Symptomatic profile of intestinal parasitic infections in the hostels of a medical college.
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Biomedical subjects
Publications and source records attributed to S K Ray.
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Oral administration of carbaryl to adult male albino rats produced a dose dependent increase in the steady state level of 5-hydroxytryptamine (5-HT) at 1.00 h in pons-medulla (PM). 5-Hydroxyindole acetic acid (5-HIAA) concentration was significantly elevated only in response to a higher dose of this pesticide under similar conditions. A time course study with carbaryl and pentylenetetrazol (PTZ) showed a characteristic elevation of the steady state level of 5-HT in PM, but the 5-HIAA level was significantly elevated at 0.5 h only after carbaryl treatment. No significant change of the 5-HIAA level was evident after administration of PTZ alone or in combination with carbaryl. Tryptophan concentration was significantly elevated in PM at 0.5 h after carbaryl treatment and at 1.0 h after carbaryl + PTZ treatment. No significant change of tryptophan concentration was evident after the administration of PTZ alone under similar conditions. Measurement of (1) pargyline induced (a) accumulation of 5-HT and (b) depletion of 5-HIAA levels, and (2) probenecid-induced accumulation of 5-HIAA level in presence and absence of carbaryl and revealed that carbaryl accelerated the synthesis as well as the breakdown of 5-HT, whereas PTZ alone or in combination with carbaryl accelerated the synthesis of 5-HT without affecting its catabolism. The potency of this pesticide in elevating the pargyline-induced accumulation of 5-HT is in the order of carbaryl + PTZ greater than PTZ congruent to carbaryl. These results suggest that the carbaryl-induced increase in the synthesis of 5-HT is potentiated, and the turnover is reduced, in PM when PTZ is administered to the carbaryl-intoxicated rats.
Acute administration of the anticholinesterase agent carbaryl to rats produced a dose-dependent increase of tremors. The carbaryl-induced tremor was significantly reduced by prior treatment of the rats with either atropine or L-DOPA and was exacerbated by haloperidol. These results suggest the possible involvement of a central cholinergic-dopaminergic interaction in the carbaryl-induced tremor.
Administration of pentylenetetrazol (PTZ) (60 mg/kg, s.c.) to normal or carbaryl (200 mg/kg, p.o.) treated adult male albino rats produced characteristic changes in the steady-state levels of striatal dopamine (DA), noradrenaline (NA) and homovanillic acid (HVA) at different time intervals (0.5, 1.0 and 2.0 hr). The elevation of striatal NA level was found to be more pronounced with PTZ than that produced by carbaryl. Treatment of rats with PTZ alone caused a significant elevation of DA levels only at 2.0 hr without any significant change in the level of HVA at any time interval. Carbaryl which did not have any significant effect on striatal DA level produced an elevation of HVA at 0.5 hr and 1.0 hr in striatum. The simultaneous administration of PTZ and carbaryl, under similar conditions, caused a marked reduction in the level of NA at 0.5 hr and DA at 1.0 hr without any significant effect on (i) both the amine levels at 2.0 hr and (ii) HVA level at any of the time intervals. Measurement of (a) alpha-methyl-p-tyrosine (alpha-MpT) (250 mg/kg, i.p.) induced depletion of striatal DA and NA, (b) FLA-63 (25 mg/kg, i.p.) induced disappearance of NA, (c) pargyline (75 mg/kg, i.p.) induced reduction and probenecid (200 mg/kg, i.p.) induced accumulation of striatal HVA in the presence or absence of PTZ and/or carbaryl revealed that: (1) PTZ or carbaryl alone caused a significant increase in the turnover of striatal DA; (2) the turnover of striatal NA was significantly increased after PTZ treatment but not after carbaryl administration; (3) the simultaneous administration of carbaryl and PTZ, on the other hand, attenuated (a) PTZ- or carbaryl-induced increase in metabolic activity of the striatal dopaminergic system, and (b) the enhanced anabolic activity of striatal noradrenergic system caused by PTZ, but failed to affect the enhanced utilization of striatal NA induced by PTZ alone.
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Carbaryl (200 mg/kg or 400 mg/kg, p.o.) significantly elevated serotonin (5-HT) (57-109%) and 5-hydroxyindoleacetic acid (5-HIAA) (60-78%) levels at 1.0 h in the hypothalamic region of adult male rat brain. Further, administration of carbaryl (200 mg/kg, p.o.) for different time intervals (0.5 h, 1.0 h, and 2.0 h) revealed that both 5-HT and 5-HIAA levels elevated maximally at 0.5 h in hypothalamus. These regional 5-HT and 5-HIAA levels were not significantly affected with pentylenetetrazol (PTZ) at any time after its treatment. But simultaneous administration of carbaryl (200 mg/kg, p.o.) and PTZ (60 mg/kg, s.c.) reduced the carbaryl-induced elevation of both 5-HT and 5-HIAA levels. Measurement of (i) probenecid-induced (200 mg/kg, i.p.) accumulation and (ii) pargyline-induced (75 mg/kg, i.p.) depletion of hypothalamic 5-HIAA level in the absence or presence of carbaryl (200 mg/kg, p.o.) and/or PTZ (60 mg/kg, s.c.) revealed that (a) carbaryl enhanced the synthesis as well as the breakdown of 5-HT, (b) PTZ had no effect on either of these processes of 5-HT, and (c) carbaryl-induced increased catabolism of 5-HT became normal in the presence of PTZ.
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Administration of a single dose (200 mg/kg, p.o.) of carbaryl to rats produced a significant rise in adrenal and plasma corticosterone levels and an increase of tyrosine alpha-ketoglutarate transaminase activity in the liver cytosol. Synaptosomal acetylcholinesterase activity of the hypothalamic and the striatal regions of rat brain was decreased by carbaryl treatment under similar conditions. Pretreatment (0.5 h) with atropine sulphate (10 mg/kg, i.p.) failed to counteract the carbaryl-induced elevation of adrenal and plasma corticosterone levels and hence the liver tyrosine alpha-ketoglutarate transaminase activity. Present results suggest that the carbaryl-induced rise in the corticosterone level in the adrenal gland and plasma is not due to a cholinergic mechanism.
A model, using stochastic processes, is developed to estimate some epidemiological parameters of malaria in a homogeneous population from longitudinal data. Assessments of transition probabilities from one state of health to the other are made taking "lost to follow-up" as a competing risk. The model is based on the assumptions that individuals are transferred at constant rate between states, and only one transition is possible between two consecutive surveys. It shows a good fit to the observed data; the model is simple to understand and can easily be used if computer facilities are not available.
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The plot of minimum inhibitory concentration (MIC) vs. 2Xv of twelve phenolic compounds delineates the congeners into three distinct classes: the most potent ortho compounds describe a parabola, para substituted compounds of intermediate potency lie in a line, while the least potent meta derivatives yield a scatter diagram. The same pattern is found for two skin pathogens, Trichophyton rubrum and Epidermophyton floccosum. From non-linear regression analysis 2Xv is found to be excellently correlated with observed MIC values of the most potent ortho compounds against both the test organisms. For both the organisms logP is found to be inferior to 2Xv in the correlation of MIC values. On the basis of regression equations the MIC values of certain ortho substituted phenols are calculated a priori, some of which are corroborated by findings reported in the literature.
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