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排序方式: 共有818条查询结果,搜索用时 15 毫秒
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目的探讨血清上皮型钙黏蛋白(E-Cad)、胃泌素-17(G-17)水平和肿瘤组织中人类表皮生长因子受体2(HER-2)表达与胃癌患者术后复发风险的相关性。方法选取行胃癌根治术治疗的胃癌患者92例,检测术前血清E-Cad、G-17水平和肿瘤组织HER-2的表达。对所有患者随访5年,以胃癌复发或随访满5年为随访终点。以胃良性病变患者92例作为对照组。收集所有胃癌患者的临床资料(性别、年龄、临床分期、分化程度、复发情况等)。采用受试者工作特征(ROC)曲线评估各项指标判断胃癌复发的效能。采用Cox回归分析评估影响胃癌患者复发的危险因素。采用Kaplan-Meier生存曲线评估胃癌患者的5年复发情况。结果胃癌组血清G-17水平和肿瘤组织HER-2阳性率均显著高于对照组(P=0.000),血清E-Cad水平显著低于对照组(P=0.000)。血清E-Cad、G-17水平及肿瘤组织HER-2阳性率与胃癌的TNM分期、分化情况及是否复发有关(P<0.05),与性别无关(P>0.05)。ROC曲线分析结果显示,E-Cad、G-17、HER-2单项检测与联合检测判断胃癌复发的曲线下面积(AUC)分别为0.775、0.822、0.603、0.950。Kaplan-Meier生存曲线分析结果显示,胃癌复发患者E-Cad低表达组复发率高于高表达组(P<0.05),而G-17低表达组、HER-2低表达组复发率低于G-17高表达组、HER-2高表达组(P<0.05)。Cox回归分析结果显示,E-Cad水平降低、G-17水平升高、HER-2表达升高均是胃癌复发的危险因素[风险比(HR)分别为0.835、1.568、3.981,95%可信区间(CI)分别为0.767~0.909、1.292~1.904、1.504~10.538]。结论E-Cad、G-17、HER-2在预测胃癌患者根治术后复发中均有重要价值。  相似文献   
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The aim of this study was to compare colorectal adenocarcinoma with mucinous component, ordinary adenocarcinoma (OA) and mucinous adenocarcinoma (MA) regarding clinicopathological parameters, survival, EGFR, MMP‐13, and E‐cadherin. We studied tumor tissue specimens from 28 patients with adenocarcinoma with mucinous component, 47 with OA, and 56 with MA, who underwent radical surgery from January 2007 to January 2012 at the Gastroenterology Centre, Mansoura University, Egypt. High density manual tissue microarrays were constructed and immunohistochemistry for EGFR, MMP‐13, and E‐cadherin was done. Colorectal adenocarcinoma with mucinous component (AWMC) was significantly associated with more perineural invasion, lower EGFR, and MMP‐13 expressions than OA, with no difference in E‐cadherin expression. Conversely, only microscopic abscess formation was significantly more with colorectal AWMC than MC with no difference in EGFR, MMP‐13 and E‐cadherin expression between both groups. Colorectal AWMC showed a better survival than MA with no difference with OA. In a univariate analysis, EGFR, MMP‐13, and E‐cadherin expressions did not show a significant impact on disease‐free or overall survival in patients with colorectal AWMC. Colorectal AWMC remains a vague entity that resembles OA in some clinicopathological and molecular respects as well as MA.  相似文献   
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Cancer stem cells (CSC) are a subpopulation of tumor cells with properties of high tumorigenicity and drug resistance, which lead to recurrence and poor prognosis. Although a better understanding of CSC is essential for developing cancer therapies, scarcity of the CSC population has hindered such analyses. The aim of the present study was to elucidate whether the E‐cadherin‐Fc chimera protein (E‐cad‐Fc) enhances cancer stem‐like properties because studies show that soluble E‐cadherin stimulates human epithelial growth factor receptor (EGFR) and downstream signaling pathways that are reported to play a crucial role in CSC. For this purpose, we used ornithine decarboxylase (ODC)‐degron–transduced (Degron(+)) KM12SM cells as a CSC model that retains relatively low CSC properties. Compared to cultures without E‐cad‐Fc treatment, we found that E‐cad‐Fc treatment further suppressed proteasome activity and largely enhanced cancer stem‐like properties of ODC‐degron–transduced KM12SM cells. These results include increased expression of stem cell markers Lgr5, Bmi‐1, SOX9, CD44, and CD44v9, aldehyde dehydrogenase (ALDH), and enhancement of robust spheroid formation, and chemoresistance to 5‐fluorouracil (5‐FU) and oxaliplatin (L‐OHP). These effects could be attributed to activation of the EGFR pathway as identified by extensive phosphorylation of EGFR, ERK, PI3K, AKT, and mTOR. In SW480 cells, E‐cad‐Fc matrix induced some CSC markers such as CD44v9 and ALDH. We also found that E‐cad‐Fc matrix showed high efficiency of inducing mesenchymal changes in colon cancer cells. Our data suggest that the E‐cad‐Fc matrix may enhance CSC properties such as enhancement of chemoresistance and sphere formation.  相似文献   
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Cell competition is a biological process by which unfit cells are eliminated from “cell society.” We previously showed that cultured mammalian epithelial Madin‐Darby canine kidney (MDCK) cells expressing constitutively active YAP were eliminated by apical extrusion when surrounded by “normal” MDCK cells. However, the molecular mechanism underlying the elimination of active YAP‐expressing cells was unknown. Here, we used high‐throughput chemical compound screening to identify cyclooxygenase‐2 (COX‐2) as a key molecule triggering cell competition. Our work shows that COX‐2‐mediated PGE2 secretion engages its receptor EP2 on abnormal and nearby normal cells. This engagement of EP2 triggers downstream signaling via an adenylyl cyclase‐cyclic AMP‐PKA pathway that, in the presence of active YAP, induces E‐cadherin internalization leading to apical extrusion. Thus, COX‐2‐induced PGE2 appears a warning signal to both abnormal and surrounding normal cells to drive cell competition.  相似文献   
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目的: 研究甘草酸二铵脂质配体(DGLL)对大鼠急性肺损伤(ALI)及肺水肿的影响。方法: 雄性SD大鼠123只,体重170~200 g,(6±1)周龄,灌胃DGLL(30、60、120 mg/kg),1 h后通过腹腔内注射脂多糖(LPS)10 mg/kg建立大鼠ALI模型。6 h后,使用HE染色技术评估肺损伤。使用肺湿干重比、支气管肺泡灌洗液(BALF)中的蛋白质含量和肺组织中的Evans蓝(EB)来评估肺水肿。用ELISA法测定肺组织中肿瘤坏死因子(TNF-α)和白细胞介素(IL-1β)的表达水平。通过免疫组织化学染色法检测髓过氧化物酶(MPO)的表达水平。Western blotting法测定细胞间黏附分子(ICAM-1)、血管内皮钙黏蛋白(VE-cadherin)、黏附蛋白(ZO-1)、连接黏附分子(JAM-1)等与肺部炎症和微血管通透性有关的蛋白表达水平。结果: MPO免疫反应性降低,大鼠肺组织中TNF-α、IL-1β和ICAM-1的表达水平下降,证明DGLL缓解了LPS诱导的ALI。此外,DGLL可以抑制LPS诱导的肺水肿,降低BALF的蛋白浓度及EB外渗。DGLL也降低了VE-cadherin的表达水平以及抑制LPS引起的肺组织中的连接蛋白,包括ZO-1、JAM-1的表达。结论: DGLL对LPS诱导的大鼠ALI表现出保护作用,同时也抑制了炎症细胞的浸润和微血管屏障的破坏。  相似文献   
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目的探究血管内皮钙黏蛋白(VE-Cad)能否预测ABO新生儿溶血病患儿血管内皮损伤及其与溶血的发生和严重程度的关系。方法选取2020年4月~2020年11月我院收集的50例ABO新生儿溶血病患儿(ABO新生儿溶血病组)、47例母婴血型匹配的健康新生儿(对照组),观察收集两组新生儿同期血红蛋白(Hb)、网织红细胞比率(Ret%)、间接胆红素(IBIL)、乳酸脱氢酶(LDH)的检测数据,并定量检测VE-Cad浓度。结果两组新生儿出生体重、胎龄及检测日龄比较差异无统计学意义(P>0.05),两组新生儿Hb、Ret、IBIL、LDH及VE-Cad水平比较差异有统计学意义(P<0.05),且VE-Cad水平与Ret%、IBIL、LDH水平呈正相关,而与Hb水平呈负相关(P<0.05)。经多重线性回归分析发现:ABO新生儿溶血病组VE-Cad水平与Hb、Ret%、IBIL、LDH水平呈现独立相关性(P<0.05)。结论VE-Cad在ABO新生儿溶血病患儿中的水平升高可用于反映患儿的内皮损伤,并有助于评估可能发生的血管功能障碍风险。  相似文献   
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