气体氮化的注意要点

通过理论分析,以及实际生产过程中的经验,总结归纳出气体氮化成功的几大要点,即温度、分解率、炉压、时间.     

不同截面尺寸Cr8Mo2SiV和Cr12Mo1V1钢的组织与性能

对不同截面尺寸Cr8Mo2SiV和Cr12Mo1V1冷作模具钢的组织,共晶碳化物尺寸及不均匀度,冲击性能进行了研究。结果表明,Cr8Mo2SiV钢和Cr12Mo1V1钢退火组织均为球状珠光体上分布着碳化物;随热轧截面尺寸的增大,碳化物尺寸变大,分布均匀性变差。适当减小试验钢的截面尺寸,能够显著减小共晶碳化物的尺寸并改善其分布不均度,提高材料的冲击性能。     

Neurotoxicity of Chronic Co-Exposure of Lead and Ionic Liquid in Common Carp: Synergistic or Antagonistic?

Previous studies have indicated that the harmful heavy metal lead (Pb) contamination in aquatic systems has caused intelligence development disorders and nervous system function abnormalities in juveniles due to the increased permeability of the blood–brain barrier. Ionic liquids (ILs) are considered “green” organic solvents that can replace traditional organic solvents. Studies have found the presence of ILs in soil and water due to chemical applications or unintentional leakage. Therefore, what would happen if Pb interacted with ILs in a body of water? Could ILs enable Pb to more easily cross the blood–brain barrier? Therefore, we examined the combined exposure of Pb and ILs in common carp at low concentration (18.3 mg L⁻¹ of Pb(CH₃COO)₂•3 H₂O and 11 mg L⁻¹ of the IL 1-methyl-3-octylimidazolium chloride, 5% of their LC₅₀) for 28 days in the present study. The result of a neurobehavioral assay showed that chronic exposure of lead at lower concentrations significantly altered fish movement and neurobehaviors, indicating that lead exposure caused neurotoxicity in the carp. Increases in the neurotransmitter dopamine levels and injuries in the fish brain accounted for neurobehavioral abnormalities induced by lead exposure. Moreover, we also found that lead could easily cross the blood–brain barrier and caused significant bioaccumulation in the brain. Particularly, our study indicated that the ionic liquid could not synergistically promote blood–brain barrier permeability and hence failed to increase the absorption of lead in the fish brain, suggesting that the combined exposure of lead and ILs was not a synergistic effect but antagonism to the neurotoxicity. The results of this study suggested that ILs could recede the Pb induced neurotoxicity in fish.     

不同地应力下的地下硐室动态特征分析

采用FLAC3D对地震动荷载作用下不同地应力状态的地下岩体硐室的动态特性进行了初步分析。分析结果表明,地震荷载作用下,硐室位移随地应力侧压系数的增加明显减小,地应力侧压系数λ<1时的硐室位移量值随侧压系数的变化幅度明显大于地应力侧压系数λ>1时的情况;当侧压系数λ<1,随剪切波入射角的变化,硐室测量点位移响应先增加后减小;而当侧压系数λ>1,随剪切波入射角的增加,硐室测点位移先减小后增加,同时随地应力侧压系数的增加有减小的趋势。     

Podocyte-Related Mechanisms Underlying Survival Benefit of Long-Term Angiotensin Receptor Blocker

We previously found that short-term treatment (week 8 to 12 after injury) with high-dose angiotensin receptor blocker (ARB) induced the regression of existing glomerulosclerosis in 5/6 nephrectomy rats. We therefore assessed the effects of long-term intervention with ARB vs. nonspecific antihypertensives in this study. Adult rats underwent 5/6 nephrectomy and renal biopsy 8 weeks later. The rats were then divided into three groups with equivalent renal function and glomerular sclerosis and treated with high-dose losartan (ARB), nonspecific antihypertensive triple-therapy (TRX), or left untreated (Control) until week 30. We found that blood pressure, serum creatinine levels, and glomerulosclerosis were lower at sacrifice in ARB and TRX vs. Control. Only ARB reduced proteinuria and maintained the density of WT-1-positive podocytes. Glomerular tufts showed more double-positive cells for CD44, a marker of activated parietal epithelial cells, and synaptopodin after ARB vs. TRX or Control. ARB treatment reduced aldosterone levels. ARB-treated rats had significantly improved survival when compared with TRX or Control. We conclude that both long-term ARB and triple-therapy ameliorate progression, but do not sustain the regression of glomerulosclerosis. ARB resulted in the superior preservation of podocyte integrity and decreased proteinuria and aldosterone, linked to increased survival in the uremic environment.     

250℃下时间效应对PAN纤维热氧稳定化反应的影响及关联

借用傅里叶变换红外光谱(FT-IR)、元素分析(EA)、X射线衍射(XRD)和示差扫描量热分析(DSC)等手段,对比研究了热氧稳定化过程中250℃下时间效应与两种聚丙烯腈(PAN)共聚纤维及其炭纤维结构和性能之间的关联。研究结果表明,PAN纤维在250℃温区内停留超过9min时,最终热氧稳定化纤维的环化度(RCI)、体密度和芳构化指数(AI)的增加速率开始变小;炭纤维的孔含量(Vp)值与内部微晶的d002值开始增大,微晶排列的规整程度变差,缺陷增多,拉伸强度开始降低。     

Glucose Metabolism,Neural Cell Senescence and Alzheimer’s Disease

Alzheimer’s disease (AD), an elderly neurodegenerative disorder with a high incidence and progressive memory decline, is one of the most expensive, lethal, and burdening diseases. To date, the pathogenesis of AD has not been fully illustrated. Emerging studies have revealed that cellular senescence and abnormal glucose metabolism in the brain are the early hallmarks of AD. Moreover, cellular senescence and glucose metabolism disturbance in the brain of AD patients may precede amyloid-β deposition or Tau protein phosphorylation. Thus, metabolic reprogramming targeting senescent microglia and astrocytes may be a novel strategy for AD intervention and treatment. Here, we recapitulate the relationships between neural cell senescence and abnormal glucose metabolism (e.g., insulin signaling, glucose and lactate metabolism) in AD. We then discuss the potential perspective of metabolic reprogramming towards an AD intervention, providing a theoretical basis for the further exploration of the pathogenesis of and therapeutic approach toward AD.