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The neuroprotective and nootropic activities of the amide form (AF) of the HLDF-6 peptide (TGENHR-NH2) were studied in transgenic mice of the B6C3-Tg(APPswe,PSEN1de9)85Dbo (Tg+) line (the animal model of familial Alzheimer’s disease (AD)). The study was performed in 4 mouse groups: group 1 (study group): Tg+ mice intranasally injected with the peptide at a dose of 250 μg/kg; group 2 (active control): Tg+ mice intranasally injected with normal saline; group 3 (control 1): Tg- mice; and group 4 (control 2): C57Bl/6 mice. The cognitive functions were evaluated using three tests: the novel object recognition test, the conditioned passive avoidance task, and the Morris water maze. The results testify to the fact that the pharmaceutical substance (PhS) based on the AF of HLDF-6 peptide at a dose of 250 μg/kg administered intranasally efficiently restores the disturbed cognitive functions in transgenic mice. These results are fully consistent with the data obtained in animal models of Alzheimer’s disease induced by the injection of the beta-amyloid (βA) fragment 25-35 into the giant-cell nucleus basalis of Meynert or by co-injection of the βA fragment 25-35 and ibotenic acid into the hippocampus, and the model of ischemia stroke (chronic bilateral occlusion of carotids, 2VO). According to the overall results, PhS based on AF HLDF-6 was chosen as an object for further investigation; the dose of 250 μg/kg was used as an effective therapeutic dose. Intranasal administration was the route for delivery.

An InAs0.89Sb0.11 photovoltaic detector that operates at room temperature in the 2.5-5 mu m mid-infrared wavelength region is reported. The photodiode has an extended spectral response compared with other currently available III-V room-temperature detectors. In order to accommodate the large lattice mismatch between the InAs0.89Sb0.11 active region and the InAs substrate, a buffer layer with an intermediate composition was introduced into the structure. In this way, we obtained room-temperature photodiodes with a cutoff wavelength near 5 mu m, a peak responsivity of 0.8 A/W, and a detectivity of 1.26 x 10(9) cm Hz(1/2)/W. These devices could be effectively used as the basis of an optical sensor for the environmental monitoring of carbon monoxide at 4.6 mu m, or as a replacement for PbSe photoconductors. (C) 2000 American Institute of Physics. [S0003-6951(00)02332-9].

The spontaneous electroluminescence emission of InAs light-emitting diodes (LEDs) operating at 3.3 µm was studied as a function of applied hydrostatic pressure. An enhancement of a factor of almost four in radiative efficiency at room temperature was observed in the range 0 to 10 kbar. Analysis of the dependence of electroluminescence emission intensity on hydrostatic pressure at constant current reveals that nonradiative Auger recombination dominates the quantum efficiency of these LEDs.

Development of a curved reflective surface on the bottom side of the LED chip based on the GaSb/GaInAsSb/GaAlAsSb heterostructure increases the emission power of LEDs in 1.9–2.0 times compared with power of the tradition LED chip. This effect was investigated for the wavelengths of 2.0–2.3 μm. We believe that the improving of LED efficiency is the result of changes of light direction by the reflection from the curved surface formed by the hemispherical pits in the crystal.

Powerful mid-infrared (1.7-4.8 /spl mu/m) light emitting diodes were manufactured by liquid phase epitaxy using GaSb-InAs compounds. Their output optical power was enhanced up to 2-3.5 mW using symmetrical double heterostructures with large band offsets. These diodes can be used as narrow bandwidth emitters for cost-reduced setups for atmospheric pollution monitoring.

The neuroprotective and nootropic activities of the amide form (AF) of the HLDF-6 peptide (TGENHR-NH2 ) were studied in transgenic mice of the B6C3-Tg(APPswe,PSEN1de9)85Dbo (Tg+) line (the animal model of familial Alzheimers disease (AD)). The study was performed in 4 mouse groups: group 1 (study group): Tg+ mice intranasally injected with the peptide at a dose of 250 g/kg; group 2 (active control): Tg+ mice intranasally injected with normal saline; group 3 (control 1): Tg- mice; and group 4 (control 2): C57Bl/6 mice. The cognitive functions were evaluated using three tests: the novel object recognition test, the conditioned passive avoidance task, and the Morris water maze. The results testify to the fact that the pharmaceutical substance (PhS) based on the AF of HLDF-6 peptide at a dose of 250 g/kg administered intranasally efficiently restores the disturbed cognitive functions in transgenic mice. These results are fully consistent with the data obtained in animal models of Alzheimers disease induced by the injection of the beta-amyloid (A) fragment 25-35 into the giant-cell nucleus basalis of Meynert or by co-injection of the A fragment 25-35 and ibotenic acid into the hippocampus, and the model of ischemia stroke (chronic bilateral occlusion of carotids, 2VO). According to the overall results, PhS based on AF HLDF-6 was chosen as an object for further investigation; the dose of 250 g/kg was used as an effective therapeutic dose. Intranasal administration was the route for delivery.