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Yu. M. Aliev N. E. Andreev L. M. Anosova G. M. Batanov K. Yu. Vagin L. M. Gorbunov S. E. Grebenshchikov A. V. Gurevich A. M. Ignatov A. I. Isakov L. M. Kovrizhnykh A. S. Malishevskiȝ R. R. Ramazashvili A. Yu. Romanov A. A. Rukhadze P. S. Strelkov S. A. Uryupin A. A. Frolov 《Plasma Physics Reports》2001,27(5):452-452
23.
Using the Connectivity Map to discover compounds influencing human osteoblast differentiation 下载免费PDF全文
24.
O. B. Schemchukova I. G. Dement’yeva N. E. Varlamov L. P. Pozdnyakova M. N. Bokov T. K. Aliev A. A. Panina D. A. Dolgikh M. P. Kirpichnikov P. G. Sveshnikov 《Moscow University Biological Sciences Bulletin》2016,71(1):24-28
Balb/С mice were immunized with recombinant Ebola virus glycoprotein. Following the selection, screening, and cloning of murine hybridomas, we obtained five genetically stable clones of monoclonal antibodies GPE118 (IgG), GPE274 (IgM), GPE325 (IgM), GPE463 (IgM), and GPE534 (IgG). These antibodies were isolated and purified from the ascitic fluid of Balb/С mice using Protein G affinity chromatography (for IgG) and euglobulin precipitation (for IgM). To select at least three candidate antibodies for testing in biological assays as components of an antibody cocktail for the prophylaxis and treatment of hemorrhagic fever, we carried out an immunochemical analysis of the epitope specificity of the isolated antibodies. Based on the data of immunoblotting and sandwich ELISA, it became evident that the epitope recognized by GPE 534 differs from the epitopes recognized by the monoclonal antibodies GPE 118 and GPE 325. The last two antibodies also have different epitope specificity: it follows from the immunoblotting data and from the data on the binding of these antibodies with the intact and oxidized (partly deglycosylated) recombinant glycoprotein. For the biological activity studies and the development of recombinant counterparts, we selected three candidate high-affinity monoclonal antibodies GPE 534, GPE 118, and GPE 325. 相似文献
25.
Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes 总被引:3,自引:0,他引:3
Klionsky DJ Abeliovich H Agostinis P Agrawal DK Aliev G Askew DS Baba M Baehrecke EH Bahr BA Ballabio A Bamber BA Bassham DC Bergamini E Bi X Biard-Piechaczyk M Blum JS Bredesen DE Brodsky JL Brumell JH Brunk UT Bursch W Camougrand N Cebollero E Cecconi F Chen Y Chin LS Choi A Chu CT Chung J Clarke PG Clark RS Clarke SG Clavé C Cleveland JL Codogno P Colombo MI Coto-Montes A Cregg JM Cuervo AM Debnath J Demarchi F Dennis PB Dennis PA Deretic V Devenish RJ Di Sano F Dice JF Difiglia M 《Autophagy》2008,4(2):151-175
Research in autophagy continues to accelerate,(1) and as a result many new scientists are entering the field. Accordingly, it is important to establish a standard set of criteria for monitoring macroautophagy in different organisms. Recent reviews have described the range of assays that have been used for this purpose.(2,3) There are many useful and convenient methods that can be used to monitor macroautophagy in yeast, but relatively few in other model systems, and there is much confusion regarding acceptable methods to measure macroautophagy in higher eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers of autophagosomes versus those that measure flux through the autophagy pathway; thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from fully functional autophagy that includes delivery to, and degradation within, lysosomes (in most higher eukaryotes) or the vacuole (in plants and fungi). Here, we present a set of guidelines for the selection and interpretation of the methods that can be used by investigators who are attempting to examine macroautophagy and related processes, as well as by reviewers who need to provide realistic and reasonable critiques of papers that investigate these processes. This set of guidelines is not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to verify an autophagic response. 相似文献
26.
Mark E. Obrenovich Ludis A. Morales Celia J. Cobb Justin C. Shenk Gina M. Méndez Kathryn Fischbach Mark A. Smith Eldar K. Qasimov George Perry Gjumrakch Aliev 《Journal of cellular and molecular medicine》2009,13(5):853-865
Alzheimer disease (AD) and stroke are two leading causes of age-associated dementia. Increasing evidence points to vascular damage as an early contributor to the development of AD and AD-like pathology. In this review, we discuss the role of G protein-coupled receptor kinase 2 (GRK2) as it relates to individuals affected by AD and how the cardiovasculature plays a role in AD pathogenesis. The possible involvement of GRKs in AD pathogenesis is an interesting notion, which may help bridge the gap in our understanding of the heart–brain connection in relation to neurovisceral damage and vascular complications in AD, since kinases of this family are known to regulate numerous receptor functions both in the brain, myocardium, and elsewhere. The aim of this review is to discuss our findings of overexpression of GRK2 in the context of the early pathogenesis of AD, because increased levels of GRK2 immunoreactivity were found in vulnerable neurons of AD patients as well as in a two-vessel occlusion (2-VO) mammalian model of ischaemia. Also, we consider the consequences for this overexpression as a loss of G-protein coupled receptor (GPCR) regulation, as well as suggest a potential role for GPCRs and GRKs in a unifying theory of AD pathogenesis, particularly in the context of cerebrovascular disease. We synthesize this newer information and attempt to put it into context with GRKs as regulators of diverse physiological cellular functions that could be appropriate targets for future pharmacological intervention. 相似文献
27.
Aliev G Liu J Shenk JC Fischbach K Pacheco GJ Chen SG Obrenovich ME Ward WF Richardson AG Smith MA Gasimov E Perry G Ames BN 《Journal of cellular and molecular medicine》2009,13(2):320-333
Brain function declines with age and is associated with diminishing mitochondrial integrity. The neuronal mitochondrial ultrastructural changes of young (4 months) and old (21 months) F344 rats supplemented with two mitochondrial metabolites, acetyl-L-carnitine (ALCAR, 0.2%[wt/vol] in the drinking water) and R-α-lipoic acid (LA, 0.1%[wt/wt] in the chow), were analysed using qualitative and quantitative electron microscopy techniques. Two independent morphologists blinded to sample identity examined and scored all electron micrographs. Mitochondria were examined in each micrograph, and each structure was scored according to the degree of injury. Controls displayed an age-associated significant decrease in the number of intact mitochondria (P = 0.026) as well as an increase in mitochondria with broken cristae (P < 0.001) in the hippocampus as demonstrated by electron microscopic observations. Neuronal mitochondrial damage was associated with damage in vessel wall cells, especially vascular endothelial cells. Dietary supplementation of young and aged animals increased the proliferation of intact mitochondria and reduced the density of mitochondria associated with vacuoles and lipofuscin. Feeding old rats ALCAR and LA significantly reduced the number of severely damaged mitochondria (P = 0.02) and increased the number of intact mitochondria (P < 0.001) in the hippocampus. These results suggest that feeding ALCAR with LA may ameliorate age-associated mitochondrial ultrastructural decay and are consistent with previous studies showing improved brain function. 相似文献
28.
Using a Monte Carlo simulation technique, we have modeled 3D diffusion of low molecular weight metabolites inside a skeletal muscle cell. The following structural elements are considered: (i) a regular lattice of actin and myosin filaments inside a myofibril, (ii) the membranes of sarcoplasmic reticulum and mitochondria surrounding the myofibrils, (iii) a set of myofibrils inside a skeletal muscle cell encircled by the outer cell membrane, and (iv) an additional set of regular intracellular structures ("macrocompartments") embedded into the cell interior. The macrocompartments are considered to simulate diffusion restrictions because of hypothetical cylindrical structures (16-22 μm in diameter) suggested earlier (de Graaf et al. Biophys J 78: 1657-1664, 2000). This model allowed us to calculate the apparent coefficients of particle diffusion in the radial and axial directions, D(app)(⊥) and D(app)(II), respectively. Particle movements in the axial direction are considered, at first approximation, as unrestricted diffusion (D(app)(II) = const). The apparent coefficient of radial diffusion, D(app)(⊥), decreases with time because of particle collisions with myofilaments and other rigid obstacles. Results of our random walk simulations are in fairly good agreement with experimental data on NMR measurements of restricted radial diffusion of phosphocreatine in white and red skeletal muscles of goldfish (Kinsey et al. NMR Biomed 12:1-7, 1999). Particle reflections from the low-permeable borders of macrocompartments (efficient diameter, D(eff)(MC) ≈ 9.2-10.4 μm) are the prerequisite for agreeing theoretical and experimental data. The low-permeable coverage of hypothetical macrocompartments (99.8% of coverage) provides the main contribution to time-dependent decrease in D(app)(⊥). 相似文献
29.
Rybchenko V. S. Balabashin D. S. Panina A. A. Solopova O. N. Yakimov S. A. Aliev T. K. Dolgikh D. A. Kirpichnikov M. P. 《Russian Journal of Bioorganic Chemistry》2020,46(3):327-333
Russian Journal of Bioorganic Chemistry - The extracellular part of the ErbB2 receptor (ecdErbB2), an oncological marker and a target for therapeutic antibodies, has been expressed in eukaryotic... 相似文献
30.