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61.
62.
In their discussion of a mechanism that I proposed to explain the apparent superluminal (that is, faster than light) tunnelling of light pulses observed in photonic barrier experiments, Büttiker and Washburn used an old 'reshaping' argument that is at variance with my model and is not supported by the bulk of the experimental tunnelling evidence. The mechanism I proposed agrees with experiment and resolves a long-standing paradox - namely, the lack of dependence of tunnelling time on barrier length for thick barriers (the Hartman effect). 相似文献
63.
Gut hormone PYY(3-36) physiologically inhibits food intake 总被引:42,自引:0,他引:42
Batterham RL Cowley MA Small CJ Herzog H Cohen MA Dakin CL Wren AM Brynes AE Low MJ Ghatei MA Cone RD Bloom SR 《Nature》2002,418(6898):650-654
Food intake is regulated by the hypothalamus, including the melanocortin and neuropeptide Y (NPY) systems in the arcuate nucleus. The NPY Y2 receptor (Y2R), a putative inhibitory presynaptic receptor, is highly expressed on NPY neurons in the arcuate nucleus, which is accessible to peripheral hormones. Peptide YY(3-36) (PYY(3-36)), a Y2R agonist, is released from the gastrointestinal tract postprandially in proportion to the calorie content of a meal. Here we show that peripheral injection of PYY(3-36) in rats inhibits food intake and reduces weight gain. PYY(3-36) also inhibits food intake in mice but not in Y2r-null mice, which suggests that the anorectic effect requires the Y2R. Peripheral administration of PYY(3-36) increases c-Fos immunoreactivity in the arcuate nucleus and decreases hypothalamic Npy messenger RNA. Intra-arcuate injection of PYY(3-36) inhibits food intake. PYY(3-36) also inhibits electrical activity of NPY nerve terminals, thus activating adjacent pro-opiomelanocortin (POMC) neurons. In humans, infusion of normal postprandial concentrations of PYY(3-36) significantly decreases appetite and reduces food intake by 33% over 24 h. Thus, postprandial elevation of PYY(3-36) may act through the arcuate nucleus Y2R to inhibit feeding in a gut-hypothalamic pathway. 相似文献
64.
采用CALPHAD技术评估了Ni-Ga二元系的相图和热力学性质.用双亚晶格模型描述2个有序相(L1 2-Ni3Ga和B2-NiGa)的热力学行为,并在优化过程中考虑了fc-(Ni)和LI2-Ni3Ga相的有序-无序转变.溶液相(液相、fcc-(Ni)固溶体)的热力学模型采用Redlich-Kister方程,其余5个中间化合物被视为整比化合物. 相似文献
65.
The mysteries of adaequare: A vindication of fermat 总被引:2,自引:0,他引:2
Herbert Breger 《Archive for History of Exact Sciences》1994,46(3):193-219
66.
Barton ES White DW Cathelyn JS Brett-McClellan KA Engle M Diamond MS Miller VL Virgin HW 《Nature》2007,447(7142):326-329
All humans become infected with multiple herpesviruses during childhood. After clearance of acute infection, herpesviruses enter a dormant state known as latency. Latency persists for the life of the host and is presumed to be parasitic, as it leaves the individual at risk for subsequent viral reactivation and disease. Here we show that herpesvirus latency also confers a surprising benefit to the host. Mice latently infected with either murine gammaherpesvirus 68 or murine cytomegalovirus, which are genetically highly similar to the human pathogens Epstein-Barr virus and human cytomegalovirus, respectively, are resistant to infection with the bacterial pathogens Listeria monocytogenes and Yersinia pestis. Latency-induced protection is not antigen specific but involves prolonged production of the antiviral cytokine interferon-gamma and systemic activation of macrophages. Latency thereby upregulates the basal activation state of innate immunity against subsequent infections. We speculate that herpesvirus latency may also sculpt the immune response to self and environmental antigens through establishment of a polarized cytokine environment. Thus, whereas the immune evasion capabilities and lifelong persistence of herpesviruses are commonly viewed as solely pathogenic, our data suggest that latency is a symbiotic relationship with immune benefits for the host. 相似文献
67.
Sometimes a larger dataset needs to be reduced to just a few points, and it is desirable that these points be representative of the whole dataset. If the future uses of these points are not fully specified in advance, standard decision-theoretic approaches will not work. We present here methodology for choosing a small representative sample based on a mixture modeling approach. 相似文献
68.
Leung JY Bennett WR Herbert RP West AK Lee PR Wake H Fields RD Chuah MI Chung RS 《Cellular and molecular life sciences : CMLS》2012,69(5):809-817
Prior studies have reported that metallothionein I/II (MT) promote regenerative axonal sprouting and neurite elongation of
a variety of central nervous system neurons after injury. In this study, we evaluated whether MT is capable of modulating
regenerative axon outgrowth of neurons from the peripheral nervous system. The effect of MT was firstly investigated in dorsal
root ganglion (DRG) explants, where axons were scratch-injured in the presence or absence of exogenous MT. The application
of MT led to a significant increase in regenerative sprouting of neurons 16 h after injury. We show that the pro-regenerative
effect of MT involves an interaction with the low-density lipoprotein receptor megalin, which could be blocked using the competitive
antagonist RAP. Pre-treatment with the mitogen-activated protein kinase (MAPK) inhibitor PD98059 also completely abrogated
the effect of exogenous MT in promoting axonal outgrowth. Interestingly, we only observed megalin expression in neuronal soma
and not axons in the DRG explants. To investigate this matter, an in vitro injury model was established using Campenot chambers,
which allowed the application of MT selectively into either the axonal or cell body compartments after scratch injury was
performed to axons. At 16 h after injury, regenerating axons were significantly longer only when exogenous MT was applied
solely to the soma compartment, in accordance with the localized expression of megalin in neuronal cell bodies. This study
provides a clear indication that MT promotes axonal regeneration of DRG neurons, via a megalin- and MAPK-dependent mechanism. 相似文献
69.
Deficiency of PORCN, a regulator of Wnt signaling, is associated with focal dermal hypoplasia 总被引:1,自引:0,他引:1
Grzeschik KH Bornholdt D Oeffner F König A del Carmen Boente M Enders H Fritz B Hertl M Grasshoff U Höfling K Oji V Paradisi M Schuchardt C Szalai Z Tadini G Traupe H Happle R 《Nature genetics》2007,39(7):833-835
Focal dermal hypoplasia (FDH) is an X-linked dominant multisystem birth defect affecting tissues of ectodermal and mesodermal origin. Using a stepwise approach of (i) genetic mapping of FDH, (ii) high-resolution comparative genome hybridization to seek deletions in candidate chromosome areas and (iii) point mutation analysis in candidate genes, we identified PORCN, encoding a putative O-acyltransferase and potentially crucial for cellular export of Wnt signaling proteins, as the gene mutated in FDH. The findings implicate FDH as a developmental disorder caused by a deficiency in PORCN. 相似文献
70.
Exercise-induced BCL2-regulated autophagy is required for muscle glucose homeostasis 总被引:3,自引:0,他引:3
He C Bassik MC Moresi V Sun K Wei Y Zou Z An Z Loh J Fisher J Sun Q Korsmeyer S Packer M May HI Hill JA Virgin HW Gilpin C Xiao G Bassel-Duby R Scherer PE Levine B 《Nature》2012,481(7382):511-515
Exercise has beneficial effects on human health, including protection against metabolic disorders such as diabetes. However, the cellular mechanisms underlying these effects are incompletely understood. The lysosomal degradation pathway, autophagy, is an intracellular recycling system that functions during basal conditions in organelle and protein quality control. During stress, increased levels of autophagy permit cells to adapt to changing nutritional and energy demands through protein catabolism. Moreover, in animal models, autophagy protects against diseases such as cancer, neurodegenerative disorders, infections, inflammatory diseases, ageing and insulin resistance. Here we show that acute exercise induces autophagy in skeletal and cardiac muscle of fed mice. To investigate the role of exercise-mediated autophagy in vivo, we generated mutant mice that show normal levels of basal autophagy but are deficient in stimulus (exercise- or starvation)-induced autophagy. These mice (termed BCL2 AAA mice) contain knock-in mutations in BCL2 phosphorylation sites (Thr69Ala, Ser70Ala and Ser84Ala) that prevent stimulus-induced disruption of the BCL2-beclin-1 complex and autophagy activation. BCL2 AAA mice show decreased endurance and altered glucose metabolism during acute exercise, as well as impaired chronic exercise-mediated protection against high-fat-diet-induced glucose intolerance. Thus, exercise induces autophagy, BCL2 is a crucial regulator of exercise- (and starvation)-induced autophagy in vivo, and autophagy induction may contribute to the beneficial metabolic effects of exercise. 相似文献