新一代载人飞船卫生区功能性空间优化设计研究

目的 开展中国新一代载人飞船卫生区的空间优化研究,探索功能性空间优化设计方法,提高载人飞船空间利用效率,同时提升航天员的舒适性体验。方法 以中国空间站卫生区的功能和结构为依据,探讨中国新一代载人飞船卫生区功能组件的构成;依据航天员在微重力状态下使用卫生区的动作与姿态,建立卫生区空间布置的初步概念;根据卫生区的舱壁布局、微重力下航天员视野区域及最佳操作空间分析,开展相关功能组件建模,基于卫生区的人机交互节点,利用JACK软件进行仿真分析与评估,结合评估结果改进设计方案,并通过追踪航天员活动轨迹产生的包络体完成卫生区的空间优化。结论 通过对比中国新一代载人飞船卫生区优化前后设计方案的舒适性、可操作性和空间尺寸,验证了功能性空间优化设计方法的有效性和可靠性,为载人航天器舒适性与集成化设计提供了参考。     

Extension of the applicable range of the implicit curve-fitting method for refrigerant thermodynamic properties to critical pressure

The method of implicit curve-fitting and explicit-calculation has been used for fast and stable calculations of thermodynamic properties of subcritical refrigerants. In order to extend that method to the critical pressure, a method of sectional implicit curve-fitting and explicit-calculation for refrigerant thermodynamic properties is introduced in this paper. The whole data range is divided into several subsections. The requirements on the continuity of thermodynamic properties and the first order derivative of thermodynamic properties in the intersection points of subsections are indicated, and the methods to meet the requirements are presented. Quadric equations are constructed instead of curve-fitting when no data can be given. With the source data obtained from REFPROP 7.1, explicit fast calculation formulae for thermodynamic properties of R410A, covering the saturated temperature of 213.15–344.51 K and superheat of 0–65 K, are given as an example. The calculation speeds of the formulae of R410A are more than 7000 times faster than those of REFPROP 7.1 while the total mean relative deviation of the fast calculation formulae from REFPROP 7.1 is only 0.04%.     

组成、粘度比及加工条件对PB／CS共混物粘度和形态的影响

研究了组成、粘度比、转速和混合时间对聚丁烯／玉米浆共混物的粘度和形态的影响。结果表明，共混物的粘度均随转速的提高而增大。在高转速下，８０／２０共混物的粘度比其它组成的共混物的粘度增长迅速。在聚丁烯和玉米浆的界面观察到复合乳化结构。分散相液滴尺寸较小时，液滴尺寸的变化对共混物的粘度有很大的影响。     

对一个群签名方案的分析与改进

分析了一个基于中国剩余定理的群签名方案,指出此方案并不安全：任何一个群成员或已被撤销的群成员都可以完全攻破此方案。针对该安全缺陷提出了一个改进的新方案。分析表明,该方案不仅可以在不改变其他群成员密钥的情况下有效地增加和撤销群成员,而且具有不可伪造性、防陷害攻击、抗联合攻击等性质。     

Reduced VDAC1, Maintained Mitochondrial Dynamics and Enhanced Mitochondrial Biogenesis in a Transgenic Tau Mouse Model of Alzheimer’s Disease

Alzheimer’s disease (AD) is one of the most common forms of neurodegeneration, defined by reduced cognitive function, which is caused by the gradual death of neurons in the brain. Recent studies have shown an age-dependent rise in the levels of voltage-dependent anion channel 1 (VDAC1) in AD. In addition, we discovered an aberrant interaction between VDAC1 and P-TAU in the brains of AD patients, which led to abnormalities in the structural and functional integrity of the mitochondria. The purpose of our study is to understand the protective effects of reduced VDAC1 against impaired mitochondrial dynamics and defective mitochondrial biogenesis in transgenic TAU mice. Recently, we crossed heterozygote VDAC1 knockout (VDAC1^+/−) mice with transgenic TAU mice to obtain double-mutant VDAC1^+/−/TAU mice. Our goal was to evaluate whether a partial decrease in VDAC1 lessens the amount of mitochondrial toxicity in transgenic Tau (P301L) mice. We found that mitochondrial fission proteins were significantly reduced, and mitochondrial fusion and biogenesis proteins were increased in double-mutant mice compared to TAU mice. On the basis of these discoveries, the current work may have significance for the development of reduced-VDAC1-based treatments for individuals suffering from AD as well as other tauopathies.     

Neuronal ApoE Regulates the Cell-to-Cell Transmission of α-Synuclein

The presence of protein inclusions, called Lewy bodies (LBs) and Lewy neurites (LNs), in the brain is the main feature of Parkinson’s disease (PD). Recent evidence that the prion-like propagation of α-synuclein (α-syn), as a major component of LBs and LNs, plays an important role in the progression of PD has gained much attention, although the molecular mechanism remains unclear. In this study, we evaluated whether neuronal ApoE regulates the cell-to-cell transmission of α-syn and explored its molecular mechanism using in vitro and in vivo model systems. We demonstrate that neuronal ApoE deficiency attenuates both α-syn uptake and release by downregulating LRP-1 and LDLR expression and enhancing chaperone-mediated autophagy activity, respectively, thereby contributing to α-syn propagation. In addition, we observed that α-syn propagation was attenuated in ApoE knockout mice injected with pre-formed mouse α-syn fibrils. This study will help our understanding of the molecular mechanisms underlying α-syn propagation.     

Crohn’s Disease,Host–Microbiota Interactions,and Immunonutrition: Dietary Strategies Targeting Gut Microbiome as Novel Therapeutic Approaches

Crohn’s disease (CD) is a complex, disabling, idiopathic, progressive, and destructive disorder with an unknown etiology. The pathogenesis of CD is multifactorial and involves the interplay between host genetics, and environmental factors, resulting in an aberrant immune response leading to intestinal inflammation. Due to the high morbidity and long-term management of CD, the development of non-pharmacological approaches to mitigate the severity of CD has recently attracted great attention. The gut microbiota has been recognized as an important player in the development of CD, and general alterations in the gut microbiome have been established in these patients. Thus, the gut microbiome has emerged as a pre-eminent target for potential new treatments in CD. Epidemiological and interventional studies have demonstrated that diet could impact the gut microbiome in terms of composition and functionality. However, how specific dietary strategies could modulate the gut microbiota composition and how this would impact host–microbe interactions in CD are still unclear. In this review, we discuss the most recent knowledge on host–microbe interactions and their involvement in CD pathogenesis and severity, and we highlight the most up-to-date information on gut microbiota modulation through nutritional strategies, focusing on the role of the microbiota in gut inflammation and immunity.     

综合体内儿童活动场所执行消防规范的问题探讨

近年来,我国城市商业综合体的总数和规模出现了前所未有的增长,各种儿童活动场所在商业综合体内遍地开花,不少商业综合体甚至主打儿童品牌,成为满足儿童游乐、教育、摄影、零售、美食等多种需求的一站式基地。但此类场所的快速发展也带来了极大的火灾风险,相对消防法规和技术标准也出现了一些不适应、难执行的情况。文章对在商业综合体内设置的儿童活动场所执行现行消防法规和技术标准存在的问题及相应的解决措施进行分析,希望可以起到借鉴作用。     

Evidence for Oxidative Pathways in the Pathogenesis of PD: Are Antioxidants Candidate Drugs to Ameliorate Disease Progression?

Parkinson’s disease (PD) is a progressive neurodegenerative disorder that arises due to a complex and variable interplay between elements including age, genetic, and environmental risk factors that manifest as the loss of dopaminergic neurons. Contemporary treatments for PD do not prevent or reverse the extent of neurodegeneration that is characteristic of this disorder and accordingly, there is a strong need to develop new approaches which address the underlying disease process and provide benefit to patients with this debilitating disorder. Mitochondrial dysfunction, oxidative damage, and inflammation have been implicated as pathophysiological mechanisms underlying the selective loss of dopaminergic neurons seen in PD. However, results of studies aiming to inhibit these pathways have shown variable success, and outcomes from large-scale clinical trials are not available or report varying success for the interventions studied. Overall, the available data suggest that further development and testing of novel therapies are required to identify new potential therapies for combating PD. Herein, this review reports on the most recent development of antioxidant and anti-inflammatory approaches that have shown positive benefit in cell and animal models of disease with a focus on supplementation with natural product therapies and selected synthetic drugs.     

I2-Imidazoline Ligand CR4056 Improves Memory,Increases ApoE Expression and Reduces BBB Leakage in 5xFAD Mice

Recent evidence suggests that I2-imidazoline ligands have neuroprotective properties in animal models of neurodegeneration, such as Alzheimer’s disease (AD). We recently demonstrated that the I2-ligand BU224 reversed memory impairments in AD transgenic mice and this effect was not because of reductions in amyloid-β (Aβ) deposition. In this study, our aim was to determine the therapeutic potential of the powerful analgesic I2-imidazoline ligand CR4056 in the 5xFAD model of AD, since this ligand has been proven to be safely tolerated in humans. Sub-chronic oral administration of CR4056 (30 mg/kg for 10 days) led to an improvement in recognition memory in 6-month-old 5xFAD mice, but not in wild-type littermates, without affecting Aβ levels or deposition. Our results also revealed a change in the profile of microglia by CR4056, resulting in a suppression of pro-inflammatory activated microglia, but increased the density of astrocytes and the expression of ApoE, which is mainly produced by these glial cells. In addition, CR4056 restored fibrinogen extravasation, affecting the distribution of markers of astrocytic end feet in blood vessels. Therefore, these results suggest that CR4056 protects against Aβ-mediated neuroinflammation and vascular damage, and offers therapeutic potential at any stage of AD.