Conservation of Epiphyte Diversity in an Andean Landscape Transformed by Human Land Use

Abstract: Epiphytes are diverse and important elements of tropical forests, but as canopy‐dwelling organisms, they are highly vulnerable to deforestation. To assess the effect of deforestation on epiphyte diversity and the potential for epiphyte conservation in anthropogenically transformed habitats, we surveyed the epiphytic vegetation of an Ecuadorian cloud forest reserve and its surroundings. Our study was located on the western slopes of the Andes, a global center of biodiversity. We sampled vascular epiphytes of 110 study plots in a continuous primary forest; 14 primary forest fragments; isolated remnant trees in young, middle‐aged, and old pastures; and young and old secondary forests. It is the first study to include all relevant types of habitat transformation at a single study site and to compare epiphyte diversity at different temporal stages of fragmentation. Epiphyte diversity was highest in continuous primary forest, followed by forest fragments and isolated remnant trees, and lowest in young secondary forests. Spatial parameters of habitat transformation, such as fragment area, distance to the continuous primary forest, or distance to the forest edge from inside the forest, had no significant effect on epiphyte diversity. Hence, the influence of dispersal limitations appeared to be negligible or appeared to operate only over very short distances, whereas microclimatic edge effects acted only in the case of completely isolated trees, but not in larger forest fragments. Epiphyte diversity increased considerably with age of secondary forests, but species assemblages on isolated remnant trees were impoverished distinctly with time since isolation. Thus, isolated trees may serve for recolonization of secondary forests, but only for a relatively short time. We therefore suggest that the conservation of even small patches of primary forest within agricultural landscape matrices is essential for the long‐term maintenance of the high epiphyte diversity in tropical cloud forests.     

Investigation on the Degradation of Natural Heritage of Singing Sand Mountain and Crescent Moon Spring at Dunhuang City, China

The main purpose of this study is to put forward a reasonable idea of the general protection for Singing Sand Mountain and Crescent Moon Spring, a rare and unique desert wonder, and of sustainable tourism development based on the research on the ecological environment around. Methods of documentation, case study and comparison were employed. Finally, aiming at solving the problems of natural environment and those existing after the exploitation of Singing Sand Mountain and Crescent Moon Spring the author puts forward three measures： the comprehensive treatment for Crescent Moon Spring （broadening resources of water and reducing expenditures, checking the decreasing depth of Crescent Moon Spring, and improving the geographical environment）, the general protection envisions for Singing Sand Mountain and Crescent Moon Spring and establishing a dynamic monitoring and early-warning system of regional ecosystem.     

海冰与孤立桩柱碰撞破碎模型

本文对辽东湾冰原冰与孤立桩相互作用过程进行了研究，根据高速率下冰原冰的非开裂挤压脆性破坏过程特点，将整个冰与桩柱相互作用过程分为三个阶段，通过一些适当的简化和假设，提出了这三个不同阶段孤立桩前冰的破碎过程模型，利用此破碎过程模型结合相应的力学模式计算冰与桩柱相互作用力随时间的变化。实测资料与模拟计算值比较，其结果符合较好，因此该破碎过程模型具有较好的可实用性。     

生产厂区封闭化管理系统解决方案

简述了为加强对石化生产厂区进出作业人员、车辆的安全管理,确保安全生产和作业人员的生命安全而实施的生产厂区封闭化管理的系统解决方案.     

氯化汞、氯化甲基汞对大鼠肾近曲小管细胞损伤机理的研究

研究了HgCl_2和CH_3HgCl对大鼠游离肾近曲小管细胞的毒性作用及其机理.结果显示,HgCl_2和CH_3HgCl均对肾细胞有明显毒性,表现为细胞内乳酸脱氢酶(LDH)和溶酶体β-葡糖苷酸酶(β-GD)漏出增加,还原型谷胱甘肽(GSH)和蛋白巯基(PSH)含量降低,同时GSH和PSH含量的降低与LDH及β-GD漏出之间呈良好的相关关系.未观察到CH_3HgCl明显诱发肾细胞脂质过氧化作用,HgCl_2仅在50μmol/L以上才出现轻度脂质过氧化效应.     

孤岛工作面支承压力影响下顶板破坏机理研究

为了探讨孤岛工作面支承压力影响下顶板破坏机理,通过采用理论分析,建立薄板力学模型,对孤岛工作面顶板弯矩分布规律进行分析,并结合实验室数值模拟手段对工作面顶板支承压力集中系数及顶板围岩塑性区演变规律进行研究。研究结果表明:在支承压力作用下,随着推进距离的增大,顶板支承压力集中系数呈现增大的趋势;工作面顶板煤壁中部弯矩显著大于煤壁两侧弯矩,该结果合理解释了工作面方向上支架工作阻力不相等的规律;顶板断裂的塑性区演变特征存在时空效应及力学特征,顶板四周所形成的横向“O”型破断与横向“X”型破断,共同构成了顶板破断的横“O-X”破断形式。     

Detection, isolation, and identification of cadmium-resistant bacteria based on PCR-DGGE

This study focused on the screening of cadmium-resistant bacterial strains from Pb-Zn tailing. We investigated the diversity of microbial community inhabiting Dong-san-cha Pb-Zn tailing in Beijing, China, by polymerase chain reaction-denaturing gradient gel electrophoresis （DGGE） of 16S rRNA gene of bacterial strain, and found two dominant strains in the DGGE profile. Using special culture media, we isolated two strong cadmium-resistant bacterial strains. On the basis of morphological, physiological, and biochemical characteristics, BIOLOG, and 16S rDNA sequencing, the two strains were identified as Bacillus cereus and Enterobacter cloacae. Minimal inhibitory concentrations （MICs） of heavy metals for the bacteria were determined. E. cloacae showed higher MIC values for heavy metals and a larger range of antibiotic resistance than B. cereus.     

叠层橡胶支座串联隔震体系抗火性能研究

对叠层橡胶隔震支座在高温作用下的温度场进行数值模拟,利用小模型试件进行温度传导及温度场分布试验。在叠层橡胶隔震支座经历420℃的高温作用后,将隔震支座模型试件与钢筋混凝土柱串联,并对串联隔震体系的力学性能进行压剪往复试验。结果表明,叠层橡胶隔震支座在高温作用下的性能退化相当明显,承载状态下的橡胶隔震支座在稍高的温度作用下就开始发生畸变。这表明在实际工程中对叠层橡胶隔震支座采取防火保护措施对保证隔震结构承载力安全非常重要。     

Toxicity of depleted uranium on isolated liver mitochondria: a revised mechanistic vision for justification of clinical complication of depleted uranium (DU) on liver

Depleted uranium (DU) is widely used in military anti-armor weapons. Recent evidence suggested that oxidative stress and mitochondrial dysfunction may contribute to DU-induced toxicity. However, the underlying mechanisms of DU toxicity in mitochondria are not well understood. In this study, liver mitochondria were obtained from Wistar rats treated with DU in the form of uranyl acetate (UA) (0.5, 1 or 2 mg/kg i.p.) using differential centrifugation. For in vitro experiments, control rat liver mitochondria were incubated with different concentrations of UA (50, 100 or 200 μM) for 1 hr. Mitochondrial reactive oxygen species (ROS) production, collapse of mitochondrial membrane potential, and mitochondrial swelling were examined by flow cytometry. Mitochondrial sources of ROS formation were determined using specific substrates and inhibitors. Extent of lipid peroxidation (LPO) and glutathione (GSH) oxidation, and also complex II and IV activities were detected via spectroscopy. Further, the concentration of ATP and ATP/ADP ratio was measured using luciferase enzyme and release of cytochrome c from mitochondria which was detected by ELISA kit. UA induced succinate-supported mitochondrial ROS production, elevated LPO levels, GSH oxidation, and mitochondrial complex II inhibition. UA also induced mitochondrial permeability transition and increase in cytochrome c release which subsequently disturbed oxidative phosphorylation and reduced the mitochondrial ATP concentration. Data suggest that mitochondrial oxidative stress and uncoupling of oxidative phosphorylation may play key roles in DU-induced hepatic toxicity.     

Toxicity of cigarette smoke on isolated lung,heart, and brain mitochondria: induction of oxidative stress and cytochrome c release

Cigarette smoking is one of the main risk factors for premature human death which is associated with a variety of respiratory and vascular diseases, and cancer due to exposure to hundreds of toxicants. Rat mitochondria were obtained by differential ultracentrifugation and incubated with different concentrations (1%, 10%, or 100%) of standardized cigarette smoke extract (CSE). Our results showed that CSE induced a rise in mitochondrial reactive oxygen species (ROS) formation, lipid peroxidation, and mitochondrial membrane potential (MMP) collapse before mitochondrial swelling ensued in isolated pulmonary mitochondria. Disturbance in oxidative phosphorylation was also confirmed by decrease in ATP concentration in the CSE-treated mitochondria. In addition, collapse of MMP and mitochondrial swelling produced release of cytochrome c via outer membrane rupture or mitochondrial permeability transition (MPT) pore opening. Our results suggested that CSE-induced toxicity in lung tissue is the result of disruptive effect on mitochondrial respiratory chain that leads to ROS formation, lipid peroxidation, MMP decline, and cytochrome c expulsion which results in apoptosis signaling and cell loss.