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Publisher: Smart Science and Technology LLC   (Total: 21 journals)   [Sort by number of followers]

Showing 1 - 21 of 21 Journals sorted alphabetically
Abdomen     Open Access  
Cancer Cell & Microenvironment     Open Access   (Followers: 10)
Cardiovascular Regenerative Medicine     Open Access  
Evidence-based Medicine & Public Health     Open Access   (Followers: 7)
Immunoendocrinology     Open Access   (Followers: 1)
Inflammation and Cell Signaling     Open Access   (Followers: 3)
Itch & Pain     Open Access   (Followers: 2)
J. of Advanced Nutrition and Human Metabolism     Open Access   (Followers: 14)
Macrophage     Open Access  
Molecular & Cellular Epilepsy     Open Access   (Followers: 2)
Musculoskeletal Regeneration     Open Access   (Followers: 3)
Neurotransmitter     Open Access  
Precision Medicine     Open Access   (Followers: 2)
Receptors & Clinical Investigation     Open Access   (Followers: 1)
RNA & Disease     Open Access   (Followers: 1)
Science Proceedings     Open Access   (Followers: 1)
Stem Cell and Translational Investigation     Open Access   (Followers: 2)
Stem Cell Epigenetics     Open Access   (Followers: 3)
Telomere and Telomerase     Open Access  
Therapeutic Targets for Neurological Diseases     Open Access   (Followers: 1)
Uterus & Ovary     Open Access  
Journal Cover
Immunoendocrinology
Number of Followers: 1  

  This is an Open Access Journal Open Access journal
ISSN (Online) 2378-3079
Published by Smart Science and Technology LLC Homepage  [21 journals]
  • Exercise improves hypothalamic function induced by high-fat diet

    • Authors: Brenton Thomas Laing, Hu Huang
      Abstract: High-fat Diet (HFD) induced obesity is known as a model of mostly closed to human obesity condition. DIO not only induces peripheral insulin resistance, and glucose intolerance but also impairs central leptin and insulin signaling pathways. Exercise training reduces adiposity by mainly increased energy expenditure, however, the underlying mechanism associated with central nervous system remains largely unknown. This article highlights the recent publication by Laing et al, who first demonstrated that voluntary exercise enhanced POMC-expressing neuron survival rate in the hypothalamus of mice by protecting from apoptosis induced by long-term HFD induced obesity, improved central leptin sensitivity, and systemic insulin sensitivity, shed a light on the central mechanism of exercise improves metabolic function.
      PubDate: 2016-11-07
      Issue No: Vol. 3 (2016)
       
  • Comparison of the Nature and Cost of Diabetes Treatment at Two Clinics in
           Japan and the United States

    • Authors: oogi inada, Yasushi Yokogawa, Kinsuke Tsuda, Yutaka Seino, Hitoshi Katsuta, Akari Inada
      Abstract: In order to compare the cost-effectiveness of diabetes treatment in Japan and the USA, we examined medical expenses per diabetes outpatient (annual and per visit) at two specialist centers, Joslin Diabetes Center (USA) and Yokogawa Clinic (Japan). At Joslin, which implements advanced, short-term, intensive education of patients about self-management, the annual medical expenses incurred per outpatient and medical expenses incurred per outpatient visit were $418 ± 272 and $204 ± 100 (mean ± SD), respectively, but costs recovered were significantly below actual costs, and this is a source of serious financial pressure. On the other hand, diabetes patients tend to attend clinics regularly throughout the year in Japan, and the corresponding expenses per outpatient at Yokogawa Clinic were $1142 ± 631 annually and $114 ± 44 per visit; in this clinic, the actual costs were almost fully recovered, due to the comprehensive national insurance system in Japan. It is noteworthy that, despite the lower cost per visit, the annual cost per patient is substantially larger in Japan, due to the habit of frequent checkups. The marked increase in the number of patients with type 2 diabetes is relatively recent in Japan, where it may be related to an increasingly westernized diet, and currently there are few facilities for education of patients. Our findings suggest that the annual cost per patient in Japan could be greatly reduced if more time were allocated for advanced education of patients about self-management of their condition, since this should reduce the need for frequent checkups, depending upon patients’ ability to take responsibility for their condition. In addition, efforts should be made to clarify the roles of doctors, staff and management so as to generate an environment in which specialists can work more effectively.
      PubDate: 2016-10-31
      Issue No: Vol. 3 (2016)
       
  • PD-1 pathway-mediated regulation of islet-specific CD4+ T cell subsets in
           autoimmune diabetes

    • Authors: Brian T. Fife, Tijana Martinov, Justin Spanier, Kristen Pauken
      Abstract: Type 1 diabetes (T1D) is a CD4+ T cell-driven autoimmune disease resulting from the destruction of insulin-producing pancreatic beta cells. Clinical evidence and studies in non-obese diabetic (NOD) mice suggest that insulin is a major autoantigen. With this in mind, we developed insulin B10-23:IAg7 tetramer reagents to track insulin-specific CD4+ T cells in mice and interrogate the role of Programmed death-1 (PD-1) for peripheral tolerance. PD-1 is a T cell inhibitory receptor necessary to maintain tolerance and prevent T1D in NOD mice. PD-1 pathway inhibitors are increasingly used in the clinic for treating malignancies, and while some patients benefit, others develop adverse autoimmune events, including T1D. We therefore sought to understand the role of PD-1 in maintaining islet-specific tolerance in diabetes-resistant strains. B6.g7 mice express the same MHC Class II allele as NOD mice, have predominantly naïve insulin-specific CD4+ T cells in the periphery, and remain diabetes-free even after PD-1 pathway blockade. Here, we examined the trafficking potential of insulin-specific CD4+ T cells in NOD and B6.g7 mice with or without anti-PD-L1 treatment, and found that PD-L1 blockade preferentially increased the number of CD44highCXCR3+ insulin-specific cells in NOD but not B6.g7 mice. Additionally, we investigated whether pancreatic islets in NOD and B6.g7 mice expressed CXCL10, a lymphocyte homing chemokine and ligand for CXCR3. Anti-PD-L1 treated and control NOD mice had detectable CXCL10 expression in the islets, while B6.g7 islets did not. These data suggest that islet tolerance may be in part attributed to the pancreatic environment and in the absence of pancreas inflammation, chemotactic cytokines may be missing. This, together with our previous data showing that PD-1 pathway blockade preferentially affects effector but not anergic self-specific T cells has implications for the use of checkpoint blockade in treating tumor patients. Our work suggests that determining tumor- and self-specific CD4+ T cell activation status (naïve, effector or anergic) prior to initiation of immunotherapy would likely help to stratify individuals who would benefit from this therapy versus those who might have adverse effects or incomplete tumor control. 
      PubDate: 2016-01-25
      Issue No: Vol. 3 (2016)
       
  • Children diagnosed with both Type 1 diabetes and Celiac disease - An
           Immunological challenge

    • Authors: Maria Faresjö
      Abstract: Type 1 diabetes (T1D) and celiac disease are both characterized by an autoimmune feature. As T1D and celiac disease share several common risk factors such as environment, genetics and immune dysregulation, patients have risk of developing the other disease subsequently. Patients with manifest T1D may have had a latent celiac disease, which is activated parallel to the anti-islet immune reactivity during the development of T1D. Contrary, a low prevalence of β-cell autoimmunity is found in young patients with celiac disease.The role of antigen-specific T cells and their relation to cytokines and chemokines is not well characterized in children with combination of T1D and celiac disease. Defective regulation and an impaired ability of responder T cells to be suppressed are suggested to contribute. We have previously shown that children suffering from these two immunological diseases in combination have a suppressed immune response to several antigens for example food antigens like gluten. Low percentages of both early and late effector memory CD8+ cells together with observations of immune aberrancies seen in the gut, in children who are prone to T1D, may suggests poor development of oral tolerance that may predispose for development of celiac disease.    This review highlights the immunological complexity in these two common pediatric immunological disorders that indicates that the combination of type 1 diabetes and celiac disease is an immunological challenge. It is obvious that we are far from understanding the immunological impact of these two autoimmune diseases in combination. This immunological challenge therefore needs to be elucidated to be able to predict and prevent these autoimmune diseases. 
      PubDate: 2016-01-11
      Issue No: Vol. 3 (2016)
       
 
 
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