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31.
Polybrominated diphenyl ethers (PBDEs) are widely used as additive flame-retardants and have been detected in human blood,
adipose tissue, and breast milk. Developmental and long-term exposures to these chemicals may pose a human health risk, especially
to children. We have previously demonstrated that polychlorinated biphenyls (PCBs), which are structurally similar to PBDEs
and cause neurotoxicity, perturb intracellular signaling events including calcium homeostasis and protein kinase C translocation,
which are critical for neuronal function and development of the nervous system. The objective of the present study was to
test whether environmentally relevant PBDE congeners 47 and 99 are also capable of disrupting Ca2 + homeostasis. Calcium buffering was determined by measuring 45Ca2 + -uptake by microsomes and mitochondria, isolated from adult male rat brain (frontal cortex, cerebellum, hippocampus, and hypothalamus).
Results show that PBDEs 47 and 99 inhibit both microsomal and mitochondrial 45Ca2 + -uptake in a concentration-dependent manner. The effect of these congeners on 45Ca2 + -uptake is similar in all four brain regions though the hypothalamus seems to be slightly more sensitive. Among the two preparations,
the congeners inhibited 45Ca2 + -uptake in mitochondria to a greater extent than in microsomes. These results indicate that PBDE 47 and PBDE 99 congeners
perturb calcium signaling in rat brain in a manner similar to PCB congeners, suggesting a common mode of action of these persistent
organic pollutants.
The research described in this article has been reviewed by the National Health and Environmental Effects Research Laboratory
of the US Environmental Protection Agency, and approved for publication. Approval does not signify that the contents necessarily
reflect the views and policies of the Agency nor does mention of trade names or commercial products constitute endorsement
or recommendation for use.
These results will be presented at the 21th Biennial Meeting of International Society for Neurochemistry and American Society
for Neurochemistry in Cancun, Mexico (August 19–24, 2007).
Special issue article in honor of Dr. Frode Fonnum. 相似文献
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Jessica L. Teo Vanesa M. Tomatis Luke Coburn Anne K. Lagendijk Irin-Maya Schouwenaar Srikanth Budnar Thomas E. Hall Suzie Verma Robert W. McLachlan Benjamin M. Hogan Robert G. Parton Alpha S. Yap Guillermo A. Gomez 《Molecular biology of the cell》2020,31(23):2557
Epithelia can eliminate apoptotic cells by apical extrusion. This is a complex morphogenetic event where expulsion of the apoptotic cell is accompanied by rearrangement of its immediate neighbors to form a rosette. A key mechanism for extrusion is constriction of an actomyosin network that neighbor cells form at their interface with the apoptotic cell. Here we report a complementary process of cytoskeletal relaxation that occurs when cortical contractility is down-regulated at the junctions between those neighbor cells themselves. This reflects a mechanosensitive Src family kinase (SFK) signaling pathway that is activated in neighbor cells when the apoptotic cell relaxes shortly after injury. Inhibiting SFK signaling blocks both the expulsion of apoptotic cells and the rosette formation among their neighbor cells. This reveals the complex pattern of spatially distinct contraction and relaxation that must be established in the neighboring epithelium for apoptotic cells to be extruded. 相似文献
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The use of inflatable breast implants 总被引:1,自引:0,他引:1
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Ronald F. Coburn Edward F. Labelle Thomas Griffiths Carl B. Baron 《Journal of cellular physiology》1997,171(3):271-283
About 25% of the total cellular PLCβ2 content was found to be associated with a sarcolemmal fraction (SARC) isolated from unstimulated porcine trachealis smooth muscle. SARC-associated PLCβ2 was located within two compartments, a detergent-extractable compartment and a nondetergent extractable compartment. SARC PLCβ2 was measured after extraction with 0.6 M KCl; therefore, PLCβ2 was not bound solely by electrostatic forces within either of these compartments. PLCβ2 was shown to translocate from cytosol to SARC during a 20-sec activation of intact muscle with a muscarinic agonist, carbachol (CARB); i.e., cytosolic total PLCβ2 content decreased significantly to 73 ± 7% of control and SARC total PLCβ2 content increased to 180 ± 15% of control value. This translocation was maintained at 5 min of CARB. CARB-evoked translocation occurred into the detergent-extractable SARC fraction, and PLCβ2 content in this fraction increased 300% compared with that in unstimulated muscle. After CARB, SARC PLCβ2 content accounted for >50% of total cellular PLCβ2 content. CARB-evoked increase in PLC activity in SARC paralleled the increase in PLCβ2 content. CARB-induced translocations of PLCβ2 from the cytosol to SARC were of a similar magnitude as occurred with phorbol ester-induced translocations of PKCα. J. Cell. Physiol. 171:271–283, 1997. © 1997 Wiley-Liss, Inc. 相似文献
40.
Borrelia burgdorferi outer surface protein C (OspC) binds complement component C4b and confers bloodstream survival
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Jennifer A. Caine Yi‐Pin Lin Julie R. Kessler Hiromi Sato John M. Leong Jenifer Coburn 《Cellular microbiology》2017,19(12)
Borrelia burgdorferi (Bb) is the causative agent of Lyme disease in the United States, a disease that can result in carditis, and chronic and debilitating arthritis and/or neurologic symptoms if left untreated. Bb survives in the midgut of the Ixodes scapularis tick, or within tissues of immunocompetent hosts. In the early stages of infection, the bacteria are present in the bloodstream where they must resist clearance by the innate immune system of the host. We have found a novel role for outer surface protein C (OspC) from B. burgdorferi and B. garinii in interactions with the complement component C4b and bloodstream survival in vivo. Our data show that OspC inhibits the classical and lectin complement pathways and competes with complement protein C2 for C4b binding. Resistance to complement is important for maintenance of the lifecycle of Bb, enabling survival of the pathogen within the host as well as in the midgut of a feeding tick when ospC expression is induced. 相似文献