OpenAdaptor原理、分析与应用

数据集成是面向服务架构SOA的基本构件,开源项目OpenAdaptor适配器框架能够快速构建数据集成功能,具有标准化快速开发、灵活、易于定制、高度复用等特点,为企业应用集成的实施奠定了基础,文中分析了OpenAdaptor的原理及实现,通过数据发布/订阅模型的适配器详述了OpenAdaptor的应用。

一种启动子克隆的改良Adaptor-PCR方法及在橡胶树上的应用实例

真核生物通过顺式作用元件和反式作用因子相互作用实现基因的转录调控,而启动子区域含有多种顺式元件,作为基因表达调控网络的枢纽控制着基因转录的起始与效率,一直是基因表达调控研究的重点[1]。本文提供了一种改良的基于Adaptor-PCR启动子克隆方法,改进了接头序列,设计了适合两步法PCR的接头引物。选取了25种限制性内切酶对橡胶树基因组DNA进行酶切,在所有酶切产物都平端化后,与改进的接头连接,成功构建了以Adaptor-PCR为基础的橡胶树基因启动子克隆文库,并利用此文库成功克隆了橡胶树6个蔗糖转运蛋白基因、1个转化酶基因和1个海藻糖合酶基因的启动子。本文研究结果为橡胶树基因启动子克隆提供了一个高效平台,也为其他生物基因启动子克隆提供了有益的参考。

信息总线的Adaptor研究

企业应用集成会遇到不同的网络、操作系统平台、应用系统等等的互连互通问题,基于TIB的企业应用集成方法让不同的系统通过Adaptor插入信息总线来实现不同系统之间的无缝连接,本文分析了Adaptor的作用与构建模型。

Expression of Chicken Toll-Like Receptors and Signal Adaptors in Spleen and Cecum of Young Chickens Infected with Eimeria tenella

Toll-like receptors （TLRs） are a group of highly conserved molecules which initiate the innate immune response to pathogens by recognizing structural motifs of microbes. Understanding the changes in chicken Toll-like receptors （ChTLRs） and signal adaptors expression that occur with Eimeria tenella infection will help to elucidate the molecular basis of immune control of coccidiosis caused by Eimeria. The present study detected the dynamic changes in the expression of ChTLRs and associated signal adaptors in the spleen and cecum ofE. tenella-infected chickens during the early stage of infection. The results showed that the expression peak for ChTLRs, MyD88 and TRIF occurred at 12 h post-infection （hpi）, ChTLR3, ChTLRI 5 and MyD88 mRNA expression in the spleen ofE. tenella infected chickens were significantly higher （P〈0.05） than that of negative control chickens, and there were similar tendencies of these molecules expression in the cecum and spleen of E. tenella-infected chickens. The expression of MyD88 was upregnlated at four time points in the cecum of E. tenella-infected chickens. The results of this study indicate that ChTLR3, ChTLR15 and MyD88 play a role in young chickens infected with E. tenella.

Adaptor Reconfiguration Analysis in Web Services Composition

Most of the existing approaches focus on identifying mismatches and synthesizing adaptors at design-time or recently at run-time. However, few works have been proposed to support adaptor reconfiguration when services in the composition evolve due to changes in business needs. To address the deficiencies, the problem of adaptor reconfiguration is targeted in the context of service composition. Firstly, the formal models for describing services and adaptors are presented. Then, under this formalization,the notion of reconfiguration compliance is proposed to determine the validity of an adaptor instance with respect to its history executions and future executions. Based on the notion,the algorithm for reconfiguration analysis of adaptors is presented and it can be used for determining the migratability of an adaptor instance and the corresponding target state of reconfiguration if migratable.Finally,feasibility of the proposed approach is validated on a realistic case study. The proposed approach improves the flexibility of adaptor-based service composition by equipping adaptors with reconfiguration capabilities.

Adaptor Protein Crk is Implicated in Mucus Formation in Mucinous Epithelial Ovarian Cancer (mEOC) Cells MCAS

Objective： The mucus production is an indicator for the histological grade of mucinous epithelial ovarian cancer （mEOC）. In our previous study, Crk expression was targeted in the human ovarian mucinous adenocarcinoma cell line MCAS through RNA interference, resulting in the establishment of Crk knock down cells. These cells exhibited decreased tumorigenic potential both in vitro and in vivo. The purpose of this study was to investigate if there is any change in the capability of forming mucus in these Crk knock down cells. Methods： Cytoplasmic periodic acid Schiff （PAS） staining and particle excluding assay were conducted to assess the mucus formation within and around cells, respectively. Additionally, the amount of mucus formed in tumor lumps from nude mice model was measured following HE and PAS staining. Results： The increased mucus production in Crk knockdown mEOC cells （MCAS） was manifested by increased number of enlarged cells filled with vacuoles-like mucus observed by phase-contrast microscope and cytoplasmic PAS staining; and enhanced mucus secretion was represented by the assembly of pericellular matrix in particle excluding assay and increased mucus area in tumor lumps from nude mice models. Conclusion： The course of carcinogenesis in mEOC is associated with the altered pattern of mucus production and secretion. The adaptor protein Crk is implicated in both pathways.

Emerging roles of the neural adaptor FE65 in neurite outgrowth

The brain is the third largest organ in the human body and consists of over80 billion neurons（Herculano-Houzel,2009）.Neurons are interconnected by neurite to form a complex neural network that allows the communication of neurons to regulate different body functions and activities.Neurites,body.

Energy Saving Adaptor

别小看电器所谓的节电模式，每年全球各种电器产品因为待机模式这种非完全关机状态而消耗的电能是非常惊人的。来自法国的设计团队Gilles Belley所推出的Energy Saving Adaptor便是为了解决这种情况。每一个Energy Saving Adaptor都是独立的，你可以根据用电器的多少将它们拼在桌子边上，它会自动检测用电器的状态，当发现用电器进入待机模式时，

衔接蛋白失能同源物2通过抑制NOD样受体热蛋白结构域相关蛋白3对结核性胸膜炎大鼠炎症和氧化应激的影响

目的:探讨衔接蛋白失能同源物2(DAB2)抑制NOD样受体热蛋白结构域相关蛋白3(NLRP3)对结核性胸膜炎大鼠炎症和氧化应激的影响。方法:按照随机数字法将60只SPF级雄性SD大鼠分为四组,每组40只。除正常对照组外,结核性胸膜炎组、DAB2组和pcDNA-NLRP3组进行建模处理,以第2天是否抽出胸腔积液为模型建立成功。正常对照组不注射结核分枝杆菌H37RV悬液,DAB2组建模后第2天静脉注射AAV9-DAB2质粒,每天1次,连续注射7 d,DAB2+pcDNA-NLRP3组在注射AAV9-DAB2质粒500μg/L的同时注射pcDNA-NLRP380μl,正常对照组和结核性胸膜炎组的大鼠尾静脉注射0.9%氯化钠溶液。进行各组呼吸功能指标测定,收集胸腔积液,记录积液量,观察3、5、7 d的胸腔积液粘连性情况,HE染色观察胸膜组织病理学情况,Western blot检测胸膜组织中肿瘤坏死因子-α(TNF-α)、白细胞介素-8(IL-8)、基质金属蛋白酶1(MMP-1)和MMP-9蛋白表达,荧光探针DCFH-DA分析检测活性氧(ROS)的水平。结果:与正常组相比,结核性胸膜炎组的大鼠的胸腔积液和胸膜厚度明显增加,用力肺活量(FVC)、最大呼气流量(PEF)、用力呼气容积(FEV)0.3和FEV0.3/FVC显著降低,TNF-α、IL-8、MMP-1和MMP-9蛋白表达显著升高,基质金属蛋白酶抑制剂(TIMP-1)蛋白表达显著降低,丙二醛(MDA)水平升高,超氧化物歧化酶(SOD)水平降低,ROS累积量明显升高(均P<0.001);与结核性胸膜炎组相比,DAB2组大鼠胸腔积液和胸膜厚度显著降低,FVC、PEF、FEV0.3和FEV0.3/FVC明显升高,DAB2组大鼠胸膜组织中的TNF-α、IL-8、MMP-1和MMP-9蛋白表达明显降低,TIMP-1水平明显升高,MDA水平降低,SOD水平升高,ROS累积量明显降低(均P<0.001);与DAB2组相比,DAB2+pcDNA-NLRP3组大鼠胸腔积液和胸膜厚度明显升高,FVC、PEF、FEV0.3和FEV0.3/FVC明显降低,DAB2+pcDNA-NLRP3组的TNF-α、IL-8、MMP-1和MMP-9蛋白表达明显升高,TIMP-1蛋白表达显著降低,MDA水平明显升高,SOD水平显著降低,ROS累积量显著升高(均P<0.001),各组大鼠在3、5、7 d的胸腔积液粘连性评分比较采用重复测量设计的方差分析,结果显示,不同时间点的胸腔积液粘连性评分比较差异具有统计学意义(均P<0.001);各组胸腔积液粘连性评分比较差异具有统计学意义(均P<0.001);各组胸腔积液粘连性评分变化趋势比较差异有统计学意义(均P<0.001);与模型组相比,DAB2组大鼠的胸膜内和肺间质内血管充血症状减轻,有少量的纤维组织增生,上皮样细胞团以及凝固型坏死也明显减少,淋巴细胞和中性粒细胞浸润也明显减少;与DAB2组相比,DAB2+pcDNA-NLRP3组大鼠的胸膜内和肺间质内血管充血症状加重,出现的纤维组织增生,上皮样细胞团以及凝固型坏死也明显增多,淋巴细胞和中性粒细胞浸润也明显增加。结论:DAB2通过抑制NLRP3的活性促进胸腔积液的吸收,降低胸膜厚度和粘连发生率,降低炎症反应和氧化应激水平,缓解结核性胸膜炎的进展。

伊伐布雷定联合常规药物治疗小儿病毒性心肌炎的临床效果分析

目的:分析伊伐布雷定联合常规药物治疗小儿病毒性心肌炎(VMC)的临床效果。方法:选取2020年7月—2022年7月淮安市妇幼保健院收治的VMC患儿94例作为研究对象,依据随机数字表法分为观察组与对照组,各47例。对照组给予常规治疗,观察组在对照组基础上应用盐酸伊伐布雷定治疗。比较两组治疗效果。结果:观察组治疗总有效率、白细胞介素-4水平高于对照组,血清γ干扰素、单核细胞趋化蛋白-1、血清淀粉样蛋白、心肌肌钙蛋白T、B型钠尿肽前体水平以及外周血Toll样受体3(TLR3)、β干扰素TIR结构域衔接蛋白(TRIF)、核因子-κBp65表达量低于对照组,差异有统计学意义(P<0.05)。两组不良反应发生率比较,差异无统计学意义(P>0.05)。结论:伊伐布雷定联合常规药物治疗VMC的效果较好,可通过抑制TLR3/TRIF信号通路减轻炎性反应,改善患者心功能,且安全性高。

Assessment of pathogenicity and functional characterization of APPL1 gene mutations in diabetic patients

BACKGROUND Adaptor protein,phosphotyrosine interacting with PH domain and leucine zipper 1(APPL1)plays a crucial role in regulating insulin signaling and glucose metabolism.Mutations in the APPL1 gene have been associated with the development of maturity-onset diabetes of the young type 14(MODY14).Currently,only two mutations[c.1655T>A(p.Leu552*)and c.281G>A p.(Asp94Asn)]have been identified in association with this disease.Given the limited understanding of MODY14,it is imperative to identify additional cases and carry out comprehensive research on MODY14 and APPL1 mutations.AIM To assess the pathogenicity of APPL1 gene mutations in diabetic patients and to characterize the functional role of the APPL1 domain.METHODS Patients exhibiting clinical signs and a medical history suggestive of MODY were screened for the study.Whole exome sequencing was performed on the patients as well as their family members.The pathogenicity of the identified APPL1 variants was predicted on the basis of bioinformatics analysis.In addition,the pathogenicity of the novel APPL1 variant was preliminarily evaluated through in vitro functional experiments.Finally,the impact of these variants on APPL1 protein expression and the insulin pathway were assessed,and the potential mechanism underlying the interaction between the APPL1 protein and the insulin receptor was further explored.RESULTS A total of five novel mutations were identified,including four missense mutations(Asp632Tyr,Arg633His,Arg532Gln,and Ile642Met)and one intronic mutation(1153-16A>T).Pathogenicity prediction analysis revealed that the Arg532Gln was pathogenic across all predictions.The Asp632Tyr and Arg633His variants also had pathogenicity based on MutationTaster.In addition,multiple alignment of amino acid sequences showed that the Arg532Gln,Asp632Tyr,and Arg633His variants were conserved across different species.Moreover,in in vitro functional experiments,both the c.1894G>T(at Asp632Tyr)and c.1595G>A(at Arg532Gln)mutations were found to downregulate the expression of APPL1 on both protein and mRNA levels,indicating their pathogenic nature.Therefore,based on the patient’s clinical and family history,combined with the results from bioinformatics analysis and functional experiment,the c.1894G>T(at Asp632Tyr)and c.1595G>A(at Arg532Gln)mutations were classified as pathogenic mutations.Importantly,all these mutations were located within the phosphotyrosinebinding domain of APPL1,which plays a critical role in the insulin sensitization effect.CONCLUSION This study provided new insights into the pathogenicity of APPL1 gene mutations in diabetes and revealed a potential target for the diagnosis and treatment of the disease.

淋巴细胞胞质蛋白2在恶性肿瘤发生与发展过程中的免疫调节机制

淋巴细胞胞质蛋白2(lymphocyte cytosolic protein 2,LCP2)是一种衔接蛋白质,在T细胞受体信号通路中扮演重要角色,激活下游信号因子以完成机体的免疫应答过程。LCP2也在恶性肿瘤的发生发展与转移中发挥重要作用,其高表达会导致不良的预后效果,降低患者生存率,其具体作用机制涉及多条信号通路。本文不仅对LCP2的分子结构以及基本功能进行了介绍,而且重点综合评述了LCP2通过参与NF-κB、MAPK、JAK/STAT以及PD-1/PD-L1信号通路调控恶性肿瘤发生与发展的分子机制。总结了LCP2作为肿瘤治疗靶点的潜在作用,为将来用于相关疾病的诊断、治疗和标志物筛选等提供理论基础和参考依据。

支持批量证明的SM2适配器签名及其分布式扩展

适配器签名,又称无脚本脚本,是解决区块链应用(如密码货币)中扩展性差、吞吐量低等问题的重要密码技术.适配器签名可看作数字签名关于困难关系的扩展,同时具有签名授权和证据提取两种功能,在区块链应用中具有以下优点:(1)降低链上成本;(2)提高交易的可替代性;(3)突破区块链脚本语言限制.SM2签名是我国自主设计的国家标准签名算法,在各种重要信息系统中有着广泛应用.基于SM2签名构造出高效的适配器签名方案,并在随机谕言机模型下给出安全性证明.所提方案结合SM2签名结构,可避免在预签名阶段生成额外的零知识证明,与现有ECDSA/SM2适配器签名相比更加高效,其中,预签名生成效率提升4倍,预签名验证效率提升3倍.随后,基于SM2协同签名,构造分布式SM2适配器签名,可避免单点故障问题,提升签名私钥安全.最后,在实际应用方面,基于SM2适配器签名构造适用于一对多场景下安全高效的批量原子交换协议.

The essential adaptors of innate immune signaling

Microbial components and the endogenous molecules released from damaged cells can stimulate germ-line-encoded pattern recognition receptors(PRRs)to transduce signals to the hub of the innate immune signaling network-the adaptor proteins MyD88/TRIF/MAVS/STING/Caspase-1,where integrated signals relay to the relevant transcription factors IRF3/IRF7/NF-κB/AP-1 and the signal transducer and activator of tran-scription 6(STAT6)to trigger the expression of typeІinterferons and inflammatory cytokines or the assem-bly of inflammasomes.Most pleiotropic cytokines are secreted and bind to specific receptors,activating the signaling pathways including JAK-STAT for the prolif-eration,differentiation and functional capacity of im-mune cells.This review focuses on several critical adaptors in innate immune signaling cascades and recent progress in their molecular mechanisms.

Fuel combustion test in constant volume combustion chamber with built-in adaptor

Combustion tests of pre-mixture of methane and air in constant volume combustion chamber(CVCC) have been carried out by means of flame propagation photo and gas pressure measurement,the effects of CVCC body temperature,intake pressure of pre-mixture of methane and air,equivalence ratio and location of the built-in adaptor have been investigated.The whole combustion chamber can be divided into two parts,i.e.the upper combustion chamber and the lower combustion chamber,by the built-in adaptor with through hole.Owing to the built-in adaptor with through hole,jet ignition or compression ignition(auto-ignition) phenomena may occur in the lower combustion chamber,which is helpful to getting higher flame propagation velocity,higher combustion peak pressure,low cycle-to-cycle variation and more stable combustion process.

Arabidopsis ECAP Is a New Adaptor Protein that Connects JAZ Repressors with the TPR2 Co-repressor to Suppress Jasmonate-Responsive Anthocyanin Accumulation

Suppression mechanisms mediated by transcriptional repressors commonly exist in diverse phytohormone signaling pathways.In Arabidopsis thaliana,JASMONATE-ZIM DOMAIN(JAZ)proteins are transcriptional repressors that function as negative regulators of diverse JA responses.Novel Interactor of JAZ(NINJA)is an adaptor protein connecting JAZs with the co-repressor,TOPLESS(TPL),to mediate gene repression in JA-dependent root growth inhibition and defense pathways.However,whether NINJA or other adaptor proteins are employed in other JA-responsive biological processes remains to be elucidated.In the present study,we demonstrate that a previously uncharacterized protein,ECAP(EAR motif-Containing Adaptor Protein),directly interacts with JAZ6 and JAZ8 and enhances their transcriptional repression activities.We provide evidence that ECAP is a novel adaptor protein for JAZ6/8 recruitment of the transcriptional co-repressor,TOPLESS-RELATED 2(TPR2),into a transcriptional repressor complex that represses the WD-repeat/bHLH/MYB complex,an important transcriptional activator in the JA-dependent anthocyanin biosynthesis pathway.Our findings,together with previous reports,reveal that specific adaptor proteins play a critical role in distinct JA responses by pairing different JAZs(which possess overlapping but also specific functions)with the general co-repressors,TPL and TPRs.

Therapeutic effect of Qinghuayin(清化饮)against chronic atrophic gastritis through the inhibition of toll or interleukin-1 receptor domain-containing adaptor inducing interferon-β signaling pathway

OBJECTIVE:To examine the efficacy of Qinghuayin(清化饮,QHY)in rat chronic atrophic gastritis(CAG)models and explored the molecular mechanism of QHY in treating CAG.METHODS:In total,65 Wistar rats were randomly divided into the control(n=10)and CAG groups(n=55).CAG model rats were further divided into five groups:model(n=10),vitacoenzyme(n=10),low-dose QHY(n=10),medium-dose QHY(n=10),and high-dose QHY groups(n=10).We analyzed histopathological changes using hematoxylin and eosin staining and measured interleukin(IL)-6 and IL-8 levels in serum using enzyme-linked immunosorbent assay(ELISA)(Boster Bio,Pleasanton,USA).In addition,gastrin(GAS),pepsinogen I(PGI),and PGII expressions were evaluated using ELISA.The protein and m RNA expression of toll-like receptor 4(TLR4)and toll or interleukin-1 receptor domaincontaining adaptor inducing interferon-β(TRIF)was detected by Western blotting and quantitative reverse transcription-polymerase chain reaction,respectively.RESULTS:Our results revealed that histopathological changes in CAG model rates could be restored by low-,medium-,and high-dose QHY.The changes in GAS and PGI/II expression demonstrated that QHY improved CAG.Serum IL-6 and IL-levels were decreased by QHY administration.TLR4 and TRIF were upregulated at the m RNA and protein levels in the model group but downregulated by QHY administration.CONCLUSION:We concluded that QHY could effectively improve the histopathological changes of the gastric mucosa induced by CAG in rats.The therapeutic mechanism of QHY may be related to inhibition of the inflammatory factors IL-6 and IL-8 and suppression of TLR4/TRIF m RNA and protein expression.

Oncogenic Signaling Adaptor Proteins

Signal transduction pathways activated by receptor tyrosine kinases （RTK） play a critical role in many aspects of cell function. Adaptor proteins serve an important scaffolding function that facilitates key signaling transduction events downstream of RTKs. Recent work integrating both structural and functional genomic approaches has identified several adaptor proteins as new oncogenes. In this review, we locus on the discovery, structure and function, and therapeutic implication of three of these adaptor oncogenes. CRKL. GAB2, and FRS2. Each of the three genes is recurrently amplified in lung adenocarcinoma or ovarian cancer, and is essential to cancer cell lines that harbor such amplification. Overexpression of each gene is able to transform immortalized human cell lines in in vitro or in vivo models. These observations identify adaptor protein as a distinct class of oncogenes and potential therapeutic targets.

A novel method for evaluating microglial activation using ionized calcium-binding adaptor protein-1 staining:cell body to cell size ratio

Aim:The aim was to validate a newly developed methodology of semi-automatic image analysis to analyze microglial morphology as marker for microglial activation in ionized calcium-binding adaptor protein-1(IBA-1)stained brain sections.Methods:The novel method was compared to currently used analysis methods,visual characterization of activation stage and optical density measurement,in brain sections of young and aged rats that had undergone surgery or remained naïve.Results:The cell body to cell size ratio of microglia was strongly correlated to the visual characterization activation stage.In addition,we observed specific surgery and age-related changes in cell body size,size of the dendritic processes and cell body to cell size ratio.Conclusion:The novel analysis method provides a sensitive marker for microglial activation in the rat brain,which is quick and easy to perform and provides additional information about microglial morphology.

Arabidopsis adaptor protein 1G is critical for pollen development

Pollen development is a,pre-requisite for sexual reproduction of angiosperms, during which various cellular activities are involved. Pollen development accompanies dynamic remodeling of vacuoles through fission and fusion, disruption of which often compromises pollen viability. We previously reported that the Y subunit of adaptor protein 1 （AP1G） mediates synergid degeneration during pollen tube reception. Here, we demonstrate that AP1G is essential for pollen development. AP1G loss-of-function resulted in male gametophytic lethality due to defective pollen development. By ultrastructural analysis and fluorescence labeling, we demonstrate that AP1G loss-of-function compromised dynamic vacuolar remodeling during pollen development and impaired vacuolar acidification of pollen. Results presented here support a key role of vacuoles in gametophytic pollen development.