Further results on H ∞ control for discrete‐time uncertain singular systems with interval time‐varying delays in state and input

This paper investigates the state feedback robust H _∞ control problem of a class of discrete‐time singular systems with norm‐bounded uncertainties and interval time‐varying delays in state and input. A new bounded real lemma for discrete‐time singular systems with a pair of time‐varying interval state delays is first investigated. Mathematical comparisons of the new bounded real lemma and two existing ones are presented. Then, on the basis of the bounded real lemma proposed here, a sufficient condition in the form of nonlinear matrix inequality, such that the considered state feedback robust H _∞ control problem is solvable, is given. In order to solve the nonlinear matrix inequality, a cone complementarity linearization algorithm is offered. Several numerical examples are presented to show the applicability of the proposed approach. Copyright © 2012 John Wiley & Sons, Ltd.     

New results on H∞ filtering for nonlinear large‐scale systems with interconnected time‐varying delays

This paper proposes a new design method of H_∞ filtering for nonlinear large‐scale systems with interconnected time‐varying delays. The interaction terms with interval time‐varying delays are bounded by nonlinear bounding functions including all states of the subsystems. A stable linear filter is designed to ensure that the filtering error system is exponentially stable with a prescribed convergence rate. By constructing a set of improved Lyapunov functions and using generalized Jensen inequality, new delay‐dependent conditions for designing H_∞ filter are obtained in terms of linear matrix inequalities. Finally, an example is provided to illustrate the effectiveness of the proposed result. Copyright © 2015 John Wiley & Sons, Ltd.     

miR-431-3p对胃癌细胞增殖和凋亡的影响及其靶向调控CTDP1基因表达机制

目的 探讨miR-431-3p对胃癌细胞增殖和凋亡的影响,阐明其可能的分子机制。 方法 取经病理诊断确诊为胃癌的68例患者的胃癌组织及其癌旁组织。采用实时荧光定量PCR（RT-qPCR）法检测胃癌组织、癌旁组织和人正常胃黏膜上皮GES-1细胞、人胃癌细胞（MKN-28、MGC-803、MKN-45、SGC-7901和HGC-27）中miR-431-3p及羧基末端结构域磷酸酶1（CTDP1）mRNA表达水平,Western blotting法检测上述细胞中CTDP1蛋白和各组SGC-7901细胞中细胞色素C（Cyt C）、B细胞淋巴瘤2（Bcl-2）和Bcl-2相关X蛋白（Bax）蛋白表达水平。采用Pearson相关分析法分析miR-431-3p与CTDP1 mRNA表达水平的相关性,双荧光素酶报告基因实验检测miR-431-3p和CTDP1的靶向关系。将miR-431-3p mimic和CTDP1过表达慢病毒分别或同时转染至SGC-7901细胞中,将细胞分为空白组、空载过表达（mimic NC）组、miR-431-3p过表达（miR-431-3p mimic）组、空载慢病毒（Vector）组、CTDP1过表达慢病毒（CTDP1过表达）组和miR-431-3p mimic+CTDP1过表达（共转染）组。MTT法检测各组SGC-7901细胞增殖活性,克隆形成实验检测各组SGC-7901细胞单克隆形成数,流式细胞术检测各组SGC-7901细胞凋亡率。 结果 与癌旁组织比较,胃癌组织中miR-431-3p表达水平降低（P<0.01）,CTDP1 mRNA表达水平升高（P<0.01）,并且二者表达水平呈负相关关系（r=－0.316,P=0.009）。与GES-1细胞比较,其他5种胃癌细胞中miR-431-3p表达水平均降低（P<0.01）,CTDP1 mRNA和蛋白表达水平均升高（P<0.05）。双荧光素酶报告系统,miR-431-3p靶向调控CTDP1表达。与空白组和mimic NC组比较,miR-431-3p组SGC-7901细胞中CTDP1和Bcl-2蛋白表达水平、细胞增殖活性和克隆形成数降低（P<0.05）,细胞凋亡率和细胞中Cyt C及Bax蛋白表达水平升高（P<0.05）。与空白组和Vector组比较,CTDP1过表达组SGC-7901细胞中CTDP1和Bcl-2蛋白表达水平、细胞增殖活性及克隆形成数升高（P<0.05）;细胞凋亡率和细胞中Cyt C及Bax蛋白表达水平降低（P<0.05）。与空白组和miR-431-3p组比较,共转染组SGC-7901细胞中CTDP1和Bcl-2蛋白表达水平、细胞增殖活性及克隆形成数水平升高（P<0.05）,细胞凋亡率和细胞中Cyt C及Bax蛋白表达水平降低（P<0.05）。 结论 miR-431-3p过表达能抑制人胃癌细胞增殖,并促进细胞凋亡,可能是与靶向下调CTDP1基因表达有关。     

测定宫颈癌不同分期及正常宫颈组织MiR-140水平的临床意义分析

目的：检测不同组织的MiR基因水平,探讨宫颈癌与该基因的关系。方法：收集2012年1月-2013年6月期间来本院及中南大学湘雅二医院治疗的宫颈疾病患者的临床资料,共62例,包括32例良性患者（良性组）和30例恶性患者（观察组）,另选择同期来两院行健康体检者30例（对照组）,测定其MiR-140水平。结果：观察组MiR-140 OD值为（0.82±0.30）,高于对照组的（0.53±0.11）和良性组的（0.61±0.15）,比较差异均有统计学意义（P〈0.05）;Ⅳ期、Ⅲ期MiR-140 OD值分别为（0.92±0.21）和（0.85±0.23）,均明显高于Ⅰ期和Ⅱ期,比较差异均有统计学意义（P〈0.05）。结论：宫颈癌患者体内MiR-140水平高表达,且病情越重越明显。     

miR-183作用于Ezrin抑制结肠癌细胞侵袭和迁移的研究

目的:探讨miR-183对结肠癌细胞SW620侵袭和迁移能力的影响及是否通过作用于其靶基因Ezrin来发挥作用。方法:采用脂质体转染细胞,高表达或沉默miR-183,用Transwell实验观察细胞侵袭和迁移能力的变化,用Western Blot分析细胞Ezrin蛋白表达的改变;通过共表达miR-18和Ezrin,以及共沉默miR-18和Ezrin,观察miR-183对细胞侵袭和迁移能力的影响的变化,进一步证实miR-183是否通过作用于其靶基因Ezrin来发挥作用。结果:高表达miR-183后,与对照组相比,细胞侵袭及迁移能力明显下降,Ezrin蛋白的表达水平降低(P0.01,P0.001);反之,沉默miR-183的表达,细胞侵袭和迁移能力明显增强,Ezrin蛋白的表达水平增高(P0.01);高表达miR-183和Ezrin蛋白,与对照组(仅高表达miR-183)相比,细胞侵袭和迁移能力增强(P0.05);沉默miR-183和Ezrin的表达,与对照组(仅沉默miR-183)相比,细胞侵袭和迁移能力降低(P0.001)。结论:miR-183能够抑制结肠癌细胞SW620的侵袭和迁移,且通过调控其靶基因Ezrin蛋白的表达发挥作用。     

MiR-129-5p通过靶定胸苷酸合成酶调节结肠癌细胞对5-氟尿嘧啶的敏感性

目的 研究miR-129-5p通过靶定胸苷酸合成酶（TYMS）调控结肠癌细胞对5-氟尿嘧啶（5-Fu）敏感性的分子机制.方法 构建结肠癌耐药细胞株LoVo/5-Fu,并用实时荧光定量聚合酶链反应（PCR）检测miR-129-5p的表达水平.流式细胞术和MTT毒性实验检测过表达miR-129-5p对LoVo/5-Fu凋亡和半数致死剂量（IC50）的影响.构建TYMS 3＇UTR区荧光素酶报告载体,验证miR-129-5p对TYMS的靶向调控作用.Western Blot检测转染miR-129-5p后LoVo/5-Fu细胞中TYMS的蛋白表达.在LoVo/5-Fu内转染miR-129-5P siRNA,抑制其表达,检测LoVo/5-Fu细胞的IC50和凋亡.结果 过表达miR-129-5p后,LoVo/5-Fu细胞用5-Fu处理后凋亡增加,IC50降低.荧光素酶活性检测表明miR-129-5p能够抑制TYMS的荧光素酶活性.在LoVo/5-Fu细胞中miR-129-5p与TYMS的表达呈负相关.敲减TYMS后,LoVo/5-Fu细胞用5-Fu处理后凋亡增加,IC50降低.结论 MiR-129-5p能够通过靶定TYMS而增加结肠癌细胞对5-Fu的敏感性.     

3D-based full-guided ridge expansion osteotomy – A case report about a new method with successive use of different surgical guides,transfer of splitting vector and simultaneous implant insertion

For horizontal bone deficiency alveolar ridge osteotomy is considered an option for augmentation. Major advantages are the option for a one-stage approach and the absence of donor site morbidity. However, the conventional technique is associated with complications such as perforations and fractures of the cortical bone.A case using a 3D based modified, full-guided alveolar ridge expansion is described to explain the technique step by step. Main features of modified technique: successive application of surgical guides for ridge osteotomy and expansion – implementation of virtually determined splitting vector, which allows guided bone splitting along a guide surface of template in an ideal direction - osteotomy as deep as implant length. The example shows that the 3D based modified alveolar ridge osteotomy is a suitable alternative to the conventional technique as it has several advantages such as fewer fractures and perforations of the cortical vestibular bone.The individualized preoperative planning helps to minimize complications. However, long-term outcomes and a study, conducted on a study group, is needed to evaluate the benefits of our presented treatment protocol.     

长链非编码RNA ZFAS1在食管癌中的表达及作用机制研究

目的探讨长链非编码RNA锌指结构反义转录本1（zinc finger antisense 1,ZFAS1）在食管癌中的表达及作用机制。方法采用实时荧光定量PCR法分别检测癌旁组织和食管癌组织、正常食管上皮细胞和食管癌细胞的ZFAS1表达水平,通过细胞增殖活性检测、细胞划痕实验及流式细胞仪检测细胞凋亡技术,评价干扰食管癌细胞表达ZFAS1对细胞增殖、迁移及凋亡的影响,采用荧光素酶报告基因验证微小RNA（microRNA,miRNA）miR-302b-3p是ZFAS1的作用靶点,Western蛋白印迹法检测ZFAS1及miR-302b-3p作用下c-Jun氨基末端激酶2（c-Jun N-terminal kinase 2,JNK2）、胰岛素样生长因子1受体（insulin-like growth factor-1 receptor,IGF-1R）、白细胞介素-1受体相关激酶4（interleukin-1 receptor-associated kinase 4,IRAK-4）和上皮细胞激酶（epithelial cell kinase 2,EphA2）蛋白的表达变化。结果与癌旁组织相比,食管癌组织表达ZFAS1水平升高（t=19.40,P<0.001）,与正常食管上皮细胞相比,食管癌细胞表达ZFAS1水平增加（t=13.80,P<0.001）,通过抑制细胞表达ZFAS1发现,与NC干扰组相比,显著降低ZFAS1干扰组细胞增殖活性（t值分别=2.933,8.568,10.04,均P<0.05,）及迁移能力（t=13.96,P<0.001）,且细胞凋亡率升高（t=10.68,P<0.001）。ZFAS1可通过靶向miR-302b-3p调节JNK2、IGF-1R、IRAK4和EphA2蛋白的表达。结论ZFAS1在食管癌组织中表达显著增加,具有促进食管癌细胞增殖、迁移,抑制凋亡的能力,且ZFAS1可通过靶向miR-302b-3p激活JNK2、IGF-1R、IRAK4和EphA2,有望成为治疗食管癌的潜在靶点。     

Serum microRNA-133b is associated with low ceruloplasmin levels in Parkinson's disease

IntroductionThe cause of low serum ceruloplasmin levels in Parkinson's disease (PD) remains to be clarified. In this study, we explored serum miR-133b expression to determine whether it correlates with serum ceruloplasmin level in PD patients.MethodsForty-six patients with PD and forty-six control subjects were evaluated for miR-133b expression using qRT-PCR. The serum ceruloplasmin levels in all of the subjects were also determined.ResultsSerum miR-133b expression levels were significantly decreased in PD patients compared with those in the control subjects. Furthermore, PD patients with low serum ceruloplasmin levels also exhibited significantly lower expression of miR-133b compared with that of patients with normal ceruloplasmin levels. MiR-133b expression was correlated with the ceruloplasmin level in patients with PD, whereas no correlation was found between miR-133b and disease severity or motor phenotype.ConclusionOur observations suggest that miR-133b might be involved in ceruloplasmin dysmetabolism in PD patients and a further investigation is warranted to confirm this hypothesis.