Novel slow dynamics of phase transition in the partially ordered frustrated magnet DyRu2Si2

DyRu2Si2 is a frustrated magnet to exhibit multiple magnetic phase transition in zero and finite magnetic fields. We investigated and characterized the phase transition between the partially-ordered antiferromagnetic phases at zero field by ac susceptibility measurements. Detailed ac susceptibility measurements reveal the novel critical dynamics of the phase transition; extremely slow dynamics with the relaxation time in the order of 10-100 msec, speed-up of the dynamics on cooling indicating its non-thermally activated origin and growing of the ferromagnetic correlations towards the phase transition temperature. On the basis of these findings, we propose the novel phase transition process, namely, the spontaneous striped-arrangement of the precedently emergent "belt-like" ferromagnetic spin texture.Comment: Accepted by JPSJ URL:https://journals.jps.jp/doi/10.7566/JPSJ.92.09470

Two Models for RHEED Specular Spot Intensity Recovery in Laser-triggered Chemical Beam Epitaxy GaP Growth

RHEED specular spot intensity (RSSI) has been observed while growing GaP by laser-triggered chemical beam epitaxy. The intensity decreases after each laser pulse, and then it recovers the original value. We present two models in order to explain the RSSI changes. The first model takes the chemisorption velocity of metalorganics as a limiting factor in RSSI recovery speed. On the other hand, the second model considers the reaction time of gallium with phosphorus as a limiting factor. The second model properly fits the experimental data and it allows a deeper understanding of chemical reactions on GaP surface during chemical beam epitaxial growth

Allele Loss in MEN 1-associated Pituitary Tumor

We have examined the allele loss of chromosome 11 in a pituitary tumor from a patient with familial multiple endocrine neoplasia type 1 (MEN 1). The extensive loss of chromosome 11, including loci of D11S149, HRAS1 and F2, was detected by the loss of heterozygosity. All of the lost alleles of these loci were transmitted from the unaffected father and not from an affected mother. This is the first evidence of allele loss of chromosome 11 in a pituitary tumor of MEN 1 and supports the idea that similar allelic deletion of MEN1 locus on chromosome 11 is the common genetic basis for tumorigenesis in the pituitary, endocrine pancreas, and parathyroid gland in MEN 1

p53 gene mutation in N-butyl-N-(4-hydroxybutyl)nitrosamine-induced urinary bladder tumors and N-methyl-N-nitrosourea-induced colon tumors of rats

We analyzed p53 mutations in 17 N-butyl-N-(4-hydroxybutyl) nitrosamine-induced bladder transitional cell carcinomas (TCCs) with or without areas of squamous cell carcinoma (SCC) of Long–Evans Cinnamon (LEC) and F344 rats, and in 7 N-methyl-N-nitrosourea-induced colon adenocarcinomas of LEC rats by polymerase chain reaction-single strand conformation polymorphism analysis and DNA sequencing. Of these bladder tumors, one TCC with moderately differentiated SCC had a T to G transversion mutation at codon 141, leading to a Val to Gly amino acid change. No p53 mutation was found in colon adenocarcinomas. Thus a p53 gene mutation seems infrequent in these rat bladder and colon carcinogenesis models even in the late stage

p53 gene mutation analysis in porokeratosis and porokeratosis-associated squamous cell carcinoma

In this and previous studies, we have shown p53 overexpression immunohistochemically in 14 of 17 porokeratotic specimens obtained from 14 lesions of nine cases, and in all six specimens of squamous cell carcinoma (SCC) arising on porokeratotic lesions of two cases. We screened mutations in exons 5 to 10 of the p53 gene in all these specimens by polymerase chain reaction-single strand conformation polymorphism analysis. Mutations of the p53 gene were detected in two of the six SCCs but not in any of the 17 porokeratotic specimens. These two mutations were C to T transitions at codons 146 and 175 in exon 5, which were a nonsense mutation at a dipyrimidine site and a missense mutation at a CG site, respectively. To our knowledge, neither of these mutations has been identified in skin cancers before. Our observations indicate that mutations of the p53 gene are not the major molecular etiology for porokeratosis, but are related to its skin carcinogenesis, and that p53 overexpression in porokeratosis is not due to p53 gene mutations

Thermally stable amorphous tantalum yttrium oxide with low IR absorption for magnetophotonic devices

Thin film oxide materials often require thermal treatment at high temperature during their preparation, which can limit them from being integrated in a range of microelectronic or optical devices and applications. For instance, it has been a challenge to retain the optical properties of Bragg mirrors in optical systems at temperatures above 700 °C because of changes in the crystalline structure of the high-refractive-index component. In this study, a ~100 nm-thick amorphous film of tantalum oxide and yttrium oxide with an yttrium-to-tantalum atomic fraction of 14% was prepared by magnetron sputtering. The film demonstrated high resistance to annealing above 850 °C without degradation of its optical properties. The electronic and crystalline structures, stoichiometry, optical properties, and integration with magnetooptical materials are discussed. The film was incorporated into Bragg mirrors used with iron garnet microcavities, and it contributed to an order-of-magnitude enhancement of the magnetooptical figure of merit at near-infrared wavelengths.National Science Foundation (U.S.) (Award ECCS-1607865

Novel and recurrent COMP gene variants in five Japanese patients with pseudoachondroplasia: skeletal changes from the neonatal to infantile periods

Pseudoachondroplasia (PSACH) is an autosomal dominant skeletal dysplasia caused by pathogenic variants of cartilage oligomeric matrix protein (COMP). Clinical symptoms of PSACH are characterized by growth disturbances after the first year of life. These disturbances lead to severe short stature with short limbs, brachydactyly, scoliosis, joint laxity, joint pain since childhood, and a normal face. Epimetaphyseal dysplasia, shortened long bones, and short metacarpals and phalanges are common findings on radiological examination. Additionally, anterior tonguing of the vertebral bodies in the lateral view is an important finding in childhood because it is specific to PSACH and normalizes with age. Here, we report five Japanese patients with PSACH, with one recurrent (p.Cys351Tyr) and four novel heterozygous pathogenic COMP variants (p.Asp437Tyr, p.Asp446Gly, p.Asp507Tyr, and p.Asp518Val). These five pathogenic variants were located in the calcium-binding type 3 (T3) repeats. In four of the novel variants, the affected amino acid was aspartic acid, which is abundant in each of the eight T3 repeats. We describe the radiological findings of these five patients. We also retrospectively analyzed the sequential changes in the vertebral body and epimetaphysis of the long bones from the neonatal to infantile periods in a patient with PSACH and congenital heart disease

Molecular Cloning and Expression Analysis of a Putative Nuclear Protein, SR-25

We cloned a full-length mouse cDNA and its human homologue encoding a novel protein designated as “SR-25.” In Northern blot analysis, SR-25 mRNA was expressed in all organs tested, and relatively abundant in testis and thymus. Deduced amino acid sequences of mouse SR-25 and human SR-25 showed 77.7% identity. SR-25 has a serine-arginine repeat (SR repeat) and two types of amino acid clusters: a serine cluster and a highly basic cluster. Based on the presence of many nuclear localizing signals and a similarity to RNA splicing proteins, SR-25 is strongly suggested to be a nuclear protein and may contribute to RNA splicing

FAMILIAL ALZHEIMER’S DISEASE

Five different types of point mutation of the β-amyloid precursor gene (APP) have been reported to cosegregate with familial Alzheimer’s disease (FAD) in each of examined pedigrees (Table 1). Here we report a screening result of the APP gene mutations in two Japanese pedigrees with FAD of an early onset type which have previously been reported (2, 3). Primer pairs corresponding respectively to each of 19 exons of the APP gene were designed. Polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) analysis was performed on genomic DNA of one affected member from each of these two pedigrees. In addition, a pair of primers was designed to assess specifically codon 717 of the APP gene even in the poorly-preserved sample of genomic DNA. PCR-SSCP analysis of all 19 exons of the APP gene of both patients did not show any mutations, but disclosed one polymorphism in the intron 9. Sequencing of exons 16 and 17 of the APP gene in both patients, where all reported pathogenic mutations are located, revealed normal sequences. The results support that the genetic defect causing FAD is heterogeneous and that most cases with FAD are apparently due to the gene-defect of other than the APP gene