全文获取类型
收费全文 | 1169篇 |
免费 | 127篇 |
国内免费 | 90篇 |
专业分类
耳鼻咽喉 | 4篇 |
儿科学 | 48篇 |
妇产科学 | 6篇 |
基础医学 | 172篇 |
口腔科学 | 59篇 |
临床医学 | 83篇 |
内科学 | 173篇 |
皮肤病学 | 7篇 |
神经病学 | 38篇 |
特种医学 | 27篇 |
外科学 | 74篇 |
综合类 | 271篇 |
现状与发展 | 1篇 |
预防医学 | 114篇 |
眼科学 | 10篇 |
药学 | 255篇 |
中国医学 | 25篇 |
肿瘤学 | 19篇 |
出版年
2024年 | 1篇 |
2023年 | 13篇 |
2022年 | 44篇 |
2021年 | 52篇 |
2020年 | 33篇 |
2019年 | 30篇 |
2018年 | 43篇 |
2017年 | 44篇 |
2016年 | 80篇 |
2015年 | 71篇 |
2014年 | 106篇 |
2013年 | 130篇 |
2012年 | 114篇 |
2011年 | 118篇 |
2010年 | 89篇 |
2009年 | 60篇 |
2008年 | 76篇 |
2007年 | 53篇 |
2006年 | 43篇 |
2005年 | 31篇 |
2004年 | 34篇 |
2003年 | 20篇 |
2002年 | 17篇 |
2001年 | 10篇 |
2000年 | 5篇 |
1999年 | 3篇 |
1998年 | 1篇 |
1997年 | 5篇 |
1996年 | 1篇 |
1995年 | 7篇 |
1994年 | 4篇 |
1993年 | 6篇 |
1992年 | 8篇 |
1991年 | 9篇 |
1990年 | 6篇 |
1989年 | 3篇 |
1988年 | 1篇 |
1987年 | 4篇 |
1986年 | 2篇 |
1985年 | 3篇 |
1982年 | 3篇 |
1980年 | 1篇 |
1979年 | 1篇 |
1978年 | 1篇 |
排序方式: 共有1386条查询结果,搜索用时 15 毫秒
91.
Dun-quan XU Cao GAO Wen NIU Yan LI Yan-xia WANG Chang-jun GAO Qian DING Li-nong YAO Wei CHAI Zhi-chao LI 《中国药理学报》2013,(12):1515-1525
Aim: To investigate the protective effects of hydrogen sulfide (H2S) against inflammation, oxidative stress and apoptosis in a rat model of resuscitated hemorrhagic shock. Methods: Hemorrhagic shock was induced in adult male SD rats by drawing blood from the femoral artery for 10 min. The mean arterial pressure was maintained at 35-40 mmHg for 1.5 h. After resuscitation the animals were observed for 200 min, and then killed. The lungs were harvested and bronchoalveolar lavage fluid was prepared. The levels of relevant proteins were examined using Western blotting and immunohistochemical analyses. NariS (28 pmol/kg, ip) was injected before the resuscitation. Results: Resuscitated hemorrhagic shock induced lung inflammatory responses and significantly increased the levels of inflammatory cytokines IL-6, TNF-a, and HMGB1 in bronchoalveolar lavage fluid. Furthermore, resuscitated hemorrhagic shock caused marked oxidative stress in lung tissue as shown by significant increases in the production of reactive oxygen species H202 and OH, the translocation of Nrf2, an important regulator of antioxidant expression, into nucleus, and the decrease of thioredoxin I expression. Moreover, resuscitated hemorrhagic shock markedly increased the expression of death receptor Fas and Fas-ligand and the number apoptotic cells in lung tissue, as well as the expression of pro-apoptotic proteins FADD, active-caspase 3, active-caspase 8, Bax, and decreased the expression of Bcl-2. Injection with NariS significantly attenuated these pathophysiological abnormalities induced by the resuscitated hemorrhagic shock. Conclusion: NariS administration protects rat lungs against inflammatory responses induced by resuscitated hemorrhagic shock via suppressing oxidative stress and the Fas/FasL apoptotic signaling pathway. 相似文献
92.
《Expert review of clinical pharmacology》2013,6(10):1031-1043
ABSTRACTNSAIDs are widely used to treat pain and rheumatic conditions, but they induce adverse events in different body systems, although the major, most frequent events occur in the upper and lower gastrointestinal (GI) tracts.Areas covered: This review is focused on damage caused by NSAIDs in the upper and lower GI tracts, the different mechanisms of damage and the GI-sparing NSAIDs designed to minimize adverse events based on understanding of these mechanisms.Expert commentary: Among the new NSAIDs, COX-2 selective inhibitors have been extensively investigated, and some were approved for human use. Celecoxib demonstrated its safety for the entire GI tract, compared to traditional NSAIDs. However, coxibs, like traditional NSAIDs, are toxic to the cardiovascular (CV) system. Other GI-sparing agents include nitric oxide-NSAIDs and phosphatidylcholine-associated NSAIDs. Testing in animal models and humans they showed GI advantages over the parent NSAID compounds, but none obtained regulatory approval or were further investigated. Hydrogen sulfide-releasing NSAIDs are currently under clinical development, and more data are needed before clinical use. Alternative therapies, such as modulating gut microbiota, are being explored. Currently, clinicians must continue prescribing traditional NSAIDs or coxibs, associated with/without proton pump inhibitor therapy, based on the presence of GI/CV risk factors. 相似文献
93.
《Cutaneous and ocular toxicology》2013,32(3):125-136
Cutaneous exposure to sulfur mustard [bis(2-chloroethyl) sulfide (SM)] produces a delayed inflammatory skin response that is followed by severe dermal injury. Assessment of anti-inflammatory therapies against SM-induced skin injury has mainly relied on qualitative histopathological evaluation. The goal of this study was to identify proinflammatory biomarkers in the hairless mouse vesicant model that could be used as additional indicators of SM-induced skin injury for evaluating anti-inflammatory treatment. SM-induced inflammation was determined at 2, 6, and 24 hr postexposure by changes in edema. Ribonuclease protection assay (RPA) was used to determine changes in gene expression of inflammatory mediators. At 2, 6, and 24 hr postexposure, a time-dependent increase in edema was observed in SM-exposed skin, which was significant at 6 and 24 hr when compared to unexposed controls. Ribonuclease protection assay analysis revealed a two-fold or greater increase in monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-2 (MIP-2), MIP-1α, tumor necrosis factor-α, and interleukin (IL)-1β following exposure to SM when compared to unexposed controls. A significant time-dependent increase was observed in MCP-1, MIP-1α, and IL-1β over the 24 hr time period. At 24 hr postexposure, skin treated with the anti-inflammatory drug olvanil showed a significant decrease in SM-induced edema. Additionally, mRNA levels of MCP-1, MIP-2, and IL-1β were decreased when compared to skin exposed to SM alone. In this study, we identified molecular biomarkers at the mRNA level, up-regulated in skin exposed to SM, which can be partially suppressed by olvanil. Further characterization of the mRNA and protein expression patterns of proinflammatory biomarkers may enable the use of other classes of anti-inflammatory drugs or therapeutic treatments against SM dermal injury. 相似文献
94.
95.
硫化氢对大鼠内毒素性急性肺损伤的影响 总被引:3,自引:2,他引:3
目的观察硫化氢(H2S)对脂多糖(LPS)所致大鼠内毒素性急性肺损伤(ALI)的影响,探讨其对肺脏的作用机制。方法♂SD大鼠共64只,随机分为8组,每组8只:Ⅰ:3h空白对照组;Ⅱ:LPS3h组;Ⅲ:6h空白对照组;Ⅳ:LPS6h组;Ⅴ:LPS+NaHS低剂量组;Ⅵ:LPS+NaHS中剂量组;Ⅶ:LPS+NaHS高剂量组;Ⅷ:LPS+PPG组。LPS3h和LPS6h组给予LPS,其相应空白对照组给予生理盐水,分别在3h或6h时处死大鼠;LPS+NaHS低、中、高剂量组和LPS+PPG组分别在给LPS3h时腹腔注射低、中、高剂量氢硫化钠(NaHS)或炔丙基甘氨酸(PPG),再观察3h后处死大鼠。光、电镜下观察肺组织形态学改变,检测肺系数、肺湿/干重比(W/D)、血浆中H2S含量、肺组织胱硫醚-γ-裂解酶(CSE)活性,以及肺组织中丙二醛(MDA)含量、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性的变化。结果LPS3h和LPS6h组与相应的空白对照组比较,光、电镜下肺组织明显受损,超微结构明显改变,肺系数、肺湿/干重比和肺组织MDA含量升高,血浆中H2S的含量、肺组织CSE以及SOD、GSH-Px活性降低。LPS+NaHS低、中、高剂量组与LPS6h组比较,光、电镜下肺组织受损情况均有不同程度改善,肺系数、肺湿/干重比和肺组织MDA含量降低,血浆H2S含量、肺组织CSE以及SOD、GSH-Px活性升高。LPS+PPG组与LPS6h组比较,光、电镜下肺组织损伤无改善,肺系数、肺湿/干重比和肺组织MDA含量升高,血浆中H2S的含量、肺组织CSE和SOD活性降低,肺组织GSH-Px活性无明显变化。结论CSE/H2S体系可能参与内毒素性ALI的病理生理过程,外源性补充H2S可减轻内毒素性ALI。 相似文献
96.
硫化氢供体对Apo E基因敲除小鼠动脉粥样硬化的调节作用 总被引:1,自引:1,他引:1
目的探讨硫化氢(H2S)供体对Apo E基因敲除小鼠(Apo E-/-)动脉粥样硬化的调节作用。方法6wk龄正常C57BL/6J和Apo E-/-小鼠分为正常对照组、ApoE-/-组和Apo E-/-+硫氢化钠(NaHS)组,每组各8只,普通饮食饲养至16wk龄。分别观察各组小鼠血清中总胆固醇(TCHO)、低密度脂蛋白(LDL-C)和高密度脂蛋白(HDL-C)含量及主动脉根部斑块面积的变化;用硫电极法测定血清中H2S的含量。结果与对照组相比,Apo E-/-小鼠血清中TCHO[(12.59±3.11vs2.32±0.40)μmol·L-1]和LDL-C[(1.33±0.43vs0.13±0.03)μmol·L-1]水平明显升高,而HDL-C水平[(0.45±0.13vs1.49±0.21)μmol·L-1]明显降低,血清中H2S的含量[(44.64±4.52)μmol·L-1]较对照组[(57.69±7.03)μmol·L-1]明显下降,主动脉根部明显出现斑块[(139316.6±30362.93vs0)μm2];给予NaHS后,Apo E-/-小鼠血清中TCHO、LDL-C和HDL-C水平无明显变化,而血清中H2S的含量明显升高[(52.21±7.24vs44.64±4.52)μmol·L-1],主动脉根部动脉粥样硬化斑块明显缩小[(85927.84±1922.73vs139316.6±30362.93)μm2]。结论新型气体信号分子H2S可以延缓动脉粥样硬化的进程,缩小动脉粥样硬化斑块形成。 相似文献
97.
目的改进和完善《居住区大气中硫化氢卫生检验标准方法亚甲蓝分光光度法》(GB11742—89),提高检测方法的稳定性和测定范围,使之更适合国家卫生标准限值的要求。方法根据国家相关卫生标准,在原检验方法的基础上,改变标准使用液的配制方法及工作曲线范围,计算方法的特性参数。结果改进后的方法,检出限0.067μg/10mL,检测下限0.20μg/10mL。若采样体积60L,空气中硫化氢的测定范围0.0033—0.050mg/m3,相对标准偏差为1.7%~8.O%,平均回收率94.1%~100.6%。结论此方法可以测定居住区大气中的硫化氢浓度,也适合测定公共场所或室内空气中的硫化氢含量。 相似文献
98.
M. Morimoto A.-L. Hagbjrk A.A. Nanji M. Ingelman-Sundberg K.O. Lindros P.C. Fu E. Albano S.W. French 《Alcohol》1993,10(6):459-464
The intragastric tube feeding model is ideal for the study of the role of dietary factors and the effect of drugs on experimental alcoholic liver disease (ALD), since the model allows us to study the effect of a single variable in the diet on the pathology of liver where the blood alcohol level (BAL) is maintained over 150 mg%. By varying the dietary fatty acid composition we showed that the pathology was worsened by increasing linoleic acid or polyunsaturated fatty acids (PUFAs) in the diet where cytochrome P4502E1 (CYP2E1) was increased posttranslationally by high BAL. Concomitant with the increase in CYP2E1 there was evidence for an increase in lipid peroxidation (LP) by microsomes. Protein adducts of the products of LP were increased in the blood. Isoniazid (INH) enhanced this process and the pathology of ALD when INH was fed at therapeutic levels with ethanol. Preliminary studies show that diallyl sulfide, which inhibits and destroys liver CYP2E1 selectively, also modified the pathologic effects of ethanol. Thus we postulate that CYP2E1 induction plays a central role in the pathogenesis of ALD. 相似文献
99.
目的 探讨骨质疏松症患者血清硫化氢(H2S)的变化及临床意义。方法 收集骨质疏松症患者128例作为骨质疏松组,另选取腰背部疼痛但排除骨质疏松的患者110例作为对照组。采用双能X线骨密度仪检测腰椎(L1~4)和双侧股骨颈骨密度,亚洲人骨质疏松自我筛查工具(OSTA)筛查骨质疏松风险。采集空腹静脉血5 mL,检测血清H2S、碱性磷酸酶(ALP)、骨特异性碱性磷酸酶(BALP)、血磷、血钙、血清骨钙素、甲状旁腺素(iPTH)、Ⅰ型原胶原N-端前肽(P1NP)、Ⅰ型胶原C-末端肽交联(P1CP)、Ⅰ型胶原羧基端肽β特殊序列(β-CTX)等骨代谢标志物水平。Pearson相关分析骨质疏松症患者血清H2S与骨代谢标志物的相关性。结果 与对照组相比,骨质疏松组患者腰椎骨密度、股骨颈骨密度、OSTA指数和血清H2S浓度下降,血清ALP、BALP、骨钙素、P1NP、P1CP、iPTH水平下降,β-CTX水平升高(P<0.05)。骨质疏松症患者血清H2S与ALP、BALP、血清骨钙素、P1NP、P1CP、iPTH呈正相关,与β-CTX呈负相关(均P<0.05)。结论 骨质疏松症患者血清H2S水平出现明显下降,检测H2S有助于评估患者骨代谢水平。 相似文献
100.
目的:研究尼扎替丁中间体N,N-二甲胺基硫代乙酰胺的合成,考察不同反应温度,反应时间对收率的影响。方法:采用硫氢化钠为催化剂,硫化氢气体直接通入原料N,N-二甲胺基乙腈中反应,然后通过过滤,减压蒸馏得粗品,用异丙醇重结晶得成品,结果:控制反应温度约50℃,通入硫化氢气体反应6小时。结论:该合成方法为N,N-二甲胺基硫代乙酰胺的工业化生产提供了一条新途径。 相似文献