Tokyo, Japan
Tokyo, Japan

Juntendo University is a private university in Japan. Its headquarters are on its campus in Bunkyo, Tokyo, for the School of Medicine and in Inzai, Chiba, for the School of Health and Sports Science. The university was established in 1838 for medical and in 1946 for other departments. It is nicknamed Jundai. Wikipedia.


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ABSTRACT: Conventional magnetic resonance images are usually evaluated using the image signal contrast between tissues and not based on their absolute signal intensities. Quantification of tissue parameters, such as relaxation rates and proton density, would provide an absolute scale; however, these methods have mainly been performed in a research setting. The development of rapid quantification, with scan times in the order of 6 minutes for full head coverage, has provided the prerequisites for clinical use. The aim of this review article was to introduce a specific quantification method and synthesis of contrast-weighted images based on the acquired absolute values, and to present automatic segmentation of brain tissues and measurement of myelin based on the quantitative values, along with application of these techniques to various brain diseases. The entire technique is referred to as “SyMRI” in this review. SyMRI has shown promising results in previous studies when used for multiple sclerosis, brain metastases, Sturge-Weber syndrome, idiopathic normal pressure hydrocephalus, meningitis, and postmortem imaging.This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. Copyright © 2017 Wolters Kluwer Health, Inc. All rights reserved.


CrowdReviews.com Partnered with Madridge Conferences to Announce International Conference on Immunology and Immunotechnology Immunology-2017 features highly enlightening and interactive sessions to encourage the exchange of ideas across a wide range of disciplines in the field of immunology. Immunology-2017 mainly showcases comprehensive approaches in immunology study and research. The field of Immunology is growing rapidly and its development is making tremendous impacts in medical sciences. Immunology-2017 invites the contributions related to immunology research. You can submit your work in these broad themes. Conference mainly focuses on: Clinical and cellular immunology Tumour and cancer immunology Neuro immunology Parasitology Autoimmunity and Therapathies Mucosal immunology Reproductive Immunology Immunobiology Infection & Inflammatory Disease Rheumatology Haematopoiesis Transplantation Immunology Virology Immunodermatology Molecular and Structural Immunology Veterinary Immunology and Immunopathology Allergology and Immunology All the abstracts should be submitted through Immunology-2017 Speakers: · Nadir Kadri, Karolinska Institute, Sweden · Pawel Gajdanowicz, Wroclaw Medical University, Poland · Joel Babdor, Stanford University School of Medicine, USA · Kwan Chow, Washington University, USA · Abdallah Badou, Cadi Ayyad University, Morocco Immunology-2017 Organizing Committee: · Carmen Fernández , Stockholm University, Sweden · Carl Borrebaeck, Lund University, Sweden · SY Seong, Seoul National University College of Medicine, South Korea · Shi, Guo-Ping, Brigham and Women's Hospital, USA · Gideon Berke, Weizmann Institute of Science, Isreal · Eyad Elkord, United Arab Emirates University, United ArabEmirates · Noah Isakov, Ben Gurion University of the Negev, Isreal · Joel Pomerantz, The Johns Hopkins University School of Medicine, USA · NanShan Chang, Institute of Molecular Medicine, Taiwan · Hisaya Akiba, Juntendo University School of Medicine, Japan · Ricardo Luiz Dantas Machado, Evandro Chagas Institute, Brazil Immunology-2017 is organizing an outstanding Scientific Exhibition/Program and anticipates the world’s leading specialists involved in Immunology Research. They welcome Sponsorship and Exhibitions from the Companies and Organizations who wish to showcase their products at this exciting event. Register for the conference and book your slots at: Contact person: Sumanjani immunology@madridge.com immunology@madridge.net Naples, FL, May 09, 2017 --( PR.com )-- International Conference Immunology and Immunotechnology is going to be held during November 1-3, 2017 in Barcelona, Spain.Immunology-2017 features highly enlightening and interactive sessions to encourage the exchange of ideas across a wide range of disciplines in the field of immunology. Immunology-2017 mainly showcases comprehensive approaches in immunology study and research. The field of Immunology is growing rapidly and its development is making tremendous impacts in medical sciences.Immunology-2017 invites the contributions related to immunology research. You can submit your work in these broad themes.Conference mainly focuses on:Clinical and cellular immunologyTumour and cancer immunologyNeuro immunologyParasitologyAutoimmunity and TherapathiesMucosal immunologyReproductive ImmunologyImmunobiologyInfection & Inflammatory DiseaseRheumatologyHaematopoiesisTransplantation ImmunologyVirologyImmunodermatologyMolecular and Structural ImmunologyVeterinary Immunology and ImmunopathologyAllergology and ImmunologyAll the abstracts should be submitted through online abstract submission or can be mailed at immunology@madridge.com Immunology-2017 Speakers:· Nadir Kadri, Karolinska Institute, Sweden· Pawel Gajdanowicz, Wroclaw Medical University, Poland· Joel Babdor, Stanford University School of Medicine, USA· Kwan Chow, Washington University, USA· Abdallah Badou, Cadi Ayyad University, MoroccoImmunology-2017 Organizing Committee:· Carmen Fernández , Stockholm University, Sweden· Carl Borrebaeck, Lund University, Sweden· SY Seong, Seoul National University College of Medicine, South Korea· Shi, Guo-Ping, Brigham and Women's Hospital, USA· Gideon Berke, Weizmann Institute of Science, Isreal· Eyad Elkord, United Arab Emirates University, United ArabEmirates· Noah Isakov, Ben Gurion University of the Negev, Isreal· Joel Pomerantz, The Johns Hopkins University School of Medicine, USA· NanShan Chang, Institute of Molecular Medicine, Taiwan· Hisaya Akiba, Juntendo University School of Medicine, Japan· Ricardo Luiz Dantas Machado, Evandro Chagas Institute, BrazilImmunology-2017 is organizing an outstanding Scientific Exhibition/Program and anticipates the world’s leading specialists involved in Immunology Research. They welcome Sponsorship and Exhibitions from the Companies and Organizations who wish to showcase their products at this exciting event.Register for the conference and book your slots at: http://immunology.madridge.com/register.php Contact person:Sumanjani


Investigations by scientists in Japan illustrate how the loss of a key mitochondrial protein facilitates the progression of Parkinson’s disease. The findings are published in Nature Communications (June 2017). There is much evidence to suggest that dysfunction within cellular components contributes to the development and progression of the neurodegenerative disorder, Parkinson’s disease. However, exactly how individual genes and proteins contribute to the degradation of this integral cellular structure is unclear. Mitochondria are sub-units within cells that help control biochemical processes such as energy production. They have a double-membrane structure, the inner membrane of which forms multiple layers or ‘cristae’. Each crista structure must remain intact in order for the mitochondria to perform their tasks effectively. Now, Hongrui Meng and Chikara Yamashita at Juntendo University Graduate School of Medicine in Tokyo, and co-workers across Japan, have shown how a mitochondrial protein called CHCHD2 plays a key role in maintaining cristae structure and mitochondria integrity. Meng and Yamashita’s team generated CHCHD2 mutant fruit flies (Drosophila), and examined what happened when CHCHD2 protein expression was lost. They found that this loss resulted in abnormal matrix structures and impairments to oxygen respiration in mitochondria. This in turn led to neuron loss through oxidative stress, and also to motor dysfunction – such as loss of climbing ability - as the flies aged. When the researchers introduced a wild-type form of human CHCHD2 and a metabolic regulator 4E-BP to the flies, the dysfunctions were reversed. Further investigations showed that CHCHD2 binds to a mitochondrial protein cytochrome c along with a cell death regulator MICS-1. This binding helps cells to function properly and ensure correct cell death signaling in both mammalian cells and Drosophila. As the team state’s in their paper published in Nature Communications, their results shed light on the role of CHCHD2 mutations in Parkinson’s disease and offer “potential therapeutic targets in Parkinson’s caused by mitochondrial dysfunction.” Background The recent discovery of a gene related to Parkinson’s disease, CHCHD2, is allowing scientists to directly investigate the molecular details behind the disorder in more depth. The gene encodes a protein, CHCHD2, the role of which Hongrui Meng and his team in Japan aimed to investigate using fruit fly and mouse models. The mutant fruit flies lacked the CHCHD2 protein, resulting in flies with shorter life spans and problems with motor function as they aged. The loss of the protein resulted in the integral structure of the flies’ mitochondria was disrupted. The researchers also discovered that, by affecting the oxygen respiration processes within mitochondria, the loss of CHCHD2 generates excess reactive oxygen species in the body. This in turn exacerbates oxidative stress and directly affects the function and survival of neurons in the body. Importantly, these phenotypes were not rescued by the reintroduction of CHCHD2 missense mutants associated with Parkinson’s disease, strongly suggesting that this disease develops by the loss of CHCHD2 function. These findings suggest that CHCHD2 is a key protein that regulates the mitochondrial respiratory function through stabilizing cytochrome c. Without it – through mutations in the CHCHD2 gene - mitochondria cannot function correctly, leading to the progression of Parkinson’s disease. The researchers believe their insights into the gene, its associated protein, and how the protein works to facilitate healthy functioning of mitochondria could inform future therapies for Parkinson’s disease and help scientists better understand the condition. Reference H. Meng, C. Yamashita, K. Shiba-Fukushima, T. Inoshita, M. Funayama, S. Sato, T. Hatta, T. Natsume, M. Umitsu, J. Takagi, Y. Imai, & N. Hattori. Loss of Parkinson’s disease-associated protein CHCHD2 affects crista structure and destabilizes cytochrome c. Mission Statement The mission of Juntendo University is to strive for advances in society through education, research, and healthcare, guided by the motto “Jin – I exist as you exist” and the principle of “Fudan Zenshin - Continuously Moving Forward”. The spirit of “Jin”, which is the ideal of all those who gather at Juntendo University, entails being kind and considerate of others. The principle of “Fudan Zenshin” conveys the belief of the founders that education and research activities will only flourish in an environment of free competition. Our academic environment enables us to educate outstanding students to become healthcare professionals patients can believe in, scientists capable of innovative discoveries and inventions, and global citizens ready to serve society. About Juntendo Juntendo was originally founded in 1838 as a Dutch School of Medicine at a time when Western medical education was not yet embedded as a normal part of Japanese society. With the creation of Juntendo, the founders hoped to create a place where people could come together with the shared goal of helping society through the powers of medical education and practices. Their aspirations led to the establishment of Juntendo Hospital, the first private hospital in Japan. Through the years the institution’s experience and perspective as an institution of higher education and a place of clinical practice has enabled Juntendo University to play an integral role in the shaping of Japanese medical education and practices. Along the way the focus of the institution has also expanded, now consisting of four undergraduate programs and three graduate programs, the university specializes in the fields of health and sports science and nursing health care and sciences, as well as medicine. Today, Juntendo University continues to pursue innovative approaches to international level education and research with the goal of applying the results to society.


Patent
The Uab Research Foundation, U.S. Army, Juntendo University and Foundation University | Date: 2014-06-27

Provided are methods of diagnosing IgA nephropathy in a subject. Optionally, the methods comprise isolating an IgG from the subject and determining whether the IgG binds to a galactose-deficient IgA1. Optionally, the methods comprise providing a biological sample from the subject and detecting in the sample a mutation in a IGH gene, wherein the mutation is in a nucleotide sequence encoding a complementarity determining region 3 (CDR3) of a IGH variable region. Optionally, the methods comprise determining a level of IgG specific for a galactose-deficient IgA1 in the subject. Also provided are methods of treating or reducing the risk of developing IgA nephropathy in a subject.


Patent
Otsuka Pharmaceutical Factory Inc. and Juntendo University | Date: 2015-10-28

The invention relates to a medicament for treating Alzheimers disease comprising as active ingredients a carbostyril derivative of the general formula:or a salt thereof; and donepezil or a salt thereof.


Yokomizo T.,Juntendo University
Journal of Biochemistry | Year: 2015

Leukotriene B4 (LTB4) is a potent inflammatory mediator derived from arachidonic acid. Two G protein-coupled receptors for LTB4 have been identified: a high-affinity receptor, BLT1, and a low-affinity receptor, BLT2. Both receptors mainly couple to pertussis toxin-sensitive Gi-like G proteins and induce cell migration. 12(S)-hydroxy-5Z,8E,10E-heptadecatrienoic acid (12-HHT) was identified to bind BLT2 with higher affinity than LTB4. Expression of BLT1 was confirmed in type 1 helper T cells, type 2 helper T cells, type 17 helper T cells, effector CD8+ T cells, dendritic cells and osteoclasts in addition to granulocytes, eosinophils and macrophages, and BLT1-deficient mice showed greatly reduced phenotypes in models of various inflammatory diseases, such as peritonitis, bronchial asthma, rheumatoid arthritis, atherosclerosis and osteoporosis. In mice, BLT2 expression is restricted to intestinal epithelial cells and epidermal keratinocytes. BLT2-deficient mice showed enhanced colitis after administration of dextran sulfate, possibly due to reduced intestinal barrier function. An aspirin-dependent reduction in 12-HHT production was responsible for delayed skin wound healing, showing that the 12-HHT/BLT2 axis also plays an important role in skin biology. BLT1 and BLT2 are therefore potential targets for the development of novel drugs. © 2014 The Authors 2014. Published by Oxford University Press on behalf of the Japanese Biochemical Society. All rights reserved.


Chiba Y.,Juntendo University
Dementia and Geriatric Cognitive Disorders | Year: 2012

Background: Non-motor symptoms are recognized to enable the early detection of Parkinson's disease (PD). It remains unknown when those symptoms appear in dementia with Lewy bodies (DLB). Method: We investigated the prevalence of 15 non-motor symptoms of PD at the onset of memory loss based on a standardized worksheet in 34 patients with DLB, 32 patients with Alzheimer's disease (AD) and 30 normal controls. Results: DLB patients exhibited a significantly higher prevalence of olfactory dysfunction, constipation, increased saliva and signs of rapid eye movement sleep behavior disorder at the onset of memory loss than AD patients and normal controls. Conclusions: Paying attention to non-motor symptoms of PD may help DLB diagnosis in the early stage, especially in terms of its differentiation from AD. Copyright © 2012 S. Karger AG, Basel.


Mizuno H.,Juntendo University
Current Opinion in Molecular Therapeutics | Year: 2010

The potential use of stem cell-based therapies for the repair and regeneration of various tissues and organs offers a paradigm shift that may provide alternative therapeutic solutions for several diseases. The clinical use of either embryonic stem cells or induced pluripotent stem cells remains limited because of cell regulations, ethical considerations and the requirement for genetic manipulation, although these cells are theoretically highly beneficial. Adipose-derived stem cells (ASCs) appear to be an ideal population of stem cells for practical regenerative medicine, given that they are plentiful, of autologous tissue origin and thus non-immunogenic, and are more easily available because of minimal ethical considerations. Although ASCs originate from mesodermal lineages, recent preclinical studies have demonstrated that the use of ASCs in regenerative medicine is not limited to mesodermal tissue, but can also extend to both exodermal and endodermal tissues and organs. This review summarizes and discusses current preclinical and clinical data on the use of ASCs in regenerative medicine and discusses the future applications of such cell-based therapies. © Thomson Reuters (Scientific) Ltd.


Inappropriate activation of the intrarenal renin-angiotensin system induces generation of reactive oxygen species and tubulointerstitial inflammation, which contribute to salt-sensitive hypertension (SSHT). Liver-type fatty acid-binding protein is expressed in proximal tubules in humans, but not in rodents, and may play an endogenous antioxidative role. The objective of the present study was to examine the antioxidative effect of liver-type fatty acid-binding protein on post-angiotensin II SSHT model in transgenic mice with selective overexpression of human liver-type fatty acid-binding protein in the proximal tubules. The transgenic mice showed marked protection against angiotensin II-induced SSHT. Overexpression of tubular liver-type fatty acid-binding protein prevented intrarenal T-cell infiltration and also reduced reactive oxygen species generation, intrarenal renin-angiotensin system activation, and monocyte chemotactic protein-1 expression. We also performed an in vitro study using the murine proximal tubular cell lines with or without recombinant liver-type fatty acid-binding protein and murine proximal tubular cell lines transfected with human liver-type fatty acid-binding protein, and found that gene transfection of liver-type fatty acid-binding protein and, in part, recombinant liver-type fatty acid-binding protein administration had significantly attenuated angiotensin II-induced reactive oxygen species generation and the expression of angiotensinogen and monocyte chemotactic protein-1 in murine proximal tubular cell lines. These findings indicated that liver-type fatty acid-binding protein in the proximal tubules may protect against angiotensin II-induced SSHT by attenuating activation of the intrarenal renin-angiotensin system and reducing oxidative stress and tubulointerstitial inflammation. Present data suggest that liver-type fatty acid-binding protein in the proximal tubules may be a novel therapeutic target for SSHT.


Takai T.,Juntendo University
Allergology International | Year: 2012

Thymic stromal lymphopoietin (TSLP) is an IL-7-like cytokine initially identified in the culture supernatant of a thymic stromal cell line. Highly expressed in the epidermis in skin lesions of atopic dermatitis patients, TSLP was subsequently found to be a critical factor linking responses at interfaces between the body and environment (skin, airway, gut, ocular tissues, and so on) to Th2 responses. Recent studies have revealed that various cell types other than epithelial cells and epidermal keratinocytes (such as mast cells, airway smooth muscle cells, fibroblasts, dendritic cells, trophoblasts, and cancer or cancer-associated cells) also express TSLP. Environmental factors such as Toll-like receptor ligands, a Nod2 ligand, viruses, microbes, allergen sources, helminths, diesel exhaust, cigarette smoke, and chemicals trigger TSLP production. Proinflammatory cytokines, Th2-related cytokines, and IgE also induce or enhance TSLP production, indicating cycles of amplification. Skin barrier injury, increased epidermal endogenous protease activity, and less epidermal Notch signaling, all of which have been reported in atopic dermatitis, and keratinocyte-specific loss of retinoid X receptors and treatment of skin with agonists for vitamin D receptor in mice induce TSLP production, Th2 response, or atopic dermatitis-like inflammation. The transcription factors NF-κB and AP-1, nuclear receptors, single nucleotide polymorphisms, microRNAs, and the peptidyl-proryl isomerase Pin1 regulate TSLP mRNA expression transcriptionally or posttranscriptionally. This review focuses on events upstream of TSLP production, which is critical in allergic diseases and important in other TSLP-related disorders i.e. production sites, cellular sources, environmental and endogenous triggers and regulatory factors, and regulatory mechanisms of gene expression. ©2012 Japanese Society of Allergology.

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