Risk Assessment for a Flood Control Engineering System Using Fuzzy Theory: A Case in China

Flood control engineering system risk assessment entails fuzziness. An assessment model is developed, based on the improved fuzzy comprehensive assessment method that developed a new index (S_fin ) to judge the assessment class. The model is used to assess the flood control engineering risk of a case in China. The results show that the proposed model in the present article can rationally determine the risk status of a flood control engineering system, and has higher resolution compared to the two conventional methods, fuzzy comprehensive assessment and matter-element model method. The proposed model is flexible and adaptable for determining flood control engineering system risk status.     

Umbilical cord-derived mesenchymal stromal/stem cells expressing IL-24 induce apoptosis in gliomas

Although much progress has been made in the treatment of gliomas, the prognosis for patients with gliomas is still very poor. Stem cell-based therapies may be promising options for glioma treatment. Recently, many studies have reported that umbilical cord-derived mesenchymal stromal/stem cells (UC-MSCs) are ideal gene vehicles for tumor gene therapy. Interleukin 24 (IL-24) is a pleiotropic immunoregulatory cytokine that has an apoptotic effect on many kinds of tumor cells and can inhibit the growth of tumors specifically without damaging normal cells. In this study, we investigated UC-MSCs as a vehicle for the targeted delivery of IL-24 to tumor sites. UC-MSCs were transduced with lentiviral vectors carrying green fluorescent protein (GFP) or IL-24 complementary DNA. The results indicated that UC-MSCs could selectively migrate to glioma cells in vitro and in vivo. Injection of IL-24-UC-MSCs significantly suppressed tumor growth of glioma xenografts. The restrictive efficacy of IL-24-UC-MSCs was associated with the inhibition of proliferation as well as the induction of apoptosis in tumor cells. These findings indicate that UC-MSC-based IL-24 gene therapy may be able to suppress the growth of glioma xenografts, thereby suggesting possible future therapeutic use in the treatment of gliomas.     

Protective role of protein kinase C epsilon activation in ischemia-reperfusion arrhythmia

PURPOSE: Ischemic heart disease carries an increased risk of malignant ventricular tachycardia (VT), fibrillation (VF), and sudden cardiac death. Protein kinase C (PKC) epsilon activation has been shown to improve the hemodynamics in hearts subjected to ischemia/reperfusion. However, very little is known about the role of epsilon PKC in reperfusion arrhythmias. Here we show that epsilon PKC activation is anti-arrhythmic and its inhibition is pro-arrhythmic. METHOD: Langendorff-perfused isolated hearts from epsilonPKC agonist (epsilonPKC activation), antagonist (epsilonPKC inhibition) transgenic (TG), and wild-type control mice were subjected to 30 min stabilization period, 10 min global ischemia, and 30 min reperfusion. Action potentials (APs) and calcium transients (CaiT) were recorded simultaneously at 37 degrees C using optical mapping techniques. The incidence of VT and VF was assessed during reperfusion. RESULTS: No VT/VF was seen in any group during the stabilization period in which hearts were perfused with Tyrode's solution. Upon reperfusion, 3 out of the 16 (19%) wild-type mice developed VT but no VF. In epsilonPKC antagonist group, in which epsilonPKC activity was downregulated, 10 out of 13 (76.9%) TG mice developed VT, of which six (46.2%) degenerated into sustained VF upon reperfusion. Interestingly, in epsilonPKC agonist mice, in which the activity of epsilonPKC was upregulated, no VF was observed and only 1 out of 12 mice showed only transient VT during reperfusion. During ischemia and reperfusion, CaiT decay was exceedingly slower in the antagonist mice compared to the other two groups. CONCLUSION: Moderate in vivo activation of epsilonPKC exerts beneficial antiarrhythmic effect vis-a-vis the lethal reperfusion arrhythmias. Abnormal CaiT decay may, in part, contribute to the high incidence of reperfusion arrhythmias in the antagonist mice. These findings have important implications for the development of PKC isozyme targeted therapeutics and subsequently for the treatment of ischemic heart diseases.     

Beta- and alpha-adrenergic cross-signaling for L-type Ca current is impaired in transgenic mice with constitutive activation of epsilonPKC

It is well established that beta-adrenoceptor stimulation activates PKA and alpha(1)-adrenoceptor stimulation activates PKC. In normal ventricular myocytes, acute activation of alpha(1)-adrenoceptors inhibits beta-adrenoceptor stimulated L-type Ca current (I(Ca-L)) and direct activation of epsilonPKC leads to I(Ca-L) inhibition. Because increased PKC activity has been observed chronically in in vivo setting such as failing human heart, we hypothesized that chronic in vivo activation of epsilonPKC alters I(Ca-L) and its response to adrenergic stimulation. Therefore, we investigated the interaction between beta- and alpha(1)-adrenoceptors vis-à-vis I(Ca-L) in myocytes from transgenic mice (TG) with cardiac specific constitutive activation of epsilonPKC (epsilonPKC agonist). Whole-cell I(Ca-L) was recorded from epsilonPKC agonist TG mice and age-matched non-TG (NTG) littermates under: (1) basal condition, (2) beta-adrenoceptor agonist, isoproterenol (ISO), and (3) ISO plus alpha(1)-adrenoceptor agonist, methoxamine. The present results are the first to demonstrate that chronic in vivo activation of epsilonPKC leads to reduced basal I(Ca-L) density. beta-adrenoceptor activation of I(Ca-L) is blunted in epsilonPKC agonist TG mice. alpha-adrenoceptor cross-talk with beta-adrenoceptor signaling pathways vis-à-vis L-type Ca channels is impaired in epsilonPKC agonist TG mice. The diminished response to ISO and methoxamine suggests a protective feedback regulatory mechanism in epsilonPKC agonist TG mice and could be vital in the settings of excessive release of catecholamines during heart failure.     

黄龙山森林植被地上碳储量时空变化及驱动力

快速准确地估计植被地上碳储量及其动态变化,对评估森林固碳能力具有重要意义。以陕西省黄龙林区森林为研究对象,基于样地实测和卫星遥感数据,建立黄龙山林区植被地上碳储量模型,实现研究区2000-2021年长时间序列的森林植被地上碳储量的反演及时空分异研究。结果表明：（1）黄龙山森林植被地上碳储量平均值总体呈波动上升趋势,碳储量高于全省平均水平。（2）研究区东部、南部、中部及西北部是植被地上碳储量高值分布地区,且呈增加趋势;而东北部、西部和西南部植被地上碳储量较低,且呈减少趋势,研究区22年间森林植被地上部分固碳量增加,生产力提升。（3）年均温、年蒸散发量、年降水量和海拔是2000-2021年影响研究区森林植被地上碳储量空间分异主要因素;任意两个因子间的交互作用对黄龙山森林地上碳储量影响都大于单个因子,表明黄龙山森林植被地上碳储量在不同时间的空间分布受多种因素共同作用。年降水量对其空间分布影响逐渐减小,森林稳定性提高。研究在信息有限的基础上提出了快速估算地区植被地上碳储量的方法,了解了地区森林植被地上碳储量时空分异情况及其驱动因素,为掌握地区植被地上碳储量信息、评估森林固碳能力提供了重要依据。     

Hemicellulose modification promotes cadmium hyperaccumulation by decreasing its retention on roots in Sedum alfredii

Plant and Soil - Plant growth in the Arctic is often nutrient limited due to temperature constraints on decomposition and low atmospheric input of nitrogen (N). Local hotspots of nutrient...     

黄土高原区主导生态风险识别及分异性研究——以黄河流域中游为例

黄河流域作为典型的生态脆弱区,其生态问题复杂多样,亟待全面的生态治理和修复。同时,黄河流域生态保护和高质量发展是当前我国发展战略之一。明确黄河流域存在的生态问题,做好区域生态修复,开展综合治理是黄河流域可持续发展的重点。因此把握黄河流域的自然条件的区域差异,开展综合性的生态风险识别与评价,明确区域风险空间异质性分布与特点,是服务于区域生态修复、促进黄河流域高质量发展的重点。结合黄河流域中游气候、地形、植被等多自然本底情况识别风险源,建立服务于研究区生态保护和修复的区域生态风险评价体系,并通过GEE和GIS平台,可视化和量化了各类生态风险,并采用空间相关分析明确了生态风险的主要成因。结果表明：1）研究区的生态风险空间分布具有显著的区域特征,各个要素的生态风险呈现明显的东南和西北的差异、不同土地覆被情况的差异、人类活动带与非人类活动带的差异以及河流沿河与非沿岸的差异;2）植被净生态系统生产力呈现东南高西北低的特征,温度植被干旱指数显示西北部、山西、陕西南部存在较高的干旱风险,土壤侵蚀风险主要存在于黄河沿岸、其他河谷地带以及西北部,防风固沙服务能力在山西省山区以及植被生长较好的地区较高;3）综合生态风险评价显示宁夏以及陕西北部多数地区属于高风险区,低风险区主要分布在研究区西南部以及山西省西部沿线地区;4）双变量的Moran''s I指数显示地表温度、植被覆盖和汛期降水是导致综合生态风险西北和东南差异的主要原因,坡度是导致局部风险差异的主要原因。     

Hydrogen sulfide attenuates homocysteine-induced osteoblast dysfunction by inhibiting mitochondrial toxicity

Homocysteine (Hcy) is detrimental to bone health in a mouse model of diet-induced hyperhomocysteinemia (HHcy). However, little is known about Hcy-mediated osteoblast dysfunction via mitochondrial oxidative damage. Hydrogen sulfide (H₂S) has potent antioxidant, anti-inflammatory, and antiapoptotic effects. In this study, we hypothesized that the H₂S mediated recovery of osteoblast dysfunction by maintaining mitochondrial biogenesis in Hcy-treated osteoblast cultures in vitro. MC3T3-E1 osteoblastic cells were exposed to Hcy treatment in the presence or absence of an H₂S donor (NaHS). Cell viability, osteogenic differentiation, reactive oxygen species (ROS) production were determined. Mitochondrial DNA copy number, adenosine triphosphate (ATP) production, and oxygen consumption were also measured. Our results demonstrated that administration of Hcy increases the intracellular Hcy level and decreases intracellular H₂S level and expression of the cystathionine β-synthase/Cystathionine γ-lyase system, thereby inhibiting osteogenic differentiation. Pretreatment with NaHS attenuated Hcy-induced mitochondrial toxicity (production of total ROS and mito-ROS, ratio of mitochondrial fission (DRP-1)/fusion (Mfn-2)) and restored ATP production and mitochondrial DNA copy numbers as well as oxygen consumption in the osteoblast as compared with the control, indicating its protective effects against Hcy-induced mitochondrial toxicity. In addition, NaHS also decreased the release of cytochrome c from the mitochondria to the cytosol, which induces cell apoptosis. Finally, flow cytometry confirmed that NaHS can rescue cells from apoptosis induced by Hcy. Our studies strongly suggest that NaHS has beneficial effects on mitochondrial toxicity, and could be developed as a potential therapeutic agent against HHcy-induced mitochondrial dysfunction in cultured osteoblasts in vitro.