全文获取类型
收费全文 | 487篇 |
免费 | 35篇 |
专业分类
耳鼻咽喉 | 3篇 |
儿科学 | 6篇 |
妇产科学 | 23篇 |
基础医学 | 62篇 |
口腔科学 | 11篇 |
临床医学 | 64篇 |
内科学 | 131篇 |
皮肤病学 | 1篇 |
神经病学 | 46篇 |
特种医学 | 11篇 |
外科学 | 60篇 |
综合类 | 21篇 |
预防医学 | 40篇 |
眼科学 | 2篇 |
药学 | 31篇 |
肿瘤学 | 10篇 |
出版年
2023年 | 4篇 |
2022年 | 4篇 |
2021年 | 11篇 |
2020年 | 7篇 |
2019年 | 8篇 |
2018年 | 13篇 |
2017年 | 12篇 |
2016年 | 6篇 |
2015年 | 10篇 |
2014年 | 24篇 |
2013年 | 19篇 |
2012年 | 46篇 |
2011年 | 51篇 |
2010年 | 27篇 |
2009年 | 24篇 |
2008年 | 30篇 |
2007年 | 27篇 |
2006年 | 20篇 |
2005年 | 16篇 |
2004年 | 14篇 |
2003年 | 16篇 |
2002年 | 19篇 |
2001年 | 6篇 |
2000年 | 8篇 |
1999年 | 10篇 |
1998年 | 6篇 |
1997年 | 6篇 |
1996年 | 2篇 |
1995年 | 5篇 |
1994年 | 2篇 |
1993年 | 3篇 |
1992年 | 10篇 |
1991年 | 2篇 |
1990年 | 7篇 |
1989年 | 7篇 |
1988年 | 5篇 |
1987年 | 7篇 |
1986年 | 3篇 |
1985年 | 6篇 |
1984年 | 2篇 |
1983年 | 2篇 |
1980年 | 2篇 |
1978年 | 1篇 |
1977年 | 3篇 |
1975年 | 1篇 |
1973年 | 1篇 |
1972年 | 1篇 |
1971年 | 1篇 |
1966年 | 1篇 |
1944年 | 1篇 |
排序方式: 共有522条查询结果,搜索用时 15 毫秒
1.
J. O’Byrne S. Eustace M. M. Stephens M. N. M. R. Farahat G. Yanni R. Posten G. S. Panayi S. Sant R. Costello M. Barry J. Hassan C. Feighery B. Bresnihan A. Whelan F. Coakley A. M. de Paor R. B. Reilly E. B. Casey V. J. Tormey G. Kearns K. Gaffney P. J. Freyne M. Callaghan O. FitzGerald D. Veale E. O’Nuallain D. Reen D. Veale M. Farrell O. FitzGerald S. Rogers L. Barnes R. J. Coughlan C. McCarthy M. McDermott D. Hourihane C. O'Morain S. O'Reilly P. Hartley E. Casey L. Clancy F. Mulcahy N. Hall A. Murphy C. Breen D. Kelleher M. Abuzakouk C. O'Farrelly 《Irish journal of medical science》1992,161(6):438-442
2.
Michaël Chopin Aaron T. Lun Yifan Zhan Jaring Schreuder Hannah Coughlan Angela D’Amico Lisa A. Mielke Francisca F. Almeida Andrew J. Kueh Ross A. Dickins Gabrielle T. Belz Shalin H. Naik Andrew M. Lew Phillipe Bouillet Marco J. Herold Gordon K. Smyth Lynn M. Corcoran Stephen L. Nutt 《Immunity》2019,50(1):77-90.e5
3.
4.
The role of the protein glycosylation state in the control of cellular transport of the amyloid beta precursor protein 总被引:5,自引:0,他引:5
The amyloid beta precursor protein can exist as both a membrane-bound and a secreted protein, with the former having the potential to generate the amyloid beta peptide present in the neuritic plaques which are characteristic of Alzheimer's disease. In this study, we have used a clone of the AtT20 mouse pituitary cell line which expresses high levels of the amyloid beta precursor protein to characterize the glycosylation state of the secreted and membrane-bound forms of the protein and to examine the role of post-translational modifications in protein processing. Lectin blot analysis of immunoprecipitated amyloid beta precursor protein demonstrated that the soluble form of the protein contains significant amounts of sialic acid, with the lectin staining being reduced in the particulate cellular fractions. Treatment of the cells with mannosidase inhibitors to interfere with the formation of complex-type N-linked glycans resulted in a decrease in secreted amyloid beta precursor protein and an increase in the level of the cellular form of the protein. The increase in amyloid beta precursor protein levels in the cellular fraction was accompanied by an increase in perinuclear staining. Furthermore, cells overexpressing the alpha2,6(N)-sialyltransferase enzyme also demonstrated an increase in amyloid beta precursor protein secretion. These results suggest that the presence of terminal sialic acid residues on complex-type N-glycans may be required for the optimal transport of the amyloid beta precursor protein from the Golgi to the cell membrane with the subsequent cleavage to generate the secreted form of the protein. 相似文献
5.
6.
W. O. Tobin J. A. Kinsella G. F. Kavanagh J. S. O’Donnell R. A. McGrath D. R. Collins T. Coughlan D. O’Neill B. Egan S. Tierney T. M. Feeley R. P. Murphy Dominick J. H. McCabe 《Journal of neurology》2013,260(2):590-596
The impact of changing antiplatelet therapy on thrombin generation potential in patients with ischaemic cerebrovascular disease (CVD) is unclear. We assessed patients within 4 weeks of TIA or ischaemic stroke (baseline), and then 14 days (14d) and >90 days (90d) after altering antiplatelet therapy. Thrombin generation was assessed in platelet poor plasma. Ninety-one patients were recruited. Twenty-four were initially assessed on no antiplatelet therapy, and then after 14d (N = 23) and 90d (N = 8) on aspirin monotherapy; 52 were assessed on aspirin monotherapy, and after 14 and 90 days on aspirin and dipyridamole combination therapy; 21 patients were assessed on aspirin and after 14 days (N = 21) and 90 days (N = 19) on clopidogrel. Peak thrombin generation and endogenous thrombin potential were reduced at 14 and 90 days (p ≤ 0.04) in the overall cohort. We assessed the impact of individual antiplatelet regimens on thrombin generation parameters to investigate the cause of this effect. Lag time and time-to-peak thrombin generation were unchanged at 14 days, but reduced 90 days after commencing aspirin (p ≤ 0.009). Lag time, peak thrombin generation and endogenous thrombin potential were reduced at both 14 and 90 days after adding dipyridamole to aspirin (p ≤ 0.01). Lag time was reduced 14 days after changing from aspirin to clopidogrel (p = 0.045), but this effect was not maintained at 90 days (p = 0.2). This pilot study did not show any consistent effects of commencing aspirin, or of changing from aspirin to clopidogrel on thrombin generation potential during follow-up. The addition of dipyridamole to aspirin led to a persistent reduction in peak and total thrombin generation ex vivo, and illustrates the diverse, potentially beneficial, newly recognised ‘anti-coagulant’ effects of dipyridamole in ischaemic CVD. 相似文献
7.
Identifying Stage B colorectal cancer patients at high risk of tumor recurrence and death 总被引:6,自引:3,他引:6
Dr. Hugh E. Mulcahy M.D. M.R.C.P.I. Mary Toner M.D. M.R.C.Path. Stephen E. Patchett M.D. M.R.C.P.I. Leslie Daly M.Sc Ph.D. Hon. M.F.P.H.M. Diarmuid P. O'Donoghue M.D. F.R.C.P. F.R.C.P.I. 《Diseases of the colon and rectum》1997,40(3):326-331
PURPOSE: This study was designed to determine clinical and pathologic variables associated with poor outcome following resection of Stage B colorectal cancer. METHODS: This was a retrospective study of 117 patients with Stage B cancer who underwent curative surgery and survived the postoperative period. Fourteen clinical and pathologic features were studied. Clinical data were extracted from a prospective colorectal cancer database, and histologic slides were retreived and examined by a pathologist blinded as to clinical details and outcome. RESULTS: After a median follow-up period of 8.2 years, bowel obstruction was significantly related to a poor prognosis (log-rank test; P=0.03). Extensive necrosis (P
=0.01) and perineural invasion (P
= 0.03) were also associated with decreased survival. Vascular invasion was associated with poor long-term outcome in the subgroup of patients with rectal (P
=0.07) but not colonic (P
=0.57) cancer. Multivariate regression analysis identified both tumor necrosis (P
=0.01) and perineural invasion (P
=0.03) as independently related to outcome. CONCLUSION: Further study of prognostic indicators might result in an algorithm to distinguish Stage B cases at high risk of tumor recurrence and death. Such patients could be included in future trials of adjuvant therapies.Presented in part at the meeting of the American Gastroenterological Association, Boston, Massachusetts, May 16 to 19, 1993. Published in abstract form in Gastroenterology 1993;104:A432. 相似文献
8.
Karl Fullam Brian Caulfield Garrett F. Coughlan Mark McGroarty Eamonn Delahunt 《Journal of Athletic Training》2015,50(9):893-904
Context
Decreased postural stability is a primary risk factor for lower limb musculoskeletal injuries. During athletic competitions, cryotherapy may be applied during short breaks in play or during half-time; however, its effects on postural stability remain unclear.Objective
To investigate the acute effects of a 15-minute ankle-joint cryotherapy application on dynamic postural stability.Design
Controlled laboratory study.Setting
University biomechanics laboratory.Patients or Other Participants
A total of 29 elite-level collegiate male field-sport athletes (age = 20.8 ± 1.12 years, height = 1.80 ± 0.06 m, mass = 81.89 ± 8.59 kg) participated.Intervention(s)
Participants were tested on the anterior (ANT), posterolateral (PL), and posteromedial (PM) reach directions of the Star Excursion Balance Test before and after a 15-minute ankle-joint cryotherapy application.Main Outcome Measure(s)
Normalized reach distances; sagittal-plane kinematics of the hip, knee, and ankle joints; and associated mean velocity of the center-of-pressure path during performance of the ANT, PL, and PM reach directions of the Star Excursion Balance Test.Results
We observed a decrease in reach-distance scores for the ANT, PL, and PM reach directions from precryotherapy to postcryotherapy (P < .05). No differences were observed in hip-, knee-, or ankle-joint sagittal-plane kinematics (P > .05). We noted a decrease in mean velocity of the center-of-pressure path from precryotherapy to postcryotherapy (P < .05) in all reach directions.Conclusions
Dynamic postural stability was adversely affected immediately after cryotherapy to the ankle joint.Key Words: postural balance, lower limb, kineticsKey Points
- A 15-minute cryotherapy application to the ankle joint decreased cutaneous temperature recorded over the anterior talofibular ligament and deltoid ligament.
- Reach distances in the anterior, posterolateral, and posteromedial directions of the Star Excursion Balance Test and center-of-pressure mean velocity decreased after cryotherapy.
- A 15-minute cryotherapy application negatively influenced dynamic postural-stability performance.
- Elite-level field-based athletes should undergo a rewarming period before returning to participation after cryotherapy to the ankle joint to ensure they are not predisposed to injury due to decreased dynamic postural stability.
9.
Diarmuid J. Cahalane Christine J. Charvet Barbara L. Finlay 《Proceedings of the National Academy of Sciences of the United States of America》2014,111(49):17642-17647
A massive increase in the number of neurons in the cerebral cortex, driving its size to increase by five orders of magnitude, is a key feature of mammalian evolution. Not only are there systematic variations in cerebral cortical architecture across species, but also across spatial axes within a given cortex. In this article we present a computational model that accounts for both types of variation as arising from the same developmental mechanism. The model employs empirically measured parameters from over a dozen species to demonstrate that changes to the kinetics of neurogenesis (the cell-cycle rate, the progenitor death rate, and the “quit rate,” i.e., the ratio of terminal cell divisions) are sufficient to explain the great diversity in the number of cortical neurons across mammals. Moreover, spatiotemporal gradients in those same parameters in the embryonic cortex can account for cortex-wide, graded variations in the mature neural architecture. Consistent with emerging anatomical data in several species, the model predicts (i) a greater complement of neurons per cortical column in the later-developing, posterior regions of intermediate and large cortices, (ii) that the extent of variation across a cortex increases with cortex size, reaching fivefold or greater in primates, and (iii) that when the number of neurons per cortical column increases, whether across species or within a given cortex, it is the later-developing superficial layers of the cortex which accommodate those additional neurons. We posit that these graded features of the cortex have computational and functional significance, and so must be subject to evolutionary selection.Changes in brain structure follow a remarkably stable pattern over ∼450 My in the vertebrate lineage: it is always the same brain parts that become enlarged when overall brain size increases (1). Moreover, in studies of individual variation in humans and other mammals, when overall brain size is larger, those same divisions as would be predicted by looking at brain enlargement across taxa are also found to be preferentially enlarged (2, 3). Such regularities in brain scaling from the individual to the taxon level suggest that the developmental mechanisms which generate central nervous systems are strongly conserved across species (4).To tease apart the features of the isocortex contributed by the scaling of conserved developmental mechanisms from those features which might be specially selected for in a given niche or species, we have created an empirically informed, mathematical model of cortical neurogenesis. The model elucidates how the dials and levers made available by conserved developmental mechanisms allow selection to shape the basic landscape of the embryonic cortex. The extent to which any particular cortical area (e.g., a visual or language area) has been a special subject of selection can be better evaluated given the baselines provided by this evolutionary developmental or “evo-devo” model.The modeling approach presented here provides an explicit structure to assimilate known data and predict unknowns, both for developmental kinetic parameters and for the resultant time courses of neuronal and progenitor cell populations, for the entire range of mammalian brain sizes and across a spatial axis within the respective cortices. Our model incorporates important insights from several previously published mathematical models of cortical neurogenesis which focus on more limited sets of species or which consider spatial variations in a single species (5–10). 相似文献