Biomedical subjects
R V Bhat
Publications and source records attributed to R V Bhat.
Exposure assessment to synthetic food colours of a selected population in Hyderabad, India.
An exposure assessment of synthetic food colours was carried out among 1-5- and 6-18-year-old individuals by the food frequency method. Children had an intake of solid food consumption in the range 2-465 g day(-1) and liquid food consumption in the range 25-840 ml day(-1) with added colours. Among the eight permitted colours in India, six were consumed by the subjects of the study. The intakes of some subjects exceeded the acceptable daily intake for colours such as tartrazine, sunset yellow and erythrosine, which is 7.5, 2.5 and 0.1 mg kg(-1) body weight, respectively. Therefore, a uniform permissible limit of 100 mg kg(-1) prescribed under the Prevention of Food Adulteration Act in India for all foods is not justified. The limits need to be revised according to the Codex Alimentarius Commission, which permits different maximum levels of additives to various food categories based on both the extent of consumption and the technological justification for its use.
An atypical case of periodic paralysis.
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Chemical poisoning in three Telengana districts of Andhra Pradesh.
Medical records of (i) toxico-medico-legal death cases from three districts of Telengana region in the state of Andhra Pradesh, viz. Hyderabad, Ranga Reddy and Medak, and (ii) clinical toxicology cases in suspected poisoning from hospitals in and around Hyderabad city were examined for a period of 5 calendar years. The age group at risk in both the types of cases is 15-24. The cause of suicides includes physical illness, family/spouse problems and financial problems. Labourers form a dominant risk group in rural and semi-urban industrial area, whereas in urban area the employees were the dominant risk group. The agricultural pesticides and household insecticides were the predominant poisons used for suicide purposes.
Differential sensitivity to lithium's reversal of amphetamine-induced open-field activity in two inbred strains of mice.
To determine whether genetic differences could contribute to the pharmacological sensitivity of lithium chloride (LiCl) to reverse amphetamine-associated changes in behavior C57BL/6nCrlBR and C3H/HenCrlBR male mice were tested for the ability of an acute dose of LiCl to reverse the locomotor enhancing effects of an acute dose of amphetamine. A series of experiments were conducted that compared dose response of LiCl, chamber lighting conditions, and chamber shape on amphetamine-induced activity in two strains of mice with different genetic backgrounds. Acute amphetamine (3 mg/kg) increased locomotor activity in C57BL/6nCrlBR mice and LiCl (1-4 mEq/kg) blocked this effect. LiCl-induced changes in baseline activity seen at high doses of LiCl were not seen for the low doses. The dark condition reduced time resting but chamber shape did not appear to alter results. In C3H/HenCrlBR mice, amphetamine did not significantly increase levels of activity but did decrease rearing behavior which suggests that genetic difference between C57BL/6nCrlBR and C3H/HenCrlBR mice may contribute to sensitivity to amphetamine. In sum, the ability of LiCl to reverse amphetamine-induced changes in locomotor activity in C57BL/6nCrlBR mice may provide a useful model to study genetic and pharmacological aspects of psychiatric illnesses such as bipolar disorder.
Quantification and validation of enzyme immunoassay for urinary aflatoxin B1-N7-guanine adduct for biological monitoring of aflatoxins.
The aflatoxin B1-N7-guanine (AFB1-N7-guanine) adduct has been established as one of the relevant biomarkers of dietary aflatoxin (AFB1) exposure. Measurement of this adduct is potentially a useful dosimeter in molecular epidemiological studies. This paper reports the application and evaluation of a sensitive indirect competitive enzyme-linked immunosorbent assay (ELISA) for the detection and quantification of urinary AFB1-N7-guanine adduct in high risk populations exposed to dietary aflatoxin. Earlier, we had reported a simple and rapid indirect ELISA method for AFB1-N7-guanine adduct in the urine and liver tissues using polyclonal antibodies specific to AFB1-N7-guanine adduct. The method was evaluated using a rodent model (Fischer 344), exposed to 1 mg kg-1 body mass of AFB1 and human urine samples obtained from a maize eating population, environmentally exposed to AFB1 through their diet. The levels of AFB1-N7-guanine adduct in rat and human urine ranged from 6.42 to 20.16 micrograms mg-1 creatinine and from 9.30 to 13.43 ng mg-1 creatinine, respectively. The level of AFB1 in the diet as estimated by ELISA ranged from 1000 to 3600 ng d-1. The interesting observation in these studies is that the females (in both rodents and human subjects) are more efficient than males at excreting the adduct. Total adduct (DNA bound adduct and guanine adduct excreted in urine) was found to be similar in male and female rats. However, 63% of the total adduct was accounted for in urine of female rats, whereas male rats excreted 47% of the total adduct in their urine. The present method may find wide application as a biochemical tool in molecular epidemiological studies with respect to human exposure to dietary aflatoxins.
Autosomal recessive polycystic kidney disease with congenital hepatic fibrosis and encephalocele.
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Regulation and localization of tyrosine216 phosphorylation of glycogen synthase kinase-3beta in cellular and animal models of neuronal degeneration.
Inactivation of glycogen synthase kinase-3beta (GSK3beta) by S(9) phosphorylation is implicated in mechanisms of neuronal survival. Phosphorylation of a distinct site, Y(216), on GSK3beta is necessary for its activity; however, whether this site can be regulated in cells is unknown. Therefore we examined the regulation of Y(216) phosphorylation on GSK3beta in models of neurodegeneration. Nerve growth factor withdrawal from differentiated PC12 cells and staurosporine treatment of SH-SY5Y cells led to increased phosphorylation at Y(216), GSK3beta activity, and cell death. Lithium and insulin, agents that lead to inhibition of GSK3beta and adenoviral-mediated transduction of dominant negative GSK3beta constructs, prevented cell death by the proapoptotic stimuli. Inhibitors induced S(9) phosphorylation and inactivation of GSK3beta but did not affect Y(216) phosphorylation, suggesting that S(9) phosphorylation is sufficient to override GSK3beta activation by Y(216) phosphorylation. Under the conditions examined, increased Y(216) phosphorylation on GSK3beta was not an autophosphorylation response. In resting cells, Y(216) phosphorylation was restricted to GSK3beta present at focal adhesion sites. However, after staurosporine, a dramatic alteration in the immunolocalization pattern was observed, and Y(216)-phosphorylated GSK3beta selectively increased within the nucleus. In rats, Y(216) phosphorylation was increased in degenerating cortical neurons induced by ischemia. Taken together, these results suggest that Y(216) phosphorylation of GSK3beta represents an important mechanism by which cellular insults can lead to neuronal death.
Thyrotoxicosis of a rare aetiology.
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Thyrotoxicosis of a rare aetiology.
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Profile of street foods sold in Asian countries.
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Street foods in Latin America.
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Immunolocalization of caspase proteolysis in situ: evidence for widespread caspase-mediated apoptosis of neurons and glia in the postnatal rat brain.
Activation of a member of the caspase family of cysteine proteases is thought to be required for the execution of apoptosis in neurons and other cell types. We describe here an antibody (Ab127) reactive with a neoantigenic site on caspase substrate proteins degraded during apoptosis, and its characterization as a biochemical and histochemical probe for apoptosis-associated proteolysis in growth factor-deprived neural cells in vitro and the developing postnatal rat brain. Neuronally differentiated PC12 cells became strongly Ab127 immunoreactive only during apoptosis following nerve growth factor withdrawal. Apoptosis-associated caspase proteolysis was detectable on western blots as markedly increased immunoreactivity of a approximately 46,000 mol. wt polypeptide, a product also generated by caspase-3 treatment of cell-free extracts. In the postnatal rat brain, intense immunoreactivity indicative of caspase activation was exhibited by small proportions of neurons and glia in distinct regional and temporal patterns. The degenerating nature of these cells was confirmed by their argyrophilia, cytoplasmic immunoreactivity for c-jun and fragmented processes. Combined immunofluorescence and Hoechst 33342 staining demonstrated that cells immunopositive for caspase activation have apoptotic nuclear morphologies. Caspase proteolysis was observed throughout the neuraxis in a minority of progenitor cells in germinal zones, postmitotic neurons in the parenchyma, and glia in the corpus callosum and other white matter tracts, but was observed rarely in the adult brain. These data characterize a new approach for evaluating apoptosis in physiological and pathological neurodegeneration, and demonstrate that caspase-associated apoptosis is a widespread mechanism for the programmed death of neurons and glia in the postnatal rat brain.
Immunolocalization of the mitogen-activated protein kinases p42MAPK and JNK1, and their regulatory kinases MEK1 and MEK4, in adult rat central nervous system.
Cell survival, death, and stress signals are transduced from the cell surface to the cytoplasm and nucleus via a cascade of phosphorylation events involving the mitogen-activated protein kinase (MAPK) family. We compared the distribution of p42 mitogen-activated protein kinase (p42MAPK) and its activator MAPK or ERK kinase (MEK1; involved in transduction of growth and differentiation signals), with c-Jun N-terminal kinase (JNK1) and its activator MEK4 (involved in transduction of stress and death signals) in the adult rat central nervous system. All four kinases were present in the cytoplasm, dendrites, and axons of neurons. The presence of p42MAPK and JNK1 in dendrites and axons, as well as in cell bodies, suggests a role for these kinases in phosphorylation and regulation of cytoplasmic targets. A high degree of correspondence was found between the regional distribution of MEK1 and p42MAPK. Immunostaining for MEK1 and p42MAPK was intense in olfactory structures, neocortex, hippocampus, striatum, midline, and interlaminar thalamic nuclei, hypothalamus, brainstem, Purkinje cells, and spinal cord. In addition to neurons, p42MAPK was also present in oligodendrocytes. Whereas MEK4 was ubiquitously distributed, JNK1 was more selective. Immunostaining for MEK4 and JNK1 was intense in the olfactory bulb, lower cortical layers, the cholinergic basal forebrain, most nuclei of the thalamus, medial habenula, and cranial motor nuclei. The distribution of MEK1 and p42MAPK proteins only partially overlapped with that of MEK4 and JNK1. This suggests that the growth/differentiation and death/stress pathways affected by these kinases may not necessarily act to counterbalance each other in response to extracellular stimuli. The differential distribution of these kinases may control the specificity of neuronal function to extracellular signals.
Differential patterns of regional c-Fos induction in the rat brain by amphetamine and the novel wakefulness-promoting agent modafinil.
We examined the neuronal targets in the rat brain for the novel wakefulness-promoting agent modafinil and for amphetamine using c-Fos immunohistochemistry. Both modafinil and amphetamine induced neuronal expression of c-Fos-like immunoreactivity in the paraventricular nucleus of the hypothalamus, anterior hypothalamus and central nucleus of the amygdala. Modafinil also increased c-Fos-like immunoreactivity in the suprachiasmatic nucleus, while amphetamine had no effect. Brain regions in which amphetamine increased c-Fos-like immunoreactivity, but modafinil had no effect, included frontal cortex, striatum, lateral habenula, supraoptic nucleus and basolateral nucleus of the amygdala. These findings suggest that the mechanism of action of modafinil is different from that of amphetamine and that the neuronal targets for modafinil in the brain include nuclei of the hypothalamus and amygdala.
Sensitive method for the detection of fumonisin B1 in human urine.
Fumonisins are a group of carcinogenic mycotoxins that occur worldwide. This paper reports a sensitive method for the detection and quantitation of fumonisin B1 in human urine. Amberlite XAD-2 non-ionic polymeric adsorbent resin is used prior to strong anion-exchange (SAX) cartridge clean-up. As much as 100 ml of undiluted human urine can be loaded onto the column. Recoveries obtained using this method were 93.6, 95.1 and 94.4% when samples were spiked with 10, 50 and 500 ng/ml of fumonisin B1, respectively. This method is highly reproducible (R.S.D.<5%) and gives good sample clean-up, which is suitable for HPLC analysis.