Effects of heat-treatments on electrical properties of boron-doped silicon crystals

The effects of heat-treatments around 1000°Ｃand subsequent annealing on the electrical properties of boron-doped silicon have been studied by electrical conductivity, Hall effect, and deep-level transient spectroscopy measurements. The high-temperature heat-treatments always induced net densities of donors. Four recovery stages, stages I-IV, of heat-treatment- induced donors were observed on isochronal annealing up to 400°Ｃ Conductivity changes in these stages can be explained as described below by the reactions of interstitial iron (Fei), its pair (Fe1Bs)with substitutional boron (Bs), and two unknown donors (D1, D2). That is, stage I (25°-100°Ｃ): D1→sink and Fei + Bs→FeiBs, stage II (100°-150°Ｃ)： FeiBs→Fei + Bs, stage III (200°-250°Ｃ):D2→sink, stage IV (250°-350°Ｃ)Fei→precipitation. Heat-treatments in an oxygen atmosphere greatly reduced the introduction of Fei and FeiBs in comparison with an argon atmosphere and mainly introduced D1 and D2 donors. The density of D2 was dependent on the heat-treatment temperature, while that of D1 showed almost no dependence. In stage I, D, was annihilated by first-order kinetics with an activation energy of 0.8 eV. It was indicated that DI and D2 have no relations to iron, copper, oxygen, nor carbon. Though their origins are still unidentified, there may be some interstitial impurities. In stage IV, Fei is suggested to precipitate at oxygen precipitates and dislocation loops formed by high-temperature heat-treatments. As to the application to iron gettering in the device fabrication process, it is proposed that annealing around 300°Ｃ is most suitable as the final heat-treatment step to remove iron and related defects from active regions of devices. Silicon wafers receive complex heat-treatments at various.</p

The C allele of JAK2 rs4495487 is an additional candidate locus that contributes to myeloproliferative neoplasm predisposition in the Japanese population

<p>Abstract</p> <p>Background</p> <p>Polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF) are myeloproliferative neoplasms (MPNs) characterized in most cases by a unique somatic mutation, <it>JAK2 </it>V617F. Recent studies revealed that <it>JAK2 </it>V617F occurs more frequently in a specific <it>JAK2 </it>haplotype, named <it>JAK2 </it>46/1 or GGCC haplotype, which is tagged by rs10974944 (C/G) and/or rs12343867 (T/C). This study examined the impact of single nucleotide polymorphisms (SNPs) of the <it>JAK2 </it>locus on MPNs in a Japanese population.</p> <p>Methods</p> <p>We sequenced 24 <it>JAK2 </it>SNPs in Japanese patients with PV. We then genotyped 138 MPN patients (33 PV, 96 ET, and 9 PMF) with known <it>JAK2 </it>mutational status and 107 controls for a novel SNP, in addition to two SNPs known to be part of the 46/1 haplotype (rs10974944 and rs12343867). Associations with risk of MPN were estimated by odds ratios and their 95% confidence intervals using logistic regression.</p> <p>Results</p> <p>A novel locus, rs4495487 (T/C), with a mutated T allele was significantly associated with PV. Similar to rs10974944 and rs12343867, rs4495487 in the <it>JAK2 </it>locus is significantly associated with <it>JAK2</it>-positive MPN. Based on the results of SNP analysis of the three <it>JAK2 </it>locus, we defined the "GCC genotype" as having at least one minor allele in each SNP (G allele in rs10974944, C allele in rs4495487, and C allele in rs12343867). The GCC genotype was associated with increased risk of both <it>JAK2 </it>V617F-positive and <it>JAK2 </it>V617F-negative MPN. In ET patients, leukocyte count and hemoglobin were significantly associated with <it>JAK2 </it>V617F, rather than the GCC genotype. In contrast, none of the <it>JAK2 </it>V617F-negative ET patients without the GCC genotype had thrombosis, and splenomegaly was frequently seen in this subset of ET patients. PV patients without the GCC genotype were significantly associated with high platelet count.</p> <p>Conclusions</p> <p>Our results indicate that the C allele of <it>JAK2 </it>rs4495487, in addition to the 46/1 haplotype, contributes significantly to the occurrence of <it>JAK2 </it>V617F-positive and <it>JAK2 </it>V617F-negative MPNs in the Japanese population. Because lack of the GCC genotype represents a distinct clinical-hematological subset of MPN, analyzing <it>JAK2 </it>SNPs and quantifying <it>JAK2 </it>V617F mutations will provide further insights into the molecular pathogenesis of MPN.</p