Impairment of long-term associative memory in aging snails (Lymnaea stagnalis).

Age-dependent impairment in learning and memory functions occurs in many animal species, including humans. Although cell death contributes to age-related cognitive impairment in pathological forms of aging, learning and memory deficiencies develop with age even without substantial cell death. The molecular and cellular basis of this biological aging process is not well understood but seems to involve a decline in the aging brain's capacity for experience-dependent plasticity. To aid in resolving this issue, we used a simple snail appetitive classical conditioning paradigm in which the underlying molecular, cellular, and neural network functions can be directly linked to age-associated learning and memory performance (i.e., the Lymnaea stagnalis feeding system). Our results indicate that age does not affect the acquisition of appetitive memory but that retention and/or consolidation of long-term memory become progressively impaired with advancing age. The latter phenomenon correlates with declining electrophysiological excitability in key neurons controlling the feeding behavior. Together, these results present the Lymnaea feeding system as a powerful paradigm for investigations of cellular and molecular foundations of biological aging in the brain. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Performance variability is related to change in cognition: Evidence from the Victoria Longitudinal Study.

Performance variability across repeated task administrations may be an important indicator of age-related cognitive functioning. In the present investigation, the authors examined whether age differences and change in inconsistency were related to 6-year (3 occasion) cognitive change. Inconsistency scores were computed from 4 reaction time tasks performed by 446 older adults (54-89 years). Replicating previous cross-sectional results, greater inconsistency was observed for older participants even after controlling for differences in response speed. New longitudinal results demonstrated (a) associations between inconsistency at baseline measurement and 6-year change in cognitive performance; (b) longitudinal change in inconsistency; and (c) intraindividual covariation between 6-year change in inconsistency and 6-year change in level of cognitive function. These findings support the view that performance variability serves as a marker of cognitive aging. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

热老化聚丙烯薄膜宏观力学性能及微观结构的研究

通过对热老化处理的聚内稀薄膜进行X射线衍射实验.对测得的实验数据采用X射线衍射线形分析理论处理,同时对热老化聚丙烯薄膜进行拉仲形变测量,得到材料的力学性质和微晶尺寸及内部点阵畸变的变化规律.从而将热老化聚丙烯材料宏观性质变化与微观结构联系起来,找出材料聚集态精细结构随老化时问而改变的微观规律.     

时效处理对 TiNi 合金相变与性能的影响

通过用ＴＥＭ等方法研究热处理制度（固溶处理、时效处理）对ＴｉＮｉ合金相变组织和性能的影响，找出了最佳热处理制度。结果表明，在４５０～５００℃进行时效处理，Ｔｉ－５０．８ａｔ％Ｎｉ的合金出现了大量的Ｔｉ３Ｎｉ４相，且恢复率最高。     

Influence of water and accelerated aging on the shear fracture properties of glass/epoxy composite

The degradation of interlaminar shear strength and shear fracture toughness of glass/epoxy composites due to uptake of distilled water and sea water has been studied. The composites were immersed in water for up to eight months at temperatures up to 70 °C. Unreinforced matrix resin samples were also immersed for periods up to 2 years. Sea water was absorbed less rapidly than distilled water. Weight gains below 1% did not influence the shear strength while higher weight gains reduced shear strength up to 25%. The loss in apparent interlaminar shear strength was uniquely related to specimen weight gain. Mode II fracture toughness, G _IIc, also decreased with increasing immersion time after an initial incubation period, but the accelerated tests were found to reduce G _IIc less than the room temperature tests at comparable weight gains.     

基于混合电场线性叠加原理的换流变压器内部电场分布规律研究

换流变压器是特高压直流输电系统中的关键设备,其阀侧承受着交直流复合电压。研究热老化对交直流电压在油纸绝缘内分布的影响,可为换流变压器油纸选型提供理论借鉴。选取了换流变压器常用的绝缘油和绝缘纸作为研究对象,并对2种不同油纸组合展开加速热老化试验,测量并分析试验过程中绝缘油和绝缘纸的介电常数和电阻率的变化规律,在此基础上通过油-绝缘纸-油有限元电场仿真模型分析,基于线性叠加原则,得到了交直流电压在热老化过程中的分布变化情况,表明热老化主要影响油纸中直流分量的分布,将显著提高油中的电场强度。     

Conventional and Unconventional Mechanisms by which Exocytosis Proteins Oversee β-cell Function and Protection

Type 2 diabetes (T2D) is one of the prominent causes of morbidity and mortality in the United States and beyond, reaching global pandemic proportions. One hallmark of T2D is dysfunctional glucose-stimulated insulin secretion from the pancreatic β-cell. Insulin is secreted via the recruitment of insulin secretory granules to the plasma membrane, where the soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) and SNARE regulators work together to dock the secretory granules and release insulin into the circulation. SNARE proteins and their regulators include the Syntaxins, SNAPs, Sec1/Munc18, VAMPs, and double C2-domain proteins. Recent studies using genomics, proteomics, and biochemical approaches have linked deficiencies of exocytosis proteins with the onset and progression of T2D. Promising results are also emerging wherein restoration or enhancement of certain exocytosis proteins to β-cells improves whole-body glucose homeostasis, enhances β-cell function, and surprisingly, protection of β-cell mass. Intriguingly, overexpression and knockout studies have revealed novel functions of certain exocytosis proteins, like Syntaxin 4, suggesting that exocytosis proteins can impact a variety of pathways, including inflammatory signaling and aging. In this review, we present the conventional and unconventional functions of β-cell exocytosis proteins in normal physiology and T2D and describe how these insights might improve clinical care for T2D.     

Increased Histone Acetylation and Decreased Expression of Specific Histone Deacetylases in Ultraviolet-Irradiated and Intrinsically Aged Human Skin In Vivo

Histone deacetylases (HDACs) are conserved enzymes that remove acetyl groups from lysine side chains in histones and other proteins and play a crucial role in epigenetic regulation. Previously, we showed that histone acetylation is implicated in ultraviolet (UV)-induced inflammation and matrix impairment. To elucidate the histone acetylation status and specific HDACs involved in skin aging, we examined the changes in histone acetylation, global HDAC activity, and the expression of HDACs and sirtuins (SIRTs) in intrinsically aged and photoaged human skin as well as in UV-irradiated human skin in vivo. Following acute UV irradiation, the acetylated histone H3 (AcH3) level was increased, but HDAC activity and the expression levels of HDAC4, HDAC11, and SIRT4 were significantly decreased. In intrinsically aged skin, AcH3 levels were increased, but HDAC activity and the expression levels of HDAC4, HDAC5, HDAC10, HDAC11, SIRT6, and SIRT7 were significantly decreased. However, histone acetylation and HDAC expression in photoaged skin were not significantly different from those in intrinsically aged skin. Collectively, HDAC4 and HDAC11 were decreased in both UV-irradiated and intrinsically aged skin, suggesting that they may play a universal role in increased histone acetylation associated with skin aging.     

Utilizing an Animal Model to Identify Brain Neurodegeneration-Related Biomarkers in Aging

Glycine N-methyltransferase (GNMT) regulates S-adenosylmethionine (SAMe), a methyl donor in methylation. Over-expressed SAMe may cause neurogenic capacity reduction and memory impairment. GNMT knockout mice (GNMT-KO) was applied as an experimental model to evaluate its effect on neurons. In this study, proteins from brain tissues were studied using proteomic approaches, Haemotoxylin and Eosin staining, immunohistochemistry, Western blotting, and ingenuity pathway analysis. The expression of Receptor-interacting protein 1(RIPK1) and Caspase 3 were up-regulated and activity-dependent neuroprotective protein (ADNP) was down-regulated in GNMT-KO mice regardless of the age. Besides, proteins related to neuropathology, such as excitatory amino acid transporter 2, calcium/calmodulin-dependent protein kinase type II subunit alpha, and Cu-Zn superoxide dismutase were found only in the group of aged wild-type mice; 4-aminobutyrate amino transferase, limbic system-associated membrane protein, sodium- and chloride-dependent GABA transporter 3 and ProSAAS were found only in the group of young GNMT-KO mice and are related to function of neurons; serum albumin and Rho GDP dissociation inhibitor 1 were found only in the group of aged GNMT-KO mice and are connected to neurodegenerative disorders. With proteomic analyses, a pathway involving Gonadotropin-releasing hormone (GnRH) signal was found to be associated with aging. The GnRH pathway could provide additional information on the mechanism of aging and non-aging related neurodegeneration, and these protein markers may be served in developing future therapeutic treatments to ameliorate aging and prevent diseases.