A neglected climate risk: The price effect of urban waterlogging.

With global warming, cities are vulnerable to extreme weather, increasing the climate risk to cities worldwide. Although existing literature has examined the ex-post impacts of extreme weather, it is less clear how climate risk affects cites before extreme weather occur. To lower the risk of urban waterlogging, which is caused by extreme weather, and improve the ability of cities to adapt to extreme weather, China launched the Sponge City Project (SCP) in 2013 to manage the urban stormwater and waterlogging. Adopting the SCP pilot in China as a quasi-natural experiment, we examine the impact of the climate risk caused by urban stormwater and waterlogging on the house price with the difference-in-differences (DID) method. We find that after implementing the SCP pilot program, the house price in pilot cities increased significantly because of the improvement in cities' resilience to climate risk. Additionally, this effect was only demonstrated in cities with a high waterlogging risk. For SCP pilot cities with lower waterlogging risk, the house price is not significantly affected by SCP implementation. This indicates that the house price in China is sensitive to the climate risk caused by the urban stormwater and waterlogging. Our findings also contribute to the understanding of the significance of the climate risk management, and provided theoretical evidence for urban governance.

Effects of ICT diffusion on environmental pollution: analysis of industrial reallocation effects in China.

The development of information and communication technology (ICT) has brought about fundamental changes in social progress worldwide. Using panel data from 288 Chinese cities for the period from 1999 to 2019, this study evaluates the effect of the pilot Broadband China Strategy (BCS) program on environmental pollution. We find that BCS significantly reduces environmental pollution, and that this effect is stronger in eastern China and in Chinese cities with higher financial progress or broadband development. Interestingly, the negative effect of BCS on environmental pollution decreases with the improvement of human capital in the cities. We further discuss industrial efficiency and reallocation mechanisms and ascertain that BCS affects environmental pollution in pilot cities not only through the efficiency mechanism as established in the existing literature but also through the industrial scale change and labor transfer between different industries, which we refer to as the industrial reallocation mechanism in this study. Specifically, via the industrial efficiency and reallocation mechanisms, the implementation of the BCS increases the scale and efficiency of the primary and tertiary industries but decreases the scale and efficiency of the secondary industry. This reduction in the secondary industry results in a decline in environmental pollution. It indicates that promoting the balanced development of a country's ICT infrastructure and pushing forward ICT diffusion can help alleviate environmental pollution by industrial reallocation and efficiency improvement, especially in nations with significant regional economic and technological differences.

Does government institutional reform deter corporate tax evasion? Evidence from China.

Exploiting the quasi-natural experiment of the social insurance collection system reform implemented in China in 2000, based on data from China's industrial enterprise database from 1998 to 2006, we use the difference-in-differences method to test the impact of changing the social insurance collection institution on corporate tax evasion. We find that changing the social insurance collection institution from the social security department to the local tax department significantly deters corporate tax evasion. A series of robustness tests also support this conclusion. The reason is changing the social insurance collection institution to the local tax department increases its' social insurance information of the enterprise, and reduces the information asymmetry between the enterprise and the collection institution. Furthermore, we find that the impact of changing the social insurance collection institution on corporate tax evasion is more evident in the samples of labor-intensive enterprises, low labor cost enterprises, and enterprises under the jurisdiction of the local tax department. These results indicate that government institutional reform is a valid way to reduce the information asymmetry between the government and enterprises, which will finally deter corporate tax evasion.

Environmental regulation and corporate tax avoidance-Evidence from China.

In this study, we used a difference-in-difference (DID) approach to analyze the effect of environmental regulation on corporate tax avoidance behavior based on China's carbon emissions trading pilot policy of 2013. Our findings were as follows: (1) Environmental regulation has led companies to adopt further tax evasion behaviors. Furthermore, the core conclusion was confirmed after a series of robust and endogenous tests, such as parallel trends and PSM-DID (propensity score matching-difference-in-difference). (2) Environmental regulations increase tax avoidance activities by reducing corporate cash flows. (3) The influence of environmental regulation on firm tax evasion is highly pronounced among non-state-owned enterprises, big-scale enterprises, and enterprises with a high degree of industry competition.

TFPIα alleviated vascular endothelial cell injury by inhibiting autophagy and the class III PI3K/Beclin-1 pathway.

Endothelium (EC) dysfunction plays an important role in vascular diseases, such as arteriosclerosis and hypoxia/reoxygenation (H/R) injury. Tissue factor pathway inhibitor (TFPI) is the only physiological inhibitor of the TF/FVIIa complex in vivo. This experiment aimed to determine the effect of TFPIα on H/R-induced EC injury and the possible mechanisms. The MIC101 hypoxia system was used to establish an EC H/R injury model in vitro. Our results showed that 6 h after reoxygenation, the EC injury in H/R group was higher than that in the control group, whereas after adding TFPIα, the EC injury was alleviate than that in H/R group. The level of ROS was higher in the H/R group than in the control group, while it was apparently lower in the H/R+TFPIα group than in the H/R group. After H/R, the number of autophagosomes and the autophagic flux were significantly increased, whereas TFPIα could decrease the autophagy level after H/R. The expressions of LC3-II/LC3-I, Beclin-1 and PI3K were obviously higher after H/R and lower after adding TFPIα. In conclusion, autophagy contributes to EC injury during the H/R period. TFPIα could decrease autophagy in ECs, and the mechanism might be class III PI3K/Beclin-1 pathway regulation.

The plasma levels of CST and BCKDK in patients with sepsis.

OBJECTIVES: CST has been recently identified as a mediator of various beneficial effects in animal models of sepsis. At present, no data are available concerning the levels of CST in sepsis patients. In sepsis the plasma amino acid pattern is characterized by decreased branced chain amino acids (BCAAs). We investigated the levels of plasma CST or branched-chain α-ketoacid dehydrogenase kinase (BCKDK) and their relationship to component traits in patients with sepsis. DESIGN AND METHODS: We studied 228 patients and divided them into two groups based on severity of infection. Blood samples were taken at study entry, and CST, BCKDK were measured. RESULTS: CST and BCKDK levels were significantly higher in patients with sepsis than in controls: the median plasma CST concentration was 103.1ng/ml (range, <83.13-189.7ng/ml) in patients with sepsis and 49.69ng/ml (range, <19.38-100.8ng/ml) in controls (p=0.0022); the median plasma BCKDK concentration was 801.7ng/ml in sepsis group and 745ng/ml in controls (p=0.0292). Additionally, there was correlation between the plasma concentrations of CST and BCKDK in sepsis patients (r2=0.6357, p<0.01). CONCLUSIONS: We conclude that the plasma levels of CST in sepsis patients were higher than in controls, and there is a relationship between CST and BCKDK in sepsis patients. Future experimental and clinical studies are needed to evaluate CST as a novel prognostic tool in sepsis patients and its potential therapeutic use in sepsis.

Tissue factor pathway inhibitor gene transfer prevents vascular smooth muscle cell proliferation by interfering with the MCP-3/CCR2 pathway.

Increased vascular smooth muscle cell (VSMC) proliferation substantially contributes to the pathogenesis of atherosclerosis and intimal hyperplasia after vascular injury. The importance of inflammation in VSMC proliferation is now being recognized. Preventing the inflammatory response is one therapeutic strategy that can be used to inhibit atherosclerosis in the clinic. The present study, using RNA interference and gene transfer techniques, was conducted to investigate the effect of monocyte chemotactic protein-3 (MCP-3) on VSMC proliferation that is a result of TNF-α stimulation, and whether overexpression of the tissue factor pathway inhibitor (TFPI) gene could prevent VSMC proliferation by blocking the MCP-3/CC chemokine receptor 2 (CCR2) pathway. Mouse VSMCs were infected in vitro with recombinant adenoviruses containing either mouse MCP-3-shRNA (Ad-MCP-3-shRNA), the TFPI gene (Ad-TFPI), or the negative control, which was shRNA encoding the sequence for EGFP (Ad-EGFP) or DMEM only. The cells were then stimulated with TNF-α for different time periods on the third day after gene transfer. The data show that VSMC proliferation in the Ad-MCP-3-shRNA and Ad-TFPI groups was markedly decreased using BrdU ELISA and MTT assays; MCP-3-shRNA and TFPI inhibited the expression of MCP-3 and CCR2 after long-term stimulation and inhibited the phosphorylation of ERK1/2 and AKT after short-term stimulation, as shown by ELISA and western blot analysis. This study provides convincing evidence that clarifies the effect of the proinflammatory factor MCP-3 in promoting VSMC proliferation. Our data also show, for the first time, that TFPI has an anti-proliferative role in TNF-α stimulated-VSMCs at least partly by interfering with the MCP-3/CCR2 pathway and then via suppression of the ERK1/2 and PI3K/AKT signaling pathways. We conclude that TFPI gene transfer may be a safe and effective therapeutic tool for treating atherosclerosis and intimal hyperplasia.

Hedge Scope Detection in Biomedical Texts: An Effective Dependency-Based Method.

Hedge detection is used to distinguish uncertain information from facts, which is of essential importance in biomedical information extraction. The task of hedge detection is often divided into two subtasks: detecting uncertain cues and their linguistic scope. Hedge scope is a sequence of tokens including the hedge cue in a sentence. Previous hedge scope detection methods usually take all tokens in a sentence as candidate boundaries, which inevitably generate a large number of negatives for classifiers. The imbalanced instances seriously mislead classifiers and result in lower performance. This paper proposes a dependency-based candidate boundary selection method (DCBS), which selects the most likely tokens as candidate boundaries and removes the exceptional tokens which have less potential to improve the performance based on dependency tree. In addition, we employ the composite kernel to integrate lexical and syntactic information and demonstrate the effectiveness of structured syntactic features for hedge scope detection. Experiments on the CoNLL-2010 Shared Task corpus show that our method achieves 71.92% F1-score on the golden standard cues, which is 4.11% higher than the system without using DCBS. Although the candidate boundary selection method is only evaluated on hedge scope detection here, it can be popularized to other kinds of scope learning tasks.

Cortistatin Inhibits NLRP3 Inflammasome Activation of Cardiac Fibroblasts During Sepsis.

BACKGROUND: Cortistatin is a recently discovered neuropeptide that has emerged as a potential endogenous antiinflammatory peptide. As a clinical syndrome, sepsis occurs when an infection becomes amplified, leading to organ dysfunction or risk for secondary infection. Human septic shock involves excessive inflammatory cytokine production. Interleukin (IL) 1ß is one of these cytokines, and it plays a pivotal role in sepsis-induced myocardial dysfunction. The aim of the present study is to evaluate whether cortistatin inhibits nucleotide-binding oligomerization domain-like receptor with a pyrin-domain 3 (NLRP3) inflammasome/caspase-1/IL-1ß pathway in cardiac fibroblasts (CFs) and whether this role can subsequently affect myocardial injury. METHODS AND RESULTS: To test these processes, a murine model of cecal ligation and puncture in vivo and lipopolysaccharide-induced cardiac fibroblasts were used in vitro. We found that pretreatment with cortistatin inhibited NLRP3-mediated ASC pyroptosome formation, caspase-1 activation, and IL-1ß secretion. Additionally cortistatin inhibits proinflammatory pathways (nuclear factor κB and pro-IL-1ß). CONCLUSIONS: This work provided the first evidence of cortistatin as a new immunomodulatory factor with the capacity to deactivate NLRP3 inflammasome activity and to protect against the myocardial injury induced by sepsis. This study has important implications for the design of new strategies to control NLRP3-related diseases.

The plasma levels of relaxin-2 and relaxin-3 in patients with diabetes.

OBJECTIVES: Relaxin-2 has been found to alleviate fibrosis in experimental diabetic cardiomyopathy. In addition, the levels of serum relaxin-3 were increased and correlated with all the component traits of metabolic syndrome. We investigated the levels of plasma relaxin-2 or relaxin-3 and their relationship to component traits in patients with diabetes. DESIGN AND METHODS: We studied 33 newly diagnosed type 2 diabetes patients and 38 age-matched healthy subjects. Blood samples were taken at study entry, and relaxin-3, relaxin-2, fasting blood glucose, total cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides, serum insulin and hemoglobin A1c (HbA1c) levels were measured. RESULTS: Relaxin-2 levels were significantly lower in patients with diabetes than in controls: the median plasma relaxin-2 concentration was 34.68 pg/mL (range, <29.00-50.81 pg/mL) in patients with diabetes and 45.80 pg/mL (range, <37.42-54.46 pg/mL) in controls (p=0.0150). However, no differences in relaxin-3 levels were observed between the diabetes group and controls (p=0.6550). The plasma levels of relaxin-2 or relaxin-3 were not correlated with systolic blood pressure (BP), diastolic BP, total cholesterol, LDL-C, HDL-C, triglyceride, fasting blood glucose, fasting insulin and HbA1c in patients with diabetes. Additionally, there was no correlation between the plasma concentrations of relaxin-2 and relaxin-3 in patients with diabetes (rs=0.225; p=0.208). CONCLUSIONS: We conclude that the plasma levels of relaxin-2 in diabetes patients were lower than in controls, however, there are no difference in plasma relaxin-3 concentrations between controls and patients with diabetes. Relaxin-2 or relaxin-3 levels are not related to component traits in patients with diabetes.