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71.
饮用水中非挥发性有机物的遗传毒性及脂质过氧化作用 总被引:9,自引:0,他引:9
用SOS显色法研究了3种不同水源自来水中非挥发性有机物的遗传毒性,以大鼠肝微粒体系统为模型研究了自来水非挥发性有机物的脂质过氧化作用。结果表明:以D湖水为水源的自来水中非挥发性有机物具有遗传毒性、且能使大鼠肝微粒体的脂质过氧化作用显著增强。 相似文献
72.
采用高压液相色谱(HPLC)测定的方法研究了有机诱变剂苯并[a]芘在实验海洋食物链(从浮游藻类褐指藻Phaeodactylum tricornutum Bohlin经中国对虾Penaeueus orientalis Kishinouye到欧氏六线鱼Hexagrammos otakii Jordan et Starks)中的流动,并对积累苯并]a[芘的中国对虾和欧氏六线鱼内脏和肌肉进行了紫露草微核(Trad-MCN)的测定,结果如下:①苯并]a[芘具有延缓褐指藻生长的作用。褐指藻中苯并[a]芘的吸着量随剂量的增大而增大。苯并[a]芯的测定量小于加入量,其损失量与剂量之间具有一定的相关性。②鱼虾内脏中积累的苯并[a]芘的浓度高于肌肉中的浓度。苯并[a]芘在中国对虾到欧氏六线鱼的传递中浓度减少,在鱼肉中很难检测到。通过显著性t测检发现,处理组和对照组虾肉之间的诱变性差异显著(P<0.05),处理组和对照组虾内脏之间的违变性差异亦显著)P<0.005)。 相似文献
73.
Di Marzio WD Sáenz ME Montivero C Alberdi JL Tortorelli MC Ambrini G 《Bulletin of environmental contamination and toxicology》2007,79(5):483-487
The genotoxicity of industrial soils was evaluated. A single cell electrophoresis assay or comet assay, using eleocyte cells
of Eisenia foetida, was performed to assess the genotoxicity of aqueous elutions. These were obtained from industrial soils containing metals.
All soil samples meet the environmental quality guidelines for metal concentrations. However, elutions have produced genotoxic
effects at dilutions as low as 6%. Total metal concentrations for each aqueous elution could express synergistic effects of
these compounds. 相似文献
74.
Marina Popal Joachim Volk Gabriele Leyhausen Werner Geurtsen 《Dental materials》2018,34(12):1783-1796
Objectives
Phenylbis(acyl) phosphine oxide (BAPO) and diphenyl(acyl) phosphine oxide (TPO) are alternative photoinitiators to camphorquinone (CQ) in dental resinous materials. Aim of this study was to investigate their cytotoxic/genotoxic potential in human oral keratinocytes (OKF6/Tert2) and Chinese hamster lung fibroblasts (V79) in comparison to CQ.Methods
Cells were exposed to different concentrations of BAPO and TPO (1–50 μM). Cytotoxicity was evaluated using H33342 and MTT assay, cell proliferation by BrdU proliferation assay and microscopy. Effects on cellular redox homeostasis were assessed by detecting intracellular levels of reactive oxygen/nitrogen species (ROS/RNS) using the DCFH2 assay and by quantification of mRNA expression of oxidatively regulated, cyto-protective enzymes. Genotoxic potential was determined by use of micronucleus (MN) assay.Results
BAPO and TPO induced a concentration-dependent decrease of cell number. BAPO and TPO showed 50- to 250-fold higher cytotoxicity than CQ. In contrast to CQ, both photoinitiators revealed no increase of intracellular ROS/RNS. However, BAPO (10 μM) at least significantly induced mRNA-expression of redox-regulated proteins after 24 h similar to 2.5 mM CQ. Additionally, BAPO significantly raised the number of micronuclei, but only in V79 cells (10 μM: 12 ± 1, 2.5 mM CQ: 15 ± 1, medium control: 6 ± 3). However, it also significantly decreased proliferation of these cells (10 μM BAPO: 19.8% ± 7.3% compared to controls).Significance
BAPO and TPO revealed concentration-dependent cytotoxic effects in human oral keratinocytes and V79 cells. However, in contrast to CQ, no generation of intracellular ROS/RNS was found. Only BAPO induced genotoxicity in V79 cells. 相似文献75.
Trichloroethylene (TCE) is a suspected genotoxic and carcinogenic compound which is usually present in the air, soil and water as pollutant. To estimate the genotoxic potential of TCE in a pure chemical form as well as an ingredient of the complex sample, Ames fluctuation test using TA98 and TA100 strains and Allium cepa genotoxicity assay were performed. For the genotoxicity analysis of TCE in natural milieu, the above mentioned tests were performed on the waste waters collected from two different stations of northern India namely Saharanpur and Aligarh, U.P., and these waste waters were supplemented with 50 and 100 mg/l of trichloroethylene. TCE alone was found to be non-genotoxic by both the testing system up to the range of 1000 mg/l concentration (data not shown). However, the test water samples supplemented with 100 mg/l of TCE, exhibited a significant increase in the genotoxicity compared with control by both the testing systems. In Ames fluctuation test, Mi(f) value was found to be increased by 41% and 53% with 100 mg/l of TCE supplemented Saharanpur and Aligarh waste water samples respectively, in the presence of S9 fraction compared with their respective controls. Allium cepa genotoxicity test also showed around 25% increase in total chromosomal aberration frequency following 100 mg/l TCE supplementation. However, supplementation of 50 mg/l TCE to the test water samples could not enhance the genotoxicity to a significant extent. From these results, we can conclude that TCE itself was non-genotoxic but it may promote mutation and/or DNA damage at a concentration of 100 mg/l under certain environmental conditions. We suggest that some chemicals in the test water samples might be interacting with TCE and/or metabolite(s) to cause the enhancement in genotoxicity. The mechanism of these synergistic effects should be explored further. 相似文献
76.
77.
The 32P-postlabeling method was adapted for the detection of DNA adducts formed by methylenediphenyl-4,4'-diisocyanate (MDI). Incubation of the 3'-phosphates of the deoxyribosides of cytosine (C), adenine (A), guanine (G) and thymine (T) with MDI in Tris buffer resulted in the formation of 5, 7, 8, and 2 reaction products, respectively. Incubation of DNA with MDI resulted in detectable levels of 5, 2, and 1 adducts attributable to C, A, and G. Analysis of DNA isolated from the epidermis of rats treated dermally with 9 mg MDI showed an adduct pattern similar to the one seen in the in vitro DNA incubation. A total adduct level of 7 per 108 nucleotides was measured, the limit of detection was 2 adducts per 1010 nucleotides. The data indicate that a minute fraction of MDI can reach DNA in vivo in a chemically reactive form. In comparison with the genotoxic skin carcinogen 7,12-dimethylbenz[a]anthracene on the other hand, the DNA-binding potency of MDI was more than 1000-fold lower. 相似文献
78.
Engelhardt G 《Archives of toxicology》2006,80(12):868-872
1-Phenylethanol is one of the major primary phase-I metabolites of ethylbenzene. In principle it may yield an electrophilic intermediate by phase-II metabolism. Because of the extensive use of ethylbenzene as a solvent, 2-year carcinogenicity inhalation studies were carried out leading to renal hyperplasia and tubular neoplasms both in male and female rats and alveolar/bronchiolar neoplasms in male mice and hepatocellular neoplasms in female mice. Whereas the mechanism underlying the increased renal tumor incidences in rats has been clarified, the mechanism of tumor formation (genotoxic or nongenotoxic mode of action) in the lung and liver of mice is still unclear. The genotoxicity data available to date for 1-phenylethanol include in vitro studies using either bacteria (Salmonella reverse mutation assay, E. coli Pol A+/Pol A− test) or mammalian cells (mouse lymphoma assay, chromosome aberration test and sister chromatid exchanges using CHO cells). These experiments, however, did not always follow current standard procedures and some of the data obtained are compromised and not always convincing. The present database thus does not allow a definitive assessment of the in vitro genotoxic potential of 1-phenylethanol. The in vitro database suggests that clastogenicity may be the most relevant genetic end point, and therefore an in vivo micronucleus assay in mouse bone marrow was carried out. The animals were given 1-phenylethanol in single oral doses up to the maximum tolerated dose of 750 mg/kg body weight. Bone marrow was sampled 24 and 48 h after treatment. Under the experimental conditions used, there was no evidence of increased micronuclei frequencies at any dose or sampling time. These findings indicate that 1-phenylethanol is not clastogenic in vivo. This information, together with other negative or inconclusive genotoxicity data available so far, suggests a nongenotoxic mode of action responsible for the lung and liver tumors observed in mice following 2 years of inhalation exposure to ethylbenzene. 相似文献
79.
Comparative evaluation of the alkaline comet assay with the micronucleus test for genotoxicity monitoring using aquatic organisms 总被引:1,自引:0,他引:1
A comparative analysis between the in vivo comet assay and the in vivo micronucleus test (MNT) was carried out in three aquatic organisms suitable for genotoxicity monitoring, carp (Cyprinus carpio), rainbow trout (Oncorhynchus mykiss), and clam (Spisula sachalinensis), using a direct-acting mutagen, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), and an indirect mutagen, benzo[a]pyrene (B[a]P). By optimizing the conditions for cell isolation, gill and liver (or digestive glands) were selected as test tissues of the comet assay for MNNG and B[a]P. The MNT employed the erythrocytes (or hemocytes), the most universal cell type for the assay. The analysis of DNA strand breaks using the comet assay and the micronucleus frequencies using the MNT revealed dose- and time-dependent increases between animals exposed to several concentrations of mutagens. But the statistical significance (P<0.05) obtained was higher by the comet assay than by the MNT. When the time profiles of genotoxic signals resulting from B[a]P exposure to carp were plotted representatively, clear distinctions between all concentrations were made in the comet assay, but not in the MNT. The correlation index defined in this study also showed a higher correlation between concentration and signal in the comet assay than in the MNT. It is suggested that the standardization of the comet assay is necessary for its methodological evaluation and use as a genotoxicity biomarker. We conclude that the comet assay has an excellent suitability for aquatic genotoxicity monitoring because of its high and reliable sensitivity. 相似文献
80.
Cytogenetic effects in children treated with methylphenidate 总被引:4,自引:0,他引:4
El-Zein RA Abdel-Rahman SZ Hay MJ Lopez MS Bondy ML Morris DL Legator MS 《Cancer letters》2005,230(2):284-291
In recent years there has been a surge in methylphenidate (Ritalin) use for treatment of attention deficit/hyperactivity disorder (ADHD) in children. However, there is a paucity of information on whether this drug poses any potential health risks, such as mutagenicity or carcinogenicity, for humans. To address this issue, we investigated whether this central nervous system stimulant produces cytogenetic abnormalities in pediatric patients at therapeutic levels. In a population composed of twelve children treated with therapeutic doses of methylphenidate, we analyzed three cytogenetic endpoints in peripheral blood lymphocytes obtained before and three months after initiation of treatment with this drug. In all participants, treatment induced a significant 3, 4.3 and 2.4-fold increase in chromosome aberrations, sister chromatid exchanges and micronuclei frequencies, respectively (P=0.000 in all cases). These findings warrant further investigations of the possible health effects of methylphenidate in humans, especially in view of the well-documented relationship between elevated frequencies of chromosome aberrations and increased cancer risk. 相似文献