Inequality characteristics and influencing factors of CO2 emissions per capita in Jiangsu Province, China.

Analyzing the inequality characteristics and influencing factors of CO2 emissions per capita (CEPC) is conducive to balancing regional development and CO2 emissions reduction. This study applied the Gini coefficient and Theil index to investigate the CEPC inequalities during 2005-2017 at the county level in Jiangsu Province, China. Considering the spatial spillover and interaction effects, the factors influencing CEPC were analyzed by a hierarchical spatial autoregressive model. The results showed that the inequalities in CEPC first increased and then decreased at the inter-regional, and inter-county levels. The spatial pattern of CEPC was stable, and there was a significantly positive spatial autocorrelation of CEPC at the county level. The High-High type counties were mainly located in Sunan (southern Jiangsu). The spatial interaction effects of the CEPC between the prefecture and county levels indicated that governments at the prefecture level should integrate their county governments to reduce the CEPC. Moreover, carbon intensity, GDP per capita, land urbanization, and industrial structure play an important role in reducing CEPC. Our findings provide a scientific basis for formulating reasonable and effective carbon emission reduction policies.

Diagnostic performance of a novel automated CT-derived FFR technology in detecting hemodynamically significant coronary artery stenoses: A multicenter trial in China.

BACKGROUND AND AIMS: Computed tomography-derived fractional flow reserve (CT-derived FFR) algorithms have emerged as promising noninvasive methods for identifying hemodynamically significant coronary artery disease (CAD). However, its broad adaption is limited by the complex workflow, slow processing, and supercomputer requirement. Therefore, CT-derived FFR solutions capable of producing fast and accurate results could help deliver time-sensitive results rapidly and potentially alter patient management. The current study aimed to determine the diagnostic performance of a novel CT-derived FFR algorithm, esFFR, on patients with CAD was evaluated. METHODS: 329 patients from 6 medical centers in China were included in this prospective study. CT-derived FFR calculations were performed on 350 vessels using the esFFR algorithm using patients' presenting coronary computed tomography angiography (CCTA) images, and results and processing speed were recorded. Using invasive FFR measurements from direct coronary angiography as the reference standard, the diagnostic performance of esFFR and CCTA in detecting hemodynamically significant lesions were compared. Post-hoc analyses were performed for patients with calcified lesions or stenoses within the CT-derived FFR diagnostic "gray zone." RESULTS: The esFFR values correlated well with invasive FFR. The sensitivity, specificity, accuracy, positive and negative predictive value for esFFR were all above 90%. The overall performance of esFFR was superior to CCTA. Coronary calcification had minimal effects on esFFR's diagnostic performance. It also maintained 85% of diagnostic accuracy for "gray zone" lesions, which historically was <50%. The average esFFR processing speed was 4.6 ± 1.3 minutes. CONCLUSIONS: The current study demonstrated esFFR had high diagnostic efficacy and fast processing speed in identifying hemodynamically significant CAD.

Assessing the Association Between Lead Pollution and Risk of Alzheimer's Disease by Integrating Multigenomics.

Alzheimer's disease (AD) is a life-threatening neurodegenerative disease of the elderly. In recent observations, exposure to heavy metals environmental may increase the risk of AD. However, there are few studies on the causal relationship between heavy metal exposure and AD. In this study, we integrated two large-scale summaries of AD genome-wide association study (GWAS) datasets and a blood lead level GWAS dataset and performed the two-sample Mendelian randomization analysis to assess the causality of blood lead level and AD risk. The results showed that there is a significantly positive causality between blood lead level and AD risk both in the inverse-variance weighted (IVW) model and the weighted median estimator (WME) model. An independent additional verification also reached a consistent conclusion. These findings further confirm the conclusions of previous studies and improve the understanding of the relationship between AD pathogenesis and the toxicity of lead in environmental pollution.

Dictyophora Polysaccharide Attenuates As-Mediated PINK1/Parkin Pathway-Induced Mitophagy in L-02 Cell through Scavenging ROS.

Arsenic (As) is common in the human living environment and a certain amount of exposure to As can lead to liver damage; this toxic effect has been proved to be closely related to intracellular PINK1/Parkin pathway-mediated mitophagy. Dictyophora is an edible fungus that extracts polysaccharides with antioxidant and hepatoprotective effects. In the present study, we demonstrated that As induced the onset of mitophagy in hepatocytes by stimulating cellular production of ROS to activate PINK1/Parkin, and the extent of damage increased with increased As-induced toxicity. Dictyophora polysaccharide (DIP) has the ability to scavenge intracellular ROS, which can inhibit oxidative stress injury and inhibit the PINK/Parkin pathway through its receptors or efficacious proteins, thus preventing mitochondrial autophagy and alleviating the hepatotoxicity of As. In conclusion, our results indicate that DIP can reduce As-induced PINK1/Parkin pathway-mediated hepatic mitophagy through scavenging ROS and exert hepatoprotective effects, providing experimental data and theoretical basis for the development of medicinal value of Dictyophora as a dual-use food and medicinal fungus.

Effect of PINK1 and Parkin gene silencing on sodium arsenite-induced mitophagy in normal rat liver cells (BRL-3A).

NaAsO2-induced liver damage leads to autophagy, which plays an important role in cell quality control. Mitophagy plays an important role in hepatocyte damage, and PINK1 and Parkin constitute an important pathway in mitophagy. PINK1 selectively degrades abnormal mitochondria, and Parkin can recognize damaged mitochondria. However, the mechanism underlying the involvement of PINK1/Parkin in NaAsO2-induced mitophagy is unclear. Transfection plasmids containing dsRNA were used to interfere with the expression of Parkin in the following groups: the empty plasmid group was established by add the empty plasmid only, the PINK1-knockdown (KD) group was established by adding 5 µg of PINK1 dsRNA and then by adding 10 mM NaAsO2, and the Parkin-KD group was established by adding 5 µg of Parkin dsRNA and then by adding 10 mM NaAsO2. The expression of PINK1 and Parkin in autophagy was detected by western blotting and immunofluorescence staining. The ultrastructures of autophagosomes and mitochondria were observed by transmission electron microscopy. The successful KD of PINK1 and Parkin aggravated the NaAsO2-induced damage to mitophagy. The degeneration of mitochondrial vacuoles and the appearance of autophagosomes were detected in the NaAsO2, NaAsO2 + PINK1-KD and NaAsO2 + Parkin-KD groups. NaAsO2 can induce mitophagy in rat hepatocytes, and the silencing of PINK1 and Parkin can aggravate mitochondrial damage during this process. This study explored the mechanism of NaAsO2-induced mitophagy in BRL-3A cells after PINK1 and Parkin gene silencing.

Protective Effect of Dictyophora Polysaccharides on Sodium Arsenite-Induced Hepatotoxicity: A Proteomics Study.

The purpose of this study is to understand the mechanism of sodium arsenite (NaAsO2)-induced apoptosis of L-02 human hepatic cells, and how Dictyophora polysaccharide (DIP) protects L-02 cells from arsenic-induced apoptosis. The results revealed that DIP pretreatment inhibited NaAsO2 induced L-02 cells apoptosis by increasing anti-apoptotic Bcl-2 expression and decreasing pro-apoptotic Bax expression. Proteomic analysis showed that arsenic treatment disrupted the expression of metabolism and apoptosis associated proteins, including ribosomal proteins (RPs). After pretreatment with DIP, the expression levels of these proteins were reversed or restored. For the first time, it was observed that the significant decrease of cytoplasmic RPs and the increase of mitochondrial RPs were related to human normal cell apoptosis induced by arsenic. This is also the first report that the protective effect of DIP on cells was related to RPs. The results highlight the relationship between RPs and apoptosis, as well as the relationship between RPs and DIP attenuating arsenic-induced apoptosis.

The effects of cages implantation on surgical and adjacent segmental intervertebral foramina.

OBJECTION: The overarching goal of our research was to compare the clinical and radiological outcomes with different sizes of cages implantation in anterior cervical discectomy and fusion (ACDF), and to evaluate the effects on surgical and adjacent segmental intervertebral foramina. METHODS: The clinical data of 61 patients were analyzed retrospectively. The radiological data included the surgical intervertebral disk space height before (H0) and after surgery (H), the preoperative mean height of adjacent segments (Hm), the area and height of the surgical and adjacent segment foramen, the surgical segmental Cobb angle (α1), and C2-7Cobb angle (α2). The calculation of clinical data was conducted by Japanese Orthopaedic Association Scores (JOA), the recovery rate of JOA scores and visual analog scales (VAS). In accordance with the different ranges of distraction (H/Hm), patients were classified into three groups: group A (H/Hm<1.20, n=13), group B (1.20≤H/Hm≤1.80, n=37), and group C (H/Hm>1.80, n=11). RESULTS: After the operation and at the final follow-up, our data has demonstrated that the area and height of surgical segmental foramen all increased by comparing those of preoperation in three groups (all P<0.05). However, except for a decrease in group C (all P<0.05), the adjacent segmental foramina showed no significant changes (all P>0.05). The area and height of the surgical segment foramen and the distraction degree were positively correlated (0

Relationship between p38 signaling pathway and arsenic-induced apoptosis: a meta-analysis.

Arsenic exposure could induce apoptosis and cause related cancer. It was reported that p38 signaling pathway played a key transcriptional regulatory factor in arsenic-induced apoptosis. However, there were certain disputable questions about this point of opinion. Therefore, the relationship between p38 signaling pathway and arsenic-induced apoptosis was systematically reviewed and analyzed by meta-analysis. Twelve essays were analyzed with StataSE15.0 and Review Manager 5.3. The regulatory variables, such as normal cells and cancer cells, arsenic exposure time and exposure dose were analyzed by the subgroup analysis. The comprehensive effects were compared and analyzed by SMD method. Publication bias, the monolithic impact and heterogeneity were inspected. Subgroup analysis showed, when arsenic exposure was ≥ 5 µmol/l, the expression of Bcl-2 and Bax was down-regulated and the expression of p38 and Caspase-3 was up-regulated. When arsenic exposure was < 5 µmol/l, the expression of Bcl-2, Bax, p38 and Caspase-3 was up-regulated. Arsenic exposure time (≥ 48 h) or arsenic exposure dose (≥ 5 µmol/l or < 5 µmol/l) can promote the expression of p38. Arsenic exposure time was ≥ 48 h or exposure dose was < 5 µmol/l in cancer cells, arsenic exposure dose was ≥ 5 µmol/l or exposure time was < 48 h in normal cells, and they are statistically significant in the expression of p38. This study evaluates the role of p38 signaling pathway in arsenic-induced apoptosis, which is helpful to provide theoretical basis for the differentiation of arsenic-induced injury and the therapeutic mechanism of arsenic-induced apoptosis.

PINK1/Parkin-mediated mitophagy is involved in NaAsO2-induced apoptosis of human hepatic cells through activation of ERK signaling.

Mitochondrial dysfunction has been demonstrated as one key event in arsenic-induced hepatic cell damage though the exact molecular target remains unknown. Here we examined NaAsO2-induced mitochondrial damage in the L-02 cell led to mitochondrial depolarization and cytochrome c release, mitophagy, apoptosis in a dose response manner. Mitophagy was measured by analysis of PINK1, Parkin, LC3-II and p62 protein. Apoptosis was assessed by measuring Annexin V. Using the mitophagy inhibitor cyclosporine A (CsA) or ERK inhibitor (PD98059), the balance between mitophagy and apoptosis were further explored. When CsA was used prior to cell exposure to NaAsO2, it was found that the levels of mitophagy were decreased as expected and apoptosis was increased in response. CsA alone had no effect on the apoptosis rate. When the ERK signaling inhibitor PD98059 was used, there was a similar result that mitophagy was reduced though in contrast with CsA the apoptosis rate was also decreased compared with NaAsO2 alone. This result, along with the increased levels of ERK measured here in response to NaAsO2, indicates that ERK activation is a second key molecular response to NaAsO2 through the activation of both apoptosis and mitophagy. Thus the results with CsA indicate that the likely key biological event in NaAsO2 toxicity is at the level of the mitochondria leading to cytochrome c release and apoptosis. Mitophagy is increased in response to a secondary effect of NaAsO2 on ERK signaling that activates both mitophagy and apoptosis. The activation of mitophagy allows the cell to avoid some apoptosis. When ERK signaling is inhibited by PD98059 both the levels of apoptosis and mitophagy are decreased compared with the response produced by NaAsO2 alone in comparison to the inhibition of mitophagy by CsA that reduced mitophagy but dramatically increased apoptosis in response.

Lycium barbarum polysaccharide alleviates oxygen glucose deprivation-induced PC-12 cells damage by up-regulating miR-24.

Objective: This research was aimed to detect the functions of Lycium barbarum polysaccharides (LBPs) on oxygen and glucose deprivation (OGD) injury and potential mechanisms at PC-12 cells. Methods: CCK-8, flow cytometry and reactive oxygen species (ROS) assays were used to detect OGD, LBPs and miR-24 effects on cell viability, apoptosis, and oxidative stress. MiR-24 was transfected and texted by transfection and qRT-PCR. Moreover, the related-protein levels of apoptosis, autophagy and pathways were tested by Western blotting. Results: LBPs significantly enhanced cell viability , inhibited cell apoptosis, autophagy and ROS level in OGD injury. In addition, miR-24 expression was declined in OGD-treated cells, while it was elevated when added LBPs. The preventive effects of LBPs on PC-12 cell damage induced by OGD were reversed by down-regulating miR-24. Furthermore, miR-24 inhibitor declined LBPs-induced change in Wnt/ß-catenin and JAK1/STAT3 pathways in OGD-injuried cells. Conclusions: LBPs exhibited preventive effects via up-regulating miR-122 and activating Wnt/ß-catenin and JAK1/STAT3 pathways in OGD-induced PC-12 cells.

Down-regulation of RAC2 by small interfering RNA restrains the progression of osteosarcoma by suppressing the Wnt signaling pathway.

Osteosarcoma (OS) is the most common primary malignancy of bone and is characterized by a high malignant and metastatic potential. Microarray-based differentially expressed gene screening determined RAC2 as the candidate gene related to OS. Highly expressed RAC2 and activated Wnt signaling pathway were determined in OS tissues using reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot analysis. The OS cells were transfected with siRNA-RAC2 or treated with BIO (activator of Wnt pathway), whereby the effects of siRNA-RAC2 on cell proliferation, invasion, cycle and apoptosis were analyzed by CCK-8, Transwell assay and flow cytometry. The mRNA and protein levels of RAC2 and the Wnt signaling pathway-, proliferation- and apoptosis-related genes in OS cells were determined by RT-qPCR and Western blot assay. Importantly, siRNA-mediated RAC2 silencing inhibited the activation of the Wnt signaling pathway in OS. siRNA-RAC2 inhibited the proliferation and invasion, while impeded OS cell cycle progression and facilitated cell apoptosis. However, activation of Wnt signaling pathway reversed the effects of siRNA-RAC2. Finally, orthotopic xenograft OS mouse model confirmed the in vivo anti-tumor effects by silencing RAC2. Taken together, RAC2 gene silencing could suppress OS progression. The mechanism was obtained by inhibiting the activation of the Wnt signaling pathway.

MicroRNA-200c promotes osteogenic differentiation of human bone mesenchymal stem cells through activating the AKT/ß-Catenin signaling pathway via downregulating Myd88.

During the human bone formation, the event of osteogenic differentiation of human bone mesenchymal stem cells (hBMSCs) is vital, and recent evidence has emphasized the important role of microRNAs (miRNAs) in osteogenic differentiation of hBMSCs. This study aims to examine the potential effects of miR-200c in osteogenic differentiation of hBMSCs and understand their underlying mechanisms. HBMSCs were obtained via human bone marrow. During osteogenic induction and differentiation, cells were transfected with different plasmids with the intention of investigating the roles of miR-200c on osteogenic differentiation, calcium salt deposition, alkaline-phosphatase (ALP) activity, mineralized nodule formation, osteocalcin (OCN) content, and proliferation of osteoblasts. Following transfection, dual luciferase reporter gene assay was conducted so as to explore the correlation between miR-200c and Myd88. Moreover, the AKT/ß-Catenin signaling pathway was blocked with an AKT/ß-Catenin inhibitor, AKTi, to investigate its involvement. The hBMSCs were successfully isolated from human bone marrow. Myd88 was determined as a target gene of miR-200c. Gain and loss-of-function assays confirmed that overexpression of miR-200c, or silencing of Myd88 promoted osteogenic differentiation, increased calcium salt deposition, ALP activity, mineralized nodule formation, and enhanced the proliferation of osteoblasts following osteogenic differentiation of hBMSCs. Meanwhile, the downregulation of miR-200c has been shown to have the opposite effect. Furthermore, these findings showed that the miR-200c overexpression activated the AKT/ß-Catenin signaling pathway by targeting Myd88. To sum up, the miR-200c upregulation induces osteogenic differentiation of hBMSCs by activating the AKT/ß-Catenin signaling pathway via the inhibition of Myd88, providing a target for treatment of bone repair.

MicroRNA-377 exerts a potent suppressive role in osteosarcoma through the involvement of the histone acetyltransferase 1-mediated Wnt axis.

It has been demonstrated that microRNAs (miRNAs) may contribute to tumorigenesis and tumor growth in osteosarcoma (OS), which is a primary malignant tumor of bone frequently diagnosed in adolescents and young people. The purpose of our investigation was to evaluate the functional relevance of miR-377 in OS and to investigate whether the mechanism was related to the histone acetyltransferase 1 (HAT1)-mediated Wnt signaling pathway. By screening differentially expressed genes in microarray GSE47572, HAT1 was found to be a candidate gene of interest. Besides, the regulatory miRNA (miR-377) of HAT1 was also selected. The interaction among miR-377, HAT1, and the Wnt signaling pathway was evaluated. In addition, the miR-377 expression was altered in OS cells (U-2OS and SOSP-9607) to assess the in vitro cell apoptosis and the in vivo tumor growth. OS tissues presented elevated HAT1 expression and decreased miR-377 expression. A putative miR-377 binding site in HAT1 3'-UTR HAT1 was verified. Cells with miR-377 overexpression or HAT1 silencing were observed to exhibit reduced HAT1 expression and promoted apoptosis, accompanied by blockade of Wnt signaling. Moreover, the in vivo experiment revealed that miR-377 overexpression or HAT1 silencing inhibited tumor growth and reduced tumor size in nude mice. Taken together, our results conclude that miR-377 may promote OS cell apoptosis through inactivation of the HAT1-mediated Wnt signaling pathway, highlighting the potential therapeutic effect of miR-377 on OS treatment.

Extract of Spatholobus suberctus Dunn ameliorates ischemia-induced injury by targeting miR-494.

Cerebral stroke is a leading cause of death and permanent disability. The current therapeutic outcome of ischemic stroke (>85% of all strokes) is very poor, thus novel therapeutic drug is urgently needed. In vitro cell model of ischemia was established by oxygen-glucose deprivation (OGD) and in vivo animal model of ischemia was established by middle cerebral artery occlusion (MCAO). The effects of Spatholobus suberctus Dunn extract (SSCE) on OGD-induced cell injury, MCAO-induced neural injury and miR-494 level were all evaluated. The possible target genes were virtually screened utilizing bioinformatics and verified by luciferase assay. Subsequently, the effects of abnormally expressed miR-494 on OGD-induced cell injury and target gene expression were determined. Additionally, whether SSCE affected target gene expression through modulation of miR-494 was studied. Finally, the effects of aberrantly expressed Sox8 on OGD-induced injury and signaling pathways were estimated. SSCE reduced OGD-induced cell injury and ameliorated MCAO-induced neuronal injury, along with down-regulation of miR-494. Then, OGD-induced cell injury was increased by miR-494 overexpression but decreased by miR-494 silence. Sox8 was a target gene of miR-494, and SSCE could up-regulate Sox8 expression via down-regulating miR-494. Afterwards, OGD-induced cell injury was proved to be increased by Sox8 inhibition but reduced by Sox8 overexpression. Finally, OGD-induced inhibition of PI3K/AKT/mTOR and MAPK pathways was further inhibited by Sox8 silence but activated by Sox8 overexpression. SSCE ameliorates ischemia-induced injury both in vitro and in vivo by miR-494-mediated modulation of Sox8, involving activations of PI3K/AKT/mTOR and MAPK pathways.

Impact of mean platelet aggregation degree on long-term clinical outcomes among patients undergoing a complex percutaneous coronary intervention.

OBJECTIVE: The aim of this study was to evaluate the association between the mean platelet aggregation degree and long-term clinical outcomes in patients receiving a complex percutaneous coronary intervention (CPCI). PATIENTS AND METHODS: We screened 2141 patients after a percutaneous coronary intervention (PCI) treated with aspirin and clopidogrel. CPCI was defined as a procedure targeted to at least one of the following: left main disease, bifurcation lesion, ostial lesion, chronic total occlusion, and small-vessel stenting. ADP-induced platelet aggregation was serially measured by light transmission aggregometry at least three times after PCI and the mean value was calculated. The population was categorized on the basis of the mean ADP degree and the presence of CPCI. The primary endpoint measured was a major adverse cardiovascular and cerebral event (MACCE). RESULTS: A total of 1245 patients enrolled in the study were divided into four groups: group A (CPCI and ADP≥40%), group B (CPCI and ADP<40%), group C (non-CPCI and ADP≥40%), and group D (non-CPCI and ADP<40%). The median follow-up was 29.9 months. The Cox multivariate analysis suggested that group A was an independent risk factor for MACCE (hazard ratio: 2.70, 95% confidence interval: 1.25-5.81; P<0.001). Compared with group A, the remaining groups (groups B, C, and D) had a lower rate of MACCE. When group C was set as the reference, groups B and D had similar risks for primary endpoints. CONCLUSION: Patients undergoing CPCI with a high mean ADP degree are at a high risk for MACCE. Serial platelet function testing is therefore important in patients receiving CPCI.

Homocysteine and all-cause mortality in hypertensive adults without pre-existing cardiovascular conditions: Effect modification by MTHFR C677T polymorphism.

BACKGROUND: Previous studies support an association between elevated total homocysteine (tHcy) levels and increased all-cause mortality. However, few prospective studies have examined this association in hypertensive patients, and/or tested any effect modification by the methylene tetrahydrofolate reductase (MTHFR) C677T genotype. METHODS: This was a post hoc analysis of the China Stroke Primary Prevention Trial. Serum tHcy and folate were measured at baseline. Individual MTHFR C677T genotype (CC, CT, and TT) was determined. Evidence for death included death certificates or home visits. Cumulative hazards of all-cause mortality by tHcy quartiles were estimated using the Kaplan-Meier method, and group differences were compared by log-rank tests. Hazard ratios (HRs) and 95% confidence intervals were estimated by Cox proportional-hazard regression models, adjusting for age, sex, baseline folate, vitamin B12, blood pressure, body mass index, smoking and alcohol drinking status, study center, total cholesterol, triglycerides, high-density lipoprotein cholesterol, fasting glucose, creatinine, and treatment group. Potential effect modification by the MTHFR genotype on the relationship between tHcy and all-cause mortality was tested. RESULTS: The analyses included 20,424 hypertensive patients (41% males) without a history of myocardial infarction or stroke. Baseline mean age (SD) was 60 ±â€Š7.5 years and mean (SD) serum tHcy was 14.5 ±â€Š8.4 µmol/L. After a mean follow-up period of 4.5 years, there were 612 (3%) all-cause deaths. Kaplan-Meier survival curves revealed a graded relationship between tHcy quartiles and all-cause mortality. The HRs, using the lowest quartile as the reference, were 1.2, 1.2, and 1.5 in Q2, Q3, and Q4, respectively. A linear trend test, using natural log-transformed tHcy, resulted in an HR of 1.5 (95% confidence interval 1.2-1.9, P < .001) after adjustment for lifestyle and health-related variables. Whereas the MTHFR genotype alone had little effect on mortality, it significantly modified the tHcy-mortality association, which was much stronger in the CC/CT genotype than in the TT genotype (P for interaction < 0.05). CONCLUSIONS: Among Chinese hypertensive patients without cardiovascular comorbidities, elevated tHcy was a significant risk marker for death from all causes, and the association was subject to effect modification by MTHFR genotypes. If confirmed that tHcy and MTHFR genotypes may serve as useful biomarkers for mortality risk assessment and targeted intervention.

Circulating endothelial microparticles and miR-92a in acute myocardial infarction.

Microparticles (MPs) and miRNAs have been shown to play important roles in coronary artery disease (CAD) by monitoring endothelial dysfunction. The present study aims to investigate the diagnostic value of endothelial MPs (EMPs) and miRNAs (miR-92a or miR-23a) as biomarkers in distinguishing patients with acute myocardial infarction (AMI) from those with CAD. Plasma samples from 37 patients with AMI, 42 patients with stable CAD (SCAD), and 35 healthy adults were collected for investigation in the present study. The numbers of CD31+/CD42b- MPs, CD31+/CD42b+ MPs, and CD31-/CD42b- MPs were measured by flow cytometry and the levels of miR-92a and miR-23a were analyzed using reverse transcription-quantitative PCR. Moreover, cardiac troponin I (cTnI) expression was detected by ELISA to serve as a routine diagnostic parameter. The number of CD31+/CD42b- was higher in AMI group than those in SCAD and healthy groups. Besides, the expression of miR-92a was higher in AMI group compared with two other groups. Furthermore, evidence showed that there was a positive correlation between the levels of CD31+/CD42b- MPs and miR-92a Finally, the receiver operating characteristic (ROC) curve revealed that the area value under the curve of CD31+/CD42b- MPs, miR-92a and cTnI was 0.893, 0.888, and 0.912 respectively. CD31+/CD42b- MPs and miR-92a might have great potential to provide diagnostic value for AMI and could probably regulate the endothelial dysfunction in AMI patients.

Convergence of carbon intensity in the Yangtze River Delta, China.

As China's industrialization and urbanization have grown rapidly in recent years, China's CO2 emissions rose from 3405.1799 Mt to 10,249.4630 Mt from 2000 to 2013, and it has reached the highest levels in the word since 2006. Chinese government has emphasized the importance of reducing carbon emissions and set the target of reducing carbon intensity to 60-65% of 2005 levels by 2030. Investigating the convergence of carbon intensity can identify the convergence rate, which is helpful in guiding allocations of carbon intensity reduction. The Yangtze River Delta is one of the key carbon emission regions in China, with higher urbanization levels and larger carbon emissions; thus, we employed prefecture-level panel data derived from grid data between 2000 and 2010 to examine whether the convergence of carbon intensity exists across prefecture-level cities in the Yangtze River Delta. Spatial panel data models were utilized to investigate ß-convergence of carbon intensity. The results indicated that carbon intensity showed divergence during 2002-2004 and σ-convergence over other periods (2000-2002 and 2004-2010). Carbon intensity exhibited stochastic convergence, indicating that the shocks to carbon intensity relative to the average level of carbon intensity are only transitory. There was a spatial spillover effect and ß-convergence of carbon intensity, suggesting that prefecture-level cities with higher carbon intensity would decrease rapidly in the Yangtze River Delta. Our results highlight the importance of considering the present state of carbon intensity, spatial factors, and socioeconomic factors such as industrial structure and economic levels during allocation planning for reducing carbon intensity.

A Preliminary Study of the Carbon Emissions Reduction Effects of Land Use Control.

Land use change not only directly influences carbon storage in terrestrial ecosystems but can also cause energy-related carbon emissions. This study examined spatiotemporal land use change across Jiangsu Province, China; calculated vegetation carbon storage loss caused by land use change and energy-related carbon emissions; analysed the relationship among land use change, carbon emissions and social-economic development; and optimized land use structure to maximize carbon storage. Our study found that 13.61% of the province's land area underwent a change in type of land use between 1995 and 2010, mainly presented as built-up land expansion and cropland shrinkage, especially in southern Jiangsu. Land use change caused a 353.99 × 104 t loss of vegetation carbon storage loss. Energy-related carbon emissions increased 2.5 times from 1995 to 2013; the energy consumption structure has been improved to some extent while still relying on coal. The selected social-economic driving forces have strong relationships with carbon emissions and land use changes, while there are also other determinants driving land use change, such as land use policy. The optimized land use structure will slow the rate of decline in vegetation carbon storage compared with the period between 1995 and 2010 and will also reduce energy-related carbon emissions by 12%.