Meiji University of Integrative Medicine is a private university in Hiyoshi, Kyoto, Japan. The predecessor of the school was founded in 1925. It was chartered as a junior college in 1978 and became a four-year college in 1983. The present name of the school was adopted in 2008. Wikipedia.
Sun L.,University of Texas Health Science Center at Tyler |
Guo J.,University of Texas Health Science Center at Tyler |
Brown R.,University of Texas Health Science Center at Tyler |
Amagai T.,Meiji University of Integrative Medicine |
And 2 more authors.
Aging Cell | Year: 2010
Age-related thymic involution may be triggered by gene expression changes in lymphohematopoietic and/or nonhematopoietic thymic epithelial cells (TECs). The role of epithelial cell-autonomous gene FoxN1 may be involved in the process, but it is still a puzzle because of the shortage of evidence from gradual loss-of-function and exogenous gain-of-function studies. Using our recently generated loxP-floxed-FoxN1(fx) mouse carrying the ubiquitous CreERT (uCreERT) transgene with a low dose of spontaneous activation, which causes gradual FoxN1 deletion with age, we found that the uCreERT-fx/fx mice showed an accelerated age-related thymic involution owing to progressive loss of FoxN1+ TECs. The thymic aging phenotypes were clearly observable as early as at 3-6 months of age, resembling the naturally aged (18-22-month-old) murine thymus. By intrathymically supplying aged wild-type mice with exogenous FoxN1-cDNA, thymic involution and defective peripheral CD4+ T-cell function could be partially rescued. The results support the notion that decline of a single epithelial cell-autonomous gene FoxN1 levels with age causes primary deterioration in TECs followed by impairment of the total postnatal thymic microenvironment, and potentially triggers agerelated thymic involution in mice. © 2010 The Authors Journal compilation © Blackwell Publishing Ltd/Anatomical Society of Great Britain and Ireland 2010.
Iwai N.,Meiji University of Integrative Medicine |
Fumino S.,Kyoto Prefectural University of Medicine
Surgery Today | Year: 2013
The goal of surgery for anorectal malformations (ARM) is to achieve good bowel, urinary, and sexual functions, as well as the ability for children to become healthy adults. Various surgical procedures and surgical management protocols have been explored or devised by pediatric surgeons. These are described in this review. Making a correct type classification by invertography, fistelography and urethrography in the neonatal period allows pediatric surgeons to select an appropriate surgical strategy. Surgery for low-type malformations is principally neonatal perineoplasty, while that for intermediate- or high-type malformations is colostomy, followed by a pull-through operation during infancy. Posterior sagittal anorectoplasty or laparoscopy-assisted surgery has recently been accepted as alternative procedures. Fecal incontinence represents a devastating problem that often prevents a patient from becoming socially accepted and may cause serious psychological sequelae. One-third of adult patients with high- or intermediate-type malformations occasionally complain of fecal incontinence after surgery. Most patients with ARM have normal urinary function if they do not have urinary tract or sacral anomalies. These associated anomalies also influence the prognosis for sexual function, especially in males. Some female patients have experienced normal vaginal delivery and had children. In patients with cloacal malformation, however, fertility or sexual problems are also often present. Based on this information, it is clear that only well-planned and systemic treatments can provide a good functional prognosis after making a correct classification in the neonatal period. © 2012 Springer Japan.
Niwa F.,Kyoto Prefectural University of Medicine |
Kuriyama N.,Kyoto Prefectural University of Medicine |
Nakagawa M.,Kyoto Prefectural University of Medicine |
Imanishi J.,Meiji University of Integrative Medicine
Geriatrics and Gerontology International | Year: 2012
Aim: To understand the characteristics of peripheral immunity in patients with Parkinson's disease (PD), we investigated the natural killer (NK) cell activity and lymphocyte subpopulations including regulatory T (Treg) cells and type 17 helper T (Th17) cells. Methods: Peripheral blood was collected from 29 PD patients (mean age 70.4 years) and 30 healthy controls (mean age 68.9 years). NK cell activity was measured by a calcein acetoxymethyl ester release assay using NK-sensitive K562 cells, peripheral NK cells and lymphocytes subsets were analyzed using flow cytometry techniques. Results: Comparison of the two groups demonstrated that the percentage of NK cells increased and that of helper T cells, particularly type 1 (Th1), decreased in patients with PD. There was no evidence of Th1/Th2 or Treg/Th17 cell predominance in PD. Moreover, the increase of NK cells and the decrease of Th1 cells correlated with Unified Parkinson's Disease Rating Scale scores and the heart-to-mediastinum ratios based on myocardial 123I-metaiodobenzylguanidine uptake, both of which represent disease severity in patients with PD. Conclusion: Our investigation indicates that a certain proportion of NK cells and other lymphocytes in the peripheral blood of patients with PD and their association with disease severity may reflect the effect of innate immunity in patients with PD in addition to the effect of dopaminergic-related agents. © 2011 Japan Geriatrics Society.
Hoshino A.,Kyoto Prefectural University |
Mita Y.,Kyoto Prefectural University |
Okawa Y.,Kyoto Prefectural University |
Ariyoshi M.,Kyoto Prefectural University |
And 6 more authors.
Nature Communications | Year: 2013
Cumulative evidence indicates that mitochondrial dysfunction has a role in heart failure progression, but whether mitochondrial quality control mechanisms are involved in the development of cardiac dysfunction remains unclear. Here we show that cytosolic p53 impairs autophagic degradation of damaged mitochondria and facilitates mitochondrial dysfunction and heart failure in mice. Prevalence and induction of mitochondrial autophagy is attenuated by senescence or doxorubicin treatment in vitro and in vivo. We show that cytosolic p53 binds to Parkin and disturbs its translocation to damaged mitochondria and their subsequent clearance by mitophagy. p53-deficient mice show less decline of mitochondrial integrity and cardiac functional reserve with increasing age or after treatment with doxorubicin. Furthermore, overexpression of Parkin ameliorates the functional decline in aged hearts, and is accompanied by decreased senescence-associated β-galactosidase activity and proinflammatory phenotypes. Thus, p53-mediated inhibition of mitophagy modulates cardiac dysfunction, raising the possibility that therapeutic activation of mitophagy by inhibiting cytosolic p53 may ameliorate heart failure and symptoms of cardiac ageing. © 2013 Macmillan Publishers Limited.
Taguchi R.,Meiji University of Integrative Medicine |
Kitakoji H.,Meiji University of Integrative Medicine
Brain Research | Year: 2010
Acupuncture is widely used to relieve pain; however, the mechanism underlying electroacupuncture analgesia (EAA) during inflammatory pain is unclear. We investigated whether endogenous peripheral opioid receptors participated in EAA during hyperalgesia elicited by carrageenan-induced inflammation. Moreover, we investigated which subtype of opioid receptor was involved in EAA. Carrageenan was subcutaneously administered by intraplanter (i.pl.) injection into the left hind paw. Nociceptive thresholds were measured using the paw pressure threshold (PPT). Rats received 3 Hz electroacupuncture (EA) for 1 h after carrageenan injection. The nonselective peripheral opioid receptor antagonist, naloxone methiodide, was administered by i.pl. injection of the inflamed paw 5 min before EA. Also, animals received i.pl. or intravenous (i.v.) injection of selective antagonists against μ(D-Phe-Cys-Tyr-D-Trp-Orn- Thr-Pen-ThrNH2, CTOP), δ(naltrindole, NTI), or κ (nor-Binaltorphimine, nor-BNI) opioid receptors 1 h before EA. PPT decreased significantly 3 h after carrageenan injection. EA resulted in significant increases of PPT, moreover, PPT elevations persisted for 9 h after carrageenan injection. PPT elevations produced by EA were antagonized by local i.pl. injection of naloxone methiodide at 3 and 5 h after cessation of EA. NTI, nor-BNI and CTOP blocked EAA from immediately, 1 h, and 3 h after EA cessation, respectively. The EAA in the inflamed paw could not be blocked by i.v. injection of NTI, nor-BNI and CTOP. These findings suggest that peripheral μ, δ and κ receptors on peripheral nerve terminals are activated by EA, although there is a time difference among these activations. © 2010 Elsevier B.V. All rights reserved.