325 research outputs found
A Rotating Fluidized Bed in a Static Geometry: Experimental Proof of Concept
The new concept of a rotating fluidized bed in a static geometry (RFB-SG) is presented (1). The rotating motion of the particle bed and the tangential fluidization of the solids are obtained by the tangential injection of the fluidization gas via multiple gas inlet slots in the outer cylindrical wall of the fluidization chamber. The new fluidization concept is experimentally investigated and proven using either large diameter, low density polymer particles or small diameter, higher density Alumina particles
Interprétation géométrique de la capacité et des performances de systÚmes à diversité
- Notre étude a pour cadre les systÚmes de transmission à diversité. Nous analysons tout d'abord l'influence d'une erreur d'estimation du canal, et déduisons l'expression analytique de la capacité ainsi dégradée d'un systÚme OPRA (Optimal Power and Rate Adaptation). Ensuite, nous proposons une interprétation géométrique de cette capacité en nous basant sur la théorie des courbes dites de Bézier. AprÚs avoir passé en revue certaines propriétés héritées de cette structure particuliÚre, nous proposons alors une expression matricielle de cette capacité, ainsi qu'une méthodologie de construction graphique. Pour conclure, nous présentons une application concernant le dimensionnement de motif de pilotes, pour des systÚmes multi-porteuse à étalement fréquentiel (Multi-Carrier Spread-Spectrum)
Nouveau décodeur à complexité réduite pour codes convolutifs de rendement 1/2
Les codes convolutifs peuvent ĂȘtre dĂ©codĂ©s de façon optimale Ă l'aide l'algorithme de Viterbi (VA). Nous proposons un dĂ©codeur Ă entrĂ©e souple dans lequel l'algorithme de Viterbi est employĂ© pour identifier le vecteur d'erreur plutĂŽt que le message d'information avec une mĂ©trique appropriĂ©e. Ce type de dĂ©codage permet d'Ă©viter la mise en oeuvre d'un nombre important d'opĂ©rations ACS (Add Compare Select). Nous montrons que les performances atteintes sont proches de l'optimum tout en bĂ©nĂ©ficiant d'une rĂ©duction de la complexitĂ© qui est d'autant plus importante que le rapport signal Ă bruit (SNR) est favorable. Par exemple, pour des SNR supĂ©rieurs Ă 3 dB et dans le cas d'une transmission avec la modulation BPSK sur canal gaussien, au moins 88% des ACS peuvent ĂȘtre Ă©vitĂ©s
Higher Plasma Levels of Advanced Glycation End Products Are Associated With Incident Cardiovascular Disease and All-Cause Mortality in Type 1 Diabetes: A 12-year follow-up study
OBJECTIVE - To investigate the associations of plasma levels of advanced glycation end products (AGEs) with incident cardiovascular disease (CVD) and all-cause mortality in type 1 diabetes and the extent to which any such associations could be explained by endothelial and renal dysfunction, low-grade inflammation, and arterial stiffness. RESEARCH DESIGN AND METHODS - We prospectively followed 169 individuals with diabetic nephropathy and 170 individuals with persistent normoalbuminuria who were free of CVD at study entry and in whom levels of N Δ -(carboxymethyl)lysine, N Δ -(carboxyethyl) lysine, pentosidine and other biomarkers were measured at baseline. The median follow-up duration was 12.3 (interquartile range 7.6-12.5) years. RESULTS - During the course of follow-up, 82 individuals (24.2%) died; 85 (25.1%) suffered a fatal (n = 48) and/or nonfatal (n = 53) CVD event. The incidence of fatal and nonfatal CVD and of all-cause mortality increased with higher baseline levels of AGEs independently of traditional CVD risk factors: hazard ratio (HR) = 1.30 (95% CI = 1.03-1.66) and HR = 1.27 (1.00-1.62), respectively. These associations were not attenuated after further adjustments for markers of renal or endothelial dysfunction, low-grade inflammation, or arterial stiffness. CONCLUSIONS - Higher levels of AGEs are associated with incident fatal and nonfatal CVD as well as all-cause mortality in individuals with type 1 diabetes, independently of other risk factors and of several potential AGEs-related pathophysiological mechanisms. Thus, AGEs may explain, in part, the increased cardiovascular disease andmortality attributable to type 1 diabetes and constitute a specific target for treatment in these patients. 2011 by the American Diabetes Association
Reductive Metabolism of AGE Precursors: A Metabolic Route for Preventing AGE Accumulation in Cardiovascular Tissue
OBJECTIVEâTo examine the role of aldo-keto reductases (AKRs) in the cardiovascular metabolism of the precursors of advanced glycation end products (AGEs). RESEARCH DESIGN AND METHODSâSteady-state kinetic parameters of AKRs with AGE precursors were determined using recombinant proteins expressed in bacteria. Metabolism of meth-ylglyoxal and AGE accumulation were studied in human umbil-ical vein endothelial cells (HUVECs) and C57 wild-type, akr1b3 (aldose reductase)-null, cardiospecific-akr1b4 (rat aldose reduc-tase), and akr1b8 (FR-1)-transgenic mice. AGE accumulation and atherosclerotic lesions were studied 12 weeks after streptozoto-cin treatment of C57, akr1b3-null, and apoE- and akr1b3-apoEâ null mice. RESULTSâHigher levels of AGEs were generated in the cytosol than at the external surface of HUVECs cultured in high glucose
Accumulation of advanced glycation end (AGEs) products in intensive care patients: an observational, prospective study
<p>Abstract</p> <p>Background</p> <p>Oxidative stress plays an important role in the course and eventual outcome in a majority of patients admitted to the intensive care unit (ICU). Markers to estimate oxidative stress are not readily available in a clinical setting. AGEs accumulation has been merely described in chronic conditions, but can also occur acutely due to oxidative stress. Since AGEs have emerged to be stable end products, these can be a marker of oxidative stress. Skin autofluorescence (AF) is a validated marker of tissue content of AGEs. We hypothesized that AGEs accumulate acutely in ICU patients.</p> <p>Methods</p> <p>We performed an observational prospective study in a medical surgical ICU in a university affiliated teaching hospital. All consecutively admitted ICU patients in a 2 month period were included. Skin AF was measured using an AGE reader in 35 consecutive ICU patients > 18 yrs. As a comparison, historical data of a control group (n = 231) were used. These were also used to calculate age-adjusted AF-levels (AF<sub>adj</sub>). Values are expressed as median and interquartile range [P<sub>25</sub>-P<sub>75</sub>]. Differences between groups were tested by non parametric tests. P < 0.05 was considered statistically significant.</p> <p>Results</p> <p>AF<sub>adj </sub>values were higher in ICU patients (0.33 [0.00 - 0.68]) than in controls (-0.07 [-0.29 - 0.24]; P < 0.001). No differences in skin AF<sub>adj </sub>were observed between acute or planned admissions, or presence of sepsis, nor was skin AF<sub>adj </sub>related to severity of disease as estimated by APACHE-II score, length of ICU, hospital stay or mortality.</p> <p>Conclusion</p> <p>Acute AGE accumulation in ICU patients was shown in this study, although group size was small. This can possibly reflect oxidative stress in ICU patients. Further studies should reveal whether AGE-accumulation will be a useful parameter in ICU patients and whether skin AF has a predictive value for outcome, which was not shown in this small study.</p
Clearance kinetics and matrix binding partners of the receptor for advanced glycation end products
Elucidating the sites and mechanisms of sRAGE action in the healthy state is vital to better understand the biological importance of the receptor for advanced glycation end products (RAGE). Previous studies in animal models of disease have demonstrated that exogenous sRAGE has an anti-inflammatory effect, which has been reasoned to arise from sequestration of pro-inflammatory ligands away from membrane-bound RAGE isoforms. We show here that sRAGE exhibits in vitro binding with high affinity and reversibly to extracellular matrix components collagen I, collagen IV, and laminin. Soluble RAGE administered intratracheally, intravenously, or intraperitoneally, does not distribute in a specific fashion to any healthy mouse tissue, suggesting against the existence of accessible sRAGE sinks and receptors in the healthy mouse. Intratracheal administration is the only effective means of delivering exogenous sRAGE to the lung, the organ in which RAGE is most highly expressed; clearance of sRAGE from lung does not differ appreciably from that of albumin. Copyright: © 2014 Milutinovic et al
Glucose metabolite glyoxal induces senescence in telomerase-immortalized human mesenchymal stem cells
Abstract Background Various by-products of the cellular metabolism, such as reactive carbonyl species (RCS) are potentially harmful to cells and tissues, and play a role in many physiological and pathological processes. Among various RCS is the highly reactive dicarbonyl glyoxal (GO), which is a natural physiological metabolite produced by the auto-oxidation of glucose, and can form covalent adducts known as advanced glycation endproducts (AGE). We have previously reported that GO accelerates ageing and causes premature senescence in normal human skin fibroblasts. Results Using a bone marrow-derived telomerase-immortalised mesenchymal stem cell line hMSC-TERT we have observed that an exposure of cells to 0.75 mM and 1 mM GO induces irreversible cellular senescence within 3 days. Induction of senescence in hMSC-TERT was demonstrated by a variety of markers, including characteristic cell morphology and enlargement, vacuolisation, multinucleation, induction of senescence associated ÎČ-galactosidase, cell cycle arrest, and increased levels of a cell cycle inhibitor p16. These changes were accompanied by increased extent of DNA breaks as measured by the comet assay, and increased levels of the AGE product, carboxymethyl-lysine (CML). Furthermore, the in vitro differentiation potential of hMSC-TERT to become functional osteoblasts was highly reduced in GO-treated stem cells, as determined by alkaline phosphatase (ALP) activity and mineralized matrix (MM) formation. Conclusions The results of our study imply that an imbalanced glucose metabolism can reduce the functioning ability of stem cells in vivo both during ageing and during stem cell-based therapeutic interventions.</p
Metabolic syndrome is associated with change in subclinical arterial stiffness - A community-based Taichung Community Health Study
<p>Abstract</p> <p>Background</p> <p>The aim of this study was to evaluate the effect of MetS on arterial stiffness in a longitudinal study.</p> <p>Methods</p> <p>Brachial-ankle pulse wave velocity (baPWV), a measurement interpreted as arterial stiffness, was measured in 1518 community-dwelling persons at baseline and re-examined within a mean follow-up period of 3 years. Multivariate linear regression with generalized estimating equations (GEE) were used to examine the longitudinal relationship between MetS and its individual components and baPWV, while multivariate logistic regression with GEE was used to examine the longitudinal relationship between MetS and its individual components and the high risk group with arterial stiffness.</p> <p>Results</p> <p>Subjects with MetS showed significantly greater baPWV at the end point than those without MetS, after adjusting for age, gender, education, hypertension medication and mean arterial pressure (MAP). MetS was associated with the top quartile of baPWV (the high-risk group of arterial stiffness, adjusted odds ratio [95% confidence interval] 1.52 [1.21-1.90]), and a significant linear trend of risk for the number of components of MetS was found (p for trend < 0.05). In further considering the individual MetS component, elevated blood pressure and fasting glucose significantly predicted a high risk of arterial stiffness (adjusted OR [95% CI] 3.72 [2.81-4.93] and 1.35 [1.08-1.68], respectively).</p> <p>Conclusions</p> <p>MetS affects the subject's progression to arterial stiffness. Arterial stiffness increased as the number of MetS components increased. Management of MetS is important for preventing the progression to advanced arterial stiffness.</p
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