基于BREW平台的多态机制实现

BREW技术是在移动数据增值应用开发领域中出现的一种新技术,开发主要是应用的C语言,但手机开发中的大量问题都与C++中实现的多态效果十分相似,如果可以利用C语言这种非面向对象的语言写出面向对象的程序,将有利于提高程序的重用性、模块化功能以及健壮性。本论文主要围绕着BREW平台应用开发中一个常见应用:页面迁移技术为例,给出了多态机制在BREW平台下的解决方案,该方案均是在BREW手机实际开发中总结出来,具有很大的可重用性。

C++的多态机制及其应用

本文总结多态机制在C++中的几种表现形式,并结合具体程序设计实例提出了“协同类”概念。

幽门螺杆菌基因多态性及其致病机制研究进展

幽门螺杆菌是一种全球范围内的慢性感染性致病菌,除导致慢性胃炎、消化性溃疡、胃癌等胃肠疾病外,还与慢性心血管疾病,肝脏及胆道疾病密切相关。研究表明,其基因结构多态性差异是导致不同临床表现的主要原因,近年来对Hp毒力因子及其基因多态性研究取得长足进展,本文对其主要的毒力基因多态性及可能的致病机制进行综述。

多态性实现机制在C++与JAVA中的比较分析

熟练使用多态性是程序设计者运用面向对象方法进行程序设计的关键,而理解多态性实现机制则是熟练使用多态性的关键。为充分理解多态性的实现机制,采用比较方法,深入分析比较了C++和JAVA的多态性在使用方法、要点、内部实现流程以及实现机制上的异同,并给出了关键代码和图形分析。结果表明:两者在多态性实现机制上,原理基本相同,但具体做法不同,C++偏向直接、速度快;JAVA偏向通用、速度慢。

Java的多态

本文是蔡学镛Java入门系列的最后一篇,介绍了Java中的多态。从下期开始蔡学镛将开设C＃系列讲座,深入浅出地介绍最绍最新的.Net,主要语言C＃。

The role of titanium at the interface of hematite photoanode in multisite mechanism:Reactive site or cocatalyst site?

Hematite(α-Fe_(2)O_(3))constitutes one of the most promising photoanode materials for oxygen evolution reaction(OER).Recent research on Fe_(2)O_(3) have found a fast OER rate dependence on surface hole density,suggesting a multisite reaction pathway.However,the effect of heteroatom in Fe_(2)O_(3) on the multisite mechanism is still poorly understood.Herein we synthesized Fe_(2)O_(3) on Ti substrates(Fe_(2)O_(3)/Ti)to study the oxygen intermediates of OER by light-dark electrochemical scans.We identified the Fe-OH species disappeared and Ti-OH intermediates appeared on Fe_(2)O_(3)/Ti when pH=11‒14,which significantly improved the OER performance of Fe_(2)O_(3)/Ti.Combined with the density functional theory calculations,we propose that Ti atom acts as cocatalyst site and captures proton from neighboring Fe-OH species under highly alkaline condition,thereby promoting the coupling of Fe=O and reducing the energy barrier of the non-electrochemical step.Our work provides a new insight into the role of heteroatom in OER multisite mechanism based on clarifying the reaction intermediates.

面向对象软件开发的单元测试

本文通过与传统结构化方法中单元测试的比较,对面向对象方法中的单元测试—类测试进行分析。

改进的单形进化算法及在神经网络上的应用研究

单形进化算法(Surface-Simplex Swarm Evolution Algorithm,简称SSSE)是一种新型群体智能优化算法,该算法通过建立粒子的单形邻域搜索算子和多角色态搜索机制,具有很好地收敛效果.为了对该算法的性能进行进一步分析与讨论,同时,为了强调全局搜索的应用场景并提高算法的勘探搜索能力,提出一种改进的单形进化算法(ISSSE),ISSSE对原算法的多态平衡搜索机制进行了两点改进;然后用8个标准测试函数进行性能测试,并同不同的算法比较;最后将ISSSE算法应用于径向基神经网络(RBF)的参数优化中.实验结果表明,改进的单形进化算法(ISSSE)在其性能上具有更好的勘探搜索能力,提高了算法的求解精度和收敛速度,并且能够很好应用于RBF的参数寻优,提高了RBF的分类正确率.

利用虚函数实现鼠标、键盘事件的模块化

虚函数是C++中实现多态性的一个重要机制,常常使用它在父类中对某种操作提供一个框架,而在不同的子类中为该框架提供不同的实现,据此特点,介绍了目前图形图像处理软件中常用的一种鼠标键盘事件的新的封装机制。该机制以面向对象的多态性及技术基础,可实现鼠标键盘事件的模块化和不同功能间的自动切换。

Phase I/II enzyme gene polymorphisms and esophageal cancer risk: A meta-analysis of the literature

AIM:Phase I/II enzymes metabolize environmental carcinogens and several functional polymorphisms have been reported in their encoding genes. Although their significance with regard to esophageal carcinogenicity has been examined epidemiologically, it remains controversial. The present systematic review of the literature was performed to clarify associations. METHODS: Eligible studies were case-control or cohort studies published until September 2004 that were written in any language. From PubMed and a manual review of reference lists in relevant review articles, we obtained 16 studies related to the CYP1A1 Ile-Val substitution in exon 7, CYP1A1 MspI polymorphisms, CYP2E1 Rsal polymorphisms, GSTM1 null type, GSTT1 null type and GSTP1 Ilel04Val. All were of case-control design. Summary statistics were odds ratios (ORs) comparing heterozygous-, homozygous-non-wild type or these two in combination with the homozygous wild type, or the null type with the non-null type for GSTM1 and GSTT1, A random effect model was used to estimate the summary ORs. A meta-regression analysis was applied to explore sources of heterogeneity. RESULTS: Individuals with the Ile-Val substitution in CYP1A1 exon 7 had increased esophageal cancer risk, with ORs (95%CI) compared with lie/lie of 1.37 (1.09-1.71), 2.52 (1.62-3.91) and 1.44 (1.17-1.78) for Ile-Val, Val/Val genotype and the combined group. No significant association was found between esophageal cancer risk and the other genetic parameters. CONCLUSION: A significant association exists between the CYP1A1 Ile-Val polymorphism and risk of esophageal cancer. Polymorphisms that increase the internal exposure to activated carcinogens may increase the risk of esophageal cancer.

Cyclooxygenase 2 polymorphism and colorectal cancer:-765G>C variant modifies risk associated with smoking and body mass index

AIM： To explore whether cyclooxygenase 2 （COX-2） -765G〉C polymorphism is associated with susceptibility of colorectal cancer （CRC） and to evaluate the risk of colorectal cancer in relation to environmental exposures and polymorphism. METHODS： We conducted a case-control study of 137 patients with colorectal cancer and 199 cancerfree controls in northeast China. Multivariate logistic regression analysis was performed to calculate the adjusted odds ratio （OR） and 95% confidence interval （95% CI）. RESULTS： The -765G〉C polymorphism was not independently associated with CRC risk. However, risk associated with the polymorphism differed by smoking and body mass index （BMI）. Smoking and BMI associated risks were stronger among those with -765GG genotype, showing that smokers had a 2.682-fold greater risk of CRC than nonsmokers （51/43 vs 68/126, P = 0.006）. Compared to those with a normal body mass index （BMI 18.5-22.9）, those with overweight （BMI 23-24.9） had a 3.909-fold higher risk of CRC （OR = 3.909, 95% CI = 2.081-7.344; P 〈 0.001）, while those with obesity （BMI 〉 25） had a 2.031- fold higher risk of CRC （OR = 1.107, 95% CI = 1.107-3.726; P = 0.022）. is not associated with an increased risk of CRC, -765GG genotype appears to be related to an increased risk in the presence of smoking and higher BMI.

Drug-induced liver injury:Is it somehow foreseeable?

The classic view on the pathogenesis of drug-induced liver injury is that the so-called parent compounds are made hepatotoxic by metabolism (formation of neosubstances that react abnormally), mainly by cytochromes P-450 (CYP), with further pathways, such as mitochondrial dysfunction and apoptosis, also playing a role. Risk factors for drug-induced liver injury include concomitant hepatic diseases, age and genetic polymorphisms of CYP. However, some susceptibility can today be predicted before drug administration, working on the common substrate, by phenotyping and genotyping studies and by taking in consideration patients' health status. Physicians should always think of this adverse effect in the absence of other clear hepatic disease. Ethical and legal problems towards operators in the health care system are always matters to consider.

Genetic polymorphisms in non-alcoholic fatty liver disease:Clues to pathogenesis and disease progression

The spectrum of non-alcoholic fatty liver disease(NAFLD) ranges from simple steatosis through steatohepatitis to advanced f ibrosis and cirrhosis.Although the reason why only a minority of patients develop progressive forms of disease still remains largely unclear,recent research has identified genetic factors as a possible basis for this variation in disease presentation.Most of the studies have been focused on f inding associations between advanced disease forms and selected single nucleotide polymorphisms in genes encoding various proteins involved in disease pathogenesis.Although there are many limitations regarding the study design and interpretation of published data,further carefully planned studies together with implementation of new genetic technologies will likely bring new insights into disease pathogenesis and potential benefits to the management of patients with NAFLD.

Kimchi and soybean pastes are risk factors of gastric cancer

AIM: This case-control study investigated the effects of kimchi,soybean paste, fresh vegetables,nonfermented alliums, nonfermented seafood, nonfermented soybean foods, and the genetic polymorphisms of some metabolic enzymes on the risk of gastric cancer in Koreans. METHODS: We studied 421 gastric cancer patients and 632 age- and sex-matched controls. Subjects completed a structured questionnaire regarding their food intake pattern. Polymorphisms of cytochrome P450 1A1 (CYP1A1), cytochrome P450 2E1 (CYP2E1), glutathione S-transferase mu 1 (GSTM1),glutathione S-transferase theta 1 (65777) and aldehyde dehydrogenase 2 (ALDH2) were investigated. RESULTS: A decreased risk of gastric cancer was noted among people with high consumption of nonfermented alliums and nonfermented seafood. On the other hand, consumption of kimchi, and soybean pastes was associated with increased risk of gastric cancer. Individuals with the CYP1A1 Ile/Val or Val/Val genotype showed a significantly increased risk for gastric cancer. Increased intake of kimchi or soybean pastes was a significant risk factor for the CYP1A1 lie/lie, the CYP2E1 c1/c1,the GSTM1 non-null, the GSTT1 non-null, or the ALDH2 *1/*1 genotype.In addition, eating soybean pastes was associated with the increased risk of gastric cancer in individuals with the GSTM1 null type. Nonfermented alliums were significant in individuals with the CYP1A1 lie/lie, the CYP2E1 c1/c2 or c2/c2, the GSTT1 null, the GSTT1 non-null, or the ALDH2 *1/*2 or *2/*2 genotype,nonfermented seafood was those with the CYP1A1 lie/lie,the CYP2E1 c1/c1, the ALDH2 *1/*1 genotype or any type of GSTM1 or GSTT1. In homogeneity tests, the odds ratios of eating kimchi for gastric cancer according to the GSTM1 or 65777 genotype were not homogeneous. CONCLUSION: Kimchi, soybean pastes, and the CYP1A1 Ile/Val or Val/Val are risk factors,and nonfermented seafood and alliums are protective factors against gastric cancer in Koreans. Salt or some chemicals contained in kimchi and soybean pastes, which are increased by fermentation,would play important roles in the carcinogenesis of stomach cancer.Polymorphisms of the CYP1A1, CYP2E1, GSTM1, GSTT1, and ALDH2 genes could modify the effects of some environmental factors on the risk of gastric cancer.

THE ASSOCIATION BETWEEN TUMOR NECROSIS FACTORαGENE POLYMORPHISM AND ASTHMA

Objective.In this study,we investigated the hypothesis that tumor necrosis factor(TNF)α-308gene polymorphism might be of the genetic predisposition to asthma and asthma phenotypes.Methods.TNFα-308gene polymorphism was genotyped in221random unrelated Northern Chinese population(comprising125asthmatics and96healthy controls)and52individuals from12asthmatic families with Han ethnic by using polymerase chain reaction(PCR)-restriction fragment length polymor-phism(RFLP).Methacholine(Mch)broncho-challenge test,bronchial reversibility test and lung function were underwent in all asthmatics.Results.TNFα-3082homozygosity was present at a significantly higher frequency in asthmatics than that in controls(20.8%vs11.4%,P<0.05,OR2.259),the TNF allele2was also higher in asthmatics compared with controls(0.42vs0.33,P<0.01).TNFα-3082homozygosity was an weak independent risk factor for asthma etiology(OR0.226,P<0.05).Moreover,patients carrying TNFα-3082homozy-gosity had less responsive to inhaledβ 2 -agonist in20minutes than patients carrying other two genotypes(24.1%vs29.5%vs38.8%,P<0.05).Linkage analysis didn’t support that TNFαgene was linked to asthma (Likelihood of odds,LOD<1)based on familial data.Conclusion These results suggest that TNFα-3082homozygosity may be of a component contribut-ing to the genetic predisposition to asthma ,and airway responsiveness toβ2 -agonist.

Loss of heterozygosity analyzed by single nucleotide polymorphism array in cancer

Neoplastic progression is generally characterized by the accumulation of multiple genetic alterations including loss of tumor suppression gene function. Loss of heterozygosity （LOH） has been used to identify genomic regions that harbor tumor suppressor genes and to characterize different tumor types, pathological stages and progression. LOH pattern has been detected by allelotyping using restriction fragment length polymorphism, and later by simple sequence length polymorphisms （SSLPs or microsatellite） for 10 years. This paper reviews the detection of LOH by recently developed single nucleotide polymorphism （SNP） arrays （all analyzed by Affymetrix array）; furthermore, its advantage and disadvantage were analyzed in several kinds of cancer.

Interaction models of CYP1A1, GSTMl polymorphisms and tobacco smoking in intestinal gastric cancer

AIM： To explore the interaction models of the cytochrome P-450 （CYP） 1A1 Valvariant and glutathione S-transferase （GST） M1 null polymorphisms with tobacco smoking in the occurrence of intestinal gastric cancer. METHODS： A community-based case-control study was conducted in Yangzhong. Subjects included 114 intestinal types of gastric cancer with endoscopic and pathological diagnosis during January 1997 and December 1998, and 693 controls selected from their spouse, siblings or siblingsin-law who had no history of digestive system cancer. Logistic regression was used to estimate the interaction models. RESULTS： The frequency of the CYPIA1 Valvariant allele in cases did not differ from that in controls. The OR of GSTM1 null genotype was 2.0 （95% confidence interval [95%CI]： 1.2-3.1, P〈0.01）. It showed a significant type 2 form of interaction model when both CYPIA1 Valvariant allele and former tobacco smoking existed （i.e., among the multiplicative effects, the disease risk is increased by the tobacco exposure alone but not by the CYPIA1 variant alone）. The interaction index y was 2.8, and OReg （95%CI） was 5.0 （1.9-13.4）. GSTM1 null genctype and former tobacco smoking were significant in a type 4 interaction model （i.e., the disease risk is increased by GSTM1 null genotype or tobacco exposure alone among the multiplicative effects）. The interaction index y and OReg （95%CI） were 3.4 and 8.4 （3.4-20.9）, respectively.CONCLUSION： Different interaction models of CYPIA1 Valvariant allele and GSTM1 null genotype with tobacco smoking will contribute to understanding carcinogenic mechanism, but there is a need to further investigate in larger scale studies.

Hereditary pancreatitis

Hereditary pancreatitis is an autosomal dominant condition,which results in recurrent attacks of acute pancreatitis,progressing to chronic pancreatitis often at a young age.The majority of patients with hereditary pancreatitis expressone of two mutations (R122H or N29I) in the cationictrypsinogen gene (PRSS1 gene). It has been hypothesisedthat one of these mutations, the R122H mutation causespancreatitis by altering a trypsin recognition site sopreventing deactivation of trypsin within the pancreas andprolonging its action, resulting in autodigestion. Families withthese two mutations have been identified in many countriesand there are also other rarer mutations, which have alsobeen linked to hereditary pancreatitis.Patients with hereditary pancreatitis present in the sameway as those with sporadic pancreatitis but at an earlierage. It is common for patients to remain undiagnosed formany years, particularly ifthey present with non-specificsymptoms. Hereditary pancreatitis should always beconsidered in patients who present with recurrent pancreatitiswith a family history of pancreatic disease. If patients withthe 2 common mutations are compared, those with theR122H mutation are more likely to present at a younger ageand are more likely to require surgical intervention than thosewith N29I. Hereditary pancreatitis carries a 40 % lifetimerisk of pancreatic cancer with those patients aged between50 to 70 being most at risk in whom screening tests maybecome important.

APOLIPOPROTEIN(a) AND CORTICAL CEREBRAL INFARCTION

Objective. The present study aimed to elucidating the correlation of apolipoprotein(a)[apo(a)] with cerebral infarction at the levels of molecule and protein. Methods. The serum Lp(a) level, by means of ELISA, the polymorphism of apo(a) protein, by SDS PAGE/Western blotting combined with silver staining assays, and the sequence polymorphisms in 5’ control region, the first exon and intron of apo(a)gene, by PCR SSCP/AFLP assays, were detected in 85 healthy controls and 42 cases of cortical cerebral infarction. Results. The serum Lp(a) level was markedly higher in the patients(152.59±3.41 mg/L)than that in the controls(56.21±3.67 mg/L)(t=4.15, P<0.001), even between the subjects with the same apo(a) phenotype. The frequency of low molecular weight phenotype was significantly higher in the patients than that in the controls(0.5238 vs. 0.2941). There were 2 sites of sequence variance in the 5’ control region of apo(a) gene in our studied population, which were of significant difference between patients and controls, and were related to the variation of serum Lp(a) level. Conclusion. Our study found that the low molecular weight phenotype of apo(a) was closely associated with cerebral infarction, suggested that the variation of serum Lp(a) level be determined by not only the size of apo(a) gene but also its sequence, which indicated that both the size and sequence of apo(a) are associated with the susceptibility to cerebral infarction.

Ppargc1α基因与肉质品质的相关性

Ppargc1α是一种核转录辅激活因子,能在棕色脂肪组织、骨骼肌等部位大量表达,而在白色脂肪组织、胰腺及大脑中的分布较少。Ppargc1α通过参与机体能量平衡和多种代谢调控过程,有效诱导线粒体生物合成并且上调线粒体生物氧化功能从而影响机体的生长、疾病的发生和生物体内各种物质的合成。肉质品质与物种的遗传因素有着密切而直接的关系。本文通过分析ppargc1α基因的作用机制,阐述了ppargc1α对骨骼肌肌纤维类型、基因型表达和多种生化过程的调控作用,体现出ppargc1α作为一种辅转录激活因子能停靠多种转录因子增强靶基因转录效率,可以通过调控线粒体表达和生物氧化等途径来影响肉质品质。