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The new compound based on Wells-Dawson-type arsenomolybdate: [{Cu 10 (pz) 11 Cl 4 }{As 2 III As 2 V Mo 6 V Mo 12 VI O 62 }]·H 2 O ( 1 ) has been hydrothermally synthesized and characterized by single-crystal X-ray diffraction analysis, X-ray powder diffraction (XRPD), XPS spectroscopy and thermogravimetric analysis (TG). Compound 1 is consisted of two As caps Wells-dawson-type arsenomolybdate and {Cu 10 (py) 11 } complexes by chloride bridge. In addition, the antitumor effects of the title compound 1 were studied on three human lung cancer cells (A549, SK-LU-1 and SW1573). The results showed that compared with the positive reference drug carboplatin, compound 1 displayed efficient antitumor activity. [ABSTRACT FROM AUTHOR]

Pulmonary hypertension (PH) mainly results from excessive proliferation of pulmonary artery smooth muscle cells (PASMCs) and displays mitochondrial abnormalities such as mitochondrial fragmentation. Epigallocatechin-3-gallate (EGCG), an efficient antiproliferative compound in green tea, has recently been demonstrated to inhibit PASMCs proliferation. However, the pre-clinical issues as to whether EGCG attenuates PH and the underlying mechanisms have yet to be addressed. The present study was undertaken to investigate the therapeutic effects of EGCG on PH and its effects on mitochondrial fragmentation in PASMCs. Rats exposed to hypoxia (10% O 2 , 3 weeks) developed PH. EGCG (50, 100 or 200 mg/kg/d, i.g.) dose-dependently attenuated right ventricular systolic pressure, pulmonary vascular remodeling and right ventricular hypertrophy, increased expression of mitochondrial fusion protein - mitofusin-2 (MFN-2), and promoted mitochondrial fusion as evidenced by decreased number and volume of mitochondria in PASMCs of pulmonary arteries. Notably, EGCG (50 μM) downregulated hypoxia-induced (3% O 2 , 48 h) PASMCs mitochondrial fragmentation and inhibited PASMCs proliferation via KLF-4/MFN-2/p-Erk signaling pathway. Collectively, our data demonstrated that EGCG exerts antiproliferative effects via regulating mitochondrial fragmentation of PASMCs and EGCG holds the promise as a drug against PH. [ABSTRACT FROM AUTHOR]

Aim Chronic hypoxia leads to right ventricular hypertrophy (RVH). RVH is believed to result from hypoxia-induced pulmonary hypertension. However, if hypoxia impacts RVH directly awaits clarification. Hypoxia triggers oxidative stress, and lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) mediates reactive oxygen species (ROS) generation in different cells. Therefore, this study aims to explore whether LOX-1-mediated oxidative stress accounts for hypoxia-induced RVH. Main methods Rats developed RVH after 3 weeks of hypoxia (10% O 2 ). Immunofluorescence staining was performed to evaluate H9C2 cell hypertrophy induced by hypoxia (3% O 2 ). Real-time PCR and Western-blot were performed to assess LOX-1, NADPH oxidases (NOX), collagen I/III, atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) expression. DCFH-DA staining was performed to measure ROS generation. Key findings Hypoxia induced RVH and cardiac fibrosis in rats, as indicated by enlarged cardiomyocytes and deposition of extracellular matrix. Interestingly, hypoxia treatment directly induced H9C2 cardiomyocyte hypertrophy, implying direct effects of hypoxia on cell hypertrophy. Rat and H9C2 hypertrophy model revealed that cell hypertrophy was accompanied by marked increase in LOX-1 expression. Knockdown of LOX-1 significantly ameliorated H9C2 cell hypertrophy. Mechanistically, hypoxia induced prominent oxidative stress in rat right ventricles and H9C2 cells, most likely as a result from increased expression of NOX2/4, contributing to RVH. Knockdown of LOX-1 significantly attenuated H9C2 cell oxidative stress, with a concomitant decrease in NOX2/4 expression. Significance LOX-1/NOX/ROS pathway could represent a novel mechanism underlying hypoxia-induced RVH. Therapeutic targeting of LOX-1 would be exploited to treat RVH owing to chronic hypoxia exposure. [ABSTRACT FROM AUTHOR]

The authors have retrieved the experimental literature on moxibustion in treatment of heat syndrome in recent years, and summarized the mechanism of moxibustion in treatment of heat syndrome from such aspects as antipyretic and anti-infective effect of moxibustion, the effect on peripheral metabolism of humoral factors and the level of central neurotransmitter, and the regulation of immune function through sorting and analysis, thus providing experimental evidences for the feasibility and effectiveness of “moxibustion can be used for heat syndrome”, and providing ideas and direction for future researches. [ABSTRACT FROM AUTHOR]

Pulmonary vascular remodeling (PVR) is the pathological basis of pulmonary hypertension (PH). Incomplete understanding of PVR etiology has hindered drug development for this devastating disease, which exhibits poor prognosis despite the currently available therapies. Endothelial-to-mesenchymal transition (EndMT), a process of cell transdifferentiation, has been recently implicated in cardiovascular diseases, including PH. But the questions of how EndMT occurs and how to pharmacologically target EndMT in vivo have yet to be further answered. Herein, by performing hematoxylin–eosin and immunofluorescence staining, transmission electron microscopy and Western blotting, we found that EndMT plays a key role in the pathogenesis of PH, and importantly that aspirin, a FDA-approved widely used drug, was capable of ameliorating PVR in a preclinical rat model of hypoxia-induced PH. Moreover, aspirin exerted its inhibitory effects on EndMT in vitro and in vivo by suppressing HIF-1α/TGF-β1/Smads/Snail signaling pathway. Our data suggest that EndMT represents an intriguing drug target for the prevention and treatment of hypoxic PH and that aspirin may be repurposed to meet the urgent therapeutic needs of hypoxic PH patients. [ABSTRACT FROM AUTHOR]

Environmental pollution and its health risks to human beings have been becoming increasingly serious in China, and the health status of the individuals is not only affected by their environment but also by their own characteristics and socio-economic status. Based on the survey data of China Family Panel Studies (2014), three hierarchical linear models at three levels of individual, family, and community were developed to investigate the influencing factors of individual health status. The results indicate that: (1) there exists significant difference among individual health status, of which 16% and 9.11% are caused by the family and community levels, respectively; (2) the average health status of men is better than that of women by 6.95%. As for the difference in health effects produced by gender, total household income can reduce this difference; (3) age has significant negative health effects, while the level of education has positive effect on individual health status; and (4) the health effects of pollution is mainly reflected by its interaction with gender; in particular, when men and women face the same level of pollution exposure, men are more susceptible. [ABSTRACT FROM AUTHOR]

Aims Pulmonary hypertension (PH) is a proliferative disorder characterized by enhanced proliferation and suppressed apoptosis of intrapulmonary vascular smooth muscle cells. Recently, network-based bioinformatics have identified let-7 family, a tumor suppressive microRNA, regulate multiple interacting targets relevant to PH. However, the role of let-7 in vascular homeostasis in PH remains unknown. Thus, we wanted to investigate the role of let-7 in hypoxia-induced PASMCs proliferation and the underlying mechanism in hypoxic pulmonary hypertension (HPH). Main methods The male Sprague–Dawley (SD) rats were exposed to hypoxia (10% O 2 ) for 21 days to induce HPH. The expression of let-7 was determined by quantitative real-time polymerase chain reaction (qRT-PCR) and in situ hybridization. Primary rat PASMCs were exposed to hypoxia (3% O 2 ). MTS and EDU were performed to evaluate PASMCs proliferation. The mRNA and protein expression of c-myc, Bmi-1 and p16 were determined by qRT-PCR and Western blotting, respectively. The functions of let-7g on PASMCs proliferation, c-myc, Bmi-1 and p16 expression were assessed by let-7g mimic and inhibitor transfection. Key findings Among let-7 family members, only let-7b and let-7g were significantly down-regulated in remodeled pulmonary artery in HPH rats. Furthermore, only let-7g level was decreased in hypoxic PASMCs. Either hypoxia or let-7g inhibitor stimulated proliferation of PASMCs, let-7g mimic inhibited hypoxia-induced PASMCs proliferation. C-myc was the target of let-7g in PASMCs. Transfect of let-7g mimic inhibited hypoxia-induced c-myc, Bmi-1 up-regulation and p16 down-regulation, which ultimately controls cell cycle progression. Significance Loss of inhibition on c-myc-Bmi-1-p16 signaling pathway by let-7g may lead to PASMCs proliferation and vascular remodeling in HPH. [ABSTRACT FROM AUTHOR]

[Display omitted] The pulmonary vascular remodeling (PVR), the pathological basis of pulmonary hypertension (PH), entails pulmonary artery smooth muscle cells (PASMCs) phenotypic switching, but appreciation of the underlying mechanisms is incomplete. Exosomes, a novel transfer machinery enabling delivery of its cargos to recipient cells, have been recently implicated in cardiovascular diseases including PH. The two critical questions of whether plasma-derived exosomes drive PASMCs phenotypic switching and what cargo the exosomes transport, however, remain unclear. Herein, by means of transmission electron microscopy and protein detection, we for the first time, characterized lectin like oxidized low-density lipoprotein receptor-1 (LOX-1) as a novel cargo of plasma-derived exosomes in PH. With LOX-1 knockout (Olr1-/-) rats-derived exosomes, we demonstrated that exosomal LOX-1 could be transferred into PASMCs and thus elicited cell phenotypic switching. Of importance, Olr1-/- rats exhibited no cell phenotypic switching and developed less severe PH, but administration of wild type rather than Olr1-/- exosomes to Olr1-/- rats recapitulated the phenotype of PH with robust PASMCs phenotypic switching. We also revealed that exosomal LOX-1 triggered PASMCs phenotypic switching, PVR and ultimately PH via ERK1/2-KLF4 signaling axis. This study has generated proof that plasma-derived exosomes confer PH by delivering LOX-1 into PASMCs. Hence, exosomal LOX-1 represents a novel exploitable target for PH prevention and treatment. [ABSTRACT FROM AUTHOR]

Previous studies demonstrated that H 2 S has an antihypertension effect on hypertension, but the mechanism involved is unclear until now. The aim of the study is to elucidate the effect of H 2 S on PH and the mechanism involved. In this study, GYY4137 (a H 2 S donor) were administered to spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) by intraperitoneally injection daily for consecutive 14 days. Systolic blood pressure (SBP), endothelial-dependent relaxation (EDR), plasma malondialdehyde (MDA), superoxide dismutase (SOD), and H 2 S levels were measured. Human umbilical vein endothelial cells (HUVECs) were also used to elucidate the mechanism involved in the protect effect of H 2 S on the injured vessels. Our results showed that GYY4137 normalized the SBP (P < 0.0001), increased EDR (P < 0.01), reduced oxidative stress (increased the content of SOD and reduced the content of MDA) of SHR. Meanwhile, GYY4137 could promote the proliferation (P < 0.01) and migration (P < 0.01) of HUVECs, increase the expression of endothelial NO synthase (eNOS) and Vascular Endothelial Growth Factor Receptor 2 (VEGFR2) both in SHR and HUVECs treated with GYY4137. In addition to the above results, the PIP3/Akt signaling pathway was activated and the expression of caspase 3 was increased by GYY4137. However, all the above effects of GYY4137 were blocked by ZD6474 (a VEGFR2 inhibitor). GYY4137 had a hypotensive and vascular protect effect on PH. This effect might be mediated through upregulating the expression of VEGFR2, which subsequently alleviating oxidant-provoked vascular endothelial dysfunction, and promoting the proliferation and migration of endothelial cells in SHR. [ABSTRACT FROM AUTHOR]

• Dynamic network data envelopment analysis and Tobit regression are used for study. • The efficiency of production process is higher than the waste treatment process. • Significant regional differences exist in the industrial eco-efficiency in China. • Industrial agglomeration impedes the eco-efficiency of industrial sector. • Industrial structure rationalization promotes the industrial eco-efficiency. The industrial sector is the largest energy consumption sector and major source of environmental pollution in China. Improving the industrial eco-efficiency is significant for China to realize high-quality development. Based on the panel data of industrial sector in China's 30 provinces from 2006 to 2015, this paper first adopts a dynamic network data envelopment analysis to evaluate the eco-efficiency of industrial sector, and then uses panel Tobit regression model to investigate the impacts of industrial policies on the eco-efficiency of industrial sector. The results reveal that, (1) the overall eco-efficiency of China's provincial industrial sector is 0.7581 during 2006–2015, and the average efficiency of the industrial production process is higher than that of the waste treatment process. (2) The eco-efficiency of the industrial sector differs greatly by region, the eastern region is the highest, followed by the western and central regions, and the northeast is the lowest. (3) Industrial agglomeration impedes the improvement of industrial eco-efficiency, while industrial structure rationalization can promote industrial eco-efficiency. (4) The influence of industrial agglomeration and industrial structure rationalization on the efficiency of industrial waste treatment process is larger than that of the industrial production process. The findings of this paper reveal the importance of improving the efficiency of industrial sub-processes, and can also offer lessons for other industrialized nations to improve the industrial eco-efficiency. [ABSTRACT FROM AUTHOR]

• A flexible and comprehensive assessment framework of ISID is proposed. • Two formulations of ISID – ISID regime and ISIDsdg9 regime are established. • MEA approach and RAM approach are utilized to measure ISID. • Current status and improving potentials of ISID for China's 30 provinces are evaluated. • Policy paths toward mainstreaming ISID for China's 30 provinces are put forward. Inclusive and sustainable industrial development (ISID) is a call for action to promote industrialization by minimizing the environmental footprint and enhancing social inclusion. This study proposes a new framework of an evaluation system to assess the ISID for 30 provinces in China (2011–2016). As there does not exist a generally accepted evaluation system of ISID, this study proposes a dual-formulation of ISID to rationalize the trade-offs among externalities brought by industrialization: (i) ISID represents the aspiration of countries to promote industrialization and consequently sustain economic growth by reducing the adverse environmental and social effects which manifest in the overall economy (ii) ISIDsdg9 considers the same aspects of ISID but limits the externalities within the industrial sector. This study applied two newly developed efficiency evaluation approaches, Multi-Directional Efficiency Analysis (MEA) and Range-Adjusted Measure (RAM), to evaluate and analyze the ISID for China. This study finds that: Among the 30 provinces, (i) Beijing and Tianjin are the benchmark provinces for promoting ISID and ISIDsdg9 regimes, respectively. (ii) Throughout the 2011–2016, the overall performance of China on ISID and ISIDsdg9 regimes has improved modestly. (iii) Based on the analysis of the barrel effect, SO 2 emission is the key binding constraint to achieving the frontier status of ISID and ISIDsd9 regimes (v) Under the evaluation of ISID and ISIDsdg9 regimes, the average annual growth potentials of industrial value added (IVA) is 280.52 billion CNY and 927.54 billion CNY, respectively. This present study recommends local government in China to advance their ISID performance by exploiting the policies targeting emission mitigation concerning fossil fuels while considering Beijing and Tianjin as the benchmark provinces. [ABSTRACT FROM AUTHOR]