994 resultados para Indeterminate form of chagas’ disease


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In this paper we present a quantitative comparisons of different independent component analysis (ICA) algorithms in order to investigate their potential use in preprocessing (such as noise reduction and feature extraction) the electroencephalogram (EEG) data for early detection of Alzhemier disease (AD) or discrimination between AD (or mild cognitive impairment, MCI) and age-match control subjects.

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BACKGROUND: We investigated changes in biomarkers of liver disease in HIV-HCV-coinfected individuals during successful combination antiretroviral therapy (cART) compared to changes in biomarker levels during untreated HIV infection and to HIV-monoinfected individuals. METHODS: Non-invasive biomarkers of liver disease (hyaluronic acid [HYA], aspartate aminotransferase-to-platelet ratio index [APRI], Fibrosis-4 [FIB-4] index and cytokeratin-18 [CK-18]) were correlated with liver histology in 49 HIV-HCV-coinfected patients. Changes in biomarkers over time were then assessed longitudinally in HIV-HCV-coinfected patients during successful cART (n=58), during untreated HIV-infection (n=59), and in HIV-monoinfected individuals (n=17). The median follow-up time was 3.4 years on cART. All analyses were conducted before starting HCV treatment. RESULTS: Non-invasive biomarkers of liver disease correlated significantly with the histological METAVIR stage (P<0.002 for all comparisons). The mean ±sd area under the receiver operating characteristic (AUROC) curve values for advanced fibrosis (≥F3 METAVIR) for HYA, APRI, FIB-4 and CK-18 were 0.86 ±0.05, 0.84 ±0.08, 0.80 ±0.09 and 0.81 ±0.07, respectively. HYA, APRI and CK-18 levels were higher in HIV-HCV-coinfected compared to HIV-monoinfected patients (P<0.01). In the first year on cART, APRI and FIB-4 scores decreased (-35% and -33%, respectively; P=0.1), mainly due to the reversion of HIV-induced thrombocytopaenia, whereas HYA and CK-18 levels remained unchanged. During long-term cART, there were only small changes (<5%) in median biomarker levels. Median biomarker levels changed <3% during untreated HIV-infection. Overall, 3 patients died from end-stage liver disease, and 10 from other causes. CONCLUSIONS: Biomarkers of liver disease highly correlated with fibrosis in HIV-HCV-coinfected individuals and did not change significantly during successful cART. These findings suggest a slower than expected liver disease progression in many HIV-HCV-coinfected individuals, at least during successful cART.

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Certain strains of fluorescent pseudomonads are important biological components of agricultural soils that are suppressive to diseases caused by pathogenic fungi on crop plants. The biocontrol abilities of such strains depend essentially on aggressive root colonization, induction of systemic resistance in the plant, and the production of diffusible or volatile antifungal antibiotics. Evidence that these compounds are produced in situ is based on their chemical extraction from the rhizosphere and on the expression of antibiotic biosynthetic genes in the producer strains colonizing plant roots. Well-characterized antibiotics with biocontrol properties include phenazines, 2,4-diacetylphloroglucinol, pyoluteorin, pyrrolnitrin, lipopeptides, and hydrogen cyanide. In vitro, optimal production of these compounds occurs at high cell densities and during conditions of restricted growth, involving (i) a number of transcriptional regulators, which are mostly pathway-specific, and (ii) the GacS/GacA two-component system, which globally exerts a positive effect on the production of extracellular metabolites at a posttranscriptional level. Small untranslated RNAs have important roles in the GacS/GacA signal transduction pathway. One challenge in future biocontrol research involves development of new strategies to overcome the broad toxicity and lack of antifungal specificity displayed by most biocontrol antibiotics studied so far.

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For persons without cardiovascular disease, the benefit of aspirin in primary prevention has been controversial until the recent publication of several major randomized controlled trials. Since then, several medical societies recommend that clinicians discuss aspirin prevention with adults at high cardiovascular risk. Patients with low cardiovascular risk are unlikely to benefit from aspirin, as potential harms (hemorrhagic strokes, gastrointestinal bleedings) may outweigh benefits. Aspirin should be recommended in primary prevention only in patients with a 10-year cardiovascular risk > or = 10% or in diabetic patients aged > or = 40 years with a concomitant cardiovascular risk factor, after assessing contraindications for aspirin and individual's preferences for the risks and benefits associated with aspirin.

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OBJECTIVES: The purpose of this study was to assess whether metabolic syndrome (MetSyn) predicts a higher risk for cardiovascular events in older adults. BACKGROUND: The importance of MetSyn as a risk factor has not previously focused on older adults and deserves further study. METHODS: We studied the impact of MetSyn (38% prevalence) on outcomes in 3,035 participants in the Health, Aging, and Body Composition (Health ABC) study (51% women, 42% black, ages 70 to 79 years). RESULTS: During a 6-year follow-up, there were 434 deaths overall, 472 coronary events (CE), 213 myocardial infarctions (MI), and 231 heart failure (HF) hospital stays; 59% of the subjects had at least one hospital stay. Coronary events, MI, HF, and overall hospital stays occurred significantly more in subjects with MetSyn (19.9% vs. 12.9% for CE, 9.1% vs. 5.7% for MI, 10.0% vs. 6.1% for HF, and 63.1% vs. 56.1% for overall hospital stay; all p < 0.001). No significant differences in overall mortality was seen; however, there was a trend toward higher cardiovascular mortality (5.1% vs. 3.8%, p = 0.067) and coronary mortality (4.5% vs. 3.2%, p = 0.051) in patients with MetSyn. After adjusting for baseline characteristics, patients with MetSyn were at a significantly higher risk for CE (hazard ratio [HR] 1.56, 95% confidence interval [CI] 1.28 to 1.91), MI (HR 1.51, 95% CI 1.12 to 2.05), and HF hospital stay (HR 1.49, 95% CI 1.10 to 2.00). Women and whites with MetSyn had a higher coronary mortality rate. The CE rate was higher among subjects with diabetes and with MetSyn; those with both had the highest risk. CONCLUSIONS: Overall, subjects over 70 years are at high risk for cardiovascular events; MetSyn in this group is associated with a significantly greater risk.

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The Common variable Immunodeficiency (CVID) is next to the selective IgA-deficiency the most frequent primary immunodeficiency syndrome. Because of its variable clinical manifestations and age of declaration, CVID can mimic different other pathologies and is therefore frequently diagnosed in a later stage of the disease. However, as a consequence of late diagnosis, irreversible organ damage can have occurred which could have been prevented by early treatment. Therefore, early diagnosis of CVID by the general practitioner in patients with recurrent infections or other typical clinical manifestations is of great importance.

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Background The global mortality caused by cardiovascular disease increases with weight. The Framingham study showed that obesity is a cardiovascular risk factor independent of other risks such as type 2 diabetes mellitus, dyslipidemia and smoking. Moreover, the main problem in the management of weight-loss is its maintenance, if it is achieved. We have designed a study to determine whether a group motivational intervention, together with current clinical practice, is more efficient than the latter alone in the treatment of overweight and obesity, for initial weight loss and essentially to achieve maintenance of the weight achieved; and, secondly, to know if this intervention is more effective for reducing cardiovascular risk factors associated with overweight and obesity. Methods This 26-month follow up multi-centre trial, will include 1200 overweight/obese patients. Random assignment of the intervention by Basic Health Areas (BHA): two geographically separate groups have been created, one of which receives group motivational intervention (group intervention), delivered by a nurse trained by an expert phsychologist, in 32 group sessions, 1 to 12 fortnightly, and 13 to 32, monthly, on top of their standard program of diet, exercise, and the other (control group), receiving the usual follow up, with regular visits every 3 months. Discussion By addressing currently unanswered questions regarding the maintenance in weight loss in obesity/overweight, upon the expected completion of participant follow-up in 2012, the IMOAP trial should document, for the first time, the benefits of a motivational intervention as a treatment tool of weight loss in a primary care setting.

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Although metabolic syndrome (MS) and systemic lupus erythematosus (SLE) are often associated, a common link has not been identified. Using the BWF1 mouse, which develops MS and SLE, we sought a molecular connection to explain the prevalence of these two diseases in the same individuals. We determined SLE- markers (plasma anti-ds-DNA antibodies, splenic regulatory T cells (Tregs) and cytokines, proteinuria and renal histology) and MS-markers (plasma glucose, non-esterified fatty acids, triglycerides, insulin and leptin, liver triglycerides, visceral adipose tissue, liver and adipose tissue expression of 86 insulin signaling-related genes) in 8-, 16-, 24-, and 36-week old BWF1 and control New-Zealand-White female mice. Up to week 16, BWF1 mice showed MS-markers (hyperleptinemia, hyperinsulinemia, fatty liver and visceral adipose tissue) that disappeared at week 36, when plasma anti-dsDNA antibodies, lupus nephritis and a pro-autoimmune cytokine profile were detected. BWF1 mice had hyperleptinemia and high splenic Tregs till week 16, thereby pointing to leptin resistance, as confirmed by the lack of increased liver P-Tyr-STAT-3. Hyperinsulinemia was associated with a down-regulation of insulin related-genes only in adipose tissue, whereas expression of liver mammalian target of rapamicyn (mTOR) was increased. Although leptin resistance presented early in BWF1 mice can slow-down the progression of autoimmunity, our results suggest that sustained insulin stimulation of organs, such as liver and probably kidneys, facilitates the over-expression and activity of mTOR and the development of SLE.

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This report is a result of the ADPER & EH division management team retreat that was held on July 30 and 31, 2015 where a gap was identified in our communication with customers, especially when it came to sharing information about planning efforts. The purpose of this report is to provide a comprehensive look at what ADPER & EH has accomplished in the past year as well as what we are working on for the future. It also serves as an annual informational resource for stakeholders, local partners, policy makers and the general public.

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Following the seminal work on personal identity of Erikson, Marcia's identity status model has been one of the most enduring paradigms. The Ego Identity Process Questionnaire (EIPQ; Balistreri, Busch-Rossnagel, & Geissinger, 1995) is a widely used measure of identity status. The purpose of this study was to evaluate the factor structure and the reliability of a French version of the EIPQ. The hypothesized structures were not confirmed. In light of the failed attempts to validate the original version, an alternative short-form version of the EIPQ (EIPQ-SF), maintaining the integrity of the original model, was developed in one sample and cross-validated in another sample. Additionally, theoretically consistent associations between the EIPQ-SF dimensions and self-esteem confirmed convergent validity. Globally, the results indicated that the French short-version of the EIPQ might be a useful instrument for the assessment of the identity statuses in adolescence and emerging adulthood.

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AbstractMyotonic dystrophy type 1 (DM1), also known as Steinert's disease, is an inherited autosomal dominant disease. DM1 is characterized by myotonia, muscular weakness and atrophy, but it has a multisystemic phenotype. The genetic basis of the disease is the abnormal expansion of CTG repeats in the 3' untranslated region of the DM protein kinase (DMPK) gene on chromosome 19. The size of the expansion correlates to the severity of the disease and the age of onset.Respiratory problems have long been recognized to be a major feature of the disease and are the main factor contributing to mortality ; however the mechanisms are only partly known. The aim of our study is to investigate whether respiratory failure results only from the involvement of the dystrophic process at the level of the respiratory muscles or comes also from abnormalities in the neuronal network that generates and controls the respiratory rhythm. The generation of valid transgenic mice displaying the human DM1 phenotype by the group of Dr. Gourdon provided us a useful tool to analyze the brain stem respiratory neurons, spinal phrenic motoneurons and phrenic nerves. We examined therefore these structures in transgenic mice carrying 350-500 CTGs and displaying a mild form of the disease (DM1 mice). The morphological and morphometric analysis of diaphragm muscle sections revealed a denervation of the end-plates (EPs), characterized by a decrease in size and shape complexity of EPs and a reduction in the density of acetylcholine receptors (AChRs). Also a strong and significant reduction in the number of phrenic unmyelinated fibers was detected, but not in the myelinated fibers. In addition, no pathological changes were detected in the cervical motoneurons and medullary respiratory centers (Panaite et al., 2008). These results suggest that the breathing rhythm is probably not affected in mice expressing a mild form of DM1, but rather the transmission of action potentials at the level of diaphragm NMJs is deficient.Because size of the mutation increases over generations, new transgenic mice were obtained from the mice with 350-500 CTGs, resulting from a large increase of CTG repeat in successive generations, these mice carry more than 1300 CTGs (DMSXL) and display a severe DM1 phenotype (Gomes-Pereira et al., 2007). Before we study the mechanism underlying the respiratory failure in DMSXL mice, we analyzed the peripheral nervous system (PNS) in these mice by electrophysiological, histological and morphometric methods. Our results provide strong evidence that DMSXL mice have motor neuropathy (Panaite et al., 2010, submitted). Therefore the DMSXL mice expressing severe DM1 features represent for us a good tool to investigate, in the future, the physiological, structural and molecular alterations underlying respiratory failure in DM1. Understanding the mechanism of respiratory deficiency will help to better target the therapy of these problems in DM1 patients. In addition our results may, in the future, orientate pharmaceutical and clinical research towards possible development of therapy against respiratory deficits associated with the DM1.RésuméLa dystrophic myotonique type 1 (DM1), aussi dénommée maladie de Steinert, est une maladie héréditaire autosomique dominante. Elle est caractérisée par une myotonie, une faiblesse musculaire avec atrophie et se manifeste aussi par un phénotype multisystémique. La base génétique de la maladie est une expansion anormale de répétitions CTG dans une région non traduite en 3' du gène de la DM protéine kinase (DMPK) sur le chromosome 19. La taille de l'expansion est corrélée avec la sévérité et l'âge d'apparition de DM1.Bien que les problèmes respiratoires soient reconnus depuis longtemps comme une complication de la maladie et soient le principal facteur contribuant à la mortalité, les mécanismes en sont partiellement connus. Le but de notre étude est d'examiner si l'insuffisance respiratoire de la DM1 est dû au processus dystrophique au niveau des muscles respiratoires ou si elle est entraînée aussi par des anomalies dans le réseau neuronal qui génère et contrôle le rythme respiratoire. La production par le groupe du Dr. Gourdon de souris transgéniques de DM1, manifestant le phénotype de DM1 humaine, nous a fourni un outil pour analyser les nerfs phréniques, les neurones des centres respiratoires du tronc cérébral et les motoneurones phréniques. Par conséquence, nous avons examiné ces structures chez des souris transgéniques portant 350-500 CTG et affichant une forme légère de la maladie (souris DM1). L'analyse morphologique et morphométrique des sections du diaphragme a révélé une dénervation des plaques motrices et une diminution de la taille et de la complexité de la membrane postsynaptîque, ainsi qu'une réduction de la densité des récepteurs à l'acétylcholine. Nous avons aussi détecté une réduction significative du nombre de fibres nerveuses non myélinisées mais pas des fibres myélinisées. Par ailleurs, aucun changement pathologique n'a été détecté pour les neurones moteurs médullaires cervicaux et centres respiratoires du tronc cérébral (Panaite et al., 2008). Ces résultats suggèrent que le iythme respiratoire n'est probablement pas affecté chez les souris manifestant une forme légère du DM1, mais plutôt que la transmission des potentiels d'action au niveau des plaques motrices du diaphragme est déficiente.Comme la taille du mutation augmente au fil des générations, de nouvelles souris transgéniques ont été générés par le groupe Gourdon; ces souris ont plus de 1300 CTG (DMSXL) et manifestent un phénotype sévère du DM1 (Gomes-Pereira et al., 2007). Avant d'étudier le mécanisme sous-jacent de l'insuffisance respiratoire chez les souris DMSXL, nous avons analysé le système nerveux périphérique chez ces souris par des méthodes électrophysiologiques, histologiques et morphométriques. Nos résultats fournissent des preuves solides que les souris DMSXL manifestent une neuropathie motrice (Panaite et al., 2010, soumis). Par conséquent, les souris DMSXL représentent pour nous un bon outil pour étudier, à l'avenir, les modifications physiologiques, morphologiques et moléculaires qui sous-tendent l'insuffisance respiratoire du DM1. La connaissance du mécanisme de déficience respiratoire en DM1 aidera à mieux cibler le traitement de ces problèmes aux patients. De plus, nos résultats pourront, à l'avenir, orienter la recherche pharmaceutique et clinique vers le développement de thérapie contre le déficit respiratoire associé à DM1.

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Numerous health benefits have been attributed to cocoa and its derived products in the last decade including antioxidant, anti-platelet and positive effects on lipid metabolism and vascular function. Inflammation plays a key role in the initiation and progression of atherosclerosis. However, cocoa feeding trials focused on inflammation are still rare and the results yielded are controversial. Health effects derived from cocoa consumption have been partly attributed to its polyphenol content, in particular of flavanols. Bioavailability is a key issue for cocoa polyphenols in order to be able to exert their biological activities. In the case of flavanols, bioavailability is strongly influenced by several factors, such as their degree of polymerization and the food matrix in which the polyphenols are delivered. Furthermore, gut has become an active site for the metabolism of procyanidins (oligomeric and polymeric flavanols). Estimation of polyphenol consumption or exposure is also a very challenging task in Food and Nutrition Science in order to correlate the intake of phytochemicals with in vivo health effects. In the area of nutrition, modern analytical techniques based on mass spectrometry are leading to considerable advances in targeted metabolite analysis and particularly in Metabolomics or global metabolite analysis. In this chapter we have summarized the most relevant results of our recent research on the bioavailability of cocoa polyphenols in humans and the effect of the matrix in which cocoa polyphenols are delivered considering both targeted analysis and a metabolomic approach. Furthermore, we have also summarized the effect of long-term consumption of cocoa powder in patients at high risk of cardiovascular disease (CVD) on the inflammatory biomarkers of atherosclerosis.

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Gluten-induced enteropathy or coeliac disease is a condition characterized by malabsorption and a variety of clinical manifestations. In adults, coeliac disease may be discovered while investigating iron-deficient anemia, bone pain or unexplained weight loss. We have recently diagnosed a case of gluten-induced enteropathy in an elderly woman whose symptoms were unusual. The patient had episodes of laryngospasm secondary to severe hypocalcemia and hypomagnesemia. The malabsorption syndrome was responsible for low levels of vitamin D, causing the electrolytic imbalance. Laryngospasm is a rare symptom of hypocalcemia and has not, to our knowledge, been described in the context of coeliac disease.

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HIV-positive adolescents face a number of challenges in dealing with their disease and its treatment. In this qualitative study, twenty-nine HIV-positive adolescents aged 13 to 20 years (22 girls), who live in Switzerland, were asked, in a semi-structured interview (duration of 40-110 minutes), to describe their perceptions and experiences with the disease itself and with therapeutic adherence. While younger adolescents most often thought of their disease as fate, older adolescents usually knew that they had received it through vertical transmission, although the topic appeared to be particularly difficult to discuss for those living with their HIV-positive mothers. Based on their attending physician's assessment, 18 subjects were judged highly adherent, 4 fairly and 7 poorly adherent. High adherence appeared linked with adequate psychological adjustment and effective coping mechanisms, as well as with the discussion and adoption of explicit medication-taking strategies. The setting and organisation of health care teams should allow for ongoing discussions with HIV-positive adolescents that focus on their perceptions of their disease, how they cope with it and with the treatment, and how they could improve their adherence.