首页 | 本学科首页   官方微博 | 高级检索  
文章检索
  按 检索   检索词:      
出版年份:   被引次数:   他引次数: 提示:输入*表示无穷大
  收费全文   39901篇
  免费   2365篇
  国内免费   1069篇
耳鼻咽喉   116篇
儿科学   1466篇
妇产科学   1404篇
基础医学   4829篇
口腔科学   402篇
临床医学   3425篇
内科学   7108篇
皮肤病学   372篇
神经病学   3633篇
特种医学   538篇
外国民族医学   6篇
外科学   3093篇
综合类   5696篇
现状与发展   6篇
预防医学   1711篇
眼科学   168篇
药学   6427篇
  15篇
中国医学   1408篇
肿瘤学   1512篇
  2024年   45篇
  2023年   340篇
  2022年   690篇
  2021年   1132篇
  2020年   954篇
  2019年   954篇
  2018年   940篇
  2017年   1067篇
  2016年   1081篇
  2015年   1183篇
  2014年   2098篇
  2013年   2631篇
  2012年   2021篇
  2011年   2332篇
  2010年   1930篇
  2009年   1820篇
  2008年   1867篇
  2007年   1854篇
  2006年   1810篇
  2005年   1662篇
  2004年   1341篇
  2003年   1267篇
  2002年   1061篇
  2001年   992篇
  2000年   890篇
  1999年   747篇
  1998年   656篇
  1997年   692篇
  1996年   644篇
  1995年   557篇
  1994年   570篇
  1993年   507篇
  1992年   511篇
  1991年   474篇
  1990年   481篇
  1989年   399篇
  1988年   339篇
  1987年   300篇
  1986年   312篇
  1985年   364篇
  1984年   310篇
  1983年   228篇
  1982年   255篇
  1981年   222篇
  1980年   177篇
  1979年   159篇
  1978年   130篇
  1977年   94篇
  1976年   72篇
  1975年   51篇
排序方式: 共有10000条查询结果,搜索用时 31 毫秒
1.
2.
3.
目的:探讨甲状旁腺激素(PTH)对大鼠牵张成骨(DO)过程中ONC、OPN、C-FOS、COL1、VEGF、RUNX2、ALP基因表达的影响。方法30只雄性大鼠制备大鼠下颌骨DO模型。随机分5组,每组6只。第1组(只有牵张无PTH),术后8周取材,应用HE染色及微CT检测,以确定成骨情况。第2组(有牵张无PTH),第3组(有牵张有PTH),第4组(无牵张有PTH),第5组(对照组:无牵张无PTH)。2、3、4组及对照组术后1周取材,RT-PCR测定ONC、OPN、C-FOS、COL1、VEGF、RUNX2、ALP基因的表达。结果第1组,新骨形成,骨质充满牵张区,骨质连续,大鼠建模成功。RT-PCR检测结果显示,2、3、4组与对照组比较,OPN、COL1、RUNX2、ALP基因表达有明显提高(P<0.05),其中第3组最为明显。ONC、C-FOS、VEGF基因2、3、4组与对照组比较差异无统计学意义(P>0.05)。结论 PTH在 DO 过程中,间歇性给以 PTH的作用只有在牵张期发挥作用,其对 OPN、COL1、RUNX2、ALP基因表达能够获得理想的协同作用。  相似文献   
4.
5.

Objective

To assay peripheral inter-ictal cytokine serum levels and possible relations with non-invasive vagus nerve stimulation (nVNS) responsiveness in migraineurs.

Methods

This double-blinded, sham-controlled study enrolled 48 subjects and measured headache severity, frequency [headache days/month, number of total and mild/moderate/severe classified attacks/month], functional state [sleep, mood, body weight, migraine-associated disability] and serum levels of inflammatory markers [inter-ictal] using enzyme-linked immunoassays at baseline and after 2 months of adjunctive nVNS compared to sham stimulation and suitably matched controls.

Results

No significant differences were observed at baseline and after 2 months for headache severity, total attacks/month, headache days/month and functional outcome [sleep, mood, disability] between verum and sham nVNS. However, the number of severe attacks/month significantly decreased in the verum nVNS group and circulating pro-inflammatory IL-1β was elevated significantly in the sham group compared to nVNS. Levels of anti-inflammatory IL-10 were significantly higher at baseline in both groups compared to healthy controls, but not at 2 months follow-up [p?<?0.05]. Concentrations of high-mobility group box-1 (HMGB-1), IL-6, tumor-necrosis factor-α (TNF-α), leptin, adiponectin, ghrelin remained unchanged [p?>?0.05]. No severe device-/stimulation-related adverse events occurred.

Conclusion

2 months of adjunctive cervical nVNS significantly declined the number of severe attacks/month. Pro-inflammatory IL-1β plasma levels [inter-ictal] were higher in sham-treated migraine patients compared to verum nVNS. However, pro- [IL-6, HMGB-1, TNF-α, leptin] and anti-inflammatory [IL-10, adiponectin, ghrelin] mediators did not differ statistically. Profiling of neuroinflammatory circuits in migraine to predict nVNS responsiveness remains an experimental approach, which may be biased by pre-analytic variables warranting large-scale biobank-based systematic investigations [omics].  相似文献   
6.
Background/objectiveObstructive sleep apnea (OSA) is independently associated with dyslipidemia, a surrogate marker of atherosclerosis. Low-density lipoprotein (LDL)-cholesterol is accepted as a major independent risk factor for cardiovascular disease. However, non-high-density lipoprotein (HDL)-cholesterol is a better marker of atherogenic dyslipidemia and recommended as a target of lipid lowering therapy. We aimed to assess the prevalence of atherogenic dyslipidemia, and relationship between OSA severity and serum LDL-cholesterol and non-HDL cholesterol levels in OSA patients.MethodsWe retrospectively evaluated treatment naïve 2361 subjects admitted to the sleep laboratory of a university hospital for polysomnography. All subjects’ lipid profile including total cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides, and non-HDL-cholesterol were measured.ResultsOut of 2361 patients (mean age 49.6 ± 11.9 years; 68.9% male, apnea-hypopnea index 36.6 ± 28.4/h), 185 (7.8%) had no OSA and 2176 (92.2%) had OSA. Atherogenic dyslipidemia prevalence was high (57–66%) in OSA patients, and especially increased in severe OSA compared to other groups (p < 0.05). Though total and LDL-cholesterol did not differ between those with and without OSA, non-HDL-cholesterol (p = 0.020), and triglycerides (p = 0.001) were higher and HDL-cholesterol levels (p = 0.018) were lower in OSA patients than non-OSA. Non-HDL-cholesterol was significantly correlated with OSA severity (p < 0.001) and hypoxia parameters (p < 0.01), whereas LDL-cholesterol showed no correlation.ConclusionsAtherogenic dyslipidemia is highly prevalent and non-HDL-cholesterol levels are significantly increased, predominantly in severe OSA patients. Non-HDL-cholesterol but not LDL-cholesterol, is significantly correlated with OSA severity and hypoxia parameters. Therefore, it could be better to use non-HDL-cholesterol, which is a guideline recommended target of lipid therapy, as a marker of atherosclerotic cardiovascular risk in OSA patients.  相似文献   
7.
8.
目的探讨参附注射液对老年重症肺炎疗效及N末端B型利钠肽原(NT-pro BNP)的影响。方法选择2016年6月—2019年6月医院收治的老年重症肺炎患者80例,以随机数表法将其分为两组,即对照组与研究组各40例。对照组患者接受常规对症治疗,研究组在此基础上应用参附注射液治疗。对比两组临床疗效,治疗前与治疗3 d、5 d时血浆NT-pro BNP水平,以及不良反应情况。结果研究组治疗的总有效率为95.00%,高于对照组77.50%(P<0.05)。治疗后3 d与5 d时研究组血浆NT-pro BNP水平均低于对照组(P<0.01)。两组治疗期间均未见明显的药物不良反应。结论参附注射液能够有效提高老年重症肺炎患者的疗效,调节脑钠肽水平。  相似文献   
9.
10.
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号