; Gandhi Bm


The Lancet | 1984

SUBCLINICAL HEPATITIS A IN NORTH INDIAN CHILDREN

Tandon Bn; Gandhi Bm; Y. K. Joshi; Hema Gupta; M. Irshad

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Tandon Bn

All India Institute of Medical Sciences

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M. Irshad

All India Institute of Medical Sciences

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Y. K. Joshi

All India Institute of Medical Sciences

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Subrat K. Acharya

All India Institute of Medical Sciences

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Hema Gupta

All India Institute of Medical Sciences

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Anand Ac

All India Institute of Medical Sciences

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Malaviya An

All India Institute of Medical Sciences

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P. Buch

All India Institute of Medical Sciences

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T.C. Chawla

All India Institute of Medical Sciences

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