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1.
采动影响下含瓦斯煤岩的损伤变形是一个极其复杂的非线性过程,单纯依靠传统经典弹塑性力学无法准确分析其破坏机理。针对此情况,通过试验研究了不同初始围压条件下含瓦斯煤岩的损伤变形特征,并分析了损伤变形与能量演化规律之间的内在联系。研究表明:初始围压越高,煤样破坏时强度越大,脆性破坏特征越明显,瓦斯流量急剧增加幅度越大,煤样破坏时积累的总能量和弹性应变能越多,且初始围压与弹性能之间满足对数函数关系。采用累积耗散能定义了煤岩损伤变量,并分析了不同阶段损伤与渗透率之间的演化关系。 相似文献
2.
AbstractThe roles of PM2.5-induced mitochondrial damage and oxidative stress on mast cell degranulation were examined in vitro. Mast cells were treated with suspensions of PM2.5 in Dulbecco’s modified Eagle’s medium at concentrations from 25 to 200?mg/L in the absence or presence of 10?mmol/L N-acetyl-L-cysteine. Biological effects and mitochondrial function were assessed by determining cell viability, β-hexosaminidase release, interleukin-4 secretion, reactive oxygen species generation, adenosine triphosphate production, potential alteration of mitochondrial membrane, and activities of mitochondrial electron transport chain complexes I and III. Exposure of mast cells to PM2.5 induced reduction of adenosine triphosphate production, collapse of mitochondrial membrane potential, and inhibition of the activity of complex III. Co-treatment of mast cells exposed to PM2.5 with N-acetyl-L-cysteine attenuated cytotoxicity and the production of reactive oxygen species, and decreased the release of β-hexosaminidase and interleukin-4. Evidently, PM2.5-induced oxidative stress plays an essential role in mitochondrial toxicity and mast cell activation. 相似文献
3.
我国的环境司法处于发展初期,有关环境纠纷的司法救济程序散落在不同的部门法中。为了维护国家环境安全和公共环境利益,构建环境司法专门化势在必行,但是在特殊的环境保护法院进行专门化的环境审判过程中,出现环境诉讼保护对象的争议性、生态环境损害责任承担的特殊性等问题亟待解决,环境民事公益诉讼和生态环境损害赔偿诉讼等特殊环境诉讼规则应运而生,虽然目前还面临着一些困境,但是整体上构建环境司法体系的进程依然在不断推进。 相似文献
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5.
低剂量镉诱导细胞氧化损伤的机理研究 总被引:1,自引:0,他引:1
镉是一种有毒重金属,能诱导酿酒酵母的氧化损伤.为了研究低剂量镉诱导细胞氧化损伤的作用,通过有葡萄糖和无葡萄糖的酵母培养基,用浓度2 μmol/L和10 μmol/L的CdCl2染毒酿酒酵母10 h后,统计酿酒酵母细胞的存活率,并用HPLC-EC法测定酿酒酵母线粒体DNA中8-OH-dG/105dG比值.结果表明:无葡萄糖条件下,10μmol/L的CdCl2染毒时酿酒酵母对Cd2 的耐受性比有葡萄糖时明显高(P<0.01),而且线粒体DNA氧化损伤程度也明显低(P<0 01);但2 μmol/L的CdCl2染毒时,酿酒酵母对Cd2 的耐受性和线粒体DNA氧化损伤程度与有葡萄糖条件下相比差异不显著(P>0.05).因此,本文认为低浓度Cr主要对酿酒酵母细胞质中蛋白造成氧化损伤,浓度升高时则对线粒体DNA也产生氧化损伤. 相似文献
6.
In order to address the risk of combustible gas explosions in sewage culverts, a numerical model was established using ANSYS/LS-DYNA software. The model consisted of a culvert and a cover plate, and was used to study the effect of cover plate thickness (ranging from 0.08 m to 0.12 m) on the dynamic response and damage of the structure under explosive loads. The results indicated that, during the loading negative pressure stage, the equivalent stress peak value of the central monitoring unit of the cover plate first increased and then decreased with increasing cover plate thickness. Additionally, the maximum principal stress peak value first decreased and then increased, while the maximum shear stress peak value first increased and then decreased. During the loading positive pressure stage, the maximum principal strain peak value of the monitoring unit decreased overall with increasing cover plate thickness. However, the equivalent plastic strain peak value initially increased and then decreased gradually. The equivalent strain indicated that plastic damage occurred in the cover plate. Beyond a thickness of 0.11 m, increasing the cover thickness did not appear to enhance its resistance to plastic damage. The damage analysis revealed that as cover plate thickness increased, the peak displacement and velocity of the monitoring unit continued to decrease, while the overall stability and explosive resistance of the cover plate increased. Additionally, the number of damaged fragments decreased. However, once the cover plate thickness reached 0.11 m, the bonding performance of the reinforced concrete structure had been fully developed, increasing the thickness of the cover plate no longer had a significant impact on the explosive resistance of the cover plate. 相似文献
7.
为了进一步研究当量加速关系,归纳了现有腐蚀损伤当量化的研究方法,详细介绍了基于电化学原理、物理参量和力学损伤的当量折算法,讨论了各种方法的优劣和所适用范围。基于电化学原理的当量加速关系研究方法适合用于制定飞机金属结构加速试验环境谱,以物理参量为基准的当量折算法适用于建立疲劳关键部位、腐蚀关键部位的涂层及金属基体等各种加速试验环境谱的当量加速关系,力学损伤对比法适合用于结构疲劳关键部位。最后得出针对不同材料、不同部位应该采用不同的当量加速关系的结论。 相似文献
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9.
Plastics such as polyvinyl chlorides (PVC) are widely used in many indoor constructed environments; however, their unbound chemicals, such as di-(2-ethylhexyl) phthalates (DEHP), can leach into the surrounding environment. This study focused on DEHP's effect on the central nervous system by determining the precise DEHP content in mice brain tissue after exposure to the chemical, to evaluate the specific exposure range. Primary neuronal-astrocyte co-culture systems were used as in vitro models for chemical hazard identification of DEHP. Oxidative stress was hypothesized as a probable mechanism involved, and therefore the total reactive oxygen species (ROS) concentration was determined as a biomarker of oxidative stress. In addition, NeuriteTracer, a neurite tracing plugin with ImageJ, was used to develop an assay for neurotoxicity to provide quantitative measurements of neurological parameters, such as neuronal number, neuron count and neurite length, all of which could indicate neurotoxic effects. The results showed that with 1 nmol/L DEHP exposure, there was a significant increase in ROS concentrations, indicating that the neuronal-astrocyte cultures were injured due to exposure to DEHP. In response, astrocyte proliferation (gliosis) was initiated, serving as a mechanism to maintain a homeostatic environment for neurons and protect neurons from toxic chemicals. There is a need to assess the cumulative effects of DEHP in animals to evaluate the possible uotake and effects on the human neuronal system from exoosure to DEHP in the indoor environment. 相似文献
10.
CdSe/ZnS量子点对稀有鮈鲫胚胎发育的影响及其氧化应激作用 总被引:1,自引:0,他引:1
本研究以稀有鮈鲫(Gobiocypris rarus)为对象,研究了不同浓度CdSe/ZnS量子点(QDs)暴露下,稀有鮈鲫胚胎发育过程中自主运动频率、内心率和体长的变化,以及利用体内超氧化物歧化酶(SOD)和丙二醛(MDA)作为毒性指标,反映CdSe/ZnS QDs暴露对稀有鮈鲫胚胎发育的氧化应激作用.结果显示:CdSe/ZnS QDs对稀有鮈鲫胚胎72 hpf(hours post fertilization)的半致死浓度(LC50)为319.629 nmol·L-1,96 hpf的半致畸浓度(EC50)为203.312 nmol·L-1.CdSe/ZnS QDs暴露不仅影响稀有鮈鲫胚胎死亡率、畸形率、自主运动频率、孵化时间和孵化率,而且使其内心率减缓、体长缩短,导致胚胎卵凝结,心包囊肿,出现脊椎弯曲等多种毒性现象.同时发现,CdSe/ZnS QDs暴露导致稀有鮈鲫体内MDA含量增加以及SOD活力的降低.这表明CdSe/ZnS QDs对稀有鮈鲫胚胎发育具有致畸、致死作用,而氧化应激可能是引起其胚胎致畸、致死的重要机制之一. 相似文献