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101.
Constância M Hemberger M Hughes J Dean W Ferguson-Smith A Fundele R Stewart F Kelsey G Fowden A Sibley C Reik W 《Nature》2002,417(6892):945-948
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Kévin Baranger Yannick Marchalant Amandine E. Bonnet Nadine Crouzin Alex Carrete Jean-Michel Paumier Nathalie A. Py Anne Bernard Charlotte Bauer Eliane Charrat Katrin Moschke Mothoharu Seiki Michel Vignes Stefan F. Lichtenthaler Frédéric Checler Michel Khrestchatisky Santiago Rivera 《Cellular and molecular life sciences : CMLS》2016,73(1):217-236
104.
Manning AK Hivert MF Scott RA Grimsby JL Bouatia-Naji N Chen H Rybin D Liu CT Bielak LF Prokopenko I Amin N Barnes D Cadby G Hottenga JJ Ingelsson E Jackson AU Johnson T Kanoni S Ladenvall C Lagou V Lahti J Lecoeur C Liu Y Martinez-Larrad MT Montasser ME Navarro P Perry JR Rasmussen-Torvik LJ Salo P Sattar N Shungin D Strawbridge RJ Tanaka T van Duijn CM An P de Andrade M Andrews JS Aspelund T Atalay M Aulchenko Y Balkau B Bandinelli S Beckmann JS Beilby JP Bellis C Bergman RN Blangero J 《Nature genetics》2012,44(6):659-669
Recent genome-wide association studies have described many loci implicated in type 2 diabetes (T2D) pathophysiology and β-cell dysfunction but have contributed little to the understanding of the genetic basis of insulin resistance. We hypothesized that genes implicated in insulin resistance pathways might be uncovered by accounting for differences in body mass index (BMI) and potential interactions between BMI and genetic variants. We applied a joint meta-analysis approach to test associations with fasting insulin and glucose on a genome-wide scale. We present six previously unknown loci associated with fasting insulin at P < 5 × 10(-8) in combined discovery and follow-up analyses of 52 studies comprising up to 96,496 non-diabetic individuals. Risk variants were associated with higher triglyceride and lower high-density lipoprotein (HDL) cholesterol levels, suggesting a role for these loci in insulin resistance pathways. The discovery of these loci will aid further characterization of the role of insulin resistance in T2D pathophysiology. 相似文献
105.
Anne Stephens 《Systemic Practice and Action Research》2012,25(1):1-14
Feminist Systems Theory (FST) is an emerging theory grounded in cultural ecofeminism and critical systems theory. FST’s contribution
is in a set of principles that contain implications for community development and social research. FST brings to the fore
the importance of valuing and considering the voices of people at the margins of social research and community development
projects and is an effort towards a new ontology and language of person and nature to adequately address environmental marginalization.
The ‘systems’ theory contribution to FST enriches our repertoires of methods and tools with an emphasis on systems thinking
characterised by the use of boundary analysis. FST is ideally situated to enhance systemic intervention practice, an application
of action research and participatory research practices. This paper will examine ‘process philosophy’ necessary to understand
the nature of boundary analysis and the implications for FST and praxis with relevant examples drawn from case studies of
current applications of FST in action research settings; (1) economic analysis and transition pathways; (2) policy analysis
of the Close the Gap strategy for Indigenous equality and equity in Australia; (3) a community food distribution system; and, (4) a community
health and diabetes prevention program. 相似文献
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Ferrón SR Charalambous M Radford E McEwen K Wildner H Hind E Morante-Redolat JM Laborda J Guillemot F Bauer SR Fariñas I Ferguson-Smith AC 《Nature》2011,475(7356):381-385
The gene for the atypical NOTCH ligand delta-like homologue 1 (Dlk1) encodes membrane-bound and secreted isoforms that function in several developmental processes in vitro and in vivo. Dlk1, a member of a cluster of imprinted genes, is expressed from the paternally inherited chromosome. Here we show that mice that are deficient in Dlk1 have defects in postnatal neurogenesis in the subventricular zone: a developmental continuum that results in depletion of mature neurons in the olfactory bulb. We show that DLK1 is secreted by niche astrocytes, whereas its membrane-bound isoform is present in neural stem cells (NSCs) and is required for the inductive effect of secreted DLK1 on self-renewal. Notably, we find that there is a requirement for Dlk1 to be expressed from both maternally and paternally inherited chromosomes. Selective absence of Dlk1 imprinting in both NSCs and niche astrocytes is associated with postnatal acquisition of DNA methylation at the germ-line-derived imprinting control region. The results emphasize molecular relationships between NSCs and the niche astrocyte cells of the microenvironment, identifying a signalling system encoded by a single gene that functions coordinately in both cell types. The modulation of genomic imprinting in a stem-cell environment adds a new level of epigenetic regulation to the establishment and maintenance of the niche, raising wider questions about the adaptability, function and evolution of imprinting in specific developmental contexts. 相似文献
109.
Coucke PJ Willaert A Wessels MW Callewaert B Zoppi N De Backer J Fox JE Mancini GM Kambouris M Gardella R Facchetti F Willems PJ Forsyth R Dietz HC Barlati S Colombi M Loeys B De Paepe A 《Nature genetics》2006,38(4):452-457
Arterial tortuosity syndrome (ATS) is an autosomal recessive disorder characterized by tortuosity, elongation, stenosis and aneurysm formation in the major arteries owing to disruption of elastic fibers in the medial layer of the arterial wall. Previously, we used homozygosity mapping to map a candidate locus in a 4.1-Mb region on chromosome 20q13.1 (ref. 2). Here, we narrowed the candidate region to 1.2 Mb containing seven genes. Mutations in one of these genes, SLC2A10, encoding the facilitative glucose transporter GLUT10, were identified in six ATS families. GLUT10 deficiency is associated with upregulation of the TGFbeta pathway in the arterial wall, a finding also observed in Loeys-Dietz syndrome, in which aortic aneurysms associate with arterial tortuosity. The identification of a glucose transporter gene responsible for altered arterial morphogenesis is notable in light of the previously suggested link between GLUT10 and type 2 diabetes. Our data could provide new insight on the mechanisms causing microangiopathic changes associated with diabetes and suggest that therapeutic compounds intervening with TGFbeta signaling represent a new treatment strategy. 相似文献
110.
Gupta GP Nguyen DX Chiang AC Bos PD Kim JY Nadal C Gomis RR Manova-Todorova K Massagué J 《Nature》2007,446(7137):765-770
Metastasis entails numerous biological functions that collectively enable cancerous cells from a primary site to disseminate and overtake distant organs. Using genetic and pharmacological approaches, we show that the epidermal growth factor receptor ligand epiregulin, the cyclooxygenase COX2, and the matrix metalloproteinases 1 and 2, when expressed in human breast cancer cells, collectively facilitate the assembly of new tumour blood vessels, the release of tumour cells into the circulation, and the breaching of lung capillaries by circulating tumour cells to seed pulmonary metastasis. These findings reveal how aggressive primary tumorigenic functions can be mechanistically coupled to greater lung metastatic potential, and how such biological activities may be therapeutically targeted with specific drug combinations. 相似文献