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991.
M. R. Mulloy M. Tan J. H. Wolf S. H. D'Annunzio H. S. Pollinger 《American journal of transplantation》2014,14(12):2883-2886
Minimally invasive surgery for removal of a failed renal allograft has not previously been reported. Herein, we report the first robotic trans‐abdominal transplant nephrectomy (TN). A 34‐year‐old male with Alport's syndrome lost function of his deceased donor allograft after 12 years and presented with fever, pain over his allograft and hematuria. The operation was performed intra‐abdominally using the Da Vinci Robotic Surgical System with four trocars. The total operative time was 235 min and the estimated blood loss was less than 25 cm3. There were no peri‐operative complications observed and the patient was discharged to home less than 24 h postoperatively. The utilization of robotic technology facilitated the successful performance of a minimally invasive, trans‐abdominal TN. 相似文献
992.
M. Haas B. Sis L. C. Racusen K. Solez D. Glotz R. B. Colvin M. C. R. Castro D. S. R. David E. David‐Neto S. M. Bagnasco L. C. Cendales L. D. Cornell A. J. Demetris C. B. Drachenberg C. F. Farver A. B. Farris III I. W. Gibson E. Kraus H. Liapis A. Loupy V. Nickeleit P. Randhawa E. R. Rodriguez D. Rush R. N. Smith C. D. Tan W. D. Wallace M. Mengel as the Banff meeting report writing committee 《American journal of transplantation》2014,14(2):272-283
993.
目的 利用Meta分析方法定量比较光面乳房假体和毛面乳房假体隆乳术后的包膜挛缩发生率.方法 以breast augmentation、capsular contracture、smooth implant、textured implant、隆乳、乳房假体等检索词在MEDLINE数据库、EMBASE数据库、Cochrane图书馆、中国生物医学文献数据库、维普生物数据库等检索,最大限度地收集毛面乳房假体和光面乳房假体隆乳的文献,提取其包膜挛缩和其他并发症的数据进行整合,以获得比值比(odds ratio,OR)合并值.各合并数据使用RevMan 5.2软件进行分析.结果 对11项研究毛面乳房假体和光面乳房假体的临床对照试验进行Meta分析后得出,包膜挛缩发生率的合并OR值为0.32,95%可信区间(CI)为0.18~0.58,P=0.0002.除包膜挛缩外,其他并发症发生率的合并OR值为1.31,95% CI为0.96~1.77,P=0.09.结论 毛面乳房假体隆乳术后发生包膜挛缩风险低于光面乳房假体. 相似文献
994.
Zhong-Bao Yang Bin Tan Ting-Bo Li Zheng Lou Jun-Lin Jiang Ying-Jun Zhou Jie Yang Xiu-Ju Luo Jun Peng 《Naunyn-Schmiedeberg's archives of pharmacology》2014,387(9):861-871
Vitexin compound B-1 (VB-1) is a novel member of the vitexins family isolated from the seeds of the Chinese herb Vitex negundo. This study aims to investigate whether VB-1 is able to protect nerve cells against oxidative injury and whether the antioxidative effects of VB-1 occur through a mechanism involving the inhibition of NADPH oxidase (NOX) in a manner of hypoxia-inducible factor 1α (HIF-1α)-dependent. To establish a neuronal in vitro model of oxidative stress, the differentiated PC12 cells were subjected to 5 h of hypoxia followed by 20 h of reoxygenation (H/R). Three dosages of VB-1 (10?8, 10?7, and 10?6 M) were chosen to evaluate the effect of VB-1 on H/R-induced injury and the underlying mechanisms. At the end of the experiments, culture mediums and cells were collected for analysis of cellular apoptosis, lactate dehydrogenase (LDH) and caspase 3/7-like activities, reactive oxygen species (ROS) levels, 4-hydroxynonenal (4-HNE) and malondialdehye (MDA) contents, and HIF-1α and NOX expression, respectively. Our results showed that cell injury (indicated by apoptosis ratio, caspase 3/7-like activity, and LDH release), oxidative stress (indicated by ROS production, 4-HNE, and MDA contents), NOX activity, and NOX expression (NOX2 and NOX4 isoforms) were dramatically increased in PC12 cells following H/R, which were attenuated in the presence of VB-1 at dosage of 10?7 or 10?6 M. There was no significant change in HIF-1α expression in all experimental groups. These results provide evidence that VB-1 is able to protect the PC12 cells against H/R-induced injury through a mechanism involving the suppression of NOX expression and subsequent reduction of ROS production. The effect of VB-1 on H/R-induced NOX expression is independent on HIF-1α inhibition. 相似文献
995.
Huibing Tan Laura G. Rosen Garye A. Ng Walter J. Rushlow Steven R. Laviolette Addiction Research Group 《Psychopharmacology》2014,231(24):4669-4679
Rationale
N-Methyl-d-aspartate (NMDA) receptors in the medial prefrontal cortex (mPFC) are involved in opiate reward processing and modulate sub-cortical dopamine (DA) activity. NMDA receptor blockade in the prelimbic (PLC) division of the mPFC strongly potentiates the rewarding behavioural properties of normally sub-reward threshold doses of opiates. However, the possible functional interactions between cortical NMDA and sub-cortical DAergic motivational neural pathways underlying these effects are not understood.Objective
This study examines how NMDA receptor modulation in the PLC influences opiate reward processing via interactions with sub-cortical DAergic transmission. We further examined whether direct intra-PLC NMDA receptor modulation may activate DA-dependent opiate reward signaling via interactions with the ventral tegmental area (VTA).Methods
Using an unbiased place conditioning procedure (CPP) in rats, we performed bilateral intra-PLC microinfusions of the competitive NMDA receptor antagonist, (2R)-amino-5-phosphonovaleric acid (AP-5), prior to behavioural morphine place conditioning and challenged the rewarding effects of morphine with DA receptor blockade. We next examined the effects of intra-PLC NMDA receptor blockade on the spontaneous activity patterns of presumptive VTA DA or GABAergic neurons, using single-unit, extracellular in vivo neuronal recordings.Results
We show that intra-PLC NMDA receptor blockade strongly activates sub-cortical DA neurons within the VTA while inhibiting presumptive non-DA GABAergic neurons. Behaviourally, NMDA receptor blockade activates a DA-dependent opiate reward system, as pharmacological blockade of DA transmission blocked morphine reward only in the presence of intra-PLC NMDA receptor antagonism.Conclusions
These findings demonstrate a cortical NMDA-mediated mechanism controlling mesolimbic DAergic modulation of opiate reward processing. 相似文献996.
Xiang Yang Zhang Da Chun Chen Yun Long Tan Mei Hong Xiu Jingyi Cui Li Hui Fu De Yang Thomas R Kosten 《Psychopharmacology》2014,231(1):305-314
Objective
Despite higher smoking rates in schizophrenia, few studies have explored the clinical–demographic correlates of different amounts of smoking exposure. Little is known about the association between smoking severity and clinical phenotypes in Chinese patients with schizophrenia.Materials and methods
We investigated differences between heavy (≥1 pack/day) and non-heavy (<1 pack/day) smoking in 550 male inpatients with schizophrenia using clinician-administered questionnaires and the Fagerstrom Test for Nicotine Dependence. They also were rated on the Positive and Negative Symptom Scale (PANSS), the Simpson and Angus Extrapyramidal Symptom Rating Scale (SAES), and the Abnormal Involuntary Movement Scale (AIMS), as well as were assayed with laboratory tests and an electrocardiogram.Results
Heavy smoking prevalence was approximately 31 %. Compared to the non-heavy smokers, the heavy smokers were younger, more with paranoid subtype but less with disorganized subtype schizophrenia, smoked at an earlier age, fewer getting clozapine or all atypical antipsychotics together, and were taking larger doses of antipsychotic drugs. The heavy smokers scored significantly lower on the PANSS negative symptom subscore and total score, and also on the SAES and AIMS scores than the non-heavy smokers. In addition, heavy smokers displayed longer rate-corrected electrocardiographic QT intervals, but without any significant differences in other laboratory tests.Conclusion
Our results suggest several clinical or demographic differences between the heavy and non-heavy smoking patients with schizophrenia in a Chinese population. Heavy smoking remains a general health risk for schizophrenia. 相似文献997.
Xia Yin Shanshan Zhou Yang Zheng Yi Tan Maiying Kong Bo Wang Wenke Feng Paul N. Epstein Jun Cai Lu Cai 《Toxicology and applied pharmacology》2014
Obstructive sleep apnea (OSA) causes chronic intermittent hypoxia (IH) to induce cardiovascular disease, which may be related to oxidative damage. Metallothionein (MT) has been extensively proved to be an endogenous and highly inducible antioxidant protein expressed in the heart. Therefore, we tested the hypotheses that oxidative stress plays a critical role in OSA induced cardiac damage and MT protects the heart from OSA-induced cardiomyopathy. To mimic hypoxia/reoxygenation events that occur in adult OSA patients, mice were exposed to IH for 3 days to 8 weeks. The IH paradigm consisted of alternating cycles of 20.9% O2/8% O2 FIO2 (30 episodes per hour) with 20 s at the nadir FIO2 for 12 h a day during daylight. IH significantly increased the ratio of heart weight to tibia length at 4 weeks with a decrease in cardiac function from 4 to 8 weeks. Cardiac oxidative damage and fibrosis were observed after 4 and 8 weeks of IH exposures. Endogenous MT expression was up-regulated in response to 3-day IH, but significantly decreased at 4 and 8 weeks of IH. In support of MT as a major compensatory component, mice with cardiac overexpression of MT gene and mice with global MT gene deletion were completely resistant, and highly sensitive, respectively, to chronic IH induced cardiac effects. These findings suggest that chronic IH induces cardiomyopathy characterized by oxidative stress-mediated cardiac damage and the antioxidant MT protects the heart from such pathological and functional changes. 相似文献
998.
Wei Gong Erling Hu Huan Dou Yuxian Song Liu Yang Jianjian Ji Erguang Li Renxiang Tan Yayi Hou 《British journal of pharmacology》2014,171(21):4866-4878
Background and Purpose
Sepsis is a clinical condition characterized by overwhelming systemic inflammation with high mortality rate and high prevalence, but effective treatment is still lacking. Toll-like receptor 3 (TLR3) is an endogenous sensor, thought to regulate the amplification of immune response during sepsis. Modulators of TLR3 have an advantage in the treatment of sepsis. Here, we aimed to explore the mechanism of a monosubstituted 1,2-benzenediamine derivative FC-99 {N1-[(4-methoxy)methyl]-4-methyl-1,2-benzenediamine}on modulating TLR3 expression and its therapeutic potential on mouse model of sepsis.Experimental Approach
Cells were pretreated with FC-99 followed by poly(I:C) or IFN-α stimulation; TLR3 and other indicators were assayed. Female C57BL/6 mice were subjected to sham or caecal ligation puncture (CLP) surgery after i.p. injection of vehicle or FC-99; serum and tissues were collected for further experiments.Key Results
FC-99 suppressed inflammatory response induced by poly(I:C) with no effect on cell viability or uptake of poly(I:C). FC-99 also inhibited TLR3 expression induced by not only poly(I:C) but also by exogenous IFN-α. This inhibition of FC-99 was related to the poly(I:C)-evoked IRF3/IFN-α/JAK/STAT1 signalling pathway. In CLP-induced model of sepsis, FC-99 administration decreased mice mortality and serum levels of inflammatory factors, attenuated multiple organ dysfunction and enhanced bacterial clearance. Accordingly, systemic and local expression of TLR3 was reduced by FC-99 in vivo.Conclusion and Implications
FC-99 reversed TLR3 expression and ameliorate CLP-induced sepsis in mice. Thus, FC-99 will be a potential therapeutic candidate for sepsis.Table of LinksTARGETS | LIGANDS | |
IFNAR1, interferon α/β receptor 1 | CCL5 | IL-6 |
TLR3, Toll-like receptor 3 | Eritoran | Poly I:C |
JAK, Janus kinase | IFN-α | TNF-α |
999.
1000.