Kanazawa Medical University

About: Kanazawa Medical University is a education organization based out in Kanazawa, Japan. It is known for research contribution in the topics: Population & Cancer. The organization has 3103 authors who have published 6322 publications receiving 144592 citations. The organization is also known as: Kanazawa ika daigaku.

Sirtuins and Type 2 Diabetes: Role in Inflammation, Oxidative Stress, and Mitochondrial Function.

Abstract: The rising incidence of type 2 diabetes mellitus (T2DM) is a major public health concern, and novel therapeutic strategies to prevent T2DM are urgently needed worldwide. Aging is recognized as one of the risk factors for metabolic impairments, including insulin resistance and T2DM. Inflammation, oxidative stress, and mitochondrial dysfunction are closely related to both aging and metabolic disease. Calorie restriction (CR) can retard the aging process in organisms ranging from yeast to rodents and delay the onset of numerous age-related disorders, such as insulin resistance and diabetes. Therefore, metabolic CR mimetics may represent new therapeutic targets for insulin resistance and T2DM. Sirtuin 1 (SIRT1), the mammalian homolog of Sir2, was originally identified as a nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase. The activation of SIRT1 is closely associated with longevity under CR, and it is recognized as a CR mimetic. Currently, seven sirtuins have been identified in mammals. Among these sirtuins, SIRT1 and SIRT2 are located in the nucleus and cytoplasm, SIRT3 exists predominantly in mitochondria, and SIRT6 is located in the nucleus. These sirtuins regulate metabolism through their regulation of inflammation, oxidative stress and mitochondrial function via multiple mechanisms, resulting in the improvement of insulin resistance and T2DM. In this review, we describe the current understanding of the biological functions of sirtuins, especially SIRT1, SIRT2, SIRT3, and SIRT6, focusing on oxidative stress, inflammation, and mitochondrial function, which are closely associated with aging.

Short-term treatment outcome study for the management of temporomandibular joint closed lock. A comparison of arthrocentesis to nonsurgical therapy and arthroscopic lysis and lavage.

Abstract: Objective The aim of this study is to compare the clinical short-term results and efficacy of arthrocentesis with those of nonsurgical treatments and arthroscopic surgery for the management of temporomandibular joint closed lock. Study Design The three groups consisted of 63 consecutive patients treated nonsurgically, 20 patients treated with arthrocentesis, and 25 patients treated with arthroscopic surgery. All patients rated their pain level on a visual analogue scale and completed a pain, jaw dysfunction, and activity-limiting questionnaire before and 6 months after the procedure. Each patient's jaw opening was also scaled. The success rate of each procedure was calculated according to our success criteria. The clinical efficacy of each procedure was evaluated in successfully treated subgroups in which the between-group and within-group differences of the obtained data were statistically tested. Results The success rate was 55.6% in the nonsurgically treated group, 70% in the arthrocentesis group, and 91% in the arthroscopy group. With respect to efficacy, all posttreatment scores showed significant improvements in within-group differences, but no between-group differences were found between the arthrocetesis group and the other two groups. Conclusion Arthrocentesis was considered as an intervening treatment modality between nonsurgical treatment and arthroscopic surgery on the basis of its short-term outcome. Although the treatment efficacy was comparable with arthroscopic surgery, this procedure was thought to be indicated for the patients with acute temporomandibular joint closed lock who were refractory to medication and mandibular manipulation rather than the alternative of arthroscopic surgery.

Role of the endothelial-to-mesenchymal transition in renal fibrosis of chronic kidney disease

Abstract: All types of progressive chronic kidney disease (CKD) inevitably induce renal fibrosis, the hallmark of which is the activation and accumulation of a large number of matrix-producing fibroblasts or myofibroblasts. The activated fibroblasts or myofibroblasts are derived from diverse origins, such as residential fibroblasts, vascular pericytes, epithelial-to-mesenchymal transition (EMT), and bone marrow (circulating fibrocytes). Recently, endothelial-to-mesenchymal transition (EndMT) or endothelial-to-myofibroblast transition has also been suggested to promote fibrosis and is recognized as a novel mechanism for the generation of myofibroblasts. Similar to EMT, during EndMT, endothelial cells lose their adhesion and apical–basal polarity to form highly invasive, migratory, spindle-shaped, elongated mesenchymal cells. More importantly, biochemical changes accompany these distinct changes in cell polarity and morphology, including the decreased expression of endothelial markers and the acquisition of mesenchymal markers. This review highlights evidence supporting the important role of EndMT in the development of renal fibrosis in CKD and its underlying mechanisms, including novel biological significance of microRNA regulation.