纤维桩核与陶瓷桩核分别治疗磨牙残根残冠的临床疗效对比分析

目的:探讨纤维桩核与陶瓷桩核治疗磨牙残根残冠的临床疗效。方法:120例(126颗牙)磨牙残根残冠患者根据个人意愿分为纤维组和陶瓷组,分别进行根管治疗、预备、纤维桩核与陶瓷桩核制作与粘固、全冠修复等。结果:两组患牙治疗成功率相近,数据经统计学比较无显著差异(P>0.05)。研究组患者主要出现牙龈红肿、患牙不适和咀嚼不适,对照组患者主要出现牙桩松动、牙根折裂和咀嚼不适,研究组患者不适发生率明显高于对照组(P<0.05)。结论:纤维桩核与陶瓷桩核治疗磨牙残根残冠都具有较好的治疗成功率和近期疗效,但纤维桩核可能存在重负荷时的潜在弯曲,造成患牙感染,而陶瓷桩核则需要更多的临床经验来熟练和完善造模技术。     

Atonal homolog 1 expression in lung cancer correlates with inhibitors of the Wnt pathway as well as the differentiation and primary tumor stage

Atonal homolog 1 (Atoh1) is crucial to the differentiation of many cell types and participates in tumorigenesis and progression. This study investigated the role of Atoh1 in lung cancer development and its correlation with key members of the Wnt pathway. We used immunohistochemistry to examine the expressions of Atoh1, β‐catenin, Axin, chibby, and Disabled‐2 (Dab2) in 118 samples of lung cancer. We also detected the cytoplasmic and nuclear expression of Atoh1 in lung cancer tissues using western blot. Atoh1 nuclear expression was negatively correlated with differentiation level (p = 0.004) and primary tumor stage (p = 0.044) of lung cancer. Nuclear Atoh1 expression was positively correlated with nuclear expression of chibby (p < 0.001) and Dab2 (p < 0.001). Cytoplasmic Atoh1 expression was positively correlated with the cytoplasmic expression of Axin (p = 0.028), chibby (p < 0.001), and Dab2 (p < 0.001). We conclude that the nuclear expression of Atoh1 was inversely correlated with the differentiation and primary tumor stage of lung cancers. The expression and localization of Atoh1 correlated with Axin, chibby, or Dab2. Atoh1 may be a potential therapeutic target for the inhibition of growth and progression of lung cancers.     

Pyroptosis: An inflammatory cell death implicates in atherosclerosis

Cell death and inflammation are the fundamental biological processes in both normal physiology and pathology. Apoptosis is the most well-studied process of cell death, but there are also many other forms of cell death such as necrosis, autophagy and pyroptosis. Cell death could be observed throughout atherosclerosis and plays an important role in determining the fate of atherosclerotic lesion. Inflammation, the primary response of innate immunity, is considered essential in initiating and driving atherosclerosis. Apoptosis and autophagy had been reported in atherosclerosis, however, the mechanism of cell death involved in atherosclerosis still remain largely unknown. Cell death and inflammation are inextricably linked with their effectors modulating the process of atherosclerosis. Therefore, we proposed hypothesis that pyroptosis, an inflammatory form of cell death, may be implicated in atherosclerosis and play an important role in lesion instability.     

探讨按摩疗法在骨科患者疼痛护理中的作用

目的:评估按摩疗法这项护理措施对骨科患者疼痛程度的影响.方法:本研究纳入了80例在我院住院的男性膝关节手术患者.研究对象随机分为两组.干预组的患者除了常规治疗外,每天接受20min的按摩治疗,同时评估按摩治疗前后的疼痛程度.结果:干预组患者按摩前后的疼痛程度评分有显著差异(P <0.001),但这种差异在对照组(P = 0.33)不存在.两组患者的疼痛程度评分在干预措施前没有显著的差异(P>0.05),在干预后有显著统计学意义(P = 0.002).结论:按摩作为一种简单、廉价和有效的护理措施,可成为一种缓解骨科患者疼痛的积极方法.     

Mitochondrial DNA control region sequences may differentiate Yanbian Koreans in China from other Asian populations

Abstract

Background: Sequence polymorphisms of mitochondrial DNA (mtDNA) are valuable in forensic medicine and anthropological genetics.

Aim: This study investigated the mtDNA control region sequences in 295 unrelated individuals living in the Yanbian Korean Autonomous Prefecture in the People’s Republic of China.

Subjects and methods: DNA was extracted from blood stained filter papers. Hypervariable regions of the mtDNA control region (HVI and HVII) were amplified and sequenced. The resulting sequences were aligned and compared with the revised Cambridge reference sequence (rCRS).

Results: A total of 182 variations were confirmed. Population comparison showed the significant difference between Yanbian Korean and other included populations.

Conclusion: These results provide useful data for human genetic studies and forensic examinations and demonstrate that the Yanbian Korean population is an endogamous Northeast Asian group.     

SNP interactions of Helicobacter pylori-related host genes PGC,PTPN11, IL1B,and TLR4 in susceptibility to gastric carcinogenesis

A series of host genes that respond to Helicobacter pylori (H. pylori) infection are involved in the process of gastric carcinogenesis. This study sought to examine interactions among polymorphisms of H. pylori-related genes PGC, PTPN11, TLR4, and IL1B and assess whether their interaction effects were modified by H. pylori infection. Thirteen polymorphisms of the aforementioned genes were genotyped by the Sequenom MassARRAY platform in 714 gastric cancer patients, 907 atrophic gastritis cases and 1276 healthy control subjects. When we considered the host genetic effects alone, gene–gene interactions consistently decreased the risks of gastric cancer and/or atrophic gastritis, including three two-way interactions: PGC rs6912200-PTPN11 rs12229892, PGC rs4711690-IL1B rs1143623 and PTPN11 rs12229892-IL1B rs1143623 and a three-way interaction: PGC rs4711690-PGC rs6912200-PTPN11 rs12229892. When the effect modification of H. pylori infection was evaluated, the cumulative effects of the aforementioned three-way interaction on atrophic gastritis susceptibility switched from being beneficial to being risky by the status of H. pylori infection. These data showed that SNP interactions among H. pylori-related genes PGC, PTPN11, and IL1B, are associated with susceptibility to gastric carcinogenesis. Moreover, we provided important hints of an effect modification by H. pylori infection on the cumulative effect of PGC and PTPN11 polymorphisms. Functional experiments and further independent large-scale studies especially in other ethnic populations are still needed to confirm our results.     

Coxsackievirus-induced acute neonatal central nervous system disease model

Coxsackievirus B (CVB) is a significant pathogen that causes pediatric central nervous system disease with acute syndromes commonly. The onset of its infection was abrupt, and after recovery there usually will be severe mental sequelae. The disease model for research was not established by the way of natural infection, although there are various investigations about the CVB-induced central nervous system (CNS) diseases. Thus, we have established an acute neonatal CNS disease mice model by CVB orally infecting. This model imitated the natural infection route and focuses the onset of CNS disease, inducing severe infection and lesion in the hippocampus and cortex regions, and the stability of the model was demonstrated. A pathology score system was developed for quantitative pathology analysis, which standardizes the CNS pathology analysis by statistics analysis. By this model, the track of CVB penetrating the blood brain barrier in vivo has been captured. One of the experimental strains CVB3/Macocy, as a new variant, was isolated, and its genomic RNA was cloned. According to its nucleotide sequence, we have characterized its genomic structure and defined its genotype. Based on the sequence, some mutations which do not change the CVB-induced CNS damage have been found. The model is an effective tool for studies on CVB-induced CNS diseases.