Preparation of Aluminum Nitride–Silicon Carbide Nanocomposite Powder by the Nitridation of Aluminum Silicon Carbide

Aluminum nitride (AlN)–silicon carbide (SiC) nanocomposite powders were prepared by the nitridation of aluminum-silicon carbide (Al₄SiC₄) with the specific surface area of 15.5 m²·g⁻¹. The powders nitrided at and above 1400°C for 3 h contained the 2H-phases which consisted of AlN-rich and SiC-rich phases. The formation of homogeneous solid solution proceeded with increasing nitridation temperature from 1400° up to 1500°C. The specific surface area of the AlN–SiC powder nitrided at 1500°C for 3 h was 19.5 m²·g⁻¹, whereas the primary particle size (assuming spherical particles) was estimated to be ∼100 nm.     

Preparation and characterisation of MgSiN2 powders

The powder preparation of MgSiN₂ was studied using several starting mixtures (Mg₃N₂/Si₃N₄, Mg/Si₃N₄ and Mg/Si) in the temperature range 800–1500°C in N₂ or N₂/H₂ atmospheres. The phase formation was followed with TGA/DTA and powder X-ray diffraction (XRD). At 1250°C Mg/Si mixtures did not yield single phase MgSiN₂ whereas for Mg/Si₃N₄ and Mg₃N₂/Si₃N₄ mixtures nearly single-phase powders were obtained. The Mg/Si₃N₄ mixtures yielded MgSiN₂ at the lowest processing temperature but the Mg₃N₂/Si₃N₄ mixtures yielded the most pure MgSiN₂ powder with respect to secondary phases. The main secondary phase detectable with XRD was MgO when starting from Mg₃N₂/Si₃N₄ or MgO and metallic Si when starting from Mg/Si₃N₄ mixtures. When the processing starting from Mg₃N₂/Si₃N₄ mixtures was optimised MgSiN₂ powders containing only 0.1 wt% O could be prepared. Using XRD the solubility of oxygen in the MgSiN₂ lattice was estimated to be at maximum 0.6 wt%. The MgSiN₂ powder was oxidation resistant in air till 830°C. The morphology and particle size were studied with the scanning electron microscope (SEM) and the sedimentation method. Two different kinds of morphology were observed determined by the morphology of the Si₃N₄ starting material.     

Maintenance of recombinant type A gamma-aminobutyric acid receptor function: role of protein tyrosine phosphorylation and calcineurin

In the present study, rundown of gamma-aminobutyric acid (GABA)-activated Cl- channels was studied in recombinant GABAA receptors stably expressed in human embryonic kidney cells (HEK 293), with conventional whole-cell and amphotericin B-perforated patch recording. When [ATP]i was lowered to 1 mM and resting [Ca++]i was buffered to a relatively high level, the response of alpha 3 beta 2 gamma 2 GABAA receptors to relatively low [GABA] (up to 50 microM) did not show rundown in the whole-cell configuration. However, high [GABA] (greater than 200 microM) induced significant rundown, which was observed by decreases in both the maximum GABA-induced current and GABA EC50. Rundown was prevented completely with a solution containing 4 mM Mg(++)-ATP and low resting [Ca++]i, or during perforated patch recording. The magnitude of rundown was comparable in alpha 1 beta 2 gamma 2 and beta 2 gamma 2 receptors. Neither stimulation nor inhibition of protein kinase A or protein kinase C had a significant effect on rundown. However, sodium metavanadate, an inhibitor of protein tyrosine phosphatase, significantly reduced rundown. In addition, inhibition of protein tyrosine kinase activity by either genistein or lavendustin A induced rundown of the GABA response. Inhibition of the Ca++/calmodulin-dependent phosphatase calcineurin with fenvalerate also prevented rundown of the response to GABA. Our results demonstrate that rundown of GABAA receptor function is concentration-dependent, due to depletion of ATP and/or unbuffered [Ca++]i, and does not depend on the presence or subtype of the alpha subunit. We propose that protein phosphorylation at a tyrosine kinase-dependent site, and a distinct unidentified site, which is dephosphorylated by calcineurin, maintains the function of GABAA receptors.     

Optical Properties of (Oxy)Nitride Materials: A Review

(Oxy)nitride materials, consisting mainly of transition metal and ionic‐covalent (oxy)nitrides, show a vast number of interesting physical and chemical properties due to their substantial structural diversity. The optical properties of these (oxy)nitrides, in combination with their excellent mechanical strength, thermal properties, and chemical stability, enable (oxy)nitrides to be used in a variety of industrial fields, such as photovoltaic, photothermal, photocatalytic, pigment, lighting and display, optoelectronic, and defense industries. The optical properties are extremely related to the electronic band structure of (oxy)nitrides, and can be varied significantly by changing the chemical composition (e.g., the oxygen to nitrogen ratio) and preparation/processing conditions. This article overviews the optical properties (including refractive index, reflectance, absorbance, band gap, photoluminescence, and transmittance) of (oxy)nitride materials that are in the form of thin films, powders, or bulk ceramics, and highlights their applications as antireflection coatings, solar spectral selectivity coatings, visible‐light‐driven photocatalysts, ecological pigments, phosphors for light‐emitting diodes, and transparent window materials.     

Creativity of undergraduates with and without family history of alcohol and other drug problems

BACKGROUND: Colonoscopic surveillance is a standard procedure in many patients with long standing, extensive ulcerative colitis (UC), in order to avoid death from colorectal cancer. No conclusive proof of its benefits has been presented however. AIMS: To evaluate the association between colonoscopic surveillance and colorectal cancer mortality in patients with UC. PATIENTS: A population based, nested case control study comprising 142 patients with a definite UC diagnosis, derived from a study population of 4664 patients with UC, was conducted. METHODS: Colonoscopic surveillance in all patients with UC who had died from colorectal cancer after 1975 was compared with that in controls matched for age, sex, extent, and duration of the disease. Information on colonoscopic surveillance was obtained from the medical records. RESULTS: Two of 40 patients with UC and 18 of 102 controls had undergone at least one surveillance colonoscopy (relative risk (RR) 0.29, 95% confidence interval 0.06 to 1.31). Twelve controls but only one patient with UC had undergone two or more surveillance colonoscopies (RR 0.22, 95% confidence interval 0.03 to 1.74), indicating a protective dose response relation. CONCLUSION: Colonoscopic surveillance may be associated with a decreased risk of death from colorectal cancer in patients with long standing UC.     

Regulation of BRCA1 and BRCA2 expression in human breast cancer cells by DNA-damaging agents

Germline mutations in the breast cancer susceptibility genes BRCA1 and BRCA2 have been linked to the development of breast cancer, ovarian cancer, and other malignancies. Recent studies suggest that the BRCA1 and BRCA2 gene products may function in the sensing and/or repair of DNA damage. To investigate this possibility, we determined the effects of various DNA-damaging agents and other cytotoxic agents on the mRNA levels of BRCA1 and BRCA2 in the MCF-7 and other human breast cancer cell lines. We found that several agents, including adriamycin (a DNA intercalator and inhibitor of topoisomerase II), camptothecin (a topoisomerase I inhibitor), and ultraviolet radiation induced significant decreases in BRCA1 and BRCA2 mRNA levels. Decreased levels of BRCA1 and BRCA2 mRNAs were observed within 6-12 h after treatment with adriamycin and persisted for at least 72 h. Adriamycin also induced decreases in BRCA1 protein levels; but these decreases required several days. U.V. radiation induced dose-dependent down-regulation of BRCA1 and BRCA2 mRNAs, with significant decreases in both mRNAs at doses as low as 2.5 J/m2, a dose that yielded very little cytotoxicity. Adriamycin-induced down-regulation of BRCA1 and BRCA2 mRNAs was first observed at doses that yielded relatively little cytotoxicity and little or no apoptotic DNA fragmentation. Adriamycin and U.V. radiation induced distinct dose- and time-dependent alterations in the cell cycle distribution; but these alterations did not correlate well with corresponding changes in BRCA1 and BRCA2 mRNA levels. However, the adriamycin-induced reduction in BRCA1 and BRCA2 mRNA levels was correlated with p53 functional status. MCF-7 cells transfected with a dominant negative mutant p53 (143 val-->ala) required at least tenfold higher doses of adriamycin to down-regulate BRCA1 and BRCA2 mRNAs than did parental MCF-7 cells or control-transfected MCF-7 clones. These results suggest that BRCA1 and BRCA2 may play roles in the cellular response to DNA-damaging agents and that there may be a p53-sensitive component to the regulation of BRCA1 and BRCA2 mRNA expression.     

Neuronal stress and injury in C57/BL mice after systemic kainic acid administration

Kainate-induced seizures are widely studied as a model of human temporal lobe epilepsy due to behavioral and pathological similarities. While kainate-induced neuronal injury is well characterized in rats, relatively little data is available on the use of kainate and its consequences in mice. The growing availability of genetically altered mice has focused attention on the need for well characterized mouse seizure models in which the effects of specific genetic manipulations can be examined. We therefore examined the kainate dose-response relationship and the time-course of specific histopathological changes in C57/BL mice, a commonly used founder strain for transgenic technology. Seizures were induced in male C57/BL mice (kainate 10-40 mg/kg i.p.) and animals were sacrificed at various time-points after injection. Seizures were graded using a behavioral scale developed in our laboratory. Neuronal injury was assayed by examining DNA fragmentation using in situ nick translation histochemistry. In parallel experiments, we examined the expression an inducible member of the heat shock protein family, HSP-72, another putative marker of neuronal injury, using a monoclonal antibody. Seizure severity paralleled kainate dosage. At higher doses DNA fragmentation is seen mainly in hippocampus in area CA3, and variably in CA1, thalamus and amygdala within 24 h, is maximal within 72 h, and is largely gone by 7 days after administration of kainate. HSP-72 expression is also highly selective, occurring in limbic structures, and it evolves over a characteristic time-course. HSP-72 is expressed mainly in structures that also manifest DNA fragmentation. Using double-labeling techniques, however, we find essentially no overlap between neurons expressing HSP-72 and DNA fragmentation. These findings indicate that DNA fragmentation and HSP-72 expression are complementary markers of seizure-induced stress and injury, and support the notion that HSP-72 expression is neuroprotective following kainate-induced seizures.