正丁基锂/2,5,8-三氧壬烷引发的α-甲基苯乙烯阴离子平衡聚合动力学及反应机理研究

以n-BuLi为引发剂,2,5,8·三氧壬烷(2G)为极性添加剂,环己烷为溶剂,在20℃进行α-甲基苯乙烯的阴离子平衡聚合反应。测定了聚合、解聚速率常数随2G浓度变化规律,讨论了不同[2G]/[BuLi]下的反应活性种及聚合、解聚反应动力学。当[2G]/[BuLi]<0.683时,聚合反应速度和单体浓度在引发阶段为二级反应;在增长阶段为一级反应;在[2G]/[BuLi]<0.683的整个聚合反应期间为一级发应。因而得到了[2G]/[BuLi]不同比值范围内的平衡单体浓度、添加剂浓度、聚合、解聚速率常数之间的关联式。当[2G]/[BuLi]<50时,提出了自由离子存在下的平衡聚合反应机理。     

端环氧基聚苯乙烯低聚的物合成与表征

采用阴离子聚合法,以正丁基锂(n-BuLi)为引发剂、乙二醇二缩水甘油醚(EGDE)为封端剂,在常压惰性气体保护下引发苯乙烯(St)聚合,制得端环氧基聚苯乙烯低聚物(PS-ep)。采用GPCI、R和1H-NMR对PS-ep进行表征,并用盐酸-二氧六环银量法测定端环氧基含量。结果表明:以EGDE为封端剂可以使端环氧基摩尔分数(xep)达到0.80左右;升高封端反应温度和延长封端反应时间有利于提高端环氧基的摩尔分数;EGDE与n-BuLi的摩尔比以4∶1为宜。     

新型引发剂引发苯乙烯聚合的动力学

采用过氧化2-乙基己基碳酸叔丁酯为引发剂,研究了苯乙烯自由基本体聚合的动力学过程,考察了引发剂浓度、温度、乙苯质量分数对聚合反应速率和聚苯乙烯分子量的影响。结果表明：在117 °C下,聚合速率（Rp)对引发剂浓度的反应级数为0.42,对苯乙烯浓度的反应级数为1,聚合反应的表观活化能为54.8 kJ/mol。引发剂浓度、温度、乙苯质量分数的提高导致聚苯乙烯数均分子量分别下降了约30%、20%和15%,其中引发剂浓度的影响最为显著。     

α-甲基苯乙烯阴离子平衡聚合动力学及反应历程研究

本文研究了以环已烷作稀释剂,n-BuLi引发α-甲基苯乙烯阴离子平衡聚合动力学和反应历程,获得了单量体和缔合体引发α-甲基苯乙烯聚合的增长反应速度常数和解聚反应速度常数及相应的活化能。     

红外光谱法研究苯乙烯原子转移自由基聚合反应动力学

利用红外光谱法测定反应转化率研究原子转移自由基聚合反应动力学。在环己酮溶液中,以卤代烃为引发剂,过渡金属卤化物与配位剂２,２‘－联吡啶为催化体系,进行了苯乙烯聚合。分别就反应温度,反应物浓度和引发体系对苯乙烯聚合速率的影响进行了动力学测定,证实了原子转移自由基聚合具有活性聚合的特征,同时计算并讨论了苯乙烯原子转移自由基聚合反应的动力学数据。     

PAN-b-PHEA的合成与表征

首先以丙烯腈（AN）为单体、2-溴异丁酸乙酯 (EBiB) 为引发剂、溴化亚铜（CuBr）以及1,10-菲罗啉为催化体系,经原子转移自由基聚合（ATRP）反应合成聚丙烯腈（PAN）,利用质量法测定了引发剂和催化剂用量对AN转换率的影响;然后以2-羟乙基丙烯酸乙酯（HEA）为单体、PAN-Br为大分子引发剂、CuBr和N,N,N′,N″,N″-五甲基二乙烯三胺（PMDETA）为催化体系,合成了PAN-b-PHEA嵌段共聚物。采用红外光谱（FT-IR）、核磁共振谱（1H-NMR）、元素分析对聚合物的结构进行了表征,并经热重分析考察了PAN-b-PHEA嵌段共聚物的热分解行为。结果表明,当n（AN）/n（EBiB）=100以及n（CuBr）/n（AN）=1%时,AN的ATRP聚合反应呈现一级动力学特征（ln(c0/ct)与时间t的线性相关系数为0.988）。PAN-b-PHEA嵌段共聚物的热分解温度为250 °C。     

分散聚合法制备甲基丙烯酸甲酯-苯乙烯共聚物微球

以聚乙烯吡咯烷酮(PVP)为分散剂，以偶氮二异丁腈(AIBN)为引发剂，在甲醇／水混合溶剂中，采用分散聚合法制备出微米级的甲基丙烯酸甲酯一苯乙烯共聚物微球，研究了分散介质组成、单体组成、引发剂浓度、分散剂浓度、反应温度等反应条件对聚合产物粒径及粒径分布的影响。     

DPE对正丁基锂及聚苯乙烯活性种缔合体的影响

以具有较大空间位阻的1,1-二苯基乙烯（DPE）作为盖帽剂,使用核磁锂谱研究了正丁基锂（n-BuLi）经其盖帽以后缔合态的变化。结果表明:DPE的加入使n- BuLi中的超大缔合体解缔合成六元缔合体,但是不会影响原有的六元缔合体。由1,1-二苯基己基锂引发的苯乙烯本体聚合实验中存在转化率突变点。在突变点前的聚合产物中存在超分子结构,并随着聚合反应的进行逐渐解缔合;突变点过后超分子结构解缔合完全,反应加速进行。     

分散聚合法制备聚丙烯酰胺水包水乳液

采用甲醇一水为分散介质，聚乙烯吡咯烷酮(PVP)为稳定剂，过硫酸钾(KPS)为引发剂，用分散聚合的方法制备了聚丙烯酰胺水包水乳液。研究了醇／水比、稳定剂的种类和用量对聚丙烯酰胺水包水乳液稳定性的影响及单体浓度、引发剂用量和聚合温度对分散聚合法制备聚丙烯酰胺反应速率及分子量的影响。     

苯乙烯阴离子高温本体聚合引发机理的新发现（二）

采用创建的一种研究方法,以正丁基锂（n-BuLi）为引发剂,研究了苯乙烯 (St) 在60 °C至140 °C下的阴离子本体聚合。结果表明,低温下 (<20 °C) 以六元缔合结构形式存在的非活性正丁基锂在高温下 (≥60 °C) 会转化为活性种。随机分布在该六元结构上的平均1.3个离子对可以引发St的阴离子聚合。然而从六元缔合结构上增长出的超分子聚合物线团又将阻碍单体继续扩散进入离子对参与聚合,从而产生一个持续时间较长的聚合转化率停滞平台 (SCP) 。由于时温等效作用,提高聚合温度可以显著地缩短SCP     

A case of PAN with positive Hbs Ag cured by immunosuppressive and antiviral therapies: a case report

Polyarteritis nodosa (PAN) first described by Kussmaul and Maier in 1866, is a multisystem necrotizing vasculitis of small and middle-sized muscular arteries. The presence of hepatitis B antigenemia (Hbs Ag) in approximately 30% of patients with PAN as well as immune complexes of Hbs Ag-Immunoglobulins and complement in the blood vessel walls strongly suggest the role of immunologic phenomena. The extremely poor prognosis of classic PAN has been modified by corticosteroid treatment with boluses of cyclophosphamide, and plasmapheresis. We report a case of PAN with renal, cardiac, central and peripheral nervous system involvement associated with active hepatitis B that got a total remission with corticosteroids, lamivudine and boluses of cyclophosphamide without plasmapheresis.     

纳米二氧化硅填充催化与分离双功能复合膜的性能

以聚丙烯腈（PAN）中空纤维膜为支撑底膜,聚乙烯醇（PVA）为渗透汽化(PV)层,全氟磺酸树脂（PFSA）为催化层,催化层中填充纳米二氧化硅,制备了催化与分离双功能中空纤维复合膜。考察了该双功能膜的一系列表面性能：亲水性、对乙酸乙酯塔顶粗酯的分离性能、力学性能以及对乙酸乙醇酯化反应的催化性能。实验结果表明：催化与分离双功能膜具有良好的力学性能和亲水性,其渗透通量可达175 g/(m2·h),相对应的分离选择性为144;相比于空白实验,双功能膜可明显提高乙酸乙醇酯化反应的转化率,缩短达到平衡转化率的时间,其平衡转化率达60%。     

多次交替浸渍法构筑簇状ZnO的PAN复合纳米纤维膜及其光催化性能

以聚丙烯腈（PAN）与氯化锌（ZnCl₂）作为前驱物,采用静电纺丝工艺制备PAN/ZnCl₂复合纳米纤维膜,分别采用多次冷热交替浸渍法和单次冷热静置浸渍法得到簇状PAN/ZnO-1和PAN/ZnO-2复合纳米纤维膜。利用扫描电镜（SEM）、傅里叶红外光谱（FT-IR）、X射线衍射（XRD）、X射线能量色散光谱（XPS）和热重分析仪（TG）对复合纳米纤维膜的表面形貌和微结构进行了表征,并以亚甲基蓝（MB）为污染物模型,评价其光催化降解性能。结果表明：经冷热交替浸渍后,纳米ZnO粒子均匀地附着在PAN纤维表面,尤其在PAN/ZnO-1复合纳米纤维膜表面还出现了花状ZnO粒子;相比单次冷热静置浸渍法处理的PAN/ZnO-2复合纳米纤维膜,经多次冷热交替浸渍的PAN/ZnO-1复合纳米纤维膜循环使用3次后对MB的降解率仍可达到90%以上,具有更好的光催化活性和循环使用性能。同时,MB溶液的初始质量浓度、催化剂用量和染料溶液的pH等因素对样品的的光催化降解率有一定影响。     

衰老,损伤与生命维护的博弈

衰老已不再是生物学的不解之谜,是种种生化副反应损伤与生物体维护之间的博弈的最终结果.尽管生物进化建立的遗传系统竭尽全力试图把生物体维持在理想状态,然而能量代谢过程仍然会引起氧应激与糖应激相关的生理性和病理性的机体损变.解密衰老之后,关于健康长寿的研究将进入全新的历史时期.     

Athletic performance and urban air pollution.

Air pollution may affect athletic performance. In Los Angeles, contaminants include carbon monoxide, ozone, peroxyacetylnitrate (PAN) and nitrogen oxides, whereas in older European cities, such as Sarajevo, "reducing smog" of sulfur dioxide is the main hazard. The carbon monoxide and ozone levels expected in Los Angeles this summer could affect the athletes' performance in endurance events at the Olympic Games. Carbon monoxide may also impair psychomotor abilities, and PAN causes visual disturbances. The only likely physiologic consequence from reducing smog is an increase in the workload of the respiratory system and thus a decrease in endurance performance. While carbon monoxide has been blamed for myocardial infarctions, nitrogen oxides for pulmonary edema and sulfur dioxide for deaths due to respiratory failure, the only illnesses that are likely to be more frequent than usual among young athletes exposed to high levels of these pollutants are upper respiratory tract infections. Therapeutic tactics include the avoidance of pollution, the administration of oxygen, vitamin C and vitamin E, and general reassurance.     

Effect of down-regulation of TRPC6 on the puromycin aminonucleoside-induced apoptosis of mouse podocytes

Eukaryotic expression vectors carrying the small hairpin RNA （shRNA） for TRPC6 mRNA were constructed, and the effects of knocking-down TRPC6 on puromycin aminonucleoside （PAN）-induced apoptosis of mouse podocytes were observed. Two eukaryotic expression vectors containing small hairpin structure targeting TRPC6 named pGCsi-TRPC6A and pGCsi-TRPC6B were designed and synthesized. The plasmids were transfected into conditionally immortalized murine podocyte cell line by liposome. The changes in the TRPC6 mRNA and protein expression were observed by RT-PCR and Western blot after 48 h. Cultured podocytes were divided into four groups： control group, PAN treatment group, PAN treatment＋shRNA transfection group, and PAN treatment＋negative control group. The expression of Bax and Bcl-2 mRNA and proteins was detected by RT-PCR and Western-blot respectively. The apoptotic rate of podocytes was measured by flow cytometry. The results showed that the expression of TRPC6 mRNA and protein was decreased in the podocytes when transfected with pGCsi-TRPC6A, and pGCsi-TRPC6B. The expression of Bax was increased, and that of Bcl-2 was decreased at protein and mRNA levels in the podocytes after treated with PAN for 48 h. These changes was attenuated by knocking-down TRPC6. Knocking-down TRPC6 could effectively decrease the PAN-induced apoptosis of podocytes. It was concluded that TRPC6 may play an important role in the PAN-induced apoptosis of podocytes. Knocking-down TRPC6 gene could effectively prevent the podocytes from apoptosis induced by PAN.     

缬沙坦对实验性肾病肾组织内皮素及其受体基因表达的影响

目的 观察血管紧张素受体拮抗剂缬沙坦(valsartan)对阿霉素肾病大鼠血浆及肾组织内皮素含量以及肾组织内皮素受体基因表达的影响。方法 SD大鼠经阿霉素诱导建立肾病综合征模型，设肾病模型组、valsartan治疗组、苯那普利(benazepril)治疗组及正常对照组。28天后比较各组大鼠间血浆及肾组织内皮素含量；应用RT-PCR技术检测大鼠肾组织内皮素-1(ET-1)及其A、B两型受体基因表达情况。结果 肾病综合征大鼠ET-1水平明显增加，肾脏内皮素A型受体表达显著增多；valsartan及benazepril治疗可使ET-A型受体表达明显下降，4组ET-B型受体mRNA表达无显著差异。结论 在肾病综合征状态下内皮素系统活性明显增强，血管紧张素受体拮抗剂valsaxtan可下调ET-A型受体mRNA表达，减轻ET-1在肾病综合征发生、发展中的作用。     

Effect of TRPC6 knockdown on puromycin aminonucleoside-induced podocyte injury

This study was aimed to construct eukaryotic expression vectors carrying the small hairpin RNA (shRNA) targeting TRPC6 gene and investigate the effect of TRPC6 knockdown on puromucin aminonucleoside (PAN)-induced podocyte injury. Two DNA sequences containing the small hairpin structure targeting TRPC6 were designed, synthesized and then inserted into the green fluorescence protein (GFP)-contained plasmids (pGC) to establish the plasmids pGCsi-TRPC6A and pGCsi-TRPC6B. Plasmids expressing scrambled shRNA were used as negative control and named pGCsi-NC. These plasmids were transfected into a conditionally immortalized murine podocyte cell line by using liposome. Flow cytometry was used to examine the transfection efficiency. TRPC6 mRNA and protein ex-pression levels were detected by RT-PCR and Western blotting. Cultured podocytes were divided into four groups: control group, PAN treatment group, PAN+TRPC6 shRNA transfected group and PAN+scrambled shRNA transfected group. The paracelluar permeability to BSA was evaluated by Millicell-PCF Inserts and cell viability was measured by the trypan blue assay. Immunofluorescent assay was used to observe the distribution of α-actinin-4 and α-tubulin. The results showed that the transfection efficiency of the shRNA expression vector was about 45%. Expression levels of TRPC6 mRNA and protein were downregulated after transfection with pGCsi-TRPC6A and pGCsi-TRPC6B. Knocking down TRPC6 gene could effectively reverse the PAN-induced increase in the paracelluar permeability to BSA. The distribution of α-actinin-4 and α-tubulin was disrupted after treatment with PAN, which was reversed by knocking down TRPC6 gene. It was concluded that knocking down TRPC6 gene could effectively prevent podocytes from the permeability increase induced by PAN, which may be related to the regulation of podocyte cytoskeleton.     

单次静脉注射嘌呤霉素氨基核苷所致大鼠肾病模型的优化及评价

目的明确大鼠嘌呤霉素氨基核苷(puromycinaminonucleoside,PAN)肾病模型的适宜条件和病程演变,为该模型更好地用于肾病综合征、肾硬化发病机制及治疗的研究奠定基础。方法用6周龄雄性Wistar大鼠,一次性颈静脉注射PAN,分别以2、3、4、5、7、9mg/100g体重的剂量给药,以等量生理盐水作对照,测定2周内不同时间点的尿蛋白排泄量;另以9mg/100g体重的剂量给药,观察28周内尿蛋白、血清胆固醇和三酰甘油的变化及肾组织的病理改变。结果各个剂量的PAN均可引起不同程度的蛋白尿,约在10~14d达到高峰,最高达(592.0±61.0)mg/24h。28周连续观察的结果显示,PAN组动物的尿蛋白呈现典型的双相曲线,即第2周达到高峰,伴有血清胆固醇及三酰甘油的升高,此后逐渐降至接近正常,但自第12周起尿蛋白再度逐渐上升,第28周可达急性期峰值的一半。结论6周龄雄性Wistar大鼠,一次性颈静脉注射适量PAN可建立不同程度的肾病模型,成功率极高,方法简单,用药量省,动物价廉易得,且急性期发病快而周期短,不失为研究人类相应疾病的良好模型。     

肾上腺髓质肽在大鼠足细胞损伤模型中调控肾小球壁层上皮细胞分化

 目的  探讨肾上腺髓质肽(adrenomedullin,AM)是否通过调控肾小球壁层上皮细胞(parietal epithelial cells,PECs)分化参与对大鼠足细胞损伤模型的保护作用及可能的分子机制。方法  雄性SD大鼠经一次性腹腔注射嘌呤霉素氨基核苷(puromycinaminonucleoside,PAN) (15 mg/100 g体重)建立足细胞损伤模型,随机分为模型组和治疗组,治疗组每天经尾静脉注射AM 蛋白质(6.6 μg/100 g体重)。分别在首次注射PAN后7、14 和21 天,观察大鼠尿蛋白水平及肾组织形态改变,并经免疫组化染色、双重或三重免疫荧光染色,检测足细胞数量、肾小球AM的表达、PECs分化以及Notch3表达变化。结果  大鼠 PAN肾病模型表现为大量蛋白尿、肾小球节段性损伤、足细胞计数显著减少。AM/claudin-1双重荧光染色显示PECs中AM表达显著增强且出现于毛细血管袢内。AM治疗可改善大鼠尿蛋白及肾组织形态,减少足细胞丢失,14天时显著增加共表达PECs(claudin-1)及足细胞特异性标志蛋白(WT-1和synaptopodin)的细胞数。Ki67与claudin-1共定位表达于PECs,但未与WT-1共表达。AM显著抑制由PAN所致的Notch3表达。结论  在大鼠PAN足细胞损伤模型中,PECs中AM表达上调提示机体的一种代偿性保护机制,AM可能通过下调Notch3信号通路而促进PECs分化,参与其促进损伤后修复的作用。