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71.
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OH Willemsen MM Snel L Kuipers CG Figdor J Greve BG De Grooth 《Canadian Metallurgical Quarterly》1999,76(2):716-724
Atomic force microscopy is one of the few techniques that allow analysis of biological recognition processes at the single-molecule level. A major limitation of this approach is the nonspecific interaction between the force sensor and substrate. We have modeled the nonspecific interaction by looking at the interaction potential between a conical Si3N4 tip with a spherical end face and a mica surface in solution, using DLVO (Derjaguin, Landau, Verwey, Overbeek) theory and numerical calculations. Insertion of the tip-sample potential in a simulation of an approach-retract cycle of the cantilever gives the well-known force-distance curve. Simulating a force-distance curve at low salt concentration predicts a discrete hopping of the tip, caused by thermal fluctuations. This hopping behavior was observed experimentally and gave rise to a novel approach to making measurements in adhesion mode that essentially works in the repulsive regime. The distance between tip and sample will still be small enough to allow spacer-involved specific interactions, and the percentage of nonspecific interactions of the bare tip with the mica is minimized. We have validated this physical model by imaging intercellular adhesion molecule 1 (ICAM-1) antigen with a tip functionalized with anti-ICAM-1 antibody. The measurement demonstrated that a significant decrease in the number of nonspecific interactions was realized, and the topographical image quality and the specific bonding capability of the tip were not affected. 相似文献
73.
S D?ppenschmitt P Langguth CG Reg?rdh TB Andersson C Hilgendorf H Spahn-Langguth 《Canadian Metallurgical Quarterly》1999,288(1):348-357
Interaction with the exsorptive transporter P-glycoprotein (P-gp) is a possible source of peculiarities in drug pharmacokinetics, including dose-dependent absorption, drug-drug interactions, intestinal secretion, and limited permeability of the blood-brain barrier. Among the established in vitro methods of the analysis of drug interactions with P-gp, none directly quantifies the affinity of ligands with P-gp. Instead, they measure the result of a membrane permeation and a receptor-binding process; this may lead to difficulties in the interpretation of results. An assay for quantification of drug affinity to the transporter is presented on the basis of the radioligand-binding assay principle. This has the advantage of directly quantifying the interaction between drugs and P-gp. Because of the reversible and competitive interaction of numerous substrates with P-gp, a radioligand-binding assay was developed by taking [3H]verapamil and [3H]vinblastine as radioligands and the human intestinal Caco-2 cells, overexpressed with P-gp by culturing in the presence of vinblastine or transfecting with multidrug resistance gene MDR-1 as receptor preparation. The assay was performed in 96-well plates and has the potential to be used as a high-throughput method. A clear induction of the expression of P-gp was demonstrated in the Caco-2 cells grown in the presence of vinblastine, as well as in the transfected cells, although to a lesser extent. Both radioligands were shown to bind to P-gp. Verapamil was the radioligand of choice for further investigations due to its lower nonspecific binding to the transporter preparation. Kinetics as well as specificity of the binding of verapamil to the P-gp preparation were demonstrated. A two-affinity model was found to adequately describe the data derived from saturation as well as from competition experiments, in accordance with previous findings on two exsorption sites for P-gp. The binding properties of [3H]verapamil and [3H]vinblastine to a P-gp preparation derived from induced Caco-2 cells are described. The concentration-dependent displacement of the radioligand by nonlabeled substrates for P-gp should be a suitable principle for the determination of drug affinity to the respective binding sites at the human intestinal multidrug transporter P-gp. 相似文献
74.
The need to defluoridate and fluoridate the water supplies in areas with drinking water naturally containing above-optimal (>/=2.5 mg/l) and suboptimal (=0.3 mg/l) fluoride concentration and caries and fluorosis prevalence of 12-year-old schoolchildren were assessed in Italy. In the low-fluoride area, 48.4% children were caries-free (DMFT = 0) and the DMFT and DMFS were 1.5 and 2.6; in the high-fluoride area, 46.8% had a DMFT = 0 and the values of the indices were 1.4 and 1.6, respectively. Multiple logistic regression analysis showed a significant association in the caries-free status according to parents' employment status (OR = 1.2, 95% CI = 1.1-1.3) and children's sweets consumption, since children who consumed sweets at least once a day had an adjusted odds ratio of 1.8 (95% CI = 1.4-2.3) compared to those with a lower consumption. Multiple linear regression analysis showed that DMFT and DMFS were significantly higher in children with a lower socioeconomic status and in those who consumed sweets at least once a day, with the DMFS significantly associated also with the area of residence. DT and FT scores were higher in the high- and low-fluoride areas, respectively. No evidence of fluorosis was reported in 94.5 and 55.3% of children in the low- and high-fluoride areas, respectively. The Community Fluorosis Index (CFI) for all permanent teeth was significantly higher in the high-fluoride area, 0.8, than the value, 0.1, found in the low-fluoride community. Our results substantiate the difficulties in defining universal guidelines for the fluoridation or defluoridation of drinking water and the need for an epidemiological approach to the decision as to fluoridate and defluoridate the water supply. 相似文献
75.
1.IntroductionHydrogenembrittlement(HE)0rhydr0gendamage(HD)ofall0ysisnotonlyrelatedt0chemicalc0mpositionsbutals0c10selyt0microstructures.Thereweres0merep0rts0ntheeffect0fmicr0structures0nHD0fsingle-phaseausteniticsteels[1-3].Themicrostructuralreas0nsofHD0fprecipitate-strengthenedausteniticsteels(PSAS),however,havereceivedlessattenti0n.Single-phaseausteniticsteelshaveproveninseveralinstancestohaveg00dresistancet0HD,butaretypicallynostr0ngerthan450MPainyieldstrength.Thus,anausteniticmatri… 相似文献
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Zhang Qian Shi Jiaoying CaiHong CAD & CG State Key Lab. Zhejiang University Foshan Enterprise Postdoctoral Workstaion 《计算机辅助绘图.设计与制造(英文版)》1997,(2)
TwoAlgorithmsforFastPolyhedronRay-TracingZhangQianShiJiaoyingCaiHongCAD&CGStateKeyLab.,ZhejiangUniversity,310027FoshanEnterpr... 相似文献
79.
A central question in Alzheimer's disease (AD) is the role of amyloid in pathogenesis. Recent discoveries implicating the longer A beta 1-42 form of amyloid in pathogenesis led us to characterize the interaction of A beta with cells to elucidate differences that might account for these observations. We characterized the adsorption, internalization and degradation of radiolabeled A beta in NGF-differentiated PC12 cells under conditions that are not acutely toxic. All A beta peptides examined absorb to the surface of PC12 cells and are internalized; however the adsorption and internalization of A beta 1-42 is significantly greater than that of A beta 1-40 and A beta 1-28. The adsorption of A beta 1-42 is decreased by treatment of the cells with neuraminidase, but not heparitinase. The fate of the internalized A beta 1-42 is also very different than shorter A beta peptides; a fraction of the internalized A beta 1-42 accumulates intracellularly and is resistant to degradation for at least 3 days while A beta 1-40 and shorter peptides are eliminated with a half life of about 1 h. A beta 1-42 does not appear to inhibit lysosomal hydrolases, since A beta 1-28 is degraded at the same rate in the presence or absence of A beta 1-42. The intracellular A beta 1-42 is located in a dense organellar compartment and colocalizes with the lysosomal markers Lucifer Yellow and horseradish peroxidase. These data indicate that there are significant differences in the cell surface adsorption, internalization and catabolism of A beta 1-42 compared to A beta 1-40 and A beta 1-28. These differences may be important for the preferential accumulation of the longer A beta 1-42 isoform and its association with AD pathogenesis. 相似文献
80.