木造建物の耐震性能の力学的評価に関する研究

八戸工業大

Structures and Magnetic Properties of Tm1-yYyMn1-xCoxO3

The structure and magnetic properties of Tm1−y Y y Mn1−x Co x O3 with 0 ≦ x ≦ 0.5 and 0 ≦ y ≦ 0.3 were investigated by X-ray diffraction, specific heat and magnetization measurements. Thulium manganite TmMnO3 prepared by solid-state synthesis at ambient pressure is hexagonal and antiferromagnetic with a Nèel temperature T N of 86 K. The substitution of Y for Tm in TmMnO3 does not greatly affect the fundamental hexagonal structure. The magnetization and specific heat measurement results for Tm1−y Y y MnO3 can be qualitatively explained in terms of the dilution effect of Tm by Y. On the other hand, the structure of TmMn1−x Co x O3 changes gradually from hexagonal to orthorhombic with the substitution of Co for Mn; hexagonal and orthorhombic phases coexist in samples for x ≦ 0.3 whereas TmMn0.6Co0.4O3 is almost a single orthorhombic phase. The magnetization of TmMn0.6Co0.4O3 in a field of 250 Oe increases rapidly at about 60K with decreasing temperature. The difference between zero-field-cooled (ZFC) and field-cooled (FC) magnetizations increases remarkably at about 60 K. Moreover, the temperature dependences of the ZFC and the FC magnetizations exhibit peaks at about 40 and 30K, respectively. Thus, TmMn1−x Co x O3 exhibits complex magnetic properties

Accumulation of Immunity in Heavy-Tailed Sexual Contact Networks Shapes Mpox Outbreak Sizes

Many countries affected by the global outbreak of mpox in 2022 have observed a decline in cases. Our mathematical model accounting for heavy-tailed sexual partnership distributions suggests that mpox epidemics can hit the infection-derived herd immunity threshold and begin to decline with less than 1% of sexually active MSM population infected regardless of interventions or behavioural changes. Consistently, we found that many countries and US states experienced an epidemic peak with cumulative cases of around 0.1-0.5% of MSM population. The observed decline in cases may not necessarily be attributable to interventions or behavioural changes primarily

An Autopsy Case of Ruptured Hepatic Angiosarcoma Treated by Transcatheter Arterial Embolization

An 80-year-old Japanese man presented to our hospital with intra-abdominal hemorrhage due to a ruptured liver tumor. Transcatheter arterial embolization (TAE) temporarily achieved hemostasis, but he died following re-rupture 4 days later. Based on autopsy findings, the liver tumor was diagnosed as hepatic angiosarcoma. Embolic agents used during embolization were identified within the hepatic small interlobular arteries. However, there were no findings of tumor cell necrosis or ischemic change in the angiosarcoma. In the present case, TAE alone did not induce ischemia-induced tumor necrosis, suggesting that TAE might be unsuitable to treat hepatic angiosarcoma. Treatment optimization for ruptured hepatic angiosarcoma is desired

Prenatal diagnosis of severe mitochondrial diseases caused by nuclear gene defects: a study in Japan

Prenatal diagnoses of mitochondrial diseases caused by defects in nuclear DNA (nDNA) or mitochondrial DNA have been reported in several countries except for Japan. The present study aimed to clarify the status of prenatal genetic diagnosis of mitochondrial diseases caused by nDNA defects in Japan. A comprehensive genomic analysis was performed to diagnose more than 400 patients, of which, 13 families (16 cases) had requested prenatal diagnoses. Eight cases diagnosed with wild type homozygous or heterozygous variants same as either of the heterozygous parents continued the pregnancy and delivered healthy babies. Another eight cases were diagnosed with homozygous, compound heterozygous, or hemizygous variants same as the proband. Of these, seven families chose to terminate the pregnancy, while one decided to continue the pregnancy. Neonatal- or infantile-onset mitochondrial diseases show severe phenotypes and lead to lethality. Therefore, such diseases could be candidates for prenatal diagnosis with careful genetic counseling, and prenatal testing could be a viable option for families

Two distinct prions in fatal familial insomnia and its sporadic form

Abstract Fatal familial insomnia is a genetic prion disease, which is associated with the aspartic acid to asparagine substitution at codon 178 of the prion protein gene. Although the hallmark pathological feature is thalamic and olivary degeneration, there is a patient with an atypical fatal familial insomnia without the hallmark feature. The cause of the pathological variability is unclear. We analysed a Japanese fatal familial insomnia kindred and compared one atypical clinicopathological fatal familial insomnia phenotype case and typical fatal familial insomnia phenotype cases with transmission studies using multiple lines of knock-in mice and with protein misfolding cyclic amplification. We also analysed the transmissibility and the amplification properties of sporadic fatal insomnia. Transmission studies revealed that the typical fatal familial insomnia with thalamic and olivary degeneration showed successful transmission only using knock-in mice expressing human–mouse chimeric prion protein gene. The atypical fatal familial insomnia with spongiform changes showed successful transmission only using knock-in mice expressing bank vole prion protein gene. Two sporadic fatal insomnia cases with thalamic and olivary degeneration showed the same transmissibility as the typical fatal familial insomnia phenotype. Interestingly, one sporadic fatal insomnia case with thalamic/olivary degeneration and spongiform changes showed transmissibility of both the typical and atypical fatal familial insomnia phenotypes. Protein misfolding cyclic amplification could amplify both typical fatal familial insomnia cases and sporadic fatal insomnia cases but not the atypical fatal familial insomnia phenotype or other sporadic Creutzfeldt–Jakob disease subtypes. In addition to clinical findings and neuropathological features, the transmission properties and the amplification properties were different between the typical and atypical fatal familial insomnia phenotypes. It is suggested that two distinct prions were associated with the diversity in the fatal familial insomnia phenotype, and these two prions could also be detected in sporadic fatal insomnia