A single-laboratory validation was performed on a wide range of food and feed products. The inter-day repeatability (%RSDr) was <3.58% (w/w) across a range of samples containing 44.1 to 88.9% available carbohydrates. The LOD and LOQ obtained were 0.054% (w/w) and 0.179% (w/w), respectively. The method is all inclusive, specific, robust and simple to use.

A unique method has been developed for the direct measurement of available carbohydrates, entailing separate measurement of glucose, fructose and galactose; information of value in determining the glycemic index of foods.

A unique method has been developed for the direct measurement of available carbohydrates, entailing separate measurement of glucose, fructose and galactose; information of value in determining the glycemic index of foods.Vascular smooth muscle cells (VSMCs) are key participants in both early and late-stage atherosclerosis. VSMCs invade the early atherosclerotic lesion from the media, expanding lesions, but also forming a protective fibrous cap rich in extracellular matrix to cover the ‘necrotic’ core. Hence, VSMCs have been viewed as plaque-stabilising, and decreased VSMC plaque content – often measured by expression of contractile markers – associated with increased plaque vulnerability. However, the emergence of lineage-tracing and transcriptomic studies has demonstrated that VSMCs comprise a much larger proportion of atherosclerotic plaques than originally thought, demonstrate multiple different phenotypes in vivo, and have roles that might be detrimental. VSMCs downregulate contractile markers during atherosclerosis whilst adopting alternative phenotypes, including macrophage-like, foam cell-like, osteochondrogenic-like, myofibroblast-like and mesenchymal stem cell-like. Selleck 2,6-Dihydroxypurine VSMC phenotypic switching can be studied in tissue culture, but also now in the media, fibrous cap and deep-core region, and markedly affects plaque formation and markers of stability. In this review, we describe the different VSMC plaque phenotypes and their presumed cellular and paracrine functions, the regulatory mechanisms that control VSMC plasticity, and their impact on atherogenesis and plaque stability.

External hemorrhage control devices (EHCDs) are effective in reducing the death risk of noncompressible torso hemorrhage (NCTH), but the pressurized area is too large to prevent serious organ damage. This study aims to establish the surface localization strategy of EHCDs based on the anatomical features of NCTH-related arteries through CT images to facilitate the optimal design and application of EHCDs.

Two hundred patients who underwent abdominal CT were enrolled. Anatomical parameters such as the length of the common iliac artery (CIA), the external iliac artery (EIA), and the common femoral artery were measured; positional relationships among the EHCD-targeted arteries, umbilicus, anterior superior iliac spine (ASIS), and pubic tubercle (PT) were determined. The accuracy of surface localization was verified by the 3D-printed mannequins of 20 real patients.

Aortic bifurcation (AB) was 7.5 ± 8.6 mm to the left of the umbilicus. The left CIA (left 46.6 ± 16.0 mm vs. right 43.3 ± 15.5 mm, P = .038) and t The data are necessary for improving EHCD design, precise hemostasis, and EHCD-related collateral injuries.Trial registration Ratification no. 2019092. Registered November 4, 2020-retrospectively registered, http://www.chictr.org.cn.

The transcription factor Tbx5 controls cardiogenesis and drives Scn5a expression in mice. We have identified two variants in TBX5 encoding p.D111Y and p.F206L Tbx5, respectively, in two unrelated patients with structurally normal hearts diagnosed with Long QT (LQTS) and Brugada (BrS) Syndrome. Here we characterized the consequences of each variant to unravel the underlying disease mechanisms.

We combined clinical analysis with in vivo and in vitro electrophysiological and molecular techniques in human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs), HL-1 cells, and cardiomyocytes from mice trans-expressing human wildtype (WT) or mutant proteins. Tbx5 increased transcription of SCN5A encoding cardiac Nav1.5 channels, while repressing CAMK2D and SPTBN4 genes encoding Ca-calmodulin kinase IIδ (CaMKIIδ) and βIV-spectrin, respectively. These effects significantly increased Na current (INa) in hiPSC-CMs and in cardiomyocytes from mice trans-expressing Tbx5. Consequently, action potential (AP) a of the electrical phenotype in LQTS and BrS patients.

In addition to peak INa, Tbx5 critically regulates INaL and the duration of repolarization in human cardiomyocytes. Our original results suggest that TBX5 variants associate with and modulate the intensity of the electrical phenotype in LQTS and BrS patients.Fruit quality depends largely on the type and amount of sugar accumulated in the fruit. In peach [Prunus persica (L.) Batsch], sorbitol is the main photosynthetic product and plays a crucial role in sugar metabolism. As a conserved energy sensor, SNF1-related kinase 1 (SnRK1) is involved in the regulation of carbon metabolism. In this study, SnRK1 was able to respond to induction by treatment with exogenous trehalose and sorbitol on ‘Ruipan 17’ peach fruit. After treatment with 100-mM trehalose for 3 h, the SnRK1 activity decreased by 18% and the activities of sorbitol dehydrogenase (SDH) and sucrose synthase (SS) also decreased significantly, but sucrose phosphate synthase (SPS) activity increased significantly; whereas sorbitol treatment under the same conditions resulted in a 12.6% increase in SnRK1 activity and the activities of SDH and SS synthase also increased significantly, compared with the control. The contents of glucose, fructose and sucrose in peach fruit increased significantly after 3 h of sorbitol treatment. In addition, the interactions between PpSnRK1α and enzymes PpSDH and PpSPS were confirmed by yeast two-hybrid method and the phosphorylation of PpSnRK1α and PpSDH was detected in vitro. Taken together, these results suggest that SnRK1 promotes sorbitol metabolism by activating SDH and it also regulates the activities of SS and SPS that enhance sucrose accumulation in peach fruit. SnRK1 protein kinase is involved in sugar metabolism and has the potential to be used for improving fruit quality.