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91.
We present a view of the neuromechanical regulation of breathing and causes of breathing instability during sleep. First, we would expect transient increases in upper airway resistance to be a major cause of transient hypopnea. This occurs in sleep because a hypotonic upper airway is more susceptible to narrowing and because the immediate excitatory increase in respiratory motor output in response to increased loads is absent in non-REM sleep. Secondly, sleep predisposes to an increased occurrence of ventilatory "overshoots", in part because abruptly changing sleep states cause transient changes in upper airway resistance and in the gain of the respiratory controller. Following these ventilatory overshoots, breathing stability will be maintained if excitatory short-term potentiation is the prevailing influence. On the other hand, apnea and hypopnea will occur if inhibitory mechanisms dominate following the ventilatory overshoot. These inhibitory mechanisms include: a) hypocapnia-if transient, will inhibit carotid chemoreceptors and cause hypopnea, but if prolonged will inhibit medullary chemoreceptors and cause apnea; b) a persistent inhibitory effect from lung stretch; c) baroreceptor stimulation, from a transient rise in systemic blood pressure immediately following termination of apnea or hypopnea may partially suppress the accompanying hyperpnea; d) depression of central respiratory motor output via prolonged brain hypoxia. Once apneas are initiated, reinitiation of inspiration is delayed even though excitatory stimuli have risen well above their apneic thresholds, and these prolonged apneas are commonly accompanied by tonic EMG activation of expiratory muscles of the chest wall and upper airway. 相似文献
92.
In the era of the nanometer CMOS technology, due to stringent system requirements in power, performance and other fundamental physical limitations (such as mechanical reliability, thermal constraints, overall system form factor, etc.), future VLSI systems are relying more on ultra-high data rates (up to 100 Gbps/pin or 20 Tbps aggregate), scalable, re-configurable, highly compact and reliable interconnect fabric. To overcome such challenges, we first explore the use of multiband RF/wireless-interconnects wh... 相似文献
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We have examined the interactions of various peptides with the mouse class II major histocompatibility complex molecule I-Ak. The peptides were derived from the model protein hen egg white lysozyme (HEL). The immunodominant peptide of HEL is a 10-mer, residues 52-61. Our previous work established that this sequence contains the key residues for binding and presentation to T cells. Now we show that the binding of this 10-mer sequence resulted in complexes of I-Ak and peptide that, in SDS/PAGE (without boiling the protein), rapidly dissociated from the component alpha and beta chains. The binding interactions were studied in vitro, by incubating purified I-Ak and radiolabeled peptide, or ex vivo, by using antigen-presenting cells incubated with peptides. Peptides with additional residues at either the amino or carboxyl terminus behaved dramatically differently. Complexes of I-Ak with the longer peptides were stable to SDS/PAGE. Very few amino acid additions result in the change from unstable to stable complexes. The important issue here is that when cultured with HEL, antigen-presenting cells selected the HEL peptides containing the 52-61 sequences that favored stability [Nelson, C. A., Roof, R. W., McCourt, D. W. & Unanue, E. R. (1992) Proc. Natl., Acad. Sci. USA 89, 7380-7383]. Also, from other studies, such sequences correlate with a high immunogenicity of the peptide. We conclude that there are structural features of peptides that change the stability of the class II molecule and that are independent of the "core" peptide seen by the T cells. 相似文献
95.
钨酸催化氧化环己酮合成己二酸 总被引:3,自引:1,他引:3
以钨酸-有机酸性添加剂为催化体系,在无有机溶剂和相转移剂的情况下,催化30%过氧化氢氧化环己酮合成己二酸。当钨酸∶有机酸性添加剂∶环己酮∶过氧化氢=11∶4∶01∶76(摩尔比,钨酸用量为2.5mmol)时,使用有机酸性添加剂来调节钨酸催化活性,结果表明以钨酸-磺酸水杨酸氧化环己酮效果最优,反应8h时己二酸分离产率达86.8%、纯度为99.9%;以间苯二酚或邻苯二酚为添加剂时,己二酸分离产率分别达到85.9%和84.5%,纯度约为100%;而不使用任何添加剂时,己二酸分离产率只有68.1%、纯度为95.2%。当使用磺酸水杨酸、草酸等为有机酸性添加剂时,随反应时间的延长,己二酸分离产率均升高。当磺酸水杨酸用量为2.5mmol时,己二酸分离产率和纯度均较高。钨酸-磺酸水杨酸和钨酸-草酸催化体系重复使用5次后,己二酸分离产率仍分别可达80.2%和80.9%。 相似文献
96.
M Harmsen TA Oosterlaken C Tangerman H Snippe CA Kraaijeveld 《Canadian Metallurgical Quarterly》1993,43(2):137-146
3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (EC 1.1.1.34) is the rate limiting step in the mevalonate pathway that produces isoprenoids and cholesterol. Inhibitors of HMG-CoA reductase are teratogenic in vivo and induce neural tube defects in rat embryo culture, effects which appear unrelated to cholesterol deficiency. This study is the first to localize HMG-CoA reductase mRNA by in situ hybridization (ISH). Expression of reductase mRNA was examined in post-implantation rat embryos, and for control purposes in rat liver and UT-1 cells, using a digoxigenin-11 (dig-11) labelled cRNA probe. Eighteen-day fetal liver showed heavy but patchy hybridization, and adult rat liver showed strong hybridization only on some periportal hepatocytes, which was absent in livers of fasted animals. UT-1 cells stimulated to overexpress HMG-CoA reductase mRNA were strongly positive with the same probe. Control hybridizations with sense strand RNA probe, or with cRNA probe on pre-RNased tissue were negative. Strong hybridization signal for HMG-CoA reductase mRNA was observed in all tissues of the post-implantation rat embryo, from egg cylinder to 30 somite stages (7 to 12 days). Heavy signal was noted in primitive ectoderm and neural tube. The wide embryonic and extraembryonic distribution and abundance of HMG-CoA reductase mRNA may reflect developmental requirements for products of the mevalonate pathway, e.g., isoprenoids for post-translational farnesylation of p21ras. 相似文献
97.
X Meng X Lu Z Li ED Green H Massa BJ Trask CA Morris MT Keating 《Canadian Metallurgical Quarterly》1998,103(5):590-599
Williams syndrome (WS) is a contiguous gene deletion disorder caused by haploinsufficiency of genes at 7q11.23. We have shown that hemizygosity of elastin is responsible for one feature of WS, supravalvular aortic stenosis (SVAS). We have also implicated LIM-kinase 1 hemizygosity as a contributing factor to impaired visual-spatial constructive cognition in WS. However, the common WS deletion region has not been completely characterized, and genes for additional features of WS, including mental retardation, infantile hypercalcemia, and unique personality profile, are yet to be discovered. Here, we present a physical map encompassing 1.5 Mb DNA that is commonly deleted in individuals with WS. Fluorescence in situ hybridization analysis of 200 WS individuals shows that WS individuals have the consistent deletion interval. In addition, we identify three novel genes from the common deletion region: WS-betaTRP, WS-bHLH, and BCL7B. WS-betaTRP has four putative beta-transducin (WD40) repeats, and WS-bHLH is a novel basic helix-loop-helix leucine zipper (bHLHZip) gene. BCL7B belongs to a novel family of highly conserved genes. We describe the expression profile and genomic structure for each of these genes. Hemizygous deletion of one or more of these genes may contribute to developmental defects in WS. 相似文献
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100.
综述了近年来稀土配合物杂化材料的制备和性能.按基质的不同,稀土配合物杂化材料可分为稀土配合物,无机杂化材料,稀土配合物,有机杂化材料以及稀土配合物,混合基质杂化材料。本文对以上3种杂化材料的优缺点进行了较为详细的分析,并提出一步法制备稀土配合物杂化材料,以简化合戍步骤,提高稀土配合物在基质分布的均匀性,因而该方法有望戍为制备稀土配合物杂化材料的一个重要发展方向。 相似文献