Risk assessment of venous thromboembolism and bleeding in COVID‐19 patients

BackgroundThe coronavirus disease 2019 (COVID‐19) is a newly recognized illness that has spread rapidly all over the world. More and more reports highlight the risk of venous thromboembolism (VTE) in COVID‐19. Our study aims to identify in‐hospital VTE risk and bleeding risk in COVID‐19 patients.MethodsWe retrospectively studied 138 consecutively enrolled patients with COVID‐19 and identified in‐hospital VTE and bleeding risk by Padua Prediction Score and Improve bleed risk assessment model. The clinical data and features were analyzed in VTE patients.ResultsOur findings identified that 23 (16.7%) patients with COVID‐19 were at high risk for VTE according to Padua prediction score and 9 (6.5%) patients were at high risk of bleeding for VTE prophylaxis according to Improve prediction score. Fifteen critically ill patients faced double high risk from thrombosis (Padua score more than 4 points in all 15 [100%] patients) and hemorrhage (Improve score more than 7 points in 9 [60.0%] patients). Thrombotic events were identified in four patients (2.9%) of all COVID‐19 patients. All of them were diagnosed with deep vein thrombosis by ultrasound 3 to 18 days after admission. Three (75.0%) were critically ill patients, which means that the incidence of VTE among critically ill patients was 20%. One major hemorrhage happened in critically ill patients during VTE treatment.ConclusionCritically ill patients with COVID‐19 suffered both a high risk of thrombosis and bleeding risks. More effective VTE prevention strategies based on an individual assessment of bleeding risks were necessary for critically ill patients with COVID‐19.     

Antioxidant vitamins reduce acute meal-induced memory deficits in adults with type 2 diabetes

Memory impairment is observed in adults with type 2 diabetes mellitus (T2DM), with further acute deficits after meal ingestion. This study explored whether postprandial oxidative stress was a contributor to these meal-induced memory deficits. Sixteen adults with T2DM (mean age, 63.5 ± 2.1 years) who were not regularly taking high-dose antioxidant supplements were fed a high-fat meal, the same test meal with vitamins C (1000 mg) and E (800 IU) tablets, or water on 3 separate occasions. After meal ingestion, a battery of cognitive tests were administered, which included measures of delayed verbal memory, assessed at 60 and 105 minutes after meal ingestion. Relative to water consumption, the high-fat meal resulted in poorer performance at 105 minutes postingestion on measures of delayed verbal recall (word list and paragraph recall) and working memory (Digit-Span Forward). Coconsumption of antioxidant vitamins and high-fat meal prevented this meal-induced deficit such that performance on these tasks was indistinguishable from that after water intake. At the same time point, a small but significant improvement on the word-naming and color-naming components of Stroop was observed after meal ingestion, relative to water, irrespective of whether antioxidants were consumed, demonstrating the specificity of meal-induced impairments to memory function. Executive function, assessed by Trails Parts A and B, was not influenced by meal or antioxidant ingestion. In adults with T2DM, coconsumption of antioxidant vitamins minimizes meal-induced memory impairment, implicating oxidative stress as a potential contributor to these decrements.     

A glucose reference curve is the optimum method to determine the glycemic glucose equivalent values of foods in humans

The glycemic index ranks carbohydrates in foods on the basis of the blood glucose response they produce for a given amount of carbohydrate. The glycemic glucose equivalents (GGEs) is the blood glucose response to a defined portion of food. The purpose of this study was to determine the best method by which to measure the GGE of a food; whether it can be estimated from 1 or 2 glucose references or if a range of glucose references should be measured. Twenty individuals without diabetes participated. The incremental area under the curve (iAUC) from fasting to at least 120 minutes after consumption of 5 foods was determined. The iAUC for different glucose amounts was also determined and a standard glucose curve of glucose level against iAUC generated. The GGE of each food was estimated from iAUC of test food using the standard curve. The study found that using a glucose reference closest to the available carbohydrate content of the food gave a mean difference (95% confidence interval) in GGEs of 3.4 (2.0-4.8) g in comparison to the standard curve. Using a 50-g glucose reference gave a mean difference in GGEs of 5.2 (4.7-5.6) g and interpolating from 2 glucose references, 3.5 (1.9-5.2) g in comparison to the standard curve. In conclusion, the best method to determine the GGE value of a food is to use the standard glucose reference curve and estimate the response of the food directly from this.     

Dihydrotestosterone and the role of 5 alpha-reductase inhibitors in benign prostatic hyperplasia

The genesis of benign prostate hyperplasia (BPH) depends on two factors: testicular androgen and the aging process. The most important androgen in the prostate is dihydrotestosterone (DHT). In the aging male the level of DHT in the prostate remains largely constant although the plasma level of testosterone decreases. DHT is formed by the reduction of testosterone by the enzyme 5-alpha-reductase, which has two isoenzymes. The 5-alpha-reductase type 2 is the predominant isoenzyme in genital tissue and thus also in the prostate. Finasteride is a 5-alpha-reductase inhibitor, which is applied in the treatment of BHP and male baldness. In the doses used finasteride acts mainly by inhibiting the 5-alpha-reductase type 2, thereby reducing the serum level of DHT by approximately 70% and by about 85-90% in the prostate. Indeed the effect of finasteride in BPH was proven in clinical studies. However, the circulating and intraprostatic DHT could be further reduced by a more effective dual 5-alpha-reductase inhibitor, which would be efficacious in the treatment of benign prostate hyperplasia and other DHT-related disorders.     

下丘脑室旁核对大鼠胃缺血/再灌注损伤保护作用的细胞机制

目的 研究电刺激下丘脑室旁核（PVN）对胃缺血/再灌注损伤（GI/RI）大鼠胃黏膜细胞凋亡和增殖的影响,探讨电刺激PVN对GI/RI保护作用的细胞机制.方法 采用电刺激、电解损毁PVN的手段,以夹闭大鼠腹腔动脉30 min、松开 动脉夹恢复血流灌注1 h制备GI/RI模型,计算胃黏膜损伤指数,检测胃黏膜细胞的凋亡和增殖情况.结果 夹闭大鼠腹腔动脉30 min,再灌注1 h后可造成胃黏膜的明显损伤,电刺激PVN后GI/RI明显减轻,而且胃黏膜细胞的增殖增加,凋亡减少.结论 电刺激PVN对GI/RI具有明显的保护作用.这种保护作用是通过促进胃黏膜细胞增殖、抑制胃黏膜细胞凋亡而实现的.