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.
News Article | June 7, 2017
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.
News Article | May 9, 2017
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 email@example.com firstname.lastname@example.org 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 email@example.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
Nakazato T.,Juntendo University
Experimental Brain Research | Year: 2013
The role of serotonin in stress and anxiety, particularly in social environments, is not well understood. Selective serotonin reuptake inhibitors are useful for patients that experience social anxiety; however, their mechanism of action has not been fully characterized. Dopamine is known to operate in different temporal modes (fast phasic, intermediate, and tonic changes). We hypothesized that serotonin may also operate in temporal modes in the context of social stress. We used wireless voltammetry (4 Hz) to investigate changes in extracellular ventral striatal serotonin and dopamine during a test of repeated social interactions between two rats. Test rats (electrode-implanted; n = 5) and counter rats (n = 6) were placed in separate sections of a partitioned box. The partitions were raised to allow interactions for 10 min; four sessions were repeated at 10-min intervals. In the first session, serotonin increased gradually, then peaked at approximately the end of the interaction, and decreased rapidly between sessions. This slow phasic increase in serotonin diminished gradually (but significantly) in subsequent interactions. Test rats received active, one-sided contacts (chasing, walking-over, and occasional attacking behavior) from counter rats. Changes in contact times were not correlated with changes in phasic serotonin increases. Dopamine levels did not increase. Citalopram caused significant suppression of slow phasic increases, caused tonic increases in basal serotonin concentrations, and caused active (chasing, all grooming), but not aggressive behavior in test rats. These findings implied that the slow phasic serotonin increase in the ventral striatum induced adaptation to social stress caused by a counter rat; moreover, the tonic increase in serotonin promoted the adaptive change and caused socially dominant behavior. © 2012 Springer-Verlag.
Imai Y.,Juntendo University |
Lu B.,Stanford University
Current Opinion in Neurobiology | Year: 2011
Parkinson's disease (PD), the most common movement disorder, is characterized by age-dependent degeneration of dopaminergic neurons in the substantia nigra of the mid-brain. Non-motor symptoms of PD, however, precede the motor features caused by dysfunction of the dopaminergic system, suggesting that PD is a systemic disorder. Mitochondrial dysfunction has long been observed in PD patients and animal models, but the mechanistic link between mitochondrial dysfunction and PD pathogenesis is not well understood. Recent studies have revealed that genes associated with autosomal recessive forms of PD such as PINK1 and Parkin are directly involved in regulating mitochondrial morphology and maintenance, abnormality of which is also observed in the more common, sporadic forms of PD, although the autosomal recessive PDs lack Lewy-body pathology that is characteristic of sporadic PD. These latest findings suggest that at least some forms of PD can be characterized as a mitochondrial disorder. Whether mitochondrial dysfunction represents a unifying pathogenic mechanism of all PD cases remains a major unresolved question. © 2011 Elsevier Ltd.
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.
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.
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.
Osaki K.,Juntendo University
Hypertension | Year: 2013
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.