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41.
The oxidative erosion of seven types of graphite has been investigated by heating in air at temperatures between 600 and 1000 K. The specimens include pyrolytic graphite, fine-grain graphites, carbon-fibre composites (CFC), and graphites doped with Si and Ti. The weight loss was measured using a microbalance, the surface morphology by scanning electron microscopy, and the composition of the surface layer by MeV ion beam techniques. Pyrolytic graphite is least affected by erosion, while pure and Si-doped CFCs erode particularly fast. Typical erosion rates for specimens with a surface area of ?4 cm2 are below 0.2 μg/m2 s at 600 K for all graphite types, and at 900 K range from 0.34 mg/m2 s for pyrolytic graphite to about 9 mg/m2 s for the strongest eroding types. The temperature dependence of the erosion rate of all types of graphite studied is well described by an activation energy of 1.7 eV. The erosion rates of these graphites are by far lower than the removal rates for deposited amorphous hydrocarbon layers. In contrast to all other types, the Ti-doped graphite absorbs a significant amount of oxygen reaching up to ?5% of its original mass. Once the oxygen uptake is saturated, it erodes with rates similar to those of the strongest eroding types.  相似文献   
42.
43.
Cubic silicon carbide (3C-SiC) thin films were grown on (100) and (111) Si substrates by CVD technique using hexamethyldisilane (HMDS) as the source material in a resistance heated furnace. HMDS was used as the single source for both Si and C though propane was available for the preliminary carbonization. For selective epitaxial growth, patterned Si (100) substrates were used. The effect of different growth parameters such as substrate orientation, growth temperature, precursor concentration, etc on growth was examined to improve the film quality. The surface morphology, microstructure and crystallinity of grown films were studied using optical microscopy, scanning electron microscopy (SEM), X-ray diffraction (XRD) analysis and X-ray photoelectron spectroscopy (XPS).  相似文献   
44.
Measurement of cell volume in living epithelial cells has become an important technique in studies of membrane transport processes that function in cell volume regulation. Planimetry of video images of optical sections enables the measurement of the cross sectional area of each section. Cell volume is calculated from the measured area of each section and the known focus displacements. In the past the measurement of cross section area has been done by manual positioning of a cursor superimposed on the video image. Each experiment generates approximately 200 images in which two or more cells may be analysed. We have developed a computer-based method that uses one image as a template, and allows automated area determination of successive images by template matching and digital image processing. This new method is comparable to the older method in speed and accuracy, but requires much less effort from the experimenter.  相似文献   
45.
Questions C. G. Watson's (see PA, Vol 52:Issue 3) attempt to explain apparent inconsistencies in findings between his and the present authors' studies in terms of sample differences. Despite Watson's reanalysis of his data by matched pairs, he fails adequately to control for differences in chronicity. (PsycINFO Database Record (c) 2010 APA, all rights reserved)  相似文献   
46.
DNA double-strand breaks (DSBs), classified as the most harmful type of DNA damage based on the complexity of repair, lead to apoptosis or tumorigenesis. In aging, DNA damage increases and DNA repair decreases. This is exacerbated in disease, as post-mortem tissue from patients diagnosed with mild cognitive impairment (MCI) or Alzheimer’s disease (AD) show increased DSBs. A novel role for DSBs in immediate early gene (IEG) expression, learning, and memory has been suggested. Inducing neuronal activity leads to increases in DSBs and upregulation of IEGs, while increasing DSBs and inhibiting DSB repair impairs long-term memory and alters IEG expression. Consistent with this pattern, mice carrying dominant AD mutations have increased baseline DSBs, and impaired DSB repair is observed. These data suggest an adaptive role for DSBs in the central nervous system and dysregulation of DSBs and/or repair might drive age-related cognitive decline (ACD), MCI, and AD. In this review, we discuss the adaptive role of DSBs in hippocampus-dependent learning, memory, and IEG expression. We summarize IEGs, the history of DSBs, and DSBs in synaptic plasticity, aging, and AD. DSBs likely have adaptive functions in the brain, and even subtle alterations in their formation and repair could alter IEGs, learning, and memory.  相似文献   
47.
Due to its essential role in cellular processes, actin is a common target for bacterial toxins. One such toxin, TccC3, is an effector domain of the ABC-toxin produced by entomopathogenic bacteria of Photorhabdus spp. Unlike other actin-targeting toxins, TccC3 uniquely ADP-ribosylates actin at Thr-148, resulting in the formation of actin aggregates and inhibition of phagocytosis. It has been shown that the fully modified F-actin is resistant to depolymerization by cofilin and gelsolin, but their effects on partially modified actin were not explored. We found that only F-actin unprotected by tropomyosin is the physiological TccC3 substrate. Yet, ADP-ribosylated G-actin can be produced upon cofilin-accelerated F-actin depolymerization, which was only mildly inhibited in partially modified actin. The affinity of TccC3-ADP-ribosylated G-actin for profilin and thymosin-β4 was weakened moderately but sufficiently to potentiate spontaneous polymerization in their presence. Interestingly, the Arp2/3-mediated nucleation was also potentiated by T148-ADP-ribosylation. Notably, even partially modified actin showed reduced bundling by plastins and α-actinin. In agreement with the role of these and other tandem calponin-homology domain actin organizers in the assembly of the cortical actin network, TccC3 induced intense membrane blebbing in cultured cells. Overall, our data suggest that TccC3 imposes a complex action on the cytoskeleton by affecting F-actin nucleation, recycling, and interaction with actin-binding proteins involved in the integration of actin filaments with each other and cellular elements.  相似文献   
48.
The endothelium has a fundamental role in the cardiovascular complications of coronavirus disease 2019 (COVID-19). Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) particularly affects endothelial cells. The virus binds to the angiotensin-converting enzyme 2 (ACE-2) receptor (present on type 2 alveolar cells, bronchial epithelial cells, and endothelial cells), and induces a cytokine storm. The cytokines tumor necrosis factor alpha, interleukin-1 beta, and interleukin-6 have particular effects on endothelial cells—leading to endothelial dysfunction, endothelial cell death, changes in tight junctions, and vascular hyperpermeability. Under normal conditions, apoptotic endothelial cells are removed into the bloodstream. During COVID-19, however, endothelial cells are detached more rapidly, and do not regenerate as effectively as usual. The loss of the endothelium on the luminal surface abolishes all of the vascular responses mediated by the endothelium and nitric oxide production in particular, which results in greater contractility. Moreover, circulating endothelial cells infected with SARS-CoV-2 act as vectors for viral dissemination by forming clusters that migrate into the circulation and reach distant organs. The cell clusters and the endothelial dysfunction might contribute to the various thromboembolic pathologies observed in COVID-19 by inducing the formation of intravascular microthrombi, as well as by triggering disseminated intravascular coagulation. Here, we review the contributions of endotheliopathy and endothelial-cell-derived extracellular vesicles to the pathogenesis of COVID-19, and discuss therapeutic strategies that target the endothelium in patients with COVID-19.  相似文献   
49.
Alterations in mitochondrial function are an important control variable in the progression of metabolic dysfunction-associated fatty liver disease (MAFLD), while also noted by increased de novo lipogenesis (DNL) and hepatic insulin resistance. We hypothesized that the organization and function of a mitochondrial electron transport chain (ETC) in this pathologic condition is a consequence of shifted substrate availability. We addressed this question using a transgenic mouse model with increased hepatic insulin resistance and DNL due to constitutively active human SREBP-1c. The abundance of ETC complex subunits and components of key metabolic pathways are regulated in the liver of these animals. Further omics approaches combined with functional assays in isolated liver mitochondria and primary hepatocytes revealed that the SREBP-1c-forced fatty liver induced a substrate limitation for oxidative phosphorylation, inducing enhanced complex II activity. The observed increased expression of mitochondrial genes may have indicated a counteraction. In conclusion, a shift of available substrates directed toward activated DNL results in increased electron flows, mainly through complex II, to compensate for the increased energy demand of the cell. The reorganization of key compounds in energy metabolism observed in the SREBP-1c animal model might explain the initial increase in mitochondrial function observed in the early stages of human MAFLD.  相似文献   
50.
We present the first demonstration of shot-noise limited supercontinuum-based spectral domain optical coherence tomography (SD-OCT) with an axial resolution of ...  相似文献   
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