基于建筑容量的城市建设用地碳汇量核算方法

城市建设中的矿物质材料开发利用活动不仅导致大量碳排放,也产生了碳吸收.以往建筑矿物质材料的碳吸收过程一直没有得到重视和科学量化.本研究采用遥感影像阴影高度反演技术,提取地块的建筑容量,识别建筑类型,以此为依据确定矿物材料用量及碳含量参数,采用热重分析法测定碳化率,基于以上步骤构建城市建筑碳汇量的核算方法,并选取沈阳市蒲河新来测试这一核算方法,同时进行不确定性分析.结果表明: 1996—2016年,沈阳市蒲河新城各类型建筑产生的碳汇总量依次为:居住建筑>公共服务建筑>其他类建筑>商业金融建筑>工业建筑;各类建筑用地的碳汇容积率依次为:商业金融建筑>居住建筑>公共服务建筑>其他类建筑>工业建筑.本研究构建的基于建筑容量提取的城市尺度的建筑碳汇量核算方法,可以快速准确地估算不同类型城市建设用地无机材料产生的碳汇量.在城市自然碳汇有限条件下,利用建筑碳汇增加城市碳汇量,能够为我国城市低碳发展提供新的思路.     

Effects of static magnetic fields on the physical and chemical properties of cell culture medium RPM1 1640

RPMI 1640 culture medium was chosen to simulate body fluids, and after exposure to 0.085 approximately 0.092 T static magnetic fields (SMF), surface tension, pH, dissolved oxygen, and UV-visible spectrum were measured. Compared with the control group in the normal geomagnetic field, the pH value increased about 0.14 units, dissolved oxygen increased about 14%, and the UV-visible spectra were different in peak intensity but without a shift in the peak. Surface tension showed no significant difference in the two groups. This data suggests that SMF can change some of the physical and chemical properties of RPM1 1640 solution, and may contribute to understanding biological effects of SMF.     

Retracted: Downregulated microRNA-224 aggravates vulnerable atherosclerotic plaques and vascular remodeling in acute coronary syndrome through activation of the TGF-β/Smad pathway

Recent studies have shown that circulating microRNAs (miRNA) play a critical role in diagnosing acute coronary syndrome (ACS). This study aims to investigate the effect of miR-224 on atherosclerotic plaques forming and vascular remodeling in ACS and its relationship with TGF-β/Smad pathway. Myocardial infarction (MI) rat model was established and lentivirus vector of miR-224 inhibitor was prepared for investigating the effect of downregulated miR-224 on the contents of nitric oxide (NO) and endothelin-1 (ET-1), blood lipid levels and inflammatory factor levels in serum as well as the TGF-β/Smad pathway. The rats suffering from MI had decreased survival rates and exhibited reduced levels of NO, high-density lipoprotein cholesterol, and lumen diameter, and Smad7 messenger RNA (mRNA) and protein expression; while had significantly increased ratio of heart weight or body weight, levels of ET-1, inflammatory factors, blood lipid indexes, vascular remodeling indexes, collagen volume fraction, vulnerable atherosclerotic plaque area, VCAM-1 and MMP-2 protein expression, TGF-β, Smad2, Smad3, and Smad4 mRNA and protein expression. After inhibiting the TGF-β/Smad pathway, the rats suffering from MI showed notably opposite trend. In conclusion, downregulation of miR-224 expression promotes the formation of vulnerable atherosclerotic plaques and vascular remodeling in ACS through activation of the TGF-β/Smad pathway. Therefore, this study provides a new therapeutic target for ACS.     

A varying‐coefficient generalized odds rate model with time‐varying exposure: An application to fitness and cardiovascular disease mortality

Varying‐coefficient models have become a common tool to determine whether and how the association between an exposure and an outcome changes over a continuous measure. These models are complicated when the exposure itself is time‐varying and subjected to measurement error. For example, it is well known that longitudinal physical fitness has an impact on cardiovascular disease (CVD) mortality. It is not known, however, how the effect of longitudinal physical fitness on CVD mortality varies with age. In this paper, we propose a varying‐coefficient generalized odds rate model that allows flexible estimation of age‐modified effects of longitudinal physical fitness on CVD mortality. In our model, the longitudinal physical fitness is measured with error and modeled using a mixed‐effects model, and its associated age‐varying coefficient function is represented by cubic B‐splines. An expectation‐maximization algorithm is developed to estimate the parameters in the joint models of longitudinal physical fitness and CVD mortality. A modified pseudoadaptive Gaussian‐Hermite quadrature method is adopted to compute the integrals with respect to random effects involved in the E‐step. The performance of the proposed method is evaluated through extensive simulation studies and is further illustrated with an application to cohort data from the Aerobic Center Longitudinal Study.     

Phloem Unloading Strategies and Mechanisms in Crop Fruits

Journal of Plant Growth Regulation - Carbohydrate produced by photosynthesis is loaded into phloem via collection phloem, translocated via the transport phloem, and unloaded by release phloem into...     

膝关节内干细胞/祖细胞在软骨再生中作用研究进展

关节软骨(AC)由于缺乏血管、神经和淋巴,一旦损伤无法自我修复.虽然以外源性细胞为基础的治疗策略在一定程度上能够再生关节软骨,但仍然存在手术间隔长、供体有限、细胞体外培养易去分化和病原体传播等风险.成人膝关节存在许多类型干细胞/祖细胞(SCPCs),当软骨损伤时,就会被动员,迁移到损伤部位,参与再生修复.因此,基于趋化...     

Periplocymarin alleviates pathological cardiac hypertrophy via inhibiting the JAK2/STAT3 signalling pathway

Pathological cardiac hypertrophy is the most important risk factor for developing chronic heart failure. Therefore, the discovery of novel agents for treating pathological cardiac hypertrophy remains urgent. In the present study, we examined the therapeutic effect and mechanism of periplocymarin (PM)‐mediated protection against pathological cardiac hypertrophy using angiotensinII (AngII)‐stimulated cardiac hypertrophy in H9c2 cells and transverse aortic constriction (TAC)‐induced cardiac hypertrophy in mice. In vitro, PM treatment significantly reduced the surface area of H9c2 cells and expressions of hypertrophy‐related proteins. Meanwhile, PM markedly down‐regulated AngII‐induced translocation of p‐STAT3 into the nuclei and enhanced the phosphorylation levels of JAK2 and STAT3 proteins. The STAT3 specific inhibitor S3I‐201 or siRNA‐mediated depleted expression could alleviate AngII‐induced cardiac hypertrophy in H9c2 cells following PM treatment; however, PM failed to reduce the expressions of hypertrophy‐related proteins and phosphorylated STAT3 in STAT3‐overexpressing cells, indicating that PM protected against AngII‐induced cardiac hypertrophy by modulating STAT3 signalling. In vivo, PM reversed TAC‐induced cardiac hypertrophy, as determined by down‐regulating ratios of heart weight to body weight (HW/BW), heart weight to tibial length (HW/TL) and expressions of hypertrophy‐related proteins accompanied by the inhibition of the JAK2/STAT3 pathway. These results revealed that PM could effectively protect the cardiac structure and function in experimental models of pathological cardiac hypertrophy by inhibiting the JAK2/STAT3 signalling pathway. PM is expected to be a potential lead compound of the novel agents for treating pathological cardiac hypertrophy.