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101.
去势后大鼠海马结构一氧化氮合酶阳性神经元的变化 总被引:8,自引:1,他引:7
目的:观察去势后大鼠海马结构一氧化氮合酶(NOS)阳性神经元的变化。方法:用黄递酶组织化学染色方法观察切除双侧卵巢后雌后SD大鼠海马结构NOS阳性神经元的形态,分布的变化,并进行计算机图像分析。结果:去势后海马结构NOS阳性神经元分布变化有区域差异性;NOS阳性神经元在下托、海马(CA)一区邻近下托的部分、CA三区、CA四区(CA4)和齿状回(DG)数目明显减少,而在CA二区数目明显明显增多,CA4和DG的NOS阳性神经元平均密度降低,胞体的平均周长和平均截面积都明显减少。结论:雌激素可能通过影响海马结构NOS的表达来影响学习和记忆。 相似文献
102.
钾通道阻断剂对低氧/复氧诱导的培养海马神经元死亡的防护作用 总被引:3,自引:0,他引:3
目的研究钾通道阻断剂对单纯低氧/复氧诱导的培养海马神经元死亡的防护作用。方法培养8 d的海马神经元置于低氧环境(95% N2/5% CO2)6 h,复氧再培养直至72 h,复氧后0.5 h培养液内分别给予不同钾通道阻断剂,用细胞计数及MTT比色法检测神经元死亡情况。结果低氧/复氧诱导培养海马神经元出现迟发性死亡;四乙铵以剂量依赖性的方式防护低氧/复氧诱导的培养海马神经元免于死亡;大电导钙激活钾通道(BK通道)阻断剂iberiotoxin(IbTX)可完全消除低氧/复氧诱导的神经元死亡(P<0.001);A型钾通道阻断剂4-氨基吡啶不能防护低氧/复氧诱导的神经元免于死亡(P>0.05)。结论钾通道阻断剂四乙铵和IbTX能防护低氧/复氧诱导的培养海马神经元免于死亡,提示某些类型的钾通道尤其是BK通道活动增强可能参与了低氧/复氧诱导的培养海马神经元死亡。 相似文献
103.
104.
Ming Zhao Cheng Simon C F Rawlinson Andrew A Pitsillides Gul Zaman Subburaman Mohan David J Baylink Lance E Lanyon 《Journal of bone and mineral research》2002,17(4):593-602
The mechanism by which mechanical strain and estrogen stimulate bone cell proliferation was investigated using monolayer cultures of human osteoblastic TE85 cells and female human primary (first-passage) osteoblasts (fHOBs). Both cell types showed small but statistically significant dose-dependent increases in [3H]thymidine incorporation in response to 17beta-estradiol and to a single 10-minute period of uniaxial cyclic strain (1 Hz). In both cell types, the peak response to 17beta-estradiol occurred at 10(-8) - 10(-7) M and the peak response to strain occurred at 3500 microstrain ((mu)epsilon). Both strain-related and 17beta-estradiol-related increases in [3H]thymidine incorporation were abolished by the estrogen receptor (ER) modulator ICI 182,780 (10-8 M). Tamoxifen (10(-9) - 10(-8) M) increased [3H]thymidine incorporation in both cell types but had no effect on their response to strain. In TE85 cells, tamoxifen reduced the increase in [3H]thymidine incorporation associated with 17beta-estradiol to that of tamoxifen alone but had no such effect in fHOBs. In TE85 cells, strain increased medium concentrations of insulin-like growth factor (IGF) II but not IGF-I, whereas 17beta-estradiol increased medium concentrations of IGF-I but not IGF-II. Neutralizing monoclonal antibody (MNAb) to IGF-I (3 microg/ml) blocked the effects of 17beta-estradiol and exogenous truncated IGF-I (tIGF-I; 50 ng/ml) but not those of strain or tIGF-II (50 ng/ml). Neutralizing antibody to IGF-II (3 microg/ml) blocked the effects of strain and tIGF-II but not those of 17beta-estradiol or tIGF-I. MAb aIR-3 (100 ng/ml) to the IGF-I receptor blocked the effects on [3H]thymidine incorporation of strain, tIGF-II, 17beta-estradiol, and tIGF-I. HOBs and TE85 cells, act similarly to rat primary osteoblasts and ROS 17/2.8 cells in their dose-related proliferative responses to strain and 17beta-estradiol, both of which can be blocked by the ER modulator ICI 182,780. In TE85 cells (as in rat primaries and ROS 17/2.8 cells), the response to 17beta-estradiol is mediated by IGF-I, and the response to strain is mediated by IGF-II. Human cells differ from rat cells in that tamoxifen does not block their response to strain and reduces the response to 17beta-estradiol in TE85s but not primaries. In both human cell types (unlike rat cells) the effects of strain and IGF-II as well as estradiol and IGF-I can be blocked at the IGF-I receptor. 相似文献
105.
中西医结合冲击治疗免疫性不孕的临床研究 总被引:5,自引:0,他引:5
目的:探讨中西医结合冲击治疗对女性免疫性不孕症病人的治疗效果。方法:应用酶联免疫吸附法(ELISA)对560例病人血清和宫颈粘液中的抗精子抗体(AsAb)、抗子宫内膜抗体(IAEmAb)、抗卵巢抗体(AOVAb、抗人绒毛膜促性腺激素抗体(AhCGAb)进行检测,采用中药,维生素E、维生素C对所有抗体阳性者进行周期性治疗,2个周期为1疗程。结果:560例病人血清中共检测中各种抗体641例例次,宫颈粘液中共检出各抗体596例次。治疗1疗程,AsAb、AEmAb、AOVAb、AhCGAb在血清的转阴率分别为87.4%、85.4%、74.0%、86.5%,在宫颈粘液中的转阴率分别为93.7%、95.0%、87.0%,94.2%,在宫内颈粘液中的转阴率分别为90.1%、94.0%、94.7%、100.0%,抗体转阴后妊娠率高达58.2%,结论:中西医结合冲击治疗对免疫性不孕抗体转阴所需时间短,转阴率和转阴后妊娠率高,对AsAb、AEmAb、AOVAb与AhCGAb等所致的免疫性不孕均有显著疗效。 相似文献
106.
HCC的早期诊断是其治疗的关键,HCC血清标志物的检测又为其诊断提供了有利的途径,并且操作简单,敏感性高和特异性强。目前常用的血清标志物为AFP、AFP变异体、AFP mRNA、AFU、GGT、DCP、AIF、GPC3等。这些标志物的联合使用有助于HCC的诊断及预后。 相似文献
107.
内镜乳晕小切口男性乳房肥大矫正术 总被引:5,自引:0,他引:5
目的探索减少男性乳房肥大整形术后瘢痕,使乳房切除更加精确,更有利于塑形,避免出血、血肿及支配乳头、乳晕感觉神经的损伤。方法对16例患者在内镜监视下,采用乳晕旁2~3.5cm切口,切除肥大的男性乳腺腺体组织,对于以脂肪增生为主者,先行肿胀吸脂术,后在内镜监视下进行残余肥大腺体切除。切除乳腺体组织量单侧为100~320g,平均为130g;吸脂量为20~130ml,平均为68ml,无血肿,切除组织病理检查为脂肪组织及腺体组织。结果术后无血肿,无皮肤坏死,乳头及皮肤的感觉良好,均获随访观察,时间为手术后5个月至3年,无复发。结论内镜外科技术能缩小乳晕切口,避免损伤乳头、乳晕,利于离乳晕较远范围的乳腺组织切除及乳房重新塑形,为男性乳房肥大矫正的一种良好选择。 相似文献
108.
目的:探讨甲状腺全切除术在治疗分化性甲状腺癌中的临床应用价值。方法:采用我院1988年1月~2001年5月甲状腺全切除术或甲状腺侧叶切除加峡部切除术治疗分化性甲状腺癌125例,对其手术并发症发生、局部复发、转移情况及术后5年生存率进行回顾性对比分析。结果:甲状腺全切除术术后并发症发生率高于甲状腺侧叶切除加峡部切除术组;局部复发、转移率低于侧叶切除加峡部切除术组;5年生存率两组无显著性差异。结论:甲状腺全切除术是治疗甲状腺癌有效的手术方式,但应掌握手术指征,改进、提高手术技术,减少并发症。 相似文献
109.
110.
Objective To test the hypothesis that p53 gene therapy combined with endostatin can enhance tumor response to radiation therapy of RM-1 mouse xenograft prostate cancer and to investigate its mechanism. Methods A mouse prostate cancer model was established. Then mice with xenograft tumor were randomly divided into group A (control), B (radiation), C (radiation and rAdp53), D (radiation and rh-endostatin) and E (radiation and rAdp53 and rh-endostatin). On day 1, rAdp53 was injected intra-tumorously with 1 × 1010 vp per animal to group C and E. From day 1 to 14, rh-endostatin was given 15 mg/kg intraperitoneally daily to group D and E. On day 4 single fraction of 15 Gy was given to tumors in groups B, C, D and E. Normal saline was injected intra-tumorously or intraperitoneaUy accordingly as control. No treatment was done to group A. Tumor volume was measured daily. Samples were collected on Days 5, 10 and 15. Ki67, CD31, p53 and VEGF were detected by means of immunohistochemistry. Results (1) Radiation alone, radiation combined with intra-tumorous injection of Adp53 and/or intraperitoneal injection of rh-endostatin resulted in tumor growth arrest of RM-1 cells in vivo (P = 0.000). Radiation combined with both rAdp53 and rh-endostatin was the most effective treatment (P < 0.05). (2) All the four treatment groups had a decreased expression of mutant type P53 (P = 0.000). The expression of Ki67 in groups B and C were equal (P 0.05) and increasing (P = 0.000), respectively. Group D had a up-down-up curve (P < 0.05), but group E had a up-down one. On day 5 the expresion of VEGF in group E was the lowest (P < 0.05). An increased expression of MVD compared with the control was shown, and MVD in groups C, D and E were always higher than that in the control (P < 0.05). Conclusions The limitation of radiotherapy could be overcome by combination with beth p53 gene therapy and endostatin on the growth of mouse prostate cancer cell. Radiation, rAdp53 and endostatin have their own role but they can be interacted with each other. 相似文献