全文获取类型
收费全文 | 1171篇 |
免费 | 84篇 |
国内免费 | 7篇 |
专业分类
耳鼻咽喉 | 10篇 |
儿科学 | 76篇 |
妇产科学 | 15篇 |
基础医学 | 225篇 |
口腔科学 | 18篇 |
临床医学 | 138篇 |
内科学 | 232篇 |
皮肤病学 | 27篇 |
神经病学 | 57篇 |
特种医学 | 92篇 |
外科学 | 111篇 |
综合类 | 13篇 |
一般理论 | 16篇 |
预防医学 | 93篇 |
眼科学 | 15篇 |
药学 | 74篇 |
中国医学 | 3篇 |
肿瘤学 | 47篇 |
出版年
2021年 | 8篇 |
2019年 | 9篇 |
2018年 | 16篇 |
2017年 | 11篇 |
2016年 | 19篇 |
2015年 | 25篇 |
2014年 | 22篇 |
2013年 | 44篇 |
2012年 | 26篇 |
2011年 | 35篇 |
2010年 | 20篇 |
2009年 | 37篇 |
2008年 | 48篇 |
2007年 | 37篇 |
2006年 | 48篇 |
2005年 | 51篇 |
2004年 | 49篇 |
2003年 | 54篇 |
2002年 | 41篇 |
2001年 | 46篇 |
2000年 | 37篇 |
1999年 | 46篇 |
1998年 | 32篇 |
1997年 | 23篇 |
1996年 | 21篇 |
1995年 | 16篇 |
1994年 | 15篇 |
1992年 | 15篇 |
1991年 | 15篇 |
1990年 | 20篇 |
1989年 | 19篇 |
1988年 | 26篇 |
1987年 | 25篇 |
1986年 | 17篇 |
1985年 | 14篇 |
1984年 | 10篇 |
1983年 | 9篇 |
1982年 | 9篇 |
1981年 | 14篇 |
1980年 | 8篇 |
1979年 | 28篇 |
1978年 | 27篇 |
1977年 | 13篇 |
1975年 | 17篇 |
1974年 | 19篇 |
1972年 | 14篇 |
1971年 | 11篇 |
1970年 | 9篇 |
1966年 | 8篇 |
1933年 | 7篇 |
排序方式: 共有1262条查询结果,搜索用时 0 毫秒
31.
R A Morey J E Dunsmoor C C Haswell V M Brown A Vora J Weiner D Stjepanovic H R Wagner III VA Mid-Atlantic MIRECC Workgroup K S LaBar 《Translational psychiatry》2015,5(12):e700
Fear conditioning is an established model for investigating posttraumatic stress disorder (PTSD). However, symptom triggers may vaguely resemble the initial traumatic event, differing on a variety of sensory and affective dimensions. We extended the fear-conditioning model to assess generalization of conditioned fear on fear processing neurocircuitry in PTSD. Military veterans (n=67) consisting of PTSD (n=32) and trauma-exposed comparison (n=35) groups underwent functional magnetic resonance imaging during fear conditioning to a low fear-expressing face while a neutral face was explicitly unreinforced. Stimuli that varied along a neutral-to-fearful continuum were presented before conditioning to assess baseline responses, and after conditioning to assess experience-dependent changes in neural activity. Compared with trauma-exposed controls, PTSD patients exhibited greater post-study memory distortion of the fear-conditioned stimulus toward the stimulus expressing the highest fear intensity. PTSD patients exhibited biased neural activation toward high-intensity stimuli in fusiform gyrus (P<0.02), insula (P<0.001), primary visual cortex (P<0.05), locus coeruleus (P<0.04), thalamus (P<0.01), and at the trend level in inferior frontal gyrus (P=0.07). All regions except fusiform were moderated by childhood trauma. Amygdala–calcarine (P=0.01) and amygdala–thalamus (P=0.06) functional connectivity selectively increased in PTSD patients for high-intensity stimuli after conditioning. In contrast, amygdala–ventromedial prefrontal cortex (P=0.04) connectivity selectively increased in trauma-exposed controls compared with PTSD patients for low-intensity stimuli after conditioning, representing safety learning. In summary, fear generalization in PTSD is biased toward stimuli with higher emotional intensity than the original conditioned-fear stimulus. Functional brain differences provide a putative neurobiological model for fear generalization whereby PTSD symptoms are triggered by threat cues that merely resemble the index trauma. 相似文献
32.
F. Gamerith G. J. Zlabinger O. Scherak G. Kolarz M. Schemper H. Heinzl J. E. Menzel 《Rheumatology international》1993,13(3):107-112
Summary In the present study the ratio of antigen-bound anti-IgG-Fab antibodies (hidden aFab) to free aFab was found to be significantly increased in patients with adult onset rheumatoid arthritis (AORA) as compared to late onset rheumatoid arthritis (LORA). The overall amount of aFab was similar in both groups. The difference was only seen in seropositive patients. Within the seropositive AORA group, the aFab ratio was correlated with the duration and the stage of disease but not with the patients' age at investigation. This might reflect a higher affinity of anti-Fab antibodies and/or a greater diversity of the idiotypic repertoire in adult onset disease resulting in the formation of immune complexes, the stability of which might be enhanced further by the presence of rheumatoid factors. Although a pathophysiological involvement of aFab cannot be concluded from our observations, it is conceivable that different immunoregulatory mechanisms could be operative in RA with onset at different ages. 相似文献
33.
Stephan Menzel Helen Rooks Diana Zelenika Siana N. Mtatiro Akshala Gnanakulasekaran Emma Drasar Sharon Cox Li Liu Mariam Masood Nicholas Silver Chad Garner Nisha Vasavda Jo Howard Julie Makani Adekunle Adekile Betty Pace Tim Spector Martin Farrall Mark Lathrop Swee Lay Thein 《Annals of human genetics》2014,78(6):434-451
34.
35.
Verena Tenten Sylvia Menzel Uta Kunter Eva-Maria Sicking Claudia R. C. van Roeyen Silja K. Sanden Michaela Kaldenbach Peter Boor Astrid Fuss Sandra Uhlig Regina Lanzmich Brigith Willemsen Henry Dijkman Martin Grepl Klemens Wild Wilhelm Kriz Bart Smeets Jürgen Floege Marcus J. Moeller 《Journal of the American Society of Nephrology : JASN》2013,24(12):1966-1980
36.
Preventing musculoskeletal disorders in nurses: a safe patient handling curriculum module for nursing schools 总被引:1,自引:0,他引:1
Nursing educators who teach outmoded manual patient handling techniques contribute to the widespread problem of musculoskeletal disorders in student and practicing nurses. The authors discuss the development and implementation of a new safe patient handling curriculum module, which was pilot tested in 26 nursing programs. The module changes the focus of patient handling education from body mechanics to equipment-assisted safe patient lifting programs that have been shown to protect nurses from injury and improve care. 相似文献
37.
The amino acid intermediate homocysteine (Hcy) is formed during the metabolism of methionine to cysteine. Hyperhomocysteinemia (HHcy) is recognized as an independent risk factor for coronary atherosclerosis. The circulating levels of total Hcy (tHcy) can increase due to intake of foods rich in methionine or deficiencies of vitamins such as folate, pyridoxine and cyanocobalamin, which are required for the metabolism of Hcy. In addition, mutations in the genes coding for Hcy metabolizing enzymes can contribute to an increase in tHcy levels. Clinical and epidemiological studies have shown that an elevated level of tHcy measured in serum or plasma is a strong predictor of cardiovascular disease risk, which appears to be greatest in patients who have HHcy following a methionine load. Intimal hyperplasia (IH) (intima/media [I/M] ratio) is the universal response of a vessel to injury and may result in vasoconstriction when left unattended. The effect of dietary HHcy on balloon catheter-injured carotid artery and its modulation (if any) by the peroxisome proliferator-activated receptor agonist gamma rosiglitazone was evaluated in 12-week-old female Sprague-Dawley rats fed either a control diet or a diet containing 1% L-methionine. Once the rats were established on the diet, the group that was fed 1% L-methionine was further subdivided and either given an aqueous preparation of 3 mg/kg/day rosiglitazone or the vehicle via oral gavage for one week. This was followed by surgically injuring the left carotid artery using a Maverick Over-The-Wire catheter (2.0 mm × 20 mm, 3.2F; Boston Scientific, USA). The rats were continued on their respective diets and drug regimen for 21 days postsurgery. On day 22 of the procedure, the rats were sacrificed for collection of blood, the carotid arteries and liver for biochemical and histological evaluation. Compared with controls there was a significant increase in both tHcy levels and I/M ratio in the rats fed 1% L-methionine (5.4±0.28 μM versus 32.8±3.01 μM, P<0.002; and 0.175±0.05 versus 1.05±0.23, P<0.005, respectively). The effect of rosiglitazone in rats fed the control diet was not prominent. On the other hand, administration of rosiglitazone to the rats on the 1% L-methionine diet significantly reduced the levels of serum tHcy (16.6±2.1 μM versus 32.8±3.01 μM, P<0.001); however, the tHcy levels remained significantly elevated compared with animals on the control diet (P<0.002). The group receiving the L-methionine diet plus rosiglitazone had an inhibition in the development of IH compared with those receiving the L-methionine diet alone (I/M of 0.278±0.041 versus 1.05±0.23, P<0.01). Moreover, the development of IH in the group receiving the L-methionine diet plus rosiglitazone treatment was not significantly different from that observed in the group on the control diet without rosiglitazone (0.278±0.041 versus 0.175±0.05, respectively). These findings may have important implications in deciphering the molecular mechanisms involved in the augmentation of IH in HHcy and modulation of this process by rosiglitazone. 相似文献
38.
Menzel T; Rahman Z; Calleja E; White K; Wilson EL; Wieder R; Gabrilove J 《Blood》1996,87(3):1056-1063
Chronic lymphocytic leukemia (CLL) is characterized by delayed senescence and slow accumulation of monoclonal, small lymphocytes. Basic fibroblast growth factor (bFGF) is a pleiotropic cytokine that plays a role in hematopoiesis and apoptosis. Elevated bFGF levels have been detected in urine from patients with a variety of neoplastic diseases including various leukemias; however, the cellular source of the bFGF has not been determined. In this study, the intracellular bFGF level in lymphocytes of 36 patients with B-CLL and 15 normal donors was determined using an enzyme-linked immunoassay. In cells derived from patients with high-risk disease, the median level of intracellular bFGF was 381.5 pg/2 x 10(5) cells, compared with a median of 90.5 pg/2 x 10(5) cells in patients with intermediate disease. In patients with low- risk disease, the median bFGF level was 4.9 pg/2 x 10(5) cells, and in normal controls, it was 6.0 pg/2 x 10(5) cells. The difference in the bFGF levels was significant for the comparison between low- and intermediate-risk (P = .00119), low- and high-risk (P < .0001), and intermediate- and high-risk disease (P = .0001). Immunofluorescent stains of peripheral blood mononuclear cells confirmed CLL lymphocytes as a cellular source of bFGF. To evaluate the potential contribution of elevated intracellular bFGF levels to the phenotype of CLL cells, leukemic cells were cultured in vitro with an apoptotic stimulus (fludarabine). CLL cells with high intracellular levels of bFGF appeared to be more resistant to fludarabine treatment. The addition of bFGF to fludarabine-treated CLL cells resulted in a delay of apoptosis and prolonged survival. These data suggest that bFGF may contribute to the resistance of CLL cells to an apoptotic stimulus. 相似文献
39.
Demonstration of antibodies to collagen and of collagen-anticollagen immune complexes in rheumatoid arthritis synovial fluids. 下载免费PDF全文
J Menzel C Steffen G Kolarz G Eberal O Frank N Thumb 《Annals of the rheumatic diseases》1975,35(5):446-450
Twenty-nine synovial fluids from patients with rheumatoid arthritis (RA) and 10 synovial fluids from patients with other joint diseases were investigated with regard to the presence of antibodies to denatured human collagen and of collagen-anticollagen immune complexes. 12 of the 29 RA synovial fluids showed anticollagen titres from 1:16 to 1:512 in passive haemagglutination. Only one patient in the group with no arthritis had a significant anticollagen titre of 1:32. Digestion of the synovial fluids with bacterial collagenase resulted in an anticollagen titre increase from two to four dilution steps in 9 of the RA fluids, while 6 previously negative RA synovial fluids showed anticollagen titres from 1:32 to 1:28 after digestion with collagenase. These results indicate the existence of collagen-anticollagen immune complexes in 15 of the 29 RA synovial fluids investigated. 相似文献
40.
Cardoso AA; Schultze JL; Boussiotis VA; Freeman GJ; Seamon MJ; Laszlo S; Billet A; Sallan SE; Gribben JG; Nadler LM 《Blood》1996,88(1):41-48
Even if neoplastic cells express tumor associated antigens they still may fail to function as antigen presenting cells (APC) if they lack expression of one or more molecules critical for the induction of productive immunity. These cellular defects can be repaired by physiologic activation, transfection, or fusion of tumor cells with professional APC. Although such defects can be repaired, antitumor specific T cells may still fail to respond in vivo if they may have been tolerized. Here, human pre-B cell acute lymphoblastic leukemia (pre-B ALL) was used as a model to determine if primary human tumor cells can function as alloantigen presenting cells (alloAPC) or alternatively whether they induce anergy. In the present report, we show that pre-B cell ALL express alloantigen and adhesion molecules but uniformly lack B7-1 (CD80) and only a subset express B7-2 (CD86). Pre-B ALL cells are inefficient or ineffective alloAPC and those cases that lack expression of B7-1 and B7-2 also induce alloantigen specific T- cell unresponsiveness. Under these circumstances, T-cell unresponsiveness could be prevented by physiologic activation of tumor cells via CD40, cross-linking CD28, or signaling through the common gamma chain of the interleukin-2 receptor on T cells. Taken together, these results suggest that pre-B ALL may be incapable of inducing clinically significant T-cell-mediated antileukemia responses. This defect may be not only due to their inability to function as APC, but also due to their potential to induce tolerance. Attempts to induce clinically significant antitumor immune responses may then require not only mechanisms to repair the antigen presenting capacity of the tumor cells, but also reversal of tolerance. 相似文献