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51.
Biagia La Pira Tarun D. Singh Alejandro A. Rabinstein Giuseppe Lanzino 《Mayo Clinic proceedings. Mayo Clinic》2018,93(12):1786-1793
Objective
To analyze trends in mortality rates, functional outcomes, and treatment in patients with aneurysmal subarachnoid hemorrhage (aSAH) over the past 3 decades.Patients and Methods
We conducted a retrospective review of consecutive patients with aSAH treated at Mayo Clinic in Rochester, Minnesota, between January 1, 1985, and December 31, 2014.Results
A total of 1173 patients identified were grouped by decade of treatment: 1985 to 1994, n=274; 1995 to 2004, n=461; and 2005 to 2014, n=438. Overall, the use of endovascular techniques increased progressively from 5.1% (14) in 1985 to 1994 to 65.5% (287) in 2005 to 2014. This corresponded to a progressive decrease in the rate of clipping from 78.8% (216) in 1985 to 2004 to 21.5% (94) in 2005 to 2014 (P<.001). The percentage of patients admitted with poor clinical grade also increased from 22.3% (61) in 1985 to 1994 to 24.1% (111) in 1995 to 2004 and 29.5% (129) in 2005 to 2014 (P=.06). The in-hospital mortality rate decreased from 22.6% (62) in 1985 to 1994 to 16.3% (75) in 1995 to 2004 and remained relatively constant at 16.7% (73) in 2005 to 2014. Good functional outcome at 3- to 6-month follow-up improved significantly from 64.8% (173) in 1985 to 1994 to 72% (332) in 1995 to 2004 and 78.8% (345) in 2005 to 2014 (P<.001).Conclusion
Outcomes in patients with aSAH have markedly improved over the past 3 decades, in terms of both in-hospital survival and functional recovery of survivors. Higher rates of endovascular coiling over time paralleled these improvements in clinical outcomes. More detailed investigation is necessary to determine whether this or other factors may directly explain the favorable trends in survival and functional recovery over time. 相似文献52.
Vitamin D Analogue: Potent Antiproliferative Effects on Cancer Cell Lines and Lack of Hypercalcemic Activity 下载免费PDF全文
53.
Brian Miller MD Rama Vunnam MD Olurotimi Mesubi MD Mark F. Smith PhD Wengen Chen MD Jagat Bandhu Mahat MD Soren M. Bentzen D.M.Sc PhD Vincent See MD Alejandro Restrepo MD Stephen Shorofsky MD PhD Vasken Dilsizian MD Timm-Michael L. Dickfeld MD PhD 《Journal of cardiovascular electrophysiology》2021,32(8):2238-2245
54.
Chade AR Rodriguez-Porcel M Rippentrop SJ Lerman A Lerman LO 《American journal of hypertension》2003,16(2):111-115
BACKGROUND: Hypercholesterolemia (HC) is a risk factor for renal disease that may activate the angiotensin II type 1 (AT1) receptor and accelerate renal damage. Early diet-induced HC impairs renal perfusion responses, but it is yet unknown whether the AT1 receptor is involved. This study tested the hypothesis that AT1 receptor blockade improved renal perfusion and functional responses in hypercholesterolemic pigs. METHODS: Regional renal hemodynamics and function in vivo were quantified bilaterally in pigs, at baseline and during vasoactive challenge (acetylcholine or sodium nitroprusside), using electron beam computed tomography after 12 weeks of normal (n = 6) or HC diet (n = 6), or HC diet supplemented (100 mg/d) with the AT1-receptor antagonist irbesartan (HC + AT1, n = 6). RESULTS: Basal cortical and medullary perfusion was similar among the groups. Basal tubular function was similar on normal and HC diets, whereas HC + AT1 showed decreased proximal and distal fluid reabsorption. Hypercholesterolemic pigs had blunted cortical perfusion (P = .22) and augmented tubular responses to acetylcholine, whereas on HC + AT1 diet, cortical perfusion (P = .002) and tubular function were similar to normal animals. This was associated with decreased systemic levels of the oxidative stress markers thiobarbituric acid reactive substances. CONCLUSIONS: The AT1 receptor blockade in HC improves renal perfusion and tubular functional responses to endothelium-dependent vasodilators, in association with a decrease in oxidative stress. These results imply involvement of the renin-angiotensin system in the blunted renal cortical perfusion responses observed in HC, and suggest a potential role for these agents in preservation of intrarenal hemodynamics and function in HC. 相似文献
55.
Liu P Liu J Huang W Li MD Dopico AM 《Alcoholism, clinical and experimental research》2003,27(10):1640-1644
BACKGROUND: Ethanol at clinically relevant concentrations increases BKCa channel activity in dorsal root ganglia neurons, GH3 cells, and neurohypophysial terminals, leading to decreases in cell excitability and peptide release. In contrast, ethanol inhibits BKCa channels from aortic myocytes, which likely contributes to alcohol-induced aortic constriction. The mechanisms that determine differential BKCa channel responses to ethanol are unknown. We hypothesized that nonconserved regions in the BKCa channel-forming subunit (slo) are major contributors to the differential alcohol responses of different BKCa channel phenotypes. METHODS: We constructed chimeras by interchanging the core and the tail domains of two BKCa channel-forming subunits (mslo and bslo) that, after expression, differentially respond to ethanol (activation and inhibition, respectively), and studied ethanol action on these mbslo and bmslo chimeric channels using single-channel, patch-clamp techniques. RESULTS AND CONCLUSION: Data from cell-free membranes patches demonstrate that the activity of channels that share a mslo-type core-linker (wt mslo and the mbslo chimera) is consistently and significantly potentiated by acute exposure to ethanol. Thus, a mslo tail is not necessary for ethanol potentiation of slo channels. In contrast, the activity of channels that share a bslo-type core-linker (wt bslo and the bmslo chimera) display heterogenous responses to ethanol: inhibition (in the majority of cases), refractoriness, or activation. Overall, our data indicate that the slo core-linker is a critical region likely contributing to the differential responses of BKCa channels to ethanol. 相似文献
56.
57.
Alejandro Castellanos-Gonzalez Miguel M. Cabada Joan Nichols Guillermo Gomez A. Clinton White Jr. 《Infection and immunity》2013,81(6):1996-2001
The study of human intestinal pathogens has been limited by the lack of methods for the long-term culture of primary human intestinal epithelial cells (PECs). The development of infection models with PECs would allow a better understanding of host-parasite interactions. The objective of this study was to develop a novel method for prolonged in vitro cultivation of PECs that can be used to study Cryptosporidium infection. We isolated intact crypts from human intestines removed during weight loss surgery. The fragments of intestinal layers were cultivated with culture medium supplemented with growth factors and antiapoptotic molecules. After 7 days, the PECs formed self-regenerating cell clusters, forming villi that resemble intestinal epithelium. The PECs proliferated and remained viable for at least 60 days. The cells expressed markers for intestinal stem cells, epithelial cells, and mature enterocytes. The PECs were infected with Cryptosporidium. In contrast to older models in which parasite numbers decay, the burden of parasites increased for >120 h. In summary, we describe here a novel method for the cultivation of self-regenerating human epithelial cells from small intestinal crypts, which contain both intestinal stem cells and mature villus cells. We present data that suggest these cells support Cryptosporidium better than existing cell lines. PECs should provide an improved tool for studying host-parasite interactions involving Cryptosporidium and other intestinal pathogens. 相似文献
58.
Lourdes Serrano Paloma Martínez-Redondo Anna Marazuela-Duque Berta N. Vazquez Scott J. Dooley Philipp Voigt David B. Beck Noriko Kane-Goldsmith Qiang Tong Rosa M. Rabanal Dolors Fondevila Purificación Mu?oz Marcus Krüger Jay A. Tischfield Alejandro Vaquero 《Genes & development》2013,27(6):639-653
The establishment of the epigenetic mark H4K20me1 (monomethylation of H4K20) by PR-Set7 during G2/M directly impacts S-phase progression and genome stability. However, the mechanisms involved in the regulation of this event are not well understood. Here we show that SirT2 regulates H4K20me1 deposition through the deacetylation of H4K16Ac (acetylation of H4K16) and determines the levels of H4K20me2/3 throughout the cell cycle. SirT2 binds and deacetylates PR-Set7 at K90, modulating its chromatin localization. Consistently, SirT2 depletion significantly reduces PR-Set7 chromatin levels, alters the size and number of PR-Set7 foci, and decreases the overall mitotic deposition of H4K20me1. Upon stress, the interaction between SirT2 and PR-Set7 increases along with the H4K20me1 levels, suggesting a novel mitotic checkpoint mechanism. SirT2 loss in mice induces significant defects associated with defective H4K20me1–3 levels. Accordingly, SirT2-deficient animals exhibit genomic instability and chromosomal aberrations and are prone to tumorigenesis. Our studies suggest that the dynamic cross-talk between the environment and the genome during mitosis determines the fate of the subsequent cell cycle. 相似文献
59.