Search

This report (I) aims to investigate defect behavior during the growth of heavily phosphorus (P)-doped Czochralski silicon (HP-Cz-Si) crystals. The defects and P chemical states in as-grown crystals with a resistivity of 0.6 mΩ cm and the wafers annealed at around 600 °C were evaluated by transmission electron microscopy and hard x-ray electron spectroscopy (HAXPES). Micro-dislocation loops (MDLs) were observed in the bottom portion of the crystal, and larger stacking faults (SFs), including complex dislocation clusters, were observed in the middle portion. HAXPES revealed two different P states, P1 and P2. P1 was attributed to a substitutional P (Ps). The P2 present in as-grown crystals was found to be electrically active, while the newly formed P2 after annealing was electrically inactive, indicating that they are in different states. HAXPES evaluation of HP-Cz-Si after electron irradiation showed similar behavior to P2 after annealing, suggesting that P-vacancy (V) clusters are formed when the crystals are held at temperatures below 600 °C during crystal growth. Combining the experimental results with our theoretical analysis in the report (II) based on density functional theory calculations, we identified the following defect formation mechanisms. Interstitial P (Pi) atoms introduced at the melting point become supersaturated during cooling to 600 °C, and MDLs are generated by the aggregation of Si self-interstitials (Is) released through a position exchange from Pi to Ps. In crystal portions with a long residence time below 600 °C, supersaturated Ps transforms into P–V clusters, and Is generated simultaneously are absorbed by the MDLs, which grow into SFs containing dislocation clusters. [ABSTRACT FROM AUTHOR]

Recent studies including our own report (I) have revealed that heavily phosphorus (P) doped Czochralski-silicon (HP-Cz-Si) exhibits peculiar defect behaviors during crystal growth. HP-Cz-Si crystals with a low resistivity of around 0.6 mΩ cm (P concentration of 1.3 × 1020 P cm−3) have interstitial-type stacking faults (SFs) and dislocations, which degrade device characteristics. The purpose of this paper is to clarify what causes the defect behavior in HP-Cz-Si through theoretical calculations. The thermal equilibrium concentrations of substitutional P (Ps), interstitial P (Pi), and (Ps)n-vacancy (V) clusters (n = 1−4) were determined by using density functional theory (DFT) calculations. The concentrations of Pi ([Pi]) and (Ps)nV ([(Ps)nV]) balanced with the given Ps concentration ([Ps]) were obtained as a function of the total P concentration ([P]) and the temperature. On the basis of the calculated results those can quantitatively explain our experimental results in the report (I), we propose a defect model that accurately represents HP-Cz-Si crystal growth. The main feature of the model is that the incorporated Pi atoms at the solid/liquid interface around [Pi] = 1017 Pi cm−3 cause the formation of SFs and dislocations during the HP-Cz-Si crystal growth with around [P] = 1020 P cm−3. Furthermore, DFT calculations were performed for Pi segregation on the SF and for the photoelectron spectra of P 1s measured by hard x-ray photoelectron spectroscopy to explain the other experimental results in the report (I). [ABSTRACT FROM AUTHOR]

Aims: This study aimed to identify the genetic risk factors from donors or recipients that contribute to postliver transplantation (LT) steatotic liver disease (SLD), focusing on the genetic risk score (GRS) based on single nucleotide polymorphisms (SNPs) in SLD patients. Methods: This retrospective study included 55 Japanese SLD recipients and their respective donors. Genotyping of PNPLA3, TM6SF2, and HSD17B13 was undertaken, and the combined GRS was calculated. The relationship between the GRS and the incidence of posttransplant SLD was also evaluated. Results: The SLD recipients had a high prevalence of post‐LT graft steatosis/steatohepatitis (76.4% and 58.2%, respectively). Although the recipients had a high frequency of risk alleles, there was no relationship between the number of risk alleles for each SNP and the incidence of posttransplant SLD. In contrast, an increased number of risk alleles for any SNP in the donor was correlated with high incidence rates of both post‐LT steatosis and steatohepatitis. A multivariable analysis showed that a high donor GRS was an independent risk factor for graft steatosis (odds ratio 8.77; 95% CI, 1.94–52.94; p = 0.009). Similarly, a high donor GRS was an independent risk factor (odds ratio 6.76; 95% CI, 1.84–30.78; p = 0.007) for post‐LT graft steatohepatitis. Conclusions: Donor risk alleles of PNPLA3, TM6SF2, and HSD17B13, rather than recipient risk alleles, have been implicated in the development of posttransplant SLD. The combination of these donor risk alleles into a GRS could predict the development of posttransplant SLD. [ABSTRACT FROM AUTHOR]

Aim: Combined hepatocellular‐cholangiocarcinoma (cHCC‐CCA) is a rare primary liver cancer that has two different tumor phenotypes in a single tumor nodule. The relationship between genetic mutations and clinicopathological features of cHCC‐CCA remains to be elucidated. Methods: Whole‐exome sequencing analyses were carried out in 13 primary and 2 recurrent cHCC‐CCAs. The whole‐exome analyses and clinicopathological information were integrated. Results: TP53 was the most frequently mutated gene in this cohort, followed by BAP1, IDH1/2, and NFE2L2 mutations in multiple cases. All tumors with diameters <3 cm had TP53 mutations. In contrast, six of seven tumors with diameters ≥3 cm did not have TP53 mutations, but all seven tumors had mutations in genes associated with various pathways, including Wnt, RAS/PI3K, and epigenetic modulators. In the signature analysis, the pattern of mutations shown in the TP53 mutation group tended to be more similar to HCC than the TP53 nonmutation group. Mutations in recurrent cHCC‐CCA tumors were frequently identical to those in the primary tumor, suggesting that those tumors originated from identical clones of the primary cHCC‐CCA tumors. Recurrent and co‐occurrent HCC tumors in the same patients with cHCC‐CCA had either common or different mutation patterns from the primary cHCC‐CCA tumors in each case. Conclusions: The study suggested that there were two subtypes of cHCC‐CCA, one involving TP53 mutations in the early stage of the carcinogenic process and the other not involving such mutations. The comparison of the variants between primary and recurrent tumors suggested that cHCC‐CCA was derived from an identical clone. [ABSTRACT FROM AUTHOR]

The fabrication of a thin-film quasi-silicon-on-insulator power MOSFET has been achieved using a reversed silicon wafer direct bonding technique. The MOSFET device has a low base resistance to the parasitic npn bipolar transistor, has a specific on-resistance of 86 micro ohms per millimeter squared and an on-state breakdown voltage of 30 volts.

Analysis of the etching of Si by ultraviolet irradiation-excited Cl radicals through native oxide diffusion on Si surfaces at 200 degrees Celsius shows that surface morphologies and Si etch rate depend on the native oxides that develop due to wet chemical treatments prior to etching. Scanning electron microscopy reveals caves on the etched Si surface, confirming that the occurrence of etching does not affect the native oxide layer as it is supported by a thermally grown thick-oxide etching mask.

Studies on a scaling theory for double-gate SOI MOSFET's reveal that the theory enables the design of SOI devices with proper subthreshold factor. The design involves selection of SOI silicon and gate oxide thicknesses, tsi and tox, respectively, for a specified gate length. Experimental results reveal that the shortest gate length depends upon the thinnest tsi value.