Copolymers of novel methacrylic and styrenic monomer based on the thiophene: synthesis,characterization, monomer reactivity ratios,thermal properties,and biological activity

The free radical copolymerization of 2-thienylmethyl 4-vinylbenzyl ether (TMVBE) with 2-oxo-2-(2-thienylmethoxy)ethyl-2-methylacrylate (TMOEM) has been carried out in 1,4-dioxane at 65?°C?±?1 and were analyzed by Fourier transform infrared, ¹H NMR, and ¹³C NMR spectroscopy. ¹H NMR analysis was used to determine the molar fractions of TMVBE and TMOEM in the copolymers. The monomer reactivity ratios were calculated according to the general copolymerization equation using Kelen–Tüdõs and Finemann–Ross linearization methods. The reactivity ratios indicated a tendency toward alternation copolymerization. The thermal behaviors of copolymers with various compositions were investigated by differential scanning calorimetry and thermogravimetric analysis. Also, the apparent thermal decomposition activation energies were calculated by the Ozawa and Kissinger methods with a Shimadzu TGA 60 thermogravimetric analysis thermobalance. All the products showed moderate activity against different strains of bacteria and fungi.     

不同表面处理方法在纳米混合树脂复合材料修复中的应用

目的： 分析不同表面处理方法和粘接剂自酸蚀功能单体对树脂-复合材料界面即时修复粘结强度和完整性的影响。方法： 采用纳米树脂复合材料制作98个树脂复合材料,随机分为A1、A2、B1、B2、C、D组,各14个试件。表面未处理的试件作为阳性对照组（14个试件）。A1组用Gluma 通用粘接剂系统抛光,A2组用Gluma 通用粘接剂系统抛光、喷砂,B1组用Tokuyama Bond ForceⅡ^TM粘结系统抛光,B2组用Tokuyama Bond ForceⅡ^TM抛光、喷砂,C组仅经抛光样品组。D组仅做喷砂。采用与底物相同的树脂复合材料,对修复后试件进行剪切粘结强度（shear bond strength,SBS）测试,所有样本均进行电子显微镜扫描、测定表面轮廓,进行失效分析。采用SPSS 20.0软件包对数据进行统计学处理。结果： D组修复粘结强度显著高于阴性对照组（P<0.05）,A1、A2、B2、B1组粘结强度显著高于C、D组（P<0.05）;B1、D或A1组相比,粘结强度无显著差异（P>0.05）;B2组、阳性对照组粘结强度无显著差异（P>0.05）。除喷砂、TBFⅡ外,阳性对照组粘合强度值显著高于A1、C组（P<0.05）。抛光后表面粘合失效率高于喷砂样本（P<0.05）;抛光、Gluma处理样品粘合失败率高于抛光、TBFⅡ处理样品（P<0.05）;喷砂、TBFⅡ处理的表面内聚破坏率高于抛光、TBFⅡ处理（P<0.05）。抛光技术的表面粗糙度与喷砂技术相比,较规则且粗糙度较低（P<0.05）。结论： 经喷砂处理的复合材料基材加TBFⅡ,其修复粘结性最强,且表面内聚破坏率较高,TBFⅡ处理粘合失败率低。但经喷砂处理后的材料易堆积食物残渣,而抛光后的材料则不易发生。使用喷砂处理的复合材料基材上加TBFⅡ的患者,需正确有效地维护口腔卫生。     

Parkinson disease-associated mutation R1441H in LRRK2 prolongs the “active state” of its GTPase domain

Mutation in leucine-rich-repeat kinase 2 (LRRK2) is a common cause of Parkinson disease (PD). A disease-causing point mutation R1441H/G/C in the GTPase domain of LRRK2 leads to overactivation of its kinase domain. However, the mechanism by which this mutation alters the normal function of its GTPase domain [Ras of complex proteins (Roc)] remains unclear. Here, we report the effects of R1441H mutation (Roc_R1441H) on the structure and activity of Roc. We show that Roc forms a stable monomeric conformation in solution that is catalytically active, thus demonstrating that LRRK2 is a bona fide self-contained GTPase. We further show that the R1441H mutation causes a twofold reduction in GTPase activity without affecting the structure, thermal stability, and GDP-binding affinity of Roc. However, the mutation causes a twofold increase in GTP-binding affinity of Roc, thus suggesting that the PD-causing mutation R1441H traps Roc in a more persistently activated state by increasing its affinity for GTP and, at the same time, compromising its GTP hydrolysis.Mutation in leucine-rich-repeat kinase 2 (LRRK2) is a common cause of Parkinson disease (PD) (1–5). LRRK2 is a large (2,527-aa) multidomain protein consisting of seven putative domains (2), including a Ras-like GTPase domain called Ras of complex proteins (Roc), followed by a domain called C-terminal of Roc (COR), which is then followed by a kinase domain (Kin). It remains unclear how perturbations of these activities result in disease; however, the most common mutation in LRRK2-associated PD, G2019S in the kinase domain, shows higher kinase activity than wild type; therefore, its overactivation might be associated with disease pathogenesis (6).The tandem Roc-COR-Kin arrangement suggests that their activities might be coupled such that the GTPase activity of Roc might modulate the kinase activity. Indeed, several studies have shown that GTP binding to the Roc domain regulates the activity of the Kin domain (7, 8). Moreover, a PD-associated mutation in the Roc domain (R1441C) has been shown to have higher kinase activity (9), thus suggesting that mutations in the Roc domain, also up-regulate kinase activity.Understanding the function of Roc and its mechanism of action is important for understanding the mechanism of PD pathogenesis and therapeutic development. However, because of the lack sufficient quantity of protein samples amendable for detailed investigations, the biochemical properties and enzymatic activities of the Roc domain of LRRK2 are poorly understood.Here, we describe a stably folded construct of human Roc domain that enabled us to investigate quantitatively its biochemical and enzymatic properties. The results revealed that a PD-causing mutation R1441H in the Roc domain renders it less active at hydrolyzing GTP, as well as having higher affinity for GTP, than its wild-type counterpart, thereby increasing the residence time of its GTP-bound “active state,” which is associated with PD pathogenesis (8).     

临时冠单体诱导颊黏膜上皮细胞凋亡的动物实验研究

目的:研究4种临时冠桥材料戴用后的单体释出对颊黏膜上皮细胞的凋亡行为的影响.方法:选用4种临时冠桥材料(丙烯酸自凝树脂、丙烯酸热凝树脂、DMG-TEMP树脂、松风SWIFT-TEMP树脂) 对犬的右侧后牙进行临时冠修复,在牙备前、戴冠时、戴冠1周、2周、1个月5个时间点,收集临时冠对应区域的颊黏膜上皮细胞,并应用流式细胞仪检测其凋亡情况.结果:自凝塑料及热凝塑料组的颊黏膜上皮细胞的凋亡率大小排序为戴冠1周>戴冠2周>戴冠1个月>牙备前、戴冠时,差异有统计学意义(P < 0.01).DMG-TEMP树脂及松风SWIFT-TEMP树脂组的颊黏膜上皮细胞凋亡率在戴冠前后均维持较低水平,差异无统计学意义(P >0.05).颊黏膜上皮细胞的凋亡率与自凝塑料及热凝塑料中的残余单体释出量呈正相关(P < 0.01).结论:自凝塑料冠及热凝塑料冠在戴冠早期均有明显的残余单体释出,并加速诱导了颊黏膜上皮细胞的凋亡.     

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义齿树脂基托是全口义齿及局部义齿的重要组成部分,由于其具有吸水性和溶解性,加之释放一些残留单体,影响了材料的综合性能,降低了材料的使用寿命,并给患者的健康造成一定的危害。本文就义齿树脂基托的吸水性和溶解性机制及相关问题做一综述。     

Durability of bond between an indirect composite veneering material and zirconium dioxide ceramics

Abstract

Objective. The purpose of the present study was to evaluate the durability of bond strength between an indirect composite material and zirconia ceramics after thermocycling (100 000 cycles) and to assess the effect of various priming agents for zirconia surface treatments. Materials and methods. A CAD/CAM system (Katana, Noritake Dental Supply) was used to fabricate 96 zirconia disks as a bonding substrate. The specimens were randomly divided into six groups (n = 16) and treated with one of the following acidic priming agents: Alloy Primer (ALP, Kuraray), Clearfil Ceramic Primer (CCP, Kuraray), Clearfil Photo Bond (CPB, Kuraray), Clearfil Photo Bond with Clearfil Porcelain Bond Activator (CPB + Activator, Kuraray), Estenia Opaque Primer (EOP, Kuraray) and Porcelain Liner M Liquid A (PLA, Sun Medical). The specimens were bonded with an indirect composite material (Estenia C&B Dentin, Kuraray). Shear bond strengths were tested before and after 100 000 thermocycles and the data were analyzed by using the Steel-Dwass test and Mann-Whitney U-test. Results. After 100 000 thermocycles, the PLA group showed the lowest bond strength (p = 0.010), whereas the CPB + Activator (23.9 MPa; p < 0.014) and CPB (22.7 MPa; p < 0.028) groups had significantly higher bond strengths than the other groups. The Mann-Whitney U-test revealed that bond strengths did not significantly decrease after thermocycling, except for specimens in the PLA (p = 0.038) and CCP (p = 0.028) groups. Conclusions. Application of a combination of hydrophobic phosphate monomer (MDP) and initiator results in a durable long-term bond between Katana zirconia and Estenia C&B composite material.     

临时冠单体释出对颊黏膜上皮细胞DNA损伤的影响

目的研究4种临时冠桥材料戴用后的单体释出对颊黏膜上皮细胞DNA损伤的影响。方法给狗的右侧后牙进行全冠牙体预备后,分别选用4种临时冠桥材料(自凝塑料、热凝塑料、DMG-TEMP树脂、松风SWIFT-TEMP树脂)进行临时冠修复。在牙备前、戴冠时及戴冠后1周、2周、1个月5个时期,收集临时冠对应区域的颊黏膜上皮细胞,应用单细胞凝胶电泳(彗星实验)检测颊黏膜上皮细胞的DNA损伤程度。结果自凝塑料组及热凝塑料组临时冠戴用后,颊黏膜上皮细胞的彗星百分率在戴冠1周>戴冠2周>戴冠1月>牙备前和戴冠时,存在显著性差异(P<0.01)。空白对照组、DMG-TEMP树脂组及松风SWIFT-TEMP树脂组的颊黏膜上皮细胞的彗星百分率在戴冠前、后均维持较低水平,无统计学差异(P>0.05)。颊黏膜上皮细胞的DNA损伤程度(以彗星百分率反应)与临时冠材料中的有机叔胺及MMA单体的释出量呈正相关性。结论自凝塑料及热凝塑料临时冠在戴冠后的早期均有残余单体释出,并导致对应区域颊黏膜上皮细胞的DNA损伤。DMG-TEMP树脂及松风SWIFT-TEMP树脂临时冠戴用后,未有显著的颊黏膜上皮细胞的DNA损伤。     

血清血小板活化因子、脂蛋白(a)、纤维蛋白单体对骨折患者发生近端深静脉血栓评估价值

目的 探讨血清血小板活化因子、脂蛋白(a)、纤维蛋白单体对骨折患者发生近端深静脉血栓评估价值.方法 选取自2018年1月至2020年1月收治的97例骨折患者为研究对象.将发生近端深静脉血栓患者纳入血栓组(n=34),未发生近端深静脉血栓患者纳入非血栓组(n=63),分析骨折患者发生近端深静脉血栓的危险因素.采用受试者工...     

糖尿病合并冠心病患者F1+2及SFMC的变化及意义

为探讨F1 2及SFMC在糖尿病合并冠心病中的变化及意义，采用酶联免疫吸附法(ELISA)检测28例糖尿病合并冠心病患者(试验组)静脉血凝血酶原片段1 2(F1 2)及纤维蛋白单体复合物(SFMC)水平，并与25例单纯糖尿病患者(对照组)进行比较。结果显示，试验组F1 2、SFMC水平均明显高于对照组(P＜0．005、＜0．01)，其它出凝血指标如凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)、纤维蛋白原(Fbg)、血浆因子Ⅶ促凝活性(FⅦ：c)等两组比较无明显差异(P＞0．05)。试验组与对照组空脂血糖(FBG)、甘油三酯（TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL—C)水平无明显差异(P＞0，05)；低密度脂蛋白胆固醇(LDL—C)水平有显著性差异(P＜0．05)。两组血流变学中全血比粘度(中切)、血浆比粘度无显著性差异(P＞0．05)，红细胞压积、红细胞聚集指数有显著性差异(P＜0.05)。提示血栓前状态与糖尿病合并冠心病有密切关系，F1 2及SFMC可以作为糖尿病患者发生冠心病的预测指标。     

新生血管特异性结合肽GX1二聚体抑制胃癌新生血管生成的实验研究

目的:探讨新生血管特异性结合肽GX1二聚体对胃癌新生血管生成的影响。方法:化学合成GX1二聚体、GX1单体、对照肽二聚体,CCK-8实验、管状结构形成实验、迁移实验研究GX1二聚体对胃癌血管内皮细胞（co-HUVEC）增殖、微管形成、迁移能力的影响,流式细胞学技术分析其对细胞周期分布和凋亡的影响。结果:CCK-8结果显示,GX1二聚体与对照肽二聚体及PBS对照组相比,100~200 μmol/L可抑制co-HUVEC增殖,具有统计学差异（P<0.05）,并呈剂量依赖性,GX1二聚体较单体抑制作用增强,并有统计学差异（P<0.05）。管状结构形成实验、细胞损伤迁移实验结果显示,与对照肽二聚体及对照组PBS 相比,GX1二聚体及GX1单体,均可抑制胃癌内皮细胞管状结构的形成及迁移,且二聚体抑制作用强于单体;对照肽二聚体仅有轻微的抑制胃癌内皮细胞管状结构的形成及迁移。流式细胞术分析显示,与对照肽二聚体及PBS对照组相比,GX1二聚体及GX1单体均可诱导细胞凋亡（P<0.05）,且GX1二聚体的诱导作用强于GX1单体（P<0.05）,而对细胞周期分布则无明显影响。结论:GX1二聚体和GX1单体均可抑制胃癌新生血管内皮细胞增殖、微管形成、迁移能力及诱导凋亡,且GX1二聚体较GX1单体作用增强。GX1二聚体有望代替单体成为胃癌新生血管靶向治疗小肽类药物。