The effect of Sn on the physical and optical properties of (Se0.6As0.1Ge0.3)100-xSnx glasses.

Chalcogenide glasses are significant materials for semiconducting and infrared imaging because of their infrared (IR) transparency. In the present study, Se-Ge-As based chalcogenide glasses with chemical composition of (Se0.6As0.1Ge0.3)100-x Snx doped with different amounts of Sn were prepared by conventional melting-quenching method. Physical properties of glasses were investigated by studying density and molar volume. Based on differential scanning calorimetry (DSC) results and density measurements, the binary role of Sn was proved. Fourier transform infrared spectroscopy (FT-IR) study of the samples approved presence of impurities. Using the UV-Vis spectra, optical properties including Fermi energy level, direct and indirect optical band gap and Urbach energy were determined. The results showed a decrease in density of glasses with the increase of Sn from 2 to 6 mol%. Increasing Sn in the glassy microstructure of samples provides a semiconducting character to Se based chalcogenide glass by reducing the direct and indirect optical band gaps of glass samples from 1.29 to 1.15 (eV) and 1.16 to 1.01 (eV), respectively.

Construction of a new selective coated disk electrode for Ag (I) based on modified polypyrrole-carbon nanotubes composite with new lariat ether.

A poly (vinyl chloride) (PVC) matrix membrane ion-selective electrode for silver (I) ion is fabricated based on modified polypyrrole - multiwalled carbon nanotubes composite with new lariat ether. This sensor has a Nernstian slope of 59.4±0.5mV/decade over a wide linear concentration range of 1.0×10(-7) to 1.0×10(-1)molL(-1) for silver (I) ion. It has a short response time of about 8.0s and can be used for at least 50days. The detection limit is 9.3×10(-8)molL(-1) for silver (I) ion, and the electrode was applicable in the wide pH range of 1.6 -7.7. The electrode shows good selectivity for silver ion against many cations such as Hg (II), which usually imposes serious interference in the determination of silver ion concentration. The use of multiwalled carbon nanotubes (MWCNTs) in a polymer matrix improves the linear range and sensitivity of the electrode. In addition by coating the solid contact with a layer of the polypyrrole (Ppy) before coating the membrane on it, not only did it reduce the drift in potential, but a shorter response time was also resulted. The proposed electrode was used as an indicator electrode for potentiometric titration of silver ions with chloride anions and in the titration of mixed halides. This electrode was successfully applied for the determination of silver ions in silver sulphadiazine as a burning cream.

Diabetes mellitus type 1 induces dark neuron formation in the dentate gyrus: a study by Gallyas' method and transmission electron microscopy.

BACKGROUND: Diabetes mellitus type 1 is a chronic endogenous stressor. We investigated the effects of a diabetes mellitus type 1 on dark neuron formation in granular layer of dentate gyrus. MATERIALS AND METHODS: Diabetes was induced by a single intraperitoneal (IP) injection of streptozotocin (STZ) at a dose of 60 mg/kg dissolved in saline. Control animals were received only saline. In the end of eight weeks, the brains were removed and hippocampi studied by Gallyas' method and transmission electron microscopy. RESULTS: The comparison between the rate of dark neurons in diabetic group (223 ± 25) and of control (5.75 ± 4.34) showed significant level of difference (p<0.05). Ultrastructurally dark neurons showed apoptotic death criteria namely: dark and electron dense appearance, chromatin condensation, margination and clumping. CONCLUSIONS: Present results suggest that STZ-induced diabetes accelerates dark neuron formation with apoptotic criteria in granule layer of dentate gyrus.

Pancreatic alpha-cell function in idiopathic reactive hypoglycemia.

Idiopathic reactive hypoglycemia (IRH) is a well-documented but overdiagnosed syndrome. The presence of transient hypoglycemia and enhanced insulin secretion and/or increased insulin sensitivity before the onset of IRH is well documented. However, the data regarding glucagon secretion are sparse. Therefore, this study assessed glucagon and insulin responses to (1) oral ingestion of 100 g glucose oral glucose tolerance test (OGTT) and (2) a 100-g protein meal after an overnight fast in a randomized sequence at intervals of 7 to 10 days in five subjects with previously well-documented IRH and six normal subjects. Basal plasma glucose and insulin levels were not significantly different in both groups. However, basal glucagon was significantly higher (P < .025) in IRH subjects (347 +/- 83 ng/L) compared with normals (135 +/- 20 ng/L). In IRH subjects during the OGTT, hypoglycemia (2.7 +/- 0.11 mmol/L) occurred at 150 +/- 16 minutes and was preceded by a markedly higher (P < .01) peak glucose concentration (11.7 +/- 0.6 mmol/L) at 36 +/- 6 minutes in comparison to normals (8.8 +/- 0.4 mmol/L), indicating the presence of impaired glucose tolerance in these subjects. Similarly, the plasma insulin increase was significantly higher (P < .01) but delayed in IRH subjects compared with normals. In contrast, glucagon suppression was not significantly different in both groups, although glucagon failed to increase following hypoglycemia in IRH. During a protein meal, plasma glucose declined in both groups, with a significantly (P < .05) greater decrease in IRH subjects (-0.8 +/- 0.2 mmol/L) compared with normals (0.5 +/- 0.1 mmol/L). However, the glucagon increase was significantly (P < .01) blunted in IRH subjects (61% +/- 15%) in comparison to normals (152% +/- 39%). Thus, basal hyperglucagonemia with normal glucose concentration may suggest the presence of a hyposensitivity of the glucagon receptor in IRH. Moreover, the lack of appropriate suppression during the OGTT despite marked hyperglycemia, the lack of an increase at the onset of hypoglycemia, and the inhibited response to a protein meal in IRH subjects compared with normals denote altered glucagon secretion in IRH. Therefore, it is likely that glucagon receptor downregulation and impaired glucagon sensitivity and secretion may contribute to postprandial hypoglycemia in IRH.