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排序方式: 共有221条查询结果,搜索用时 968 毫秒
31.
Egging D van den Berkmortel F Taylor G Bristow J Schalkwijk J 《Archives of dermatological research》2007,298(8):389-396
Tenascin-X (TNX) is a large 450 kDa extracellular matrix protein expressed in a variety of tissues including skin, joints and blood vessels. Deficiency of TNX causes a recessive form of Ehlers–Danlos syndrome characterized by joint hypermobility, skin fragility and hyperextensible skin. Skin of TNX deficient patients shows abnormal elastic fibers and reduced collagen deposition. The mechanism by which TNX deficiency leads to connective tissue alterations is unknown. Here we report that C-terminal domains of human TNX bind to major dermal fibrillar collagens and tropoelastin. We have mapped these interactions to the fibronectin type III repeat 29 (FNIII29) and the C-terminal fibrinogen domain (FbgX) of TNX. In addition we found that FNIII29 of TNX accelerates collagen fibrillogenesis in vitro. We hypothesize that TNX contributes to matrix stability and is possibly involved in collagen fibril formation.Electronic supplementary material Supplementary material is available in the online version of this article at and is accessible for authorized users. 相似文献
32.
目的观察感染性休克患者血浆中弹性蛋白肽(EP)水平的变化,探讨其在感染性休克期间血流动力学改变中所起的作用。方法采集18例感染性休克患者的血样,同时采集同期住院的36例非感染性疾病患者和18名正常人的血样,采用ELISA技术测量血浆弹性蛋白肽的浓度。结果与非感染性疾病患者及正常人相比,感染性休克患者休克期间血浆EP水平明显增高,而非感染性休克患者与正常人之间差异无统计学意义,感染性休克患者在休克好转后血浆EP水平较休克期间明显降低(P〈0.05)。结论感染性休克患者在休克期间血浆EP水平明显增高,增高的EP可能参与了感染性休克血流动力学改变的病理生理过程。 相似文献
33.
N. El ioglu C. Mackie-Ogilvie M. Daker A. C. Berry 《Acta paediatrica (Oslo, Norway : 1992)》1998,87(1):48-53
Williams syndrome is a rare neurodevelopmental disorder with variable phenotypic expression and a contiguous gene syndrome caused by deletion of the elastin gene. In our study, hemizygosity at the elastin locus was investigated using FISH analyses in 16 sporadic cases with a firm clinical diagnosis of Williams syndrome, and the characteristic features were evaluated. Fourteen patients were found to have deletions; 2 further patients did not have deletions of the elastin gene, but did have the clinical features. The presence of two copies of the elastin gene locus in a patient does not rule out Williams syndrome as a diagnosis. Since deletion of the elastin gene, which continues to be a useful confirmatory diagnostic test, cannot account for several features found in Williams syndrome, the non-deletion patients will be valuable in further delineation of the critical region responsible for the Williams syndrome phenotype. 相似文献
34.
Time course of respiratory mechanics and pulmonary structural remodelling in acute lung injury 总被引:2,自引:0,他引:2
Rocco PR Facchinetti LD Ferreira HC Negri EM Capelozzi VL Faffe DS Zin WA 《Respiratory physiology & neurobiology》2004,143(1):49-61
The aim of this study was to evaluate the time course of in vivo and in vitro respiratory mechanics and examine whether these parameters could reflect the temporal changes in lung parenchyma remodelling in paraquat (PQ)-induced lung injury. Measurements were done 1, 3 and 8 weeks after the intraperitoneal (i.p.) injection of saline (control) or paraquat (7mgkg(-1)) in rats. Airway and tissue resistances increased from control in PQ1 and PQ3 and returned to control values in PQ8, in accordance with the magnitude of bronchoconstriction. Viscoelastic/inhomogeneous pressure, tissue elastance, the number of polymorphonuclear cells, and collagen fibre content in lung parenchyma increased in PQ1 and remained elevated in PQ3 and PQ8. Static elastance increased in PQ1, returned to control values after 3 weeks, and was correlated with the volume fraction of collapsed alveoli. In conclusion, there is a restoration of normal alveolar-capillary lung units with a gradual improvement in airway and tissue resistances and static elastance. However, the on-going fibrotic process kept elevated tissue elastance and viscoelastic/inhomogeneous pressure. 相似文献
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38.
C. Herbert Pratt Christopher S. Potter Raoul V. Kuiper Son Yong Karst Soheil S. Dadras Derry C. Roopenian John P. Sundberg 《Experimental and molecular pathology》2017,102(1):128-132
Mus pahari is a wild-derived, inbred mouse strain. M. pahari colony managers observed fragility of this strain's skin resulting in separation of tail skin from the mouse if handled incorrectly. Tail skin tension testing of M. pahari resulted in significantly lowered force threshold for caudal skin rupture and loss in comparison to closely related inbred mouse species and subspecies and even more than a model for junctional epidermolysis bullosa. Histologically, the tail skin separated at the subdermal level with the dermis firmly attached to the epidermis, excluding the epidermolysis bullosa complex of diseases. The dermal collagen bundles were abnormally thickened and branched. Elastin fiber deposition was focally altered in the dermis adjacent to the hair follicle. Collagens present in the skin could not be differentiated between the species in protein gels following digestion with pepsin. Together these data suggest that M. pahari have altered extracellular matrix development resulting in separation of the skin below the level of the dermis with moderate force similar to the African spiny mouse (Acomys spp.). 相似文献
39.
血管钙化是由于高钙磷环境以及局部或全身矿化诱导子上调、抑制子下调所导致的骨特异性羟基磷灰石结晶主动沉积在血管壁的病理过程.在这一过程中,血管壁矿化防御机制被耗竭,平滑肌细胞等间叶细胞丢失原有表型而获得成骨表型,释放矿化脂质小泡.脂质小泡(在动脉壁至少存在基质小泡和凋亡小体两种形式)为钙化结晶提供了合适的成核微环境,而血管壁弹性蛋白则为羟基磷灰石沉积提供了支架结构.因此在钙沉积(成骨细胞样细胞介导)与钙吸收(破骨细胞样细胞介导)之间的平衡被打破后,血管壁内膜、中膜或主动脉瓣膜就可能形成异位钙化.针对钙化形成的机制及钙化危险因素进行干预和调控,有可能对血管钙化的逆转和消退带来有益的影响,尤其是对钙化灶内破骨细胞或破骨细胞样细胞数量与活性的上调可能是一个更有效的治疗策略.但由于骨-血管轴钙化异象的存在,如何将正位骨形成与异位钙吸收有机的协调在一起尚是今后研究的一个难题. 相似文献
40.
Jong-Beom Park Chae-Gwan Kong Kyung-Hwan Suhl Eun-Deok Chang K. Daniel Riew 《Clinics in Orthopedic Surgery》2009,1(2):81-89