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991.
MDMA (3,4-methylenedioxymethamphetamine) induces thermogenesis in a mitochondrial uncoupling protein 3-dependent manner. There is evidence that this hyperthermia is mediated in part by the lipolytic release of free fatty acids, that subsequently activate uncoupling protein 3 in skeletal muscle mitochondria. We hypothesize that atrial natriuretic peptide (ANP), a strong lipolytic mediator, may contribute to the induction and maintenance of MDMA-induced thermogenesis. The specific aims of this study were to (1) determine if ANP is released following MDMA administration, and (2) use the ANP receptor antagonist, Anantin, to ascertain the role of ANP in MDMA-induced hyperthermia. ANP levels were measured in plasma at baseline, 10, 20, 30 and 60 min following MDMA (40 mg/kg, sc) administration in 16 male Sprague-Dawley rats. A robust increase in ANP was seen within 10 min of MDMA administration. ANP levels returned to baseline at 20 min and then gradually rose over the 60 min monitoring period. The administration of Anantin (40 mg, ip), 15 min before and after MDMA, significantly attenuated the MDMA-induced hyperthermia. We conclude that ANP signaling contributes to the hyperthermia induced by MDMA. 相似文献
992.
microRNA are small noncoding RNAs that translationally repress their target messenger RNAs. Many microRNAs are expressed at
reduced levels in tumors. microRNAs with reduced expression in cancer often regulate oncogenes, resulting in enhanced tumor
growth. One therapeutic option is to restore microRNA levels in the tumor to that of the non-diseased tissue. This is possible
by delivering microRNA to the tumor in the form of an oligonucleotide mimic or by expressing the microRNA in the cancer using
a gene vector. This article surveys the field of oligonucleotide mimics and gene vector approaches to restore microRNA levels
in tumors and reviews the literature on experimental and pre-clinical studies that have used these approaches to treat cancer. 相似文献
993.
994.
Jagessar SA Gran B Heijmans N Bauer J Laman JD 't Hart BA Constantinescu CS 《Journal of neuroimmune pharmacology》2012,7(1):253-265
The core pathogenic process in the common marmoset model of multiple sclerosis (MS) is the activation of memory-like T cells
specific for peptide 34 to 56 derived from the extracellular domain of myelin/oligodendrocyte glycoprotein (MOG34-56). Immunization with MOG34-56 in incomplete Freund’s adjuvant is a sufficient stimulus for in vivo activation of these T cells, together with the induction
of MS-like disease and CNS pathology. Ex vivo functional characteristics of MOG34-56 specific T cells are specific cytolysis of peptide pulsed target cells and high IL-17A production. To indentify possible
functions in this new model of T helper 1 cells, which play a central pathogenic role in MS models induced with complete Freund’s
adjuvant, we tested the effect of human interferon-γ (IFNγ) administration during disease initiation of the disease (day 0–25)
and around the time of disease expression (psd 56–81). The results show a clear modulatory effect of early IFNγ treatment
on humoral and cellular autoimmune parameters, but no generalized mitigating effect on the disease course. These results argue
against a prominent pathogenic role of T helper 1 cells in this new marmoset EAE model. 相似文献
995.
We have designed a dual-aptamer complex specific to both prostate-specific membrane antigens (PSMA) (+) and (-) prostate cancer cells. In the complex, an A10 RNA aptamer targeting PSMA (+) cells and a DUP-1 peptide aptamer specific to PSMA (-) cells were conjugated through streptavidin. Doxorubicin-loaded onto the stem region of the A10 aptamer was delivered not only to PSMA (+) cells but to PSMA (-) cells, and eventually induced apoptosis in both types of prostate cancer cells. Cell death was monitored by measuring guanine concentration in cells using differential pulse voltammetry (DPV), a simple and rapid electrochemical method, and was further confirmed by directly observing cell morphologies cultured on the transparent indium tin oxide (ITO) glass electrode and checking their viabilities using a trypan blue assay. To investigate the in vivo application of the dual-aptamer system, both A10 and DUP-1 aptamers were immobilized on the surface of thermally cross-linked superparamagnetic iron oxide nanoparticles (TCL-SPION). Selective cell uptakes and effective drug delivery action of these probes were verified by Prussian blue staining and trypan blue staining, respectively. 相似文献
996.
Introduction
Tobacco quitlines (QLs) are efficacious and have assisted many smokers in achieving tobacco abstinence. However, most smokers are not able to achieve tobacco abstinence with QL services. QL counseling interventions for smokers who do not quit on their target quit date (TQD) and decline to set a new TQD after missing their TQD have not been systematically evaluated.Methods
A telephone survey of tobacco QLs in the United States (US) was conducted to examine systematic approaches used with smokers who do not quit on their TQD and decline to set a new TQD. Tobacco QLs service providers were identified through the North American Quitline Consortium (NAQC).Results
Fourteen service providers managing QLs of all 50 US states were identified and completed the voluntary survey. All providers recommended setting a new quit TQD if smokers did not achieve smoking cessation by their initial TQD. Six percent of US state QLs used brief motivational interviewing utilizing the “5R's” (relevance, risk, rewards, roadblocks, repetition). However, 90% of QLs had intervention protocols emphasizing smoking rate reduction.Conclusion
Although some US QLs utilized the “5Rs,” the majority provided smoking reduction interventions for smokers not achieving tobacco cessation by their initial TQD and declining to set a new TQD. Research is needed to evaluate the efficacy of smoking rate reduction methods implemented through QLs for increasing smoking abstinence rates. 相似文献997.
The U.S. Environmental Protection Agency (EPA) has instituted the Chemical Safety for Sustainability (CSS) research program for assessing the health and environmental impact of manufactured chemicals. This is a broad program wherein one of the tasks is to develop high throughput screening (HTS) methods and follow-up confirmation for toxicity at realistic environmental exposure levels. The main tools under this task are in vitro toxicity testing, in silico molecular modeling, and in vivo (systemic) measurements documentation. The in vivo research component is intended to support and corroborate in vitro chemical toxicity prioritization with observations of systemic perturbations and statistical parameters derived from intact (living) organisms. Based on EPA's Biomonitoring Framework for human health research, such observations are intended to link environmental exposures to a cascade of biomarker chemicals to help identify and clarify adverse outcome pathways within the context of systems biology. This commentary discusses the issues regarding interpretation of in vitro changes from HTS as an adverse result, an adaptive (non-adverse) response, or a random/irrelevant occurrence. A second goal is to inform in vitro strategies as to relevant dosing (potency) levels at the cellular level that reflect realistic systemic exposures. Although we recognize the high value of in vivo animal toxicity testing, herein we focus on observational (minimally invasive) human biomonitoring methods and propose complementary in vivo testing that could help guide the design of high-throughput analyses and the ultimate interpretation of their outcomes. 相似文献
998.
999.
Hjelm BE Rosenberg JB Szelinger S Sue LI Beach TG Huentelman MJ Craig DW 《Neuroscience letters》2011,502(3):219-224
Human induced pluripotent stem cells (iPSCs) have become an intriguing approach for neurological disease modeling, because neural lineage-specific cell types that retain the donors’ complex genetics can be established in vitro. The statistical power of these iPSC-based models, however, is dependent on accurate diagnoses of the somatic cell donors; unfortunately, many neurodegenerative diseases are commonly misdiagnosed in live human subjects. Postmortem histopathological examination of a donor's brain, combined with premortem clinical criteria, is often the most robust approach to correctly classify an individual as a disease-specific case or unaffected control. In this study, we describe iPSCs generated from a skin biopsy collected postmortem during the rapid autopsy of a 75-year-old male, whole body donor, defined as an unaffected neurological control by both clinical and histopathological criteria. These iPSCs were established in a feeder-free system by lentiviral transduction of the Yamanaka factors, Oct3/4, Sox2, Klf4, and c-Myc. Selected iPSC clones expressed both nuclear and surface antigens recognized as pluripotency markers of human embryonic stem cells (hESCs) and were able to differentiate in vitro into neurons and glia. Statistical analysis also demonstrated that fibroblast proliferation was significantly affected by biopsy site, but not donor age (within an elderly cohort). These results provide evidence that autopsy donor-derived fibroblasts can be successfully reprogrammed into iPSCs, and may provide an advantageous approach for generating iPSC-based neurological disease models. 相似文献
1000.
Meader N Mitchell AJ Chew-Graham C Goldberg D Rizzo M Bird V Kessler D Packham J Haddad M Pilling S 《The British journal of general practice》2011,61(593):e808-e820