Observation of machined surface and subsurface structure of hinoki (Chamaecyparis obtusa) produced in slow-speed orthogonal cutting using X-ray computed tomography

First online: 01 January 2015X-ray computed tomography (CT) was applied to non-destructive observation of machined surface and subsurface structure of hinoki (Chamaecyparis obtusa) produced in slow-speed orthogonal cutting. The cutting experiments were conducted under several cutting conditions and the chip formations were observed with a high-speed camera to be classified into four chip types. The difference in the quality of the machined surfaces produced in four types of chip formation was investigated. During type 0 chip formation, the workpiece was cut almost exactly at the path of the cutting edge, so no deformation was found on and beneath the machined surface. During type I chip formation, the direction of the fore-split, which is dependent on the arrangement of cells, determined the machined surface. During type II chip formation, the cutting tool sometimes tore part of the workpiece below the path of the cutting edge and the tore part was then compressed by the tool, remaining on the machined surface. During type III chip formation, part of the workpiece above the path of the cutting edge was compressed by the tool, instead of being removed as a chip, so the compression occurred in wide area. The relationship between the formation of the machining defects such as torn grain or the compressed cells and the way chip is separated, deformed, or removed was clarified in this study

『ドン・キホーテ』の人物像に関する一考察

博士(文学)神戸市外国語大

Causes and consequences of stress generation : Longitudinal associations of negative events, aggressive behaviors, rumination, and depressive symptoms

The present study examined the causes and consequences of stress generation in university students in Japan. A two-wave longitudinal study with an 8- or 9-week interval was conducted in the fall of 2020. Undergraduate and graduate students at four universities in Japan (N = 201) completed self-report measures assessing experiences of negative interpersonal dependent events, negative non-interpersonal events, and negative independent events at two times. At the same time, they also responded to measures of aggressive behaviors, trait rumination, and depressive symptoms. Path analyses revealed that baseline aggressive behaviors were positively associated with an increase in subsequent negative interpersonal dependent events, even after controlling for the influences of negative interpersonal dependent events, rumination, and depressive symptoms at baseline. However, aggressive behaviors were not significantly associated with subsequent negative non-interpersonal dependent events or negative independent events. These findings suggest that aggressive behaviors may have been a factor leading to interpersonal stress generation. Furthermore, all categories of negative event experiences predicted an increase in subsequent depressive symptoms, but not subsequent rumination, and rumination was not significantly associated with subsequent depressive symptoms. This research extends previous studies on the causes and consequences of stress generation conducted in the US by using specific measures of aggressive behaviors and including a non-restricted sample of university students in Japan

α1-Syntrophin–deficient skeletal muscle exhibits hypertrophy and aberrant formation of neuromuscular junctions during regeneration

α1-Syntrophin is a member of the family of dystrophin-associated proteins; it has been shown to recruit neuronal nitric oxide synthase and the water channel aquaporin-4 to the sarcolemma by its PSD-95/SAP-90, Discs-large, ZO-1 homologous domain. To examine the role of α1-syntrophin in muscle regeneration, we injected cardiotoxin into the tibialis anterior muscles of α1-syntrophin–null (α1syn−/−) mice. After the treatment, α1syn−/− muscles displayed remarkable hypertrophy and extensive fiber splitting compared with wild-type regenerating muscles, although the untreated muscles of the mutant mice showed no gross histological change. In the hypertrophied muscles of the mutant mice, the level of insulin-like growth factor-1 transcripts was highly elevated. Interestingly, in an early stage of the regeneration process, α1syn−/− mice showed remarkably deranged neuromuscular junctions (NMJs), accompanied by impaired ability to exercise. The contractile forces were reduced in α1syn−/− regenerating muscles. Our results suggest that the lack of α1-syntrophin might be responsible in part for the muscle hypertrophy, abnormal synapse formation at NMJs, and reduced force generation during regeneration of dystrophin-deficient muscle, all of which are typically observed in the early stages of Duchenne muscular dystrophy patients

Role of the VEGF-Flt-1-FAK pathway in the pathogenesis of osteoclastic bone destruction of giant cell tumors of bone

BACKGROUND: Giant cell tumors (GCTs) of bone are primary benign bone tumors that are characterized by a high number of osteoclast-like multinuclear giant cells (MNCs). Recent studies suggest that the spindle-shaped stromal cells in GCTs are tumor cells, while monocyte-like cells and MNCs are reactive osteoclast precursor cells (OPCs) and osteoclasts (OCs), respectively. In this study, we investigated the pathogenesis of osteoclastic bone destruction in GCTs by focusing on the role of the vascular endothelial growth factor (VEGF)-Flt-1 (type-1 VEGF receptor)-focal adhesion kinase (FAK) pathway. METHODS: The motility of OPCs cells was assessed by a chemotaxis assay and the growth of OPCs was examined using a cell proliferation assay. The expression of VEGF and activation of Flt-1 and FAK in clinical GCT samples and in OPCs were detected by immunohistochemistry and immunoblotting. The correlation between the expression levels of activated Flt-1 and FAK and clinical stages of GCTs was investigated by immunohistochemistry. RESULTS: In GCT samples, CD68, a marker of OPCs and OCs, co-localized with Flt-1. Conditioned media from GCT tissue (GCT-CM) enhanced the chemotaxis and proliferation of OPCs. GCT-CM also stimulated FAK activation in OPCs in vitro. Moreover, there was a correlation between the clinical stage of GCTs and the expression of tyrosine-phosphorylated Flt-1 and FAK. CONCLUSIONS: Our results suggest that the VEGF-Flt-1-FAK pathway is involved in the pathogenesis of bone destruction of GCTs

Vaccination and Infection as Causative Factors in Japanese Patients With Rasmussen Syndrome: Molecular Mimicry and HLA Class I

Rasmussen syndrome is an intractable epilepsy with a putative causal relation with cellular and humoral autoimmunity. Almost half of the patients have some preceding causative factors, with infections found in 38.2%, vaccinations in 5.9% and head trauma in 8.9% of Japanese patients. In a patient with seizure onset after influenza A infections, cross-reaction of the patient's lymphocytes with GluRε2 and influenza vaccine components was demonstrated by lymphocyte stimulation test. Database analyses revealed that influenza A virus hemagglutinin and GluRε2 molecules contain peptides with the patient's HLA class I binding motif (HLA − A*0201). The relative risks of HLA class I genotypes for Rasmussen syndrome are 6.1 (A*2402), 6.4 (A*0201), 6.3 (A*2601) and 11.4 (B*4601). The relative risks of HLA class I-A and B haplotypes are infinity (A*2601+B*5401), 21.1 (A*2402+B*1501), 13.3 (A*2402+B*4801) and 5.1 (A*2402+B*5201). Some alleles and haplotypes of HLA class I may be the risk factors in Japanese patients. Cross-reactivity of cytotoxic T lymphocytes may contribute to the processes leading from infection to the involvement of CNS