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目的 探讨间歇性腹膜透析对长期维持腹膜透析患者尿毒症脑病的治疗效果。方法 选择2013年1月-2018年12月本院肾内科长期维持腹膜透析出现尿毒症脑病患者46 例,并随机分为持续性不卧床腹膜透析(Continuous ambulatory peritoneal dialysis,CAPD)组及间歇性腹膜透析(Intermittent peritoneal dialysis,IPD)组,在治疗前及治疗7 d后分别采血进行血肌酐(Scr)、尿素氮(BUN)、甲状旁腺激素(iPTH)、白细胞介素6(IL-6)、β2微球蛋白(β2-MG)、超敏C反应蛋白(CRP)水平的检测,采用阳性与阴性症状量表评分表(PAN - SS)评价患者的疗效。结果 CAPD组治疗后血BUN、Scr、iPTH、IL-6、β2-MG、CRP水平与治疗前比较无明显变化(P>0.05); IPD组治疗后血BUN、Scr水平与治疗前比较无明显变化(P>0.05),而iPTH、IL-6、β2-MG、CRP水平较治疗前明显下降(P<0.05); 治疗后IPD组iPTH、IL-6、β2-MG、CRP水平与CAPD组比较有明显差异(P<0.05); PAN-SS显示,IPD组与CAPD组阳性症状、阴性症状、一般精神症状等方面均有明显差异(P<0.05); CAPD组无效8例,好转12例,显著进步4例,基本痊愈2例; IPD组无效2例,好转14例,显著进步5例,基本痊愈5例。结论 规律腹膜透析患者出现尿毒症脑病时应用间歇性腹膜透析治疗效果优于持续不卧床腹膜透析 相似文献
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Aim: We report two patients with Panayiotopoulos syndrome (PS) who developed encephalopathy related to status epilepticus during slow sleep (ESES) at the peak of their clinical course. Methods: Clinical charts and EEG data were reviewed. Results: The patients exhibited nocturnal autonomic seizures and occipital EEG foci, the latter of which later evolved into multifocal EEG foci with synchronous frontopolar and occipital spikes (Fp‐O EEG foci), and finally into continuous spikes‐waves during sleep (CSWS; spike‐wave index >85% based on whole‐night sleep recording) at eight years and seven years of age, respectively. The occipital spikes always preceded frontopolar spikes by 30~50 mseconds based on the analysis of CSWS. Neuropsychological ability, including IQ, deteriorated during the CSWS period in both patients. The autonomic seizures and focal to bilateral tonic‐clonic seizures were initially resistant to antiepileptic drugs (AEDs), and occurred more than 10 times in both patients. However, the seizures and EEG findings gradually resolved, and AEDs were successfully terminated in both patients. Conclusion: PS can progress to ESES if the clinical course exhibits atypical evolution. The initial autonomic symptom of the seizures and interictal Fp‐O EEG foci should be carefully monitored in patients with CSWS or ESES. 相似文献
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Melatonin alleviates brain injury in mice subjected to cecal ligation and puncture via attenuating inflammation,apoptosis, and oxidative stress: the role of SIRT1 signaling 下载免费PDF全文
Lei Zhao Rui An Yang Yang Xiangmin Yang Haixiao Liu Liang Yue Xia Li Yan Lin Russel J. Reiter Yan Qu 《Journal of pineal research》2015,59(2):230-239
Sepsis is a systemic inflammatory response to infection that causes severe neurological complications. Previous studies have suggested that melatonin is protective during sepsis. Additionally, silent information regulator 1 (SIRT1) was reported to be beneficial in sepsis. However, the role of SIRT1 signaling in the protective effect of melatonin against septic encephalopathy remains unclear. This study aimed to investigate the role of SIRT1 in the protective effect of melatonin. EX527, a SIRT1 inhibitor, was used to reveal the role of SIRT1 in melatonin's action. Cecal ligation and puncture or sham operation was performed in male C57BL/6J mice. Melatonin was administrated intraperitoneally (30 mg/kg). The survival rate of mice was recorded for the 7‐day period following the sham or CLP operation. The blood–brain barrier (BBB) integrity, brain water content, levels of inflammatory cytokines (TNF‐α, IL‐1β, and HMGB1), and the level of oxidative stress (superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA)) and apoptosis were assessed. The expression of SIRT1, Ac‐FoxO1, Ac‐p53, Ac‐NF‐κB, Bcl‐2, and Bax was detected by Western blot. The results suggested that melatonin improved survival rate, attenuated brain edema and neuronal apoptosis, and preserved BBB integrity. Melatonin decreased the production of TNF‐α, IL‐1β, and HMGB1. Melatonin increased the activity of SOD and CAT and decreased the MDA production. Additionally, melatonin upregulated the expression of SIRT1 and Bcl‐2 and downregulated the expression of Ac‐FoxO1, Ac‐p53, Ac‐NF‐κB, and Bax. However, the protective effects of melatonin were abolished by EX527. In conclusion, our results demonstrate that melatonin attenuates sepsis‐induced brain injury via SIRT1 signaling activation. 相似文献
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《Annals of hepatology》2020,19(2):190-196
Introduction and objectivesZinc deficiency has been associated with poor prognosis in chronic liver disease. This systematic review and meta-analysis aimed to evaluate the role of zinc supplementation in the management of chronic liver diseases.Materials and methodsWe searched MEDLINE, LILACS, EMBASE, and Cochrane CENTRAL databases from inception to August 2018. We included randomized controlled trials evaluating adult patients with chronic liver disease of any etiology receiving zinc supplementation. Studies with other designs or evaluating chronic conditions other than liver disease were excluded. Two reviewers independently screened and extracted data from eligible studies. Study quality was assessed using the Cochrane Collaboration's tool for assessing risk of bias in randomized studies.ResultsOf 1315 studies screened, 13 were included. Six assessed chronic hepatitis C treatment, with a relative risk of 0.83 indicating no protective effect of zinc supplementation on the improvement of sustained virological response. Three evaluated response to hepatic encephalopathy treatment, with a relative risk of 0.66 indicating a favorable effect of zinc supplementation on clinical improvement of this condition. Of four studies evaluating the management of cirrhosis, two analyzed the effect of zinc supplementation on serum albumin levels, with no statistical difference between zinc and placebo groups.ConclusionsClinical trials assessing zinc supplementation in liver diseases do not show benefits in terms of clinical improvement or disease halting. There are possible benefits of zinc supplementation on hepatic encephalopathy, however, this is based on limited evidence. This research question is still open for evaluation in larger, well-designed, clinical trials. 相似文献