全文获取类型
收费全文 | 25735篇 |
免费 | 1246篇 |
国内免费 | 176篇 |
专业分类
耳鼻咽喉 | 200篇 |
儿科学 | 525篇 |
妇产科学 | 439篇 |
基础医学 | 2814篇 |
口腔科学 | 618篇 |
临床医学 | 2052篇 |
内科学 | 6754篇 |
皮肤病学 | 486篇 |
神经病学 | 2968篇 |
特种医学 | 776篇 |
外科学 | 3880篇 |
综合类 | 43篇 |
一般理论 | 5篇 |
预防医学 | 1082篇 |
眼科学 | 451篇 |
药学 | 1448篇 |
中国医学 | 30篇 |
肿瘤学 | 2586篇 |
出版年
2024年 | 26篇 |
2023年 | 172篇 |
2022年 | 389篇 |
2021年 | 747篇 |
2020年 | 443篇 |
2019年 | 616篇 |
2018年 | 691篇 |
2017年 | 550篇 |
2016年 | 620篇 |
2015年 | 690篇 |
2014年 | 1010篇 |
2013年 | 1268篇 |
2012年 | 1993篇 |
2011年 | 1988篇 |
2010年 | 1155篇 |
2009年 | 1067篇 |
2008年 | 1745篇 |
2007年 | 1806篇 |
2006年 | 1670篇 |
2005年 | 1645篇 |
2004年 | 1627篇 |
2003年 | 1349篇 |
2002年 | 1318篇 |
2001年 | 192篇 |
2000年 | 114篇 |
1999年 | 147篇 |
1998年 | 249篇 |
1997年 | 210篇 |
1996年 | 194篇 |
1995年 | 170篇 |
1994年 | 128篇 |
1993年 | 130篇 |
1992年 | 112篇 |
1991年 | 89篇 |
1990年 | 86篇 |
1989年 | 65篇 |
1988年 | 66篇 |
1987年 | 63篇 |
1986年 | 56篇 |
1985年 | 56篇 |
1984年 | 78篇 |
1983年 | 44篇 |
1982年 | 45篇 |
1981年 | 43篇 |
1980年 | 33篇 |
1979年 | 20篇 |
1978年 | 16篇 |
1977年 | 30篇 |
1976年 | 17篇 |
1974年 | 15篇 |
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
81.
Environmental enrichment potentiates neural plasticity, enhancing acquisition and consolidation of memory traces. In the sensory cortices, after cortical circuit maturation and sensory function acquisition are completed, neural plasticity declines and the critical period 'closes'. In the visual cortex, this process can be prevented by dark-rearing, and here we show that environmental enrichment can promote physiological maturation and consolidation of visual cortical connections in dark-reared rats, leading to critical period closure. 相似文献
82.
Tancredi M Sensi E Cipollini G Aretini P Lombardi G Di Cristofano C Presciuttini S Bevilacqua G Caligo MA 《European journal of human genetics : EJHG》2004,12(9):775-777
Germ-line mutations in the BRCA1 gene cause hereditary predisposition to breast and ovarian cancer. BRCA1 and BRCA2 mutations account for about 40% of high-risk families. Mutation-screening methods generally focus on genomic DNA and are usually PCR based; they enable the detection of sequence alterations such as point mutations and small deletions and insertions. However, they do not allow the detection of partial or entire exon(s) loss, because the presence of the homologous allele results in a positive PCR signal, giving rise to a false-negative result. Identification of unusual haplotypes in patient samples by an expectation maximization algorithm has recently been suggested as a method for identifying hemizygous regions caused by large intragenic deletions. Using a similar approach, we identified a novel BRCA1 genomic rearrangement in a breast/ovarian cancer family negative at the first mutation screening; we detected a deletion encompassing exons 14-19, probably due to replication slippage between Alu sequences. 相似文献
83.
Lanari M Papa I Venturi V Lazzarotto T Faldella G Gabrielli L Guerra B Landini MP Salvioli GP 《Journal of medical virology》2003,70(4):628-632
Human herpesvirus 6 (HHV 6) has neurotropic and neuroinvasive properties. The virus has been found in the cerebrospinal fluid of many children with aseptic meningoencephalitis. Intrauterine transmission has been documented by HHV 6 DNA detection in cord blood specimens of apparently healthy newborns and in fetuses following spontaneous abortions. A patient is described with early neonatal afebrile seizures resulting from a congenital HHV 6 variant B infection disclosed by repeated detection of viral genome by polymerase chain reaction (PCR) in cerebrospinal fluid in the first days of life. At follow-up, magnetic resonance imaging (MRI) studies disclosed hyperintensities in the periventricular white matter and basal ganglia, associated with cerebral atrophy. Further follow-up at 18 months revealed poor neurological outcome with mild neurodevelopmental retardation, strabismus and hypertonia of legs. This report provides evidence of neurological involvement after HHV 6 vertical transmission, and the association with neurological sequelae. 相似文献
84.
Fazzi E Signorini SG Uggetti C Bianchi PE Lanners J Lanzi G 《American journal of medical genetics. Part A》2005,(1):13-19
Leber congenital amaurosis (LCA) is the most severe form of inherited retinal dystrophy that presents in infancy. LCA is both clinically and genetically heterogeneous. The aim of our study was to clarify the clinical aspects of LCA and to contribute to improved characterization of the disorder. We studied 40 children affected by LCA (mean age at first observation: 19 months, range: 8-50 months), who underwent a comprehensive evaluation that included: neurophthalmological evaluation, electroretinogram (ERG), and visual evoked potentials (VEPs), general and neurological examinations, developmental assessment using scales for visually impaired children, neuroradiological examinations, hepatic and renal function and metabolic investigations, brainstem auditory evoked potentials (BAEPs), EEG, and hand radiographs. Analyses of known LCA genes are ongoing. The subjects are still being followed up at 6-/12-month intervals. All the subjects fulfilled De Laey's criteria for LCA. The neurological examination was abnormal in 31 cases (hypotonia, ataxia with/without associated cerebellar signs). Cognitive development was normal in 24 cases, borderline in five, and subnormal in 11. Mild and nonspecific alterations on MRI were present in seven cases, and "molar tooth" sign in four; all the others had a normal neuroradiological picture. Among the subjects presenting with neurological signs, a subgroup (13 patients) emerged that was characterized by systemic (skin, kidney, liver) involvement. Our data confirm that LCA is a heterogeneous entity that can present as an isolated ocular manifestation, or in association with neurological and systemic abnormalities and support the need for a multidisciplinary approach to this entity and for genotype-phenotype studies. 相似文献
85.
Federica Cavallo Alfonso Martin-Fontecha Matteo Bellone Silvia Heltai Evelina Gatti Paola Tornaghi Massimo Freschi Guido Forni Paolo Dellabona Giulia Casorati 《European journal of immunology》1995,25(5):1154-1162
Although the transfection of B7-1 cDNA into a few mouse tumor cell lines can induce anti-tumor T cell immunity, its expression alone is ineffective in many other tumor cell lines tested. We were interested to study what factors limit B7-1 co-stimulatory activity, and decided to investigate whether B7-1 requires the cooperation of ICAM-1 to provide the minimal co-stimulatory signal for establishing an efficient anti-tumor immunity. We show that the transfection of B7-1 cDNA into three ICAM-1+ (plasmocytoma J558L, T lymphomas EL-4 and RMA), but not into two ICAM-1? tumor cell lines (adenocarcinoma TS/A and melanoma B16.F1), is sufficient to induce their complete rejection in syngeneic mice. The expression of ICAM-1 is necessary for the rejection of the B7 expressing tumors, since the primary response elicited by B7-1+ EL-4 and RMA clones expressing reduced levels of ICAM-1 is severely reduced. Furthermore, super-transfection of ICAM-1 cDNA into B7-1+ adenocarcinoma and melanoma clones optimizes their primary rejection. Histologic examination of transfected tumors reveals that B7-1 and ICAM-1 exert a potent pro-inflammatory activity. The intra-tumor infiltration is composed of both eosinophils and lymphomono-cytes, and is already massive 5 days after the tumor challenge. The primary rejection of the B7-1+ ICAM-1+ tumors depends critically on CD8+ T cells, natural killer cells and granulocytes, but is independent of CD4+ T cells. Remarkably, in addition to its effects on the early phases of the immune response, the co-expression of ICAM-1 and B7-1 on tumors is also necessary for the efficient induction of a memory response. In fact, only the primary challenge with B7-1+, ICAM-1+ tumor cells protects the majority of the mice from a second injection of parental tumor cells. Collectively, our findings indicate that B7-1 and ICAM-1 are fundamental components for triggering the primary rejection of tumors and establishing a protective memory response. These findings may help to define new strategies for the rational application of co-stimulation in tumor immunotherapy. 相似文献
86.
Alessandro Daniotti Gaetano Povolo Agata Barchitta Aierken Abudureheman Paolo Cardaioli Cristina Basso 《Cardiovascular pathology》2004,13(6):330-333
A 51-year-old woman suffered rapidly irreversible cardiogenic shock with left hemiparesis. Transesophageal echocardiography, which represents an essential imaging tool in the emergency room, ruled out aortic dissection involving branch vessels but did not allow an in vivo diagnosis of spontaneous coronary dissection. The in vivo diagnosis of spontaneous coronary dissection is rather difficult because of the dramatic clinical presentation and selective coronary angiography requirement. 相似文献
87.
88.
Paolo Ghia Alois Gratwohl Erich Signer Thomas H. Winkler Fritz Melchers Antonius G. Rolink 《European journal of immunology》1995,25(11):3108-3114
The capacity of bone marrow-derived surface immunoglobulin-positive (sIg+) human and mouse immature B cells, generated either in vitro or in vivo, to change their light (L) chain expression, has been assayed by the number of cells which change in vitro from one type of L chain to the other type, or to no sIg at all. Immature sIg+ B cells were generated in vitro from sIg? precursor cells from human or mouse bone marrow. The immature sIg+ cells expressed RAG-1. Human sIg+ cells expressed xfr; and λ L chains in ratios between 1:1 and 3:1, whereas in mouse cells, this ratio ranged from 10:1 to 20:1. Upon reculture of the human and mouse xfr;+sIg+ cells, about half of them remained xfr;+, a quarter became λ+, and another quarter became sIg?. Between 1 and 3% expressed both xfr; and λ chains. Of the human λ+ cells, about two-thirds remained λ+, only 1 to 2% became xfr;+, while the other third became sIg?. Again, between 1 and 3% expressed both xfr; and λ L chains. These results indicate that expression of sIgM in the B cell membrane does not terminate L chain gene rearrangement, and that some order exists in xfr; versus λ gene rearrangements. Hence, human and mouse xfr;+ immature B cells can become λ+, but very few of the λ+ cells can become xfr;+, and both can become sIg?. Further, human CD10+/sIg+ xfr;+ and λ+ cells and mouse B220low/sIglow xfr;+ cells enriched from bone marrow, i.e. immature B cells differentiated in vivo, changed their Ig phenotype upon in vitro culture, but in lower frequencies. By contrast, human and mouse mature B cells did not change their L chain or Ig phenotype. Hence, at least a part of the sIg+ immature B cells in bone marrow retain the capacity to change their L chain and Ig phenotype, and this capacity is lost when they become mature, peripheral B cells. 相似文献
89.
90.
Ligand and cytokine dependence of the immunosuppressive pathway of tryptophan catabolism in plasmacytoid dendritic cells 总被引:3,自引:0,他引:3
Fallarino F Orabona C Vacca C Bianchi R Gizzi S Asselin-Paturel C Fioretti MC Trinchieri G Grohmann U Puccetti P 《International immunology》2005,17(11):1429-1438
Murine plasmacytoid dendritic cells (pDCs) have been credited with a unique ability to express indoleamine 2,3-dioxygenase (IDO) function and mediate immunosuppression in specific settings; yet, the conditions of spontaneous versus induced activity have remained unclear. We have used maneuvers known to up-regulate IDO in different cell types and have examined the relative efficacy and mechanisms of the induced activity in splenic pDCs, namely, after specific receptor engagement by CTLA-4-Ig, CD200-Ig or CD28-Ig, the latter in combination with silenced expression of the suppressor of cytokine signaling 3 (SOCS3) gene. We found that pDCs (CD11c+ mPDCA-1+ 120G8+) do not express IDO and are not tolerogenic under basal conditions. B7-1 engagement by CTLA-4-Ig, CD200R1 engagement by CD200-Ig and B7-1/B7-2 engagement by CD28-Ig in SOCS3-deficient pDCs were each capable of initiating IDO-dependent tolerance via different mechanisms. IFN-gamma was the major cytokine responsible for CTLA-4-Ig effects, and type I IFNs for those of CD200-Ig. Immunosuppression by CD28-Ig in the absence of SOCS3 required IFN-gamma induction and IFN-like actions of IL-6. Therefore, although pDCs do not mediate IDO-dependent tolerance constitutively, multiple ligands and cytokines will contribute to the expression of a tolerogenic phenotype by pDCs in the mouse. 相似文献