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Publisher: Smart Science and Technology LLC   (Total: 20 journals)   [Sort by number of followers]

Showing 1 - 20 of 20 Journals sorted alphabetically
Abdomen     Open Access  
Cancer Cell & Microenvironment     Open Access   (Followers: 9)
Cardiovascular Regenerative Medicine     Open Access  
Evidence-based Medicine & Public Health     Open Access   (Followers: 7)
Immunoendocrinology     Open Access   (Followers: 1)
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  
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Number of Followers: 1  

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ISSN (Online) 2378-3079
Published by Smart Science and Technology LLC Homepage  [20 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)
  • H2S and glucose metabolism, how does the stink regulate the sweet'

    • Authors: Guangdong Yang
      Abstract: Hydrogen sulfide (H2S), once regarded as a toxic gas with a very bad smell of rotten eggs, now is recognized as an important gasotransmitter and regulates numerous physiological and pathophysiological processes in our body.  Recent studies have demonstrated that H2S is able to directly alter protein activity by modifying the free thiol groups in the target cysteine residue(s) to form persulfides, a process termed as protein S-sulfhydration, which mediates the major bioactivities of H2S in cellular functions.  Compared with all other tissues, liver generates huge amount of H2S mainly from the enzyme cystathionine gamma-lyase.  H2S participates in the regulation of liver functions and attenuates fatty liver development.  In this research highlight, I discuss the latest published findings on H2S regulation of liver glucose generation and metabolism via posttranslational modification of gluconeogenic enzymes.
      PubDate: 2015-12-15
      Issue No: Vol. 3 (2015)
  • Preservation of Residual Beta Cell Function with Vitamin D Supplementation
           in Type 1 Diabetes

    • Authors: Devi Dayal, Naresh Sachdeva
      Abstract: Preservation of residual β-cell function (RBCF) at diagnosis of Type 1 diabetes (T1D) is important for major benefits in short and long term outcomes as endogenous insulin secretion is associated with better glycemic control, reduced risk of diabetes related complications and positive effects on physical development in children. Several immunotherapeutic interventions including nonspecific immunosuppression, epitope or antigen specific immunomodulation, cellular and β-cell trophic therapies have been tried for preservation of RBCF in T1D.Immunological interventions targeting the T cells that include therapies resulting in partial depletion or modulation of effector T cells (Teffs) and preservation or augmentation of regulatory T cells (Tregs) have shown the best potential. Recent evidence suggests that vitamin D is an effective agent for increasing the numbers as well as promoting the functions of Tregs in patients with T1D. A number of in vitro and in vivo studies have shown that vitamin D may prevent pancreatic β-cell destruction through its immunomodulatory effects when the blood concentrations are in the optimal ranges. However, clinical trials on patients with T1D have shown variable results. The authors conducted a case control interventional study on 30 children with T1D. After an oral cholecalciferol dose of 2000 IU per day for 6 months, a trend towards lesser decline of RBCF was seen. The percent decrease in stimulated C-peptide was also lower in the intervention group as compared to the control group. Three (20%) patients progressed to undetectable stimulated C-peptide over the study period as compared to 1 (6%) in the intervention group. The results were similar to the recently conducted similar studies but the effect size was lower. A number of limitations in the authors’ work as well as in the previous studies will need to be addressed in the future studies of vitamin D supplementation for preserving RBCF. These issues are related to dosage and type of vitamin D, C-peptide concentration at inclusion, glycemic control during supplementation, duration of supplementation, sunexposure quantification and assessment of epitope specific T cell frequencies. Depending upon the results of subsequent larger studies, vitamin D supplementation may emerge as an important arm of the combination therapies for preservation of RBCF.
      PubDate: 2015-11-30
      Issue No: Vol. 3 (2015)
  • The role of p53 in pancreatic β-cell apoptosis

    • Authors: Clara Ortega-Camarillo, Luis Antonio Flores-Lopez, Alejandro Avalos-Rodriguez
      Abstract: β-cells regulate glucose serum levels by means of synthesis and secretion of insulin. Chronic hyperglycemia diminishes the pancreatic β-cell mass due to an increase in the rate of apoptosis. Although the precise mechanism of glucotoxicity on the β-cells is not fully known, several mechanisms have been proposed, the most outstanding being: the increase of Reactive Oxygen Species (ROS), the loss of the mitochondrial membrane potential, and the activation of the intrinsic route of the apoptosis due to p53. This paper will focus on the mobilization and phosphorylation of p53 towards the mitochondrion, and the activation of the intrinsic route of the apoptosis by hyperglycemia. Since p53 has important functions over the regulation of the cellular cycle, proliferation, and apoptosis, it is subject to strict regulation. The degradation of p53 occurs in the proteasome, and depends on its ubiquitination by Mdm2 (murine double minute 2). Hyperglycemia affects the concentration, ubiquitination and phosphorylation of Mdm2, as well as the phosphorylation of p53, therefore also affecting its average life. Studies made by our group demonstrated that the increase of glucose promotes the interaction between p53 and Mdm2; however, the ubiquitination of p53 diminishes. Thus, it is likely that hyperglycemia interferes with the capacity of Mdm2 to ubiquitinate p53, and leads it to degradation, which allows for p53 to move towards the mitochondria, and for apoptosis activation. Knowing what mechanisms activate the death of the pancreatic β-cells, will allow proposing alternative treatment to prevent dysfunction and decreased of pancreatic β-cell. 
      PubDate: 2015-11-23
      Issue No: Vol. 3 (2015)
  • Exercise Training and Caloric Restriction Reduce Adiposity Index and
           Hepatic Lipids in Obese Rats

    • Authors: Rogério Antonio Laurato Sertié, Ellena Christina Paulino, Patricia Chakur Brum, Sandra Andreotti, Fabio Bessa Lima, Carlos Eduardo Negrão
      Abstract: Objective: Obesity is a multifactorial disorder associated with dyslipidemia and hepatic insulin resistance as the consequence of fatty liver accumulation. In the present study, we tested the hypothesis that exercise training or caloric restriction would reduce hepatic steatosis in obese rats. In addition, we investigated whether exercise training associated with caloric restriction would cause a more intense reduction in hepatic steatose than exercise training or caloric restriction alone. Subjects: Male Wistar rats were fed with cafeteria diet with high-fat content for 25 weeks. Then, they were randomly divided into four groups: high-fat-diet (n=13), high-fat-diet submitted to running exercise training (60% peak VO2, n=13), caloric restriction (-20 % of Kcal/day, n=14), and caloric restriction plus training (n=14). This period lasted 10 weeks. Results:           Exercise training significantly decreased adiposity index (-23%) and leptin level (-31%) and significantly increased peak oxygen uptake (23%), but caused no changes in body weight and hepatic triglycerides and cholesterol contents.            Caloric restriction decreased body weight (-18%), adiposity index (-50%), hepatic triglycerides content (-53%) and leptin (-61%) levels.            Exercise training associated with caloric restriction caused decrease in body weight (-22%), adiposity index (-61%), hepatic triglycerides (-54%) and leptin (-75%) levels and, in addition, hepatic cholesterol content (-26%).                Exercise associated with caloric restriction caused no significant changes serum lipids, glucose and insulin levels and HOMA-IR. Conclusion: Exercise training associated with caloric restriction is an important nonpharmacological strategy to reduce adiposity index and hepatic lipids in obese rats.
      PubDate: 2015-11-09
      Issue No: Vol. 3 (2015)

    • Authors: Seiho Nagafuchi, Antonio Toniolo
      Abstract: Diabetes mellitus (DM) is on the rise worldwide, and is associated with improvement in socioeconomic conditions, increasing wealth, high caloric and fat intake, and reduced physical activity. Accumulating evidence also suggests a causal/triggering link with environmental factors, such as toxins and viruses.A variety of viral infections have been associated with the development of diabetes. There might be no ‘diabetes virus’, but there might be a variety of ‘diabetogenic viruses’ that contribute to diabetes in people who are particularly susceptible due to genetic or physiologic conditions. Increasing evidence is showing that human enteroviruses (EVs) are prominent among possible causal candidates for type 1 diabetes mellitus (T1D). However, evidence for diabetogenicity of viruses is still missing. For a pathogen, causality should fulfill the etiologic criteria known as ‘modified Koch’s postulates’.Recently, we presented evidence that mutations of Tyk2 gene are responsible for diabetes susceptibility of mice infected with the diabetogenic D strain of encephalomyocarditis virus (EMC-D). Observations have been extended to identify the human polymorphism of TYK2 gene associated with increased risk for virus-induced diabetes in humans. An update is given on the possible diabetogenic role of EVs with reference to experimental work in animals and to human studies (viral serology, pancreas histopathology, virus detection in blood and in tissues of diabetic patients). For the identification of a diabetogenic virus, the development of a sensitive experimental model is imperative. In vivo assay systems should include an animal model appropriately simulating a susceptible human and carrying susceptibility genes or factors. This work summarizes current knowledge on virus-induced diabetes together with evidence from experimental models, susceptibility genes in mice, candidate diabetogenic viruses and susceptibility genes in humans. Perspectives on the identification of diabetogenic viruses - which may possibly lead to innovative strategies for the cure or prevention of diabetes – are also presented. 
      PubDate: 2015-10-19
      Issue No: Vol. 3 (2015)
  • Adipokines and Adipose Tissue Angiogenesis in Obesity

    • Authors: Raghu Adya, Shervanthi Homer-Vanniasinkam
      Abstract: Initially described as an inert fat store, adipose tissue (AT) has been extensively studied in recent years and shown to have multifaceted roles in appetite regulation, vascular homeostasis, energy balance and systemic inflammation in chronic diseases. Composed mainly of adipocytes and stromal vascular fraction (SVCs), comprising preadipocytes, macrophages, mesenchymal stem cells (MSCs), T cells, B cells, mast cells and endothelial progenitor cells (EPCs), AT performs an endocrine role in secretion of growth factors and cytokines (termed adipocytokines).AT is extensively vascularized and, as in other tissues and organs, the growth and maintenance of AT is critically dependent on angiogenic processes.The microvasculature network surrounding the adipocytes provides efficient pathways for crosstalk with the surrounding environment. AT undergoes constant expansion and shrinkage during its entire life span. To cope with this increased metabolic demand during expansion, AT vasculature undergoes extensive remodelling, and changes to vessel density are observed. To facilitate these processes, AT secretes angiogenic/growth factors. Dysregulation in the secretion of these factors is known to play an important role in obesity and insulin-resistant states. In this article we will discuss novel therapeutic strategies to combat obesity and inflammation by inducing changes to the AT vascular network.
      PubDate: 2015-08-03
      Issue No: Vol. 3 (2015)
  • Diabetes affects rat visceral yolk sac cells viability and cell markers

    • Authors: Marlúcia Bastos Aires
      Abstract: Rodents have a well-developed visceral yolk sac (VYS) that acts as an active region for metabolic exchange and nutrition uptake until final fetal development in rats and may be affected by diabetes. Using Wistar rats, diabetes was induced by a single injection of alloxan at gestational day 8 (8 gd) and at 15 gd the collection of VYS was made. Flow cytometry was performed for VYS cell characterization, determination of mitochondrial activity, cell proliferation, DNA ploidy, cell cycle phases and caspase-3 activity. Fetal weight was reduced in the diabetic group. CD34, CCR2, and OCT3/4 expressions were significantly reduced, and CD90, CD117, and CD14 expressions were increased in the diabetic group. VYS cells with inactive mitochondria, activated caspase-3, and low proliferation were present in the diabetic condition. Severe hyperglycemia due to maternal diabetes was shown to have negative effects on pregnancy, VYS viability, and cell marker expression.
      PubDate: 2015-05-24
      Issue No: Vol. 3 (2015)
  • Epitope specific T cells in type 1 diabetes: From detection to

    • Authors: Naresh Sachdeva
      Abstract: Monitoring autoreactive T cells, directed towards immunodominant epitopes is useful in assessment of disease progression and distinguishing different forms of autoimmune diabetes. In a recent work, the authors reported that individuals with slower progression of autoimmune diabetes, i.e. latent autoimmune diabetes in adults (LADA) harbour lower frequency of preproinsulin (PPI) specific CD8+ T cells compared to those with typical type 1 diabetes (T1D). Further, the PPI specific CD8+ T cells of T1D subjects showed higher proliferation potential and greater proportion of cells with effector phenotype. Besides highlighting the differences in the repertoire of PPI specific peripheral CD8+ T cells between T1D and LADA subjects, this study also demonstrates that autoreactive CD8+ T cells directed towards immunodominant epitopes persist over a period of time in these subjects and hence present as attractive targets for immunotherapy. Generating epitope specific CD4+ regulatory T cells (Tregs) directed towards the same antigen can counter regulate effector CD4+ T cells and further limit the frequency and actions of such autoreactive CD8+ T cells.Recent animal studies have indeed shown that islet antigen specific Tregs can in fact reverse autoimmune diabetes by targeting T cells that infiltrate pancreas. Therefore, combining the approaches of identification of epitope specific T cells using MHC multimers and Treg specific markers, can facilitate the scope of epitope specific immunotherapy in human T1D.
      PubDate: 2015-04-14
      Issue No: Vol. 3 (2015)
  • Nitric oxide and insulin resistance

    • Authors: Jun Kobayashi
      Abstract: Obesity with increased visceral adiposity is a low grade inflammatory state leading to insulin resistance. Because the insulin signaling pathway is coupled with endothelial nitric oxide synthase (eNOS) activation, insulin resistance is always associated with impaired nitric oxide (NO) bioavailability. Recently, accumulating evidence has suggested that physical exercise and dietary nitrate/nitrite diets rich in vegetables improve the features of insulin resistance by enhancing NO availability, and thus provide potential options for prevention and therapy for these patients. This review discusses the mechanisms by which insulin resistance develops in the presence of increased adiposity, the causative relationship between impaired NO availability and insulin resistance, and the implications of life-style changes to prevent insulin resistance.
      PubDate: 2015-03-11
      Issue No: Vol. 3 (2015)
  • The effect of genetic and non genetic factors on the association of T1D
           with PTPN22 genotype and with the ACP1-ADA1 joint genotype.

    • Authors: Fulvia Gloria-Bottini, Patrizia Saccucci, Maria Luisa Manca Bitti, Anna Neri, Andrea Magrini, Egidio Bottini
      Abstract: Background: We have recently observed that the joint genotype Acid Phosphatase locus 1-Adenosine deaminase locus 1 (ACP1- ADA1) cooperate with Phospho Tyrosine Phosphatase, non-receptor type 22 (PTPN22) in the susceptibility to Type 1 Diabetes (T1D) . Since T1D has been found associated with sex, maternal age at birth, Adenosine Deaminase locus 2 (ADA2) genotype and p53 codon 72 genotype we have investigated the possible effects of these variables on the association of T1D  with PTPN22  and with ACP1-ADA1 joint genotype.Methods: We have reexamined the data on 314 children with T1D and on 700 controls from the White population of Rome. PTPN22, ADA2 and p53 codon 72 genotypes were determined by DNA analysis. Statistical analysis were carried out by commercial software (SPSS).Results: The genetic and non genetic variables considered, in particular ADA2*2 carrier, p53 codon 72 *Pro carrier, male sex and maternal age greater than 32 years, have a positive effect on the strength of association between PTPN22  and T1D but tend to have a negative effect on the strength of association between ACP1-ADA1 joint genotype and T1D.Conclusions: The results suggest that although PTPN22 and ACP1-ADA1 genetic complex cooperate in the susceptibility to T1D, the mechanisms underlying the association of the two genetic systems with the disease are different. 
      PubDate: 2015-03-11
      Issue No: Vol. 3 (2015)
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