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The kinetics of the exchange between56Mn-labelled manganese dioxide and cations in aqueous solution was studied by measuring the β activity acquired by the solution. The results of the exchange between a chemical γ MnO2 and a divalent M2+ ion (M=Mn, Co, Cu or Zn) or a trivalent M3+ ion (M=Ga, Fe, In, Rh or Al) indicate a fast initial process followed by a diffusion—controlled exchange. It is assumed that M2+ ions exchange with Mn2+ ions and M3+ ions exchange with Mn3+ ions in MnO2. The process depends on the radii of the host and substituent ions and on consideration of crystal field stabilisation energies. It seems that the γ MnO2 studied contains more Mn3+ than Mn2+ ions. The possibility of the exchange between Mn ions and cations of a different charge cannot be ruled out. The exchange between Co2+ ions and MnO2 was enhanced in presence of pyrophosphate, which stabilises Mn(III) as a complex. The fraction of Mn in different samples of MnO2 exchanged with a given cation depends on the type and not on the surface area of the sample.

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DSC curves of polyster/cotton blends indicate that the glass transition temperature,T g, of cotton varies with the blend composition. Standard curves for quality control purposes are presented and are based on either the cotton or PET transition peak areas. Factors that contribute to the size of the peak areas were determined: a composition coefficient factor and a thermal coefficient factor.

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Acta Biologica Hungarica
Authors: C. Pekcetin, Muge Kiray, B. Ergur, K. Tugyan, H. Bagriyanik, G. Erbil, Basak Baykara, and U. Camsari

Cerebral ischemia leads to cognitive decline and neuronal damage in the hippocampus. Reactive oxygen species (ROS) play an important role in the neuronal loss after cerebral ischemia and reperfusion injury. Carnosine has both antioxidant and neuroprotective effects against ROS. In the present study, the effects of carnosine on oxidative stress, apoptotic neuronal cell death and spatial memory following transient cerebral ischemia in rats were investigated. Transient ischemia was induced by occlusion of right common carotid artery of rats for 30 min and reperfusion for 24 h or 1 week. Rats received intraperitoneal injection of 250 mg/kg carnosine or saline 30 min prior to experiment. Determination of antioxidant enzyme activities was performed spectrophotometrically. To detect apoptotic cells, TUNEL staining was performed using an In Situ Cell Death Detection Kit. Carnosine treatment elicited a significant decrease in lipid peroxidation and increase in antioxidant enzyme activities in ischemic rat brains. The number of TUNEL-positive cells was decreased significantly in carnosine-treated group when compared with the ischemia-induction group. Carnosine treatment did not provide significant protection from ischemia induced deficits in spatial learning. The results show that carnosine is effective as a prophylactic treatment for brain tissue when it is administered before ischemia without affecting spatial memory.

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