Biomedical subjects

Diptendu Chatterjee

Publications and source records attributed to Diptendu Chatterjee.

6 recordsLinked to original sources

PubMed2006

Age and sex variation of body mass index and waist circumference among the Santal children of Jharkhand, India.

Central body fat (CBF) as measured by waist circumference (WC) etc. has now been considered as risk factor for chronic disease, disability, and death. It has been assumed that one's characteristic level of body fat, as measured by body mass index (BMI), and CBF unfolds during the normal course of growth and development. However, studies of the development of CBF show relatively weak consistency in comparison to body fat. But to the best of our knowledge, no study in this aspect has been undertaken on any Indian population to study the effect of age and sex on body fat and CBF during development. In view of the above consideration, the present work has been undertaken among 179 Santal (a tribal population) children (Boys = 107, Girls = 72) of the Galudih area in East Singbhum, Jharkhand, India. Anthropometric measurements of height, weight, and circumference of waist were taken from each subject using standard procedure. The mean ages of boys and girls were 10.94 years and 9.48 years, respectively. The mean BMI for boys and girls were 14.48 kg/m2 and 13.78 kg/m2 Percent of variance explained by age was much greater for BMI (> 50%) as compared to WC (7-10%) in both sexes. Two way ANOVA showed that BMI had a significant (p < 0.05) effect of age and not of sex, whereas age-sex interaction had a significant impact on WC. The results of the present cross-sectional study indicated that during growth and development unfolding of CBF and BMI is independent of one another. Different set(s) of gene(s), onset of growth hormones during the normal development or their interaction could have been considered for this differentiation.

Age Distribution↗

PubMed2005

Decrease in brain POMC mRNA expression and onset of obesity in guinea pigs exposed to 2-chloroethyl ethyl sulfide, a mustard analogue.

The full spectrum of physiological effects resulting from exposure to sulfur mustard and its analogs is currently unknown. In a guinea pig model, initially selected to study the role of an inflammatory cytokine cascade in mustard gas induced lung injury, we observed significant body weight gain in guinea pigs exposed to an intratracheally injected single dose of 2-chloroethyl ethyl sulfide, a mustard analog. The body weight gain was not associated with any apparent change in appetite. To further elucidate a molecular basis for the observed weight gain, we evaluated candidate genes for the obese phenotype by quantitative RT-PCR. We observed a time- and dose-dependent decrease in guinea pig pro-opiomelanocortin (POMC) message following treatment with mustard gas. This reduction in POMC message is consistent with the onset of obesity in the animals. We hypothesize that the POMC melanocortin pathway provides a mechanistic basis for the observed effects of sulfur mustard on body weight.

Animals↗

PubMed2005

Developmental changes in the neuronal protein composition: a study by high resolution 2D-gel electrophoresis.

Cerebellar granular neurons were grown in culture up to 21 days and the protein compositions of undifferentiated (day 1), partially differentiated (day 7) and fully differentiated (day 21) neurons were analyzed by high-resolution 2D-gel electrophoresis. During neuronal differentiation there were not only increase in the amount of several known proteins, viz. actin, tubulin (both alpha and beta subunits), myosin (heavy and light chains), but very interesting changes were also observed in the expressions of different subunits and isoforms of those proteins. Furthermore, both in the acidic (pI 4.0-4.5) and alkaline (pI 7.0-8.5) regions interesting up and down regulations of several unidentified proteins were observed during the neuronal differentiation. These results indicated that there were several unidentified proteins that might be very valuable targets for studying regulation of neuronal differentiation. Research is going on for further characterization of those proteins using recently developed proteomics technology.

Animals↗

PubMed2004

Evidence of hair loss after subacute exposure to 2-chloroethyl ethyl sulfide, a mustard analog, and beneficial effects of N-acetyl cysteine.

Mustard gas has been used as a vesicant chemical warfare agent. However, a suitable biomarker for monitoring mustard gas exposure is not known. We observed that the hairs of the guinea pigs exposed intratracheally to subacute doses of 2-chloroethyl ethyl sulfide (CEES), a mustard analog, came out very easily though there was no sign of skin lesions or skin damage. Also the hairs looked rough and dry and lost the shiny glaze. There was no recovery from this hair loss, though the animals never became hairless, following CEES exposure. Hairs were observed in this study both visually and with light microscopy. Treatment with N-acetylcysteine (NAC) prior to CEES exposure could prevent the hair loss completely. Hence, sudden hair loss might be a good biomarker for subacute exposure of mustard gas to subjects at risks when the victims might have no other visible symptom of toxicity.

Acetylcysteine↗

PubMed2003

Signal transduction events in lung injury induced by 2-chloroethyl ethyl sulfide, a mustard analog.

Sulfur mustard has been used as a vesicant chemical warfare agent. To understand the mechanism by which mustard gas exposure causes respiratory damage, we have used 2-chloroethyl ethyl sulfide (CEES) as a mustard analog. Our initial studies have shown that guinea pigs exposed to CEES intratracheally accumulate high levels of TNF-alpha. Accumulation of TNF-alpha leads to activation of both acid and neutral sphingomyelinases, resulting in high accumulation of ceramides, a second messenger involved in cell apoptosis. In addition, NF-kappa B was activated for a short period (1-2 h after exposure) as determined by mobility shift assay. Supershift assays indicated that both p50 and p65 of NF-kappa B were activated due to CEES exposure. However, NF-kappa B rapidly disappeared after 2 h. It is possible that the initial activation of NF-kappa B was an adaptive response to protect the cells from damage since NF-kappa B is known to inhibit TNF-alpha/ceramide-induced cell apoptosis. Since NF-kappa B disappeared after 2 h, the cells continued being damaged owing to accumulation of ceramides and activation of several caspases, leading to apoptosis.

Administration, Inhalation↗

PubMed2003

Prophylactic protection by N-acetylcysteine against the pulmonary injury induced by 2-chloroethyl ethyl sulfide, a mustard analogue.

Mustard gas exposure causes adult respiratory distress syndrome associated with lung injury. The purpose of this study was to investigate whether an antioxidant, such as N-acetylcysteine (NAC), has any protective effect. Guinea pigs were given single exposure (0.5-6 mg/kg body weight) of 2-chloroethyl ethyl sulfide (CEES) as a mustard analogue intratracheally and maintained for various lengths of time (1 h to 21 days). Within 1 h of CEES infusion at 4 mg/kg, high levels of tumor necrosis factor alpha (TNF-alpha), ceramides, and nuclear factor kappaB accumulated in lung and alveolar macrophages. Both acid and neutral sphingomyelinases were activated within 4 h. These signal transduction events were associated with alteration in the oxygen defense system. Within 1 h of exposure to CEES (6 mg/kg body weight), there was 10-fold increase in the (125)I-BSA leakage into lung tissue, indicating severe lung injury. Although low level of CEES exposure (0.5 mg/kg body weight) produced symptoms of chemical burn in lung as early as 1 h after exposure, the severity of edema, congestion, hemorrhage, and inflammation increased progressively with time (1 h to 21 days). Feeding of single dose of NAC (0.5 g) by gavage just before the CEES infusion was ineffective to counteract these effects. However, consumption of the antioxidant in drinking water for 3 or 30 days prior to CEES exposure significantly inhibited the induction of TNF-alpha, activation of neutral and acid sphingomyelinases, production of ceramides, activation of caspases, leakage of (125)I-bovine serum albumin ((125)I-BSA) into lung tissue, and histological alterations in lung. Pretreatment with NAC for 3 and 30 days protected against 69-76% of the acute lung injury. Therefore, NAC may be an antidote for CEES-induced lung injury.

Acetylcysteine↗