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John A. Nyakatura Vivian R. Allen Jonas Laustr?er Amir Andikfar Marek Danczak Hans-Jürgen Ullrich Werner Hufenbach Thomas Martens Martin S. Fischer 《PloS one》2015,10(9)
Orobates pabsti, a basal diadectid from the lower Permian, is a key fossil for the understanding of early amniote evolution. Quantitative analysis of anatomical information suffers from fragmentation of fossil bones, plastic deformation due to diagenetic processes and fragile preservation within surrounding rock matrix, preventing further biomechanical investigation. Here we describe the steps taken to digitally reconstruct MNG 10181, the holotype specimen of Orobates pabsti, and subsequently use the digital reconstruction to assess body mass, position of the centre of mass in individual segments as well as the whole animal, and study joint mobility in the shoulder and hip joints. The shape of most fossil bone fragments could be recovered from micro-focus computed tomography scans. This also revealed structures that were hitherto hidden within the rock matrix. However, parts of the axial skeleton had to be modelled using relevant isolated bones from the same locality as templates. Based on the digital fossil, mass of MNG 10181 was estimated using a model of body shape that was varied within a plausible range to account for uncertainties of the dimension. In the mean estimate model the specimen had an estimated mass of circa 4 kg. Varying of the mass distribution amongst body segments further revealed that Orobates carried most of its weight on the hind limbs. Mostly unrestricted joint morphology further suggested that MNG 10181 was able to effectively generate propulsion with the pelvic limbs. The digital reconstruction is made available for future biomechanical studies. 相似文献
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Cytochrome c reductase is inhibited by p-chlorophenyl-methoxybenzyl-ketoxime (CPMB-oxime). CPMB-oxime induces a red-shift of the reduced spectrum of cytochrome b. The inhibitor blocks the oxidation of ubihydroquinone at the QP center of this enzyme in a non-competitive way. The binding stoichiometry equals one inhibitor molecule per Qp center. The apparent Kd in a red-shift assay was 6.9 +/- 0.6 microM. All binding characteristics analysed in this study were very similar to those of the E-beta-methoxyacrylate inhibitors, although the chemical structure is different from these inhibitors. This result is interpreted as a support for the inhibitory mechanism based on the model of a 'catalytic switch' proposed recently for the E-beta-methoxyacrylate inhibitors (MOA-inhibitors (Brandt and von Jagow, Eur. J. Biochem. 相似文献
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U Z Muratova V T Bornikov A Kh Abdukaiumova T S Saatov 《Biokhimii?a (Moscow, Russia)》1991,56(2):320-325
The activity of phospholipase A2 in blood platelets of healthy donors and IHD patients was examined. The enzyme activity was found to be increased 3-fold in platelets possessing a high level of functional activity (IHD) and by one order of magnitude in patients with myocardial infarction as compared with healthy donors. An enzyme preparation possessing a phospholipase activity was isolated from platelets by using salt extraction (KCl) and sonication. Purification of the enzyme by affinity chromatography resulted in two protein peaks both having a phospholipase A2 activity, the purification and molecular masses of these fractions being 768- and 2200-fold, and 13.5 and 15 kDa, respectively. It was supposed that these proteins are substrate-specific forms of phospholipase A2. 相似文献
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Amylin, a 37-residue polypeptide with a single disulfide bond originally isolated from the pancreas of type-II diabetic patients, has been shown to cause peripheral insulin resistance and to attenuate the inhibition of hepatic glucose output by insulin. We have also shown that amylin is present in the rat hypothalamus and that it inhibits food intake by rats. In order to further investigate the anorectic properties we synthesized both human and rat amylin by the solid phase method and purified to homogeneity in an overall yield of 10-20%. Structural analyses indicated that human amylin exhibited predominantly a beta-sheet structure at both acidic and alkaline pH, whereas no ordered structure was evident in the case of rat amylin. Intrahypothalamic injection of rat amylin resulted in a potent dose-dependent inhibitory effect on the food intake by rats adapted to eat their daily ration of food in an eight-hour period. Human amylin was less effective as an anorectic agent. Furthermore, rat amylin completely blocked the potent orexigenic effect of neuropeptide Y (NPY). These investigations show that there is a fundamental difference in the secondary structures of human and rat amylin and that rat amylin is a potent inhibitor of both basal and NPY-induced feeding by rats. 相似文献
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S. Kleinle U. Wiesmann A. Superti-Furga S. Krähenbühl E. Boltshauser J. Reichen S. Liechti-Gallati 《Human genetics》1997,100(5-6):643-650
We used a strategy based on long PCR (polymerase chain reaction) for detection and characterization of mitochondrial DNA (mtDNA)
rearrangements in two patients with clinical signs suggesting Pearson syndrome and Kearns-Sayre syndrome (KSS), respectively,
and one patient with myopathic symptoms of unidentified origin. Mitochondrial DNA rearrangements were detected by amplification
of the complete mitochondrial genome (16.6 kb) using long PCR with primers located in essential regions of the mitochondrial
genome and quantified by three-primer PCR. Long PCR with deletion-specific primers was used for identification and quantitative
estimation of the different forms of rearranged molecules, such as deletions and duplications. We detected significant amounts
of a common 7.4-kb deletion flanked by a 12-bp direct repeat in all tissues tested from the patient with Pearson syndrome.
In skeletal muscle from the patient with clinical signs of KSS we found significant amounts of a novel 3.7-kb rearrangement
flanked by a 4-bp inverted repeat that was present in the form of deletions as well as duplications. In the patient suffering
from myopathic symptoms of unidentified origin we did not detect rearranged mtDNA in blood but found low levels of two rearranged
mtDNA populations in skeletal muscle, a previously described 7-kb deletion flanked by a 7-bp direct repeat and a novel 6.6-kb
deletion with no repeat. These two populations, however, were unlikely to be the cause of the myopathic symptoms as they were
present at low levels (10–40 ppm). Using a strategy based on screening with long PCR we were able to detect and characterize
high as well as low levels of mtDNA rearrangements in three patients.
Received: 10 March 1997 / Accepted: 20 May 1997 相似文献
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