全文获取类型
收费全文 | 1139篇 |
免费 | 72篇 |
国内免费 | 10篇 |
专业分类
耳鼻咽喉 | 43篇 |
儿科学 | 71篇 |
妇产科学 | 59篇 |
基础医学 | 148篇 |
口腔科学 | 16篇 |
临床医学 | 99篇 |
内科学 | 259篇 |
皮肤病学 | 10篇 |
神经病学 | 141篇 |
特种医学 | 29篇 |
外科学 | 130篇 |
综合类 | 4篇 |
一般理论 | 1篇 |
预防医学 | 60篇 |
眼科学 | 10篇 |
药学 | 32篇 |
肿瘤学 | 109篇 |
出版年
2024年 | 1篇 |
2023年 | 7篇 |
2022年 | 11篇 |
2021年 | 24篇 |
2020年 | 11篇 |
2019年 | 17篇 |
2018年 | 32篇 |
2017年 | 21篇 |
2016年 | 13篇 |
2015年 | 25篇 |
2014年 | 37篇 |
2013年 | 52篇 |
2012年 | 81篇 |
2011年 | 85篇 |
2010年 | 55篇 |
2009年 | 42篇 |
2008年 | 88篇 |
2007年 | 88篇 |
2006年 | 83篇 |
2005年 | 81篇 |
2004年 | 68篇 |
2003年 | 60篇 |
2002年 | 55篇 |
2001年 | 9篇 |
2000年 | 20篇 |
1999年 | 11篇 |
1998年 | 9篇 |
1997年 | 11篇 |
1996年 | 10篇 |
1995年 | 8篇 |
1994年 | 6篇 |
1993年 | 3篇 |
1992年 | 5篇 |
1991年 | 10篇 |
1990年 | 8篇 |
1989年 | 9篇 |
1988年 | 12篇 |
1987年 | 6篇 |
1986年 | 3篇 |
1985年 | 5篇 |
1984年 | 4篇 |
1983年 | 2篇 |
1982年 | 5篇 |
1980年 | 9篇 |
1979年 | 9篇 |
1978年 | 5篇 |
1977年 | 1篇 |
1975年 | 2篇 |
1973年 | 1篇 |
1971年 | 1篇 |
排序方式: 共有1221条查询结果,搜索用时 31 毫秒
1.
Toshiro Hara Rony Chanoch-Myers Nathan D. Mathewson Chad Myskiw Lyla Atta Lillian Bussema Stephen W. Eichhorn Alissa C. Greenwald Gabriela S. Kinker Christopher Rodman L. Nicolas Gonzalez Castro Hiroaki Wakimoto Orit Rozenblatt-Rosen Xiaowei Zhuang Jean Fan Tony Hunter Inder M. Verma Kai W. Wucherpfennig Itay Tirosh 《Cancer cell》2021,39(6):779-792.e11
- Download : Download high-res image (228KB)
- Download : Download full-size image
2.
Rats exposed on their first postnatal day to 100% nitrogen for 25 min developed hyperactivity and lower performance in passive avoidance task during development. Administration of MK-801 (0.5 mg/kg i.p.) 1 h before anoxia or (0.25 and 0.5 mg/kg) 1 h after completely reversed this behavioral impairment. Senescent rats (24-26 months) exposed to hypoxia (92% N2 + 8% O2) for 5 h failed in their performance in C.A.R., 30 days later. Pretreatment with MK-801 (1 mg/kg i.p.) completely reversed this impairment. These data suggest that activation of endogenous NMDA receptors produces different behavioral consequences in neonatal and senescent rats and that MK-801 administration close to exposure of animals to anoxia or hypoxia can prevent such damage, thus preventing behavioral impairments in postnatal as well as in senescent rats. 相似文献
3.
4.
Samuel Szomstein Orit Kaidar-Person Kristoff Naberezny Marcia Cruz-Correa Raul Rosenthal 《Surgery for obesity and related diseases》2006,2(6):617-621
BACKGROUND: Anastomotic stenosis presents as one of the most common late complications in the postoperative period after bariatric surgery. It is often diagnosed by upper gastrointestinal series (UGIS) and/or upper endoscopy (UE). The aim of this study was to determine whether a correlation exists between the Gastrografin UGIS and UE findings in the determination of gastrojejunal anastomotic strictures after Roux-en-Y gastric bypass (RYGB). METHODS: Between July 2001 and October 2003, all medical records of patients who underwent RYGB at our institution were retrospectively reviewed. The medical records of patients who underwent UE because of symptoms suggestive of gastric outlet obstruction and those of patients who were initially evaluated by Gastrografin UGIS before UE were evaluated further. RESULTS: Of 535 morbidly obese patients who underwent RYGB, 52 (9.7%) had UE and were included in this study. The mean number of UEs performed per patient was 2.67. Of these 52 patients, 30 underwent Gastrografin UGIS before UE. The mean diameter of the anastomosis on the first UE was 5.97 mm and on Gastrografin UGIS was 6.83 mm. A good correlation was found between the Gastrografin UGIS and UE findings using Pearson's correlation coefficient (0.44, P = .02) and single linear regression analysis using the endoscopic diameter as the outcome and radiographic findings as the predictor (beta = 0.27, P = .025, 95% confidence interval 0.30-0.49). CONCLUSION: In our study, the Gastrografin UGIS findings correlated positively with the endoscopic gastrojejunal anastomosis findings in patients with anastomotic stricture who had undergone RYGB. 相似文献
5.
Dagan O Hochner H Levi H Raas-Rothschild A Sagi M 《American journal of medical genetics》2002,114(2):137-143
Autism is a complex genetic disorder. Chromosome 15 is of particular interest in this disorder, because of previous reports of individuals with autism with chromosomal abnormalities in the 15q11-q13 region. Transmission disequilibrium between polymorphisms in this region and autism has been also been reported in some, but not all studies. Recently, a novel maternally expressed gene, ATP10C, was characterized and mapped to the chromosome 15q11-q13 region, 200 kb distal to UBE3A. It encodes a putative aminophospholipid translocase likely to be involved in the asymmetric distribution of proteins in the cell membrane. Preferential maternal expression has been demonstrated in fibroblasts and brain. Because of its physical location and imprinting pattern, ATP10C was considered to be a candidate gene for chromosome 15-associated autism. In an effort to find the genes responsible for autism in this chromosomal region, 1.5 kb of the 5' flanking region, as well as the coding and splicing regions of ATP10C, were screened for sequence variants. Several polymorphic markers including five nonsynonymous SNPs were identified. To investigate transmission disequilibrium between ATP10C and autism, a family-based association study was conducted for 14 markers in 115 autism trios. No significant transmission disequilibrium was found, suggesting ATP10C is unlikely to contribute strongly to susceptibility to autism in these families. However, due to limited power to detect genes of modest effect, the possible functional role of the nonsynonymous SNPs and the functional implications of the SNPs identified from 5' flanking region and intron 2 splicing region may be evaluated in further studies. 相似文献
6.
Fidder HH Olschwang S Avidan B Zouali H Lang A Bardan E Picard O Bar-Meir S Colombel JF Chowers Y 《American journal of medical genetics. Part A》2003,(3):240-244
Ulcerative colitis (UC) and Crohn's disease (CD) are heterogeneous disorders characterized by chronic intestinal inflammation. Genetic predisposition is a major risk factor in both diseases. The CARD15 (NOD2) gene has been implied as a candidate gene in the pathogenesis CD. Our aim was to delineate the frequency of three missense and one frameshift variant of CARD15 in Israeli Jewish CD and UC patients. DNA was extracted from blood samples from 238 unrelated inflammatory bowel disease (IBD) patients, 68 with UC and 170 with CD. The DNA was genotyped for two missense mutations, R675W and G881R, and one frameshift mutation, 980FS981X. Mutations in CARD15 were observed with significantly greater frequency in CD patients (46/170, 27%) than in UC patients (7/68, 10%) (P = 0.005). Homozygous and compound heterozygous carriers were restricted to seven (4%) patients with CD as compared to none of the UC patients (P = 0.01). Similar rates in Ashkenazi and non-Ashkenazi Jewish patients were observed. Age-of-onset of disease was lower in Ashkenazi mutation carriers as compared to non-carriers of Ashkenazi origin (18.7 +/- 8.6 years vs. 25.8 +/- 13.4 years, respectively, P = 0.03). No other phenotypic characteristics could distinguish mutation carriers from non-carriers. We conclude that germline mutations in the CARD15 gene are more frequently found in CD than UC patients and appear to predict an earlier age-of-onset in Ashkenazi Jewish patients. No association could be demonstrated between CARD15 mutations and specific disease course or behavior. 相似文献
7.
Angelo Agostoni Bianca Marasini Marco Cicardi Giancarlo Martignoni Lilj Uziel Maurezio Pietrogrande 《Allergy》1978,33(4):216-221
Prophylactic treatment with antifibrinolytic agents, epsilon-aminocapriod and tranexamic acid, reduces the incidence and severits of attacks in patients with hereditary angioedema. Long-term ellectivenessor risk of antifibrinolytic agents has not been established. Sixteen patients needing continuous prophylaxis because of frequency and severity of attacks were treated with tranexamic acid. In four patients this treatment was ineffective and the drug was withdrawn after 2 months. A remission or reduction in the frequency or serverity of attacks was observed in 12 patients treated for a period ranging from 8 to 34 months. Hepatic tests and blood fibrinolytic activity were not influenced by long term oral treatment with tranexamic acid. 相似文献
8.
Phialemonium curvatum arthritis of the knee following intra-articular injection of a corticosteroid.
Michael Dan Orit Yossepowitch David Hendel Orna Shwartz Deanna A Sutton 《Medical mycology》2006,44(6):571-574
Phialemonium curvatum arthritis of the knee developed in a diabetic man following intra-articular injection of a corticosteroid. Cure was achieved with a 6-week course of intravenous amphotericin B deoxycholate. P.curvatum is commonly found in the environment and is often considered a contaminant; yet, its pathogenic potential should be seriously considered in selected patients. 相似文献
9.
Predominance of null mutations in ataxia-telangiectasia 总被引:15,自引:4,他引:15
Gilad S; Khosravi R; Shkedy D; Uziel T; Ziv Y; Savitsky K; Rotman G; Smith S; Chessa L; Jorgensen TJ; Harnik R; Frydman M; Sanal O; Portnoi S; Goldwicz Z; Jaspers NG; Gatti RA; Lenoir G; Lavin MF; Tatsumi K; Wegner RD; Shiloh Y; Bar-Shira A 《Human molecular genetics》1996,5(4):433-439
Ataxia-telangiectasia (A-T) is an autosomal recessive disorder involving
cerebellar degeneration, immunodeficiency, chromosomal instability,
radiosensitivity and cancer predisposition. The responsible gene, ATM, was
recently identified by positional cloning and found to encode a putative
350 kDa protein with a Pl 3-kinase-like domain, presumably involved in
mediating cell cycle arrest in response to radiation-induced DNA damage.
The nature and location of A-T mutations should provide insight into the
function of the ATM protein and the molecular basis of this pleiotropic
disease. Of 44 A-T mutations identified by us to date, 39 (89%) are
expected to inactivate the ATM protein by truncating it, by abolishing
correct initiation or termination of translation, or by deleting large
segments. Additional mutations are four smaller in-frame deletions and
insertions, and one substitution of a highly conserved amino acid at the Pl
3-kinase domain. The emerging profile of mutations causing A-T is thus
dominated by those expected to completely inactivate the ATM protein. ATM
mutations with milder effects may result in phenotypes related, but not
identical, to A-T.
相似文献
10.
Immune-deficient SCID and NOD/SCID mice models as functional assays for studying normal and malignant human hematopoiesis 总被引:3,自引:0,他引:3
T. Lapidot Yfat Fajerman Orit Kollet 《Journal of molecular medicine (Berlin, Germany)》1997,75(9):664-673
Many events and requirements of the developmental program of human hematopoietic stem cells have not yet been discovered.
A major impediment has been the lack of an appropriate experimental system. At present the conditions for maintaining human
stem cells in vitro are not fully known. As a result within a short period the small stem cell pool is lost due to differentiation,
making it difficult to examine the correlation between these cells and their function in vivo. Most of our knowledge of hematopoietic
stem cells is from animal models in which purified stem cell canididates are assayed based on their functional ability to
rescue lethally conditioned recipients. The permanent correction of many genetic disorders of the hematopoietic system requires
efficient methods for introducing genes into stem cells in vitro. However, progress has been hindered by the absence of preclinical
models that assay the repopulating capacity of primitive human cells. In addition, the development of therapy for malignant
diseases also requires assays to identify the target leukemic stem cells based on their ability to initiate the disease. The
recent development of methods to transplant or implant both normal and leukemic cells into immune-deficient mice provides
the foundation for human stem cell assays. These models assay the repopulating capacity of primitive human cells and provide
an important approach to identify and characterize human stem cells, both normal and leukemic. This review focuses on the
development of functional assays for normal and leukemic human stem cells and on the new insights that these models are beginning
to provide on the organization of the human stem cell hierarchy.
Received: 27 January 1997 / Accepted: 3 April 1997 相似文献