Effect of Ammonia-Nitrogen Stress on Non-specific Immunity of Hybrid Tilapia(Oreochromis niloticus× Oreochromis areus)

The juveniles of hybrid tilapia （ Oreochromis niloticus x Oreochromis areus） were exposed to ananonia-nitrogen （N） （0, 2.5, 5, 10 and 20 mg/L） for 0, 12, 24, 48 and 72 h to evaluate the effect of ammonia-N stress on their non-specific immunity. Results show that the activity of serum lysozyme decreased signifi- candy with extension of stress time （P 〈 0.05）. The total antioxidant capacity （T-AOC） and activity of antioxidase in liver were significantly affected. The activi- ty of T-AOC and total superoxide dismutase （T-SOD） of fish exposed to ammonia-N were initially decreasing then increasing （ P 〈 0.05 ）. Activities of catalase （CAT） and glutathione peroxidase （GSH-Px） were correlated with concentrations of ammonia-N. Fish exposed to lower concentrations （2.5 mg/L or 5 mg/L） showed decreased CAT activity within 24 h （P 〈 0.05 ）, while those exposed to higher concentrations （10 mg/L or 20 mg/L） initially showed increased then decreased activity of CAT. Except for the highest concentration groups, fish exposed to ammonia-N showed inductive activity of GSH-Px （ P 〈 0.05 ）. Under the ex- perimental conditions, non-specific immunity of tilapia was affected by ammonia-N stress, and the impact was increased with increased concentration and extension of time.

N-乙酰半胱氨酸对热胁迫香菇菌丝活性氧代谢及糖酵解的影响

为探究外源N-乙酰半胱氨酸(NAC)对热胁迫香菇(Lentinula edodes)菌丝活性氧代谢和糖酵解的影响,本研究以耐热性较弱菌株为供试菌株,设置不同浓度的外源NAC添加至培养基中,于37℃热胁迫处理下筛选出最佳添加浓度。采用此浓度,于37℃下进行热胁迫(胁迫0、6、12、24 h),以及热胁迫后恢复生长(胁迫24 h后于25℃下恢复培养6 h)处理,测定菌丝活性氧代谢和糖酵解相关指标。结果表明,0.1 mmol·L^(-1)为最佳添加浓度。在热胁迫中,与未添加NAC(对照)相比,添加NAC处理超氧阴离子、过氧化氢、蛋白质羰基、硫代巴比妥酸反应物含量的峰值分别显著降低40.94%、41.97%、53.21%、47.62%;超氧化物歧化酶、过氧化氢酶、过氧化物酶、抗坏血酸过氧化物酶、己糖激酶、丙酮酸激酶活性和还原型谷胱甘肽含量的峰值分别显著提高19.21%、43.98%、12.36%、21.95%、25.42%、54.41%、31.93%。同时,在热胁迫恢复生长中,添加NAC处理的菌丝活性氧物质和氧化损伤产物含量仍显著低于对照,而超氧化物歧化酶、过氧化物酶、抗坏血酸过氧化物酶、己糖激酶、丙酮酸激酶活性以及还原型谷胱甘肽含量仍显著高于对照。NAC有效维持了胁迫中菌丝活性氧稳态,使抗氧化酶活性和还原型谷胱甘肽含量保持在较高水平,并减缓氧化损伤程度和进程,加快菌丝糖酵解途径。多因素方差分析表明,NAC主要对还原型谷胱甘肽、硫代巴比妥酸反应物、超氧阴离子含量和己糖激酶、过氧化氢酶、抗坏血酸过氧化物酶活性等指标具有显著效应。本研究结果为外源NAC在热胁迫环境下食用菌中的应用推广提供了新思路。

Clear correspondence between gated-diode R-G current and performance degradation of SOI n-MOSFETs after F-N stress tests

A clear correspondence between the gated-diode generation-recombination （R-G） current and the performance degradation of an SOI n-channel MOS transistor after F-N stress tests has been demonstrated. Due to the increase of interface traps after F-N stress tests, the R-G current of the gated-diode in the SOI-MOSFET architecture increases while the performance characteristics of the MOSFET transistor such as the saturation drain current and sub-threshold slope are degraded. From a series of experimental measurements of the gated-diode and SOI-MOSFET DC characteristics, a linear decrease of the drain saturation current and increase of the threshold voltage as well as a like-line rise of the sub-threshold swing and a corresponding degradation in the trans-conductance are also observed. These results provide theoretical and experimental evidence for us to use the gated-diode tool to monitor SOI-MOSFET degradation.

Antagonistic Effects of N-acetylcysteine on Mitogen-activated Protein Kinase Pathway Activation, Oxidative Stress and Inflammatory Responses in Rats with PM2.5 Induced Lung Injuries

Objective To evaluate the antagonistic effects of N-acetylcysteine(NAC)on mitogen-activated protein kinases(MAPK)pathway activation,oxidative stress and inflammatory responses in rats with lung injury induced by fine particulate matter(PM2.5).Methods Forty eight male Wistar rats were randomly divided into six groups:blank control group(C1),water drip control group(C2),PM2.5 exposed group(P),low-dose NAC treated and PM2.5 exposed group(L),middle-dose NAC treated and PM2.5 exposed group(M),and high-dose NAC treated and PM2.5 exposed group(H).PM2.5 suspension(7.5 mg/kg)was administered tracheally once a week for four times.NAC of 125 mg/kg,250 mg/kg and 500 mg/kg was delivered intragastrically to L,M and H group respectively by gavage(10 ml/kg)for six days before PM2.5 exposure.The histopathological changes and human mucin 5 subtype AC(MUC5AC)content in lung tissue of rats were evaluated.We investigated IL-6 in serum and bronchoalveolar lavage fluid(BALF)by Enzyme-linked immunosorbent assay(ELISA),MUC5AC in lung tissue homogenate by ELISA,glutathione peroxidase(GSH-PX)in serum and BALF by spectrophotometry,and the expression of p-ERK1/2,p-JNK1/2 and p-p38 proteins by Western blot.All the measurements were analyzed and compared statistically.Results Lung tissue of rats exposed to PM2.5 showed histological destruction and increased mucus secretion of bronchial epithelial cells.Rats receiving NAC treatment showed less histological destruction and mucus secretion.Of P,L,M and H group,MUC5AC in lung tissue,IL-6 in serum and BALF were higher than controls(C1 and C2)(all P<0.05),with the highest levels found in the P group and a decreasing trend with increase of NAC dose.The activity of GSH-PX in serum and BALF of PM2.5 exposed rats(P,L,M and H)was lower than that of controls(all P<0.05),with higher activities found in NAC treated rats(L,M,and H),and an increasing trend with increase of NAC dose.The expressions of p-ERK1/2,p-JNK1/2 and p-p38 proteins in PM2.5 exposed lung tissue(P,L,M and H)was higher than controls(all P<0.05),with decreased levels and dose dependent downregulation found in NAC treated rats.Conclusion NAC can antagonize major MAPK pathway activation,lung oxidative stress and inflammatory injury induced by PM2.5 in rats.

基于断裂力学的腐蚀钢丝疲劳S-N曲线研究

高强冷拔钢丝因其优异的力学性能被广泛应用于缆索承重结构,服役过程中钢丝腐蚀与断裂威胁着结构安全。钢丝腐蚀后表面的蚀坑因应力集中效应易产生疲劳裂纹,因此腐蚀钢丝剩余疲劳寿命主要取决于裂纹的扩展阶段,且裂纹扩展受到腐蚀程度(初始损伤)的显著影响。精确表征腐蚀程度并准确评估服役期钢丝腐蚀后的剩余寿命,仍是亟待解决的维修难题。首先采用蚀坑最大深度表征钢丝腐蚀程度,以应力强度因子幅作为裂纹扩展驱动力指标,基于断裂力学的Paris公式建立受拉钢丝裂纹扩展理论模型,进而推导腐蚀钢丝的疲劳S-N曲线。大量既有的腐蚀钢丝疲劳试验结果与理论预测值的比较验证了所提理论模型及疲劳S-N曲线的合理性和有效性。含多个蚀坑的钢丝裂纹扩展有限元模拟表明,等效单裂纹适用于多腐蚀坑钢丝疲劳寿命的简化分析。参数分析表明,蚀坑深度和腐蚀环境是腐蚀钢丝疲劳强度的关键影响因素,而应力比和疲劳加载频率影响较小,所提出的S-N曲线在钢丝常规服役条件下适用于评估其剩余寿命,可得到合理的预测结果。基于断裂力学所提的理论方法和疲劳S-N曲线可为腐蚀钢丝的疲劳强度和寿命评估提供参考。

N-acetylcysteine protects against cadmium-induced germ cell apoptosis by inhibiting endoplasmic reticulum stress in testes

Cadmium （Cd） is a reproductive toxicant that induces germ cell apoptosis in the testes. Previous studies have demonstrated that endoplasmic reticulum （ER） stress is involved in Cd-induced germ cell apoptosis. The aim of the present study was to investigate the effects of N-acetylcysteine （NAC）, an antioxidant, on Cd-induced ER stress and germ cell apoptosis in the testes. Male CD-1 mice were intraperitoneally injected with CdCl2 （2.0 mg kg^-1）. As expected, acute Cd exposure induced germ cell apoptosis in the testes, as determined by terminal dUTP nick-end labelling （TUNEL）. However, the administration of NAC alleviated Cd-induced germ ceil apoptosis in the testes. Further analysis showed that NAC attenuated the Cd-induced upregulation of testicular glucose-regulated protein 78 （GRP78）, an important ER molecular chaperone. Moreover, NAC inhibited the Cd-induced phosphorylation of testicular eukaryotic translation initiation factor 2a （elF2a）, a downstream target of the double-stranded RNA-activated kinase-like ER kinase （PERK） pathway. In addition, NAC blocked the Cd-induced activation of testicular X binding protein （XBP）-1, indicating that NAC attenuates the Cd-induced ER stress and the unfolded protein response （UPR）. Interestingly, NAC almost completely prevented the Cd-induced elevation of C/EBP homologous protein （CHOP） and phosphorylation of c-Jun N-terminal kinase （.INK）, two components of the ER stress-mediated apoptotic pathway. In conclusion, NAC protects against Cd-induced germ cell apoptosis by inhibiting endoplasmic reticulum stress in the testes.

Myocardial reperfusion injury and oxidative stress: Therapeutic opportunities

Acute myocardial infarction(AMI) is the leading cause of death worldwide. Its associated mortality, morbidity and complications have significantly decreased with the development of interventional cardiology and percutaneous coronary angioplasty(PCA) treatment, which quick-ly and effectively restore the blood flow to the area previously subjected to ischemia. Paradoxi-cally, the restoration of blood flow to the ischemic zone leads to a massive production of reactive oxygen species(ROS) which generate rapid and severe damage to biomolecules, generating a phenomenon called myocardial reperfusion injury(MRI). In the clinical setting, MRI is associated with multiple complications such as lethal reperfusion, no-reflow, myocardial stunning, and reperfusion arrhythmias. Despite significant advances in the understanding of the mechanisms accounting for the myocardial ischemia reperfusion injury, it remains an unsolved problem. Although promising results have been obtained in experimental studies(mainly in animal models), these benefits have not been translated into clinical settings. Thus, clinical trials have failed to find benefits from any therapy to prevent MRI. There is major evidence with respect to the contribution of oxidative stress to MRI in cardiovascular diseases. The lack- of consistency between basic studies and clinical trials is not solely based on the diversity inherent in epidemiology but is also a result of the methodological weak-nesses of some studies. It is quite possible that pharmacological issues, such as doses, active ingredients, bioavailability, routes of administration, co-therapies, startup time of the drug intervention,and its continuity may also have some responsibility for the lack- of consistency between different studies. Furthermore, the administration of high ascorbate doses prior to reperfusion appears to be a safe and rational therapy against the development of oxidative damage associated with myocardial reperfusion. In addition, the association with N-acetylcysteine(a glutathione donor) and deferoxamine(an iron chelator) could improve the antioxidant cardioprotection by ascorbate, mak-ing it even more effective in preventing myocardial reperfusion damage associated with PCA following AMI.

Effect of atorvastatin on serum oxidative stress and N-terminal brain natriuretic peptide expression in rats

Objective:To investigate the effect of atorvastatin on serum oxidative stress and N-terminal brain natriuretic peptide expression in rats.Methods:A total of 40 healthy male SD rats were randomly divided into the sham group(Croup A,n=10,saline 5 mL/d),ischemia-reperfusion group(Group B,n=10,saline S mL/d),atorvastatin group(Group C,n=10.atorvastatin 20 mg/kg·d),atorvastatin + N-amino-arginine group(Group D,n=10,atorvastatin 20 mg/kg·d + N-amino arginine 15 mg/kg).Myocardial ischemia-reperfusion rat model was eslablished after 3 days of gavage.N-amino arginine 15 mg/kg was given by tail vein injection 15 min before ischemia.After reperfusion,enzymology indicators such us creatine kinase(CK) and lactate dehydrogenase and the oxidative stress parameters such as nitric oxide(NO),malondialdehyde(MDA) and total superoxide dismutase(TSOD),and n-terminal pro-brain natriuretic peptide(NT-proBNP)expression was detected by immunohistochemistry.Results:LDH and CK levels of group A were significantly lower than the outer three groups,and group B was the highest.There was significant difference between group B and group C(P<0.05),and no significant difference between group B and group D(P>0.05).MDA levels in group B were significantly higher than the other three groups.The lowest was group A,followed by group C,the difference among groups was significantly(P<0.05).TSOD and NO levels in group B was the lowest,the level in group A was the highest,followed by group C,the difference among groups was significant(P<0.05).NT-proBNP level in group B was significantly higher than the other three groups,the lowest was group A,followed by group C,the difference among groups was significant(P<0.05).Conclusions:Atorvastatin has a protective effect on the myocardial injury in the myocardial ischemia and reperfusion rats.It can increase NO synthesis and decrease MDA content,increase serum TSOD activity and the oxidative stress effect,meanwhile protect myocardial cells and reduce myocardial injury.

Induction of Mitochondrial Pathways and Endoplasmic Reticulum Stress for Increasing Apoptosis in Ectopic and Orthotopic Neuroblastoma Xenografts

Cancers are characterized by deregulation of multiple signaling pathways and thus monotherapies are hardly effective. Neuroblastoma, which often occurs in adrenal glands, is the most common childhood malignancy. Malignant neuroblastoma resists traditional treatments and further studies are needed for effective therapeutic interventions. We evaluated synergistic efficacy of N-(4-hydroxyphenyl) retinamide (4-HPR) and genistein (GST) for induction of apoptosis in human malignant neuroblastoma SH-SY5Y and SK-N-BE2 cells in culture and activation of multiple pathways for increasing apoptosis in ectopic and orthotopic neuroblastoma xenografts in nude mice. Combination of 4-HPR and GST synergistically reduced cell viability, caused subG1 accumulation, increased caspase-3 activity for apoptosis in vitro and reduced tumor growth in vivo. Western blotting indicated that combination therapy down regulated Id2 to induce differentiation, increased pro-apoptotic Bax and decreased anti-apoptotic Bcl-2 leading to an increase in Bax:Bcl-2 ratio, increased mitochondrial Bax level, caused mitochondrial release of Smac/Diablo, down regulation of the baculovirus inhibitor-of-apoptosis repeat containing (BIRC) proteins such as BIRC-2 and BIRC-3, and activation of calpain and caspase-3 in SH-SY5Y xenografts. Accumulation of apoptosis-inducing-factor (AIF) in cytosol and increase in caspase-4 activation suggested involvement of mitochondrial pathway and endoplasmic reticulum (ER) stress, respectively, for apoptosis in SH-SY5Y xenografts. In situ immunofluorescent labelings of SH-SY5Y and SK-N-BE2 xenograft sections showed overexpression of calpain, caspase-12, and caspase-3, and AIF, suggesting induction of mitochondrial caspase-dependent and caspase-independent pathways for apoptosis. Collectively, synergistic effects of 4-HPR and GST induced mitochondrial pathways and also ER stress for increasing apoptosis in ectopic and orthotopic neuroblastoma xenografts in nude mice.

Effect of Water Deficit Stress on Isotope ^15N Uptake and Nitrogen Metabolism of Newhall Orange and Yamasitaka Mandarin Seedling

Soil water content significantly influenced uptake and distribution of ^15N in both Newhall and Yamasitaka. The content of ^15N uptake in treated plants was less than that in controlled plants, under 20% soil water content, ^15N was only taken up 16.02% by Newhall and 10.11% by Yamasitaka. The most ^15N was detained in root and old shoots under water stress. Protein concentration in two cultivars significantly decreased by water deficit stress, protein content of Newhall and Yamasitaka in controlled plants was 16.29 mg/g fresh weight and 15.89 mg/g fresh weight, but at 20% of water content, these were 9.60 mg/g fresh weight and 9.02 mg/g fresh weight. Water stress increased concentration of NH3-NH4^＋, Arginine and Proline. Compared with control plants, concentrations of NH3-NH4^＋ in both Newhall and Yamasitaka at 20% water content treatment increased 5.83 fold and 5.71 fold, Arginine increased 197% and 205%, and Proline increased 112% and 132%.

Parametric Equation of Stress Concentration Factor for Circular X-Joints Under Axial Loads

In engineering practice, tubular X-joints have been widely used in offshore structures. The fatigue failure of tubular X-joints in offshore engineering is mainly caused by axial tensile stress. In this study, the stress concentration factor distribution along the weld toe in the hot spot stress region for tubular X-joints subject to axial loads have been analyzed by use of finite element method. Through numerical analysis, it has been found that the peak stress concentration factor is located at the saddle position. Thereafter, 80 models have been analyzed, and the effect of the geometric parameters of a tubular X-joint on the stress concentration factor has been investigated. Based on the experimental values of the numerical stress concentration factor, a parametric equation to calculate the stress concentration factor of tubular X-joints has been proposed. The accuracy of this equation has been verified against the requirement of the Fatigue Guidance Review Panel, and the proposed equation is found capable of producing reasonably accurate stress concentration factor values for tubular X-joints subject to axial loads.

The effect of Nb additive on Te-induced stress corrosion cracking in Ni alloy: a first-principles calculation

Nb can improve the resistance of Ni-based Hastelloy N alloy to Te-induced intergranular embrittlement.First-principles calculations are performed to research this mechanism by simulating the Ni(111) surface and the 5(012) grain boundary. The calculated adsorption energy suggests that Te atoms prefer diffusing along the grain boundary to forming the surface-reaction layer with Nb on surface of the Ni alloy. First-principles tensile tests show that the Nb segregation can enhance the cohesion of grain boundary. The strong Nb-Ni bonding can prevent the Te migration into the inside of the alloy. According to the Rice-Wang model, the strengthening/embrittling energies of Nb and Te are calculated, along with their mechanical and chemical components.The chemical bonds and electronic structures are analyzed to uncover the physical origin of the different effects of Te and Nb. Our work sheds lights on the effect of Nb additive on the Te-induced intergranular embrittlement in Hastelloy N alloy on the atomic and electronic level.

缺口对34CrNi3Mo合金钢的扭转疲劳性能的影响

以船舶主轴为实验对象,研究34CrNi3Mo合金钢作为船舶主轴时法兰与主轴连接处的疲劳寿命.利用实验将法兰与主轴连接处简化成带U型缺口的扭转疲劳试样,基于小样本量中值S-N实验法对应力集中系数为1.45的34CrNi3Mo合金钢在扭转荷载作用下进行疲劳分析,测定其在不同应力幅值下的疲劳寿命并绘制S-N曲线,估算其疲劳极限.将绘制出的S-N曲线与光滑试样的S-N曲线进行对比,结果发现疲劳寿命差别较大.利用ABAQUS软件和Fe-safe软件进行数值模拟,将试验结果与所绘的S-N曲线对比表明,S-N曲线的方程与试验结果很接近,验证了所建立的数值模型的正确性.

Advanced glycation end products induce neural tube defects through elevating oxidative stress in mice

Our previous study showed an association between advanced glycation end products （AGEs） and neural tube defects （NTDs）. To understand the molecular mechanisms underlying the effect of AGEs on neural tube development, C57BL/6 female mice were fed for 4 weeks with com- mercial food containing 3% advanced glycation end product bovine serum albumin （AGE-BSA） or 3% bovine serum albumin （BSA） as a control. After mating mice, oxidative stress markers including malondialdehyde and H202 were measured at embryonic day 7.5 （E7.5） of ges- tation, and the level of intracellular reactive oxygen species （ROS） in embryonic cells was determined at E8.5. In addition to evaluating NTDs, an enzyme-linked immunosorbent assay was used to determine the effect of embryonic protein administration on the N-（carboxymethyl） lysine reactivity of acid and carboxyethyl lysine antibodies at E10.5. The results showed a remarkable increase in the incidence of NTDs at El0.5 in embryos of mice fed with AGE-BSA （no hyperglycemia） compared with control mice. Moreover, embryonic protein administration resulted in a noticeable increase in the reactivity of N-（carboxymethyl） lysine and N（ε）-（carboxyethyl） lysine antibodies. Malondialdehyde and H2O2 levels in embryonic cells were increased at E7.5, followed by increased intracellular ROS levels at E8.5. Vitamin E supplementation could partially recover these phenomena. Collectively, these results suggest that AGE-BSA could induce NTDs in the absence of hyperglycemia by an underlying mechanism that is at least partially associated with its capacity to increase embryonic oxidative stress levels.

Uniaxial stress influence on lattice,band gap and optical properties of n-type ZnO:first-principles calculations

The lattice, the band gap and the optical properties of n-type ZnO under uniaxial stress are investigated by first- principles calculations. The results show that the lattice constants change linearly with stress. Band gaps are broadened linearly as the uniaxial compressive stress increases. The change of band gap for n-type ZnO comes mainly from the contribution of stress in the c-axis direction, and the reason for band gap of n-type ZnO changing with stress is also explained. The calculated results of optical properties reveal that the imaginary part of the dielectric function decreases with the increase of uniaxial compressive stress at low energy. However, when the energy is higher than 4.0 eV, the imaginary part of the dielectric function increases with the increase of stress and a blueshift appears. There are two peaks in the absorption spectrum in an energy range of 4.0-13.0 eV. The stress coefficient of the band gap of n-type ZnO is larger than that of pure ZnO, which supplies the theoretical reference value for the modulation of the band gap of doped ZnO.

Di-(n-butyl)-phthalate-induced Oxidative Stress and Depression-like Behavior in Mice with or without Ovalbumin Immunization

Objective To investigate the relationship between atopic allergy and depression and the role of DBP in the development of depression. Methods BALB/c mice were randomly divided into eight groups：saline;ovalbumin （OVA）-immunized;saline＋DBP （0.45 mg/kg·183;d）; saline＋DBP （45 mg/kg·d）; DBP （0.45 mg/kg·d） OVA-immunized; DBP （45 mg/kg·d） OVA-immunized; saline＋hydrocortisone （30 mg/kg·d）; and hydrocortisone （30 mg/kg·d）-exposed OVA-immunized. Behavior （e.g. open-field, tail suspension, and forced swimming tests）, viscera coefficients （brain and spleen）, oxidative damage [e.g. reactive oxygen species （ROS）, malondialdehyde （MDA）, and glutathione （GSH）], as well as levels of IgE and IL-4, were then analyzed. Results In the saline and OVA groups, the degree of depression symptoms in mice increased with increasing DBP concentration. Additionally, the OVA-immunity groups were associated with more serious depressive behavior compared with the same exposure concentration in the saline group. Oxidative damage was associated with a dose-dependent increase in DBP in the different groups. IL-4 and IgE levels were associated with low-dose DBP stimulation, which changed to high-dose inhibition with increasing DBP exposure, possibly due to spleen injury seen at high DBP concentrations.Conclusion Development of an atopic allergy has the potential to increase the risk of depression in mice, and it seems that DBP helps OVA to exert its effect in our present model. Moreover, the results of our study implicate a certain connection between brain oxidative stress and depression, which deserves a further exploration.

Neuroprotective effects of Activin A on endoplasmic reticulum stress-mediated apoptotic and autophagic PC12 cell death

Activin A, a member of the transforming growth factor-beta superfamily, plays a neuroprotective role in multiple neurological diseases. Endoplasmic reticulum（ER） stress-mediated apoptotic and autophagic cell death is implicated in a wide range of diseases, including cerebral ischemia and neurodegenerative diseases. Thapsigargin was used to induce PC12 cell death, and Activin A was used for intervention. Our results showed that Activin A significantly inhibited morphological changes in thapsigargin-induced apoptotic cells, and the expression of apoptosis-associated proteins [cleaved-caspase-12, C/EBP homologous protein（CHOP） and cleaved-caspase-3] and biomarkers of autophagy（Beclin-1 and light chain 3）, and downregulated the expression of thapsigargin-induced ER stress-associated proteins [inositol requiring enzyme-1（IRE1）, tumor necrosis factor receptor-associated factor 2（TRAF2）, apoptosis signal-regulating kinase 1（ASK1）, c-Jun N-terminal kinase（JNK） and p38]. The inhibition of thapsigargin-induced cell death was concentration-dependent. These findings suggest that administration of Activin A protects PC12 cells against ER stress-mediated apoptotic and autophagic cell death by inhibiting the activation of the IRE1-TRAF2-ASK1-JNK/p38 cascade.

Study on Fatigue Lifetimes and Their Variation of Mg Alloy AZ61 at Various Stress Ratios

In this study, fatigue tests under different R ratios were conducted on the AZ61 Mg alloy to investigate its fatigue lifetimes and fatigue crack growth (FCG) behavior. The fracture surface of the failed specimens was investigated using a scanning electron microscope to study the size of the intermetallic compounds from which the pioneer fatigue crack initiated and led to the final failure of the specimen. To determine the maximum size of the intermetallic compounds existing within the cross section of the specimen at higher risk, Gumbel’s extreme-value statistics were utilized. In the present study, the intermetallic compounds contained within the specimen were assumed to be the initial cracks existing in the material before the fatigue tests. A modified linear elastic fracture-mechanics parameter, M, proposed by McEvily et al., was used to analyze the short FCG behavior under different stress ratios, R. The relation between the rate of FCG and M parameter was found to be useful and appropriate for predicting the fatigue lifetimes under different R ratios. Moreover, the probabilistic stress-fatigue life (P-S-N) curve of the material under different R ratios could be predicted with this method, which utilizes both the FCG law and a statistical distribution of sizes of the most dangerous intermetallic compounds. The evaluated results were in good agreement with the experimental ones. This correspondence indicates that the estimation method proposed in the present study is effective for evaluation of the probabilistic stress-fatigue life (P-S-N) curve of the material under different R ratios.

N-乙酰半胱氨酸在缺血性脑卒中的作用及机制

缺血性脑卒中(CIS)是指因脑部血液循环障碍,缺血、缺氧所致的局限性脑组织的缺血性坏死或软化,其发病率在脑血管病中占据首位。氧气和营养供应的减少会导致神经元的严重丧失,并导致中风患者脑功能的缺陷。开发缺血性脑卒中的治疗方法仍然是临床医学的重要挑战。抗氧化剂N-乙酰半胱氨酸(NAC)是谷胱甘肽前体物质,缺血性脑卒中动物模型及一些临床研究的证据表明,NAC可以有效地保护大脑免受缺血损伤。本文从抗氧化、抑制炎症、保护脑神经和线粒体功能、稳定动脉斑块及溶栓功能等多方面阐述NAC在CIS中的作用机制,旨在从基础层面深入探究NAC与CIS的关系,为NAC进一步应用于缺血性脑卒中患者的防治提供理论依据。

FEM simulation on residual stress distribution during diffusion bonding between Ti （ C, N） metallic ceramic/interlayer/40Cr steel

Based on ANSYS FEM software, the distribution of residual stress in the diffusion bonding joints between Ti（ C,N） metallic ceramic/interlayer/4OCr steel was calculated and experimentally ver^ed. The results showed that the trend on the distribution of residual stress field in the joints was not changed with the use of interlayer. The maximum residual stress was always located in metallic ceramic with area ranging from 1 mm to 4 mm to the interlayer. The maximum residual stress in the joints was also affected by diffusion temperature. The satellite pulse current during the initial stage on diffusion bonding can promote the formation of liquid film at the interface, by which diffusion temperature and loading pressure can be greatly decreased. The crack initiation was easily produced at the corner of Ti （ C, N） metallic ceramic close to the interlayer. If a higher residual stress produced in the joints, the crack was propagated into the whole ceramic.