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41.
吉西他滨联合铂类药物治疗晚期胰腺癌的疗效观察 总被引:1,自引:1,他引:1
目的 观察吉西他滨(健择)联合顺铂/草酸铂(GP/GEM-OX方案)治疗晚期不能手术或手术后复发的胰腺癌患者的疗效与不良反应。方法 28例患者分别给予GP或GEM-OX方案2~13周期。按WHO标准评定疗效和不良反应。结果 26例可评价疗效,无一例完全缓解(CR,0%),部分缓解(PR)7例(26.9%),稳定(SD)10例(38.5%),进展(PD)9例(34.6%)。可评价临床受益反应(CBR)27例,有效率为70.4%(19/27)。中位疾病进展时间为4.2个月,中位生存时间为9.3个月。结论 健择联合顺铂/草酸铂是治疗晚期胰腺癌患者的安全有效方案,并能较好改善疾病相关症状,毒副反应可以耐受。 相似文献
42.
43.
Previous work has shown that sustained increased and decreased cell
proliferation, induced by dietary zinc deficiency and caloric restriction
respectively, influence the course of N- nitrosomethylbenzylamine
(NMBA)-induced esophageal carcinogenesis in rats. The present study
considered whether the increased cell proliferation and esophageal tumor
incidence induced by zinc deficiency are reversed upon zinc replenishment.
Weanling rats were maintained initially on a deficient diet containing 4
p.p.m. zinc. After 5 weeks, carcinogen-treated animals were given six
intragastric doses of NMBA (2 mg/kg twice weekly). Controls were untreated.
After the second NMBA dose, the rats were divided into three dietary
groups. One group was continued on the deficient diet, while the other two
groups were switched to diets containing either 75 or 200 p.p.m. zinc, with
half of the members in each group fed ad libitum and half pair-fed with
deficient rats. NMBA-untreated controls were similarly replenished. At
various time points, esophageal cell proliferation was assessed in five
animals from each group by immunohistochemical detection of cells in S
phase, with in vivo 5-bromo-2'deoxyuridine labeling. At 11 weeks after the
first dose, esophageal tumor incidence was greatly reduced, from 100% in
the deficient group to 26 and 14% respectively in the replenished groups
fed ad libitum 75 and 200 p.p.m. zinc and to 14 and 11% respectively in the
replenished groups pair-fed 75 and 200 p.p.m. zinc. In addition, the number
of tumors per esophagus was reduced from 9.93 +/- 4.25 in deficient rats,
to a range of 0.11 +/- 0.31-0.30 +/- 0.54 in replenished animals. Following
zinc replenishment, esophageal cell proliferation, as measured by labeling
index (LI), the number of labeled cells and the total number of cells, was
markedly decreased in NMBA-untreated and -treated esophagi as compared with
those in corresponding deficient esophagi. Thus, the esophageal cell
proliferation induced by zinc deficiency is reversed by zinc replenishment
and replenished animals have a markedly lower incidence of esophageal
tumors.
相似文献
44.
Computer-aided 3-D reconstruction and measurement of the optic canal and intracanalicular structures
Traumaticopticneuropathyisavision threateningdisorder Autopsiesafterheadtraumahaveshownthattheopticnervesareoftendamagedmostseverelywithintheopticcanal 1 Althoughvariouskindsofmicrosurgicaldecompressionoftheopticcanalhavebeenadvocatedastheeffectivemeth… 相似文献
45.
Objective To investigate the effects of Donglian Capsule(the combination of Ophiopogonis Tuber Polysaccharide with Rhizoma Coptidis Alkaloids, OPRA for short, Component of Chinese medicine)on early insulin resistance in experimental diabetic rats. Methods The animal model of insulin resistance in 2 type diabetic was established by injecting low dose of STZ in 60 high fat-fed SD rats. After one week, the successful models were randomly divided into 4 groups: untreated, high and low OPRA-treated, mefformin-treated group, Meanwhile, a normal control group was designed. After four weeks, the differences of FBG, PG, INS and C-P were compared among the groups. Results The OPRA can significantly reduced the level of serum TC and FBG, increased the C-E ]Lightened the IRI(P<0.01). Conclusion The OPRA can reduce the level of serum TG and FBG, and decrease insulin resistance to protect the β-cell function. 相似文献
46.
47.
目的应用前庭诱发的肌源性电位(vestibular evoked myogenic potentials,VEMPs),观察Tullio现象与Ramsay Hunt综合征的电位特点,为诊断提供客观依据.方法Tullio现象与Ramsay Hunt综合征各1例,通过已经建立的VEMPs检查方法观察两者的电位引出情况.结果正常人VEMP刺激声在阈上85dB nHL可引出VEMPs.本文Tullio现象患者在刺激强度降至39dB nHL时仍可引出.而健侧在69dB nHL时就已不能引出.Ramsay Hunt综合征在阈上105dBHL右侧不能引出VEMP;而左侧可以引出.结论VEMPs可用来了解前庭下神经的功能状态.由于VEMPs的检查特点,可用于动态观察前庭神经病变后的恢复情况. 相似文献
48.
目的对恩施地区2003年3月上、中旬发生的两起流感局部暴发流行进行病原学分析。方法采集患者咽拭子进行病毒分离鉴定,采集急性期和恢复期双份血进行抗流感病毒IgG抗体测定。结果证实湖北恩施地区出现的流感局部暴发流行是由B型流感病毒引起的,分离的B型流感病毒的抗原性与2001年香港分离株(B/香港/维多利亚30/2001)和浙江分离株(B/浙江/2/2001)很接近,而与1999年四川分离株(B/四川/397/1999)和2001年上海分离株(B/上海/20/2001)相差甚远。结论湖北省恩施地区2003年3月流感局部暴发流行是由流感病毒B型引起的。 相似文献
49.
目的 :探讨非小细胞肺癌(NSCLC)中NM23/NDPK的表达及其在NSCLC发生、转移及预后中的意义。方法:采用S P免疫组化染色技术,检测69例NSCLCNM23/NDPK的表达情况。结果:肺癌原发灶NM23/NDPK阳性表达率与NSCLC淋巴结转移及临床分期有关,NM23/NDPK的表达与患者的生存率有关,但与组织学分级及分化程度无关。NM23/NDPK阳性率在NSCLC伴淋巴结阳性组低于淋巴结阴性组(P<0.01)。随着临床分期的增高,阳性率逐渐降低(P<0.05)。NM23/NDPK阳性患者术后1,3年生存率明显高于阴性者(P<0.05)。结论:对NSCLC进行NM23/NDPK的检测,有助于预测NSCLC进展程度和淋巴结转移的诊断,以及评估NSCLC患者的预后。 相似文献
50.
To observe the effects of simvastatin on nuclear factor kappaB (NF-kB)-DNA binding activity and on the expression of monocyte chemoattractant protein-1 (MCP-1) in atherosclerotic plaque in rabbits and to explore the anti-atherosclerotic properties beyond its lipid-lowering effects. Thirty-six New Zealand male rabbits were randomly divided into low-cholesterol group (LC), high- cholesterol group (HC), high-cholesterol+ simvastatin group (HC+S) and then were fed for 12 weeks. At the end of the experiment, standard enzymatic assays, electrophoretic mobility shift as- say (EMSA), immunohistochemical staining, and morphometry were performed to observe serum lipids, NF-kB-DNA binding activity, MCP-1 protein expression, intirna thickness and plaque area of aorta respectively in all three groups. Our results showed that the serum lipids, NF-kB-DNA binding activity, expression of MCP-1 protein, intima thickness, and plaque area of aorta in the LC and HC+S groups were significantly lower than those in the HC group (P〈0.05). There was no significant difference in the serum lipids between the LC and HC+S groups (P〉0.05), but the NF-kB-DNA binding activity, the expression of MCP-1 protein and the intirna thickness and plaque area of aorta in the HC+S group were significantly decreased as compared to the LC group (P〈0. 05). This study demonstrated that simvastatin could decrease atherosclerosis by inhibiting the NF-kB-DNA binding activity and by reducing the expression of MCP-1 protein. 相似文献