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61.
Alfonso Pompella Aldo Paolicchi Silvia Dominici Mario Comporti Roberto Tongiani 《Histochemistry and cell biology》1996,106(3):275-282
A number of studies indicate that cell proliferation can be modulated by changes in the redox balance of (soluble and protein)
cellular thiols. Free radical processes, including lipid peroxidation (LPO), can affect such a balance, and a role for LPO
in multistage carcinogenesis has been envisaged. The present study was aimed to assess the relationships between the protein
thiol redox status and the LPO process in chemically induced preneoplastic tissue. The Solt-Farber's initiation-promotion
model of chemical carcinogenesis in the rat liver was used. In fresh cryostat sections, preneoplastic lesions were identified
by the reexpression of γ-glutamyltranspeptidase (GGT) activity. In serial sections, different classes of protein thiols were
stained; in additional sections, LPO was elicited by various prooxidant mixtures and determined thereafter by the hydroxynaphthoic
hydrazide-Fast Blue B procedure. The incubation of sections in the presence of chelated iron plus substrates for GGT activity
leads to the development of LPO in selected section areas closely corresponding to GGT-positive lesions, indicating the ability
of GGT activity to initiate LPO. Protein-reactive thiols, as well as total protein sulfur, were decreased by 20–25% in cells
belonging to GGT-positive preneoplastic nodules, suggesting the occurrence of oxidative conditions in vivo. The incubation
of additional adjacent sections with the prooxidant mixture H2O2 plus iron(II), in order to induce the complete oxidation of lipid present in the section, showed a decreased basal concentration
of oxidizable lipid substrate in GGT-rich areas. The decreased levels of both protein thiols and lipid-oxidizable substrate
in GGT-positive nodules suggest that the observed GGT-dependent path-way of LPO initiation can be chronically operative in
vivo during early stages of chemical carcinogenesis, in cells expressing GGT as part of their transformed phenotype. 相似文献
62.
63.
Stuart L. Pimm 《Biodiversity and Conservation》1996,5(9):1059-1067
During their colonization by Polynesians and later by Europeans, the Hawaiian islands suffered a massive loss of species. All the extinctions are indirectly attributable to human impact. Nonetheless, it has proved extremely difficult to specify which of several possible mechanisms caused each particular extinction. This seems to admit defeat in the battle to understand past extinctions. Such understanding could guide our efforts to protect species that are now threatened with extinction. Will it be easier to understand the causes of future extinctions? Surveys of future extinctions stress habitat destruction as the simple and dominant mechanism. This contrasts to its secondary (and generally confused) role in past extinctions. I argue that this contrast between the complexity of the past and the apparent simplicity of the future arises because extinction mechanisms are inherently synergistic. Once extensive species losses begin, it may be impossible to separate the mechanisms and thus manage an individual species as if its decline had a single cause. 相似文献
64.
James B. Hoying Carl A. Boswell Stuart K. Williams 《In vitro cellular & developmental biology. Animal》1996,32(7):409-419
Summary During angiogenesis, the microvasculature displays both vessel remodeling and expansion under the control of both cellular
and extracellular influences. We have evaluated the role of angiogenic and angiostatic molecules on angiogenesis in anin vitro model that more appropriately duplicates the cellular and extracellular components of this process. Freshly isolated microvessel
fragments from rat adipose tissue (RFMF) were cultured within three-dimensional collagen I gels. These fragments were characterized
at the time of isolation and were composed of vessel segments observed in the microvasculature of fatin situ (i.e., arterioles, venules, and capillaries). Fragments also exhibited characteristic ablumenally associated cells including
smooth muscle cells and pericytes. Finally, fragments were encased in an extracellular matrix composed of collagen type IV
and collagen type I/III. The elongation of microvascular elements was subsequently evaluated using morphologic and immunocytochemical
techniques. The proliferation, migration, and elongation of cellular elements in microvessel fragments from rat adipose tissue
was dependent on initial fragment density, matrix density, and required serum. Inclusion of endothelial cell growth factors
to microvessel fragments from rat adipose tissue 3-D cultures resulted in the accelerated elongation of tube structures and
the expression of von Willebrand factor in cells constituting these tubes. Molecules with reported angiostatic capacity (e.g.,
transforming growth factor and hydrocortisone) inhibited vessel tube elongation.
In vitro methods have been developed to evaluate numerous mechanisms associated with angiogenesis, including endothelial cell proliferation,
migration, and phenotypic modulation. Microvascular endothelial cell fragments described in this study represent anin vitro population of cells that accurately duplicate thein vivo microcirculatory elements of fat. The proliferation of cells and elongation of microvascular elements subsequently observed
in three-dimensional cultures provides anin vitro model of angiogenesis. Microvascular formation in this system results from pre-existing microvessel fragments unlike tube
formation observed when cultured endothelial cells are placed in three-dimensional gels. This form of tube formation from
cultured endothelium is more characteristic of vasculogenesis. Thus, the formation of microvascular elements from microvessel
fragments provides the opportunity to examine the mechanisms regulating angiogenesis in anin vitro system amenable to precise experimental manipulation. 相似文献
65.
Stuart Knutton 《Bioscience reports》1995,15(6):469-479
EnteropathogenicEscherichia coli (EPEC), first described in the 1940's and 1950's, remain an important cause of severe infantile diarrhoea in many parts of the developing world. EPEC do not produce enterotoxins and are not invasive; instead their virulence depends upon exploitation of host cell signalling pathways and the host cell cytoskeleton both as a means of colonizing mucosal surfaces of the small intestine and causing diarrhoea. Following initial mucosal attachment, EPEC secrete signalling proteins and expresss a surface adhesin, intimin, to produce attaching & effacing lesions in the enterocyte brush border membrane characterised by localised destruction of brush border microvilli, intimate bacterial adhesion and cytoskeletal reorganisation and accretion beneath attached bacteria. The pathophysiology of EPEC diarrhoea is also complex and probably results from a combination of epithelial cell responses including both electrolyte secretion and structural damage. 相似文献
66.
Yuan-Pu Di Elizabeth Repasky Andrei Laszlo Stuart Calderwood John Subjeck 《Journal of cellular physiology》1995,165(2):228-238
The percentage of T and B lymphocytes expressing a distinct cytoplasmic aggregate enriched in spectrin, ankyrin, and in several other proteins including protein kinase C greatly increases following various activation protocols. Members of the 70 kDa family of heat shock proteins (hsp70) temporarily bind to and stabilize unfolded segments of other proteins, a function apparently required for proper protein folding and assembly. Considering the multiprotein and dynamic nature of the lymphocyte aggregate, the possibility that hsp70 also might be associated with componets of this structure is considered here. Double immunofluorescence analysis indicates that hsp70 is a component of the lymphocyte aggregate and is coincident with spectrin in a subpopulation of freshly isolated, untreated lymphocytes from various murine tissues and in a T-lymphocyte hybridoma. When cell lysates of lymph node T cells are immunoprecipitated using an antibody against hsp70 or spectrin and then analyzed by Western blot utilizing the alternate antibody, it was found that hsp70 and spectrin coprecipitated with one another. Moreover, this coprecipitation could be abolished by addition of ATP. This latter observation was extended to lymphoid cells using a transient permeabilization procedure, and it was shown that addition of exogenous ATP results in the dissipation of the aggregate structure itself. Finally, conditions that result in T-cell activation and aggregate formation, i.e., treatment with the phorbol ester PMA or T-cell receptor cross-linking, also lead to the repositioning of hsp70 into the aggregate from a membrane/cytosolic locale in congruence with spectrin. These data suggest that hsp70 is an active component of the aggregate and that it may function in the interactions believed to occur in this unique activation-associated organelle. © 1995 Wiley-Liss, Inc. 相似文献
67.
Summary 1. The cloning of the mammalian gonadotropin-releasing hormone receptor sets the stage for rapid progress in understanding the structure of the receptor, its interaction with ligand, and its mechanisms of activation.2. The receptor is a 327 to 328-amino acid seven-transmembrane domain G protein-coupled receptor.3. Recent site-direct mutagenesis studies have provided considerable insight into glycosylation of the receptor, the arrangement of the helices, and the ligand binding domains. 相似文献
68.
69.
Colin V. Beechey Simon T. Ball K. M. Stuart Townsend Janet Jones 《Mammalian genome》1997,8(4):236-240
Mouse Chromosome (Chr) 7 distal to band F3 on the physical map is known to be subject to imprinting, maternal duplication
(MatDp) of the region leading to a late embryonic lethality, while paternal duplication (PatDp) causes death in utero before
11.5 dpc. Using a new mouse reciprocal translocation T(7;11)65H to produce MatDp for distal Chr 7, we have mapped the region
subject to imprinting more precisely to bands 7F4/F5 on the cytogenetic map. Fluorescence in situ hybridization (FISH) studies
on mitotic and meiotic chromosomes of a T65H heterozygote show that the imprinted gene Igf2 is located in the same region. This was confirmed by the finding that embryos with MatDp of bands 7F4/F5 did not express
Igf2. We suggest that other members of the imprinted domain containing Igf2, namely Mash2, H19, Ins2, and p57
K1P2
, are also located in 7F4/F5 and that some or all of these genes may be responsible for the two imprinting lethalities seen
with MatDp and PatDp for this region.
Received: 13 October 1996 / Accepted: 8 December 1996 相似文献
70.
At thirteen sites in northern and central Alaska, full factonal and partial factonal NPK fertilizer experiments were completed in wet and moist tundras The effects of the fertilizers on N and P concentrations in leaves, leaf mass per tiller, tilling, and flowering of the dominant sedge species ( Eriophorum vaginatum. E angustifolium, and Carex aquatilis ) were documented for 3–10 yr at each site Almost all sites showed at least some response to the fertilizer treatment, but the specific treatments and elements that caused the responses varied greatly among sites There also was no consistent difference in responses between wet and moist sites There was, however, a consistent temporal pattern to the responses observed, starting with increases in N and P concentration in leaves in the year that fertilizer was added, followed by growth and tilling responses in the second year, and increased flowering in the third year The increases in N concentration generally only appeared in the first year, while increased P concentrations were sustained for 3–4 yr Effects of fertilizer on flowering were still significant after 6 years in some cases Results are discussed in terms of the role of "nutrient limitation" arctic plant communities and detemuning their productivity following disturbance or fertilization 相似文献