共享经济在农村的模式创新

当今社会是共享的社会,共享经济在人们的生活中越来越普遍。文中运用文献研究法、案例分析法、数据分析法等方法对共享经济在农村的应用进行研究,分析现有的农村共享经济模式以及与传统农村经济发展方式相比发生的变化,分析共享经济给农村带来的好处,帮助农民增产增收,转变经济增长方式,增加额外收入,创造新的就业方式,最后,对今后农村地区的发展提出建议。

Pretreatment with Tongxinluo protects porcine myocardium from ischaemia/reperfusion injury through a nitric oxide related mechanism

Background The traditional Chinese medicine injury, but the mechanism of its action is not we protective role of Tongxinluo. Tongxinluo can protect myocardium against documented. We examined the involvement schaemia/reperfusion of nitric oxide in the Methods Miniswine were randomized to four groups of seven： sham, control, Tongxinluo and Tongxinluo coadministration with a nitric oxide synthase inhibitor N^ωnitro-L-arginine （L-NNA, 10 mg/kg i.v.）. Three hours after administration of Tongxinluo, the animals were anaesthetised and the left anterior descending coronary artery ligated and maintained in situ for 90 minutes followed by 3 hours of reperfusion before death. Area of no reflow and necrosis and risk region were determined pathologically by planimetry. The degree of neutrophil accumulation in myocardium was obtained by measuring myeloperoxidase activity and histological analysis. Myocardial endothelial nitric oxide synthase activity and vascular endothelial cadherin content were measured by colorimetric method and immunoblotting analysis respectively. Results Tongxinluo significantly increased the local blood flow and limited the infarct and size of no reflow. Tongxinluo also attenuated myeloperoxidase activity and neutrophil accumulation in histological sections and maintained the level of vascular endothelial cadherin and endothelial nitric oxide synthase activity in the reflow region when compared with control group. The protection of Tongxinluo was counteracted by coadministration with L-NNA. Conclusions Tongxinluo may limit myocardial ischaemia and protect the heart against reperfusion injury. Tongxinluo regulates synthesis of nitric oxide by altering activity of endothelial nitric oxide synthase.

Protein kinase A-mediated cardioprotection of Tongxinluo relates to the inhibition of myocardial inflammation, apoptosis, and edema in reperfused swine hearts

Background Our previous studies have demonstrated that Tongxinluo （TXL）, a traditional Chinese medicine, can protect hearts against no-reflow and reperfusion injury in a protein kinase A （PKA）-dependent manner. The present study was to investigate whether the PKA-mediated cardioprotection of TXL against no-reflow and reperfusion injury relates to the inhibition of myocardial inflammation, edema, and apoptosis. Methods In a 90-minute ischemia and 3-hour reperfusion model, minipigs were randomly assigned to sham, control, TXL （0.05 g/kg, gavaged one hour prior to ischemia）, and TXL ＋ H-89 （a PKA inhibitor, intravenously and continuously infused at 1.0 μg/kg per minute） groups. Myocardial no-reflow, necrosis, edema, and apoptosis were determined by pathological and histological studies. Myocardial activity of PKA and myeloperoxidase was measured by colorimetric method. The expression of PKA, phosphorylated cAMP response element-binding protein （p-CREB） （Ser133）, tumor necrosis factor a （TNF-a）, P-selectin, apoptotic proteins, and aquaporins was detected by Western blotting analysis. Results TXL decreased the no-reflow area by 37.4% and reduced the infarct size by 27.0% （P〈0.05）. TXL pretreatment increased the PKA activity and the expression of Ser133 p-CREB in the reflow and no-reflow myocardium （P 〈0.05）. TXL inhibited the ischemia-reperfusion-induced elevation of myeloperoxidase activities and the expression of TNF-a and P-selectin, reduced myocardial edema in the left ventricle and the reflow and no-reflow areas and the expression of aquaporin-4, -8, and -9, and decreased myocytes apoptosis by regulation of apoptotic protein expression in the reflow and no-reflow myocardium. However, addition of the PKA inhibitor H-89 counteracted these beneficial effects of TXL. Conclusion PKA-mediated cardioprotection of TXL against no-reflow and reperfusion injury relates to the inhibition of myocardial inflammation, edema, and apoptosis in the reflow and no-reflow myocardium.

Severe coronary artery disease in Chinese patients with abdominal aortic aneurysm： prevalence and impact on operative mortality

Background Little is known about the prognosis of coronary artery disease （CAD） in Chinese patients with abdominal aortic aneurysm （AAA）. The aim of this study was to evaluate the predictors of in-hospital all-cause mortality of severe CAD in Chinese patients who were hospitalized for AAAs. Methods From January 2003 to August 2009, 368 patients were operated on for AAAs. The clinical characteristics were retrospectively collected. The primary outcome was the in-hospital all-cause mortality. The clinical risk factors were subjected to a multivariate analysis to determine the predictors of in-hospital all-cause mortality. Results During their hospitalization, 23% （85/368） of the patients underwent coronary angiography, which revealed significant lesions in 93% （79/85） of the patients. In 25 cases, coronary artery bypass grafting （CABG） was performed before the AAA repair and in 16 cases of percutaneous coronary intervention （PCI） was performed. Ten patients with AAA alone died before discharge, and eight patients diagnosed with AAA combined with CAD died. There was no statistical difference in the postoperative death between the two groups. The logistic analysis showed that age 〉70 years and CAD （vessels ≥2） were the significant factors in predicting the adverse clinical outcome. Conclusions The prevalence of severe CAD in Chinese patients with AAAs seemed lower than those that were reported. Myocardial evaluation and subsequent revascularization before AAA surgery could improve the clinical outcome for these patients who have severe CAD.

Tacrolimus-related hypertrophic cardiomyopathy in an adult cardiac transplant patient

Left ventricular hypertrophy associated with the use of tacrolimus is a rare complication of solid organ transplantation in adult recipients. We present a cardiac transplant recipient who developed severe concentric left ventricular hypertrophy with congestive heart failure related to myocardial hypertrophy on tacrolimus. Hypertrophy improved when the drug was discontinued and replaced with sirolimus.