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81.
Hedley CA Emsley Craig J Smith Carole M Gavin Rachel F Georgiou Andy Vail Elisa M Barberan Karen Illingworth Sylvia Scarth Vijitha Wickramasinghe Margaret E Hoadley Nancy J Rothwell Pippa J Tyrrell Stephen J Hopkins 《BMC neurology》2007,7(1):1-12
Background
As critical mediators of local and systemic inflammatory responses, cytokines are produced in the brain following ischaemic stroke. Some have been detected in the circulation of stroke patients, but their role and source is unclear. Focusing primarily on interleukin(IL)-1-related mechanisms, we serially measured plasma inflammatory markers, and the production of cytokines by whole blood, from 36 patients recruited within 12 h and followed up to 1 year after acute ischaemic stroke (AIS).Results
Admission plasma IL-1 receptor antagonist (IL-1ra) concentration was elevated, relative to age-, sex-, and atherosclerosis-matched controls. IL-1β, soluble IL-1 receptor type II, tumour necrosis factor (TNF)-α, TNF-RII, IL-10 and leptin concentrations did not significantly differ from controls, but peak soluble TNF receptor type I (sTNF-RI) in the first week correlated strongly with computed tomography infarct volume at 5–7 days, mRS and BI at 3 and 12 months. Neopterin was raised in patients at 5–7 d, relative to controls, and in subjects with significant atherosclerosis. Spontaneous IL-1β, TNF-α and IL-6 gene and protein expression by blood cells was minimal, and induction of these cytokines by lipopolysaccharide (LPS) was significantly lower in patients than in controls during the first week. Minimum LPS-induced cytokine production correlated strongly with mRS and BI, and also with plasma cortisol.Conclusion
Absence of spontaneous whole blood gene activation or cytokine production suggests that peripheral blood cells are not the source of cytokines measured in plasma after AIS. Increased plasma IL-1ra within 12 h of AIS onset, the relationship between sTNF-RI and stroke severity, and suppressed cytokine induction suggests early activation of endogenous immunosuppressive mechanisms after AIS. 相似文献82.
Yuansha Chen Peter Bystricky Jacob Adeyeye Pinaki Panigrahi Afsar Ali Judith A Johnson CA Bush JG MorrisJr OC Stine 《BMC microbiology》2007,7(1):20
Background
In V. cholerae, the biogenesis of capsule polysaccharide is poorly understood. The elucidation of capsule structure and biogenesis is critical to understanding the evolution of surface polysaccharide and the internal relationship between the capsule and LPS in this species. V. cholerae serogroup O31 NRT36S, a human pathogen that produces a heat-stable enterotoxin (NAG-ST), is encapsulated. Here, we report the covalent structure and studies of the biogenesis of the capsule in V. cholerae NRT36S. 相似文献83.
84.
85.
Principal component models for sparse functional data 总被引:5,自引:0,他引:5
86.
玉米叶片生长部位渗透调节和生长的生物物理参数变化 总被引:6,自引:0,他引:6
玉米叶片生长部位随着水分胁迫加剧ψ_w降低、LER减慢。LER从最大到零,快速干旱处理的ψw从-0.55降至-0.85 MPa;缓慢干旱处理ψ_w从-0.88降至-1.13 MPa。在任何一种LER下,缓慢干旱处理的ψ_s比快速干旱处理更低,生长停止时,前者为-1.57 MPa,而后者为-1.30MPa。缓慢干旱叶片尽管在更低ψ_w下,仍能维持一定膨压,保持一定的生长速率。经历长时间水分胁迫会改变细胞延伸生长的生物物理参数,增大临界膨压(0.08~0.09 MPa)。这是水分胁迫植株,在一定ψ_p下生长速率减慢的原因。 相似文献
87.
入侵种喜旱莲子草和莲子草的营养生长和光合作用对温度的响应 总被引:2,自引:0,他引:2
比较温度对入侵种喜旱莲子草(Alternantheraphiloxeroides(Mart.)Griseb.)和其本土近缘种莲子草(A.sessilis(L.)DC.)的营养生长、叶片光合作用及叶绿素荧光的影响。实验将生长均衡的这两种植物放在不同温度(10℃、15℃、20℃、25℃、30℃)的光照培养箱中处理28d。结果表明,喜旱莲子草营养生长的速率和对温度的响应明显不同于莲子草:前者主茎生长的有效积温明显低于后者,分别是11.6d℃和27.0d℃;而新叶萌发的有效积温高于后者,分别是12.1d℃和6.7d℃。入侵种主茎和叶的发育起点温度都比本土种低,分别是10.4℃、11.0℃和12.8℃、14.9℃,表明喜旱莲子草的发育对低温反应不及莲子草敏感。对两种植物叶片的光合作用和叶绿素荧光的测定结果还表明:入侵种比本土种有较高的最大净光合速率和光饱和点,尤其在25℃时;10-30℃的温度范围内喜旱莲子草的最大光化学效率Fv/Fm没有显著变化,而莲子草在10℃低温条件下Fv/Fm值显著降低。较快的主茎生长速率、较宽的温度适应范围以及较高的光合能力可能使喜旱莲子草比本地种具有更强的竞争力,从而在其入侵过程中起了重要作用。 相似文献
88.
Lívia CA Ribeiro Lívia C Massimino Araceli C Durante Aline Tansini Ana C Urbaczek Heloísa S Selistre-de-Araújo Iracilda Z Carlos 《Cell Adhesion & Migration》2014,8(1):60-65
Integrin αvβ3 is most likely the foremost modulator of angiogenesis among all known integrins. Recombinant disintegrin DisBa-01, originally obtained from snake venom glands, binds to αvβ3, thereby significantly inhibiting adhesion and generating in vivo anti-metastatic ability. However, its function in mediator production is not clear. Here, we observed that the mediators VEGF-A, IL-8, and TGF-β are not produced by human umbilical vein endothelial cells (HUVEC cell line) or monocyte/macrophage cells (SC cell line) when cells adhered to vitronectin. However, when exposed to DisBa-01, HUVECs produced higher levels of TGF-β, and SC cells produced higher levels of VEGF-A. Nonetheless, HUVECs also showed an enhancement of apoptosis after losing adherence when exposed to disintegrin, which is a characteristic of anoikis. We propose that disintegrin DisBa-01 could be used to modulate integrin αvβ3 functions. 相似文献
89.
Background
The impact of circle of Willis anatomical variation upon the presentation of stroke is probably underrecognised. 相似文献90.
Steenvoorden MM Tolboom TC van der Pluijm G Löwik C Visser CP DeGroot J Gittenberger-DeGroot AC DeRuiter MC Wisse BJ Huizinga TW Toes RE 《Arthritis research & therapy》2006,8(6):R165-10
The healthy synovial lining layer consists of a single cell layer that regulates the transport between the joint cavity and the surrounding tissue. It has been suggested that abnormalities such as somatic mutations in the p53 tumor-suppressor gene contribute to synovial hyperplasia and invasion in rheumatoid arthritis (RA). In this study, expression of epithelial markers on healthy and diseased synovial lining tissue was examined. In addition, we investigated whether a regulated process, resembling epithelial to mesenchymal transition (EMT)/fibrosis, could be responsible for the altered phenotype of the synovial lining layer in RA. Synovial tissue from healthy subjects and RA patients was obtained during arthroscopy. To detect signs of EMT, expression of E-cadherin (epithelial marker), collagen type IV (indicator of the presence of a basement membrane) and alpha-smooth muscle actin (alpha-sma; a myofibroblast marker) was investigated on frozen tissue sections using immunohistochemistry. Fibroblast-like synoviocytes (FLSs) from healthy subjects were isolated and subjected to stimulation with synovial fluid (SF) from two RA patients and to transforming growth factor (TGF)-beta. To detect whether EMT/fibrotic markers were increased, expression of collagen type I, alpha-sma and telopeptide lysylhydroxylase (TLH) was measured by real time PCR. Expression of E-cadherin and collagen type IV was found in healthy and arthritic synovial tissue. Expression of alpha-sma was only found in the synovial lining layer of RA patients. Stimulation of healthy FLSs with SF resulted in an upregulation of alpha-sma and TLH mRNA. Collagen type I and TLH mRNA were upregulated after stimulation with TGF-beta. Addition of bone morphogenetic protein (BMP)-7 to healthy FLS stimulated with SF inhibited the expression of alpha-sma mRNA. The finding that E-cadherin and collagen type IV are expressed in the lining layer of healthy and arthritic synovium indicates that these lining cells display an epithelial-like phenotype. In addition, the presence of alpha-sma in the synovial lining layer of RA patients and induction of fibrotic markers in healthy FLSs by SF from RA patients indicate that a regulated process comparable to EMT might cause the alteration in phenotype of RA FLSs. Therefore, BMP-7 may represent a promising agent to counteract the transition imposed on synoviocytes in the RA joint. 相似文献