Cs2CO3-Initiated Trifluoro-Methylation of Chalcones and Ketones for Practical Synthesis of Trifluoromethylated Tertiary Silyl Ethers.

It was found that 1,2-trifluoromethylation reactions of ketones, enones, and aldehydes were easily accomplished using the Prakash reagent in the presence of catalytic amounts of cesium carbonate, which represents an experimentally convenient, atom-economic process for this anionic trifluoromethylation of non-enolisable aldehydes and ketones.

Epigallocatechin-3-gallate protects HUVECs from PM2.5-induced oxidative stress injury by activating critical antioxidant pathways.

Endothelial dysfunction and oxidative stress likely play roles in PM2.5-induced harmful effects. Epigallocatechin-3-gallate (EGCG), the major polyphenolic constituent of green tea, is a potent antioxidant that exerts protective effects on cardiovascular diseases (CVDs) in part by scavenging free radicals. The exposure to ambient fine particulate matter (PM2.5) is responsible for certain CVDs. The aim of the present study was to investigate whether EGCG could also inhibit PM2.5-induced oxidative stress by activating the nuclear factor E2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway in human umbilical vein endothelial cells (HUVECs). PM2.5 (200 µg/mL) increased both cell death and intracellular ROS levels significantly, whereas EGCG (50-400 µM) inhibited these effects in a concentration-dependent manner. Western blotting and PCR demonstrated that EGCG increased Nrf2 and HO-1 expression in HUVECs that had been exposed to PM2.5. PD98059 (a selective inhibitor of extracellular signal regulated kinase [ERK]-1/2) and SB203580 (a selective inhibitor of p38 MAPK), but not SP600125 (a selective inhibitor of c-jun N-terminal kinase [JNK]), attenuated the EGCG-induced Nrf2 and HO-1 expression. In addition, silencing Nrf2 abolished EGCG-induced Nrf2 and HO-1 upregulation and enhancement of cell viability. The present study suggests that EGCG protects HUVECs from PM2.5-induced oxidative stress injury by upregulating Nrf2/HO-1 via activation of the p38 MAPK and the ERK1/2 signaling pathways.

The clinical effects of a new management mode for hypertensive patients: a randomized controlled trial.

BACKGROUND: The Internet, smartphones, and the application of health technology have great potential for hypertension management. We aim to evaluate a new mode of mobile health management with a social network application to guide blood pressure management in patients with hypertension. METHODS: Using a randomized controlled trial design, 120 hypertensive patients in the First Hospital of Shanxi Medical University who volunteered to participate in the study were randomly divided into an experimental group and a control group. The experimental group was divided into low, middle, or high-risk groups according to the cardiovascular risk stratification. The blood pressures of both the experimental group (the WeChat-guided new mode group) and the control group (the conventional mode group) were administered for three months. RESULTS: With intervention, both systolic blood pressure (SBP) and diastolic blood pressure (DBP) in the experimental group were significantly lower than those in the control group (P=0.016). The SBP and DBP of the experimental group after intervention were lower than those before intervention (P<0.001), which was not observed in the control group (P=0.056). There was no difference in the SBP drops in the low-risk, middle-risk, and high-risk groups (P=0.402). Similarly, no difference in DBP drop was observed (P=0.628). There were no differences in Colorado Pretrial Assessment Tool (CPAT) scores between the experimental group and the control group before intervention (P=0.509). After intervention, CPAT scores in the experimental group were higher than those in the control group (P<0.001). Before intervention, there was no significant difference in the Hypertension Patients Self-Management Behavior Rating Scale (HPSMBRS) scores, blood lipid, body mass index (BMI), and urinary microalbumin between the experimental group and the control group (P>0.05). After intervention, the HPSMBRS score in the experimental group was significantly higher than that in the control group (P<0.05). The HPSMBRS score of the experimental group after intervention was higher than before intervention, and BMI, urinary microalbumin, TC, LDL-C were lower than before intervention (P<0.05). CONCLUSIONS: This new mode of mobile health management has a good effect on blood pressure control in patients with hypertension. It provides evidence for the application of mobile information technology for hypertension patients in clinical practice.

Ginsenoside Rg1 reduces toxicity of PM(2.5) on human umbilical vein endothelial cells by upregulating intracellular antioxidative state.

Ambient airborne particulate matter (PM) is an important environmental pollutant responsible for many human diseases. Oxidative stress is suggested to be involved in PM-induced cell injury. The present study is designed to study unsalutary effects of the organic extracts of PM with an aerodynamic diameter of less than 2.5µm (PM(2.5)) and protective effect of Ginsenoside Rg1 (Rg1) against PM(2.5) on human umbilical vein endothelial cells (HUVECs) in vitro. Cytotoxic effects of the organic extract PM(2.5) on HUVECs were measured by means of HUVEC cell viability and the generation of intracellular reactive oxygen species (ROS). Expression of heme oxygenase-1(HO-1) and Nuclear factor-erythroid 2-related factor 2 (Nrf2) and Nrf2 cytoplasm-nucleus location were assayed. The present results showed that PM(2.5) (50-800µg/ml) decreased HUVEC viability and increased intracellular generation of ROS and malondialdehyde (MDA) in a concentration dependent manner, but increased HO-1 expression without concentration dependence. Rg1 (10 and 40µg/ml) diminished PM(2.5)-induced HUVEC viability, decrease ROS and MDA generation, increased HO-1 and Nrf2 expression and promoted Nrf2 translocation to nucleus in a concentration dependent manner. These results suggested that organic extracts of PM(2.5) increase oxidative stress and decrease cell viability; Rg1 antagonize PM(2.5)-induced excess oxidative stress; HO-1 expression increase and Nrf2 translocation to nucleus may be involved in the effects of both PM(2.5) and Rg1 on HUVECs.

Isoflurane preconditioning confers cardioprotection by activation of ALDH2.

The volatile anesthetic, isoflurane, protects the heart from ischemia/reperfusion (I/R) injury. Aldehyde dehydrogenase 2 (ALDH2) is thought to be an endogenous mechanism against ischemia-reperfusion injury possibly through detoxification of toxic aldehydes. We investigated whether cardioprotection by isoflurane depends on activation of ALDH2.Anesthetized rats underwent 40 min of coronary artery occlusion followed by 120 min of reperfusion and were randomly assigned to the following groups: untreated controls, isoflurane preconditioning with and without an ALDH2 inhibitor, the direct activator of ALDH2 or a protein kinase C (PKCε) inhibitor. Pretreatment with isoflurane prior to ischemia reduced LDH and CK-MB levels and infarct size, while it increased phosphorylation of ALDH2, which could be blocked by the ALDH2 inhibitor, cyanamide. Isolated neonatal cardiomyocytes were treated with hypoxia followed by reoxygenation. Hypoxia/reoxygenation (H/R) increased cardiomyocyte apoptosis and injury which were attenuated by isoflurane and forced the activation of ALDH2. In contrast, the effect of isoflurane-induced protection was almost abolished by knockdown of ALDH2. Activation of ALDH2 and cardioprotection by isoflurane were substantially blocked by the PKCε inhibitor. Activation of ALDH2 by mitochondrial PKCε plays an important role in the cardioprotection of isoflurane in myocardium I/R injury.

[The historical review of cardio pulmonary resuscitation].

Cardio pulmonary resuscitation is the main method to rescue sudden cardiac arrest, which involved the aspects of opening airway, artificial ventilation, cardiac compression, defibrillation and pacing. By reviewing the developmental process of each aspect of the above and analyzing the historical role of academic background, important events and outstanding figures could contribute to conclude the experience and discipline in this historical process so as to grasp the developmental sequence of cardio pulmonary resuscitation and understand deeply and further perfect and develop the cardio pulmonary resuscitation.