On Complemented Subsystems of Commutative Jordan Quadruple Systems

We extend the notions of commutativity,ideals,anisotropy,and complemented subtriples of Jordan triple systems to those of Jordan quadruple systems.We show that if S is a complemented subsystem of an anisotropic commutative Jordan quadruple system U,then S and its annihilator S^(⊥)are orthogonal ideals and U=S⊕S^(⊥).We also prove that the range of a structural projection on an anisotropic commutative Jordan quadruple system is a complemented ideal and,conversely,a complemented subsystem of an anisotropic commutative Jordan quadruple system is the range of a unique structural projection.

Antibodies elicited by Newcastle disease virus-vectored H7N9 avian influenza vaccine are functional in activating the complement system

H7N9 subtype avian influenza virus poses a great challenge for poultry industry.Newcastle disease virus(NDV)-vectored H7N9 avian influenza vaccines(NDV_(vec)H7N9)are effective in disease control because they are protective and allow mass administration.Of note,these vaccines elicit undetectable H7N9-specific hemagglutination-inhibition(HI)but high IgG antibodies in chickens.However,the molecular basis and protective mechanism underlying this particular antibody immunity remain unclear.Herein,immunization with an NDV_(vec)H7N9 induced low anti-H7N9 HI and virus neutralization titers but high levels of hemagglutinin(HA)-binding IgG antibodies in chickens.Three residues(S150,G151 and S152)in HA of H7N9 virus were identified as the dominant epitopes recognized by the NDV_(vec)H7N9 immune serum.Passively transferred NDV_(vec)H7N9 immune serum conferred complete protection against H7N9 virus infection in chickens.The NDV_(vec)H7N9 immune serum can mediate a potent lysis of HA-expressing and H7N9 virus-infected cells and significantly suppress H7N9 virus infectivity.These activities of the serum were significantly impaired after heat-inactivation or treatment with complement inhibitor,suggesting the engagement of the complement system.Moreover,mutations in the 150-SGS-152 sites in HA resulted in significant reductions in cell lysis and virus neutralization mediated by the NDV_(vec)H7N9 immune serum,indicating the requirement of antibody-antigen binding for complement activity.Therefore,antibodies induced by the NDV_(vec)H7N9 can activate antibody-dependent complement-mediated lysis of H7N9 virus-infected cells and complement-mediated neutralization of H7N9 virus.Our findings unveiled a novel role of the complement in protection conferred by the NDV_(vec)H7N9,highlighting a potential benefit of engaging the complement system in H7N9 vaccine design.

Repetitive traumatic brain injury–induced complement C1–related inflammation impairs long-term hippocampal neurogenesis

Repetitive traumatic brain injury impacts adult neurogenesis in the hippocampal dentate gyrus,leading to long-term cognitive impairment.However,the mechanism underlying this neurogenesis impairment remains unknown.In this study,we established a male mouse model of repetitive traumatic brain injury and performed long-term evaluation of neurogenesis of the hippocampal dentate gyrus after repetitive traumatic brain injury.Our results showed that repetitive traumatic brain injury inhibited neural stem cell proliferation and development,delayed neuronal maturation,and reduced the complexity of neuronal dendrites and spines.Mice with repetitive traumatic brain injuryalso showed deficits in spatial memory retrieval.Moreover,following repetitive traumatic brain injury,neuroinflammation was enhanced in the neurogenesis microenvironment where C1q levels were increased,C1q binding protein levels were decreased,and canonical Wnt/β-catenin signaling was downregulated.An inhibitor of C1 reversed the long-term impairment of neurogenesis induced by repetitive traumatic brain injury and improved neurological function.These findings suggest that repetitive traumatic brain injury–induced C1-related inflammation impairs long-term neurogenesis in the dentate gyrus and contributes to spatial memory retrieval dysfunction.

Association of complement components with risk of colorectal cancer:A systematic review and meta-analysis

BACKGROUND Complement components could contribute to the tumor microenvironment and the systemic immune response.Nevertheless,their role in colorectal cancer(CRC)remains a contentious subject.AIM To elucidate the relationship between complement components and CRC risk and clinical characteristics.METHODS Searches were conducted in PubMed,the Cochrane Library,and the China National Knowledge Infrastructure database until June 1,2023.We included cohort studies encompassing participants aged≥18 years,investigating the association between complement components and CRC.The studies were of moderate quality or above,as determined by the Agency for Healthcare Research and Quality.The meta-analysis employed fixed-effects or random-effects models based on the I^(2)test,utilizing risk ratio(RR)and their corresponding 95%confidence interval(CI)for outcomes.Sensitivity and subgroup analyses were performed to validate the robustness of the collective estimates and identify the source of heterogeneity.RESULTS Data from 15 studies,comprising 1631 participants that met the inclusion criteria,were included in the meta-analysis.Our findings indicated that protein levels of cluster of differentiation 46(CD46)(RR=3.66,95%CI:1.75-7.64,P<0.001),CD59(RR=2.86,95%CI:1.36-6.01,P=0.005),and component 1(C1)(RR=5.88,95%CI:1.75-19.73,P=0.004)and serum levels of C3(standardized mean difference=1.82,95%CI:0.06-3.58,P=0.040)were significantly elevated in patients with CRC compared to healthy controls.Strong expression of CD55 or CD59 was associated with a higher incidence of lymph node metastasis,whereas strong CD46 expression correlated with a higher incidence of tumor differentiation compared to low CD46 expression(P<0.05 for all).Although specific pooled results demonstrated notable heterogeneity,subgroup analyses pointed to regional differences as the primary source of inconsistency among the studies.CONCLUSION Our analysis underscores that increased levels of specific complement components are associated with a heightened risk of CRC,emphasizing the potential significance of monitoring elevated complement component levels.

Complement factor Ⅰ knockdown inhibits colon cancer development by affecting Wnt/β-catenin/c-Myc signaling pathway and glycolysis

BACKGROUND Colon cancer(CC)occurrence and progression are considerably influenced by the tumor microenvironment.However,the exact underlying regulatory mechanisms remain unclear.AIM To investigate immune infiltration-related differentially expressed genes(DEGs)in CC and specifically explored the role and potential molecular mechanisms of complement factor I(CFI).METHODS Immune infiltration-associated DEGs were screened for CC using bioinformatics.Quantitative reverse transcription polymerase chain reaction was used to examine hub DEGs expression in the CC cell lines.Stable CFI-knockdown HT29 and HCT116 cell lines were constructed,and the diverse roles of CFI in vitro were assessed using CCK-8,5-ethynyl-2’-deoxyuridine,wound healing,and transwell assays.Hematoxylin and eosin staining and immunohistochemistry staining were employed to evaluate the influence of CFI on the tumorigenesis of CC xenograft models constructed using BALB/c male nude mice.Key proteins associated with glycolysis and the Wnt pathway were measured using western blotting.RESULTS Six key immune infiltration-related DEGs were screened,among which the expression of CFI,complement factor B,lymphoid enhancer binding factor 1,and SRY-related high-mobility-group box 4 was upregulated,whereas that of fatty acid-binding protein 1,and bone morphogenic protein-2 was downregulated.Furthermore,CFI could be used as a diagnostic biomarker for CC.Functionally,CFI silencing inhibited CC cell proliferation,migration,invasion,and tumor growth.Mechanistically,CFI knockdown downregulated the expression of key glycolysis-related proteins(glucose transporter type 1,hexokinase 2,lactate dehydrogenase A,and pyruvate kinase M2)and the Wnt pathway-related proteins(β-catenin and c-Myc).Further investigation indicated that CFI knockdown inhibited glycolysis in CC by blocking the Wnt/β-catenin/c-Myc pathway.CONCLUSION The findings of the present study demonstrate that CFI plays a crucial role in CC development by influencing glycolysis and the Wnt/β-catenin/c-Myc pathway,indicating that it could serve as a promising target for therapeutic intervention in CC.

RELATIVELY COMPLEMENTED DISTRIBUTIVE LATTICE

In this paper, we have proved that for a relatively complemented distributive lattice L,there exists one and only one completion ? of L such that for every ξ∈?, there exists afamily {Sα}α∈△ of non-vacuous subsets of L satisfying ξ= ∨[∧f（Sα）]. Such a completion? is called the entire completion of L. We have in this paper extended the homomorphic extension theorem of a generalizedBoolean lattice to that of a relatively complemented distributive lattice and proved that the lat-tice of the congruences on a relatively complemented distributive lattice is isomorphicwith the lattice of the convex sublattices containing a fixed element and that the entire comple-tion of a relatively complemented distributive lattice L, the lattice of the completable con-gruences on L and the lattice of the completable convex sublattices of L containing a fixed ele-ment are isomorphic.

Finite p-Groups with a Class of Complemented Normal Subgroups

Assume G is a finite group and H a subgroup of G. If there exists a subgroup K of G such that G = HK and H ∩ K = 1, then K is said to be a complement to H in G. A finite p-group G is called an NC-group if all its proper normal subgroups not contained in de（G） have complements. In this paper, some properties of NC-groups are investigated and some classes of NC-groups are classified. Keywords Finite p-groups, normal subgroups, subgroup complement

Tandem Mass Tag-based proteomics analysis reveals the vital role of inflammation in traumatic brain injury in a mouse model

Proteomics is a powerful tool that can be used to elucidate the underlying mechanisms of diseases and identify new biomarkers.Therefore,it may also be helpful for understanding the detailed pathological mechanism of traumatic brain injury(TBI).In this study,we performed Tandem Mass Tag-based quantitative analysis of cortical proteome profiles in a mouse model of TBI.Our results showed that there were 302 differentially expressed proteins in TBI mice compared with normal mice 7 days after injury.Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses showed that these differentially expressed proteins were predominantly involved in inflammatory responses,including complement and coagulation cascades,as well as chemokine signaling pathways.Subsequent transcription factor analysis revealed that the inflammation-related transcription factors NF-κB1,RelA,IRF1,STAT1,and Spi1 play pivotal roles in the secondary injury that occurs after TBI,which further corroborates the functional enrichment for inflammatory factors.Our results suggest that inflammation-related proteins and inflammatory responses are promising targets for the treatment of TBI.

Different serum levels of IgG and complements and recurrence rates in IgG4-positive and negative lacrimal gland benign lymphoepithelial lesion

·AIM:To analyze the differences in immune indicators and prognosis between Ig G4-positive and negative lacrimal gland benign lymphoepithelial lesion(LGBLEL).·METHODS:This was a single-center retrospective clinical study including 105 cases of Ig G4-positive LGBLEL and 41 cases of Ig G4-negative LGBLEL.Basic information,related indicators of peripheral venous blood samples using immunoscattering turbidimetry,treatment(partial surgical excision and glucocorticoid therapy)and prognosis(recurrence and death)were collected.Survival curves for recurrence were created using the Kaplan-Meier analysis.Univariate analysis and multivariate regression analysis were used to analyze prognostic factors.·RESULTS:The mean age was 50.10±14.23y and 44.76±11.43y(P=0.033)in Ig G4-positive and negative group respectively.The serum C3 and C4 was lower in Ig G4-positive group(P=0.005,P=0.002),while the serum Ig G and Ig G2 was higher in Ig G4-positive group(P=0.000 and P=0.008).Twenty-one cases had recurrence in Ig G4-positive group and 3 cases recurrence in Ig G4-negative group.The 5-year recurrence-free cumulative percentages of Ig G4-positive group was 81.85%,and 83.46%in the Ig G-negative group(P=0.216).The history of preoperative glucocorticoid therapy,serum C4,Ig G1 and Ig G2 were the factors affecting recurrence in Ig G4-positive group,while serum C4,and Ig G1 were the factors affecting recurrence of LGBLEL.·CONCLUSION:Serum C4 and Ig G1 are the factors affecting recurrence of LGBLEL,while the Ig G4 does not affect recurrence of LGBLEL.

Association of C-reactive protein and complement factor H gene polymorphisms with risk of lupus nephritis in Chinese population

BACKGROUND Complement overactivation is a major driver of lupus nephritis(LN).Impaired interactions of C-reactive protein(CRP)with complement factor H(CFH)have been shown as a pathogenic mechanism that contributes to the overactivation of complement in LN.However,genetic variations of neither CRP nor CFH show consistent influences on the risk of LN.AIM To examine whether genetic variations of CRP and CFH in combination can improve the risk stratification in Chinese population.METHODS We genotyped six CRP single nucleotide polymorphisms(SNPs)(rs1205,rs3093062,rs2794521,rs1800947,rs3093077,and rs1130864)and three CFH SNPs(rs482934,rs1061170,and rs1061147)in 270 LN patients and 303 healthy subjects.RESULTS No linkage was found among CRP and CFH SNPs,indicating lack of genetic interactions between the two genes.Moreover,CRP and CFH SNPs,neither individually nor in combination,are associated with the risk or clinical manifestations of LN.Given the unambiguous pathogenic roles of the two genes.CONCLUSION These findings suggest that the biological effects of most genetic variations of CRP and CFH on their expressions or activities are not sufficient to influence the disease course of LN.

苦参素联合阿德福韦酯对慢性乙肝患者HBV复制及C3、C-反应蛋白的影响

目的:观察苦参素联合阿德福韦酯治疗对慢性乙肝(CHB)患者补体C3、CRP水平及乙型肝炎病毒(HBV)复制的影响。方法:164例CHB患者按随机数字表法分为观察组84例和对照组80例,两组均给予阿德福韦酯治疗48周,观察组在疗程的前24周联用苦参素。在治疗前、24周和48周分别检测补体C3、CRP及HBV-DNA水平。结果:治疗后24周及48周察组HBV-DNA转阴率均高于对照组(P<0.05);治疗后两组补体C3、CRP水平与治疗前比较均有统计学差异,且观察组补体C3水平高于对照组,CRP水平低于对照组,差异有统计学意义(P<0.05)。结论:苦参素联合阿德福韦酯治疗CHB可显著提高疗效,改善肝脏炎症活动和器官免疫功能。

CD11c分子及其在抗肿瘤免疫中作用的研究进展

树突状细胞（Dendritic cells,DCs）是目前所知体内功能最强大的专职抗原提呈细胞,是连接天然免疫应答和适应性免疫应答的桥梁,也是体内唯一能够激活初始T细胞的APC（Antigen presenting cell）。

Gc、Tf和C_3表型的同步检测

血清蛋白多态性的同步检测可节省检材、简化操作步骤、省时省力.本文用醋酸纤维素薄膜电泳免疫固定法同步检测血清型特异成份（Group-Specific component,Gc）、转铁蛋白（Transferrin,Tf）和补体第三成份（Complment 3,C3）的表型,调查了成都地区汉族116名无亲缘关系的健康献血员的表型频率,现将结果报导如下:

ASYMPTOTICALLY ISOMETRIC COPIES OF l_P (1≤P<∞) AND c_0 IN BANACH SPACES

Let X be a Banach space. If there exists a quotient space of X which is asymptotically isometric to l^1, then X contains complemented asymptotically isometric copies of l^1. Every infinite dimensional closed subspace of l1. contains a complemented subspace of l1 which is asymptotically isometric to l1. Let X be a separable Banach space such that X^＊ contains asymptotically isometric copies of lp （1 〈 p 〈∞）. Then there exists a quotient space of X which is asymptotically isometric to lq （1/p ＋ 1/q=1）. Complemented asymptotically isometric copies of co in K（X, Y） and W（X, Y） are discussed. Let X be a Gelfand-Phillips space. If X contains asymptotically isometric copies of co, it has to contain complemented asymptotically isometric copies of co.

英藏“补语”比较及Complement一词藏译略考

在汉语基础薄弱的偏远藏族农牧区的英文教学中,进行英藏语法直接的比较,对该地区英语教学效果的提高具有积极意义。本文以英文语法教学为主体,旨在通过对英藏基础句法中"Complement"一词的直接对比和语法术语的藏译探讨,望能帮助解决农牧区藏族学生英文教学中对该语法盲点的理解困扰。

STAT3及XRCC4基因多态性与肝细胞癌易感性的关系研究

目的：探讨转录激活因子3（STAT3）及X线修复交叉互补基因4（XRCC4）基因多态性与中国人群肝细胞癌（HCC）易感性的关系。方法采用病例对照研究，以确诊的200例乙型肝炎病毒（HBV）感染相关 HCC 为肝癌组，207例性别及年龄匹配的 HBsAg阳性患者为非肝癌组。采用PCR-限制性长度多态性技术检测STAT3 rs2292152和XRCC4 rs1805377多态性位点的基因型，Logistic回归分析比较不同基因型与 HCC易感风险的关系。结果（1）STAT3 rs2293152位点3种基因型（CC、CG和GG型）在肝癌组分布频率分别为17％（34／200）、49．5％（99／200）和33．5％（67／200），在非肝癌组中分别为18．4％（38／207）、56．5％（117／207）和25．1％（52／207），各基因型在两组之间的差异无统计学意义（P＞0．05）；以CC基因型作参照，携带rs2293152 GG型的个体 HCC患病风险差异无统计学意义（OR＝1．440，95％ CI＝0．800～2．592，P＝0．224）。（2）XRCC4 rs1805377位点3种基因型（AA、GA和GG 型）在肝癌组分布频率分别为61％（122／200）、30％（60／200）和9％（18／200），在非肝癌组中分别为59．9％（124／207）、31．9％（66／207）和8．2％（17／207），各基因型在两组之间的差异无统计学意义（P＞0．05）；以 AA 基因型作参照，携带rs1805377 GG型的个体 HCC 患病风险差异无统计学意义（OR＝1．076，95％ CI＝0．530～2．185，P＝0．839）。结论 STAT3 rs2292152和XRCC4 rs1805377多态性位点可能与中国人群HBV 相关HCC 易感性无密切关系。

FHR4抗体的制备与初步鉴定

目的制备Complemen tfactorH4(FHR4/CFHL4)多克隆和单克隆抗体(mAb),并进行特性鉴定。方法以成人肝cDNA表达文库为模板,构建重组表达质粒pGEX-4T-1-FHR4和PET-32a-FHR4。GST-FHR4融合蛋白在大肠杆菌中高效表达,作为免疫原制备兔多抗和鼠单抗。采用ELISA法和Westernblot鉴定抗FHR4兔抗血清在重组蛋白和天然蛋白中的特异性。采用蛋白印迹,间接免疫荧光,免疫组化鉴定mAb的特异性。结果 GST-FHR4融合蛋白在相对分子质量约58000处呈现明显表达条带。Westernblot鉴定表明,制备的抗FHR4兔多克隆抗体可特异地识别成人肝总蛋白中相对分子质量约37000和45000的FHR4蛋白。获得2株可稳定分泌抗FHR4的杂交瘤细胞株可识别重组人FHR4蛋白,同时可特异性结合HepG2细胞浆中的蛋白和成人肝脏组织肝细胞浆中的蛋白。结论成功制备出兔抗人FHR4抗血清和2株抗FHR4的mAbs,为进一步研究FHR4的功能奠定了基础。

补体在适应性免疫中的调节作用

补体系统在一百多年前被发现,因其在杀菌和吞噬过程中的辅助作用被命名为补体（Complement）,是连接天然和特异性免疫的桥梁。随着研究深入,补体的功能早已超越最初的含义,不再只是免疫系统的配角。肝脏合成的称作系统补体,其他组织细胞产生的则称作局部补体,细胞内部通过其他途径产生的低水平补体被称作细胞内补体,他们在免疫调节中扮演着不同的角色。

中外学习者使役结构使用对比研究——以“make+object+complement”结构为例

中国大学英语学习者在表达使役关系的时候多倾向于使用"make+object+complement"结构,但对中国学生在使用这一结构和本族语者使用这一结构存在哪些差异及其原因的研究却不多。利用WordNeighbors数据库对本族语者使用这一结构的情况进行了调查研究,结果显示:就使用频率而言,本族语者也比较频繁地使用这一结构,但在具体用法上与汉语存在两点不同之处。究其原因,主要是受母语负迁移的影响。研究表明,输入的匮乏是造成中国学习者过度依赖母语的一个原因。