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.

Apigenin relaxes rat intrarenal arteries, depresses Ca2+-activated Cl- currents and augments voltage-dependent K+ currents of the arterial smooth muscle cells.

The vasorelaxant effect of apigenin (API) has been demonstrated in a number of vascular beds. We aimed to study the possible involvement of Cl- channels and K+ channels in API-induced vasorelaxation in intrarenal arteries. The vascular tone of isolated rat intrarenal arteries (RIRAs) was measured with a myograph. The myocyte transmembrane Cl- currents through Ca2+ activated Cl- channels (CaCCs) and the K+ currents through voltage-dependent (Kv) K+ channels were recorded using a patch clamp in the single arterial smooth muscle cells (ASMCs) isolated freshly from RIRAs. Preincubation with API (10-100 µM) concentration-dependently depressed the contractions induced by KCl, thromboxane A2 analog U46619, phenylephrine and vasopressin. The IC50 values were 13.27-26.26 µM. Instant application of API elicited immediate relaxations in RIRAs precontracted with these vasoconstrictors. The RC50 values were 5.80-24.33 µM. Chloride deprivation, Cl- channel blockers, Kv blocker and nitric oxide synthase inhibitor attenuated API-induced RIRA relaxation. At 10-100 µM, API depressed CaCC currents, but augmented Kv currents. Taken together, the present study demonstrated that API depresses contractions induced by various vasoconstrictors in RIRAs, suppresses CaCC currents and augments Kv currents in RIRA ASMCs.

Statin Attenuated Myocardial Inflammation Induced by PM2.5 in Rats.

BACKGROUND: Here, the study aims to explore the effect of PM2.5 exposure on atherosclerosis in rats. MATERIALS AND METHODS: 32 Wistar rats were selected in our study. An atherosclerosis model was established. All rats were evenly divided into four groups, including normal control group (NC), model control group (MC), model PM2.5 group (PM2.5) and model Atorvastatin group (Atorvastatin). The rats in NC and model control group were treated with saline 1 ml/kg body weight by tail intravenous injection, while the rats in PM2.5 group were exposed to PM2.5 suspension. The rats in atorvastatin group were given atorvastatin by gavage with 10 mg·kg-1·per day for 12 weeks until PM2.5 injection. After 24 h, all rats in each group were sacrificed. Pathological analysis, immunohistochemistry (IHC) and electrophoretic mobility shift assays (EMSA) were carried out. RESULTS: PM2.5 exposure significantly reduced the levels of triglyceride (TG), high density lipoprotein (HDL) and superoxide dismutase (SOD), but promoted the levels of total cholesterol (TC), low density lipoprotein (LDL), atherosclerosis index (AI), malondialdehyde (MDA), tumor necrosis factor-α (TNF-α) and high-sensitivity C-reactive protein (hs-CRP) in the rats of PM2.5 group than MC group (p < 0.05). PM2.5 group showed activated nuclear factor-kappa B (NF-κB), seriously damaged myocardial coronary branches and the highest nuclear translocation rate. Atorvastatin significantly improved the levels of TG, HDL, SOD, interleukin-6 (IL-6), and reduced the levels of TC, LDL, AI, MDA, TNF-α, hs-CRP, oxidized low-density lipoprotein (ox-LDL) and blood pressure, even the nuclear translocation rate. CONCLUSIONS: PM2.5 exposure contributes to atherosclerosis in rats, which correlate with the levels of cholesterol, oxidative stress and inflammatory response. Atorvastatin could attenuate myocardial inflammation caused by PM2.5 exposure in rats.

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.

The IL-24 gene protects human umbilical vein endothelial cells against H2O2-induced injury and may be useful as a treatment for cardiovascular disease.

The aim of the present study was to investigate the protective effects of interleukin-24 (IL-24) on hydrogen peroxide (H2O2)-induced vascular endothelial injury and to examine the association between IL-24 and cardiovascular disease. Human umbilical vein endothelial cells (HUVECs) were exposed to increasing concentrations of H2O2 in the presence or absence of IL-24, which was introduced via Lipofectamine® 2000-mediated transfection. The successful uptake of the IL-24 plasmid was confirmed by RT-PCR at 24 h post-transfection. The effects of H2O2 and IL-24 on the proliferation and migration of the HUVECs was determined using cell migration assays. Cell viability was determined using a Cell Counting Kit-8 (CCK-8). Apoptosis and the measurement of the intracellular reactive oxygen species (ROS) levels were determined by flow cytometry, and the levels of caspase-3, which is associated with apoptosis, were determined by western blot analysis. Real­time PCR and western blot analysis were also used to measure the levels of multiple cardiovascular disease­associated factors. In vivo experiments were also performed using a rat model of hypertension which was constructed by angiotensin II infusion using an osmotic pump. The mRNA and protein levels of IL-24 were measured in both the control and hypertensive rats; the effects of treatment with enalapril and nifedipine on the IL-24 levels were also examined. Our results revealed that IL-24 protected against the H2O2-mediated abnormal increase in HUVEC proliferation. IL-24 also antagonized H2O2 by reducing the content of ROS in the cells, thus decreasing cellular oxidative damage, improving the cellular survival rate, reducing apoptosis and decreasing the expression of cardiovascular disease-related factors. The results from our in vivo animal experiments revealed that IL-24 expression was lower in the hypertensive rats compared to the healthy controls. Additionally, the IL-24 levels increased following anti-hypertensive therapy. The findings of our study indicate that IL-24 protects against H2O2-mediated endothelial cell damage and may thus provide a novel therapeutic strategy for treatment of cardiovascular disease.

Overproduction of reactive oxygen species and activation of MAPKs are involved in apoptosis induced by PM2.5 in rat cardiac H9c2 cells.

Epidemiological studies show a positive correlation between the air levels of fine particulate matter (PM2.5) and cardiovascular disorders, but how PM2.5 affects cardiomyocytes has not been studied in great deal. The aim of the present study was to obtain an insight into the links among intracellular levels of reactive oxygen species (ROS), apoptosis and mitogen-activated protein kinases (MAPKs) in rat cardiac H9c2 cells exposed to PM2.5. H9c2 cells were incubated with PM2.5 at 100-800 µg ml(-1) to evaluate the effects of PM2.5 on cell viability, cell apoptosis, intracellular levels of ROS and expression of apoptosis-related proteins as well as activation of MAPKs. PM2.5 decreased cell viability, increased the cell apoptosis rate and intracellular ROS production in a concentration-dependent manner. PM2.5 decreased the Bcl-2/Bax ratio and increased cleaved caspase-3 levels. A Western blots study showed up-regulation of phosphorylated MAPKs including extracellular signal-regulated protein kinases (ERKs), c-Jun NH2-terminal kinases (JNKs) and p38 MAPK in the PM2.5-treated cells. The p38 MAPK inhibitor SB239063 attenuated whereas the ERKs inhibitor PD98059 augmented the effects of PM2.5 on apoptosis and the expression of related proteins. In conclusion, PM2.5 decreases cell viability and increases apoptosis by enhancing intracellular ROS production and activating the MAPKs signaling pathway in H9c2 cells. The MAPKs signaling pathway could be a new promising target for clinical therapeutic strategies against PM2.5-induced cardiac injury.

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.

Combination of IL-24 and cisplatin inhibits angiogenesis and lymphangiogenesis of cervical cancer xenografts in a nude mouse model by inhibiting VEGF, VEGF-C and PDGF-B.

The aim of the present study was to investigate the synergistic inhibitory effects of recombinant IL-24 delivered by pDC316-hIL-24 transfection and cisplatin (DDP) on angiogenesis and lymphangiogenesis in a cervical cancer xenograft model established in nude mice. Thirty-six mice (successful model) were randomly divided into six groups (n=6 in each): i) phosphate-buffered saline control; ii) empty plasmid; iii) half-dose DDP; iv) recombinant interleukin (IL)-24; v) full-dose DDP; and vi) combined treatment. Tumor growth and animal weight were measured every 3 days. Animals were sacrificed by cervical dislocation at 2 weeks after the cessation of treatment. Tumor inhibition was compared after intervention. Lymph node metastasis was evaluated by immunohistochemical (IHC) analysis of vascular endothelial growth factor (VEGF), VEGF-C and VEGFR-3. Platelet-derived growth factor (PDGF)-B expression was also investigated by western blot analysis. Microvessel density was evaluated by IHC analysis of CD34 expression. The tumor growth was slower or reduced in the IL-24 and half-dose DDP+IL-24 groups. The expression of VEGF and microvessel density in the IL-24 group was significantly lower than that in the other groups. VEGF (VEGF-A), VEGF-C, VEGFR-3 and PDGF-B expression was significantly decreased in the IL-24 and half-dose DDP+IL-24 groups compared with that in the other groups (P<0.001). The recombinant plasmid pDC316-hIL-24 acts synergistically with cisplatin to inhibit tumor growth and angiogenesis. Our data indicate that these effects are mediated by downregulation of VEGF, VEGF-C and PDGF-B expression. Thus, IL-24 may enhance tumor chemosensitivity to cisplatin, which may be an important strategy for reducing the side-effects of this chemotherapy.

Effects of ß-adrenoceptor subtypes on cardiac function in myocardial infarction rats exposed to fine particulate matter (PM 2.5).

The pathophysiological mechanisms of heart failure (HF) stems were mainly from longstanding overactivation of the sympathetic nervous system and renin-angiotensin-aldosterone system. Recent studies highlighted the potential benefits of ß1-adrenoceptor (ß1-AR) blocker combined with ß2-adrenergic receptor (ß2-AR) agonist in patients with HF. Long-term exposure to fine particulate air pollution, such as particulate matter ≤ 2.5 µm in diameter (PM2.5), has been found associated with acute myocardial infarction (AMI) which is the most common cause of congestive HF. In this study, we have investigated the effect of combined metoprolol and terbutaline on cardiac function in a rat model of AMI exposed to PM2.5. Our results demonstrated that short-term exposure to PM2.5 contributes to aggravate cardiac function in rats with myocardial infarction. The combined use of ß1-AR blocker and ß2-AR agonist is superior to ß1-AR blocker alone for the treatment of AMI rats exposed to PM2.5. The combination of ß1-AR blocker and ß2-AR agonist may decrease the mortality of patients with myocardial infarction who have been exposed to PM2.5.

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.

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.

[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.