Effect of inflammation on adhesive interaction between keratinocytes

Institute of Biochemistry and Physiology of the Cell, Research-Production Center for Medical Biotechnology, Moscow. (Presented by Academician of the Russian Academy of Medical Sciences A. D. Ado). Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 114, No. 7, pp. 32–34, July, 1992.     

中枢、神经—肌肉接头、肌肉疲劳的实验模型及其应用研究

目的：建立研究中枢、神经－肌肉接头和肌肉疲劳动物模型,为各种因素对运动性疲劳的影响及机制的研究,提供一种新的实验方法。方法：用铂金电极刺激蟾蜍脊髓,保护电极刺激坐骨神经干,直刺电极刺激腓肠肌,用MS302实验系统记录坐骨神经干的动作电位和腓肠肌的收缩曲线。观察丹参和生脉注射液对上述疲劳的影响。结果：中枢出现疲劳时间最短;神经－肌肉接头次之;肌肉出现疲劳时间最长。丹参和生脉注射液使中枢、神经－肌肉接头和肌肉出现疲劳时间都相应延长。结论：运动性疲劳首先发生在中枢,其次是神经－肌肉接头,最后是肌肉疲劳,丹参和生脉具有抗疲劳的作用。     

犬陈旧性心肌梗死时连接蛋白43的分布

目的：探讨陈旧性心肌梗死时心肌缝隙连接蛋白43（connexin 43,Cx43)的分布特征。方法：结扎犬冠状动脉造成心肌梗死,术后恢复40－50d,用改良的免疫细胞化学法显示心肌梗死区,边缘带及非缺血区Cx43的分布,半定量分析不同部位Cx43的分布密度。结果：与正常心肌相比,梗死病灶及其邻近区域Cx43的分布出现明显紊乱：梗死中心区Cx43完全消失;边缘带Cx43呈现不均匀消失,少量Cx43分布于岛状或半岛状尚存活的心肌;心肌细胞端－端相接处的Cx43严重消失,而细胞侧－侧相接处的Cx43仍有部分存在。非缺血区Cx43的密度和分布与正常心肌相比无明显改变。结论：陈旧性心肌梗死时Cx43的数量和分布呈现高度不均一性,尤其在边缘带Cx43的分布特点是形成局部传导阻滞和折返性心律失常的结构基础。     

The Wolff-Parkinson-White syndrome: the cellular substrate for conduction in the accessory atrioventricular pathway

The longstanding quest for the anatomical basis of the Wolff-Parkinson-White syndrome has left many unanswered questions. The ultrastructuralmorphology of the myocytes comprising accessory atrioventricularpathways, which are capable of rapid and variable conduction,is central to understanding the development and behaviour ofthis congenital anomaly, but remains unknown. Examination ofthree surgically resected pathways was performed to determinetheir underlying cellular morphology and the pattern of intercellularcoupling, by correlative light microscopy, electron microscopyand confocal scanning laser microscopy combined with immunohistochemicallocalization of the cardiac gap-junctional protein, connexin43. Two left-sided pathways were composed of myocardium of ‘normalworking ventricular’ type. The right-sided pathway wascomposed almost entirely of highly abnormal myocytes characterizedby aberrant myofibril organisation, with a lack of A-band materialand abnormal mitochondria, but normal intact intercalated disksno different from those seen in left-sided pathways. The gapjunctions of all pathways were composed of connexin43 distributedas in ventricular myocardium, and not as found in atrial oratrioventricular nodal tissues. While myocytes of abnormal structure were present in one ofthe accessory atrioventricular pathways examined, all pathwayshad morphologically normal gap junctions, the structures responsiblefor efficient intercellular coupling, with a pattern of distributionsuggestive of working ventricular myocardium.     

High Cervical Disc Lesions in Elderly Patients – Presentation and Surgical Approach

Summary  The incidence of high cervical disc lesions is extremely rare, and the mechanism of their development is unclear. We report these three cases, and discuss the possible mechanisms. We also describe surgical strategies for these lesions.  The first and second cases were an 82-year-old male and an 84-year-old male with retro-odontoid disc hernia. The third was an 83-year-old female with a herniated disc at C2/C3. To investigate Aetiological mechanisms of these lesions, we examined the findings on cervical images in extension and flexion, and compared the results in a younger than 80-year-old group and an older than 80-year-old group.  The patients underwent surgery via a posterolateral intradural approach. Wide laminectomy and incision of the dentate ligaments enabled access to the ventral space of the upper cervical spinal canal and sufficient decompression. All patients became ambulatory postoperatively without special fixation of the cervical spine. In the younger group, the level mostly loaded during cervical movement was C5/6, however, the levels in the older group were C2/3 and C3/4.  In elderly patients, less mobilization of the middle and/or lower cervical spine due to spondylotic change causes overloading at higher levels resulting in high cervical disc lesions. Retro-odontoid disc lesions can be caused by a herniated disc at C2/C3, which migrates upward. Regarding surgical strategy, the posterolateral intradural approach is less invasive and more advantageous for these lesions.     

Expression, distribution and ultrastructural localization of the synapse-organizing molecule agrin in the mature avian retina

At the vertebrate neuromuscular junction the extracellular matrix molecule agrin is responsible for the formation, maintenance and regeneration of most if not all postsynaptic specializations. Several agrin isoforms are generated by alternative splicing which differ in their function and which are all expressed in the CNS. To analyse the role of agrin in the CNS, we investigated the expression and ultrastructural localization of agrin in the posthatched chick retina. In situ hybridization revealed the presence of agrin mRNA in all cellular layers of the mature retina, indicating that most if not all major retinal cell types synthesize agrin. Pan-specific as well as isoform-specific antiagrin antisera stained the optic fibre layer and the outer plexiform layer. However, only the pan-specific antiserum additionally stained the inner limiting membrane. Immunoelectron microscopy showed that in the optic fibre layer agrin was associated with ganglion cell axons and that at least part of this agrin corresponds to a neuronal isoform of agrin. In the outer plexiform layer, agrin was localized in the cleft between the photoreceptor terminals and the invaginating horizontal and bipolar cell dendrites. In the synapse-containing inner plexiform layer both antisera revealed punctate immunoreactivity. This staining corresponded to agrin concentrated in the synaptic cleft of conventional synapses as determined by preembedding immunoelectron microscopy. Agrin is thus concentrated at mature interneuronal synapses as it is at the neuromuscular junction, consistent with a role of agrin during formation and/or maintenance of synapses in the CNS.     

Effects of dexamethasone on the differentiation of membrane structure in cultured astrocytes.

Astrocytic processes investing vascular structures or forming the surface of mammalian brain have large numbers of orthogonally packed aggregates of intramembrane particles, termed "assemblies." Similar particle aggregates are expressed by astrocytes derived from neonatal rat forebrain in secondary culture, but they are much more uniformly distributed across the membranes of the cultured cells. Dexamethasone, a potent glucocorticoid, affects the differentiation of astrocyte membrane structure in two patterns, depending on the rate of proliferation in the culture. When confluent secondary cultures of astrocytes are exposed to 5 microM dexamethasone, the densities of assemblies increase, and in some cells approach the values present in the glial limitans in vivo. However, when rapidly proliferating astrocytes are exposed to dexamethasone during the first week of secondary culture, most of the astrocytes fail to express any assemblies. The rate of astrocyte proliferation is slowed, and a lower cell density is reached during the first 2 weeks of secondary culture in dexamethasone. The suppression of assemblies is transient: as the cultures approach confluence, the proportion of cells expressing assemblies increases to nearly control levels, and the density of assemblies increases to greater than control values in some astrocytes. Certain of the effects of dexamethasone on cultured astrocytes may have relevance for understanding the mechanism(s) of its action in treating cerebral edema.