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671.

Background  

With the increasing availability of live cell imaging technology, tracking cells and other moving objects in live cell videos has become a major challenge for bioimage informatics. An inherent problem for most cell tracking algorithms is over- or under-segmentation of cells – many algorithms tend to recognize one cell as several cells or vice versa.  相似文献   
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The aim of this study was to investigate the combined influence of 3 independent variables in the preparation of piroxicam proniosomes by the slurry method. A 3-factor, 3-level Box-Behnken design was used to derive a second-order polynomial equation and construct contour plots to predict responses. The independent variables selected were molar ratio of Span 60:cholesterol (X(1)), surfactant loading (X(2)), and amount of drug (X(3)). Fifteen batches were prepared by the slurry method and evaluated for percentage drug entrapment (PDE) and vesicle size. The transformed values of the independent variables and the PDE (dependent variable) were subjected to multiple regression to establish a full-model second-order polynomial equation. F was calculated to confirm the omission of insignificant terms from the full-model equation to derive a reduced-model polynomial equation to predict the PDE of proniosome-derived niosomes. Contour plots were constructed to show the effects of X(1), X(2) and X(3) on the PDE. A model was validated for accurate prediction of the PDE by performing checkpoint analysis. The computer optimization process and contour plots predicted the levels of independent variables X(1), X(2), and X(3) (0, -0.158 and -0.158 respectively), for maximized response of PDE with constraints on vesicle size. The Box-Behnken design demonstrated the role of the derived equation and contour plots in predicting the values of dependent variables for the preparation and optimization of piroxicam proniosomes.  相似文献   
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An environmentally benign and efficient route of synthesis of polyacrylic acid grafted carboxymethyl cellulose (CMC-g-PAA) is developed using microwave radiation alone to initiate the grafting reaction. The synthesis is optimized in terms of percentage grafting and intrinsic viscosity, by varying the microwave irradiation time and monomer (acrylic acid) concentration. The grafted product has been characterized by various physicochemical characterization techniques (intrinsic viscosity measurement, FTIR spectroscopy, SEM morphology study and elemental analysis). FTIR spectroscopy confirmed that free radicals are formed on polysaccharide backbone by cleavage of 1°-OH bond, indicating microwave effect and not thermal decomposition as the cause of free radical generation. The application of the grafted product as flocculant for river water clarification, towards augmentation of drinking water supply has been investigated.  相似文献   
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Functional & Integrative Genomics - Zea mays defense response is well-crafted according to the physical and chemical weapons utilized by their invaders during the coevolutionary period. Maize...  相似文献   
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The common food additive carrageenan (CGN) predictably induces intestinal inflammation in animal models. Mechanisms of CGN-induced nuclear factor κB and interleukin-8 (IL-8) stimulation include an immune-mediated pathway involving toll-like receptor 4 (TLR4) and B-cell lymphoma/leukemia 10 (BCL10) and a reactive oxygen species (ROS)-mediated pathway. To determine how the structure of CGN contributes to its initiation of inflammation through these two distinct mechanisms, we treated CGNs with galactosidases and carrageenases (CGNases) and determined the impact on IL-8 secretion and BCL10 production. Hydrolysis of CGN by the enzyme α-1→(3,6)-galactosidase significantly reduced increases in IL-8 and BCL10, but other galactosidases tested, including α-1→6-galactosidase, β-1→4-galactosidase and β-1→3,6-galactosidase, had no effect. In contrast, specific κ-CGNases or ι-CGNases, which hydrolyze β-1,4-galactosidic bonds, produced increases in IL-8 and BCL10 attributable to increased exposure of the immunogenic α-1→3-galactosidic epitope of CGN to TLR4. These results were consistent with induction of innate immune response by an interaction of TLR4 with the unusual α-d-Gal-(1→3)-d-Gal epitope present in CGN. Activation of the ROS-mediated pathway was unaffected by treatment of κ-CGN with either κ-CGNase (3 mg/L), α-1→(3,6)-galactosidase (20 mU/ml) or these enzymes in combination, indicating that changes in IL-8 production were attributable to the effects of induction of inflammation on the TLR4–BCL10-mediated innate immune pathway. These findings provide new information about the specificity of carbohydrate–protein interaction between CGN and TLR4 and may help to devise treatments that modify the immune reactivity induced by carbohydrate antigens.  相似文献   
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Aging is associated with insulin resistance, often attributable to obesity and inactivity. Recent evidence suggests that skeletal muscle insulin resistance in aging is associated with mitochondrial alterations. Whether this is true of the senescent myocardium is unknown. Twelve young (Y, 4 years old) and 12 old (O, 11 years old) dogs, matched for body mass, were instrumented with left-ventricular pressure gauges, aortic and coronary sinus catheters, and flow probes on left circumflex artery. Before surgery, all dogs participated in a 6-wk exercise program. Dogs underwent measurements of hemodynamics and plasma substrates before and during a 2-h hyperinsulinemic-euglycemic clamp to measure whole body and myocardial glucose and nonesterified fatty acid uptake. Following the protocol, myocardial and skeletal samples were obtained to measure components of the insulin-signaling cascade and mitochondrial structure. There was no difference in plasma glucose (Y, 90 +/- 4 mg/dl; O, 87 +/- 4 mg/dl), but old dogs had higher (P < 0.02) nonesterified fatty acids (Y, 384 +/- 48 micromol/l; O, 952 +/- 97 micromol/l) and plasma insulin (Y, 39 +/- 11 pmol/l; O, 108 +/- 18 pmol/l). Old dogs had impaired total body glucose disposition (Y, 11.5 +/- 1 mg x kg(-1) x min(-1); O, 8.0 +/- 0.5 mg x kg(-1) x min(-1); P < 0.05) and insulin-stimulated myocardial glucose uptake (Y, 3.5 +/- 0.3 mg x min(-1) x g(-1); O, 1.8 +/- 0.3 mg x min(-1) x g(-1); P < 0.05). The impaired insulin action was associated with altered insulin signaling and glucose transporter (GLUT4) translocation. There were myocardial mitochondrial structural changes observed in association with decreased expression of uncoupling protein-3. Aging is associated with both whole body and myocardial insulin resistance, independent of obesity and inactivity, but involving altered mitochondrial structure and impaired cellular insulin action.  相似文献   
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