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131.
Chang Wang Chongwo Li Qingzhu JiaCollege of Material Science & Chemical Engineering Tianjin University of Science & Technology Dagunan Road Tianjin City P.R. China 《天津科技大学学报》2004,19(Z2)
INTRODUCTIONPlant consists essentially of three main polymers:lignin, cellulose, and hemicellulose, which are themost abundant and renewable hydrocarbon resourceson the earth. The annual yield of rice straw, wheatstraw, bagasse, reed, and bamboo in our country hasexceeded 1 billion tons. 30% of the yield of ricestraw and wheat straw are used for papermaking, which occupy 70-80% of the raw material. However, it is the difficulty in papermaking waste liquid treatment as well as the lack of c… 相似文献
132.
ZHAO Wei HU Ke KIMOTO Akitsu MIZUYAMA Takahisa . Institute of Environmental Science Beijing Normal University Beijing China . College of Earth Sciences Jilin University Changchun Jilin China . Laboratory of Erosion Control Graduate School of Agriculture Kyoto University Kyoto Japan 《武汉大学学报:自然科学英文版》2004,9(4):527-532
0 IntroductionManystudieshavebeendoneonthesedimentdischargeinMt.Tanakami .Thosestudiesconcerntheamountofsedi mentsandfewdiscussionsabouttheprocessonly .Andthesedi mentyieldmechanismindevastatedslopeinMt.Tanakamiisnotfullyunderstood.Inordertorecordthewholeprocessofsoilero sionfromthebeginningofprecipitation ,totheendofsedimentmovement,asimulatingexperimentbyusingartificialrainiscon ducted .Basedonthisexperiment,andbyfurthercomparingwiththepreviousdataofsedimentsinthisarea,somebasicdataaboutc… 相似文献
133.
结合工程实际,通过室内模型试验方法,研究锥柱式桩基础明挖基坑回填土在模拟实际环境温度条件下的回冻过程.结果表明,在模拟平均温度为-2.71℃的环境温度条件下,正温极值时刻表层土体融化深度约6.1 cm,回填土冻结深度随着冻融次数的增加而增厚,经历13次冻融循环,冻结层厚度达20.0 cm;桩基沿着水平向和纵向对回填土回冻过程产生影响,但其影响范围有限;土体和桩基与空气界面温度存在差异,桩基和空气界面处温度接近低温试验箱内空气温度,土体和空气界面处与空气温度差别较大,正温极值状态,空气温度高于土表温度5.0℃,负温极值状态,空气温度低于土表温度6.7℃.试验结果有助于进一步认识此类桩基回填土实际回冻过程,为确定模型试验控温条件及数值模拟边界条件提供参考. 相似文献
134.
Selective functionalization of mesoporous silica nanospheres (MSNs) is crucial for nanoengineering of MSNs.
Herein, we have combined “surface-protected etching strategy” and “cationic surfactant assisted etching
strategy” to prepare functionalized MSNs with externally attached amino groups. The externally attached NH2
groups endow the catalysts with excellent catalytic performance for nitroaldol reaction between nitromethane
and benzaldehyde. In addition, those NH2-MSNs can also be used to support gold nanoparticles, which display
very good catalytic performance for reduction of 4-nitrophenol. It can be envisioned that the synthesis protocol
developed in this work could also be extended to nanoengineered MSNs, which provides opportunities for nanoreactors
design. 相似文献
135.
The pedigrees of three sequenced rice cultivars were analyzed to show that a majority of the genetic composition of 'Nipponbare' originates from japonica cultivars while the minority originates from indica cultivars. In contrast, '93-11' is derived mainly from indica cultivars with a smaller contribution from japonica cultivars. All ancestors of 'Guang lu ai 4' appeared to be indica lines. A set of molecular markers (46 InDels and 53 SSRs) polymorphic between 'Nipponbare' and '93-11' were examined in 46 typical indica and 47 typical japonica cultivars selected from 443 accessions according to Cheng's index. All cultivars were divided into indica and japonica groups without overlapping when clustered by Cheng's index, InDels and SSRs. Much higher InDel and SSR diversity between groups than within groups implies that the marker polymorphisms between 'Nipponbare' and '93-11' represent a large proportion of inter-subspecific diversity. About 85% of indica cultivars and more than 90% of japonica cultivars were confirmed to have the same PCR banding patterns as '93-11' and 'Nipponbare', respectively. Some polymorphic loci between 'Nipponbare' and '93-11' cannot be validated in other indica and japonica cultivars, either as subspecies-specific but not predominant alleles, or alleles not specific between the two groups. It was concluded that molecular markers developed from sequence polymorphism between 'Nipponbare' and '93-11' often represent inter-subspecific diversity, although some exceptions were sensitive to either particular marker loci or particular cultivars. 相似文献
136.
变数据窗阻抗算法的频域分析方法研究 总被引:1,自引:1,他引:0
分析典型变数据窗阻抗算法的估计原理和特点 ,提出了一种适用于不同阻抗估计算法的新型频率响应计算方法 ,为不同算法的频域特性分析和比较提供了共同的基础 .该方法也可用于对算法抑制非周期分量的性能进行分析研究 相似文献
137.
Mitochondrial dysfunction and apoptosis in myopathic mice with collagen VI deficiency 总被引:13,自引:0,他引:13
Irwin WA Bergamin N Sabatelli P Reggiani C Megighian A Merlini L Braghetta P Columbaro M Volpin D Bressan GM Bernardi P Bonaldo P 《Nature genetics》2003,35(4):367-371
Collagen VI is an extracellular matrix protein that forms a microfilamentous network in skeletal muscles and other organs. Inherited mutations in genes encoding collagen VI in humans cause two muscle diseases, Bethlem myopathy and Ullrich congenital muscular dystrophy. We previously generated collagen VI-deficient (Col6a1-/-) mice and showed that they have a muscle phenotype that strongly resembles Bethlem myopathy. The pathophysiological defects and mechanisms leading to the myopathic disorder were not known. Here we show that Col6a1-/- muscles have a loss of contractile strength associated with ultrastructural alterations of sarcoplasmic reticulum (SR) and mitochondria and spontaneous apoptosis. We found a latent mitochondrial dysfunction in myofibers of Col6a1-/- mice on incubation with the selective F1F(O)-ATPase inhibitor oligomycin, which caused mitochondrial depolarization, Ca2+ deregulation and increased apoptosis. These defects were reversible, as they could be normalized by plating Col6a1-/- myofibers on collagen VI or by addition of cyclosporin A (CsA), the inhibitor of mitochondrial permeability transition pore (PTP). Treatment of Col6a1-/- mice with CsA rescued the muscle ultrastructural defects and markedly decreased the number of apoptotic nuclei in vivo. These findings indicate that collagen VI myopathies have an unexpected mitochondrial pathogenesis that could be exploited for therapeutic intervention. 相似文献
138.
139.
Mutations in the gene encoding pejvakin, a newly identified protein of the afferent auditory pathway, cause DFNB59 auditory neuropathy 总被引:5,自引:0,他引:5
Delmaghani S del Castillo FJ Michel V Leibovici M Aghaie A Ron U Van Laer L Ben-Tal N Van Camp G Weil D Langa F Lathrop M Avan P Petit C 《Nature genetics》2006,38(7):770-778
Auditory neuropathy is a particular type of hearing impairment in which neural transmission of the auditory signal is impaired, while cochlear outer hair cells remain functional. Here we report on DFNB59, a newly identified gene on chromosome 2q31.1-q31.3 mutated in four families segregating autosomal recessive auditory neuropathy. DFNB59 encodes pejvakin, a 352-residue protein. Pejvakin is a paralog of DFNA5, a protein of unknown function also involved in deafness. By immunohistofluorescence, pejvakin is detected in the cell bodies of neurons of the afferent auditory pathway. Furthermore, Dfnb59 knock-in mice, homozygous for the R183W variant identified in one DFNB59 family, show abnormal auditory brainstem responses indicative of neuronal dysfunction along the auditory pathway. Unlike previously described sensorineural deafness genes, all of which underlie cochlear cell pathologies, DFNB59 is the first human gene implicated in nonsyndromic deafness due to a neuronal defect. 相似文献
140.
Purification and cloning of amyloid precursor protein beta-secretase from human brain 总被引:40,自引:0,他引:40
Sinha S Anderson JP Barbour R Basi GS Caccavello R Davis D Doan M Dovey HF Frigon N Hong J Jacobson-Croak K Jewett N Keim P Knops J Lieberburg I Power M Tan H Tatsuno G Tung J Schenk D Seubert P Suomensaari SM Wang S Walker D Zhao J McConlogue L John V 《Nature》1999,402(6761):537-540
Proteolytic processing of the amyloid precursor protein (APP) generates amyloid beta (Abeta) peptide, which is thought to be causal for the pathology and subsequent cognitive decline in Alzheimer's disease. Cleavage by beta-secretase at the amino terminus of the Abeta peptide sequence, between residues 671 and 672 of APP, leads to the generation and extracellular release of beta-cleaved soluble APP, and a corresponding cell-associated carboxy-terminal fragment. Cleavage of the C-terminal fragment by gamma-secretase(s) leads to the formation of Abeta. The pathogenic mutation K670M671-->N670L671 at the beta-secretase cleavage site in APP, which was discovered in a Swedish family with familial Alzheimer's disease, leads to increased beta-secretase cleavage of the mutant substrate. Here we describe a membrane-bound enzyme activity that cleaves full-length APP at the beta-secretase cleavage site, and find it to be the predominant beta-cleavage activity in human brain. We have purified this enzyme activity to homogeneity from human brain using a new substrate analogue inhibitor of the enzyme activity, and show that the purified enzyme has all the properties predicted for beta-secretase. Cloning and expression of the enzyme reveals that human brain beta-secretase is a new membrane-bound aspartic proteinase. 相似文献