Pressure-induced phase transition of Bi2Te3 into the bcc structure

The pressure-induced phase transition of bismuth telluride, Bi2Te3, has been studied by synchrotron x-ray diffraction measurements at room temperature using a diamond-anvil cell (DAC) with loading pressures up to 29.8 GPa. We found a high-pressure body-centered cubic (bcc) phase in Bi2Te3 at 25.2 GPa, which is denoted as phase IV, and this phase apperars above 14.5 GPa. Upon releasing the pressure from 29.8 GPa, the diffraction pattern changes with pressure hysteresis. The original rhombohedral phase is recovered at 2.43 GPa. The bcc structure can explain the phase IV peaks. We assumed that the structural model of phase IV is analogous to a substitutional binary alloy; the Bi and Te atoms are distributed in the bcc-lattice sites with space group Im-3m. The results of Rietveld analysis based on this model agree well with both the experimental data and calculated results. Therefore, the structure of phase IV in Bi2Te3 can be explained by a solid solution with a bcc lattice in the Bi-Te (60 atomic% tellurium) binary system.Comment: 12 pages, 5 figure

Fasting insulin and risk of cerebral infarction in a Japanese general population: The Jichi Medical School Cohort Study

Abstract Objective: We investigated the relation between fasting insulin (FI) and risk of cerebral infarction in a Japanese general population. Methods: The subjects were 2,610 men and women without past history of stroke or myocardial infarction and under treatment for diabetes, examined between 1992 and 1995 as part of the Jichi Medical School Cohort Study. The FI level was measured once at the baseline. Subjects were divided into quintiles by FI levels, and Cox's proportional hazard model was used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for cerebral infarction. Results: During an average of 11.1 years of follow-up, 87 participants developed cerebral infarction. Crude incidence rates of FI quintiles 1-5 were 4.69, 2.35, 1.85, 2.77 and 3.30 per 1,000 person-years, respectively. The multivariate-adjusted HRs for cerebral infarction were 2.33 (95% CI, 1.10 -4.96) in quintile 1 (Q1), 1.25 (95% CI, 0.55 -2.84) in Q2, 1.68 (95% CI, 0.76 -3.70) in Q4 and 2.06 (95% CI, 0.94 -4.47) in Q5, using Q3 as the reference. Conclusions: The lowest FI level was associated with increased risk of cerebral infarction and the association between FI and risk of cerebral infarction appeared to be a U-shaped relationship

Differential gene expression profiles in neurons generated from lymphoblastoid B-cell line-derived iPS cells from monozygotic twin cases with treatment-resistant schizophrenia and discordant responses to clozapine

Schizophrenia is a chronic psychiatric disorder with complex genetic and environmental origins. While many antipsychotics have been demonstrated as effective in the treatment of schizophrenia, a substantial number of schizophrenia patients are partially or fully unresponsive to the treatment. Clozapine is the most effective antipsychotic drug for treatment-resistant schizophrenia; however, clozapine has rare but serious side-effects. Furthermore, there is inter-individual variability in the drug response to clozapine treatment. Therefore, the identification of the molecular mechanisms underlying the action of clozapine and drug response predictors is imperative. In the present study, we focused on a pair of monozygotic twin cases with treatment-resistant schizophrenia, in which one twin responded well to clozapine treatment and the other twin did not. Using induced pluripotent stem (iPS) cell-based technology, we generated neurons from iPS cells derived from these patients and subsequently performed RNA-sequencing to compare the transcriptome profiles of the mock or clozapine-treated neurons. Although, these iPS cells similarly differentiated into neurons, several genes encoding homophilic cell adhesion molecules, such as protocadherin genes, showed differential expression patterns between these two patients. These results, which contribute to the current understanding of the molecular mechanisms of clozapine action, establish a new strategy for the use of monozygotic twin studies in schizophrenia research

Mutant analyses reveal different functions of fgfr1 in medaka and zebrafish despite conserved ligand–receptor relationships

AbstractMedaka (Oryzias latipes) is a small freshwater teleost that provides an excellent developmental genetic model complementary to zebrafish. Our recent mutagenesis screening using medaka identified headfish (hdf) which is characterized by the absence of trunk and tail structures with nearly normal head including the midbrain–hindbrain boundary (MHB). Positional-candidate cloning revealed that the hdf mutation causes a functionally null form of Fgfr1. The fgfr1hdf is thus the first fgf receptor mutant in fish. Although FGF signaling has been implicated in mesoderm induction, mesoderm is induced normally in the fgfr1hdf mutant, but subsequently, mutant embryos fail to maintain the mesoderm, leading to defects in mesoderm derivatives, especially in trunk and tail. Furthermore, we found that morpholino knockdown of medaka fgf8 resulted in a phenotype identical to the fgfr1hdf mutant, suggesting that like its mouse counterpart, Fgf8 is a major ligand for Fgfr1 in medaka early embryogenesis. Intriguingly, Fgf8 and Fgfr1 in zebrafish are also suggested to form a major ligand–receptor pair, but their function is much diverged, as the zebrafish fgfr1 morphant and zebrafish fgf8 mutant acerebellar (ace) only fail to develop the MHB, but develop nearly unaffected trunk and tail. These results provide evidence that teleost fish have evolved divergent functions of Fgf8–Fgfr1 while maintaining the ligand–receptor relationships. Comparative analysis using different fish is thus invaluable for shedding light on evolutionary diversification of gene function

Defective repair of radiation-induced DNA damage is complemented by a CHORI-230-65K18 BAC clone on rat chromosome 4

AbstractThe Long Evans cinnamon (LEC) rat is highly susceptible to X-irradiation due to defective DNA repair and is thus a model for hepatocellular carcinogenesis. We constructed a bacterial artificial chromosome (BAC) contig of rat chromosome 4 completely covering the region associated with radiation susceptibility. We used transient and stable transfections to demonstrate that defective DNA repair in LEC cells is fully complemented by a 200-kb BAC, CHORI-230-65K18. Further analysis showed that the region associated with radiation susceptibility is located in a 128,543-bp region of 65K18 that includes the known gene Rpn1. However, neither knockdown nor overexpression of Rpn1 indicated that this gene is associated with radiation susceptibility. We also mapped three ESTs (TC523872, TC533727, and CB607546) in the 128,543-bp region, suggesting that 65K18 contains an unknown gene associated with X-ray susceptibility in the LEC rat

Report of Health Promotion Collaboration Project for the Faculty and Staff at Hokusho University

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