缝隙接合部

摘要： 胎膜早破(premature rupture of membranes,PROM)是产科最常见的早产原因之一,可诱发新生儿呼吸窘迫综合征、绒毛膜羊膜炎、胎盘早剥、败血症等不良结局.间隙连接通讯是细胞间最常见的信息交互及物质交换途径,其功能主要由间隙连接蛋白实现,间隙连接蛋白43(Connexin43,Cx43)是间隙连接蛋白家族中最常见且最重要的一类间隙连接蛋白,Cx43的半通道结构可在细胞间进行连接,形成细胞间的完整传输通道,在细胞间缝隙连接、细胞间信息和物质交流及胎膜完整性中发挥重要作用,Cx43在胎膜中的表达与胎膜中Ⅰ、Ⅲ型胶原表达水平有密切关系,并可通过影响Ⅰ、Ⅲ型胶原数量及交联方式而致胎膜薄弱,进而导致胎膜早破.Cx43降低可致胎膜微裂隙发生及扩大进而导致胎膜早破发生,本文就Cx43与胎膜早破的相关性进行综述,以期对胎膜早破的发生机制及防治有进一步认识.

摘要： 脑组织细胞之间存在广泛的缝隙连接蛋白和泛连接蛋白.由神经元、神经胶质细胞和血管细胞构成的神经血管单元通过缝隙连接蛋白和泛连接蛋白构成的细胞膜通道整合和处理信息,从而维持神经系统的动态平衡.脑缺血后,细胞膜通道通过参与兴奋毒性、炎症反应、血脑屏障损伤等病理机制在缺血性脑损伤中发挥着重要作用.因此,维持缝隙连接蛋白和泛连接蛋白的正常功能对于保护神经元免受缺血性脑损伤至关重要.

摘要： 缝隙连接是细胞间信号转导的重要方式.缝隙连接及其所组成的蛋白结构和(或)功能改变与多种疾病相关.运动障碍性疾病作为中枢神经系统的常见疾病,与缝隙连接有一定的关联性,其已成为国内外研究中枢神经系统疾病发病与治疗机制的关键因素.本文就缝隙连接及其与运动障碍性疾病的相关性进行概述.

摘要： Background Connexin43(Cx43) is the major protein of gap junction in the heart.A series of cardiac pathologic processes,such as heart failure and arrhythmias,facilitate Cx43 redistribution to the lateral membrane of the cardiomyocytes from the intercalated disc.The occurrence of gap junctions uncoupling after Cx43 lateralization can lead to reentrant arrhythmias and cardiac dysfunction.Objective To elaborate the molecular mechanisms of myocardial Cx43 lateralization through the process of Cx43 transportation and location.Content The lateralization of Cx43 was proposed to be closely associated with the loss of coupling with connexins (Cxs),i.e.,N-cadherin,desmosomes,Zonula Occludens-1 (ZO-1),and cytoskeletal proteins-mediated forward trafficking of Cx43.Moreover,phosphorylation or acetylation of Cx43 was also involved in its lateralization.This review focusess on the Cxs,cytoskeletal proteins,phosphorylation,and acetylation of Cx43 to show the probable molecular mechanisms of Cx43 lateralization.Trend To provide new ideas and molecular mechanisms for further research into the mechanisms of Cx43 lateralization and the therapy of reentrant arrhythmias.%背景 缝隙连接蛋白43(connexin43,Cx43)是心肌缝隙连接的主要结构,多种心脏病理过程(如缺血/再灌注等)均可使Cx43重分布至侧膜而发生侧膜化.这种侧膜化使缝隙连接脱耦连,导致折返性心律失常,严重影响心脏的功能.目的 旨在从Cx43转运及定位过程来阐述心肌Cx43侧膜化的分子机制.内容 Cx43侧膜化与闰盘处N钙黏蛋白、桥粒、紧密连接蛋白-1(zonulaoccludens-1,ZO-1)等连接蛋白(connexins,Cxs)的解耦连,以及细胞骨架蛋白介导的Cx43重定向转运密切相关;此外,Cx43的磷酸化、乙酰化也参与了侧膜化的过程.从Cxs、细胞骨架蛋白、磷酸化、乙酰化4个方面就Cx43侧膜化的分子机制展开具体讨论.趋向 为进一步研究Cx43侧膜化机制及临床治疗折返性心律失常提供相关思路及分子基础.

摘要： 目的：探讨17β雌二醇（17β-E2）对子宫腺肌病患者子宫内膜-肌层交界区（EMI）平滑肌细胞内游离Ca2+浓度（[Ca2+]i）的调节作用及可能机制。方法选择2011年9月至2012年12月在首都医科大学附属北京妇产医院妇科微创中心因子宫腺肌病行子宫全切除术的患者28例为腺肌病组，选择同期因子宫颈上皮内瘤变（CIN）Ⅲ行子宫全切除术者31例为对照组，对两组患者的EMI平滑肌细胞进行分离及原代培养。应用Ca2+荧光探针Fluo-4/AM负载平滑肌细胞，采用细胞外钙阻断实验、细胞内钙释放阻断实验、细胞膜钙通道阻断实验、细胞膜钙激活钾通道阻断实验阻断引起[Ca2+]i变化的各个环节，利用激光共聚焦显微镜观察17β-E2诱导后的两组患者EMI平滑肌细胞内[Ca2+]i的变化，其变化程度以ΔF[Ca2+]i表示。结果（1）在常规有Ca2+培养基中，17β-E2诱导后腺肌病组和对照组EMI平滑肌细胞内Ca2+荧光强度均明显高于其17β-E2诱导前，腺肌病组ΔF[Ca2+]i为384±26，对照组ΔF[Ca2+]i为235±20，两组比较，差异有统计学意义（P=0.001）；细胞外钙阻断实验显示，细胞外无Ca2+时，腺肌病组ΔF[Ca2+]i为207±17，对照组ΔF[Ca2+]i为221±19，两组比较，差异无统计学意义（P=0.731）。腺肌病组ΔF[Ca2+]i在细胞外有Ca2+时明显高于无Ca2+时，差异有统计学意义（P=0.000）；而对照组两者比较，差异无统计学意义（P=0.060）。（2）细胞内钙释放阻断实验显示，阻断肌质网钙库上三磷酸肌醇（IP3）敏感的钙释放通道、肌质网利阿诺定（Ryanodine）受体（RyR）钙释放通道、肌质网钙泵释放后，腺肌病组和对照组ΔF[Ca2+]i分别与其阻断前相比均明显降低（P0.05）。结论17β-E2通过内源性钙库释放Ca2+和细胞膜L-型钙通道介导的Ca2+内流导致子宫腺肌病患者EMI平滑肌细胞内游离[Ca2+]i异常增高，[Ca2+]i调节异常导致的子宫收缩功能障碍可能参与子宫腺肌病的发生、发展。%Objective To investigate the regulation mechanism of estrogen on the free calcium of smooth muscle cells at the endometrial-myometrial interface (EMI) in uteri with adenomyosis. Methods From September 2011 to November 2012, 59 uterine myometrial specimens were obtained from 59 cases underwent hysterectomy, including 28 adenomyosis patients as adenomyosis (ADS) group and 31 patients with cervical intraepithelial neoplasia Ⅲ as control group. EMI smooth muscle cells were cultured and loaded with calcium ion fluorescent probe fluo-4/AM. After treated with trisphosphate (IP3) receptor antagonist, blocker of sarcoplasmic reticulum calcium-adenosine triphosphate (ATP), depleted agent of the ryanodine receptor-operated Ca2+, inhibitor of L-type calcium channel, inhibitor of Na+-Ca2+exchanger, the labeled cells were stimulated with estrogen. The changes of intracellular Ca2+fluorescence intensity were detected by laser scanning microscopy. The changes of intracellular Ca2+concentration was indicated byΔF[Ca2+]i. Results (1) Under normal calcium conditions, after the stimulation of estrogen, intracellular Ca2+fluorescence intensity in ADS group and control group both increased than those without estrogen. TheΔF[Ca2+]i in ADS group was 384±26, and in the control groupΔF[Ca2+]i was 235±20. TheΔF[Ca2+]i in ADS group was higher than that in the control (P0.05). But, the ΔF[Ca2 +]i in ADS group was significantly reduced after treatment compared to before treatment, (211 ± 19 vs 384 ± 28; P=0.001). The increase in control group was almost the same with before (203±16 vs 234±22, P=0.141). (4) After treated with inhibitor of Na+-Ca2+exchanger, theΔF[Ca2+]i in ADS group was 357 ± 24 and in the controlΔF[Ca2+]i was 209±19. The increase in ADS group was significant higher than that in the control (P=0.000). Compared withΔF[Ca2+]i on the condition without treating with inhibitor of Na+-Ca2+exchanger,ΔF[Ca2+]i was 363±21 in ADS group andΔF[Ca2+]i was 237±20 in control group after treatment. When compared with before treatment, there was no significant difference in both groups (P>0.05). Conclusions The increase of intracellular Ca2+induced by estrogen at EMI smooth muscle cells in adenomyosis patients was mostly from the release of arcoplasmic reticulum, and also from the Ca2+influx controlled by L-type calcium channel. The increase of Ca2+inducing abnormal contraction of EMI muscle may have relationship with the development of adenomyosis.

摘要： 缝隙连接参与了细胞间电信号传递的电偶联和物质交换的代谢偶联,长期高血糖导致患者缝隙连接蛋白结构及表达发生改变,机体神经再生、血管生理功能及伤口愈合发生障碍,同时促进血管动脉粥样硬化形成.这些病变是糖尿病患者足部发生溃疡或坏疽的重要原因.本文就缝隙连接在糖尿病足发生发展中的研究进展进行文献综述.

摘要： 目的探讨缝隙连接功能异常在左旋多巴诱发异动症( LID)发生机制中的作用。方法对6-羟多巴胺制备的偏侧帕金森病大鼠模型重复腹腔注射左旋多巴(20 mg/kg )和卞丝肼(10 mg/kg)共21 d,以建立左旋多巴诱发异动症模型。将实验动物分为3组：LID组、帕金森病组、正常对照组。通过腹腔注射甘珀酸和侧脑室注射奎宁来观察缝隙连接阻断剂对异动症大鼠行为学的影响。免疫双标法分析脑啡肽阳性纹状体传出神经元及小清蛋白( parvalbumin)阳性中间神经元缝隙连接蛋白36(connexin 36,Cx36)的表达情况。蛋白质印迹检测纹状体及运动皮质Cx36蛋白水平的表达。结果行为学研究显示大剂量(>60 mg/kg )的甘珀酸腹腔注射和奎宁侧脑室注射(0.5、1.0、2.0μmol/L,>2.5μmol/L)能减少异动症大鼠的不自主运动评分,蛋白质印迹检测显示异动症大鼠损毁侧纹状体和运动皮质Cx36表达水平分别为219.56%依18.12%、226.03%依16.33%,高于正常对照组(104.05%依3.82%,t=15.389,P60 mg/kg) intraperitoneal injection and intracerebroventricular injection of quinine ( 0.5, 1.0, 2.0 μmol/L, > 2.5 μmol/L ) could decrease the AIM score of LID rats. Western blotting indicated that expression of Cx36 in lesioned striatum and motor cortex of LID rat model was 219.56% ±18.12% and 226.03% ±16.33%, respectively, which induced a significant upregulation in comparison with the normal control group (104.05% ±3.82%, t=15.389, P<0.01;105.27% ±2.82%,t=8.074, P<0.01) and untreated PD group (119.31% ±8.92%, t=13.356, P<0.01; 138.20% ±17.88%, t=5.872, P<0.01). Double immunofluorescence labeling staining revealed that Cx36 expression was increased in Enk-positive striatum neurons in LID model ( 57.59% ±5.36%) compared with that in normal control group (32.67% ±4.22%) and PD group (37.24% ±0.86%, F=78.060, P<0.01). The expression of Cx36 in PV-positive interneurons was also elevated in LID group (68.49% ±11.60%) in comparison with normal control group ( 40.43% ± 2.30%) and PD group ( 31.92% ± 5.68%, F = 39.567, P < 0.01 ).Conclusions The Cx36 expression is generally increased in lesioned striatum and motor cortex of LID rat model. In the striatum, the up-regulation of Cx36 is specifically observed in Enk-positive striatum neurons and in PV-positive interneurons. The dyskinesia behavior of LID rats can be significantly reduced by treatment with gap junction blockade. All these results suggest that gap junction dysfunction may play an important role in the pathogenesis of LID.

摘要： Background The mechanism of myocardial ischemia/reperfusion (I/R) involves in peroxidation,calcium overload,mitochondria injury,myocardial cells apoptosis and so on.Recent sdudies indicate that the gap junctional(GJ) intercellular communication of myocardial cells may play a role in myocardial I/R injury.Objective This article summarized the relationship between the GJ connexin (Cx) 43 and myocardial I/R injury.Content Cx43 could protected myocardium from I/R injury.The mechanism may be related with calcium overload,mitochondria injury,myocardial cells apoptosis and so on.Trend Researches in future should be taken to further explore of the relation between Cx43 and apoptosis,and strengthen the cilinial applications.%背景 研究表明,心肌缺血/再灌注(ischemia/reperfusion,I/R)损伤的发病机制与氧自由基过量产生、钙超载、线粒体损伤及心肌细胞凋亡等密切相关,最新研究发现缝隙连接(gap junction,GJ)也参与心肌I/R损伤. 目的 现主要针对GJ连接蛋白(connexin,Cx)43与心肌I/R损伤的关系作一综述. 内容 Cx43在心肌I/R损伤中参与心肌保护作用,其机制可能与钙超载、在线粒体中的分布及细胞凋亡等因素相关. 趋向 未来研究需要进一步探究Cx43与心肌细胞凋亡之间的关系,同时为临床实际工作提供依据.

摘要： 目的 观察缝隙连接蛋白36(Cx36)在帕金森病模型大鼠纹状体和运动皮质区的表达变化,并探讨缝隙连接功能异常与帕金森病基底节环路功能紊乱间的关系.方法 采用6-羟多巴胺注射法建立帕金森病动物模型,免疫组织化学染色及Western blotting法检测纹状体及运动皮质区Cx36表达变化,免疫荧光双标染色进一步分析纹状体脑啡肽阳性传出神经元及Parvalbumin阳性中间神经元Cx36表达变化.结果 (1)免疫组织化学染色显示,帕金森病组大鼠右侧纹状体及运动皮质区Cx36表达水平高于正常对照组(均P＜0.05).(2)免疫荧光双标染色显示,纹状体脑啡肽阳性神经元数目和Cx36表达水平高于正常对照组(均P＜ 0.05),而Parvalbumin阳性神经元数目和Cx36表达水平低于正常对照组(均P＜0.05).(3)Western blotting法检测显示,帕金森病组大鼠右侧纹状体[(119.31±8.92)％]及运动皮质区[(138.20± 17.88)％] Cx36表达水平高于正常对照组[(104.05±3.82)和(105.27±2.82)％,均P＜0.05].结论 帕金森病大鼠右侧纹状体及运动皮质区Cx36表达水平升高,纹状体脑啡肽阳性传出神经元Cx36表达上调,Parvalbumin阳性中间神经元Cx36表达下调.提示缝隙连接异常可能参与帕金森病皮质-基底节-皮质环路功能紊乱的发生机制.%Objective To observe the expression of connexin 36 (Cx36) in the striatum and motor cortex of rat model of Parkinson's disease (PD) in order to explore whether gap junction is involved in the pathogenesis of the cortex-basal ganglia circuit disturbances in PD.Methods Hemi-parkinsonian rat model was produced by stereotaxically injecting 6-hydroxydopamine (6-OHDA) to right medial forebrain bundle (MFB).Immunohistochemical staining and Western blotting analysis were used to observe the expression changes of Cx36 in the striatum and motor cortex.Double immunofluorescence labeling was used to analyze the expression of Cx36 in enkephalin (ENK) positive medium spiny neurons and Parvalbumin (PV) positive interneurons in the striatum.Results Immunohistochemical staining showed Cx36 expression was elevated in the right striatum as well as right motor cortex of PD group compared with normal control group (t =2.474,P =0.048; t=2.614,P =0.040).Double immunofluorescence labeling staining revealed that ENK-positive striatum neurons were elevated (t =3.987,P =0.007) and Cx36 expression was increased in ENK-positive striatum neurons (t =3.271,P =0.017) in PD group compared with normal control group.While PV-positive interneurons decreased (t =2.777,P =0.032) and Cx36 expression was down-regulated in PV-positive interneurons (t =2.624,P =0.039) compared with the normal control group.Western blotting indicated that the 6-OHDA lesion induced a significant upregulation of Cx36 to (119.31 ± 8.92)％ in comparison with the normal group [(104.05 ± 3.82)％] in right striatum (t =3.516,P =0.024).In right motor cortex Cx36 increased to (138.20 ± 17.88)％,induced a significant upregulation of Cx36 in the right motor cortex in comparison with the normal control group [(105.27 ± 2.82)％; t =4.068,P =0.015].Conclusion The Cx36 expression was generally increased in the striatum and motor cortex of PD rat model,with upregulation in ENK-positive striatum neurons but downregulation in PV-positive interneurons,suggesting that gap junction dysfunction may play an important role in the disturbance of cortex-basal ganglia pathway in PD.

摘要： 目的:探讨纳米银中可溶性银离子对皮肤细胞HaCaT间隙连接通讯的影响.方法:将1 g/L纳米银储备液于4°C,20 000 ×g离心2h后,吸取上清作为银离子储备液,采用电感耦合等离子体质谱法测定其中银离子含量.采用细胞划痕染料标记示踪技术检测细胞间隙连接通讯的改变；分别采用蛋白免疫印迹和实时荧光定量PCR技术检测连接蛋白43(connexin 43,Cx43)及其mRNA表达的变化.结果:不同浓度银离子(0.01、0.1和1.0 mg/L)对HaCaT细胞间隙连接通讯无明显影响.进一步的研究发现,经上述不同浓度银离子作用后,细胞Cx43蛋白及mRNA水平均无明显改变.结论:纳米银材料中可溶性银离子对HaCaT细胞间隙连接通讯的影响及其作用特征可能与纳米银不同.%Objective:To further investigate the effects of silver ion (Ag +) dissolved from silver nanoparticles (AgNps) on gap junctional intercellular communication (GJIC) between HaCaT cells.Methods:In this study,20 000 × g of 1 g/L AgNps suspension were centrifuged at 4 C for 2 h,then the supernatant was collected as Ag+ stock solution and measured by inductively coupled plasma massspectrometry (ICP-MS) ; GJIC was detected by the scrape loading/dye transfer assay; connexin 43(Cx43) protein and mRNA level were estimated by Western-blot and RT-PCR,respectively.Results:Different concentrations of Ag+ (0.01,0.1 and 1.0 mg/L) did not affect the GJIC significantly.No notable changes were observed in expression of Cx43 protein and mRNA.Conclusion:The characteristics of Ag+ and the effects on gap junctional intercellular communication between HaCaT cells may be different from those of AgNps.

摘要： 本发明涉及一种方法，用于连接两个利用纤维增强的塑料材料构成的机身部段(1，2，21，22)、特别是飞机机舱的被卷绕的机身部段(1，2，21，22)，机身部段在形成横向接合部(5，30)的情况下具有多个在内部彼此平行均匀间隔分布地布置在蒙皮(3，4，25，26)上的纵梁(10，11，35，36)。特别为了可以接合被卷绕的CFK机身部段，其中在连续的、工业的制造过程中能够实现简单的公差补偿，根据本发明的方法包括的步骤是：将第一和第二机身部段(1，2，21，22)彼此对齐；这样地加热和调整至少一个利用纤维增强的热塑性的塑料材料构成的横向连接板(9，23)，即可以在第一和第二机身部段(1，2，21，22)的有偏差的横截面几何结构之间实现公差补偿或者加热利用纤维增强的热塑性的塑料材料构成的第二机身部段(2，22)的至少一个端部区域(27)；和将两个机身部段(1，2，21，22)接合在一起。

摘要： 本公开提供了一种总成，该总成包括齿形上基板，该齿形上基板限定多个交替的槽和脊。下基板设置于邻近齿形上基板处，以及粘合材料设置于齿形上基板和下基板之间。紧固件延伸穿过齿形上基板的槽、穿过粘合材料并进入下基板内。本公开还提供一种装配上基板和下基板的方法，其包括使齿形上基板塑性变形以减少基板间的空气吸入。

摘要： 本发明涉及铰链接合部、将其装配的方法和带铰链接合部的眼镜。在此，铰链接合部具有：‑罐形的圆柱体，其具有圆柱体轴线；‑铰链销，其在已装配的状态中以如下方式布置在圆柱体中，即，铰链销纵轴线基本上沿着圆柱体轴线取向并且铰链销能绕圆柱体轴线转动；‑衬套，其在已装配的状态中布置在圆柱体中，以便与配对支座一起固定住铰链销在圆柱体中的取向，其中，罐形的圆柱体具有底部，配对支座构造在该底部中，并且其中，罐形的圆柱体具有沿着圆柱体的周长延伸的圆柱体周面凹口，为了装配铰链接合部，能经由该圆柱体周面凹口将铰链销引入到圆柱体中。

摘要： 本发明涉及一种方法，用于连接两个利用纤维增强的塑料材料构成的机身部段(1，2，21，22)、特别是飞机机舱的被卷绕的机身部段(1，2，21，22)，机身部段在形成横向接合部(5，30)的情况下具有多个在内部彼此平行均匀间隔分布地布置在蒙皮(3，4，25，26)上的纵梁(10，11，35，36)。特别为了可以接合被卷绕的CFK机身部段，其中在连续的、工业的制造过程中能够实现简单的公差补偿，根据本发明的方法包括的步骤是：将第一和第二机身部段(1，2，21，22)彼此对齐；这样地加热和调整至少一个利用纤维增强的热塑性的塑料材料构成的横向连接板(9，23)，即可以在第一和第二机身部段(1，2，21，22)的有偏差的横截面几何结构之间实现公差补偿或者加热利用纤维增强的热塑性的塑料材料构成的第二机身部段(2，22)的至少一个端部区域(27)；和将两个机身部段(1，2，21，22)接合在一起。

摘要： 一种用于将第一部件(10)紧固到第二部件(30)的接合部(20)，包括由复合材料制成的紧固套管(22)和紧固插入件(24)，该紧固套管旨在至少包覆模制在第一部件(10)的一部分上并且包括旨在支承在第二部件(30)上的支承表面(22c)，所述紧固插入件沿着与套管(22)的支承表面(22c)基本垂直的延伸轴线(Y2‑Y2)延伸并用于紧固到第二部件(30)，所述紧固套管(22)围绕所述插入件(24)包覆模制。

摘要： 具备焊料接合部的寿命预测部件的控制装置(10)具备：温度传感器(3)，测量驱动加热器(7)及马达(9)的电子电路基板的焊料接合部的温度；存储部(51)，存储基准加速系数，该基准加速系数是基于搭载电子电路基板的电子设备的热冲击试验的试验条件及电子设备的使用环境下的基准条件的加速系数；运算部(52)，根据从加热器(7)或马达(9)的驱动的开始至结束为止的1个循环中的焊料接合部的温度变化幅度及最高到达温度计算实际加速系数，针对从负载的驱动的开始至结束为止的每1个循环，累计将实际加速系数除以基准加速系数得到的加速系数比，求出加速系数比的累计值；及判定部(53)，比较加速系数比的累计值与阈值，预测焊料接合部的寿命。

摘要： 公开了一种用于包括结构部件(1、2)的离岸框架构筑物的结构接合部。在结构部件(1、2)之间的结构接合部包括叉部(3)、耳部(4)和销钉(5)。所述叉部和所述耳部包括孔，孔设置为用于容纳所述销钉。还公开了一种用于组装包括结构部件(1、2)的离岸框架构筑物的方法，以及结构接合部在离岸风力涡轮机基础中用于结构的柱体和支架之间连接的应用。

摘要： 公开了机翼与机身接合部和包括该接合部的飞机。一种飞机，包括：具有外机身蒙皮的机身，该外机身蒙皮至少部分地限定机身的外表面；以及机翼组件，经由机翼与机身接合部可操作地耦接至机身。机翼组件包括具有左下翼区域蒙皮和左上翼区域蒙皮的左翼区域、具有下右翼区域蒙皮和上右翼区域蒙皮的右翼区域以及具有下中心翼区域蒙皮的中心翼区域。外机身蒙皮与下中心翼区域蒙皮共同延伸。

摘要： 目的在于使得能够将金属线制带状构件以稳定的状态收纳于模具内。准备模具，该模具具备形成有凹部的下模具和形成有凸部的上模具，凸部能够以封堵凹部内的上方空间的方式配置在凹部内，凹部的内表面包括中央模具面和一对弯曲引导模具面，中央模具面形成于凹部的底部的宽度方向中央，一对弯曲引导模具面在中央模具面的两侧相连设置，并以向外侧凸出的方式弯曲，中央模具面形成为平面或比一对弯曲引导模具面更平缓地弯曲的面。将金属线制带状构件的接合加工部分对折而配置在凹部内，在凸部与凹部之间将金属线彼此接合。

摘要： 本公开提供了一种总成，该总成包括齿形上基板，该齿形上基板限定多个交替的槽和脊。下基板设置于邻近齿形上基板处，以及粘合材料设置于齿形上基板和下基板之间。紧固件延伸穿过齿形上基板的槽、穿过粘合材料并进入下基板内。本公开还提供一种装配上基板和下基板的方法，其包括使齿形上基板塑性变形以减少基板间的空气吸入。