全文获取类型
收费全文 | 31321篇 |
免费 | 2321篇 |
国内免费 | 458篇 |
专业分类
耳鼻咽喉 | 634篇 |
儿科学 | 512篇 |
妇产科学 | 677篇 |
基础医学 | 4452篇 |
口腔科学 | 485篇 |
临床医学 | 2577篇 |
内科学 | 7109篇 |
皮肤病学 | 956篇 |
神经病学 | 2165篇 |
特种医学 | 1616篇 |
外科学 | 4250篇 |
综合类 | 523篇 |
一般理论 | 15篇 |
预防医学 | 1275篇 |
眼科学 | 920篇 |
药学 | 2743篇 |
中国医学 | 339篇 |
肿瘤学 | 2852篇 |
出版年
2023年 | 174篇 |
2022年 | 342篇 |
2021年 | 991篇 |
2020年 | 497篇 |
2019年 | 817篇 |
2018年 | 948篇 |
2017年 | 679篇 |
2016年 | 906篇 |
2015年 | 1237篇 |
2014年 | 1461篇 |
2013年 | 1676篇 |
2012年 | 2450篇 |
2011年 | 2528篇 |
2010年 | 1521篇 |
2009年 | 1302篇 |
2008年 | 1846篇 |
2007年 | 1759篇 |
2006年 | 1591篇 |
2005年 | 1523篇 |
2004年 | 1278篇 |
2003年 | 1244篇 |
2002年 | 1129篇 |
2001年 | 755篇 |
2000年 | 678篇 |
1999年 | 636篇 |
1998年 | 246篇 |
1997年 | 226篇 |
1996年 | 200篇 |
1995年 | 171篇 |
1994年 | 150篇 |
1993年 | 98篇 |
1992年 | 305篇 |
1991年 | 230篇 |
1990年 | 264篇 |
1989年 | 257篇 |
1988年 | 243篇 |
1987年 | 198篇 |
1986年 | 177篇 |
1985年 | 161篇 |
1984年 | 140篇 |
1983年 | 111篇 |
1982年 | 79篇 |
1981年 | 71篇 |
1980年 | 69篇 |
1979年 | 124篇 |
1978年 | 82篇 |
1977年 | 66篇 |
1975年 | 59篇 |
1974年 | 53篇 |
1972年 | 49篇 |
排序方式: 共有10000条查询结果,搜索用时 31 毫秒
921.
Glenn M. Stewart Courtney M. Wheatley‐Guy Bruce D. Johnson Win K. Shen Chul‐Ho Kim 《Journal of clinical hypertension (Greenwich, Conn.)》2020,22(6):1083-1089
The present study investigated the impact of 12 weeks of pulsed electromagnetic field (PEMF) therapy on peripheral vascular function, blood pressure (BP), and nitric oxide in hypertensive individuals. Thirty hypertensive individuals (SBP > 130 mm Hg and/or MAP > 100 mm Hg) were assigned to either PEMF group (n = 15) or control group (n = 15). During pre‐assessment, participants underwent measures of flow‐mediated dilation (FMD), BP, and blood draw for nitric oxide (NO). Subsequently, they received PEMF therapy 3x/day for 12 weeks and, at conclusion, returned to the laboratory for post‐assessment. Fifteen participants from the PEMF group and 11 participants from the control group successfully completed the study protocol. After therapy, the PEMF group demonstrated significant improvements in FMD and FMDNOR (normalized to hyperemia), but the control group did not (P = .05 and P = .04, respectively). Moreover, SBP, DBP, and MAP were reduced, but the control group did not (P = .04, .04, and .03, respectively). There were no significant alterations in NO in both groups (P > .05). Twelve weeks of PEMF therapy may improve BP and vascular function in hypertensive individuals. Additional studies are needed to identify the mechanisms by which PEMF affects endothelial function. 相似文献
922.
Raymond Chuen-Chung Chang Yuen-Shan Ho Shun Wong Stephen M. Gentleman Ho-Keung Ng 《Acta neuropathologica》2014,127(1):53-69
It is well established that cigarette smoking is hazardous to health and is a risk factor for many chronic diseases. However, its impact on the brain, whether it be from prenatal exposure to maternal cigarette smoking, cerebrovascular disease, Alzheimer’s disease (AD) or Parkinson’s disease, is still not very clear. Neuroimaging and neuropathological investigations suggest that there are heterogeneous effects of cigarette smoking on the brain. On the one hand, it is quite clear that cigarette smoking causes damage to endothelial cells, resulting in increased risk of cerebrovascular disease. On the other hand, it seems to be associated with different Alzheimer’s pathologies in post-mortem brains and experimental models, despite the fact that epidemiological studies clearly indicate a positive correlation between cigarette smoking and increased risk for AD. Interestingly, cigarette smoking appears to be associated with reduced Parkinson’s pathology in post-mortem brains. However, although nicotine in cigarettes may have some neuroprotective actions, the effects of all the other toxic compounds in cigarettes cannot be ignored. It is, therefore, our aim to summarize what is known about the neuropathology of cigarette smoking and, in particular, its implications for neurodegenerative diseases. 相似文献
923.
924.
HH Chang YM Huang CP Wu YC Tang CW Liu CH Huang LT Ho LY Wu YC Kuo YH Kao 《General and comparative endocrinology》2012,178(3):450-458
Endothelin (ET)-1 and suppressor of cytokine signaling (SOCS)-3 were respectively found to regulate energy metabolism and hormone signaling in fat cells. Although ET-1 can also regulate the expression of SOCS-3-stimulating hormones, it is still unknown whether ET-1 regulates SOCS-3 gene expression. This study investigated the pathways involved in ET-1's modulation of SOCS-3 gene expression in 3T3-L1 adipocytes. ET-1 upregulated SOCS-3 mRNA and protein expression in dose- and time-dependent manners. The concentration of ET-1 that increased SOCS-3 mRNA levels by 250-400% was ~100nM with 2-4h of treatment. Treatment with actinomycin D prevented ET-1-stimulated SOCS-3 mRNA expression, suggesting that the effect of ET-1 requires new mRNA synthesis. Pretreatment with the ET type A receptor (ET(A)R) antagonist, BQ-610, but not the ET type B receptor (ET(B)R) antagonist, BQ-788, prevented the stimulatory effect of ET-1 on SOCS-3 gene expression. The specific inhibitors of either MEK1 (U-0126 and PD-98059), JAK (AG-490), JNK (SP-600125), or PI3K (LY-294002 and wortmannin) reduced ET-1-increased levels of SOCS-3 mRNA and respectively inhibited ET-1-stimulated activities of MEK1, JAK, JNK, and PI3K. These results imply that the ET(A)R, ERK, JAK, JNK, and PI3K are functionally necessary for ET-1's stimulation of SOCS-3 gene expression. Moreover, ET-1 was observed to upregulate expressions of SOCS-1, -2, -3, -4, -5, and -6 mRNAs, but not SOCS-7 or cytokine-inducible SH2-containing protein-1 mRNAs. This suggests that ET-1 selectively affects particular types of SOCS family members. Changes in SOCS gene expressions induced by ET-1 may help explain the mechanism by which ET-1 modulates hormone signaling of adipocytes. 相似文献
925.
Shin DH Lee MJ Kim SJ Oh HJ Kim HR Han JH Koo HM Doh FM Park JT Han SH Yoo TH Kang SW 《The Journal of clinical endocrinology and metabolism》2012,97(8):2732-2740
Context: Subclinical hypothyroidism is not a rare condition, but the use of thyroid hormone to treat subclinical hypothyroidism is an issue of debate. Objective: This study was undertaken to investigate the impact of thyroid hormone therapy on the changes in estimated glomerular filtration rate (eGFR) in subclinical hypothyroidism patients with stage 2-4 chronic kidney disease. Patients: A total of 309 patients were included in the final analysis. Main Outcome Measure: The changes in eGFR over time were compared between patients with and without thyroid hormone replacement therapy using a linear mixed model. Kaplan-Meier curves were constructed to determine the effect of thyroid hormone on renal outcome, a reduction of eGFR by 50%, or end-stage renal disease. The independent prognostic value of subclinical hypothyroidism treatment for renal outcome was ascertained by multivariate Cox regression analysis. Results: Among the 309 patients, 180 (58.3%) took thyroid hormone (treatment group), whereas 129 (41.7%) did not (nontreatment group). During the mean follow-up duration of 34.8 ± 24.3 months, the overall rate of decline in eGFR was significantly greater in the nontreatment group compared to the treatment group (-5.93 ± 1.65 vs. -2.11 ± 1.12 ml/min/yr/1.73 m(2); P = 0.04). Moreover, a linear mixed model revealed that there was a significant difference in the rates of eGFR decline over time between the two groups (P < 0.01). Kaplan-Meier analysis also showed that renal event-free survival was significantly lower in the nontreatment group (P < 0.01). In multivariate Cox regression analysis, thyroid hormone replacement therapy was found to be an independent predictor of renal outcome (hazard ratio, 0.28; 95% CI, 0.12-0.68; P = 0.01). Conclusion: Thyroid hormone therapy not only preserved renal function better, but was also an independent predictor of renal outcome in chronic kidney disease patients with subclinical hypothyroidism. 相似文献
926.
DB Foster AS Ho J Rucker AO Garlid L Chen A Sidor KD Garlid B O'Rourke 《Circulation research》2012,111(4):446-454
Rationale: Activation of the mitochondrial ATP-sensitive potassium channel (mitoK(ATP)) has been implicated in the mechanism of cardiac ischemic preconditioning, yet its molecular composition is unknown. Objective: To use an unbiased proteomic analysis of the mitochondrial inner membrane to identify the mitochondrial K(+) channel underlying mitoK(ATP). Methods and Results: Mass spectrometric analysis was used to identify KCNJ1(ROMK) in purified bovine heart mitochondrial inner membrane and ROMK mRNA was confirmed to be present in neonatal rat ventricular myocytes and adult hearts. ROMK2, a short form of the channel, is shown to contain an N-terminal mitochondrial targeting signal, and a full-length epitope-tagged ROMK2 colocalizes with mitochondrial ATP synthase β. The high-affinity ROMK toxin, tertiapin Q, inhibits mitoK(ATP) activity in isolated mitochondria and in digitonin-permeabilized cells. Moreover, short hairpin RNA-mediated knockdown of ROMK inhibits the ATP-sensitive, diazoxide-activated component of mitochondrial thallium uptake. Finally, the heart-derived cell line, H9C2, is protected from cell death stimuli by stable ROMK2 overexpression, whereas knockdown of the native ROMK exacerbates cell death. Conclusions: The findings support ROMK as the pore-forming subunit of the cytoprotective mitoK(ATP) channel. 相似文献
927.
928.
929.
930.