Carisolv去龋对牙本质黏结强度影响的实验研究

目的：研究Carisolv去龋对牙本质黏结强度的影响：方法：选择30颗新鲜拔除的[牙合]面中度龋损的第三磨牙，每个牙的龋洞分成两半，一半用Carisolv去龋，另一半用慢速球钻去龋，而后随机分成3组，分别使用Prime＆Bond NT＋Dyract AP复合体黏结；Uni—Etch（320ml／L磷酸）＋One—Step Plus＋Renew树脂黏结：Prompt—L—Pop＋Z100树脂黏结。测试微抗拉强度（MTBS）：结果：Cafisolv组3种黏结系统MTBS分别为：（17．22±7．95）MPa、（25．40±8．44）MPa、（17．66±8．33）MPa，车针组分别为：（16．01±7．43）MPa、（23.45±7．55）MPa、（16.26±7.97）MPa：2种去龋方法间差异无显著性。结论：Carisolv去龋法对以上3种黏结系统与牙本质的黏结强度无不利影响：     

腭裂患者喉塞音的声学特征初探

目的:探讨腭裂患者喉塞音的声学特征。方法:检测存在病理性喉塞音的男性腭裂患儿及正常男性儿童各20名发含口塞音的语句时的语图,观察患者喉塞音声学特征并与正常对照组相比较。结果:腭裂患者喉塞音出现与原塞音的伴随情况不同,可以表现出包括冲直条、嗓音起始时间(VOT)、共振峰转接、冲直条频谱等各种声学指标的异常。结论:塞音的声学特征复杂,应该结合语图形态及各参数的数值共同诊断。     

Carisolv去龋对牙本质粘结界面影响的实验研究

目的:研究Carisolv去龋对牙本质粘结界面的影响。方法:24颗新鲜拔除的中度龋损的第三磨牙,随机分成ABCD4组。每个牙的龋洞分成两半,一半用Carisolv去龋,另一半用涡轮车针去龋后,做如下处理:A组不处理;B组320ml/L磷酸酸蚀,扫描电镜观察牙本质表面形态;C组不酸蚀,DyractAP复合体充填;D组320ml/L磷酸酸蚀后复合树脂充填,扫描电镜观察牙本质-充填体界面。结果:A组:Carisolv去龋后牙本质表面玷污层少,大部分牙本质小管口开放,清晰可见,表面粗糙不平;涡轮车针去龋后牙本质表面覆盖较厚玷污层,牙本质小管口堵塞,很少见到开口。B组:Carisolv去龋组和涡轮车针去龋组均去除了玷污层,牙本质小管口开放,但Carisolv组牙本质小管无管塞,而涡轮车针组牙本质小管残留部分管塞。C组:观察牙本质-复合体界面见Carisolv去龋组有较多树脂突形成,深入牙本质小管及管周;而涡轮车针去龋组未见明显树脂突起形成。D组:观察牙本质-树脂界面见2组树脂突的密度和长度无明显差异,但Carisolv去龋组树脂突之间的侧枝连接较涡轮车针去龋组多见。结论:Carisolv去龋后牙本质表面玷污层少,牙本质小管口开放,表面粗糙不规则,利于粘结,尤其在使用不需酸蚀的复合体充填时优势突出。     

艾叶水提物对山东山地丘陵丹参种植区7种主要杂草种子萌发的抑制作用研究

目的 通过种子萌发实验,研究艾叶水提物对山东山地丘陵丹参种植区7种主要杂草种子萌发的抑制作用。方法 蒸馏水提取艾粉得到艾叶水提物,稀释不同浓度后对杂草种子进行处理,在恒温培养箱中观察8 d,记录种子发芽率。结果 艾叶水提物在质量浓度为25 mg·mL^–1时对莎草、藜、反枝苋种子的发芽抑制率分别为97.33%、98.00%、100.00%,在质量浓度为50 mg·mL^–1时对狗尾草、画眉草、马齿苋、牛筋草种子的发芽抑制率分别为92.67%、94.67%、73.33%、82.00%。结论 艾叶水提物对山东山地丘陵丹参种植区杂草种子萌发有明显的抑制作用,可在丹参苗期杂草未萌发前结合雨天或灌溉等农艺措施撒施适量艾粉以达到生态除草的目的。     

Subpicomolar diphenyleneiodonium inhibits microglial NADPH oxidase with high specificity and shows great potential as a therapeutic agent for neurodegenerative diseases

Activation of microglial NADPH oxidase (NOX2) plays a critical role in mediating neuroinflammation, which is closely linked with the pathogenesis of a variety of neurodegenerative diseases, including Parkinson's disease (PD). The inhibition of NOX2‐generated superoxide has become an effective strategy for developing disease‐modifying therapies for PD. However, the lack of specific and potent NOX2 inhibitors has hampered the progress of this approach. Diphenyleneiodonium (DPI) is a widely used, long‐acting NOX2 inhibitor. However, due to its non‐specificity for NOX2 and high cytotoxicity at standard doses (µM), DPI has been precluded from human studies. In this study, using ultra‐low doses of DPI, we aimed to: (1) investigate whether these problems could be circumvented and (2) determine whether ultra‐low doses of DPI were able to preserve its utility as a potent NOX2 inhibitor. We found that DPI at subpicomolar concentrations (10^?14 and 10^?13 M) displays no toxicity in primary midbrain neuron‐glia cultures. More importantly, we observed that subpicomolar DPI inhibited phorbol myristate acetate (PMA)‐induced activation of NOX2. The same concentrations of DPI did not inhibit the activities of a series of flavoprotein‐containing enzymes. Furthermore, potent neuroprotective efficacy was demonstrated in a post‐treatment study. When subpicomolar DPI was added to neuron‐glia cultures pretreated with lipopolysaccharide, 1‐methyl‐4‐phenylpyridinium or rotenone, it potently protected the dopaminergic neurons. In summary, DPI's unique combination of high specificity toward NOX2, low cytotoxicity and potent neuroprotective efficacy in post‐treatment regimens suggests that subpicomolar DPI may be an ideal candidate for further animal studies and potential clinical trials. GLIA 2014;62:2034–2043     

The p.R229Q variant of the NPHS2 (podocin) gene in focal segmental glomerulosclerosis and steroid-resistant nephrotic syndrome: a meta-analysis

While many previous studies have reported an association between the p.R229Q variant of the NPHS2 gene and focal segmental glomerulosclerosis (FSGS) or steroid-resistant nephrotic syndrome (SRNS), a conclusive relationship has not been defined. In this study, we performed a meta-analysis of the published data to investigate the impact of the p.R229Q polymorphism on FSGS and SRNS patients. Despite significant heterogeneity within some of the comparisons, the results revealed significantly higher risks of SRNS in individuals homozygous for the variant allele (OR 7.411, 95 % confidence interval 1.876–29.436, p = 0.004) compared to homozygous non-variant individuals. However, the carrier rate of the p.R229Q variant was not significantly different between SRNS patients and steroid-sensitive nephrotic syndrome patients. No statistically significant differences in the p.R229Q carrier rate were observed between FSGS patients and controls or FSGS patients and patients with different pathology classifications. No notable differences in the p.R229Q carrier rate were found between patients and controls in any group with early-onset disease (onset age < 18). In conclusion, our meta-analysis suggests that for adult-onset disease (onset age > 18), the homozygous variant could be a potential predictor of hereditary nephrotic syndrome and that the p.R229Q allele cannot currently be considered a risk factor for predicting FSGS.