Heavy metal phosphate nanophases in silica: influence of radiolysis probed via f-electron state properties

We have assessed the feasibility of carrying out time- and wavelength-resolved laser-induced fluorescence measurements of radiation damage in glassy silica. The consequences of alpha decay of Es-253 in LaPO₄ nanophases embedded in silica were probed based on excitation of 5f states of Cm³⁺, Bk³⁺, and Es³⁺ ions. The recorded emission spectra and luminescence decays showed that alpha decay of Es-253 ejected Bk-249 decay daughter ions into the surrounding silica and created radiation damage within the LaPO₄ nanophases. This conclusion is consistent with predictions of an ion transport code commonly used to model ion implantation. Luminescence from the ⁶D_7/2 state of Cm³⁺was used as an internal standard. Ion-ion energy transfer dominated the dynamics of the observed emitting 5f states and strongly influenced the intensity of observed spectra. In appropriate sample materials, laser-induced fluorescence provides a powerful method for fundamental investigation of alpha-induced radiation damage in silica.     

基于微结构损伤的珠光体材料本构行为研究

珠光体材料由许多随机取向的珠光体团组成,每一珠光体团又由铁素体片和渗碳体片交替 叠合而成. 实验表明具有较小片层间距的珠光体材料具有较高的强度和寿命. 通过分析构成 珠光体团的各相及界面的损伤特征,利用损伤耗散功的概念,得到了铁素体、渗碳体与界面 损伤的具有统一形式的演化规律,将其嵌入基于细片层微结构和非经典塑性理论的珠光体团 的弹塑性本构方程,利用Hill自洽方法,得到了珠光体材料的损伤本构描述. 所得到的损 伤本构描述显含表征微结构特征的片层间距,容易证明具有较小片层间距的珠光体材料具有 较好的综合力学性能. 对珠光体材料的拉伸和循环拉压特性进行了分析,得到了与实验一 致的结果.     

Mulberry Ethanol Extract and Rutin Protect Alcohol-Damaged GES-1 Cells by Inhibiting the MAPK Pathway

Mulberry extract has been proven to have the effect of resisting alcohol damage, but its mechanism is still unclear. In this study, the composition of mulberry ethanol extract (MBE) was identified by LC-MS/MS and the main components of MBE were ascertained by measuring. Gastric mucosal epithelial (GES-1) cells were used to elucidate the mechanism of MBE and rutin (the central part of MBE) helped protect against alcohol damage. The results revealed that phenolics accounted for the majority of MBE, accounting for 308.6 mg/g gallic acid equivalents and 108 substances were identified, including 37 flavonoids and 50 non-flavonoids. The treatment of 400 μg/mL MBE and 320 μM rutin reduced early cell apoptosis and the content of intracellular reactive oxygen species, malondialdehyde and increased glutathione. The qPCR results indicated that the MBE inhibits the expression of genes in the mitogen-activated protein kinase (MAPK) pathway, including p38, JNK, ERK and caspase-3; rutin inhibits the expression of p38 and caspase-3. Overall, MBE was able to reduce the oxidative stress of GES-1 cells and regulated apoptosis-related genes of the MAPK pathway. This study provides information for developing anti-ethanol injury drugs or functional foods.     

Phenolic Constituents,Antioxidant and Cytoprotective Activities,Enzyme Inhibition Abilities of Five Fractions from Vaccinium dunalianum Wight

The bud of Vaccinium dunalianum Wight has been traditionally consumed as health herbal tea by “Yi” people in Yunnan Province, China, which was locally named “Que Zui tea”. This paper studied the chemical constituents of five fractions from Vaccinium dunalianum, and their enzyme inhibitory effects of α-glucosidase and pancreatic lipase, antioxidant activity, and cytoprotective effects on H₂O₂-induced oxidative damage in HepG2 cells. The methanol extract of V. dunalianum was successively partitioned with petroleum ether (PF), chloroform (CF), ethyl acetate (EF), n-butanol (BF), and aqueous (WF) to obtain five fractions. The chemical profiling of the five fractions was analyzed by ultra-high-performance liquid chromatography coupled with a tandem mass spectrometry (UHPLC-MS/MS), and 18 compounds were tentatively identified. Compared to PF, CF, BF and WF, the EF revealed the highest total phenols (TPC) and total flavonoids (TFC), and displayed the strongest enzyme inhibition ability (α-glucosidase and pancreatic lipase) and antioxidant capacity (DPPH, ABTS and FRAP). Furthermore, these five fractions, especially EF, could effectively inhibit reactive oxygen species (ROS) production and cell apoptosis on H₂O₂-induced oxidative damage protection in HepG2 cells. This inhibitory effect might be caused by the up-regulation of intracellular antioxidant enzyme activity (CAT, SOD, and GSH). The flavonoids and phenolic acids of V. dunalianum might be the bioactive substances responsible for enzyme inhibitory, antioxidant, and cytoprotective activities.     

PROGRESSIVE DAMAGE ARREST MECHANISM IN TAILORED LAMINATED PLATES WITH A CUTOUT

This study addresses the effectiveness of a simple stiffness tailoring concept to delay damage initiation, control damage progression, and improve residual strength in tensile-loaded composite plates with a central circular cutout. The tailoring concept is to simply reposit all axially oriented （0°） material into regions near the edge of the plate away from the cutout. This tailoring is done in a way so as not to affect the weight of the plate. This accomplishes several beneficial changes in the way that the plate resists loading with no increases in material cost or weight. Lowering the axial stiffness of the laminate surrounding the cutout lowers the stress concentration. Increasing the axial stiffness near edges of the plate attracts loading away from the vicinity of the cutout to further lower stresses in the critical cutout region. This study focuses on in-plane response including damage progression and residual strength as a function of the degree of tailoring and cutout size. Strength and stiffness properties typical of IM7/8551-7 preperg material were assumed and a modified version of the Hashin failure criteria was used to identify the local damage. Results show that tailoring can significantly increase the damage initiation load and the residual strength. In some cases, observed evidence shows that tailoring performs as a damage arrest mechanism.     

复合材料单层板损伤分析

研究了复合材料单层板在远场均匀拉应力作用下，基体中微裂纹损伤，利用Ⅰ、Ⅱ型复合裂纹应力强度因子，分析了沿裂纹面的拉伸型损伤变量和剪切型损伤变量，应用能量释放率的概念建立了损伤条件下的应力应变关系，并给出了正交各向异性单向层板在损伤条件下的有效偏轴柔度系数计算公式。通过算例分析可知，由于复合材料单层板中微裂纹的存在，有效偏轴柔度系数S‘11和S‘61增大，而S‘21减小。     

电场的增强作用对介质膜光栅损伤形貌的影响

研究了电场在介质膜光栅结构中的增强效应对其抗激光损伤阈值的影响.使用傅里叶模式方法计算了电场在介质膜光栅浮雕结构内的分布.数值分析表明：电场在介质膜光栅中增强的最大值为入射光的2倍,其最大的位置出现在相对于入射光对面的光栅槽侧壁。实验测试介质膜光栅样品在1 064 nm和12 ns, 51.2°和TE偏振光入射时,其抗激光损伤阈值为6.61 J/cm2.对损伤形貌进行扫描电镜精确分析,发现介质膜光栅的初始损伤产生于电场在介质膜光栅内增强最大的位置处.     

Antioxidant Activity of Ruthenium Cyclopentadienyl Complexes Bearing Succinimidato and Phthalimidato Ligands

In these studies, we investigated the antioxidant activity of three ruthenium cyclopentadienyl complexes bearing different imidato ligands: (η⁵-cyclopentadienyl)Ru(CO)₂-N-methoxysuccinimidato (1), (η⁵-cyclopentadienyl)Ru(CO)₂-N-ethoxysuccinimidato (2), and (η⁵-cyclopentadienyl)Ru(CO)₂-N-phthalimidato (3). We studied the effects of ruthenium complexes 1–3 at a low concentration of 50 µM on the viability and the cell cycle of peripheral blood mononuclear cells (PBMCs) and HL-60 leukemic cells exposed to oxidative stress induced by hydrogen peroxide (H₂O₂). Moreover, we examined the influence of these complexes on DNA oxidative damage, the level of reactive oxygen species (ROS), and superoxide dismutase (SOD) activity. We have observed that ruthenium complexes 1–3 increase the viability of both normal and cancer cells decreased by H₂O₂ and also alter the HL-60 cell cycle arrested by H₂O₂ in the sub-G1 phase. In addition, we have shown that ruthenium complexes reduce the levels of ROS and oxidative DNA damage in both cell types. They also restore SOD activity reduced by H₂O₂. Our results indicate that ruthenium complexes 1–3 bearing succinimidato and phthalimidato ligands have antioxidant activity without cytotoxic effect at low concentrations. For this reason, the ruthenium complexes studied by us should be considered interesting molecules with clinical potential that require further detailed research.     

Two localized CO2 laser treatment methods for mitigation of UV damage growth in fused silica

Two methods：high-power,short-time,single-shot irradiation（Method A） and low-power,long-time,multi-shot irradiation（Method B） are investigated to mitigate the UV damage growth in fused silica by using a 10.6-μm CO2 laser.To verify the mitigation effect of the two methods,the laser induced damage thresholds（LIDTs） of the mitigated sites are tested with a 355-nm,6.4-ns Nd：YAG laser,and the light modulation of the mitigation sites are tested with a 351-nm continuous Nd：YLF laser.The mitigated damaged sites treated with the two methods have almost the same LIDTs,which can recover to the level of pristine material.Compared with Method A,Method B produces mitigated sites with low crater depth and weak light modulation.In addition,there is no raised rim or re-deposited debris formed around the crater edge for Method B.Theoretical calculation is utilized to evaluate the central temperature of the CO2 laser beam irradiated zone and the radius of the crater.It is indicated that the calculated results are consistent with the experimental results.     

“天光”一号MOPA系统光学元件加工与镀膜的进展

本文阐述了在中国原子能科学研究院“天光一号”ＫｒＦ激光核聚变实验装置上，ＭＯＰＡ系统光学元件加工与镀膜研究工作的进展。实验测量结果表明，加工后的基片表面均方根粗糙度对于Ｋ９光学玻璃与熔融石英玻璃来说分别为σｒｍｓ＝１．８±０．５ｎｍ，σｒｍｓ＝２．０±０．４ｎｍ。镀ＨｆＯ２／ＳｉＯ２高反射膜的光学元件的反射率与破坏阈值分别为Ｒ＞９９．５％，Ｅｔｈ＝１．３０～１．３３Ｊ／ｃｍ２。镀Ａｌ２Ｏ３／ＭｇＦ２增透膜的光学元件的透射率与破坏阈值分别为Ｔ＞９９．５％，Ｅｔｈ＝１．３～１．９７Ｊ／ｃｍ２。