The Wenzhou Municipality in Zhejiang Province is spearheading China' marketization and development of private enterprises. Its successful development trajectory, centered on family‐owned small businesses embedded in thick local institutions, resembles Marshallian industrial districts (MIDs). However, with China' changing institutional environment and intensifying competition, Wenzhou has been facing challenges. Since the late 1980s, Wenzhou has gone through two major rounds of restructuring (from family enterprises to shareholding cooperatives to shareholding enterprises), that have included four major types of strategic response: institutional change, technological upgrading, industrial diversification, and spatial restructuring. Firms in Wenzhou have gone through localization and delocalization, and locational choices reflect the dual destinations of globalizing cities and interior cities. The formation of new firms and clusters has been accompanied by mergers, acquisitions, and the emergence of multiregional enterprises (MREs), some of which have relocated their headquarters and specialized functions to metropolitan areas, especially Shanghai and Hangzhou. More recently, Wenzhou' growth has slowed, leading some to question the sustainability of the Wenzhou model. We argue that Wenzhou' development is in danger of regional lock‐ins—relational, intergenerational, and structural. Wenzhou' experience challenges the orthodox concept of MIDs and calls for “scaling up” regional development.

BackgroundAcute heart failure, which requires urgent evaluation and treatment, is a leading cause for admission to the emergency department. The aim of this meta-analysis was to evaluate the effects of tolvaptan on acute heart failure and compare them with the effects of conventional therapy or placebo.MethodsThe electronic databases PubMed, EMBASE, and the Cochrane Controlled Trial registry were searched from their starting dates to October 24, 2016. Two authors independently read the trials and extracted related information from the included studies. We used fixed-effects or random-effects models to assess the overall combined risk estimates according to I2 statistics. Analysis to determine sensitivity and publication bias was conducted.ResultsSix randomised controlled trials from eight articles, with a total of 746 patients, were included for analysis. Compared with the control, tolvaptan reduced body weight in two days (WMD 1.35; 95% CI 0.75 to 1.96), elevated sodium level in two days (WMD 2.33; 95% CI 1.08 to 3.57) and five days (WMD 1.57; 95% CI 0.04 to 3.09), and ameliorated symptoms of dyspnoea (RR 0.82; 95% CI 0.71–0.95). However, tolvaptan did not improve long-term (RR 1.04; 95% CI 0.66–1.62) or short-term all-cause mortality (RR 0.89; 95% CI 0.45–1.76), incidence of clinical events (worsening heart failure, RR 0.75; 95% CI 0.50–1.12 and worsening renal function, RR 0.97; 95% CI 0.75–1.27), and length of hospital stay in patients (WMD 0.14; 95% CI -0.29 to 2.38) with acute heart failure.ConclusionTolvaptan can decrease body weight, increase serum sodium level, and ameliorate some of the congestion symptoms in patients with acute heart failure, which may help avoid the overdose of loop diuretics, especially in patients with renal dysfunction.Electronic supplementary materialThe online version of this article (doi:10.1186/s12872-017-0598-y) contains supplementary material, which is available to authorized users.

Abstract. The aim of the present study was to explore the effect of naringenin on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in a mouse model, as well as the underlying mechanism. The animals were randomly assigned to four groups: PBS-treated healthy control (Control), LPS-induced ALI (LPS), vehicle-treated ALI (LPS + Vehicle), and naringenin-treated ALI (LPS + Nar) group. Naringenin (100 mg/kg) was administered orally for 4 consecutive days, starting 3 days prior to induction of ALI. The survival rates of mice, lung wet/dry weight ratios, lung injury score, protein levels of bronchoalveolar lavage fluid (BALF), lactate dehydrogenase (LDH) activity in the BALF, lung myeloperoxidase (MPO) activity, the number of infiltrated neutrophils and reactive oxygen species (ROS) levels (H 2 O 2 and malondialdehyde) were assessed. In addition, the serum and BALF levels of inflammatory cytokines [tumor necrosis factor-α, interleukin (IL)-1β, IL-6 and macrophage inflammatory protein 2] were determined, along with the total and the phosphorylated protein levels of phosphatidylinositol 3-hydroxy kinase (PI3K) and AKT in lung tissues. The results showed that naringenin pre-treatment significantly increased the survival rate, improved histopathologic changes, alleviated pulmonary edema and lung vascular leak, downregulated the levels of ROS and reduced neutrophil infiltration as well as the levels of inflammatory cytokines in the serum and BALF. Moreover, naringenin pre-treatment reduced the total and the phosphorylated protein levels of PI3K and AKT. The present study suggested that naringenin pre-treatment ameliorated LPS-induced ALI through its anti-oxidative and anti-inflammatory activity and by inhibition of the PI3K/AKT pathway in mice.

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