春季连阴雨对江苏省夏收作物产量的影响

分析了江苏省40年(1960～1999)春季连阴雨的发生概率、发展趋势及其时空分布规律。研究发现,春季连阴雨累计日数、总雨量与夏粮产量呈显著负相关关系,且累计日数≥30d时,夏粮减产非常明显,这种情况的发生概率达59．1％。     

降低地下矿深孔爆破落矿大块率的技术措施

降低深孔爆破落矿大块率是矿山凿岩中的一个重要课题。笔者对地下矿深孔爆破落矿中大块产生位置及原因进行分析;探讨在炸药单耗、孔网布置、装药结构、堵塞长度、微差间隔、起爆方式等方面对其产生影响的规律;提出地下矿深孔爆破落矿中通过优化爆破参数降低大块率的技术措施。该优化技术措施主要有:减少地质构造对深孔落矿的影响,合理确定炸药单耗的方法,使用大孔距小抵抗线落矿技术,采用多种装药结构技术,采用多排微差起爆技术,加强深孔的施工管理和加强爆破施工的现场管理。这些措施在工程实践中获得了良好的应用效果。     

WATER QUALITY FROM TWO SMALL FORESTED WATERSHEDS IN SOUTHERN ILLINOIS1

Two intermittent streams on oak-hickory watersheds in southern Illinois were gaged with a V-notched weir and sampled with an automatic water sampler. For three years data were collected on flow volume and water quality. Flow volumes show large variations between years and watersheds. Samples were analyzed for Na⁺, K⁺, Ca⁺⁺, Mg⁺⁺, P, and NO^-₃. Water quality was consistently high, although there were significant differences between watersheds. A baseline for water quality has been established for comparison after one of the watersheds is clearcut at a later date.     

HYDROLOGIC EFFECTS OF THE TONKAWA CREEK FLOOD ABATEMENT PROGRAM1

ABSTRACT: Floodwater-retarding impoundments, controlling 68 percent of the drainage area of Tonkawa Creek, a Washita River tributary in southwestern Oklahoma, have reduced the total flow volume about 36 percent over a 5-year period. Analyses showed the reduction occurred primarily in the less-than-2.5-cfs flow range, indicating the base flow regime has been altered. However, channelizing the downstream, mild-sloped, 3.6 miles of Tonkawa Creek that flows across a Washita River terrace increased the flow volume fourfold at the outlet. A double-masscurve analysis of water yield from a 1,127-square-mile Washita basin segment versus an untreated tributary showed the yield has not changed after 25 percent of the tributary area had been treated. Therefore, the flow reduction caused by structures is being offset by increased yields from channelization.     

Thimerosal in childhood vaccines contributes to accumulating mercury toxicity in the kidney

Mercury (Hg) is a hazardous chemical that accumulates in many cells and tissues, thereby producing toxicity. The kidney is a key target organ for Hg accumulation and toxicity. The contributing factors to Hg accumulation in humans include: (1) elemental and inorganic Hg exposure, often occurring by inhalation of Hg vapors; (2) exposure to methyl Hg (meHg), for example, through contaminated seafood; and (3) exposure to ethyl mercury (etHg) via thimerosal-containing vaccines. Systematic investigations on the toxic effects of etHg/thimerosal on the nervous system were carried out, and etHg/thimerosal emerged as a possible risk factor for autism and other neurodevelopmental disorders. There is, however, little known about the mechanisms and molecular interactions underlying toxicity of etHg/thimerosal in the kidney, which is the focus of the current review. Susceptible populations such as infants, pregnant women, and the elderly are exposed to etHg through thimerosal-containing vaccines, and in-depth study of the potential adverse effects on the kidney is needed. In general, toxicity occurring in association with different forms of Hg is related to: intracellular thiol metabolism and oxidative stress reactions; mitochondrial function; intracellular distribution and build-up of calcium; apoptosis; expression of stress proteins; and also interaction with the cytoskeleton. Available evidence for the etHg-induced toxicity in the kidney was examined, and the main mechanisms and molecular interactions of cytotoxicity of etHg/thimerosal exposure in kidney described. Such accumulating knowledge may help to indicate molecular pathways that, if modulated, may better handle Hg-mediated toxicity.     

Managing forest ecosystem services for hydropower production

In many countries, hydropower development is rapidly becoming a focus of green growth policies. This represents a significant opportunity for ecosystem services-based land management that integrates environmental and development goals to benefit the hydropower sector and support economic growth. In this study, we present an approach for targeting ecosystem-provision investment in hydropower catchments coupled with hydrologic modeling to quantify the benefits of soil and water conservation activities. We demonstrate the application of this approach in five hydropower facility catchments in the state of Himachal Pradesh, India. The results show that there is a high potential for targeted soil and water conservation to increase sediment retention services that benefit hydropower facilities (up to a 44% reduction in sediment transported from uplands into streams), although this benefit is distributed non-uniformly across catchments and levels of investment. The extent to which services can be improved is strongly driven by current land use and management practices that impact how and where conservation activities can be located. Iterative use of the method described here, in a process of stakeholder engagement and capacity-building, enables policy makers to determine the optimal mix of land management strategies and budget allocation to maximize service improvements that support hydropower production.     

A SUPERCRITICAL FLUME FOR MEASURING SEDIMENT-LADEN STREAMFLOW1

ABSTRACT: After 25 years of operation on ephemeral streams in the semiarid Southwest, this supercritical flume has provided more than 350 station-years of reliable streamflow data, even under freezethaw conditions experienced at elevations of 1,500 to 2,100 m, in Arizona. The flume has also provided streamflow data during flood periods produced by high intensity summer thunderstorm conditions, where considerable sediment and other debris was moved downstream.     

地表载荷对硬岩区埋地管道应力应变影响分析

为研究地表载荷对硬岩区埋地管道力学性能的影响,建立了管-土耦合三维数值模型,分析了地表载荷大小、作用面积、管道压力、管道径厚比及回填土弹性模量对管道应力分布、塑性应变、椭圆度的影响。结果表明:地表压载作用下,高应力区首先出现在管道顶部且呈椭圆形;随着地表载荷及其作用面积的增大,管道高应力区逐渐扩大,管道截面左右两侧也出现应力集中;随着回填土弹性模量、管道壁厚及内压的增加,管道顶部高应力区及最大等效应力均减小。塑性应变首先出现在管顶,且塑性区随地表载荷、载荷作用长度增加而增大,随回填土体弹性模量及管道壁厚增大而逐渐减小;当内压为0~4MPa时,管道塑性应变及塑性区随内压的增大而减小。管道椭圆度随回填土体弹性模量、管道内压、壁厚增加而逐渐减小,随地表压载增大而增大。     

前车突然切入时驾驶人应激生理特性研究

为研究前车突然切入对驾驶人生理负荷的影响,利用MP150生理监测系统对22名被试进行虚拟驾驶试验。采集记录前车突然切入时被试的生理参数。研究驾驶人心率增长率和心率变异性(HRV)指标与车速、应激距离之间的关系。结果表明:自车速度为100 km/h时,随着前车切入距离从55.6 m减小到27.8 m,被试的平均心率增长率从16.21%增大到23.27%,HRV参数低频(LF)值也呈现下降趋势。前车切入距离一定,随着自车车速从60 km/h增加到120 km/h,被试的平均心率增长率存在显著性差异,平均从13.05%上升到21.85%。差异性检验结果表明,前车切入距离和自车速度发生变化时驾驶人的生理负荷变化趋势一致,但自车速度因素对驾驶人生理负荷的影响程度高于切入距离因素。     

Involvement of mitochondrial-mediated caspase-3 activation and lysosomal labilization in acrylamide-induced liver toxicity

Acrylamide (ACR) is a chemical frequently used in both industrial and synthetic processes and may be produced during food processing. ACR at very high concentrations is postulated to exert its toxicity through the stimulation of an oxidative stress. ACR in excessive doses induces the central nervous system, reproduction, and genetic toxicity. However, ACR effects on the liver, a major organ of drug metabolism, have not been adequately explored. In addition, the role of mitochondria in an ACR-mediated hepatotoxicity is still unclear. The aim of this study was to investigate the cytotoxic mechanisms attributed to ACR using isolated rat hepatocytes. Hepatocytes were isolated by the collagenase perfusion method and incubated with an EC50_2hr concentration of ACR for 3 hr. The EC50_{2 hr} of ACR on isolated rat hepatocytes was determined to be 1 mM. Based on our results, hepatocytes cytotoxicity of ACR (1 mM) was mediated by a reactive oxygen species formation and lipid peroxidation. Incubation of hepatocytes with ACR produced rapid hepatocyte glutathione depletion which is another marker of the cellular oxidative stress. ACR cytotoxicity was also associated with mitochondrial injury as evidenced by the decline of mitochondrial membrane potential and lysosomal membrane leakiness. Our results also showed that ACR induced caspase-3 activation, the final mediator of apoptosis signaling. These findings contribute to a better understanding underlying mechanisms involved in ACR hepatotoxicity originating from the oxidative stress and ending in mitochondrial/lysosomal damage and cell death signaling.