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231.
The ability to expand normal pancreatic islet
β cells in culture would significantly advance
the prospects of cell therapy for diabetes. A
number of growth factors can stimulate limited
islet cell replication, however other factors may
exist which are more effective β-cell-specific
mitogens. The search for novel β-cell growth
factors has been hampered by the lack of a β-cell-specific proliferation assay. We developed a
simple and sensitive assay for β-cell growth factors
based on a conditionally-transformed
mouse β-cell line (βTC-tet). These cells express
the SV40 T antigen (Tag) oncoprotein under
control of the tetracycline (Tc) operon regulatory
system. In the presence of Tc, Tag expression
is tightly shut off and the cells undergo
complete growth arrest. Here we show that the
growth-arrested cells can proliferate in
response to growth factors in the absence of Tag. Using this assay, a number of growth factors
previously shown to be mitogenic to a
mixed islet cell population were found to
induce proliferation of pure β cells. We conclude
that growth-arrested βTC-tet cells can be
employed in a survey of factors from various
sources for identifying novel factors with β-cell
mitogenic activity. 相似文献
232.
Models that explain the sustainability of an exploiter–victim ecosystem admit, generally, a coexistence state of both species
in the well-mixed limit. Even if this state is unstable, the extinction-prone system may acquire stability on spatial domains
where different patches oscillate incoherently around the coexistence state. New experiments, however, suggest that a spatially
segregated system may be stable even in the absence of such a coexistence state. Here we revisit the hawk–dove (case 3) model
of Durrett and Levin, which has been shown to support persistent population for system of interacting particles. It turns
out that this model does not admit a (stable or unstable) coexistence state on a single habitat. We analyze the peculiar mechanism
that leads to persistence in this case and the role of demographic stochasticity with and without self-interaction, using
numerical simulations and exact solutions in the infinite diffusion limit. 相似文献
233.
234.
David Israeli David Tanne Dianne Daniels David Last Ran Shneor David Guez Efrat Landau Yiftach Roth Aharon Ocherashvilli Mati Bakon Chen Hoffman Amit Weinberg Talila Volk Yael Mardor 《International journal of biological sciences》2011,7(1):1-8
The development of imaging methodologies for detecting blood-brain-barrier (BBB) disruption may help predict stroke patient''s propensity to develop hemorrhagic complications following reperfusion. We have developed a delayed contrast extravasation MRI-based methodology enabling real-time depiction of subtle BBB abnormalities in humans with high sensitivity to BBB disruption and high spatial resolution. The increased sensitivity to subtle BBB disruption is obtained by acquiring T1-weighted MRI at relatively long delays (~15 minutes) after contrast injection and subtracting from them images acquired immediately after contrast administration. In addition, the relatively long delays allow for acquisition of high resolution images resulting in high resolution BBB disruption maps. The sensitivity is further increased by image preprocessing with corrections for intensity variations and with whole body (rigid+elastic) registration. Since only two separate time points are required, the time between the two acquisitions can be used for acquiring routine clinical data, keeping the total imaging time to a minimum.A proof of concept study was performed in 34 patients with ischemic stroke and 2 patients with brain metastases undergoing high resolution T1-weighted MRI acquired at 3 time points after contrast injection. The MR images were pre-processed and subtracted to produce BBB disruption maps. BBB maps of patients with brain metastases and ischemic stroke presented different patterns of BBB opening. The significant advantage of the long extravasation time was demonstrated by a dynamic-contrast-enhancement study performed continuously for 18 min. The high sensitivity of our methodology enabled depiction of clear BBB disruption in 27% of the stroke patients who did not have abnormalities on conventional contrast-enhanced MRI. In 36% of the patients, who had abnormalities detectable by conventional MRI, the BBB disruption volumes were significantly larger in the maps than in conventional MRI.These results demonstrate the advantages of delayed contrast extravasation in increasing the sensitivity to subtle BBB disruption in ischemic stroke patients. The calculated disruption maps provide clear depiction of significant volumes of BBB disruption unattainable by conventional contrast-enhanced MRI. 相似文献
235.
A qualitative difference in the requirement of mouse helper and cytotoxic T lymphocytes for interleukin 2 (IL-2) was revealed by offering such cells IL-2 synthesized in Xenopus laevis oocytes that had been microinjected with messenger RNA (mRNA) encoding human IL-2. While both helper and cytotoxic mouse T-cell lines proliferate in response to the IL-2 present in medium conditioned by stimulated human lymphocytes, only helper-T-cell lines respond to human IL-2 secreted from oocytes. This result demonstrates a difference between helper and cytotoxic T lymphocytes in their response to IL-2. The growth response of murine cells shows that IL-2 secreted from human cells has properties not found in the IL-2 secreted from oocytes, even though a monoclonal antibody directed against the human IL-2 receptor blocks the activity of both types of IL-2. Quite possibly, this difference results from a post-translational modification. 相似文献
236.
AAA-ATPase p97/Cdc48p, a Cytosolic Chaperone Required for Endoplasmic Reticulum-Associated Protein Degradation 下载免费PDF全文
Efrat Rabinovich Anat Kerem Kai-Uwe Frhlich Noam Diamant Shoshana Bar-Nun 《Molecular and cellular biology》2002,22(2):626-634
Endoplasmic reticulum-associated degradation (ERAD) disposes of aberrant proteins in the secretory pathway. Protein substrates of ERAD are dislocated via the Sec61p translocon from the endoplasmic reticulum to the cytosol, where they are ubiquitinated and degraded by the proteasome. Since the Sec61p channel is also responsible for import of nascent proteins, this bidirectional passage should be coordinated, probably by molecular chaperones. Here we implicate the cytosolic chaperone AAA-ATPase p97/Cdc48p in ERAD. We show the association of mammalian p97 and its yeast homologue Cdc48p in complexes with two respective ERAD substrates, secretory immunoglobulin M in B lymphocytes and 6myc-Hmg2p in yeast. The membrane 6myc-Hmg2p as well as soluble lumenal CPY*, two short-lived ERAD substrates, are markedly stabilized in conditional cdc48 yeast mutants. The involvement of Cdc48p in dislocation is underscored by the accumulation of ERAD substrates in the endoplasmic reticulum when Cdc48p fails to function, as monitored by activation of the unfolded protein response. We propose that the role of p97/Cdc48p in ERAD, provided by its potential unfoldase activity and multiubiquitin binding capacity, is to act at the cytosolic face of the endoplasmic reticulum and to chaperone dislocation of ERAD substrates and present them to the proteasome. 相似文献
237.
Elisha Efrat 《Human ecology: an interdisciplinary journal》1993,21(3):281-293
The results of a comparison of agricultural settlement and land-use and local precipitation patterns in the arid region of the Arava in Israel indicated that as the number of settlements and the area of cultivated land has increased since the 1950s, the albedo effect in the region has decreased, and the amounts of precipitation at the first October rains have increased. It is suggested that the albedo effect in desert areas is influenced by extended agricultural land-use. 相似文献
238.
Shimon Efrat 《Experimental diabetes research》2003,4(1):1-5
Insulin resistance is the primary cause of type 2 diabetes. However, if compensated by increased insulin production, insulin resistance by itself does not lead to overt disease. Type 2 diabetes develops when this compensation is insufficient, due to defects in β-cell function and in regulation of the β-cell mass. β-Cell transplantation, as well as approaches that replenish or preserve the endogenous β-cell mass, may facilitate the treatment of type 2 diabetes in patients requiring exogenous insulin. 相似文献
239.