全文获取类型
收费全文 | 1135篇 |
免费 | 96篇 |
国内免费 | 2篇 |
专业分类
耳鼻咽喉 | 13篇 |
儿科学 | 36篇 |
妇产科学 | 9篇 |
基础医学 | 112篇 |
口腔科学 | 30篇 |
临床医学 | 235篇 |
内科学 | 168篇 |
皮肤病学 | 21篇 |
神经病学 | 31篇 |
特种医学 | 80篇 |
外科学 | 138篇 |
综合类 | 18篇 |
一般理论 | 1篇 |
预防医学 | 231篇 |
眼科学 | 2篇 |
药学 | 61篇 |
1篇 | |
肿瘤学 | 46篇 |
出版年
2021年 | 13篇 |
2020年 | 10篇 |
2019年 | 12篇 |
2018年 | 13篇 |
2017年 | 14篇 |
2016年 | 10篇 |
2015年 | 33篇 |
2014年 | 29篇 |
2013年 | 34篇 |
2012年 | 59篇 |
2011年 | 57篇 |
2010年 | 39篇 |
2009年 | 28篇 |
2008年 | 29篇 |
2007年 | 59篇 |
2006年 | 47篇 |
2005年 | 45篇 |
2004年 | 27篇 |
2003年 | 30篇 |
2002年 | 27篇 |
2001年 | 23篇 |
2000年 | 24篇 |
1999年 | 30篇 |
1998年 | 34篇 |
1997年 | 28篇 |
1996年 | 35篇 |
1995年 | 18篇 |
1994年 | 22篇 |
1993年 | 17篇 |
1992年 | 39篇 |
1991年 | 36篇 |
1990年 | 43篇 |
1989年 | 37篇 |
1988年 | 21篇 |
1987年 | 15篇 |
1986年 | 20篇 |
1985年 | 14篇 |
1984年 | 12篇 |
1983年 | 9篇 |
1982年 | 7篇 |
1981年 | 8篇 |
1979年 | 14篇 |
1977年 | 9篇 |
1976年 | 7篇 |
1975年 | 7篇 |
1973年 | 9篇 |
1972年 | 7篇 |
1968年 | 7篇 |
1967年 | 9篇 |
1966年 | 8篇 |
排序方式: 共有1233条查询结果,搜索用时 15 毫秒
1.
2.
Elliot Carlisle MD Mario Luna MD Paul M. Tsou MD Jeffrey C. Wang MD 《The spine journal》2005,5(6):608-614
BACKGROUND CONTEXT: There is limited information describing the correlation between the initial quantitative measurements on magnetic resonance imaging (MRI) scans of disc herniation area, canal cross-section areas, percent canal compromise, and disc herniation location to the need for surgery. PURPOSE: Our aim is to determine if the size of disc herniation area, canal cross-section area, percent canal compromise, and disc herniation location taken from MRI images of patients with symptomatic single-level lumbar herniated intervertebral discs upon initial presentation to a spine surgeon, were predictive of the need for surgical treatment. STUDY DESIGN/SETTING: This is a retrospective case matched study of patient MRI images in the senior author's private practice. PATIENT SAMPLE: From a pool of 332 patients with sciatica caused by lumbar intervertebral disc herniations at our institution, 65 patients had surgery, of which MRI images were available and analyzed on 44 patients. Forty-four additional patients were randomly selected from the remaining 267 original group as nonoperative controls. METHODS: The axial MRI image showing the largest canal compromise by the herniated disc was selected for measurements. Using T1- and T2-weighted images, the areas of interest were digitally scanned at high resolution. The canal area and disc herniation area measurement were calculated from the total number of pixels per cross-sectional area, multiplied by a scan correction factor, mm(2) /pixel. Disc herniation locations were classified into either central or paracentral. The percent canal compromise was obtained by disc herniation area divided by canal cross-section area and multiplied by 100. RESULTS: The surgical group's overall mean herniated disc area was 219.6 square millimeter (mm(2)), 179.8 at L4-5, and 267.4 at L5-S1. The nonoperative group's overall mean herniated disc area was 178.4 mm(2), 135.1 at L2-3, 160.3 at L4-5, and 207.4 at L5-S1. The surgical group's overall mean canal cross-sectional area was 471.8 mm(2), 418.6 at L4-5, and 535.6 at L5-S1. The nonoperative group's overall mean canal cross-sectional area was 541.3 mm(2), 518.1 at L2-3, 446.8 at L4-5, and 669.9 at L5-S1. The overall percent canal compromise ratio in the surgery group was 46.7%, 44.1% at L4-5, and 49.8% at L5-S1. The overall percent canal compromise in the nonoperative group was 34.2%, 34.1% at L2-3, 36.1% at L4-5, and 31.8% at L5-S1. The percent canal compromise in central herniations at L4-5 level was 53.0% in the surgical group, and 32.8% in the nonoperative group; at the L5-S1 level surgical group percent canal compromise was 64.1% and in the nonoperative group canal compromise was 27%. L4-L5 level paracentral herniations canal compromise was 36.7% in the surgical group compared with 42.5% canal compromise in the nonoperative group. At the L5-S1 level the canal compromise was 45% in the surgical group and 34.8% in the nonoperative group. CONCLUSIONS: Our findings show a trend for patients treated with surgery to have larger disc herniation areas and smaller canal cross-section areas, corresponding to larger percent canal compromise than the nonoperative group. Centrally located herniations followed this trend closely at all levels studied. However, the paracentral herniation at the L4-5 level does not follow this trend, possibly because paracentral disc herniation clinical course is determined more by herniation location rather than the overall herniation size. 相似文献
3.
4.
5.
E. J. Carlisle J. D. Allen W. G. Kernohan W. Leahey A. A. Adgey 《British journal of pharmacology》1990,100(3):530-534
1. The effects of anti-arrhythmic drugs on the power spectrum of established ventricular fibrillation induced by endocardial electrical stimulation, have been studied in greyhounds anaesthetized with sodium pentobarbitone (35 mg kg-1, i.v.). 2. In dogs receiving no drug, initial recording of ventricular fibrillation showed a dominant frequency of 9.9 +/- 0.7 Hz (lead II) and 10.0 +/- 0.6 Hz (endocardium). After 3.3 min the frequency had fallen to 4.0 +/- 0.4 Hz in lead II, but remained high in the endocardium (10.7 +/- 0.5 Hz). 3. Lignocaine significantly reduced the dominant frequency for fibrillation recorded from lead II at (0-80 s), and for endocardial fibrillation at (0-200 s). 4. Pretreatment with propranolol or bretylium had little effect on the time course of the dominant frequency of fibrillation in lead II or the endocardium. 5. Verapamil prevented the fall in frequency seen in lead II after 80 s in the no drug group. A significantly higher frequency was maintained in both lead II (14.7 +/- 0.9 Hz) and the endocardium (14.8 +/- 0.9 Hz) for 3.3 min, compared with the no drug group (P less than 0.01). 6. Activation of fast sodium channels may determine the rapid frequency of the initial stages of ventricular fibrillation. The rapid fall in dominant frequency in lead II after fibrillation for 80 s can be prevented by calcium channel blockade and may be due to intracellular accumulation of calcium. 相似文献
6.
Golli M; Van Nhieu JT; Mathieu D; Zafrani ES; Cherqui D; Dhumeaux D; Vasile N; Rahmouni A 《Radiology》1994,190(3):741
7.
8.
9.
10.
Inhibition of 2-nitropropane-induced rat liver DNA and RNA damage by benzyl selenocyanate 总被引:5,自引:2,他引:3
We observed that pretreatment of male F344 rats with benzyl selenocyanate,
a versatile organoselenium chemopreventive agent in several animal model
systems, decreases the levels of DNA and RNA modifications produced in the
liver by the hepatocarcinogen 2- nitropropane. To clarify the mechanisms
involved, we pretreated male F344 rats with either benzyl selenocyanate,
its sulfur analog benzyl thiocyanate, phenobarbital or cobalt
protoporphyrin IX; the latter is a depletor of P450. We then determined (1)
the ability of liver microsomes to denitrify 2-nitropropane, (2) effects on
2-nitropropane- induced liver DNA and RNA modifications and (3) amount of
nitrate excreted in rat urine following administration of the carcinogen.
Pretreatment with benzyl selenocyanate or phenobarbital increased the
denitrification activity of liver microsomes by 217 and 765%, respectively,
increased liver P4502B1 by 31- and 435-fold, respectively, decreased the
levels of 2-nitropropane-induced modifications in liver DNA (29-70% and
17-30%, respectively) and RNA (67-85% and 30-50%, respectively), and
increased the 24-h urinary excretion of nitrate by 157 and 209%,
respectively. Pretreatment with benzyl thiocyanate had no significant
effect on any of these parameters. Pretreatment with cobalt protoporphyrin
IX decreased liver P4502B 1 by 87%, decreased the denitrification activity
of liver microsomes by 76%, decreased the 24 h urinary excretion of nitrate
by 88.5%, but increased the extent of 2-nitropropane-induced liver nucleic
acid modifications by 17-67%. These results indicate that the metabolic
sequence from 2-nitropropane to the reactive species causing DNA and RNA
modifications does not involve the removal of the nitro group. Moreover,
they suggest that benzyl selenocyanate inhibits 2-NP-induced liver nucleic
acid modifications in part by increasing its detoxication through induction
of denitrification, although it is evident that other mechanisms must also
be involved.
相似文献