Wakayama-shi, Japan
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.


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The thalamic reticular nucleus (TRN), a cluster of GABAergic cells, is thought to regulate bottom-up and top-down streams of sensory processing in the loop circuitry between the thalamus and cortex. Provided that sensory inputs of different modalities interact in the TRN, the TRN could contribute to fast and flexible cross-modal modulation of attention and perception that incessantly takes place in our everyday life. Indeed, diverse subthreshold interactions of auditory and visual inputs have been revealed in TRN cells (Kimura, 2014). To determine whether such sensory interaction could extend across modalities as a universal neural mechanism, the present study examined TRN cell activities elicited by auditory and cutaneous electrical stimulations in anesthetized rats. Juxta-cellular recording and labeling techniques were used. Recordings were obtained from 129 cells. Auditory or somatosensory responses were modulated by subthreshold electrical stimulation or sound (noise burst) in the majority of recordings (77 of 85 auditory and 13 of 15 somatosensory cells). Additionally, 22 bimodal cells and seven cells that responded only to combined stimulation were recognized. Suppression was predominant in modulation that was observed in both early and repeatedly evoked late responses. Combined stimulation also induced de novo cell activities. Further, response latency and burst spiking were modulated. Axonal projections of cells showing modulation terminated in first- or higher-order thalamic nuclei. Nine auditory cells projected to somatosensory thalamic nuclei. These results suggest that the TRN could regulate sensory processing in the loop circuitry between the thalamus and cortex through the sensory interaction pervasive across modalities. © 2017 Elsevier B.V.


Patent
Wakayama Medical University and SBI Biotech Co. | Date: 2013-05-10

A monoclonal antibody against oncostatin M specific receptor beta subunit, a hybridoma capable of producing the same and a medicament for treating atopic dermatitis comprising the same.


Patent
Kyoto University, Wakayama Medical University, Ito, Shinkokai Medical Corporation and Toyo Kohan Co. | Date: 2016-07-20

The present invention provides a test method and an evaluation kit for determining the risk of antithyroid drug-induced agranulocytosis. More particularly, it provides a test method for determining the risk of antithyroid drug-induced agranulocytosis, including testing susceptibility polymorphism to antithyroid drug-induced agranulocytosis, and determining the risk of antithyroid drug-induced agranulocytosis, and an evaluation kit for the risk of antithyroid drug-induced agranulocytosis, containing a polynucleotide capable of detecting susceptibility polymorphism to antithyroid drug-induced agranulocytosis.


Patent
Kyoto University, Wakayama Medical University, Shinkokai Medical Corporation and Toyo Kohan Co. | Date: 2014-09-11

The present invention provides a test method and an evaluation kit for determining the risk of antithyroid drug-induced agranulocytosis. More particularly, it provides a test method for determining the risk of antithyroid drug-induced agranulocytosis, including testing susceptibility polymorphism to antithyroid drug-induced agranulocytosis, and determining the risk of antithyroid drug-induced agranulocytosis, and an evaluation kit for the risk of antithyroid drug-induced agranulocytosis, containing a polynucleotide capable of detecting susceptibility polymorphism to antithyroid drug-induced agranulocytosis.


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.


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.


Kokado M.,Wakayama Medical University
Investigative ophthalmology & visual science | Year: 2013

To investigate the effects of gene ablation of epiplakin on the homeostasis of corneal epithelium in mice. Light and transmission electron microscopic histology, immunohistochemistry, and real-time RT-PCR were carried out to evaluate the effects of the loss of epiplakin on structure and gene expression of cell-cell adhesion-related components in mice. Integrity against mechanical intervention and wound-healing response of corneal epithelium were also tested. Epiplakin protein was detected in the cells of the basal layer of corneal epithelium. Morphologically basal-like cells were observed in the suprabasal layer of adult epiplakin-null corneal epithelium, suggesting an impaired intraepithelial cell differentiation. Such abnormality was not detected in mice before the age of postnatal day 14. Epiplakin-deficient epithelium exhibits fragility against mechanical intervention as compared with wild-type epithelium. Although cell proliferation is suppressed, migration-dependent wound healing is promoted in epiplakin-null epithelium. E-cadherin expression was suppressed by the loss of epiplakin in the epithelium. Lacking epiplakin affects cell differentiation of the corneal epithelium, as well as its proliferation activity and its structural integrity. The mechanism of acceleration of cell migration in the epiplakin-null corneal epithelium is to be further investigated, although suppression of expression of E-cadherin might be included.


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.


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.


Our attention to a sensory cue of a given modality interferes with attention to a sensory cue of another modality. However, an object emitting various sensory cues attracts attention more effectively. The thalamic reticular nucleus (TRN) could play a pivotal role in such cross-modal modulation of attention given that cross-modal sensory interaction takes place in the TRN, because the TRN occupies a highly strategic position to function in the control of gain and/or gating of sensory processing in the thalamocortical loop. In the present study cross-modal interactions between visual and auditory inputs were examined in single TRN cells of anesthetised rats using juxta-cellular recording and labeling techniques. Visual or auditory responses were modulated by subthreshold sound or light stimuli, respectively, in the majority of recordings (46 of 54 visual and 60 of 73 auditory cells). However, few bimodal sensory cells were found. Cells showing modulation of the sensory response were distributed in the whole visual and auditory sectors of the TRN. Modulated cells sent axonal projections to first-order or higher-order thalamic nuclei. Suppression predominated in modulation that took place not only in primary responses but also in late responses repeatedly evoked after sensory stimulation. Combined sensory stimulation also evoked de-novo responses, and modulated response latency and burst spiking. These results indicate that the TRN incorporates sensory inputs of different modalities into single cell activity to function in sensory processing in the lemniscal and non-lemniscal systems. This raises the possibility that the TRN constitutes neural pathways involved in cross-modal attentional gating. © 2014 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.

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