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IntroductionSerum levels of FGF23 have been associated with adverse outcomes in cardiovascular diseases in patients with and without impaired renal function. Hence, this study aimed to explore the prognostic relevance of intact FGF23 (iFGF23) and its derivate C-terminal FGF23 (cFGF23) in patients undergoing transcatheter aortic valve replacement (TAVR) with regard to renal function.MethodsA total of 274 patients undergoing transfemoral TAVR were enrolled in this study. Blood samples were obtained preinterventionally and analyzed for iFGF23 and cFGF23 by means of enzyme linked immunosorbent assay (ELISA). Follow-up was obtained for 12 months.ResultsSerum levels of cFGF23 and iFGF23 both correlated positively with serum creatinine and inversely with estimated glomerular filtration rate (eGFR). Cox regression analysis revealed a significant association of cFGF23 with 1-year-mortality in patients with eGFR ≥45ml/min/1.73m², but not in patients with an eGFR <45ml/min/1.73m². A cut-off was calculated for cFGF23 (6.82 pmol/l) and patients with eGFR ≥45ml/min/1.73m² were retrospectively divided into two groups (above/below cut-off). Patients above the cut-off had a significantly worse 1-year-mortality than patients below the cut-off (33.3% vs. 19.6%; OR 2.05 (95%CI 1.03-4.07), p= 0.038). The association of cFGF23 with 1-year-mortality in patients with eGFR ≥45ml/min/1.73m² remained statistically significant even after correction for possible confounders in a multivariate Cox regression analysis.ConclusioncFGF23 could be an individual risk factor for mortality in patients undergoing TAVR with an eGFR ≥45ml/min/1.73m². 相似文献
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上腔静脉起源快速心律失常的电生理特征和射频消融治疗 总被引:3,自引:0,他引:3
目的:上腔静脉内存在由右心房肌延伸产生的肌袖,由此产生的电活动可能导致阵发性快速房性心律失常,该研究探讨一种以往认为罕见的心律失常,即上腔静脉起源房性心律失常的电生理特点和射频消消融治疗。方法:1998年1月至今,因房性心动过速(房速)和心房颤动(房颤)而接受射频治疗共21例,其中3例源于上腔静脉,分别为1例房速,2例房颤伴房速,结果:3例患者房速时心电图的特点是PaVL呈负向,PI为正向,伴发房颤的患者,房速时频率快,临床多种抗心律失常药物治疗无效,3例患者的常规标测心内激动顺序为:高位右房→希氏束→冠状窦远端→冠状窦近端。1例房速采用最早激动点标测消融成功,2例房速伴房颤分别采用解剖隔离上腔静脉和电隔离上腔静脉消融成功,分别随访31,10,2.5个月无复发。结论:上腔静脉是房速和房颤的起源部位之一,药物治疗效果不满意时射频消融可望获得有效治疗。 相似文献
997.
丹参银杏复方制剂治疗高血脂症的临床评价 总被引:3,自引:2,他引:1
目的:比较辛伐他汀(舒降之)、血脂康与丹参银杏复方制剂降血脂的临床疗效。方法:310例高脂血症患者随机分为4组。安慰剂组(n=30):给予安慰剂胶囊2粒,每日3次;辛伐他汀组(n=50):给予辛伐他汀20mg,每晚1次;血脂康组(n=50):给予血脂康2粒,每日2次;丹参银杏复方制剂组(n=180):给予丹参银杏复方制剂2粒,每日2次。除丹参银杏复方制剂组70例延长至24周,其余病例疗程均为12周。结果:丹参银杏复方制剂在降低总胆固醇、甘油三酯等方面均有显著疗效,对低密度脂蛋白的降低作用与阳性药相当,在升高高密度脂蛋白方面,短期内逊于辛伐他汀组和血脂康组,24周后有明显改善。结论:作为保健品丹参银杏复方制剂在降脂方面与血脂康、辛伐他汀疗效相当,随着服用时间的延长,还可显著改善高血脂症状。目前的实验结果显示:短期及长期(24周)服用,不良反应很轻微。 相似文献
998.
目的为比较内镜下与显微镜下经鼻-蝶窦入路的解剖标志和显露范围差异。方法对9例汉族成人灌注尸头采用经鼻-蝶窦入路进行解剖,其中4例行显微解剖,5例采用内镜下解剖,在内镜与显微镜下分别对入路的解剖标志和显露范围进行比较。结果在蝶窦内,内镜下可以观察到更多的解剖标志以确定鞍底、海绵窦等重要结构的位置;内镜经鼻-蝶窦入路更易于向颅前窝底、鞍旁海绵窦和斜坡方向扩展。内镜与显微镜下的操作存在较大差异。结论内镜经鼻-蝶窦入路鞍区及其周围的显露范围较显微镜下更大。 相似文献
999.
《Pancreatology》2007,7(5-6):403-408
Nitric oxide (NO) is a gaseous neurotransmitter, a vasodilator and paracrine regulator. In the pancreas, NO regulates normal pancreatic exocrine secretion, endocrine pancreatic insulin secretion and pancreatic microvascular blood flow. NO has multiple species and is produced de novo by 3 NO synthase enzymes. Endothelial NO synthase reduces the severity of the initial phase of experimental acute pancreatitis (AP). Cigarette smoking and chronic alcohol use disrupt normal NO pathways and are associated with pancreatitis and pancreatic cancer. The aims of this minireview are to describe normal intrapancreatic NO pathways, perturbations during experimental AP and due to epidemiological factors associated with pancreatic pathology, and the clinical implications Of NO On AP. 相似文献
1000.
Hydroxysafflor yellow A (HSYA), is a component of the flower, Carthamus tinctorius L. In this study, we investigated its effect on Human Umbilical Vein Endothelial Cells (HUVECs) under hypoxia. We evaluated cell viability using the MTT kit. The cell cycle distribution was analyzed by PI staining flow cytometric analysis. PI AnnexinV-FITC detection and the TUNEL assay were performed to evaluate the apoptosis rate. Nitric oxide (NO) generation in cell supernatant was measured by the Griess assay. RT-PCR, Western blot and Immunocytochemistry analysis were used to evaluate the changes of Bcl-2, Bax, p53 and eNOS. Our data showed that HSYA inhibited cell apoptosis and cell cycle G1 arrest induced by hypoxia. HSYA treatment increased the Bcl-2/Bax ratio of protein and mRNA, reduced p53 protein expression in cell nucleus. In addition, HSYA enhanced the NO content of cell supernatant under hypoxia, accompanied with upregulating eNOS mRNA expression and protein level. Taken together, these results demonstrate that HSYA could protect HUVECs from hypoxia induced injuries by inhibiting cell apoptosis and cell cycle arrest. These findings have partly revealed the molecular mechanism of HSYA on treating of ischemic heart disease. We expected our experiments might provide some clues for further research. 相似文献