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151.
Degradation mechanism of Direct Pink 12B treated by iron-carbon micro-electrolysis and Fenton reaction 总被引:1,自引:0,他引:1
The Direct Pink 12B dye was treated by iron-carbon micro-electrolysis (ICME) and Fenton oxidation. The degradation pathway of Direct Pink 12B dye was inferred by ultraviolet visible (UV-Vis), infrared absorption spectrum (IR) and high performance liquid chromatography-mass spectrometry (HPLC-MS). The major reason of decolorization was that the conjugate structure was disrupted in the iron-carbon micro-electrolysis (ICME) process. However, the dye was not degraded completely because benzene rings and naphthalene rings were not broken. In the Fenton oxidation process, the azo bond groups surrounded by higher electron cloud density were first attacked by hydroxyl radicals to decolorize the dye molecule. Finally benzene rings and naphthalene rings were mineralized to H2O and CO2 under the oxidation of hydroxyl radicals. 相似文献
152.
利用2011—2015年安徽省遥感影像土地利用类型解译数据,结合地面调查和统计资料,依据生态环境状况评价系统对安徽省"十二五"期间生态环境状况进行动态监测与评价。结果表明,"十二五"末安徽省各市生态环境状况等级为"优"的有4个市,为"良"的有12个市;"十二五"期间,各市等级均保持不变;"十二五"始末相比,有8个市生态环境状况变化度为"略有变好"等级,生态环境状况波动度为"波动"级别,其余8个市的变化度为"无明显变化"等级,波动度为"稳定"级别;省域EI增加了0.76,生态环境质量呈现稳中向好的趋势。 相似文献
153.
The dilemma of chromosomal mosaicism in chorionic villus sampling—‘direct’ versus long-term cultures
R. Nisani Dr J. Chemke R. Voss Z. Appelman B. Caspi A. Lewin H. Dar A. Reiter 《黑龙江环境通报》1989,9(4):223-226
Chromosomal mosaicism is one of several unanswered dilemmas in first-trimester prenatal diagnosis. We report the course of a pregnancy in which a normal karyotype was detected on direct CVS preparation and fetal blood, 100 per cent trisomy 21 in one long-term CVS culture, and low-rate trisomy 21 mosaicism in a second long-term CVS culture and amniocentesis. The phenotypically normal infant had a 6 per cent mosaicism of trisomy 21. It appears that a persistent low-rate mosaicism in different tissues may be indicative of the true status of the fetus. 相似文献
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157.
Two cases with trisomy 16 confined to the placenta are presented. Prenatal diagnosis was indicated because of fetal growth retardation. In case 1, a phenotypically normal but small-for-date boy was born. In case 2, the fetus turned out to be triploid on cordocentesis. In both instances the trisomy 16 was recovered from the placenta. Recovery indicates that the abnormality was present in the placenta during the time of fetal growth retardation, which supports an aetiological relationship. Strict appliance of the current models cannot readily explain the observed discrepancies. In case 2, a chimeric placenta as a result of a vanishing twin is assumed. Cases of placental trisomy 16 published after 1988 are reviewed. It is concluded that confined placental trisomy 16 can cause intrauterine growth retardation if present in both the direct preparation and the villus culture. The chances of finding a chromosomally abnormal fetus (mosaic trisomy 16, triploidy) after diagnosis of trisomy 16 in chorionic villi are low but warrant further investigations. 相似文献
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159.
Y. L. Zheng M. A. Ferguson-Smith J. P. Warner M. E. Erguson-Smith C. A. Sargent N. P. Carter 《黑龙江环境通报》1992,12(11):931-943
A comparison of the use of chromosome 21-specific libraries, DOP-PCR 21 paints, yeast artificial chromosome (YAC) clones, single cosmids, and a 21q cosmid contig as probes for the detection of the copy number of chromosome 21 in interphase cells by fluorescence in situ hybridization shows that the cosmid contig is a satisfactory probe for interphase analysis of chromosome 21. The contig cCMP21.a, which is 55 kb in length, is highly chromosome 21-specific and produces intense, compact signals in a high proportion of interphase cells. A retrospective blind analysis of coded uncultured amniotic fluid samples correctly detected four trisomy 21 cases out of 49 samples. 相似文献
160.
Children with a genetic absence of transcobalarnin 2 (TC2) are clinically asymptomatic at birth but develop severe megaloblastic anemia early in life. We have examined the incorporation of [57Co]-CN-B12 in the absence of any exogenous source of TC2 in control amniotic fluid derived cells and cultured diploid fibroblasts, and in fibroblasts from a patient with TC2 deficiency. Both control fibroblasts and arnniocytes incorporated labelled B12, into TC2-B12, and the proportion of labelled TC2-B12 could be increased by growing cells in the presence of chloroquine which prevents intralysosomal hydrolysis of the TC2-B12 complex. In contrast, fibroblasts from the patient with TC2 deficiency incorporated almost no label as TC2-B12. These studies suggest that TC2 deficiency either due to aberrant production of TC2 or because of the production of an abnormal TC2 which does not bind B12 can be diagnosed before birth. 相似文献