Showing papers by "Institute of Chartered Accountants of Nigeria published in 2015"
St. Michael's Hospital1, University of Toronto2, University of Saskatchewan3, Harvard University4, University of Copenhagen5, Lund University6, University of Sydney7, University of Parma8, University of Bonn9, University of Barcelona10, University of Milan11, Brown University12, Institute of Chartered Accountants of Nigeria13, French Institute of Health and Medical Research14, National and Kapodistrian University of Athens15
TL;DR: There is an urgent need to communicate information on GI and GL to the general public and health professionals, through channels such as national dietary guidelines, food composition tables and food labels.
Abstract: Background and aims The positive and negative health effects of dietary carbohydrates are of interest to both researchers and consumers. Methods International experts on carbohydrate research held a scientific summit in Stresa, Italy, in June 2013 to discuss controversies surrounding the utility of the glycemic index (GI), glycemic load (GL) and glycemic response (GR). Results The outcome was a scientific consensus statement which recognized the importance of postprandial glycemia in overall health, and the GI as a valid and reproducible method of classifying carbohydrate foods for this purpose. There was consensus that diets low in GI and GL were relevant to the prevention and management of diabetes and coronary heart disease, and probably obesity. Moderate to weak associations were observed for selected cancers. The group affirmed that diets low in GI and GL should always be considered in the context of diets otherwise understood as healthy, complementing additional ways of characterizing carbohydrate foods, such as fiber and whole grain content. Diets of low GI and GL were considered particularly important in individuals with insulin resistance. Conclusions Given the high prevalence of diabetes and pre-diabetes worldwide and the consistency of the scientific evidence reviewed, the expert panel confirmed an urgent need to communicate information on GI and GL to the general public and health professionals, through channels such as national dietary guidelines, food composition tables and food labels.
461 citations
TL;DR: The CASINO (Community And Systems-level INteractive Optimization) toolbox is described, a comprehensive computational platform for analysis of microbial communities through metabolic modeling that could quantitatively describe altered fecal and serum amino acid levels in response to diet intervention.
328 citations
French Institute of Health and Medical Research1, Pierre-and-Marie-Curie University2, Institute of Chartered Accountants of Nigeria3, Harvard University4, Leiden University5, University of Minnesota6, Mayo Clinic7, University of Washington8, Aix-Marseille University9, Ottawa Hospital Research Institute10, Icahn School of Medicine at Mount Sinai11, National Institute for Health Research12, University of Leicester13, French Alternative Energies and Atomic Energy Commission14, King Abdulaziz University15, University of Bordeaux16, University of Montpellier17, University of California, Los Angeles18, Karolinska Institutet19, Group Health Cooperative20, Lille University of Science and Technology21, VA Office of Research and Development22
TL;DR: A meta-analysis of genome-wide association studies to identify additional VTE susceptibility genes uncovered unexpected actors of VTE etiology and pave the way for novel mechanistic concepts of V TE pathophysiology.
Abstract: Venous thromboembolism (VTE), the third leading cause of cardiovascular mortality, is a complex thrombotic disorder with environmental and genetic determinants. Although several genetic variants have been found associated with VTE, they explain a minor proportion of VTE risk in cases. We undertook a meta-analysis of genome-wide association studies (GWASs) to identify additional VTE susceptibility genes. Twelve GWASs totaling 7,507 VTE case subjects and 52,632 control subjects formed our discovery stage where 6,751,884 SNPs were tested for association with VTE. Nine loci reached the genome-wide significance level of 5 × 10−8 including six already known to associate with VTE (ABO, F2, F5, F11, FGG, and PROCR) and three unsuspected loci. SNPs mapping to these latter were selected for replication in three independent case-control studies totaling 3,009 VTE-affected individuals and 2,586 control subjects. This strategy led to the identification and replication of two VTE-associated loci, TSPAN15 and SLC44A2, with lead risk alleles associated with odds ratio for disease of 1.31 (p = 1.67 × 10−16) and 1.21 (p = 2.75 × 10−15), respectively. The lead SNP at the TSPAN15 locus is the intronic rs78707713 and the lead SLC44A2 SNP is the non-synonymous rs2288904 previously shown to associate with transfusion-related acute lung injury. We further showed that these two variants did not associate with known hemostatic plasma markers. TSPAN15 and SLC44A2 do not belong to conventional pathways for thrombosis and have not been associated to other cardiovascular diseases nor related quantitative biomarkers. Our findings uncovered unexpected actors of VTE etiology and pave the way for novel mechanistic concepts of VTE pathophysiology.
236 citations
University of Lincoln1, Queen Mary University of London2, King's College London3, Heidelberg University4, University Hospital Heidelberg5, Cleveland Clinic6, Vanderbilt University Medical Center7, ARUP Laboratories8, University of Utah9, Columbia University Medical Center10, French Institute of Health and Medical Research11, Institute of Chartered Accountants of Nigeria12, University of Cambridge13, University of Paris-Sud14, Quest Diagnostics15, Vanderbilt University16
TL;DR: These analyses represent the largest comprehensive compilation of BMPR2 and associated genetic risk factors for PAH, comprising known and novel variation, and with the inclusion of an allelic series of locus‐specific variation in BMPR1 provide a key resource in data interpretation and development of contemporary therapeutic and diagnostic tools.
Abstract: Pulmonary arterial hypertension (PAH) is an often fatal disorder resulting from several causes including heterogeneous genetic defects. While mutations in the bone morphogenetic protein receptor type II (BMPR2) gene are the single most common causal factor for hereditary cases, pathogenic mutations have been observed in approximately 25% of idiopathic PAH patients without a prior family history of disease. Additional defects of the transforming growth factor beta pathway have been implicated in disease pathogenesis. Specifically, studies have confirmed activin A receptor type II-like 1 (ACVRL1), endoglin (ENG), and members of the SMAD family as contributing to PAH both with and without associated clinical phenotypes. Most recently, next-generation sequencing has identified novel, rare genetic variation implicated in the PAH disease spectrum. Of importance, several identified genetic factors converge on related pathways and provide significant insight into the development, maintenance, and pathogenetic transformation of the pulmonary vascular bed. Together, these analyses represent the largest comprehensive compilation of BMPR2 and associated genetic risk factors for PAH, comprising known and novel variation. Additionally, with the inclusion of an allelic series of locus-specific variation in BMPR2, these data provide a key resource in data interpretation and development of contemporary therapeutic and diagnostic tools.
188 citations
TL;DR: Few studies have investigated determinants of sedentary behaviour in older adults and these have to date mostly focussed on personal factors, and qualitative studies were mostly lacking.
Abstract: Background: Older adults are the most sedentary segment of society and high sedentary time is associated with poor health and wellbeing outcomes in this population. Identifying determinants of sedentary behaviour is a necessary step to develop interventions to reduce sedentary time. Methods: A systematic literature review was conducted to identify factors associated with sedentary behaviour in older adults. Pubmed, Embase, CINAHL, PsycINFO and Web of Science were searched for articles published between 2000 and May 2014. The search strategy was based on four key elements: (a) sedentary behaviour and its synonyms; (b) determinants and its synonyms (e.g. correlates, factors); (c) types of sedentary behaviour (e.g. TV viewing, sitting, gaming) and (d) types of determinants (e.g. environmental, behavioural). Articles were included in the review if specific information about sedentary behaviour in older adults was reported. Studies on samples identified by disease were excluded. Study quality was rated by means of QUALSYST. The full review protocol is available from PROSPERO (PROSPERO 2014: CRD42014009823). The analysis was guided by the socio-ecological model framework. Results: Twenty-two original studies were identified out of 4472 returned by the systematic search. These included 19 cross-sectional, 2 longitudinal and 1 qualitative studies, all published after 2011. Half of the studies were European. The study quality was generally high with a median of 82 % (IQR 69–96 %) using Qualsyst tool. Personal factors were the most frequently investigated with consistent positive association for age, negative for retirement, obesity and health status. Only four studies considered environmental determinants suggesting possible association with mode of transport, type of housing, cultural opportunities and neighbourhood safety and availability of places to rest. Only two studies investigated mediating factors. Very limited information was available on contexts and sub-domains of sedentary behaviours. Conclusion: Few studies have investigated determinants of sedentary behaviour in older adults and these have to date mostly focussed on personal factors, and qualitative studies were mostly lacking. More longitudinal studies are needed as well as inclusion of a broader range of personal and contextual potential determinants towards a systems-based approach, and future studies should be more informed by qualitative work.
159 citations
TL;DR: This study opens new perspectives in understanding the physiology of human EAT and its local interaction with neighbouring structures.
Abstract: Aims Human epicardial adipose tissue (EAT) is a visceral and perivascular fat that has been shown to act locally on myocardium, atria, and coronary arteries. Its abundance has been linked to coronary artery disease (CAD) and atrial fibrillation. However, its physiological function remains highly debated. The aim of this study was to determine a specific EAT transcriptomic signature, depending on its anatomical peri-atrial (PA), peri-ventricular (PV), or peri-coronary location.
Methods and results Samples of EAT and thoracic subcutaneous fat, obtained from 41 patients paired for cardiovascular risk factors, CAD, and atrial fibrillation were analysed using a pangenomic approach. We found 2728 significantly up-regulated genes in the EAT vs. subcutaneous fat with 400 genes being common between PA, PV, and peri-coronary EAT. These common genes were related to extracellular matrix remodelling, inflammation, infection, and thrombosis pathways. Omentin ( ITLN1 ) was the most up-regulated gene and secreted adipokine in EAT (fold-change >12, P < 0.0001). Among EAT-enriched genes, we observed different patterns depending on adipose tissue location. A beige expression phenotype was found in EAT but PV EAT highly expressed uncoupled protein 1 ( P = 0.01). Genes overexpressed in peri-coronary EAT were implicated in proliferation, O - N glycan biosynthesis, and sphingolipid metabolism. PA EAT displayed an atypical pattern with genes implicated in cardiac muscle contraction and intracellular calcium signalling pathway.
Conclusion This study opens new perspectives in understanding the physiology of human EAT and its local interaction with neighbouring structures.
153 citations
TL;DR: Obesity triggers T-cell-mediated inflammation and enterocyte insulin resistance in the jejunum with potential broader systemic implications, and statistical links between T cell densities and BMI, NAFLD, or lipid metabolism suggest tissue crosstalk.
129 citations
Imperial College London1, St George's, University of London2, University of the Witwatersrand3, University of São Paulo4, University of Manchester5, University of Western Australia6, Saint Joseph's University7, Sultan Qaboos University8, Medical University of Łódź9, Instituto Nacional de Saúde Dr. Ricardo Jorge10, Institute of Chartered Accountants of Nigeria11, Nanyang Technological University12, Innsbruck Medical University13, Hebrew University of Jerusalem14, Masaryk University15, University of Lisbon16, McGill University17, Ege University18, National University of Singapore19, University of Latvia20, Saarland University21, University of Ioannina22, Linköping University23, Copenhagen University Hospital24, Mashhad University of Medical Sciences25, Technische Universität München26, United Arab Emirates University27, National Taiwan University28, University of Helsinki29, University of Milan30
TL;DR: Although early detection and treatment with statins and other LDL-C lowering therapies can improve survival, FH remains widely underdiagnosed and undertreated, thereby representing a major global public health challenge.
123 citations
TL;DR: Evaluated sedative, antibiotic and immunosuppressive drug loss in ECMO circuit using ex-vivo and in-vitro experiments observed important losses of propofol and midazolam, while cyclosporine concentration decreased slowly and moderately, and vancomycin concentration remained unchanged in the ex- vivo EC MO circuit primed with whole human blood.
Abstract: Introduction: As a result of drug sequestration and increased volume of distribution, the extracorporeal membrane oxygenation (ECMO) procedure might lead to a decrease in drug concentrations during a patient's treatment. The aim of this study was to evaluate sedative, antibiotic and immunosuppressive drug loss in ECMO circuit using ex-vivo and in-vitro experiments. Methods: Blood concentrations of propofol, midazolam, cyclosporine and vancomycin were measured in an ex-vivo ECMO circuit primed with whole human blood, and compared to controls stored in polypropylene tubes. In vitro experiments were also conducted to further explore the role of temperature, oxygen exposure and polyvinylchloride surfaces on propofol loss in the ECMO circuit. Results: Propofol concentration decreased rapidly; 70% of its baseline concentration was lost after only 30 minutes, and only 11% remained after five hours (P <0.001 for the comparison with control polypropylene tube propofol concentration). Further experiments demonstrated that oxygen exposure and contact with polyvinylchloride tubing were respectively responsible for 70% and 85% of propofol loss after 45 minutes. Midazolam concentration also rapidly decreased in the ECMO circuit, with only 54% and 11% of baseline concentration being detected at 30 minutes and 24 hours respectively (P = 0.01 versus control). Alternatively, cyclosporine concentration remained stable for the five first hours, then decreased to 78% and 73% of the baseline value after 24 hours and 48 hours, (P = 0.35 versus control). Lastly, vancomycin concentration remained stable in the ECMO circuit for the 48-hour experimental protocol. Conclusions: We observed important losses of propofol and midazolam, while cyclosporine concentration decreased slowly and moderately, and vancomycin concentration remained unchanged in the ex-vivo ECMO circuit primed with whole human blood. These data might help intensive care unit physicians planning clinical trials with a final objective to better adapt doses of these drugs while treating critically ill ECMO patients.
101 citations
St George's, University of London1, Vanderbilt University2, University of Amsterdam3, National Research Foundation of South Africa4, University of Copenhagen5, Novo Nordisk6, Leo Pharma7, French Institute of Health and Medical Research8, University of Paris9, Institute of Chartered Accountants of Nigeria10, Mayo Clinic11, University of Pavia12
TL;DR: Rare variants in the screened QRS-associated genes (including SCN10A) are not responsible for a significant proportion of SCN5A mutation negative BrS, as did rare variants in isolated patients.
Abstract: Aims Brugada syndrome (BrS) remains genetically heterogeneous and is associated with slowed cardiac conduction. We aimed to identify genetic variation in BrS cases at loci associated with QRS duration.
Methods and results A multi-centre study sequenced seven candidate genes ( SCN10A , HAND1 , PLN , CASQ2 , TKT , TBX3 , and TBX5 ) in 156 Caucasian SCN5A mutation-negative BrS patients (80% male; mean age 48) with symptoms (64%) and/or a family history of sudden death (47%) or BrS (18%). Forty-nine variants were identified: 18 were rare (MAF <1%) and non-synonymous; and 11/18 (61.1%), mostly in SCN10A , were predicted as pathogenic using multiple bioinformatics tools. Allele frequencies were compared with the Exome Sequencing and UK10K Projects. SKAT methods tested rare variation in SCN10A finding no statistically significant difference between cases and controls. Co-segregation analysis was possible for four of seven probands carrying a novel pathogenic variant. Only one pedigree (I671V/G1299A in SCN10A ) showed co-segregation. The SCN10A SNP V1073 was, however, associated strongly with BrS [66.9 vs. 40.1% (UK10K) OR (95% CI) = 3.02 (2.35–3.87), P = 8.07 × 10–19]. Voltage-clamp experiments for NaV1.8 were performed for SCN10A common variants V1073, A1073, and rare variants of interest: A200V and I671V. V1073, A200V and I671V, demonstrated significant reductions in peak I Na compared with ancestral allele A1073 (rs6795970).
Conclusion Rare variants in the screened QRS-associated genes (including SCN10A ) are not responsible for a significant proportion of SCN5A mutation negative BrS. The common SNP SCN10A V1073 was strongly associated with BrS and demonstrated loss of NaV1.8 function, as did rare variants in isolated patients.
99 citations
University of Lübeck1, University of California, Los Angeles2, Technische Universität München3, Icahn School of Medicine at Mount Sinai4, French Institute of Health and Medical Research5, Pierre-and-Marie-Curie University6, Institute of Chartered Accountants of Nigeria7, University of Leicester8, Karolinska Institutet9, Scripps Health10
TL;DR: It is concluded that the great majority of causal variations affecting CAD risk occur in noncoding regions, with 41% affecting gene expression robustly versus 6% leading to amino acid changes.
Abstract: Objective—Genome-wide association studies have to date identified 159 significant and suggestive loci for coronary artery disease (CAD). We now report comprehensive bioinformatics analyses of sequence variation in these loci to predict candidate causal genes. Approach and Results—All annotated genes in the loci were evaluated with respect to protein-coding single-nucleotide polymorphism and gene expression parameters. The latter included expression quantitative trait loci, tissue specificity, and miRNA binding. High priority candidate genes were further identified based on literature searches and our experimental data. We conclude that the great majority of causal variations affecting CAD risk occur in noncoding regions, with 41% affecting gene expression robustly versus 6% leading to amino acid changes. Many of these genes differed from the traditionally annotated genes, which was usually based on proximity to the lead single-nucleotide polymorphism. Indeed, we obtained evidence that genetic variants at ...
TL;DR: Circulatory (portal and systemic) phospholipid profiling and clinical data defines NASH signature in morbid obesity, and weak contribution of visceral adipose tissue to NASH-related portal lipid alterations is reported, suggesting possible contribution from other organs draining into hepatic portal system.
TL;DR: There is evidence that stair-use interventions are effective to increase stair climbing in public settings, but evidence of such effect is limited in worksites.
TL;DR: Four-month treatment with a dietary supplement containing cinnamon, chromium and carnosine decreased FPG and increased fat-free mass in overweight or obese pre-diabetic subjects, which might open up new avenues in the prevention of diabetes.
Abstract: Background
Preventing or slowing the progression of prediabetes to diabetes is a major therapeutic issue.
Objectives
Our aim was to evaluate the effects of 4-month treatment with a dietary supplement containing cinnamon, chromium and carnosine in moderately obese or overweight pre-diabetic subjects, the primary outcome being change in fasting plasma glucose (FPG) level. Other parameters of plasma glucose homeostasis, lipid profile, adiposity and inflammatory markers were also assessed.
Methods
In a randomized, double-blind, placebo-controlled study, 62 subjects with a FPG level ranging from 5.55 to 7 mmol/L and a body mass index ≥25 kg/m2, unwilling to change their dietary and physical activity habits, were allocated to receive a 4-month treatment with either 1.2 g/day of the dietary supplement or placebo. Patients were followed up until 6 months post-randomization.
Results
Four-month treatment with the dietary supplement decreased FPG compared to placebo (-0.24±0.50 vs +0.12±0.59 mmol/L, respectively, p = 0.02), without detectable significant changes in HbA1c. Insulin sensitivity markers, plasma insulin, plasma lipids and inflammatory markers did not differ between the treatment groups. Although there were no significant differences in changes in body weight and energy or macronutrient intakes between the two groups, fat-free mass (%) increased with the dietary supplement compared to placebo (p = 0.02). Subjects with a higher FPG level and a milder inflammatory state at baseline benefited most from the dietary supplement.
Conclusions
Four-month treatment with a dietary supplement containing cinnamon, chromium and carnosine decreased FPG and increased fat-free mass in overweight or obese pre-diabetic subjects. These beneficial effects might open up new avenues in the prevention of diabetes.
TL;DR: After 1 year of follow-up in patients with a BMI ≥ 50 kg/m², LRYGB provides better weight loss and resolution in diabetes than LSG with similar postoperative morbidity.
TL;DR: T2DM remains a disease of major concern: compared with the non-diabetic population, all parameters surveyed showed unfavourable ratings, particularly for women.
TL;DR: The METADAP, a 6-month prospective, multicentric, real-world treatment observational cohort study of 624 patients with a diagnosis of major depressive disorder and a current major depressive episode, addressed the incidence of MetS in patients with major depressiveepisode treated with antidepressants.
TL;DR: The combined analysis of a large number of obesity phenotypes has provided insight in the genetic architecture of the molecular mechanisms underlying these traits indicating that QTLs underlying similar phenotypes are clustered in the genome.
Abstract: The pig is a well-known animal model used to investigate genetic and mechanistic aspects of human disease biology. They are particularly useful in the context of obesity and metabolic diseases because other widely used models (e.g. mice) do not completely recapitulate key pathophysiological features associated with these diseases in humans. Therefore, we established a F2 pig resource population (n = 564) designed to elucidate the genetics underlying obesity and metabolic phenotypes. Segregation of obesity traits was ensured by using breeds highly divergent with respect to obesity traits in the parental generation. Several obesity and metabolic phenotypes were recorded (n = 35) from birth to slaughter (242 ± 48 days), including body composition determined at about two months of age (63 ± 10 days) via dual-energy x-ray absorptiometry (DXA) scanning. All pigs were genotyped using Illumina Porcine 60k SNP Beadchip and a combined linkage disequilibrium-linkage analysis was used to identify genome-wide significant associations for collected phenotypes. We identified 229 QTLs which associated with adiposity- and metabolic phenotypes at genome-wide significant levels. Subsequently comparative analyses were performed to identify the extent of overlap between previously identified QTLs in both humans and pigs. The combined analysis of a large number of obesity phenotypes has provided insight in the genetic architecture of the molecular mechanisms underlying these traits indicating that QTLs underlying similar phenotypes are clustered in the genome. Our analyses have further confirmed that genetic heterogeneity is an inherent characteristic of obesity traits most likely caused by segregation or fixation of different variants of the individual components belonging to cellular pathways in different populations. Several important genes previously associated to obesity in human studies, along with novel genes were identified. Altogether, this study provides novel insight that may further the current understanding of the molecular mechanisms underlying human obesity.
TL;DR: In obese patients presenting high CRP levels with no obvious explanation, age, gender, BMI, fat mass proportion, OSA, and WAT inflammation should be taken into account to decide to perform further additional medical investigations.
University of Paris1, Harvard University2, Helsinki University Central Hospital3, Aalto University4, Queen's University Belfast5, University of Pennsylvania6, Steno Diabetes Center7, University of Copenhagen8, Aarhus University9, Jagiellonian University Medical College10, Novo Nordisk11, University of California, Los Angeles12, Belfast City Hospital13, French Institute of Health and Medical Research14, Institute of Chartered Accountants of Nigeria15, Baker IDI Heart and Diabetes Institute16, University of Poitiers17
TL;DR: In this paper, the genetic determinants of diabetic nephropathy remain poorly understood, and the authors aimed to identify novel susceptibility genes for diabetic kidney disease, but their work was unsuccessful.
Abstract: Aims/hypothesis
The genetic determinants of diabetic nephropathy remain poorly understood. We aimed to identify novel susceptibility genes for diabetic nephropathy.
TL;DR: In this article, the role of the MAGUK protein SAP97 in regulating the QT interval was assessed in vivo by generating a genetically modified mouse model in which SAP97 is suppressed exclusively in cardiomyocytes.
TL;DR: The main pharmacological characteristics of the new direct anti‐Xa and anti‐IIa agents are summarized.
Abstract: The new oral anticoagulants are announced as an important therapeutic revolution, particularly after their approval by authorities for stroke prevention in atrial fibrillation. However, the pharmacology of these new drugs is not homogeneous. In this review, we summarize the main pharmacological characteristics of the new direct anti-Xa and anti-IIa agents.
University of Leicester1, University of Ottawa2, University of Pennsylvania3, University of Lübeck4, Federation University Australia5, Institute of Chartered Accountants of Nigeria6, University of Paris7, French Institute of Health and Medical Research8, NHS Blood and Transplant9, Wellcome Trust Sanger Institute10, Technische Universität München11
TL;DR: Evidence is provided for an excess of homozygosity in coronary artery disease in outbred populations and the potential biological relevance of ROHs in cells of importance to the pathogenesis of atherosclerosis is suggested.
Abstract: Runs of homozygosity (ROHs) are recognized signature of recessive inheritance. Contributions of ROHs to the genetic architecture of coronary artery disease and regulation of gene expression in cells relevant to atherosclerosis are not known. Our combined analysis of 24,320 individuals from 11 populations of white European ethnicity showed an association between coronary artery disease and both the count and the size of ROHs. Individuals with coronary artery disease had approximately 0.63 (95% CI: 0.4–0.8) excess of ROHs when compared to coronary-artery-disease-free control subjects (p = 1.49 × 10−9). The average total length of ROHs was approximately 1,046.92 (95% CI: 634.4–1,459.5) kb greater in individuals with coronary artery disease than control subjects (p = 6.61 × 10−7). None of the identified individual ROHs was associated with coronary artery disease after correction for multiple testing. However, in aggregate burden analysis, ROHs favoring increased risk of coronary artery disease were much more common than those showing the opposite direction of association with coronary artery disease (p = 2.69 × 10−33). Individual ROHs showed significant associations with monocyte and macrophage expression of genes in their close proximity—subjects with several individual ROHs showed significant differences in the expression of 44 mRNAs in monocytes and 17 mRNAs in macrophages when compared to subjects without those ROHs. This study provides evidence for an excess of homozygosity in coronary artery disease in outbred populations and suggest the potential biological relevance of ROHs in cells of importance to the pathogenesis of atherosclerosis.
TL;DR: Matched for FM, PWS subjects have a better metabolic profile, a phenotype that could be linked to changes in scAT remodeling and promotion of adipocyte growth.
Abstract: Context: Prader-Willi syndrome (PWS), the most frequent syndrome of obesity, is a model of early fat mass (FM) development, but scarce data exist on adipose tissue characteristics. Objective: The objective of the study was to compare metabolic, fat distribution, and transcriptomic signatures of sc adipose tissue (scAT) in PWS adults, with matched obese adults with primary obesities. Main Outcomes and Measures: Hormonal and metabolic assessments, systemic inflammation, and gene expression in scAT were compared between PWS patients and obese controls (OCs). Each 42nd PWS patient was matched with one randomly paired control with primary obesity. Matching factors were age, gender, fat mass (percentage), and diabetic status. Results: Compared with OCs, the PWS group had a decreased percentage of trunk FM and a better metabolic profile with decreased insulin and homeostasis model assessment, an index of insulin-resistance, and increased concentrations of serum adiponectin and ghrelin. Adipocyte size relative to...
TL;DR: According to %IWL and rate of partial or complete remission of diabetes and hypertension, the study shows similar outcomes for LRYGB in SSO and non-SSO patients 5 years after surgery, but the %EWL does not seem to be an adequate indicator for evaluation of LryGB outcomes in patients with extreme obesity, such as SSO.
TL;DR: Despite achieving a high rate of reperfusion with pPCI using mainly radial access, similar to that achieved in younger patients, hospital mortality was higher in nonagenarians.
TL;DR: Patients carrying a mutation affecting the cytoplasmic tail of BMPRII were characterized by an older age at diagnosis compared with other BMPR2 mutation carriers, less severe hemodynamic characteristics, and a greater chance of being a long-term responder to calcium channel blockers.
TL;DR: A combined chemoinformatic approach for objective and systematic analysis of untargeted (1)H NMR-based metabolic profiles in quantitative genetic contexts is introduced and implemented in the powerful R/Bioconductor framework.
Abstract: High-throughput (1)H nuclear magnetic resonance (NMR) is an increasingly popular robust approach for qualitative and quantitative metabolic profiling, which can be used in conjunction with genomic techniques to discover novel genetic associations through metabotype quantitative trait locus (mQTL) mapping. There is therefore a crucial necessity to develop specialized tools for an accurate detection and unbiased interpretability of the genetically determined metabolic signals. Here we introduce and implement a combined chemoinformatic approach for objective and systematic analysis of untargeted (1)H NMR-based metabolic profiles in quantitative genetic contexts. The R/Bioconductor mQTL.NMR package was designed to (i) perform a series of preprocessing steps restoring spectral dependency in collinear NMR data sets to reduce the multiple testing burden, (ii) carry out robust and accurate mQTL mapping in human cohorts as well as in rodent models, (iii) statistically enhance structural assignment of genetically determined metabolites, and (iv) illustrate results with a series of visualization tools. Built-in flexibility and implementation in the powerful R/Bioconductor framework allow key preprocessing steps such as peak alignment, normalization, or dimensionality reduction to be tailored to specific problems. The mQTL.NMR package is freely available with its source code through the Comprehensive R/Bioconductor repository and its own website ( http://www.ican-institute.org/tools/ ). It represents a significant advance to facilitate untargeted metabolomic data processing and quantitative analysis and their genetic mapping.
TL;DR: After 5 years of follow-up, pLryGB provides greater weight loss than rLRYGB with similar rates of improvement and remission of coexisting conditions, and patients and surgeons should be aware of such results before primary and revisional bariatric surgery.
TL;DR: Time-updated heart rate is more strongly related with adverse cardiovascular outcomes than baseline heart rate, and heart rate should be measured to assess cardiovascular risk at all assessments of patients with left ventricular systolic dysfunction.