193 research outputs found

    Which is a better marker for overweight: waist height ratio or waist circumference?

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    Background: The global prevalence of obesity has been increasing. Body mass index, waist circumference and waist height ratio have been widely used for nutritional assessment. Waist height ratio has the advantage of taking into account abdominal obesity as well as height associated with body fat accumulation or distribution. The objective of this study was to suggest cut off points for waist circumference and waist height ratio to identify overweight in Omani adults.Methods: Weight, height, waist circumference and waist height ratio were measured for all participants. Pearsonā€™s correlation was used to determine correlation of BMI with waist circumference and waist height ratio. ROC curve was used to identify AUC and specific cut off point for anthropometric indicators.Results: The largest proportion of overweight was picked up by waist height ratio across both the genders. Correlation of BMI with waist height ratio was stronger (r=0.699) than correlation with waist circumference (r=0.589) for both the genders. Maximum AUC was for waist height ratio in males (AUC=0.833, 95% CI=0.791-0.875). The specific cut off point for waist circumference in males and females was 89.5cm and 87.6cm respectively. The specific cut off point for waist height ratio in males and females was 0.53 and 0.57 respectively.Conclusions: Maximum participants were found overweight by waist height ratio followed by waist circumference and the least by BMI. The higher cut off points should be used in this population for identifying overweight people

    The predictive value of the antioxidative function of HDL for cardiovascular disease and graft failure in renal transplant recipients

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    AbstractBackgroundProtection of low-density lipoproteins (LDL) against oxidative modification is a key anti-atherosclerotic property of high-density lipoproteins (HDL). This study evaluated the predictive value of the HDL antioxidative function for cardiovascular mortality, all-cause mortality and chronic graft failure in renal transplant recipients (RTR).MethodsThe capacity of HDL to inhibit native LDL oxidation was determined inĀ vitro in a prospective cohort of renal transplant recipients (RTR, nĀ =Ā 495, median follow-up 7.0 years).ResultsThe HDL antioxidative functionality was significantly higher in patients experiencing graft failure (57.4Ā Ā±Ā 9.7%) than in those without (54.2Ā Ā±Ā 11.3%; PĀ =Ā 0.039), while there were no differences for cardiovascular and all-cause mortality. Specifically glomerular filtration rate (PĀ =Ā 0.001) and C-reactive protein levels (PĀ =Ā 0.006) associated independently with antioxidative functionality in multivariate linear regression analyses. Cox regression analysis demonstrated a significant relationship between antioxidative functionality of HDL and graft failure in age-adjusted analyses, but significance was lost following adjustment for baseline kidney function and inflammatory load. No significant association was found between HDL antioxidative functionality and cardiovascular and all-cause mortality.ConclusionThis study demonstrates that the antioxidative function of HDL (i) does not predict cardiovascular or all-cause mortality in RTR, but (ii) conceivably contributes to the development of graft failure, however, not independent of baseline kidney function and inflammatory load

    PENGARUH PEMBERIAN DEKOK DAUN SIRSAK, KUNYIT PUTIH, DAN DAUN KERSEN SERTA KOMBINASINYA DALAM AIR MINUM TERHADAP PERFORMANS DAN KOLESTEROL DARAH AYAM PETELUR JANTAN YANG DIINFEKSI BAKTERI ESCHERICHIA COLI

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    The purpose of this study was to determine the effect of soursop leaf (Annona muricata), saffron white (Curcuma mangga Val.) and cherry leaves (Muntingia calabura L.) and theirs combinations in drinking water on performances and blood cholesterol  of  laying roosters that infected by Escherichia coli. This study was designed using  completely randomized design (CRD) with 11 treatments and 3 replications and each treatment using the 4 roosters. That obtained 33 experimental units. The treatments were the drinking water contain decoction of  soursop leaves (DS), saffron white (KP) and cherry leaves (DK), and combinations were as follows: R0: without decoction of herbs (control), R1: 6% of DS decoction, R2: 6% of KP decoction, R3: 6 % of  DK decoction, R4: 2% of  DS decoction + 4% of KP decoction, R5: 2% of  DS decoction + 4% of DK decoction, R6: 2%  of KP decoction + 4% of DS decoction, R7: 2% of KP decoction  + 4% of DK decoction, R8: 2% of DK decoction + 4% of DS decoction, R9: 2% of  DK decoction + 4% of KP decoction, R10: 2%  of DS decoction + 2% of KP decoction + 2% of DK decoction. Parameters of  performance were: feed consumption, water intake, body weight gain, feed conversion. The result showed that the treatment had no effect on the performances (feed consumption, water consumption, body weight gain, feed conversion)

    The anti-inflammatory function of HDL is impaired in type 2 diabetes:Role of hyperglycemia, paraoxonase-1 and low grade inflammation

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    Abstract Background Functional properties of high density lipoproteins (HDL) are increasingly recognized to play a physiological role in atheroprotection. Type 2 diabetes mellitus (T2DM) is characterized by low HDL cholesterol, but the effect of chronic hyperglycemia on the anti-inflammatory capacity of HDL, a metric of HDL function, is unclear. Therefore, the aim of the present study was to establish the impact of T2DM on the HDL anti-inflammatory capacity, taking paraoxonase-1 (PON-1) activity and low grade inflammation into account. Methods The HDL anti-inflammatory capacity, determined as the ability to suppress tumor necrosis factor-Ī± (TNF-Ī±) induced vascular cell adhesion molecule-1 (VCAM-1) mRNA expression in endothelial cells in vitro (higher values indicate lower anti-inflammatory capacity), PON-1 (arylesterase) activity, hs-C-reactive protein (hs-CRP), serum amyloid A (SAA) and TNF-Ī± were compared in 40 subjects with T2DM (no insulin or statin treatment) and 36 non-diabetic subjects. Results T2DM was associated with impaired HDL anti-inflammatory capacity (3.18 vs 1.05 fold increase in VCAM-1 mRNA expression; PĀ <Ā 0.001), coinciding with decreased HDL cholesterol (PĀ =Ā 0.001), apolipoprotein A-I (PĀ =Ā 0.038) and PON-1 activity (PĀ =Ā 0.023), as well as increased hs-CRP (PĀ =Ā 0.043) and TNF-Ī± (PĀ =Ā 0.005). In all subjects combined, age- and sex-adjusted multivariable linear regression analysis demonstrated that impaired HDL anti-inflammatory capacity was associated with hyperglycemia (Ī²Ā =Ā 0.499, PĀ <Ā 0.001), lower PON-1 activity (Ī²Ā =Ā āˆ’Ā 0.192, PĀ =Ā 0.030) and higher hs-CRP (Ī²Ā =Ā 0.220, PĀ =Ā 0.016). Conclusions The HDL anti-inflammatory capacity is substantially impaired in T2DM, at least partly attributable to the degree of hyperglycemia, decreased PON-1 activity and enhanced low grade chronic inflammation. Decreased anti-inflammatory protection capacity of HDL conceivably contributes to the increased atherosclerosis risk associated with T2DM

    Drug-eluting stents versus bare-metal stents for stable ischaemic heart disease

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    This is a protocol for a Cochrane Review (Intervention). The objectives are as follows: To assess the benefits and harms of drugā€eluting stents versus bareā€metal stents in participants with stable ischaemic heart disease

    Targeting of Epigenetic Co-dependencies Enhances Anti-AML Efficacy of Menin Inhibitor in AML with MLL1-R or Mutant NPM1

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    Monotherapy with Menin inhibitor (MI), e.g., SNDX-5613, induces clinical remissions in patients with relapsed/refractory AML harboring MLL1-r or mtNPM1, but most patients either fail to respond or eventually relapse. Utilizing single-cell RNA-Seq, ChiP-Seq, ATAC-Seq, RNA-Seq, RPPA, and mass cytometry (CyTOF) analyses, present pre-clinical studies elucidate gene-expression correlates of MI efficacy in AML cells harboring MLL1-r or mtNPM1. Notably, MI-mediated genome-wide, concordant, log2 fold-perturbations in ATAC-Seq and RNA-Seq peaks were observed at the loci of MLL-FP target genes, with upregulation of mRNAs associated with AML differentiation. MI treatment also reduced the number of AML cells expressing the stem/progenitor cell signature. A protein domain-focused CRISPR-Cas9 screen in MLL1-r AML cells identified targetable co-dependencies with MI treatment, including BRD4, EP300, MOZ and KDM1A. Consistent with this, in vitro co-treatment with MI and BET, MOZ, LSD1 or CBP/p300 inhibitor induced synergistic loss of viability of AML cells with MLL1-r or mtNPM1. Co-treatment with MI and BET or CBP/p300 inhibitor also exerted significantly superior in vivo efficacy in xenograft models of AML with MLL1-r. These findings highlight novel, MI-based combinations that could prevent escape of AML stem/progenitor cells following MI monotherapy, which is responsible for therapy-refractory AML relapse

    Evidence for overwintering and autochthonous transmission of Usutu virus to wild birds following its redetection in the United Kingdom

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    Usutu virus (USUV) is an emerging zoonotic arbovirus in Europe, where it primarily impacts Eurasian blackbirds (Turdus merula). For mosquito-borne viruses to persist in temperate areas, transovarial transmission in vectors or overwintering in either hosts or diapausing vectors must occur to facilitate autochthonous transmission. We undertook surveillance of hosts and vectors in 2021 to elucidate whether USUV had overwintered in the United Kingdom (UK) following its initial detection there in 2020. From 175 dead bird submissions, we detected 1 case of USUV infection, in a blackbird, from which a full USUV genome was derived. Using a molecular clock analysis, we demonstrate that the 2021 detection shared a most recent common ancestor with the 2020 Greater London, UK, USUV sequence. In addition, we identified USUV-specific neutralizing antibodies in 10 out of 86 serum samples taken from captive birds at the index site, demonstrating in situ cryptic infection and potential sustained transmission. However, from 4966 mosquitoes, we detected no USUV RNA suggesting that prevalence in the vector community was absent or low during sampling. Combined, these results suggest that USUV overwintered in the UK, thus providing empirical evidence for the continued northward expansion of this vector-borne viral disease. Currently, our detection indicates geographically restricted virus persistence. Further detections over time will be required to demonstrate long-term establishment. It remains unclear whether the UK, and by extension other high-latitude regions, can support endemic USUV infection

    Targeting of epigenetic co-dependencies enhances anti-AML efficacy of Menin inhibitor in AML with MLL1-r or mutant NPM1

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    Monotherapy with Menin inhibitor (MI), e.g., SNDX-5613, induces clinical remissions in patients with relapsed/refractory AML harboring MLL1-r or mtNPM1, but most patients either fail to respond or eventually relapse. Utilizing single-cell RNA-Seq, ChiP-Seq, ATAC-Seq, RNA-Seq, RPPA, and mass cytometry (CyTOF) analyses, present pre-clinical studies elucidate gene-expression correlates of MI efficacy in AML cells harboring MLL1-r or mtNPM1. Notably, MI-mediated genome-wide, concordant, log2 fold-perturbations in ATAC-Seq and RNA-Seq peaks were observed at the loci of MLL-FP target genes, with upregulation of mRNAs associated with AML differentiation. MI treatment also reduced the number of AML cells expressing the stem/progenitor cell signature. A protein domain-focused CRISPR-Cas9 screen in MLL1-r AML cells identified targetable co-dependencies with MI treatment, including BRD4, EP300, MOZ and KDM1A. Consistent with this, in vitro co-treatment with MI and BET, MOZ, LSD1 or CBP/p300 inhibitor induced synergistic loss of viability of AML cells with MLL1-r or mtNPM1. Co-treatment with MI and BET or CBP/p300 inhibitor also exerted significantly superior in vivo efficacy in xenograft models of AML with MLL1-r. These findings highlight novel, MI-based combinations that could prevent escape of AML stem/progenitor cells following MI monotherapy, which is responsible for therapy-refractory AML relapse
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