Gap Balancing Sacrifices Joint-Line Maintenance to Improve Gap Symmetry: A Randomized Controlled Trial Comparing Gap Balancing and Measured Resection

A total knee arthroplasty can be completed using two techniques; measured resection or gap balancing. A prospective blinded randomized controlled trial was completed with 103 patients randomized to measured resection (n=52) or gap balancing (n=51). Primary outcome measure was femoral component rotation. Secondary outcome measures were joint-line change, gap symmetry and function and quality-of-life outcomes. Gap balancing resulted in a significantly raised joint-line compared to measured resection. Gap symmetry was significantly better using gap balancing. Functional outcomes and quality-of-life were not significantly different at 24 months. Using computer navigation, gap balancing significantly raises the joint-line in order to improve gap symmetry. This does not result in a clinical difference in function or quality of life at 24 months.     

Difficult esophageal atresia: Trick and treat

Although most patients with esophageal atresia (EA) and tracheo-esophageal fistula (TEF) may benefit from “standard” management, which is deferred emergency surgery, some may present unexpected elements that change this paradigm. Birth weight, associated anomalies, and long gap can influence the therapeutic schedule of the patients with EA/TEF and can make their treatment tricky. As a consequence, detailed information on these aspects gives the power to develop a decision-making process as correct as possible. In this article, we will review the most important factors influencing the treatment of patients with EA/TEF and will share our experience on the diagnostic and therapeutic tips that may provide pivotal help in the management of such patients.     

氧化苦参碱对大鼠急性心肌梗死诱发室性心律失常的影响

目的探讨氧化苦参碱（OMT）对急性心肌梗死（MI）大鼠诱发室性心律失常（VA）的影响及其可能机制。 方法健康雄性SD大鼠75只,使用数字表法随机分为假手术组（Sham组）、MI组和OMT干预组（OMT组）,每组25只。MI组和OMT组通过结扎冠状动脉左前降支建立MI模型,假手术组开胸但不结扎冠状动脉。OMT组在模型建立前2周及模型建立后2周连续给予OMT（100 mg/kg）灌胃处理。模型建立后2周,行心脏超声检查评估左心功能,酶联免疫吸附法检测血浆N-末端脑钠肽前体（NT-proBNP）和超敏肌钙蛋白T（hs-TnT）水平,分别使用RT-PCR和Western blotting检测心肌缝隙连接蛋白43（Cx43）mRNA和蛋白的表达,采用Burst刺激诱发VA。 结果OMT组NT-proBNP、hs-TnT水平［（256.45±38.55）、（89.55±13.39）ng/L］与MI组［（371.93±41.23）、（132.63±20.12）ng/L］比较明显降低（P＜0.01）。Sham组、MI组与OMT组Cx43 mRNA相对表达量依次为0.93±0.16、0.47±0.06和0.71±0.12,3组Cx43蛋白相对表达量依次为0.77±0.11、0.50±0.07和0.61±0.08,3组p-Cx43蛋白相对表达量依次为0.62±0.09、0.32±0.05和0.50±0.07,差异均有统计学意义（P均＜0.05）。此外,OMT组与MI组比较VA诱发率明显降低（21.4% vs 64.3%,P＜0.05）。 结论OMT可降低MI大鼠心肌的损伤和VA的发生率,其机制可能与OMT调整MI后心肌的Cx43表达有关。     

Ultrastructure of melanocytes in the dark cell area of human vestibular organs: Functional implications of gap junctions,isolated cilia,and annulate lamellae

Background: It is known that melanocytes exist in almost all parts of the inner ear, such as the cochlear duct, stria vascularis, Reissner's membrane, modiolus, vestibular organs in the region surrounding the cristae and maculae, semicircular canals, and pars rugosa of the endolymphatic sac. But there have been few studies using human materials, because of the difficulty of obtaining materials. We attempted to investigate the detailed ultrastructure of melanocytes in the vestibular organs of human inner ear. Methods: Eight surgical specimens obtained from patients with vestibular schwannoma were studied by light microscopy and electron microscopy. Results: Melanocytes were found in the subepithelial layer of the dark cell area. Melanocytes had round or spindle-shaped nuclei and clear cytoplasm with brown pigment granules. Besides melanocytes, there were melanophages, fibroblasts, and small blood vessels. Through electron microscopy we found melanocytes with round-shaped melanosomes in various stages of pigmentation, well-developed Golgi apparatus and endoplasmic reticulum in the cytoplasm, and many cytoplasmic processes. Gap junctions were occasionally found between the cytoplasmic processes. And there were pinocytotic vesicles just under the limiting membrane of melanocytes, and intermediate filaments were abundant in the cytoplasm. Isolated cilia of melanocytes, annulate lamellae, and fusiform banded structures in the connective tissue area around melanocytes were found. Conclusions: Melanocytes in human vestibular organs actively synthesize melanosomes. Frequent findings of isoalted cilia and fusiform banded structures and the incidental existence of annulate lamellae may be an indicator of this metabolically activated state of melanocytes. Moreover, monitoring environmental changes by isolated cilia, melanocytes in the human inner ear could act not only as one cell but also as a group to achieve their physiological functions by means of information transmission through gap junctions. © 1994 Wiley-Liss, Inc.     

间隙连接蛋白43与胎膜早破的相关性

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...     

Cell mediated calcification in collagen gel cultures of fetal rat calvaria cells. Loss of gap junctions precedes calcification

Summary To analyze the mechanism of initiation of cell-mediated calcification in hard tussue and its relationship to the frequency of gap junctions, enzymatically isolated cells from fetal rat calvaria cultured in collagen gels were observed ultrastructurally over a time course. Calcification was observed at 2–3 weeks after the initiation of culture when the seeding cellularity and the concentration of β-glycerophosphate were sufficiently high. In the collagen gels, round cells (R), spindle or stellate cells (S), and fat cells (F) were characterised morphologically. The ultrastructural features of initial calcification could be classified into 4 subtypes: 1) a large mass greater than 10 μm in diameter (Type I), 2) deposition associated with dead R cells or matrix vesicles (Type II), 3) intracellular deposition (Type III), and 4) other than Types I–III (Type IV). Type II was the most frequent (44.5%) and Type III was the least (6.8%). Gap junction was observed frequently between 1) R cells, 2) S cells, 3) between R cells and S cells. The frequency of gap junctions in collagen gels decreased statistically (X²-test; p<0.001), when calcification was initiated. This cell culture system can be regarded as a useful model to analyze the initiation of cell mediated calcification in hard tissue. Gap junctions might function in cell communication and a decrease in their numbers could lead to cell death and, subsequently to calcification.     

血吸虫可溶性虫卵抗原诱发脑血管内皮细胞缝隙连接蛋白Cx37mRNA及蛋白的表达

目的 通过观察血吸虫可溶性虫卵抗原(SEA)孵育培养的脑血管内皮细胞缝隙连接(GJ)蛋白的表达和分布,探讨脑动脉GJ在脑血吸虫病病理发生中的作用。方法 使用血吸虫SEA孵育培养幼兔脑基底动脉血管内皮细胞,实验分对照组、SEA 1～5组：加入SEA（质量浓度分别为10.0％、5.0％、3.3％、2.5％、2.0％）,应用逆转录—聚合酶链式反应(RT-PCR)技术测定兔脑血管内皮细胞GJ蛋白Cx37 mRNA的表达;应用Western 印迹技术测定兔脑血管内皮细胞GJ蛋白Cx37蛋白的表达。结果 对照组和SEA 1 ～5组的GJ蛋白Cx37 mRNA水平分别为0.239±0.037、0.260±0.043、0.218±0.310、0.647±0.040、0.419±0.036、0.513±0.038;其中SEA 3～5组的GJ蛋白Cx37 mRNA水平高于对照组（P均＜0.05）。对照组和SEA 1～5组GJ 蛋白Cx37蛋白表达分别为0.401±0.045、0.485±0.048、0.749±0.052、1.119±0.063、1.015±0.057、0.605±0.047,其中SEA 2 ～5组Cx37蛋白表达高于对照组（P均＜0.05）。结论 血吸虫SEA孵育培养的兔脑血管内皮细胞GJ蛋白Cx37 mRNA及其蛋白水平高于对照组,提示GJ蛋白在SEA及其分泌物浸润脑动脉沉积于脑组织,从而在诱发脑血吸虫病的病理发生机制中可能起重要的作用。     

Cell degeneration is not a primary causer for Connexin26 (GJB2) deficiency associated hearing loss

Connexin26 (Cx26, GJB2) mutations can induce congenital deafness and are responsible for ∼50% of nonsyndromic hearing loss in children. Mouse models show that Cx26 deficiency induces cochlear development disorder, hair cell loss, and spiral ganglion (SG) neuron degeneration. Hair cell loss and cell degeneration have been considered as a primary causer responsible for Cx26 deficiency associated hearing loss. In this study, by coincidental examination of cochlear postnatal development with recording of auditory brainstem response (ABR) and hair cell function, we found that occurrence of hearing loss in Cx26 knockout (KO) mice was ahead of hair cell loss and cochlear cell degeneration. ABR was absent at the whole-frequency range (8–40 kHz) after birth. However, cochlear cells including SG neurons had no significant degeneration throughout postnatal development. Severe cochlear hair cell loss and SG neuron degeneration were only visible in middle and basal turns, i.e., in middle and high frequency regions, in the adult Cx26 KO mouse cochlea. Functional tests show that hair cells in Cx26 KO mice functioned normally; outer hair cells retained electromotility. These data suggest that cell degeneration is not a primary causer of Cx26 deficiency associated hearing loss. Some mechanisms other than cell degeneration, such as cochlear development disorders, may play an essential role in this common hereditary deafness.