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991.
Constance Duchesne Sébastien Banzet Jean-Jacques Lataillade Antoine Rousseau Nadira Frescaline 《The Journal of pathology》2019,249(3):368-380
Treatment with cold atmospheric plasma (CAP) has been reported to promote wound healing in animals. However, how this process is mediated remains unclear. In this study we examined the mechanisms which underlie the improved wound healing effects of CAP and the roles of associated reactive oxygen and nitrogen species (RONS), which are generated by plasma. By using in vitro models which mimicked various steps of angiogenesis, we demonstrated that CAP triggered the production of nitric oxide (NO), and enhanced cell migration and the assembly of endothelial cells into vessel-like structures. These are both hallmarks of the proliferative phase of wound healing. Using a mouse model of a third-degree burn wound, we went on to show that CAP treatment was associated with enhanced angiogenesis, characterised by accelerated in vivo wound healing and increased cellular proliferation. Here, CAP significantly increased the in vivo production of endothelial NO synthase (eNOS), an enzyme that catalyses NO synthesis in endothelial cells, and significantly increased the expression of pro-angiogenic PDGFRβ and CD31 markers in mouse wounds. Mechanistically, we showed that CAP induced eNOS phosphorylation and activation, thereby increasing the levels of endogenous NO in endothelial cells. Increased NO generation facilitated by CAP further stimulated important pro-angiogenic VEGFA/VEGFR2 signalling in vitro. This proof-of-concept study may guide future efforts aimed at addressing the use of physical plasma and its therapeutic applications in a variety of pathological scenarios. © 2019 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. 相似文献
992.
993.
Egemen Altan Kerem Aydin Omer Erkocak Hakan Senaran Serdar Ugras 《International orthopaedics》2014,38(6):1321-1328
Purpose
This study investigated the efficacy of platelet-rich plasma (PRP) on articular surfaces on which the mosaicplasty technique was performed. Our hypothesis was that PRP can accelerate the osseointegration process and enhance the quality of articular integrity after the mosaicplasty procedure.Methods
Standard defects were created in the femoral groove of both patellofemoral joints of 12 New Zealand rabbits. PRP solution was placed inside the defect before fixation of the osteochondral autografts and injected inside the involved joint after capsular closure of the tested knees. The contralateral knees served as the control sides. The animals were euthanized three or six weeks after mosaicplasty, and both limbs were assessed according to Pineda’s histological grading scale. Significance level was set at p ≤ 0.05 a priori, and the Mann–Whitney U test was used for statistical analysis.Results
Histologic findings at the interface between the transferred autograft and the original cartilage revealed better integration of the adjacent surfaces in the mosaicplasty with PRP group three weeks after the procedure; the difference was significant (p < 0.05). However, no significant difference in the transition zone was observed between the groups six weeks after the experiment (p = 0.59).Conclusions
Our animal model showed that adjunctive use of PRP produced a better healing response and resulted in superior histological scores after three weeks compared with the mosaicplasty-only procedure. Interpretation of our results is important in terms of rapid return to previous activity levels. Thus, application of PRP can represent a valid therapeutic option for improving the efficacy of mosaicplasty by stimulating the local healing response. 相似文献994.
Ho‐Joong Kim Jin S. Yeom Yong‐Gon Koh Jee‐Eun Yeo Kyoung‐Tak Kang Young‐Mi Kang Bong‐Soon Chang Choon‐Ki Lee 《Journal of orthopaedic research》2014,32(4):551-556
The purpose of this study was to investigate the anti‐inflammatory effect of platelet‐rich plasma (PRP) with collagen matrix on human nucleus pulposus (NP) cell in response to pro‐inflammatory cytokines such as tumor necrosis factor‐alpha (TNF‐α) and interleukin‐1 (IL‐1). NP cells from human disks were cultured in a monolayer and maintained in the collagen matrix prior to the addition of recombinant human IL‐1 and TNF‐α. After applying IL‐1 and TNF‐α, PRP prepared by using a commercially available platelet concentration system was added. The response was investigated using real‐time PCR for mRNA expression of type II collagen, aggrecan, matrix metalloproteinase‐3 (MMP‐3), and cyclooxygenase‐2 (COX‐2). The combination of IL‐1β and TNF‐α led to decrease of matrix synthesis gene expression such as collagen type II and aggrecan and increase of the degradation gene expression of COX‐2 and MMP‐3, compared to the control. Consecutive PRP exposure significantly recovered the down‐regulated gene expression of collagen type II and aggrecan and significantly reduced the increased MMP‐3 and COX‐2 gene expression, compared to that of control groups with pro‐inflammatory cytokines. The administration of PRP with collagen matrix markedly suppressed cytokine‐induced pro‐inflammatory degrading enzymes and mediators in the NP cell. It also rescued gene expression concerning matrix synthesis, thereby stabilizing NP cell differentiation. © 2013 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 32:551–556, 2014. 相似文献
995.
996.
Krista O'Shaughnessey Andrea Matuska Jacy Hoeppner Jack Farr Mark Klaassen Christopher Kaeding Christian Lattermann William King Jennifer Woodell‐May 《Journal of orthopaedic research》2014,32(10):1349-1355
The objective of this clinical study was to test if blood from osteoarthritis (OA) patients (n = 105) could be processed by a device system to form an autologous protein solution (APS) with preferentially increased concentrations of anti‐inflammatory cytokines compared to inflammatory cytokines. To address this objective, APS was prepared from patients exhibiting radiographic evidence of knee OA. Patient metrics were collected including: demographic information, medical history, medication records, and Knee Injury and Osteoarthritis Outcome Score (KOOS) surveys. Cytokine and growth factor concentrations in whole blood and APS were measured using enzyme‐linked immunosorbent assays. Statistical analyses were used to identify relationships between OA patient metrics and cytokines. The results of this study indicated that anti‐inflammatory cytokines were preferentially increased compared to inflammatory cytokines in APS from 98% of OA patients. APS contained high concentrations of anti‐inflammatory proteins including 39,000 ± 20,000 pg/ml IL‐1ra, 21,000 ± 5,000 pg/ml sIL‐1RII, 2,100 ± 570 pg/ml sTNF‐RI, and 4,200 ± 1,500 pg/ml sTNF‐RII. Analysis of the 82 patient metrics indicated that no single patient metric was strongly correlated (R2 > 0.7) with the key cytokine concentrations in APS. Therefore, APS can be prepared from a broad range of OA patients. © 2014 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 32:1349–1355, 2014. 相似文献
997.
Roza Chaireti Rupesh Rajani Annika Bergquist Tor Melin Inga-Lill Friis-Liby Marjo Kapraali Stergios Kechagias Tomas L. Lindahl Sven Almer 《Thrombosis research》2014
Introduction
In recent years there have been increasing evidence associating liver disease with hypercoagulability, rather than bleeding. The aim of the study was to evaluate the haemostatic potential in patients with liver disease.Patients and methods
We measured thrombin generation in the presence and absence of thrombomodulin in patients with portal vein thrombosis (PVT, n = 47), Budd-Chiari syndrome (BCS, n = 15) and cirrhosis (n = 24) and compared the results to those obtained from healthy controls (n = 21). Fifteen patients with PVT and 10 patients with BCS were treated with warfarin and were compared to an equal number of patients with atrial fibrillation matched for prothrombin time-international normalized ratio. We assessed resistance to thrombomodulin by using ratios [marker measured in the presence/absence of thrombomodulin].Results
There were no differences in thrombin generation between patients on warfarin treatment and their controls. Cirrhotic patients generated more thrombin in the presence of thrombomodulin and exhibited thrombomodulin resistance compared to controls [p = 0.006 for endogenous thrombin potential (ETP) and p < 0.001 for peak thrombin and both ratios ETP and peak] and patients with non-cirrhotic PVT (p = 0.001, p = 0.006, p < 0.001, p < 0.001 for ETP, peak, ratio ETP, ratio peak, respectively). The patients with cirrhotic PVT exhibited higher ETP (p = 0.044) and peak (p = 0.02) in the presence of thrombomodulin than controls, as well as thrombomodulin resistance (ETP and peak ratios: p = 0.001).Conclusions
Hypercoagulability and thrombomodulin resistance in patients with cirrhosis were independent of the presence of splanchnic vein thrombosis. The hypercoagulability in patients with cirrhotic PVT could have implications for considering longer or more intensive treatment with anticoagulants in this group. 相似文献998.
Joseph A. Jakubowski Dominick J. Angiolillo Chunmei Zhou David S. Small Brian A. Moser Jurrien M. ten Berg Patricia B. Brown Stefan James Kenneth J. Winters David Erlinge 《Thrombosis research》2014
Introduction
Patients treated with clopidogrel who have higher body size exhibit greater platelet reactivity than patients with lower body size. In a retrospective analysis of the FEATHER trial, we examined the relationship between platelet response to thienopyridines clopidogrel 75 mg (Clop-75), prasugrel 5 mg (Pras-5), and prasugrel 10 mg (Pras-10) using 3 body size indices: body weight (BW), body mass index (BMI), and body surface area (BSA). Relationships were assessed as continuous variables and as 4 incremental body size groups.Materials and Methods
Aspirin-treated patients with stable coronary artery disease (N = 72) and a BW range of 45-134 kg received Clop-75, Pras-5, and Pras-10 in a 3-period, blinded, cross-over study. Platelet assays included maximum platelet aggregation (MPA) to 20 μM ADP by light transmission aggregometry, VerifyNow-P2Y12 reaction units (PRU), and vasodilator-associated stimulated phosphoprotein (VASP) phosphorylation platelet reactivity index (PRI). Exposure to active metabolites (AMs) was also assessed.Results
Body size was a determinant of AM exposure and residual platelet reactivity regardless of type and dose of thienopyridine. BW and BSA demonstrated marginally stronger correlations with platelet reactivity; VASP-PRI demonstrated a stronger correlation with the body size than the other tests. Correlation coefficients ranged from a high of 0.64 (BW vs. PRI on Pras-5) to a low of 0.34 (BMI vs. MPA on Pras-10), but all were statistically significant (p < 0.01).Conclusions
Using a comprehensive selection of body size indices, AM exposures, platelet function tests, and thienopyridine doses, we demonstrated a consistent inverse relationship between body size and response to clopidogrel and prasugrel. 相似文献999.
Yuanyuan Zheng Limin Wang Zhixiang Zhu Xinxin YanLane Zhang Pingxiang XuDali Luo 《Thrombosis research》2014
Introduction
Downregulation of calsequestrin (CSQ), a major Ca2 + storage protein, may contribute significantly to the hyperactivity of internal Ca2 + ([Ca2 +]i) in diabetic platelets. Here, we investigated changes in CSQ-1 abundance, Ca2 + signaling and aggregation responses to stimulation with the progression of diabetes, especially the mechanism(s) underlying the exaggerated Ca2 + influx in diabetic platelets.Materials and methods
Type 1 diabetes was induced by streptozotocin in rats. Platelet [Ca2 +]i and aggregation responses upon ADP stimulation were assessed by fluorescence spectrophotometry and aggregometry, respectively. CSQ-1 expression was evaluated using western blotting.Results
During the 12-week course of diabetes, the abundance of CSQ-1, basal [Ca2 +]i and ADP-induced Ca2 + release were progressively altered in diabetic platelets, while the elevated Ca2 + influx and platelet aggregation were not correlated with diabetes development. 2-Aminoethoxydiphenyl borate, the store-operated Ca2 + channel blocker, almost completely abolished ADP-induced Ca2 + influx in normal and diabetic platelets, whereas nifedipine, an inhibitor of the nicotinic acid adenine dinucleotide phosphate receptor, showed no effect. Additionally, inhibition of Na+/Ca2 + exchange induced much slower Ca2 + extrusion and more Ca2 + influx in normal platelets than in diabetic platelets. Furthermore, under the condition of Ca2 +-ATPase inhibition, ionomycin caused greater Ca2 + mobilization and Ca2 + influx in diabetic platelets than in normal platelets.Conclusions
These data demonstrate that platelet hyperactivity in diabetes is caused by several integrated factors. Besides the downregulation of CSQ-1 that mainly disrupts basal Ca2 + homeostasis, insufficient Na+/Ca2 + exchange also contributes, at least in part, to the hyperactive Ca2 + response to stimulation in diabetic platelets. 相似文献1000.
Javier Merayo-Chalico Roberta Demichelis-Gómez Sandra Rajme-López Luis Aparicio-Vera Ana Barrera-Vargas Jorge Alcocer-Varela Diana Gómez-Martín 《Thrombosis research》2014