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101.
Metalworking fluids (MWFs), which have a long history of use in industry and are in constant and ever-increasing use in parallel with advancements in mechanisation, are emulsions prepared with water. MWFs prepared as a 1/20 (MWF: water) mixture in practice, contain a large amount of water within their structure, and may become an aquatic toxic mixture in an ecosystem. In this study, half maximal effective concentration (EC50) values for MWFs were determined using the Allium cepa test, an accepted ecotoxicological biomonitor, and test solutions were prepared (1/250, 1/500 and 1/1000). Depending on the MWF ratio at each concentration, a decrease in the mitotic index (MI), irregularities in the phase distribution and aberrations in the chromosomes were observed. When the amount of MWF in the water increased, chromosomal abnormalities such as stickiness were observed to occur; whereas abnormalities such as c-mitosis, fragments, bridges, vagrants and micronucleus increased as the amount of the MWF decreased. Over a second 24-h period, it was observed that values, in particular MI, showed a tendency to return to normal.  相似文献   
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本文根据组合模式原理提出了一种用小震调制比(rm)异常区出现高频次的空间异常图,进行强地震中短期预报的方法,简称rs法。该方法在预报强震地点和时间上可望取得较好效果。本文在介绍该方法的基础上,应用该法对3次7级以上大震进行了回顾性检验。  相似文献   
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利用我国160个台站1951—2010年逐月降水观测资料,分析了我国1990—2009年夏季(6—8月)降水的变化特征,对其代表性雨型进行了分类,重点分析了1990年代和2000年代主要多雨带的变化特征。此外还分析了1990年代和2000年代的北半球500 hPa大尺度环流背景和气温及海温背景的差异,从而探讨了夏季降水...  相似文献   
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除草剂异丙莠诱发蚕豆根尖细胞遗传损伤的研究   总被引:1,自引:1,他引:0  
以蚕豆根尖为材料,研究除草剂异丙莠对蚕豆根尖细胞的遗传毒性效应。采用蚕豆根尖微核技术,以不同浓度的异丙莠为诱变剂,测定蚕豆根尖细胞的有丝分裂指数、微核率和染色体畸变率。结果表明,异丙莠能诱发较高频率的微核率,即在一定浓度范围内,其微核率随异丙莠处理浓度的升高而增加,但随着异丙莠浓度进一步升高而呈下降趋势;异丙莠能降低蚕豆根尖细胞有丝分裂指数并诱导染色体产生多种类型的畸变。一定剂量的除草剂异丙莠对蚕豆根尖细胞具有明显的遗传毒性。  相似文献   
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We report on the prenatal diagnosis and ultrasonographic findings of a second-trimester fetus with jumping translocation involving chromosome 22. A 28-year-old gravida 2, partus 1, Turkish woman was referred for genetic counselling and ultrasonographic examination at 18 weeks' gestation because of a high risk of trisomy 21 in triple test. Prenatal ultrasonography showed tetralogy of Fallot with a diverticular dilatation of the pulmonary artery, flattened brow, complete absence of the right upper limb, hypospadias, oligodactyly (three digits) in left hand and in both feet, and hyperechogenic abdominal foci. Amniocentesis revealed a karyotype of 46,XY[4]/46,XY,−8,+ der(8),t(8;22)(q24.3;q11.21)[2]/45, XY,−22,−8,+ der(8)t(8;22)(q24.3;q11.21)[22]/45,XY,−22,−5,+ der(5)t(5;22)(q35.3;q11.21)[44]. A C-banding and FISH study with a specific centromeric probe (D14Z1/D22Z1) for chromosome 22 was made. In our case, partial monosomy for the regions 22q11.21→22pter, 8q24.3→8qter and 5q35.3→5qter may partially explain the fetal malformations. Copyright © 2005 John Wiley & Sons, Ltd.  相似文献   
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The short-stature homeobox-containing gene (SHOX) on chromosome Xp22.3 was recently identified as an important determinant of the stature phenotype. Deletions of the SHOX gene, some of them due to structural chromosome abnormalities, have been described in patients with idiopathic short stature and Leri-Weill syndrome. Additionally, haploinsufficiency of SHOX is a main cause for short stature seen in patients with Turner syndrome. Here we report an unusual X-chromosome abnormality, which was detected during a fetal karyotyping performed because of a previous child with Down syndrome. GTG banding demonstrated an extra chromosome segment on the terminal part of the short arm of chromosome X in the index case (karyotype: 46,X,Xp+). The same chromosomal abnormality was found in the mother and the maternal grandmother. All carriers of this chromosomal abnormality presented with short stature but no other associated symptoms. Whole chromosome painting of X revealed a homogeneous painting of the abnormal X chromosome indicating that no other chromosome was involved. Additional FISH studies with probe DXS1140 (Kallmann probe at Xp22.3), Quint-Essential X-Specific DNA (DMD probe at Xp21.2), XIST (at Xq13.2), and Tel Xq/Yq were performed, and no abnormality was observed in the intensities or the localizations of the probes signals. However, applying a specific SHOX gene probe (derived from cosmid LLNONO3M34F5) showed a loss of signal on the derivative X chromosome. Our results show that the Xp+ generation led to a deletion of the complete SHOX gene and caused short stature in the presented family. Copyright © 2003 John Wiley & Sons, Ltd.  相似文献   
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