Adaptive neuro-fussy based control surface fault detection and reconfiguration

The aircraft becomes unstable due to fault in actuator or if there is a loss of control surface13; effectiveness due to damaged or blown surfaces. One of the popular methods to detect and reconfigure13; the surface fault is model based approach e.g. Extended Kalman filter (EKF). Using EKF, the parameters13; of control distribution matrix are estimated as augmented states of the system which are subsequently13; used to compute feedback gain to reconfigure the impaired system In this paper, detection and13; reconfiguration of surface fault in elevator of an aircraft is demonstrated using Adaptive Neuro - Fuzzy13; Inference System ANFIS . Under this approach, i) ANFIS is trained using time history of i/o data i.e.13; inputs as errors between nominal (healthy) states of aircraft and its faulty states (noise free) for different13; fault conditions and output as parameters of control distribution matrix and ii) trained ANFIS is13; subsequently used to estimate the parameters of control distribution matrix for the actual fault condition13; and the reconfiguration is carried out by computing new feedback gain using pseudo-inverse technique

A922 Sequential measurement of 1 hour creatinine clearance (1-CRCL) in critically ill patients at risk of acute kidney injury (AKI)

Meeting abstrac

The effects of varying protein and energy intakes on the growth and body composition of very low birth weight infants

<p>Abstract</p> <p>Objective</p> <p>To determine the effects of high dietary protein and energy intake on the growth and body composition of very low birth weight (VLBW) infants.</p> <p>Study design</p> <p>Thirty-eight VLBW infants whose weights were appropriate for their gestational ages were assessed for when they could tolerate oral intake for all their nutritional needs. Thirty-two infants were included in a longitudinal, randomized clinical trial over an approximate 28-day period. One control diet (standard preterm formula, group A, n = 8, 3.7 g/kg/d of protein and 129 kcal/kg/d) and two high-energy and high-protein diets (group B, n = 12, 4.2 g/kg/d and 150 kcal/kg/d; group C, n = 12, 4.7 g/kg/d and 150 kcal/kg/d) were compared. Differences among groups in anthropometry and body composition (measured with bioelectrical impedance analysis) were determined. An enriched breast milk group (n = 6) served as a descriptive reference group.</p> <p>Results</p> <p>Groups B and C displayed greater weight gains and higher increases in fat-free mass than group A.</p> <p>Conclusion</p> <p>An intake of 150 kcal/kg/d of energy and 4.2 g/kg/d of protein increases fat-free mass accretion in VLBW infants.</p

Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol

The presence of Fc-receptor-blocking factors in the sera of normal and insulin-dependent diabetic pregnant women was investigated by means of an antibody-dependent cell-mediated cytotoxicity assay. Sera from normal pregnant women induced a significant depression of antibody dependent cell-mediated cytotoxicity when compared with sera from normal and diabetic non-pregnant women (p less than 0.0001; p less than 0.002, respectively). The effect of sera from diabetic pregnant women, however, was not different from that observed with sera from normal and diabetic non-pregnant women. Thus, we confirm the presence of Fc-receptor-blocking factors in the sera of normal pregnant women. The higher cytotoxicity levels measured in the presence of sera from pregnant women with insulin-dependent diabetes suggests that the titres of such factors are reduced in this conditio

Assessment of insulin resistance by a 13C glucose breath test: a new tool for early diagnosis and follow-up of high-risk patients

<p>Abstract</p> <p>Background/Aims</p> <p>Insulin resistance (IR) plays an important role in the pathogenesis of diabetes and non-alcoholic fatty liver disease (NAFLD). Current methods for insulin resistance detection are cumbersome, or not sensitive enough for early detection and follow-up. The BreathID^®system can continuously analyse breath samples in real-time at the point-of-care. Here we determined the efficacy of the BreathID^®using the ¹³C-Glucose breath test (GBT) for evaluation of insulin resistance.</p> <p>Methods</p> <p>Twenty healthy volunteers were orally administered 75 mg of ¹³C-glucose 1-¹³C. An oral glucose tolerance test (OGTT) was performed immediately; followed by serum glucose and insulin level determinations using GBT. GBT and OGTT were repeated following exercise, which alters insulin resistance levels.</p> <p>Results</p> <p>Within-subject correlations of GBT parameters with serum glucose and serum insulin levels were high. Before and after exercise, between-subjects correlations were high between the relative insulin levels and the % dose recoveries at 90 min (PDR 90), and the cumulative PDRs at 60 min (CPDR 60). Pairwise correlations were identified between pre-exercise Homeostasis Model Assessment (HOMA) IR at 90 min and PDR 90; HOMA B (for beta cell function) 120 and CPDR 30; HOMA IR 60 and peak time post-exercise; and HOMA B 150 with PDR 150.</p> <p>Conclusions</p> <p>The non-invasive real-time BreathID^®GBT reliably assesses changes in liver glucose metabolism, and the degree of insulin resistance. It may serve as a non-invasive tool for early diagnosis and follow up of patients in high-risk groups.</p

Insulin resistance, lipotoxicity, type 2 diabetes and atherosclerosis: the missing links. The Claude Bernard Lecture 2009

Insulin resistance is a hallmark of type 2 diabetes mellitus and is associated with a metabolic and cardiovascular cluster of disorders (dyslipidaemia, hypertension, obesity [especially visceral], glucose intolerance, endothelial dysfunction), each of which is an independent risk factor for cardiovascular disease (CVD). Multiple prospective studies have documented an association between insulin resistance and accelerated CVD in patients with type 2 diabetes, as well as in non-diabetic individuals. The molecular causes of insulin resistance, i.e. impaired insulin signalling through the phosphoinositol-3 kinase pathway with intact signalling through the mitogen-activated protein kinase pathway, are responsible for the impairment in insulin-stimulated glucose metabolism and contribute to the accelerated rate of CVD in type 2 diabetes patients. The current epidemic of diabetes is being driven by the obesity epidemic, which represents a state of tissue fat overload. Accumulation of toxic lipid metabolites (fatty acyl CoA, diacylglycerol, ceramide) in muscle, liver, adipocytes, beta cells and arterial tissues contributes to insulin resistance, beta cell dysfunction and accelerated atherosclerosis, respectively, in type 2 diabetes. Treatment with thiazolidinediones mobilises fat out of tissues, leading to enhanced insulin sensitivity, improved beta cell function and decreased atherogenesis. Insulin resistance and lipotoxicity represent the missing links (beyond the classical cardiovascular risk factors) that help explain the accelerated rate of CVD in type 2 diabetic patients

Polymorphisms within the Novel Type 2 Diabetes Risk Locus MTNR1B Determine β-Cell Function

BACKGROUND:Very recently, a novel type 2 diabetes risk gene, i.e., MTNR1B, was identified and reported to affect fasting glycemia. Using our thoroughly phenotyped cohort of subjects at an increased risk for type 2 diabetes, we assessed the association of common genetic variation within the MTNR1B locus with obesity and prediabetes traits, namely impaired insulin secretion and insulin resistance. METHODOLOGY/PRINCIPAL FINDINGS:We genotyped 1,578 non-diabetic subjects, metabolically characterized by oral glucose tolerance test, for five tagging single nucleotide polymorphisms (SNPs) covering 100% of common genetic variation (minor allele frequency > 0.05) within the MTNR1B locus (rs10830962, rs4753426, rs12804291, rs10830963, rs3781638). In a subgroup (N = 513), insulin sensitivity was assessed by hyperinsulinemic-euglycemic clamp, and in a further subgroup (N = 301), glucose-stimulated insulin secretion was determined by intravenous glucose tolerance test. After appropriate adjustment for confounding variables and Bonferroni correction for multiple comparisons, none of the tagging SNPs was reliably associated with measures of adiposity. SNPs rs10830962, rs4753426, and rs10830963 were significantly associated with higher fasting plasma glucose concentrations (p < 0.0001) and reduced OGTT- and IVGTT-induced insulin release (p < or = 0.0007 and p < or = 0.01, respectively). By contrast, SNP rs3781638 displayed significant association with lower fasting plasma glucose levels and increased OGTT-induced insulin release (p<0.0001 and p < or = 0.0002, respectively). Moreover, SNP rs3781638 revealed significant association with elevated fasting- and OGTT-derived insulin sensitivity (p < or = 0.0021). None of the MTNR1B tagging SNPs altered proinsulin-to-insulin conversion. CONCLUSIONS/SIGNIFICANCE:In conclusion, common genetic variation within MTNR1B determines glucose-stimulated insulin secretion and plasma glucose concentrations. Their impact on beta-cell function might represent the prevailing pathomechanism how MTNR1B variants increase the type 2 diabetes risk