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1.
目的分析成人血液系统恶性肿瘤患者接受强烈化疗后中性粒细胞减少性肠炎(NE)的发生率、危险因素及预后情况。方法收集2004至2013年接受化疗的1804例血液系统恶性肿瘤患者,记录患者血常规、凝血检测和血液生化检测结果,并记录患者年龄、性别、原发病、既往化疗次数、既往化疗方案中是否使用阿糖胞苷、临床症状、肠壁厚度、中性粒细胞最低计数、中性粒细胞缺乏持续时间、NE的治疗方法和预后等,探讨NE起病诱因、临床特征、腹部B超特点、症状的预后意义及化疗药物对发病的影响等。结果1804例患者中226例(12.5%)化疗后合并NE,化疗后10~19d起病,中位起病时间为化疗后第14天。发生NE后26例患者死亡,病死率11.5%。化疗药物包括阿糖胞苷、临床症状≥4项、中性粒细胞缺乏持续超过7d以及B超下肠壁厚度≥10mm的患者病死率相对较高。结论NE是接受强烈化疗的血液系统肿瘤患者的严重的并发症,发生NE后患者病死率较高。  相似文献   
2.
《Urologic oncology》2015,33(5):217-225
Although both surgery and radiation are potential curative options for men with clinically localized prostate cancer, a significant proportion of men with high-risk and locally advanced disease will demonstrate biochemical and potentially clinical progression of their disease. Neoadjuvant systemic therapy before radical prostatectomy (RP) is a logical strategy to improve treatment outcomes for men with clinically localized high-risk prostate cancer. Furthermore, delivery of chemotherapy and other systemic agents before RP affords an opportunity to explore the efficacy of these agents with pathologic end points.Neoadjuvant chemotherapy, primarily with docetaxel (with or without androgen deprivation therapy), has demonstrated feasibility and safety in men undergoing RP, but no study to date has established the efficacy of neoadjuvant chemotherapy or neoadjuvant chemohormonal therapies. Other novel agents, such as those targeting the vascular endothelial growth factor receptor, epidermal growth factor receptor, platelet-derived growth factor receptor, clusterin, and immunomodulatory therapeutics, are currently under investigation.  相似文献   
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4.
白血病病人骨髓抑制期实施防感染措施时机的研究   总被引:5,自引:0,他引:5  
目的 :研究白血病病人在化疗期间 ,不同时间实施预防感染护理的效果。方法 :对照组在化学疗法结束后给予预防感染的护理措施 ,实验组在化学疗法开始前 3~ 7d实施预防性护理措施。观察两组病人感染发生率。结果 :感染发生率实验组明显低于观察组。结论 :在化学疗法开始前实施预防性护理措施有助于降低感染发生率  相似文献   
5.
泰素蒂加顺铂治疗进展期NSCLC的临床研究   总被引:5,自引:0,他引:5  
目的观察泰素蒂加顺铂方案治疗进展期非小细胞肺癌的临床疗效、毒副作用。方法收集可评价疗效的进展期非小细胞肺癌50例,以泰素蒂加顺铂方案进行化疗,泰素蒂75 mg/m2静脉滴注,第1天;顺铂25 mg/m2~30 mg/m2静脉滴注,第2天~第5天,每3周为一个周期,2~3周期后评价疗效和毒副反应并随访。结果50例患者中,总有效率为50.0 %,其中初治病例为53.1 %,复治病例为44.4 %,初复治病例间差异无显著性(P >0.05)。中位缓解期为5个月。中位生存期为9.5个月,1年生存率为61.0 %。毒副反应主要为骨髓抑制,白细胞下降达Ⅲ度、Ⅳ度者52.0 %,血小板下降达Ⅲ度、Ⅳ度者为14.0 %。血红蛋白下降不严重。其他毒副反应还有脱发、过敏反应、水钠潴留、静脉炎、末梢神经炎、口腔炎、腹泻等,但发生率均较低。结论泰素蒂加顺铂方案治疗进展期非小细胞肺癌,特别是复发病例,临床疗效比较满意,毒副反应能够耐受。辅以G蛳CSF可防治重度的骨髓抑制,有较好的临床应用价值。  相似文献   
6.
目的:比较康泉及康泉合用地塞米松预防急性白血病化疗所致的胃肠道反应的效果。方法:在同一方案的不同疗程,分别单用康泉或康泉合用地塞米松,随机对照,共观察110疗程。结果:康泉及康泉合用地塞米松对预防化疗所致急性呕吐有效率分别为69.5%和95.1%,有明显差异(P<0.01);对于迟发性呕吐两组的有效率分别为74.555%和91.83%,亦有明显差异。结论:康泉和地塞米松合用对控制急性和迟发性恶性呕吐优于康泉单用  相似文献   
7.
The aim of this prospective randomized study was to determine whether additional doxorubicin chemotherapy improves outcome in patients with hepatocellular carcinoma (HCCA) treated by liver transplantation. Stratification parameters were tumor stage (UICC I-IVa), gender, age 50 years, α-fetoprotein 20 ng/mL, cirrhosis and HbsAg status. For pre-operative chemotherapy doxorubicin (15 mg/m2) was given biweekly, intra-operative chemotherapy was a single dose administered before surgical manipulation. Post-operative chemotherapy from day 10 was as given preoperatively for a total dosage of 300 mg/m2. Outcome parameters were overall survival (OS) and disease-free survival. Of the 75 consecutive patients who received liver transplantation for treatment of HCCA, 62 patients were enrolled. Thirty-four patients were randomized in the chemotherapy group; 28 patients were in the control group and transplanted only. OS rates at 5 years were 38% in the chemotherapy group and 40% in the control group, disease-free survival rates at 5 years 43% and 53%, respectively. Tumor stage and vascular invasion were identified as independent risk factors for recurrence of disease. Doxorubicin chemotherapy did not improve organ survival and disease-free survival in patients undergoing liver transplantation for HCCA.  相似文献   
8.
Two different hepatoma cell lines were incubated for 48h with chemotherapeutic drugs cisplatin, paclitaxel and 5-FU to determine their ability to induce cytotoxicity and DNA fragmentation as well as to modify the expression of some cell death-related genes that could be involved in the resistance to therapy. We observed that cisplatin and paclitaxel induced cytotoxicity, but significant differences between both cell lines, were found only in the case of paclitaxel. At 48h, apoptosis was clearly present in Hep3B cells treated with cisplatin and HepG2 cells treated with paclitaxel. 5-FU induced cytotoxicity in both cell lines but only at higher concentrations than the other two drugs, triggering apoptosis and necrosis in HepG2 cells and only necrosis in Hep3B. When a time course was performed for the first 8h of treatment to elucidate the initial mechanism of cell death responsible for DNA fragmentation, we observed that 5-FU in Hep3B, and cisplatin in both cell lines, induces primary necrosis, whereas at the concentration tested here, paclitaxel clearly triggers apoptosis in both cell lines. HepG2 cells were weakly sensitive to 5-FU in the first 8h of treatment, so the primary mechanism of cell death was not clear, but results seem to indicate that it could be apoptosis. At 48h, Bax was not up-regulated with any of the treatments, whereas cisplatin was able to induce Bcl-xL down-regulation in both cell lines. Treatment with 5-FU also down-regulated Bcl-xL in HepG2 cells. We also measured variations in the expression of survivin, an inhibitor of apoptosis that has also been involved in mitototic catastrophe. Hep3B cells seem to show an increase in protein levels with all treatments. Exposure to paclitaxel resulted in the highest effect. In the case of HepG2 cells, there was a decrease in survivin expression when cells were treated with 5FU and paclitaxel, both treatments showing complete loss of the protein. Using an antibody that recognizes unprocessed caspase-3, we observed that the enzyme was assumingly activated in HepG2 cells treated with 5FU and paclitaxel, but only weakly after treatment with cisplatin. Hep3B cells did not show activation since the levels of the pro-enzyme remained the same as that in the control. In conclusion, the three drugs tested in this study could induce cell death, with paclitaxel being more effective inducing apoptosis. 5FU was only effective at high doses and its mechanism seems to be primarily related to necrosis in Hep3B and probably apoptosis in HepG2. Cisplatin mechanism of cell death is probably mediated by the decrease in anti-apoptotic protein Bcl-xL whereas paclitaxel and 5FU are decreasing the apoptosis inhibitor survivin. According to pro-enzyme levels, caspase-3 was only activated in HepG2 cells, whereas in the case of Hep3B cells the mechanisms of toxicity appear to be caspase-3-independent at the time and concentrations tested in this study. The resistance of Hep3B cells to death induced by chemotherapy could be related to an increase in the expression of IAP survivin, which can decrease cell response to the treatment or even switch the type of death from apoptosis to another kind, making therapy less efficient.  相似文献   
9.
目的探讨高能聚焦超声刀加氟脲嘧啶、四氢叶酸治疗晚期胰腺癌临床疗效及毒副作用。方法30例经病理学或细胞学确诊的晚期胰腺癌病人先用高能聚焦超声刀(HIFU)治疗,再予氟脲嘧啶、四氢叶酸联合化疗。氟脲嘧啶500mg/m^2加入5%GNS500ml静滴持续6小时以每天1次连用5天,CF(四氢叶酸)100mg/m^2加入生理盐水250ml静滴每天1次连用5天,28天为1周期,至少治疗2个周期。结果CR1例;PR9例;MR9例;NC5例;PD6例。总有效率63%。毒副作用主要消化道反应,其他副作用轻微。结论应用HIFU局部治疗胰腺癌同时合用四氢叶酸加氟脲嘧啶全身化疗近期疗效提高明显,止痛明显达75%,副反应小,值得应用。  相似文献   
10.
目的研究低浓度5-Fu 24-小时持续化疗和高浓度5-Fu短时间化疗对BEL-7402肝癌细胞株的细胞周期的影响:方法用低浓度(1000.0μg/L)的5.Fu对BEL-7402肝癌细胞株进行持续24小时的培养(A组),用高浓度(50000.0μg/L)的5-Fu对BEL-1 7402肝癌细胞株进行2小时培养(B组),在培养后的不同时间点用流式细胞技术检测细胞周期的变化。结果A组结果显示:0h、4h、8h、12h、16h、20h和24h的S期细胞的百分数分别为25.23%、32.35%、39.28%、41.05%、46.02%、47.00%及47.14%。B组结果显示:0h、4h、8h、12h、16h、20h和24h的S期细胞的百分数分别为24.68%、68.43%、46.67%、43.67%、35.42%、33.22%及32.96%。结论5-Fu引起的S期细胞周期阻滞不但和浓度相关,也和作用时间相关。低浓度(1000.0μg/L)的5-Fu持续化疗较高浓度(50000.0μg/L)的5-Fu短时间(2小时)化疗更容易引起BEL-7402肝癌细胞株S期阻滞。  相似文献   
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