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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Kiguchi N.,Wakayama Medical University | Kobayashi Y.,Wakayama Medical University | Kishioka S.,Wakayama Medical University
Current Opinion in Pharmacology | Year: 2012

There has been recent evidence showing the correlation between neuroinflammation owing to the chemokine-cytokine network and neuropathic pain. Chemokines and cytokines are derived from several types of cells in the peripheral and central nervous systems following nerve injury, and are largely involved in the pathogenesis of neuropathic pain. The roles of typical inflammatory cytokines such as interleukin-1β have become the recent center of attention. There is growing evidence that inflammatory chemokines (CCL2, CCL3, and fractalkine) play pivotal roles in neuropathic pain. Further investigations concerning the functions of the chemokine-cytokine network-mediated regulation of neuroinflammation may lead to novel therapeutic strategies against intractable neuropathic pain. © 2011 Elsevier Ltd. All rights reserved.


Exposure to stressors causes substantial effects on the perception and response to pain. In several animal models, chronic stress produces hyperalgesia. The insular (IC) and anterior cingulate cortices (ACC) are the regions exhibiting most reliable pain-related activity. And the IC and ACC play an important role in pain modulation via descending pain modulatory system. In the present study we examined the expression of phospho-cAMP response element-binding protein (pCREB) and δFosB and the acetylation of histone H3 in the IC and ACC after forced swim stress (FS) and complete Freund's adjuvant (CFA) injection to clarify changes in the cerebral cortices that affect the activity of the descending pain modulatory system in rats with stress-induced hyperalgesia. CFA injection into the hindpaw or FS (day 1, 10. min; days 2-3, 20. min) induced a significant increase in the expression of pCREB and δFosB and the acetylation of histone H3 in the IC. Quantitative image analysis showed that the numbers of δFosB-immunoreactivity (IR) cells in the bilateral anterior and posterior IC (AIC and PIC) were significantly higher in the CFA group (AIC R, 548.0. ±. 98.6; AIC L, 433.5. ±. 89.4; PIC R, 546.1. ±. 72.8; PIC L, 415.5. ±. 53.5) than those in the naive group (AIC R, 86.6. ±. 14.8; AIC L, 85.5. ±. 24.7; PIC R, 124.5. ±. 29.9; PIC L, 107.0. ±. 19.8, p<. 0.01). However the FS prior to the CFA injection enhanced the mechanical hyperalgesia and attenuated the expression of pCREB and δFosB and the acetylation of histone H3 in the IC. There was no significant difference in the numbers of δFosB-IR cells in the bilateral PIC between the FS. +. CFA and naive groups. These findings suggest neuroplasticity in the IC after the FS, which may be involved in the enhancement of CFA-induced mechanical hyperalgesia through dysfunction of the descending pain modulatory system. © 2015 IBRO.


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.


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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