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Gauzere B.-A.,Center Hospitalier Felix Guyon
Revue Francophone des Laboratoires | Year: 2011

The chikungunya virus infection in the indian Ocean : what lessons Chikungunya virus is an emerging alphavirus that has caused major epidemics in India and islands off the east coast of Africa since 2005, particularly in Réunion, a french territory. Lessons have been learned the hard way in the field of the severe emerging presentations of the disease and its vector the tiger mosquito that is expending worldwide. Importations into Europe including one that led to epidemic transmission in Italy during 2007, underscore the risk of endemic establishment elsewhere. Several research programmes are being conducted, boosting previously declining virology and medical entomology. © 2011 - Elsevier Masson SAS - Tous droits réservés. Source


Hoareau L.,University of Reunion Island | Bencharif K.,University of Reunion Island | Rondeau P.,University of Reunion Island | Murumalla R.,University of Reunion Island | And 5 more authors.
Journal of Inflammation | Year: 2010

Background. The development of obesity has been linked to an inflammatory process, and the role of adipose tissue in the secretion of pro-inflammatory molecules such as IL-6 or TNFalpha has now been largely confirmed. Although TNFalpha secretion by adipose cells is probably induced, most notably by TLR ligands, the activation and secretion pathways of this cytokine are not yet entirely understood. Moreover, given that macrophagic infiltration is a characteristic of obesity, it is difficult to clearly establish the level of involvement of the different cellular types present within the adipose tissue during inflammation. Methods. Primary cultures of human adipocytes and human peripheral blood mononuclear cells were used. Cells were treated with a pathogen-associated molecular pattern: LPS, with and without several kinase inhibitors. Western blot for p38 MAP Kinase was performed on cell lysates. TNFalpha mRNA was detected in cells by RT-PCR and TNFalpha protein was detected in supernatants by ELISA assays. Results. We show for the first time that the production of TNFalpha in mature human adipocytes is mainly dependent upon two pathways: NFkappaB and p38 MAP Kinase. Moreover, we demonstrate that the PI3Kinase pathway is clearly involved in the first step of the LPS-pathway. Lastly, we show that adipocytes are able to secrete a large amount of TNFalpha compared to macrophages. Conclusion. This study clearly demonstrates that the LPS induced activation pathway is an integral part of the inflammatory process linked to obesity, and that adipocytes are responsible for most of the secreted TNFalpha in inflamed adipose tissue, through TLR4 activation. © 2010 Hoareau et al; licensee BioMed Central Ltd. Source


Roche R.,University of Reunion Island | Festy F.,University of Reunion Island | Fritel X.,Center Hospitalier Felix Guyon
Journal of Cellular and Molecular Medicine | Year: 2010

Stress urinary incontinence (SUI), the most common type of incontinence in women, is a frequent and costly ailment responsible for an alteration in the quality of life. Although medical treatment gives some rather deceiving results, surgical techniques that include colposuspension or tension-free vaginal tape, employed in cases of urethral support defect, give a 5-year cure rate of more than 80%. However, these techniques could lead to complications or recurrence of symptoms. Recently, the initiation of urethral cell therapy has been undertaken by doctors and researchers. One principal source of autologous adult stem cells is generally used: muscle precursor cells (MPCs) which are the progenitors of skeletal muscle cells. Recently, a few research groups have shown interest in the MPCs and their potential for the treatment of urinary incontinence. However, using MPCs or fibroblasts isolated from a striated muscle biopsy could be questionable on several points. One of them is the in vitro cultivation of cells, which raises issues over the potential cost of the technique. Besides, numerous studies have shown the multipotent or even the pluripotent nature of stromal vascular fraction (SVF) or adipose-derived stem cells (ASCs) from adipose tissue. These cells are capable of acquiring in vitro many different phenotypes. Furthermore, recent animal studies have highlighted the potential interest of SVF cells or ASCs in cell therapy, in particular for mesodermal tissue repair and revascularization. Moreover, the potential interest of SVF cells or ASCs for the treatment of urinary incontinence in women is supported by many other characteristics of these cells that are discussed here. Because access to these cells via lipoaspiration is simple, and because they are found in very large numbers in adipose tissue, their future potential as a stem cell reservoir for use in urethral or other types of cell therapy is enormous. © 2009 The Authors Journal compilation © 2010 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd. Source


Le Dour C.,Institute National Of La Sante Et Of La Recherche Medicale Unite Mixte Of Recherche Umr S938 | Le Dour C.,University Pierre and Marie Curie | Schneebeli S.,Groupe Hospitalier Sud Reunion | Bakiri F.,Center Hospitalier Felix Guyon | And 15 more authors.
Journal of Clinical Endocrinology and Metabolism | Year: 2011

Context: Mutations in LMNA, encoding A-type lamins, lead to multiple laminopathies, including lipodystrophies, progeroid syndromes, and cardiomyopathies. Alterations in the prelamin-A posttranslational maturation, resulting in accumulation of farnesylated isoforms, cause human progeroid syndromes. Accumulation of mutant nonfarnesylated prelamin-A leads to cardiomyopathy or progeria in mice, but no data have been provided in humans. Objective, Design, Setting, and Patients: We searched for LMNA mutations in seven women originating from Reunion Island who were referred for a severe lipodystrophic syndrome. Clinical, molecular, genealogical, and cellular studies were performed in probands and relatives. Results: The seven probands showed a severe partial lipodystrophic syndrome with diabetes and/or acanthosis nigricans, liver steatosis, hypertriglyceridemia, and low serum leptin and adiponectin levels. Three probands also had severe cardiac rhythm and conduction disturbances. We identified in all probands a homozygousLMNAp.T655fsX49 mutation leading to expression of a mutated prelamin-A with 48 aberrant C-terminal amino acids, preventing its physiological posttranslational farnesylation and maturation. Genealogical and haplotype analyses were consistent with a founder mutation transmitted from a common ancestor in the 17th century. In probands' cultured fibroblasts, mutated prelamin-A was associated with typical laminopathic nuclear dysmorphies, increased oxidative stress, and premature senescence. Heterozygous relatives were asymptomatic or partially affected, in favor of a codominant transmission of the disease with incomplete penetrance in heterozygotes. Conclusions: We reveal that a homozygous mutation of prelamin-A preventing its farnesylation leads to a severe lipodystrophic laminopathy in humans, which can be associated with cardiac conduction disturbances, stressing the pathogenicity of nonfarnesylated prelamin-A in human laminopathies. Copyright © 2011 by The Endocrine Society. Source


Guerin-Dubourg A.,University of Reunion Island | Guerin-Dubourg A.,Center Hospitalier Felix Guyon | Catan A.,University of Reunion Island | Bourdon E.,University of Reunion Island | Rondeau P.,University of Reunion Island
Diabetes and Metabolism | Year: 2012

Aim: Albumin, a major protein in the blood circulation, can undergo increased glycation in diabetes. From recent studies, it has become evident that glycation has important implications for albumin actions and impact on cell functioning. This study compares the structural and functional properties of albumin glycated by glucose and methylglyoxal (MGO) with those of albumin purified from diabetic patients. Methods: Human serum albumin (HSA) was purified from diabetic patients and control subjects using affinity chromatography, and oxidation parameters in various albumin preparations were determined. Tryptophan and 1-anilino-8-naphthalene sulphonic acid (ANSA) probe fluorescence, redox state, antioxidant and copper-binding capacities of the different preparations of albumin were also determined and compared. Results: Occurrence of oxidative modifications was enhanced in albumin whether purified from diabetic patients, or glycated by glucose or MGO, after determination of their fructosamine and free thiol and amino group contents, carbonyl content and antioxidant activities. Whereas more quantitative changes in oxidative and structural parameters were observed in the glucose- and MGO-modified albumins, significant impairment of albumin function (free-radical-scavenging and copper-binding capacities) were demonstrated in the HSA purified from diabetics. These findings reveal different structural and functional features of diabetic HSA compared with in vitro models. Conclusion: This study provides new information supporting albumin as an important biomarker for monitoring diabetic pathophysiology. In addition, it reconfirms the influence of experimental conditions in which advanced glycation end-products (AGEs) are generated in tests designed to mimic the pathological conditions of diabetes. © 2011 Elsevier Masson SAS. Source

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