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Wakayama-shi, Japan

Wakayama Medical University is a public university in Wakayama, Wakayama, Japan. The predecessor of the school was founded in 1945, and it was chartered as a university in 1948. Wikipedia.

Kanazawa N.,Wakayama Medical University
Journal of Dermatological Science | Year: 2012

Hereditary autoinflammatory syndromes are monogenic disorders with an inborn error of innate immunity, and include periodic fever syndromes such as familial Mediterranean fever (FMF), tumor necrosis factor receptor-associated periodic syndrome and cryopyrin-associated periodic syndromes (CAPS), pyogenic diseases such as pyogenic arthritis, pyoderma gangrenosum and acne syndrome (PAPAS), and granulomatous diseases such as Blau syndrome. By identifying the genetic abnormalities and subsequent analyses of the molecular mechanisms underlying these disorders, several critical in vivo pathways for inflammatory processes have been discovered. In this review, three categories of autoinflammatory disorders are discussed: inflammasomopathies, receptor antagonist deficiencies and proteasome disability syndromes. Inflammasomopathies are diseases with dysregulated NLRP3 inflammasome activation, and include CAPS with NLRP3, FMF with MEFV, and PAPAS with PSTPIP1 mutations. Analyses of these diseases have clarified some critical pathways regulating NLRP3 inflammasome signaling. Receptor antagonist deficiencies include the newly defined deficiency for interleukin-1 receptor antagonist resulting in sterile multifocal osteomyelitis with periostosis and pustulosis, and deficiency for interleukin-36 receptor antagonist resulting in generalized pustular psoriasis. The identification of these genetic abnormalities has revealed a critical role for receptor antagonists of IL-1 family cytokines in regulating neutrophil activation/recruitment. Finally, proteasome disability syndromes with PSMB8 mutations include Nakajo-Nishimura syndrome and related disorders distributed globally. Analyses of these diseases have unexpectedly shown a critical role of the ubiquitin-proteasome system in the regulation or homeostasis of inflammation/metabolism. Since there still remain a number of predicted but undefined hereditary autoinflammatory syndromes, further clinical and genetic approaches are required to discover novel in vivo critical inflammatory pathways. © 2012 Japanese Society for Investigative Dermatology. Source

Minamide A.,Wakayama Medical University
Journal of neurosurgery. Spine | Year: 2013

The authors undertook this study to document the clinical outcomes of microendoscopic laminotomy, a minimally invasive decompressive surgical technique using spinal endoscopy for lumbar decompression, in patients with lumbar spinal stenosis (LSS). A total of 366 patients were enrolled in the study and underwent microendoscopic laminotomy between 2007 and 2010. Indications for surgery were single- or double-level LSS, persistent neurological symptoms, and failure of conservative treatment. Microendoscopy provided wide visualization through oblique lenses and allowed bilateral decompression via a unilateral approach, through partial resection of the base of the spinous process, thereby preserving the supraspinous and interspinous ligaments and contralateral musculature. Clinical symptoms and signs of low-back pain were evaluated prior to and following surgical intervention by applying the Japanese Orthopaedic Association (JOA) scoring system, Roland-Morris Disability Questionnaire (RMDQ), Japanese Orthopaedic Association Back Pain Evaluation Questionnaire (JOABPEQ), and 36-Item Short Form Health Survey (SF-36). These items were evaluated preoperatively and 2 years postoperatively. Effective circumferential decompression was achieved in all patients. The 2-year follow-up evaluation was completed for 310 patients (148 men and 162 women; mean age 68.7 years). The average recovery rate based on the JOA score was 61.3%. The overall results were excellent in 34.9% of the patients, good in 34.9%, fair in 21.7%, and poor in 8.5%. The mean RMDQ score significantly improved from 11.3 to 4.8 (p < 0.001). In all categories of both JOABPEQ and SF-36, scores at 2 years' follow-up were significantly higher than those obtained before surgery (p < 0.001). Twelve surgery-related complications were identified: dural tear (6 cases [1.9%]), wrong-level operation (1 [0.3%]), transient neuralgia (4 [1.3%]), and infection (1 [0.3%]). All patients recovered, and there were no serious postoperative complications. Microendoscopic laminotomy is a safe and very effective minimally invasive surgical technique for the treatment of degenerative LSS. Source

Ino K.,Wakayama Medical University
Current Opinion in Obstetrics and Gynecology | Year: 2011

Purpose of Review: Ovarian cancer is the leading cause of cancer death among gynecologic malignancies despite significant advances in cytoreductive surgery and chemotherapy, and novel therapeutic approaches are urgently needed. Immunotherapy is one of these strategies; however, its clinical applications have shown limited efficacy. This may be attributed to tumor-induced immune tolerance, and much attention has been paid to overcoming these immune resistance mechanisms. This review focuses on the immunoregulatory enzyme indoleamine 2,3-dioxygenase (IDO) and shows the role of IDO and its clinical potential in ovarian cancer. Recent Findings: IDO suppresses the proliferation of effector T cells or natural killer cells and their killer functions. In ovarian cancer, high IDO expression in tumor cells was correlated with a reduced number of tumor-infiltrating lymphocytes. The IDO expression was also correlated with advanced surgical stage and impaired survival. Preclinical studies in mice demonstrated that oral administration of IDO inhibitors suppressed peritoneal dissemination and potentiated the antitumor efficacy of chemotherapeutic agents. Summary: IDO induces immune tolerance and promotes ovarian cancer progression. Tumoral IDO expression is correlated with impaired clinical outcome. IDO inhibition may therefore be a promising strategy to restore host antitumor immunity and to enhance the antitumor potential of current chemotherapy or immunotherapy for advanced ovarian cancer. © 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins. Source

Nishimoto N.,Wakayama Medical University
Clinical Pharmacology and Therapeutics | Year: 2010

Interleukin (IL)-6 is a multifunctional cytokine that regulates immune response, inflammation, and hematopoiesis. Although IL-6 plays several important physiological roles, deregulated overproduction of IL-6 causes various clinical symptoms and abnormalities in laboratory test results. Overproduction of IL-6 has been shown to underlie a number of autoimmune and inflammatory diseases, including rheumatoid arthritis (RA), systemic-onset juvenile idiopathic arthritis (soJIA), and Castleman's disease, as well as malignancies such as multiple myeloma and mesothelioma. Blocking of IL-6 signaling may be therapeutic in diseases characterized by pathological IL-6 overproduction. This review provides an overview of IL-6 as a therapeutic target in candidate inflammatory diseases. © 2010 American Society2010 American Society for Clinical Pharmacology and Therapeutics. Source

Kanazawa N.,Wakayama Medical University
Allergology International | Year: 2012

Nakajo-Nishimura syndrome (ORPHA2615; also registered as Nakajo syndrome in OMIM#256040) is a distinct inherited inflammatory and wasting disease, originally reported from Japan. This disease usually begins in early infancy with a pernio-like rash, especially in winter. The patients develop periodic high fever and nodular erythema-like eruptions, and gradually progress lipomuscular atrophy in the upper body, mainly the face and the upper extremities, to show the characteristic thin facial appearance and long clubbed fingers with joint contractures. So far about 30 cases have been reported from Kansai, especially Wakayama and Osaka, Tohoku and Kanto areas. At present, about 10 cases are confirmed to be alive only in the Kansai area, including one infant case in Wakayama. However, more cases are expected to be added in the near future. Although cause of the disease has long been undefined, a homozygous mutation of the PSMB8 gene, which encodes the β5i subunit of immunoproteasome, has been identified to be responsible in 2011. By analyses of the patientsderived cells and tissues, it has been suggested that accumulation of ubiquitinated and oxidated proteins due to immunoproteasome dysfunction causes hyperactivation of p38 mitogen-activated protein kinase and interleukin-6 overproduction. Since similar diseases with PSMB8 mutations have recently been reported from Europe and the United States, it is becoming clear that Nakajo-Nishimura syndrome and related disorders form proteasome disability syndromes, a new category of autoinflammatory diseases distributed globally. ©2012 Japanese Society of Allergology. Source

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