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671.
Photosynthetica - The effect of water on the primary photosynthetic activity of purple bacterium Rhodospirillum rubrum was studied in Hexadecane-Tween-Spane (HTS)- and phospholipid (PLC)-reverse... 相似文献
672.
Charis E. Teh Alissa K. Robbins Darren C. Henstridge Grant Dewson Sarah T. Diepstraten Gemma Kelly Mark A. Febbraio Sarah S. Gabriel Lorraine A. OReilly Andreas Strasser Daniel H. D. Gray 《Cell death and differentiation》2020,27(12):3374
FOXP3+ regulatory T (Treg) cells are essential for maintaining immunological tolerance. Given their importance in immune-related diseases, cancer and obesity, there is increasing interest in targeting the Treg cell compartment therapeutically. New pharmacological inhibitors that specifically target the prosurvival protein MCL-1 may provide this opportunity, as Treg cells are particularly reliant upon this protein. However, there are two distinct isoforms of MCL-1; one located at the outer mitochondrial membrane (OMM) that is required to antagonize apoptosis, and another at the inner mitochondrial membrane (IMM) that is reported to maintain IMM structure and metabolism via ATP production during oxidative phosphorylation. We set out to elucidate the relative importance of these distinct biological functions of MCL-1 in Treg cells to assess whether MCL-1 inhibition might impact upon the metabolism of cells able to resist apoptosis. Conditional deletion of Mcl1 in FOXP3+ Treg cells resulted in a lethal multiorgan autoimmunity due to the depletion of the Treg cell compartment. This striking phenotype was completely rescued by concomitant deletion of the apoptotic effector proteins BAK and BAX, indicating that apoptosis plays a pivotal role in the homeostasis of Treg cells. Notably, MCL-1-deficient Treg cells rescued from apoptosis displayed normal metabolic capacity. Moreover, pharmacological inhibition of MCL-1 in Treg cells resistant to apoptosis did not perturb their metabolic function. We conclude that Treg cells require MCL-1 only to antagonize apoptosis and not for metabolism. Therefore, MCL-1 inhibition could be used to manipulate Treg cell survival for clinical benefit without affecting the metabolic fitness of cells resisting apoptosis.Subject terms: Disease genetics, Immune cell death 相似文献
673.
Human clinical and psychophysical observations suggest that the taste
system is able to compensate for losses in peripheral nerve input, since
patients do not commonly report decrements in whole mouth taste following
chorda tympani nerve damage or anesthesia. Indeed, neurophysiological data
from the rat nucleus of the solitary tract (NST) suggests that a release of
inhibition (disinhibition) may occur centrally following chorda tympani
nerve anesthesia. Our purpose was to study this possibility further. We
recorded from 59 multi- and single- unit taste-responsive sites in the rat
NST before, during and after recovery from chorda tympani nerve anesthesia.
During anesthesia, average anterior tongue responses were eliminated but no
compensatory increases in palatal or posterior tongue responses were
observed. However, six individual sites displayed increased taste
responsiveness during anesthesia. The average increase was 32.9%.
Therefore, disinhibition of taste responses was observed, but infrequently
and to a small degree in the NST At a subset of sites, chorda
tympani-mediated responses decreased while greater superficial
petrosal-mediated responses remained the same during anesthesia. Since this
effect was accompanied by a decrease in spontaneous activity, we propose
that taste compensation may result in part by a change in signal-to-noise
ratio at a subset of sites.
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674.
FADD/MORT1 is a cytosolic adaptor protein which is critical for signalling from CD95 (Fas/APO-1) and certain other members of the tumour necrosis factor receptor (TNF-R) family (called 'death receptors'). Two protein interaction domains have been identified in FADD/MORT1. The C-terminal 'death domain' is needed for recruitment of FADD/MORT1 to ligated 'death receptors' and the N-terminal 'death effector domain' mediates oligomerisation and activation of caspase-8 zymogens. Caspase-8 activates other cysteine proteases by cleavage and this starts a proteolytic cascade which constitutes the 'point of no return' in apoptosis signalling. Experiments in mice lacking FADD/MORT1 function proved that this adaptor is required for CD95- and TNF-RI-transduced cell death but is dispensable for other pathways to apoptosis. Surprisingly, FADD/MORT1 is also essential for mitogen-induced proliferation of T-lymphocytes. Therapeutic activation of FADD/MORT1 function may be used to kill unwanted cells in cancer or autoimmunity and its suppression may help prevent cell death in certain degenerative disorders. 相似文献