Effect of various stressors on the levels of lipid peroxide,antioxidants and Na+, K+-ATPase actrivity in rat brain

The level of malondialdehyde (MDA), an index of lipid peroxidation, and the antioxidants superoxide dismutase (SOD) and glutathione (GSH), as well as the activity of Na⁺, K⁺-ATPase, were assessed in whole rat brain after immobilization, anemic hypoxia (NaNO₂) and 72 h starvation. The effect of these stressors on plasma glucose and corticosterone levels was also observed. Hypoxia and starvation stimulated the lipidj peroxide formation in braini as indicated by an increase in the level of MDA, being higher after starvation than hypoxia. Brain SOD activity was also increased in response to hypoxia and starvation while GSH content was only diminished ini hypoxia. However, neither MDA nor antioxidants were affected by immobilization. On the other hand, the activity of brain Na⁺, K⁺-ATPase was significantly increased by immobilization and hypoxia but decreased in starvation. A similar pattern of change was also observed in plasma glucose and corticosterone levels in response to these stressors. These results elucidate differences in the biochemical response of animals towards various types of stress, with increased lipid peroxide formation in hypoxia and starvation.     

Effect of different deformation and annealing procedures on non-magnetic textured Cu<Subscript>60</Subscript>Ni<Subscript>40</Subscript> alloy substrates

In this work, a series of specimens was prepared by the casting method. Sharp cube-textured substrates were processed by heavy cold rolling and recrystallization annealing (i.e., the rolling-assisted biaxially textured substrates (RABiTS) method). Both the rolling and the recrystallization texture in the alloy tapes were investigated by X-ray diffraction and electron back-scatter diffraction, respectively. The results showed that a strong copper-type deformation texture was obtained in the heavy cold-rolled substrate. In addition, the recrystallization annealing process was found to be very important for the texture transition in the Cu–Ni alloy substrates. The cube texture content in the Cu₆₀Ni₄₀ alloy substrates reached 99.7% (≤10°) after optimization of the cold-rolling procedure and the recrystallizing heat-treatment process, whereas the content of low-angle grain boundaries (from 2° to 10° misorientation) in the substrate reached 95.1%.     

Effect of different deformation and annealing procedures on non-magnetic textured Cu_(60)Ni_(40) alloy substrates

In this work,a series of specimens was prepared by the casting method.Sharp cube-textured substrates were processed by heavy cold rolling and recrystallization annealing(i.e.,the rolling-assisted biaxially textured substrates(RABi TS) method).Both the rolling and the recrystallization texture in the alloy tapes were investigated by X-ray diffraction and electron back-scatter diffraction,respectively.The results showed that a strong copper-type deformation texture was obtained in the heavy cold-rolled substrate.In addition,the recrystallization annealing process was found to be very important for the texture transition in the Cu–Ni alloy substrates.The cube texture content in the Cu60 Ni40 alloy substrates reached 99.7%(≤10°) after optimization of the cold-rolling procedure and the recrystallizing heat-treatment process,whereas the content of low-angle grain boundaries(from 2° to 10° misorientation) in the substrate reached 95.1%.     

WDR62 is associated with the spindle pole and is mutated in human microcephaly

Autosomal recessive primary microcephaly (MCPH) is a disorder of neurodevelopment resulting in a small brain. We identified WDR62 as the second most common cause of MCPH after finding homozygous missense and frame-shifting mutations in seven MCPH families. In human cell lines, we found that WDR62 is a spindle pole protein, as are ASPM and STIL, the MCPH7 and MCHP7 proteins. Mutant WDR62 proteins failed to localize to the mitotic spindle pole. In human and mouse embryonic brain, we found that WDR62 expression was restricted to neural precursors undergoing mitosis. These data lend support to the hypothesis that the exquisite control of the cleavage furrow orientation in mammalian neural precursor cell mitosis, controlled in great part by the centrosomes and spindle poles, is critical both in causing MCPH when perturbed and, when modulated, generating the evolutionarily enlarged human brain.     

Dominant and recessive deafness caused by mutations of a novel gene, TMC1, required for cochlear hair-cell function

Positional cloning of hereditary deafness genes is a direct approach to identify molecules and mechanisms underlying auditory function. Here we report a locus for dominant deafness, DFNA36, which maps to human chromosome 9q13-21 in a region overlapping the DFNB7/B11 locus for recessive deafness. We identified eight mutations in a new gene, transmembrane cochlear-expressed gene 1 (TMC1), in a DFNA36 family and eleven DFNB7/B11 families. We detected a 1.6-kb genomic deletion encompassing exon 14 of Tmc1 in the recessive deafness (dn) mouse mutant, which lacks auditory responses and has hair-cell degeneration. TMC1 and TMC2 on chromosome 20p13 are members of a gene family predicted to encode transmembrane proteins. Tmc1 mRNA is expressed in hair cells of the postnatal mouse cochlea and vestibular end organs and is required for normal function of cochlear hair cells.