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Engberg Kehoe posted an update 2 days, 9 hours ago
Because it is not visible on the 12-lead ECG, few if any electrocardiographers have seen the waveform of sinus node (SN) depolarization. Yet, SN depolarization is present before every P wave during all sinus rhythms. Herein, a case is presented in which a recorded SN depolarization waveform is observed.Purpose To determine whether an association exists between dry eye disease (DED) and statin use and/or dyslipidemia. Design Retrospective, case-control study. Methods -SETTING University of North Carolina (UNC) affiliated healthcare facilities. -study population 72,931 patients seen at UNC ophthalmology clinics over a 10 year period. -main outcome measures Odds ratios (ORs) calculated between DED and a history of low, moderate, or high-intensity statin use; and ORs calculated between DED and abnormal lipid panel values. Results 39,336 individuals (53.9% female) were analyzed after exclusion of individuals with confounding risk factors for DED. Of these, 3,399 patients (8.6%) carried a diagnosis of DED. Low, moderate, and high intensity statin regimens were used by 751 (1.9%), 2,655 (6.8%), and 1,036 (2.6%), respectively. Lipid abnormalities were identified as follows total cholesterol >200, 4,558 (11.6%); HDL 150 were 1.66 (1.52,1.82), 1.45 (1.26,1.67), 1.55 (1.39,1.74), and 1.43 (1.27,1.61), respectively. Conclusions A history of statin use or dyslipidemia is associated with an increased odds of having a DED diagnosis. Further studies are needed to determine whether statin use and/or dyslipidemia increase the risk of DED.Neat epigallocatechin gallate (EGCG) has low bioavailability and tuna oil (TO) is prone to oxidation. Broccoli byproducts (BBP) were used for preparing TO-BBP (25% oil, dry basis) and TO-EGCG-BBP (20% oil and 20% EGCG, dry basis) powders. The gross composition and surface fat of powders and morphology of reconstituted emulsions were characterized. Oxipres® data (80 °C, 5 bar oxygen pressure) showed that the TO-EGCG-BBP formulation was more oxidatively stable [Induction period (IP) > 100 h] than TO-BBP (IP ~ 20 h). During in vitro digestion, 90% of EGCG was recovered in the whole intestinal digesta of the TO-EGCG-BBP formulation compared to 76% for the EGCG-BBP formulation and 66% for the neat EGCG. The use of BBP for co-delivering EGCG and TO increases oxidative stability of TO and improves EGCG stability during in vitro digestion. This study highlights the potential for formulating functional ingredient with BBP and contribute to food waste reduction.Producing an accurate atomic model of biomolecule-ligand interactions from maps generated by cryoelectron microscopy (cryo-EM) often presents challenges inherent to the methodology and the dynamic nature of ligand binding. Here, we present GemSpot, an automated pipeline of computational chemistry methods that take into account EM map potentials, quantum mechanics energy calculations, and water molecule site prediction to generate candidate poses and provide a measure of the degree of confidence. The pipeline is validated through several published cryo-EM structures of complexes in different resolution ranges and various types of ligands. In all cases, at least one identified pose produced both excellent interactions with the target and agreement with the map. GemSpot will be valuable for the robust identification of ligand poses and drug discovery efforts through cryo-EM.Adipose dysfunction and inflammation with or without hepatic defects underlie metabolic obesity. Glutamine (GLU) improves glucoregulation and metabolic indices but its effects on adipose function and hepatic lipid deposition in estrogen-progestin oral contraceptive (EPOC) users are unknown. Therefore, we hypothesized that GLUT supplementation would protect against adipose dysfunction and excess hepatic lipid influx and deposition in EPOC-treated animals by suppressing adenosine deaminase/xanthine oxidase (ADA/XO) activity and improving glucose-6-phosphate dehydrogenase (G6PD)-dependent antioxidant defense. Female Wistar rats weighing 150-180 g were allotted into control, GLUT, EPOC and EPOC + GLUT groups (six rats/group). The groups received vehicle (distilled water, p.o.), GLUT (1 g/kg), EPOC containing 1.0 µg ethinylestradiol plus 5.0 µg levonorgestrel and EPOC plus GLUT, respectively, daily for 8 weeks. Results showed that the administration of EPOC caused glucose dysregulation and increased triglyceride-glucose index and visceral adiposity, but the body weight and liver weight were not affected. However, EPOC significantly decreased adipose lipid, G6PD and glutathione and increased glycogen synthesis, ADA, XO, uric acid, lipid peroxidation, lactate production and gamma-glutamyl transferase activity (GGT). 8-Cyclopentyl-1,3-dimethylxanthine mouse On the other hand, EPOC increased hepatic lipid, ADA, XO, uric acid, lipid peroxidation and lactate production and decreased glycogen synthesis, G6PD and glutathione. Nevertheless, supplementation with glutamine attenuated these alterations. Collectively, the present results indicate that EPOC causes metabolically induced obesity which is associated with adipose dysfunction and hepatic metabolic disturbance. The findings also suggest that glutamine confers metabo-protection with corresponding improvement in adipose and hepatic metabolic function by suppression of ADA/XO activity and enhancement of G6PD-dependent antioxidant defense.Glutathione (GSH) is a potential inhibitor for acrylamide (AA) in heated food. In the present study, the inhibition pathways of GSH on AA were investigated in the asparagine(Asn)/glucose(Glc)/GSH model system. In comparison to the Asn/Glc model system, three unique molecular ions (m/z 470, 379, and 193) were identified in the Asn/Glc/GSH model system. Those molecular ions were confirmed as the Amadori rearrangement products which formed in the reaction between Glc and GSH, as well as the addition reaction products between AA and the sulfhydryl group (-SH) of GSH and cysteine (Cys). The competition between Asn and GSH for Glc in the competitive reactions was assumed to be the major pathway. Additionally, the elimination reaction between AA and GSH or between AA and Cys also played a minor role in the inhibition of AA. The variances of precursors, intermediates, and final products provided quantitative evidence for the above pathways.