Validation of Two Portable Instruments to Measure Iron Concentration in Groundwater in Rural Bangladesh.

Iron is ubiquitous in natural water sources used around the world for drinking and cooking. The health impact of chronic exposure to iron through water, which in groundwater sources can reach well above the World Health Organization’s defined aesthetic limit of 0.3 mg/L, is not currently understood. To quantify the impact of consumption of iron in groundwater on nutritional status, it is important to accurately assess naturally-occurring exposure levels among populations. In this study, the validity of iron quantification in water was evaluated using two portable instruments: the HACH DR/890 portable colorimeter (colorimeter) and HACH Iron test-kit, Model IR-18B (test-kit), by comparing field-based iron estimates for 25 tubewells located in northwestern Bangladesh with gold standard atomic absorption spectrophotometry analysis. Results of the study suggest that the HACH test-kit delivers more accurate point-of-use results across a wide range of iron concentrations under challenging field conditions.

Study on the 3HAcetylcholine Release Induced by Oxygen-Glucose Deprivation in Rat Cerebral Cortical Slices

BACKGROUND: It has been shown that cerebral ischemia alters brain acetylcholine (Ach) metabolism. In an attempt to elucidate the mechanisms for ischemia-induced release of Ach in vitro, the effects of drugs which can influence the cholinergic neurotransmission on the ischemia-induced release of [3H]Ach from cerebral cortical slices of the rat were examined. METHODS: The cortices of decapitated rats were chopped and dispersed in artificial CSF. Then, the tissue suspensions were incubated with [3H]choline. The tissues were transferred and incubated in washing, hypoglycemic (deprivation of glucose), ischemic (deprivation of oxygen and glucose) and extracting plates sequently. Ischemia-induced release of [3H]Ach was expressed as percentage of the total [3H]Ach present in the slices. RESULTS: Ischemia induced significant release (about 9.3% of total tissue content) of [3H]Ach from cerebral cortical slices in vitro. This [3H]Ach release was significantly attenuated by tetrodotoxin, a voltage-sensitive Na+-channel blocker, and Mg2+, a physiological N-methyl-D-aspartate (NMDA) receptor blocker. Vesamicol (1 M), a blocker of vesicular transport of Ach, MK-801 and ketamine, NMDA receptor antagonists, 6,7-nitroquinoxaline-2,3-dione (DNQX) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), kainate/AMPA receptor antagonists, and 6-nitro-7-sulphamoylbenzo[f]quinoxaline-2,3-dione (NBQX), a AMPA receptor blocker attenuated the [3H]Ach. Nitrendipine, nimodipine, inhibitor of L-type Ca2+ channels, and -conotoxin GVIA, an inhibitor of N-type Ca2+ channels, significantly attenuated the ischemia-induced release of [3H]Ach. Omission of Ca2+ from incubation media attenuated the ischemia-induced [3H]Ach release. Inhibitors of intracellular Ca2+ release, dantrolene and TMB-8, and a cell-permeable calcium chelator, 1,2-bis (2-aminophenoxy)-ethane-N, N, N+, N+-tetraacetic acid tetrakis (acetoxymethyl) ester (BAPTA-AM), inhibited the ischemia-evoked [3H]Ach release. CONCLUSION: These results suggest that the ischemia can induce Ach rele.