Gastric band Surgery In France The potential results of how Sitting down can build fat around your organs, according to a new study. Besides the ever-so-annoying belly fat, there’s also a much more “invisible” – but just as harmful – kind of fat: one that sits around our internal organs. What causes this, and is it possible to get rid of it? A new study has some answers. Too much sitting down can build ‘invisible’ fat, says new study. For one thing, we need get off our tushies, and pronto! Sedentary time correlates directly with how much fat we build around our organs, according to the new study, which was published in the journal Obesity. For another, we need to exercise. The research shows that sitting has an even more harmful effect for those who don’t work out enough. You might be tempted to think, “Thank you, Captain Obvious,” but actually, few people are aware of the importance of body fat distribution and the fact that the fat around our organs puts us at serious risk of chronic illness. The new study was led by Dr. Joe Henson, research associate at the University of Leicester in the United Kingdom, who comments on the importance of the study, saying, “We know that spending long periods of time sedentary is unhealthy and a risk factor for chronic illnesses, such as type 2 diabetes and heart disease.” “Likewise, the amount of fat deposited around our internal organs may also predispose us to these diseases,” Dr. Henson says, and he’s not the only one. In a previous study we reported on, visceral fat inside the abdominal cavity was shown to raise the risk of heart disease. For FREE No Obligation Information about the cost of Gastric Band Surgery in France Click here Or Click the Image Below to visit our Special offer Page to see if you Qualify for any Discounts Read more……>click Here< Read more... Read more…

Gastric band Surgery In France Siderophore Vaccine Conjugates Protect Against Uropathogenic Escherichia Coli Urinary Tract Infection. Significance Urinary tract infections (UTIs) are primarily caused by uropathogenic Escherichia coli (UPEC), and 1 in 40 women experience chronic UTIs during their lifetime. The antibiotic courses required to treat infections promote antibiotic resistance, and current vaccine options offer limited protection. We have pioneered a strategy using small iron-chelating compounds called siderophores as vaccine antigens. These siderophores are not produced by commensal bacteria and are required for UTI. The siderophore vaccines reported here are easy to formulate and reduce bacterial burdens in a murine model of UTI. This report highlights the untapped resource of bacteria-specific small molecules as potential vaccine antigens and provides a proof of principle for incorporating these compounds into multicomponent vaccines for the prevention of bacterial infections. Abstract Uropathogenic Escherichia coli (UPEC) is the primary cause of uncomplicated urinary tract infections (UTIs). Whereas most infections are isolated cases, 1 in 40 women experience recurrent UTIs. The rise in antibiotic resistance has complicated the management of chronic UTIs and necessitates new preventative strategies. Currently, no UTI vaccines are approved for use in the United States, and the development of a highly effective vaccine remains elusive. Here, we have pursued a strategy for eliciting protective immunity by vaccinating with small molecules required for pathogenesis, rather than proteins or peptides. Small iron-chelating molecules called siderophores were selected as antigens to vaccinate against UTI for this vaccine strategy. These pathogen-associated stealth siderophores evade host immune defenses and enhance bacterial virulence. Previous animal studies revealed that vaccination with siderophore receptor proteins protects against UTI. The poor solubility of these integral outer-membrane proteins in aqueous solutions limits their practical utility. Because their cognate siderophores are water soluble, we hypothesized that these bacterial-derived small molecules are prime vaccine candidates. To test this hypothesis, we immunized mice with siderophores conjugated to an immunogenic carrier protein. The siderophore-protein conjugates elicited an adaptive immune response that targeted bacterial stealth siderophores and protected against UTI. Our study has identified additional antigens suitable for a multicomponent UTI vaccine and highlights the potential use of bacterial-derived small molecules as antigens in vaccine therapies. Both the physical and financial burdens of urinary tract infections (UTIs) are staggering. Half of all women experience a symptomatic UTI in their lifetime (1). And of those women, almost half suffer a reoccurrence within the next year (1). In the United States, where the annual societal cost of UTI is likely

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Gastric band Surgery In France Weight loss breakthrough: Sunlight is key Sign in Log in with your Medical News Today account to create or edit your custom homepage, catch-up on your opinions notifications and set your newsletter preferences. Sign in Register for a free account For FREE No Obligation Information about the cost of Gastric Band Surgery in France Click here Or Click the Image Below to visit our Special offer Page to see if you Qualify for any Discounts Read more……>click Here< Read more... Read more…

Gastric band Surgery In France The sleep diet: Could this work? Sign in Log in with your Medical News Today account to create or edit your custom homepage, catch-up on your opinions notifications and set your newsletter preferences. Sign in Register for a free account For FREE No Obligation Information about the cost of Gastric Band Surgery in France Click here Or Click the Image Below to visit our Special offer Page to see if you Qualify for any Discounts Read more……>click Here< Read more... Read more…

Research ArticleNeuroscience Free access | 10.1172/JCI88321 Nigel A. Calcutt,1 Darrell R. Smith,2 Katie Frizzi,1 Mohammad Golam Sabbir,2 Subir K. Roy Chowdhury,2 Teresa Mixcoatl-Zecuatl,1 Ali Saleh,2 Nabeel Muttalib,1 Randy Van der Ploeg,2 Joseline Ochoa,1 Allison Gopaul,1 Lori Tessler,2 Jürgen Wess,3 Corinne G. Jolivalt,1 and Paul Fernyhough2,4 1Department of Pathology, UCSD, La Jolla, California, USA. 2Division of Neurodegenerative Disorders, St. Boniface Hospital Research Centre, Winnipeg, Manitoba, Canada. 3Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland, USA. 4Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Manitoba, Canada. Address correspondence to: Paul Fernyhough, R4046 – 351 Taché Avenue, St. Boniface Hospital Research Centre, Winnipeg, Manitoba, R2H 2A6, Canada. Phone: 204.235.3692; E-mail: pfernyhough@sbrc.ca. Find articles by Calcutt, N. in: JCI | PubMed | Google Scholar 1Department of Pathology, UCSD, La Jolla, California, USA. 2Division of Neurodegenerative Disorders, St. Boniface Hospital Research Centre, Winnipeg, Manitoba, Canada. 3Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland, USA. 4Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Manitoba, Canada. Address correspondence to: Paul Fernyhough, R4046 – 351 Taché Avenue, St. Boniface Hospital Research Centre, Winnipeg, Manitoba, R2H 2A6, Canada. Phone: 204.235.3692; E-mail: pfernyhough@sbrc.ca. Find articles by Smith, D. in: JCI | PubMed | Google Scholar 1Department of Pathology, UCSD, La Jolla, California, USA. 2Division of Neurodegenerative Disorders, St. Boniface Hospital Research Centre, Winnipeg, Manitoba, Canada. 3Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland, USA. 4Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Manitoba, Canada. Address correspondence to: Paul Fernyhough, R4046 – 351 Taché Avenue, St. Boniface Hospital Research Centre, Winnipeg, Manitoba, R2H 2A6, Canada. Phone: 204.235.3692; E-mail: pfernyhough@sbrc.ca. Find articles by Frizzi, K. in: JCI | PubMed | Google Scholar 1Department of Pathology, UCSD, La Jolla, California, USA. 2Division of Neurodegenerative Disorders, St. Boniface Hospital Research Centre, Winnipeg, Manitoba, Canada. 3Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland, USA. 4Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Manitoba, Canada. Address correspondence to: Paul Fernyhough, R4046 – 351 Taché Avenue, St. Boniface Hospital Research Centre, Winnipeg, Manitoba, R2H 2A6, Canada. Phone:

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Gastric band Surgery In France Does green tea help weight loss? Sign in Log in with your Medical News Today account to create or edit your custom homepage, catch-up on your opinions notifications and set your newsletter preferences. Sign in Register for a free account For FREE No Obligation Information about the cost of Gastric Band Surgery in France Click here Or Click the Image Below to visit our Special offer Page to see if you Qualify for any Discounts Read more……>click Here< Read more... Read more…

Abstract Bladder inflammation frequently causes cystitis pain and lower urinary tract dysfunction (LUTD) such as urinary frequency and urgency. Although mast cells have been identified to play a critical role in bladder inflammation and pain, the role of mast cells in cystitis-associated LUTD has not been demonstrated. Interstitial cystitis/bladder pain syndrome (IC/BPS) is a chronic and debilitating inflammatory condition of the urinary bladder characterized by the hallmark symptoms of pelvic pain and LUTD. In this study we investigated the role of mast cells in LUTD using a transgenic autoimmune cystitis model (URO-OVA) that reproduces many clinical correlates of IC/BPS. URO-OVA mice express the membrane form of the model antigen ovalbumin (OVA) as a self-antigen on the urothelium and develop bladder inflammation upon introduction of OVA-specific T cells. To investigate the role of mast cells, we crossed URO-OVA mice with mast cell-deficient KitW-sh mice to generate URO-OVA/KitW-sh mice that retained urothelial OVA expression but lacked endogenous mast cells. We compared URO-OVA mice with URO-OVA/KitW-sh mice with and without mast cell reconstitution in response to cystitis induction. URO-OVA mice developed profound bladder inflammation with increased mast cell counts and LUTD, including increased total number of voids, decreased mean volume voided per micturition, and decreased maximum volume voided per micturition, after cystitis induction. In contrast, similarly cystitis-induced URO-OVA/KitW-sh mice developed reduced bladder inflammation with no mast cells and LUTD detected. However, after mast cell reconstitution URO-OVA/KitW-sh mice restored the ability to develop bladder inflammation and LUTD following cystitis induction. We further treated URO-OVA mice with cromolyn, a mast cell membrane stabilizer, and found that cromolyn treatment reversed bladder inflammation and LUTD in the animal model. Our results provide direct evidence for the role of mast cells in cystitis-associated LUTD, supporting the use of mast cell inhibitors for treatment of certain forms of IC/BPS. Citation: Wang X, Liu W, O’Donnell M, Lutgendorf S, Bradley C, Schrepf A, et al. (2016) Evidence for the Role of Mast Cells in Cystitis-Associated Lower Urinary Tract Dysfunction: A Multidisciplinary Approach to the Study of Chronic Pelvic Pain Research Network Animal Model Study. PLoS ONE 11(12): e0168772. https://doi.org/10.1371/journal.pone.0168772 Editor: Jayoung Kim, Cedars-Sinai Medical Center, UNITED STATES Received: October 11, 2016; Accepted: November 16, 2016; Published: December 21, 2016 Copyright: © 2016 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Data Availability: All relevant data are within the paper and its Supporting Information files. Funding: This work

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Making beta cells from people with type 1 diabetes Research Update Dec. 27, 2016 Scientists generated functional β (beta) cells from the skin cells of people with type 1 diabetes. In type 1 diabetes, a misguided attack by the immune system leads to destruction of insulin-producing β cells found in clusters called islets in the pancreas. Although administration of insulin via injections or a pump is life-saving, it does not mimic the exquisite blood glucose (sugar) control of the pancreas. Therefore, scientists are pursuing strategies to replace the destroyed β cells. One way to do that is through islet transplantation-an experimental procedure using islets from a cadaveric donor. The procedure has shown promise for people with difficult-to-control diabetes, but has significant challenges: donor islet tissue is limited, and immunosuppressive medications, which have toxic side effects, are required to prevent rejection of tissue transplanted from another individual. Toward overcoming the first barrier, scientists recently developed a new laboratory production method to make large quantities of β cells-called stem-cell derived β (SC-β) cells-from human stem cells. This method could, with further development, be used to make β cells from a sample of cells from a person with type 1 diabetes in the quantities needed for transplantation back into that same person. These cells would likely require protection from the autoimmune attack, but might not require toxic immunosuppressive medications to prevent rejection of the tissue. To investigate this possibility, in new research, scientists used skin cells from three people with type 1 diabetes (T1D cells) and three people without diabetes (ND cells). By introducing specific factors into these cells and using the new large-scale production method they developed, they made the skin cells become stem cells-cells that could subsequently become any cell type. They then, by introducing other factors, coaxed these stem cells to become SC-β cells (T1D SC-β cells and ND SC-β cells). Cells from the two different origins showed no differences in the ability to become SC-β cells, indicating for the first time that cells from a person with type 1 diabetes could be used to make SC-β cells. Next, the scientists demonstrated that the T1D SC-β cells functioned like healthy β cells. For example, in laboratory culture, T1D SC-β cells secreted insulin in response to glucose; they also released insulin in response to diabetes drugs that are known to stimulate insulin secretion, demonstrating their potential for use in screening for new diabetes drugs. The T1D SC-β also functioned in live animals: when T1D SC-β cells were transplanted into male mice, they produced insulin in response to glucose and controlled the animals’ blood glucose levels. Many research questions remain before an SC-β cell transplant procedure will be ready for testing in humans. First, it remains possible that differences between T1D

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Gastric band Surgery In France Being overweight may be more harmful than you thought Sign in Log in with your Medical News Today account to create or edit your custom homepage, catch-up on your opinions notifications and set your newsletter preferences. Sign in Register for a free account For FREE No Obligation Information about the cost of Gastric Band Surgery in France Click here Or Click the Image Below to visit our Special offer Page to see if you Qualify for any Discounts Read more……>click Here< Read more... Read more…

Genome-Wide Association Study of Primary Sclerosing Cholangitis Identifies New Risk Primary sclerosing cholangitis (PSC) is a rare progressive disorder leading to bile duct destruction; ∼75% of patients have comorbid inflammatory bowel disease (IBD). We undertook the largest genome-wide association study of PSC (4,796 cases and 19,955 population controls) and identified four new genome-wide significant loci. The most associated SNP at one locus affects splicing and expression of UBASH3A, with the protective allele (C) predicted to cause nonstop-mediated mRNA decay and lower expression of UBASH3A. Further analyses based on common variants suggested that the genome-wide genetic correlation (rG) between PSC and ulcerative colitis (UC) (rG = 0.29) was significantly greater than that between PSC and Crohn’s disease (CD) (rG = 0.04) (P = 2.55 × 10-15). UC and CD were genetically more similar to each other (rG = 0.56) than either was to PSC (P < 1.0 × 10-15). Our study represents a substantial advance in understanding of the genetics of PSC. Read more......>click Here< Read more... Read more…