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991.
Comparative proteomic analysis of Helicobacter pylori strains associated with iron deficiency anemia
Park SA Lee HW Hong MH Choi YW Choe YH Ahn BY Cho YJ Kim DS Su Kim D Lee NG 《Proteomics》2006,6(4):1319-1328
Helicobacter pylori is known to cause chronic gastritis, peptic ulcer, and gastric cancer, and has also been linked to iron deficiency anemia (IDA). To determine whether H. pylori clinical isolates correlate with the prevalence of H. pylori-associated IDA, we compared the proteomic profiles of H. pylori strains isolated from antral biopsy specimens of H. pylori-positive patients with or without IDA. Fifteen strains, including eight non-IDA and seven IDA strains, were cultured under iron-rich and iron-depleted conditions and then analyzed for protein expression profiles by 2-DE. The distances between two H. pylori strains were determined on the basis of similarities between their expression patterns of 189 protein spots, and a phylogenetic tree was constructed. The results revealed that the IDA strains formed a cluster separate from that of six non-IDA strains, with two non-IDA strains between the clusters. H. pylori strain 26695 was located in the non-IDA cluster. Protein spots displaying similar expression patterns were clustered, and 18 spots predominantly expressed in IDA strains were identified by MALDI-TOF analysis. These data indicate that the non-IDA and IDA strains can be distinguished by their protein expression profiles, suggesting that the polymorphism of H. pylori strains may be one of the factors determining the occurrence of H. pylori-associated IDA. 相似文献
992.
We have developed a surface plasmon resonance (SPR)-based protein microarray to study protein-protein interactions in a high-throughput mode. As a model system, triple protein interactions have been explored with human papillomaviral E6 protein, tumor suppressor p53, and ubiquitin ligase E6AP. Human papillomavirus (HPV) is known to be a causative agent of cervical cancer. Upon infection, the viral E6 protein forms a heterotrimeric protein complex with p53 and E6AP. The formation of the complex eventually results in the degradation of p53. In the present study, a GST-fused E6AP protein was layered onto a glutathione (GSH)-modified gold chip surface. The specific binding of GST-E6AP protein onto the gold chip surface was facilitated through the affinity of GST to its specific ligand GSH. The interacting proteins (E6 and/or p53) were then spotted. Detection of the interaction was performed using a SPR imaging (SPRI) technique. The resulting SPRI intensity data showed that the protein-protein interactions of E6AP, E6, and p53 were detected in a concentration-dependent manner, suggesting that the SPRI-based microarray system can be an effective tool to study protein-protein interactions where multiple proteins are involved. 相似文献
993.
In this protocol we describe how to perform the Multi-Source Interference Task (MSIT), a validated functional magnetic resonance imaging (fMRI) task that reliably and robustly activates the cingulo-frontal-parietal cognitive/attention network (CFP network) within individual subjects. The MSIT can be used to (i) identify the cognitive/attention network in normal volunteers and (ii) test its integrity in people with neuropsychiatric disorders. It is simple to perform, can be completed in less than 15 min and is not language specific, making it appropriate for children, adults and the elderly. Since its validation, over 100 adults have performed the task. The MSIT produces a robust and temporally stable reaction time interference effect (range 200-350 ms), and single runs of the MSIT have produced CFP network activation in approximately 95% of tested subjects. The robust, reliable and temporally stable neuroimaging and performance data make the MSIT a useful task with which to study normal human cognition and psychiatric pathophysiology. 相似文献
994.
The Rey-Osterrieth Complex Figure Test (ROCF), which was developed by Rey in 1941 and standardized by Osterrieth in 1944, is a widely used neuropsychological test for the evaluation of visuospatial constructional ability and visual memory. Recently, the ROCF has been a useful tool for measuring executive function that is mediated by the prefrontal lobe. The ROCF consists of three test conditions: Copy, Immediate Recall and Delayed Recall. At the first step, subjects are given the ROCF stimulus card, and then asked to draw the same figure. Subsequently, they are instructed to draw what they remembered. Then, after a delay of 30 min, they are required to draw the same figure once again. The anticipated results vary according to the scoring system used, but commonly include scores related to location, accuracy and organization. Each condition of the ROCF takes 10 min to complete and the overall time of completion is about 30 min. 相似文献
995.
Pasarica M Shin AC Yu M Ou Yang HM Rathod M Jen KL MohanKumar S MohanKumar PS Markward N Dhurandhar NV 《Obesity (Silver Spring, Md.)》2006,14(11):1905-1913
Objective: Human adenovirus 36 (Ad‐36) increases adiposity and reduces serum lipids in chicken, mouse, and non‐human primate models, and it is linked to obesity in sero‐epidemiological studies in humans. Involvement of the central nervous system (CNS) or adipose tissue in the mechanism of Ad‐36‐induced adiposity is unknown. The effects of Ad‐36 on adiposity and on the neuroendocrine system were investigated in a rat model. Research Methods and Procedures: Five‐week‐old male Wistar rats were inoculated intraperitoneally with Ad‐36 or medium. Results: Despite similar food intakes, infected rats attained significantly greater body weight and fat pad weight by 30 weeks post‐inoculation. Epididymal‐inguinal, retroperitoneal, and visceral fat pad weights of the infected group were greater by 60%, 46%, and 86%, respectively (p < 0.00001). The fasting serum insulin level and homeostasis model assessment index indicated greater insulin sensitivity in the infected group. Visceral adipose tissue expression of glycerol 3‐phosphate dehydrogenase, peroxisome proliferator‐activated receptor γ, and CCAAT/enhancer‐binding protein α and β was markedly increased in the infected animals compared with controls. Ad‐36 decreased norepinephrine levels significantly in the paraventricular nucleus in infected vs. control rats (mean ± standard error, 8.9 ± 1.1 vs. 12.8 ± 1.2 pg/μg protein; p < 0.05). Ad‐36 markedly decreased serum corticosterone in infected vs. control rats (mean ± standard error, 97 ± 41.0 vs. 221 ± 111 ng/mL; p < 0.005). Discussion: The results suggest that the pro‐adipogenic effect of Ad‐36 may involve peripheral as well as central effects. The male Wistar rat is a good model for the elucidation of metabolic and molecular mechanisms of Ad‐36‐induced adiposity. 相似文献
996.
Kenichiro Shirao Satoshi Okada Go Tajima Miyuki Tsumura Keiichi Hara Shin’ichiro Yasunaga Motoaki Ohtsubo Ikue Hata Nobuo Sakura Yosuke Shigematsu Yoshihiro Takihara Masao Kobayashi 《Human genetics》2010,127(6):619-628
Short-chain acyl-CoA dehydrogenase (SCAD) is a mitochondrial enzyme involved in the β-oxidation of fatty acids. Genetic defect of SCAD was documented to cause clinical symptoms such as progressive psychomotor retardation, muscle hypotonia, and myopathy in early reports. However, clinical significance of SCAD deficiency (SCADD) has been getting ambiguous, for some variants in the ACADS gene, which encodes the SCAD protein, has turned out to be widely prevailed among general populations. Accordingly, the pathophysiology of SCADD has not been clarified thus far. The present report focuses on two suspected cases of SCADD detected through the screening of newborns by tandem mass spectrometry. In both subjects, compound heterozygous mutations in ACADS were detected. The mutated genes were expressed in a transient gene expression system, and the enzymatic activities of the obtained mutant SCAD proteins were measured. The activities of the mutant SCAD proteins were significantly lower than that of the wild-type enzyme, confirming the mechanism underlying the diagnosis of SCADD in both subjects. Moreover, the mutant SCAD proteins gave rise to mitochondrial fragmentation and autophagy, both of which were proportional to the decrease in SCAD activities. The association of autophagy with programed cell death suggests that the mutant SCAD proteins are toxic to mitochondria and to the cells in which they are expressed. The expression of recombinant ACADS-encoded mutant proteins offers a technique to evaluate both the nature of the defective SCAD proteins and their toxicity. Moreover, our results provide insight into possible molecular pathophysiology of SCADD. 相似文献
997.
Sun Mi Shin Kyu Suk Cho Min Sik Choi Sung Hoon Lee Seol-Heui Han Young-Sun Kang Hee Jin Kim Jae Hoon Cheong Chan Young Shin Kwang Ho Ko 《Neurochemical research》2010,35(7):976-985
In response to brain injury, microglia migrate and accumulate in the affected sites, which is an important step in the regulation
of inflammation and neuronal degeneration/regeneration. In this study, we investigated the effect of urokinase-type plasminogen
activator (uPA) on the BV-2 microglial cell migration. At resting state, BV-2 microglial cells secreted uPA and the release
of uPA was increased by ATP, a chemoattractant released from injured neuron. The migration of BV-2 cell was significantly
induced by uPA and inhibited by uPA inhibitors. In this condition, uPA increased the activity of matrix metalloproteinase
(MMP-9) and the inhibition of MMP activity with pharmacological inhibitors against either uPA (amiloride) or MMP (phenanthrolene
and SB-3CT) effectively prevented BV2 cell migration. Interestingly, the level of MMP-9 protein and mRNA in the cell were
not changed by uPA. These results suggest that the increase of MMP-9 activity by uPA is regulated at the post-translational
level, possibly via increased activation of the enzyme. Unlike the uPA inhibitor, plasmin inhibitor PAI-1 only partially inhibited
uPA-induced cell migration and MMP-9 activation. The incubation of recombinant MMP-9 with uPA resulted in the activation of
MMP-9. These results suggest that uPA plays a critical role in BV-2 microglial cell migration by activating pro-MMP-9, in
part by its direct action on MMP-9 and also in part by the activation of plasminogen/plasmin cascade. 相似文献
998.
Masanori Noguchi Tatsuyuki Kakuma Hirotsugu Uemura Yasutomo Nasu Hiromi Kumon Yasuhiko Hirao Fukuko Moriya Shigetaka Suekane Kei Matsuoka Nobukazu Komatsu Shigeki Shichijo Akira Yamada Kyogo Itoh 《Cancer immunology, immunotherapy : CII》2010,59(7):1001-1009
Personalized peptide vaccination (PPV) combined with chemotherapy could be a novel approach for many cancer patients. In this randomized study, we evaluated the anti-tumor effect and safety of PPV plus low-dose estramustine phosphate (EMP) as compared to standard-dose EMP for HLA-A2- or -A24-positive patients with castration resistant prostate cancer. Patients were randomized into groups receiving either PPV plus low-dose EMP (280 mg/day) or standard-dose EMP (560 mg/day). After disease progression, patients were switched to the opposite regime. The primary end point was progression-free survival (PFS). We randomly assigned 28 patients to receive PPV plus low-dose EMP and 29 patients to receive standard-dose EMP. Nineteen events in the PPV group and 20 events in the EMP group occurred during the first treatment. Median PFS for the first treatment was 8.5 months in the PPV group and 2.8 months in the EMP group with a hazard ratio (HR) of 0.28 (95% CI, 0.14–0.61; log-rank P = 0.0012), while there was no difference for median PFS for the second treatment. The HR for overall survival was 0.3 (95% CI, 0.1–0.91) in favor of the PPV plus low-dose EMP group (log-rank, P = 0.0328). The PPV plus low-dose EMP was well tolerated without major adverse effects and with increased levels of IgG and cytotoxic-T cell responses to the vaccinated peptides. PPV plus low-dose EMP was associated with an improvement in PSA-based PFS as compared to the standard-dose EMP alone. 相似文献
999.
In Koo Hwang Sun Shin Yi Jae Hoon Shin Ki-Yeon Yoo Jung Hoon Choi Choong Hyun Lee Je Kyung Seong Yeo Sung Yoon Jeong Ho Park Moo-Ho Won 《Neurochemical research》2010,35(3):465-472
In the present study, we observed the effects of cyclosporine A (CsA), an efficient immunosuppressant, on cell proliferation
and neuroblast differentiation in the subgranular zone of the dentate gyrus (SZDG) in normal C57BL/6 mice using Ki67 and doublecortin
(DCX) immunohistochemical staining, respectively. At 8 weeks of age, vehicle (physiological saline) or CsA was daily administered
(40 mg/kg, i.p.) for 1 week. Animals were sacrificed at 2 weeks after last administration. CsA treatment did not show any
influences in neurons, astrocytes and microglia based on immunohistochemistry for its markers, respectively. However, in the
CsA-treated group, Fluoro-Jade B, a marker for neurodegeneration, positive cells were found in the SZDG, not in the vehicle-treated
group. In the vehicle-treated group, Ki67 immunoreactive (+) nuclei were clustered in the SZDG, whereas in the CsA-treated group Ki67+ nuclei were scattered in the SZDG, showing no difference in cell numbers. Numbers of DCX+ neuroblasts with well-developed processes (tertiary dendrites) were much lower in the CsA-treated group than those in the
vehicle-treated group; however, numbers of DCX+ neuroblasts with secondary dendrites were similar in both the groups. These results suggest that CsA significantly reduces
dendritic outgrowth and complexity from neuroblasts in the SZDG without any affecting in neurons, astrocytes and microglia
in normal mice. 相似文献
1000.
Hyung‐Ju Cho Jae Young Choi Yu‐Mi Yang Jeong Hee Hong Chang‐Hoon Kim Heon Young Gee Hyun Jae Lee Dong Min Shin Joo‐Heon Yoon 《Journal of cellular biochemistry》2010,109(6):1254-1263
Adequate fluid secretion from airway mucosa is essential for maintaining mucociliary clearance, and fluid hypersecretion is a prominent feature of inflammatory airway diseases such as allergic rhinitis. House dust mite extract (HDM) has been reported to activate protease‐activated receptors (PARs), which play various roles in airway epithelia. However, the role of HDM in regulating ion transporters and fluid secretion has not been investigated. We examined the effect of HDM on ion transport in human primary nasal epithelial cells. The Ca2+‐sensitive dye Fura2‐AM was used to determine intracellular Ca2+ concentration ([Ca2+]i) by means of spectrofluorometry in human normal nasal epithelial cells (NHNE). Short‐circuit current (Isc) was measured using Ussing chambers. Fluid secretion from porcine airway mucosa was observed by optical measurement. HDM extract (10 µg/Ml) effectively cleaved the PAR‐2 peptide and induced an increase of [Ca2+]i that was abolished by desensitization with trypsin, but not with thrombin. Apical application of HDM‐induced Isc sensitive to both a cystic fibrosis transmembrane conductance regulator (CFTR) inhibitor and a Ca2+‐activated Cl? channel (CaCC) inhibitor. HDM extract also stimulated fluid secretion from porcine airway mucosa. HDM extract activated PAR‐2 and apical Cl? secretion via CaCC and CFTR, and HDM‐induced fluid secretion in porcine airway mucosa. Our results suggest a role for PAR‐2 in mucociliary clearance and fluid hypersecretion of airway mucosa in response to air‐borne allergens such as HDM. J. Cell. Biochem. 109: 1254–1263, 2010. © 2010 Wiley‐Liss, Inc. 相似文献