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排序方式: 共有208条查询结果,搜索用时 15 毫秒
1.
A strain of Aspergillus fumigatus has been isolated from sediments of a mussel bed. When cultured in hyper saline conditions (with sea-water), it produces a cytotoxic and immunosuppressive toxin, gliotoxin, which is excreted in an exudate. In order to know if this toxin could represent a risk for shellfish consumers, an experiment of bioaccumulation of gliotoxin in mussel has been carried out. After 6 days of contamination, toxin was accumulated in the meat of the mussels, at a level up to 2.9 microg/mg of extract weight, with a mode of contamination different to the classical digestive process described for a majority of marine toxins, but similar to the contamination mode of domoic acid. 相似文献
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目的 探讨女工二硫化碳(CS2)接触水平与胚胎早期发育障碍之间的剂量-反应关系。方法 前瞻观察生育女工妊娠所需的月 经周期数;收集每个月经周期胚胎植入期尿样,检测绒毛膜促性腺激素含量;监测女工作业地点CS2浓度。结果 257名接触组经临床确诊妊娠的女工,各月经周期妊娠机率低于366名对照组女工,时间妊娠率随女工CS2接触水平(CS2接触浓度以CS2接触工龄)升高而降低:妊娠率=0.7033-0.0 相似文献
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Reqia Sagou Rachid Amanhir Hamid Taleb Paulo Vale Mohamed Blaghen Mohamed Loutfi 《Toxicon》2005,46(6):612-618
At the western Mediterranean coast of Morocco, the cockle (Acanthocardia tuberculatum) contained persistent high levels of paralytic shellfish toxins for several years, while other bivalve molluscs such as sweet clam (Callista chione) from the same vicinity were contaminated seasonally to a much lesser extent. In order to understand the causes of this prolonged contamination, a comparative study on PSP decontamination between sweet clam and cockle was conducted from November 2001 until June 2002. PSP toxicity was analysed by automated pre-column oxidation (Prechromatographic oxidation and LC-FD) in several organs of both species, namely digestive gland, foot, gill, mantle, muscle and siphon for sweet clams. The results showed that cockle sequester PSP toxins preferably in non-visceral organs (Foot, gill and mantle) contrary to sweet clam that sequester them in visceral tissues (digestive gland). The toxin profile of cockle organs indicated dominance of dcSTX, whereas sweet clam tissues contained especially C-toxins. Substantial differences in toxin profile between cockle and sweet clam, from the same area as well as from the composition of PSP toxin producer, Gymnodinium catenatum, confirm the bioconversion of PSP toxins in cockle. 相似文献
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《Environmental toxicology and pharmacology》2014,37(1):348-353
Changes in cadmium (Cd) accumulation, distribution, and chemical form in rice seedling in the joint presence of different concentrations of sulfur (S) remain almost unknown. Therefore, the indoor experiments were performed to determine the accumulation, sub-cellular distribution and chemical forms of Cd under three S levels in rice seedling for the first time. The result showed that Cd accumulation in rice roots was more than in shoots. Sub-cellular distribution of Cd in rice roots and shoots indicated that the largest proportion of Cd accumulated in cell walls and soluble fractions. As S supply increased, the proportion of Cd in cell walls reduced, while it increased in the soluble fractions. The majority of Cd existed in inorganic form, and then gradually changed to organic forms that included pectates and proteins with increased S supply. The results showed that S supply significantly influenced Cd accumulation, distribution, and chemical forms, suggesting that S might provide the material for the synthesis of sulfhydryl protein and thereby affect Cd stress on plants. These observations provided a basic understanding of potential ecotoxicological effects of joint Cd and S exposure in the environment. 相似文献
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目的 观察高糖对THP-1巨噬细胞清道夫受体CD36表达和脂质蓄积的影响。方法 用不同浓度的D-葡萄糖(分别为5.6、11、20、30及35 mmol/L)、50 mg/L氧化型低密度脂蛋白(ox-LDL)、50 mg/L ox-LDL+20 mmol/L D-葡萄糖孵育THP-1巨噬细胞24 h,油红O染色观察细胞内脂质蓄积情况,高效液相色谱分析法检测细胞内总胆固醇水平,定量PCR与免疫印迹分析法分别检测THP-1巨噬细胞CD36 mRNA和蛋白的表达。结果 随着D-葡萄糖处理THP-1巨噬细胞浓度的增加,CD36 mRNA和蛋白的表达逐渐增加(P<0.05);高糖可协同ox-LDL诱导THP-1巨噬细胞CD36 mRNA和蛋白的表达上调(P<0.05),并增加细胞内总胆固醇水平(P<0.05)。结论 高糖可诱导THP-1巨噬细胞CD36的表达上调,并促进细胞内脂质蓄积。 相似文献
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南方某地妇女儿童血液中多氯联苯蓄积水平调查 总被引:1,自引:0,他引:1
目的了解我国南方某多氯联苯(PCBs)高暴露地区的妇女、儿童体内PCBs的蓄积水平。方法采集当地某小学中符合条件的50对母子的血液,用GC-MS法进行PCBs含量的测定。结果儿童血液中所测的13种PCBs的浓度最大值为505ng/g类脂,几何均数为192ng/g类脂;母亲血液中所测的13种PCBs的总浓度的最大值为461 ng/g类脂,几何均数为176 ng/g类脂;儿童和母亲血液中PCBs含量的相关系数为0.74。结论该地区妇女和儿童血液中检测出较高水平的PCBs,儿童和母亲血液中PCBs含量呈现较好的线性关系。 相似文献
10.
Effect of Ulinastatin, a human urinary trypsin inhibitor, on the oleic acid-induced acute lung injury in rats via the inhibition of activated leukocytes 总被引:24,自引:0,他引:24
BACKGROUND: The acute respiratory distress syndrome (ARDS) is often caused by fat tissue embolism. One of the most common animal models of ARDS is produced by direct administration of oleic acid (OA). Activated leukocytes are critically involved in the pathological mechanism in this model. Human urinary trypsin inhibitor (UTI) is known to inhibit production of tumor necrosis factor (TNF)-alpha, which potently stimulates leukocyte activation. The purpose of this study was to clarify whether UTI improves OA-induced lung injury in rats by inhibiting activated leukocytes via TNF-alpha production. MATERIALS AND METHODS: Rats were subjected to a single intravenous administration of OA into the pedicle vein. Acute lung injury was evaluated by arterial blood gases and histological changes in lungs. Pulmonary vascular permeability, accumulation of neutrophils, and the levels of TNF-alpha in lung tissues were also examined. Rats were divided into four experimental groups: a sham operated, OA, OA + UTI, and OA + nitrogen mustard (NM)-induced leukocytopenia group. UTI was intravenously administered 30 min before OA administration. Leukocytopenia was induced by the administration of NM. RESULTS: UTI significantly improved the OA-induced histological changes for 4 h after OA administration. The OA-induced reduction of PaO2, the increase of pulmonary vascular permeability, and the levels of MPO activity and TNF-alpha in lung tissues were significantly improved in rats administrated UTI. The effects in the leukocytopenia group were similar to those in the UTI-administered group. CONCLUSION: Leukocytes play a critical role in the development of OA-induced lung injury. It was suggested that UTI contributed to the reduction in the OA-induced lung injury by inhibiting TNF-alpha and thereby suppressing leukocyte. 相似文献