Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury.

Myocardial ischemia and reperfusion injury (MIRI), induced by coronary heart disease (CHD), causes damage to the cardiomyocytes. Furthermore, evidence suggests that thrombolytic therapy or primary percutaneous coronary intervention (PPCI) does not prevent reperfusion injury. There is still no ideal animal model for MIRI. This study aims to improve the MIRI model in rats to make surgery easier and more feasible. A unique method for establishing MIRI is developed by using a soft tube during a key step of the ischemic period. To explore this method, thirty rats were randomly divided into three groups: sham group (n = 10); experimental model group (n = 10); and existing model group (n = 10). Findings of triphenyltetrazolium chloride staining, electrocardiography, and percent survival are compared to determine the accuracies and survival rates of the operations. Based on the study results, it has been concluded that the improved surgery method is associated with a higher survival rate, elevated ST-T segment, and larger infarct size, which is expected to mimic the pathology of MIRI better.

Astragaloside IV stimulates angiogenesis and increases nitric oxide accumulation via JAK2/STAT3 and ERK1/2 pathway.

Astragaloside IV (AS-IV), one of the major active constituents of Astragalus membranaceus in Traditional Chinese Medicine, has been widely used to treat ischemic diseases. However, the potential mechanism is this action is unclear. In this study, we tested the hypothesis that AS-IV might promote angiogenesis through multiple signaling pathways. Our data indicate that AS-IV treatment promotes umbilical vein endothelial cells (HUVEC) proliferation, migration, and tube formation. AS-IV treatment also activates JAK2/STAT3 and ERK1/2 signaling pathways, and up-regulates endothelial nitric oxide synthase (eNOS) expression and nitric oxide (NO) production. AS-IV-induced angiogenesis in HUVECs is significantly blocked by specific kinase inhibitors. Our study indicated that AS-IV is a key regulator of NO and angiogenesis through the JAK2/STAT3 and ERK1/2 pathways, which provides a mechanistic basis for the potential use of this compound in the treatment of clinical ischemic diseases.

Effects of salvianolic acid and notoginseng triterpenes on angiogenesis in EA-hy926 cells in vitro.

AIM: To investigate the different effects of salvianolic acid and notoginseng triterpenes on proliferation, angiogenesis and expression of vascular endothelial growth factor in EA-hy926 cells in vitro. METHODS: EA-hy926 cells were cultured in vitro. Salvianolic acid and notoginseng triterpenes at concentrations of 0.4, 0.8 and 1.2 mg·L(-1) were used to culture EA-hy926 cells. EA-hy926 cells in a blank control group were grown in culture solution only. Viability of cells was assessed by CCK-8, and after treated for 12 h, capillary-like structures were examined. After 24 h culture, the expression of VEGF was detected by real-time PCR. RESULTS: Salvianolic acid at 0.4, 0.8 mg·L(-1), the same as notoginseng triterpenes, increased VEGF content in EA-hy926 cells. Expression of VEGF protein in the salvianolic acid at 1.2 mg·L(-1) group, was up-regulated as compared with notoginseng triterpenes group (P < 0.05). CONCLUSION: Salvianolic acid and notoginseng triterpenes can promote EA-hy926 cell proliferation, angiogenesis and expression of VEGF protein. This analysis also provided evidence that salvianolic acid had the better effects as compared with notoginseng triterpenes.

[A case-control study of an influenza A (H1N1) outbreak in a hospital].

OBJECTIVE: This study aimed to explore the epidemiological factors of an influenza A (H1N1) outbreak in a hospital. METHODS: General data were collected via face-to-face interview and telephone survey. Total 132 individuals including medical and nursing staffs (37), in-patients (39) and patients' family members (56) who were exposed to the pediatric surgery ward during August 11 - 18, 2009, were investigated. The case group included 35 cases according to the diagnostic criteria for influenza A (H1N1). The other 97 persons were grouped as control. A case-control study was then conducted to explore the epidemic factors, and layering analysis was applied to determine the interactions among these factors. RESULTS: The overall incidence in this study was 26.5% (35/132), which included 12 confirmed and 23 suspected cases, and there was no severe case. The first case was a child with the influenza-like symptoms before admission on August 11. The onsets of these cases were during August 7 - 17. The cases were distributed in 9 of 13 rooms, and there was no room aggregation in the cases distribution (χ(2) = 0.00, P > 0.05). Twelve of 25 oropharyngeal swabs were influenza A (H1N1) nucleic acid positive. The case-control study showed that exposure to the enema room accounted for 93.10% (27/29) in cases and 72.73% (48/66) in control; OR = 5.06, 95%CI = 1.01 - 34.23), long time exposure to ward was 71.43% (25/35) in cases and 44.33% (43/97) in control; OR = 3.14, 95%CI = 1.27 - 7.90), and short distance contact with the nurse LIU (76.46% (26/34) in cases and 50.52% (49/97) in control; OR = 3.18, 95%CI = 1.22 - 8.54) were the risk factors. However, keeping the window open (27.59% (8/29) in cases and 68.18% (45/66) in control; OR = 0.14, 95%CI = 0.05 - 0.39) and hand washing (25.71% (9/35) in cases and 76.29% (74/97) in control; OR = 0.11, 95%CI = 0.04 - 0.28) were the protective factors. The longer time exposure to ward had the higher risk (ratios of cases to control were 4:20 (0 - 1 day), 6:34 (2 - 4 days) and 25:43 (≥ 5 days); χ(2)(trend) = 5.737, P < 0.05). In contrast, hand washing with more frequencies (ratios of cases to control were 26:23 (0 - 1 time one day), 7:9 (2 - 3 times one day) and 2:65 (≥ 4 times one day); χ(2)(trend) = 37.136, P < 0.01) and the longer time window opening (ratios of cases to control were 21:21 (no), 4:13 (a few) and 4:32 (often); χ(2)(trend) = 13.830, P < 0.01) had the lower risk. Nevertheless, layering analysis excluded long time exposure to ward from the risk factors (for individuals with more frequent hand washing, 6.90% (2/29) exposed in cases, 7.14% (1/14) exposed in control, OR = 0.97, 95%CI = 0.06 - 29.51; for individuals keeping window open, 21.21% (7/33) exposed in cases, 8.33% (1/12) exposed in control, OR = 2.55, 95%CI = 0.26 - 60.87), indicating the main risk factors in this outbreak were exposure to the enema room and short distance contagion with the infected nurse. CONCLUSION: The influenza A (H1N1) outbreak in this hospital was induced by an inpatient infected with influenza A (H1N1) virus before admission. Infected medical staffs keeping on work and exposure to the same place, e.g.the enema room in this study might spread the influenza A (H1N1) virus, and frequent hand washing and keeping the window open are the most effective and economic methods to prevent influenza A (H1N1) infection.