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Mihai Moldovan Volodymyr Pinchenko Oksana Dmytriyeva Stanislava Pankratova K?re Fugleholm Jorg Klingelhofer Elisabeth Bock Vladimir Berezin Christian Krarup Darya Kiryushko 《Molecular medicine (Cambridge, Mass.)》2013,19(1):43-53
We recently found that S100A4, a member of the multifunctional S100 protein family, protects neurons in the injured brain and identified two sequence motifs in S100A4 mediating its neurotrophic effect. Synthetic peptides encompassing these motifs stimulated neuritogenesis and survival in vitro and mimicked the S100A4-induced neuroprotection in brain trauma. Here, we investigated a possible function of S100A4 and its mimetics in the pathologies of the peripheral nervous system (PNS). We found that S100A4 was expressed in the injured PNS and that its peptide mimetic (H3) affected the regeneration and survival of myelinated axons. H3 accelerated electrophysiological, behavioral and morphological recovery after sciatic nerve crush while transiently delaying regeneration after sciatic nerve transection and repair. On the basis of the finding that both S100A4 and H3 increased neurite branching in vitro, these effects were attributed to the modulatory effect of H3 on initial axonal sprouting. In contrast to the modest effect of H3 on the time course of regeneration, H3 had a long-term neuroprotective effect in the myelin protein P0 null mice, a model of dysmyelinating neuropathy (Charcot-Marie-Tooth type 1 disease), where the peptide attenuated the deterioration of nerve conduction, demyelination and axonal loss. From these results, S100A4 mimetics emerge as a possible means to enhance axonal sprouting and survival, especially in the context of demyelinating neuropathies with secondary axonal loss, such as Charcot-Marie-Tooth type 1 disease. Moreover, our data suggest that S100A4 is a neuroprotectant in PNS and that other S100 proteins, sharing high homology in the H3 motif, may have important functions in PNS pathologies. 相似文献
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Rheal A. Towner Nataliya Smith Debra Saunders Patricia Coutinho De Souza Leah Henry Florea Lupu Robert Silasi-Mansat Marilyn Ehrenshaft Ronald P. Mason Sandra E. Gomez-Mejiba Dario C. Ramirez 《生物化学与生物物理学报:疾病的分子基础》2013,1832(12):2153-2161
Free radicals play a major role in gliomas. By combining immuno-spin-trapping (IST) and molecular magnetic resonance imaging (mMRI), in vivo levels of free radicals were detected within mice bearing orthotopic GL261 gliomas. The nitrone spin trap DMPO (5,5-dimethyl pyrroline N-oxide) was administered prior to injection of an anti-DMPO probe (anti-DMPO antibody covalently bound to a bovine serum albumin (BSA)–Gd (gadolinium)-DTPA (diethylene triamine penta acetic acid)–biotin MRI contrast agent) to trap tumor-associated free radicals. mMRI detected the presence of anti-DMPO adducts by either a significant sustained increase (p < 0.001) in MR signal intensity or a significant decrease (p < 0.001) in T1 relaxation, measured as %T1 change. In vitro assessment of the anti-DMPO probe indicated a significant decrease (p < 0.0001) in T1 relaxation in GL261 cells that were oxidatively stressed with hydrogen peroxide, compared to controls. The biotin moiety of the anti-DMPO probe was targeted with fluorescently-labeled streptavidin to locate the anti-DMPO probe in excised brain tissues. As a negative control a non-specific IgG antibody covalently bound to the albumin–Gd-DTPA–biotin construct was used. DMPO adducts were also confirmed in tumor tissue from animals administered DMPO, compared to non-tumor brain tissue. GL261 gliomas were found to have significantly increased malondialdehyde (MDA) protein adducts (p < 0.001) and 3-nitrotyrosine (3-NT) (p < 0.05) compared to normal mouse brain tissue, indicating increased oxidized lipids and proteins, respectively. Co-localization of the anti-DMPO probe with either 3-NT or 4-hydroxynonenal was also observed. This is the first report regarding the detection of in vivo levels of free radicals from a glioma model. 相似文献
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Nataliya Di Donato Ying Y. Jean A. Murat Maga Briana D. Krewson Alison B. Shupp Maria I. Avrutsky Achira Roy Sarah Collins Carissa Olds Rebecca A. Willert Agnieszka M. Czaja Rachel Johnson Jessi A. Stover Steven Gottlieb Deborah Bartholdi Anita Rauch Amy Goldstein Victoria Boyd-Kyle Kimberly A. Aldinger Ghayda M. Mirzaa Anke Nissen Karlla W. Brigatti Erik G. Puffenberger Kathleen J. Millen Kevin A. Strauss William B. Dobyns Carol M. Troy Robert N. Jinks 《American journal of human genetics》2016,99(5):1117-1129
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Dmitriev Alexey A. Kudryavtseva Anna V. Krasnov George S. Koroban Nadezhda V. Speranskaya Anna S. Krinitsina Anastasia A. Belenikin Maxim S. Snezhkina Anastasiya V. Sadritdinova Asiya F. Kishlyan Natalya V. Rozhmina Tatiana A. Yurkevich Olga Yu. Muravenko Olga V. Bolsheva Nadezhda L. Melnikova Nataliya V. 《BMC plant biology》2016,16(3):139-146
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Voznesenskaya T Makogon N Bryzgina T Sukhina V Grushka N Alexeyeva I 《Reproductive biology》2007,7(3):207-220
Experimental immune ovarian failure induced in CBA mice by either administration of xenogenic anti-ovarian antibodies or immunization with allogenic ovarian extracts impaired the meiotic maturation of oocytes and increased apoptosis of follicular cells. Immunization was accompanied with the inflammation and active immune reaction, as shown by the enlargement of regional lymph nodes, the increase of apoptosis in cultured lymph node cells and the increase of band and segmented neutrophil percentage in the blood. Triple injections of melatonin (5 mg/kg of the body weight) an hour before antibodies administration restored the meiotic maturation of oocytes and supported the survival of follicular and lymph node cells. In contrast, melatonin application upon immunization was not effective to prevent the ovary impairment and cell death. It is concluded that melatonin protects against immune ovary failure induced by xenogenic anti-ovarian antibodies. 相似文献
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Nicanor I. Moldovan Florea Lupu Leni Moldovan Nicolae Simionescu 《Cell biology international》1994,18(10):985-992
Cultured bovine aortic endothelial cells (BAEC) were incubated for 5 days with 10?5 4-hydroxynonenal (HN). HN treated BAEC and controls were either (i) further incubated with 125I-polymyxin B (IPxB) or with radioiodinated, inactivated coagulation factor Xa (IFXai) as markers of membrane phospholipid perturbation, or (ii) assayed for the synthesis of prostacyclin (PGI2) and thromboxane A2 (TXA2). Rabbit blood mononuclear cells enriched in monocytes (MC) were isolated and assayed for chemotactic response to HN. The results showed six - fold increases of IPxB and IFXai binding to BAEC treated with HN, as compared to untreated controls. We also found in HN treated cells a marked inhibition of PGI2 synthesis, but an unmodified TXA2 production. In addition, HN in the 10-5-10-10 M range induced oriented migration of MC. 相似文献