美军炮位侦校雷达新进展

详细介绍美军炮位侦察雷达的改进情况以及新型炮位侦察雷达的研制情况。     

壳寡糖对体外诱导的非酒精性脂肪肝细胞模型的降脂机理研究

为探讨壳寡糖在体外对肝脂质积累的抑制效果及潜在作用机制,选用油酸钠诱导HepG2细胞建立非酒精性脂肪肝细胞模型,通过油红O染色及各试剂盒检测胞内总脂质积累、甘油三酯、总胆固醇、高低密度脂蛋白胆固醇及游离脂肪酸的含量,实时定量PCR及western blot检测细胞内脂代谢相关基因和蛋白的表达。结果发现,4.0mg/mL的壳寡糖对肝脂质蓄积具有明显的抑制作用,并降低了二酰基甘油酰基转移酶2(DGAT2)、肝X受体α(LXRα)、过氧化物酶体增殖物激活受体-γ(PPARγ)、孕烯醇酮X受体(PXR)和分化簇36(CD36)的mRNA水平和蛋白水平的表达。研究结果表明,壳寡糖可以通过调节脂肪酸吸收和甘油三酯合成通路从而降低非酒精性脂肪肝细胞模型中的脂质积累。希望本研究能够为利用壳寡糖开发具有降脂护肝功能的膳食补充剂提供理论参考。     

Empagliflozin Ameliorates Free Fatty Acid Induced-Lipotoxicity in Renal Proximal Tubular Cells via the PPARγ/CD36 Pathway in Obese Mice

High serum levels of free fatty acids (FFAs) could contribute to obesity-induced nephropathy. CD36, a class B scavenger receptor, is a major receptor mediating FFA uptake in renal proximal tubular cells. Empagliflozin, a new anti-diabetic agent, is a specific inhibitor of sodium-glucose co-transporter 2 channels presented on renal proximal tubular cells and inhibits glucose reabsorption. In addition, empagliflozin has shown renoprotective effects. However, the mechanism through which empagliflozin regulates CD36 expression and attenuates FFA-induced lipotoxicity remains unclear. Herein, we aimed to elucidate the crosstalk between empagliflozin and CD36 in FFA-induced renal injury. C57BL/6 mice fed a high-fat diet (HFD) and palmitic acid-treated HK-2 renal tubular cells were used for in vivo and in vitro assessments. Empagliflozin attenuated HFD-induced body weight gain, insulin resistance, and inflammation in mice. In HFD-fed mice, CD36 was upregulated in the tubular area of the kidney, whereas empagliflozin attenuated CD36 expression. Furthermore, empagliflozin downregulated the expression of peroxisome proliferator-activated receptor (PPAR)-γ. Treatment with a PPARγ inhibitor (GW9662) did not further decrease PPARγ expression, whereas a PPARγ antagonist reversed this effect; this suggested that empagliflozin may, at least partly, decrease CD36 by modulating PPARγ. In conclusion, empagliflozin can ameliorate FFA-induced renal tubular injury via the PPARγ/CD36 pathway.     

Synthesis of aromatic poly(ether ketone)s containing C36 aliphatic unsaturated groups in the main chain

Aromatic poly(ether ketone)s (PEKs) were modified with various amount of C36 dimer acid Pripol 1017 obtained from polymerization of unsaturated C18 fatty acids. To obtain modified PEKs, polycondensation was carried out using various dicarboxylic acids with diphenylether at 75°C in phosphorus pentoxide/methanesulfonic acid as condensing agent and solvent. The reduced viscosities of polymers are relatively low, up to 0.13 dL/g. PEK with a structure (molar ratio of aliphatic to aromatic segment: 0.33) is soluble in organic polar solvents and can be cast from a tetrahydrofuran solution with cobalt naphthenate air dryer in order to obtain crosslinked film at room temperature. © 1997 John Wiley & Sons, Inc. J Appl Polym Sci 63: 1275–1278, 1997     

低成本高焊接性能船板钢EH36的开发

工业化试制了3种厚度规格(20,26和36mm)的新型低成本高焊接性能船板钢EH36。试制钢板的显微组织由多边形铁素体和针状铁素体构成,其力学性能满足EH36级别船板要求并具有优异的低温韧性。采用焊接热模拟评价了钢板的焊接性能,当热输入由30kJ/cm升高至160kJ/cm时,粗晶区原奥氏体晶粒尺寸逐渐增大,其组织也逐渐由粒状贝氏体向晶界铁素体+晶内针状铁素体+晶内多边形铁素体转变,维氏硬度逐渐下降,低温韧性优异。得益于TiN粒子对奥氏体晶粒长大的抑制作用,微量B元素对先共析铁素体转变的抑制作用以及BN粒子对晶内铁素体形核的促进作用,焊接粗晶区获得了有利于韧性的细化组织,保证了粗晶区具有优异的低温韧性。双丝埋弧焊试验也验证了钢板具有优异的焊接性能。     

WB36厚壁无缝钢管低倍组织气泡分析及工艺研究

采用扫描电镜、磁粉和超声探伤以及性能测试等方式对WB36厚壁无缝钢管低倍“气泡”形成的原因和实际影响进行了分析研究。结果表明：低倍组织气泡产生的原因主要有脱氧不良、浇注温度高、钢包和耐火材料受潮等,气泡在宏观下呈短线状暗色条纹,微观下为圆形或椭圆形孔洞,主要分布于对应钢锭头部接近冒口端部的钢管近内壁至1/2壁厚处。轻微的气泡采用磁粉、渗透、超声波探伤均无法检出,对钢管的室温力学性能影响较小。WB36钢浇注温度控制在1590℃以下,保证VD精炼67 Pa保持时间不少于15 min、发热剂和保温材料水分含量小于0.1%能够有效防止低倍组织气泡缺陷产生。     

元坝高含硫气井油套环空正常起压规律

对于元坝这种高含硫并于近期大幅度提产的气井来讲,温度效应引起的环空压力也是一类不容忽视的井筒安全威胁。首先结合元坝气井产水并且产气中含非烃成分的实际生产情况,建立了考虑非烃校正的气液两相流井筒温度、压力计算模型和温度效应引起环空压力预测模型,通过实例计算和参数敏感性分析获得了油套环空正常起压规律,并提出了相应的环空压力控制措施。然后通过不同产气量和产水量情形的模拟计算,建立了油套环空起压类型判断图版,并将该图版进行了现场应用,实现了元坝3口重点井的起压类型判断。结果表明：降低环空流体热膨胀系数、提高环空流体等温压缩系数和油套管变形系数都是控制环空压力的有效方法;投产初期预留一定环空气腔高度有利于降低环空压力。     

船用大厚度高强高韧钢焊接工艺研究

为了合理选择船用厚板高强钢焊后热处理的药芯焊丝,针对DH36钢母材特点和工程应用项目的要求,采用DWA-55LSR和GFL-71NiSR两种牌号药芯焊丝对壁厚60 mm的DH36钢板进行了焊后热处理气体保护药芯焊工艺评定,通过外观无损检验、拉伸、弯曲、冲击、硬度和宏观金相检测等试验对焊接接头的力学性能进行了研究。试验结果显示,焊接接头各项性能指标均满足相关标准及项目要求。研究表明,采用适宜的焊接工艺方案,两种牌号焊材焊接接头均具有细小铁素体弥散着的粒状渗碳体和少量珠光体显微组织,均可获得良好的力学性能。     

Caspase-1 Inhibition Impacts the Formation of Chondrogenic Nodules,and the Expression of Markers Related to Osteogenic Differentiation and Lipid Metabolism

Caspase-1, as the main pro-inflammatory cysteine protease, was investigated mostly with respect to inflammation-related processes. Interestingly, caspase-1 was identified as being involved in lipid metabolism, which is extremely important for the proper differentiation of chondrocytes. Based on a screening investigation, general caspase inhibition impacts the expression of Cd36 in chondrocytes, the fatty acid translocase with a significant impact on lipid metabolism. However, the engagement of individual caspases in the effect has not yet been identified. Therefore, the hypothesis that caspase-1 might be a candidate here appears challenging. The primary aim of this study thus was to find out whether the inhibition of caspase-1 activity would affect Cd36 expression in a chondrogenic micromass model. The expression of Pparg, a regulator Cd36, was examined as well. In the caspase-1 inhibited samples, both molecules were significantly downregulated. Notably, in the treated group, the formation of the chondrogenic nodules was apparently disrupted, and the subcellular deposition of lipids and polysaccharides showed an abnormal pattern. To further investigate this observation, the samples were subjected to an osteogenic PCR array containing selected markers related to cartilage/bone cell differentiation. Among affected molecules, Bmp7 and Gdf10 showed a significantly increased expression, while Itgam, Mmp9, Vdr, and Rankl decreased. Notably, Rankl is a key marker in bone remodeling/homeostasis and thus is a target in several treatment strategies, including a variety of fatty acids, and is balanced by its decoy receptor Opg (osteoprotegerin). To evaluate the effect of Cd36 downregulation on Rankl and Opg, Cd36 silencing was performed using micromass cultures. After Cd36 silencing, the expression of Rankl was downregulated and Opg upregulated, which was an inverse effect to caspase-1 inhibition (and Cd36 upregulation). These results demonstrate new functions of caspase-1 in chondrocyte differentiation and lipid metabolism-related pathways. The effect on the Rankl/Opg ratio, critical for bone maintenance and pathology, including osteoarthritis, is particularly important here as well.