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985.
Warwick F. Vincent 《Journal of phycology》1979,15(4):429-434
An inverse linear relationship between chlorophyll fluorescence yield (R) and light intensity was recorded in the near-surface waters of six lakes (New Zealand, England) of greatly different trophic status and phytoplankton species composition. This surface depression of R values could be removed by incubation of samples in dim light or darkness and was not observed in situ below a threshold irradiance (146 μEin ·m?2·s?1 for Lake Taupo, New Zealand). The time course of chlorophyll fluorescence depression and recovery in response to light treatment was measured in samples from Lake Windermere (England). Fluorescence exponentially decreased upon exposure to bright light and the response was 100% (5 m samples) or 83% (dim light-adapted 0 m samples) complete within 2 min. An increase in R values in the dim light occurred after a lag of 60 s and the rate of increase decreased exponentially with time. Full recovery took 15 min or more. Deep (6.5 m) populations from Lake Windermere exhibited large, time-dependent variations in chlorophyll fluorescence over the first 25 s of exposure to 450 nm light, whereas surface populations did not. These data were interpreted in terms of decreased spillover from PSII to PSI with increasing depth, to a minimum at the threshold light intensity below which cells are in light state 1. 相似文献
986.
David Tsang Cindy S. Y. Tung Vincent T. F. Yeung Clive S. Cockram 《Regulatory peptides》1997,70(2-3):91-96
The effect of endothelin-3 (ET-3) on C-type natriuretic peptide (CNP)-induced guanosine 3′,5′-cyclic monophosphate (cGMP) was examined in C6 glioma cells, CNP-induced cGMP formation was both time- and dose-dependent, with an EC50 value of about 10 nM. While ET-3 and phorbol 12-myristate 13-acetate (PMA) had no effect on basal cGMP production, both compounds were potent inhibitors of CNP-induced cGMP formation, with IC50 values of approximately 10 and 2 nM, respectively. Although protein kinase C (PKC) inhibitors had no effect on basal cGMP formation, Ro 31-8220, a PKC inhibitor, reversed the ET-3 inhibition on CNP-induced cGMP formation by 63% and that of PMA almost completely. Our findings suggest that stimulation of cGMP formation by CNP in C6 glioma cells is negatively modulated by PKC activation, and that the inhibitory action of ET-3 on CNP-stimulated cGMP formation is mediated partly by PKC. 相似文献
987.
Ilaria Donelli Paola Taddei Philippe F. Smet Dirk Poelman Vincent A. Nierstrasz Giuliano Freddi 《Biotechnology and bioengineering》2009,103(5):845-856
The purpose of this study was to investigate the changes induced by a lypolytic enzyme on the surface properties of polyethylene terephthalate (PET). Changes in surface hydrophilicity were monitored by means of water contact angle (WCA) measurements. Fourier Transform Infrared spectroscopy (FTIR) in the Attenuated Total Reflectance mode (ATR) was used to investigate the structural and conformational changes of the ethylene glycol and benzene moieties of PET. Amorphous and crystalline PET membranes were used as substrate. The lipolytic enzyme displayed higher hydrolytic activity towards the amorphous PET substrate, as demonstrated by the decrease of the WCA values. Minor changes were observed on the crystalline PET membrane. The effect of enzyme adhesion was addressed by applying a protease after‐treatment which was able to remove the residual enzyme protein adhering to the surface of PET, as demonstrated by the behavior of WCA values. Significant spectral changes were observed by FTIR–ATR analysis in the spectral regions characteristic of the crystalline and amorphous PET domains. The intensity of the crystalline marker bands increased while that of the amorphous ones decreased. Accordingly, the crystallinity indexes calculated as band intensity ratios (1,341/1,410 cm?1 and 1,120/1,100 cm?1) increased. Finally, the free carboxyl groups formed at the surface of PET by enzyme hydrolysis were esterified with a fluorescent alkyl bromide, 2‐(bromomethyl)naphthalene (BrNP). WCA measurements confirmed that the reaction proceeded effectively. The fluorescence results indicate that the enzymatically treated PET films are more reactive towards BrNP. FTIR analysis showed that the surface of BrNP‐modified PET acquired a more crystalline character. Biotechnol. Bioeng. 2009;103: 845–856. © 2009 Wiley Periodicals, Inc. 相似文献
988.
Vincent Cottin 《BMC research notes》2013,6(Z1):S2
Background
Combined idiopathic pulmonary fibrosis (IPF) with pulmonary emphysema (CPFE) is a syndrome with a characteristic presentation of upper lobe emphysema and lower lobe fibrosis. While CPFE is a strong determinant of secondary precapillary pulmonary hypertension (PH), there is limited evidence regarding the management of patients with CPFE and PH.Case presentation
A 63 year-old male presented in 2006 with dyspnoea on exertion having quit smoking in 2003. Clinical examination, together with high resolution computed tomography, bronchoalveolar lavage, and echocardiographic assessments, suggested a diagnosis of CPFE without PH. In 2007, the patient received intravenous cyclophosphamide, N-acetylcysteine, and short-term anticoagulation treatment. Due to remission of acute exacerbations, the patient received triple combination therapy (prednisone, N-acetylcysteine and azathioprine). Upon progressive clinical worsening, long-term supplemental oxygen therapy was initiated in 2009. Repeated right heart catheterisation in 2011 confirmed PH and worsening pulmonary haemodynamics, and off-label ambrisentan therapy was initiated. Dyspnoea remained at follow-up, although significant haemodynamic improvement was observed.Conclusion
CFPE is a distinct but under-recognized and common syndrome with a characteristic presentation. Further studies are needed to ascertain the etiology, morbidity, and mortality of CPEF with or without PH, and to evaluate novel management options.989.
George A. Cook Vincent H. Gattone Andrew P. Evan Robert A. Harris 《Biochimica et Biophysica Acta (BBA)/Molecular Cell Research》1983,763(4):356-367
The structural changes accompanying digitonin-induced release of enzymes and metabolites from isolated hepatocytes have been studied by scanning and transmission electron microscopy. In the initial phase, characterized by total release of the cytosolic marker enzyme, lactate dehydrogenase, the plasma membrane was immediately damaged, rapidly followed by extensive damage to the endoplasmic reticulum. The shape of the cell, however, was maintained, and the mitochondria and nucleus remained tightly held together by the cytoskeleton. Mitochondria remained intact initially, whereas the cytosol became less electron dense and the nuclear chromatin was more dispersed. An intermediate phase was characterized by total release of adenylate kinase and most of the glucose-6-phosphatase, marker enzymes for the mitochondrial intermembrane space and the endoplasmic reticulum, respectively. The outer mitochondrial membrane was ruptured, but mitochondria maintained their normal matrix electron density. In the final phase, characterized by the beginning of citrate synthase release from the mitochondrial matrix space, the mitochondria became swollen, and only the nucleus, inner and outer mitochondrial membranes, and the cytoskeleton could be clearly distinguished. Although the plasma membrane could not be readily discerned in electron micrographs after the initial phase, the plasma membrane marker enzyme 5′-nucleotidase remained associated with digitonin-treated hepatocytes. Acetyl-CoA carboxylase was released much more slowly than lactate dehydrogenase, indicating some severe restriction on its release. The release of acetyl-CoA carboxylase closely paralleled the release of glucose-6-phosphatase. The controlled exposure of hepatocytes to digitonin, therefore, leads to the sequential release of soluble, compartmentalized cellular components and some membrane-bound components, but the mitochondrial membrane, cytoskeleton and the nucleoskeleton survive even long-term digitonin treatment. 相似文献
990.
The role of progesterone in regulation of uteroovarian venous concentrations of prostaglandins F2 α (PGF2α) and E2 (PGE2) during days 13 to 16 of the ovine estrous cycle or early pregancy was examined. At estrus, ewes were either mated to a fertile ram or unmated. On day 12 postesturus, ewes were laparotomized and a catheter was inserted into a uteroovarian vein. Six mated and 7 unmated ewes received no further treatment. Fifteen mated and 13 unmated ewes were ovariectomized on day 12 and of these, 7 mated and 5 unmated ewes were given 10 mg progesteron sc and an intravaginal pessary containing 30 mg of progesterone. Uteroovarian venous samples were collected every 15 min for 3 h on days 13 to 16 postestrus. Mating resulted in higher mean daily concentrations of PGE2 in the uterovarian vein than in unmated ewes. Ovariectomy prevented the rise in PGE2 with day in mated ewes but had no effect in unmated ewes. Progesterone treatment restored PGE2 in ovariectomized, mated ewes with intact embros. Mating had no effect on mean daily concentrations of PGF2α or the patterns of the natural logarithm (ln) of the invariance of PGF2α. Ovariectomy resulted in higher mean concentrations and ln invariances of PGF2α on day 13 and lower mean concentrations and ln invariances of PGF2α on days 15 and 16. Replacement with progesterone prevented these changes in patters of mean concentrations and ln variances of PGF2α following ovariectomy. It is concluded that progesterone regulates the release of PGF2α from the uterus, maintaining high concentrations while also preventing the occurrence of the final peaks of PGF2α which are seen with falling concentrations of progesterone. This occurs in both pregnant and non-pregnant ewes. Progesterone is also needed to maintain increasing concentrations of PGE2 in mated ewes. 相似文献