Hypoxia effects on vascular endothelial growth factor derived epithelial cells of nasal polyps]

OBJECTIVE: To understand the role of nasal mucous epithelial cells to hypoxia in early stage of nasal polyps(NP) formation. METHODS: Epithelial cells of NP and inferior turbinate (IT) were cultured without serum under normal oxygen and hypoxia, and stimulus of inflammatory cytokines. Erythropoietin (EPO) was regarded as hypoxia mark, and expression of vascular endothelial growth factor(VEGF) mRNA and protein derived from epithelial cells were detected respectively by in situ hybridization and ELISA. RESULTS: 1. Under hypoxia, EPO mRNA was expressed intensely in epithelial cells from NP and IT, and there was no significant difference between both of them. This result suggested that EPO might be regarded as a hypoxic mark. 2. The ability of producing VEGF mRNA increased with cytokines stimulation, especially under hypoxia. Protein level of VEGF from epithelial cells of NP and IT increased with cytokines stimulation, especially in hypoxia and was time-dependent. CONCLUSION: Epithelial cells actively produce vast VEGF under hypoxia. The VEGF induced by hypoxia of the mucosa in middle meatus is of importance in the formation of nasal polyps(NP) in early stage, which may be the major cause of NP formation in middle meatus.     

胸腰段脊柱脊髓损伤减压与固定相关问题探讨（附166例报告）

目的 对胸腰段脊柱脊髓，马尾神经损伤患者的外科治疗及几种内固定方法的疗效进行探讨。方法 对166例患者的治疗进行回顾分析。该组患者中椎体爆裂性骨折37例，椎体压缩骨折超二分之一109例，椎体骨折脱位14例，多节段或跳跃骨折6例，脊髓损伤按Frankel分级，A级59例，B级46例，C级42例，D级19例，治疗采用后路减压复位122例，前路减压复位，髂骨植骨融合44例。结果 术后123例获3-18个月随访，随访患者中随4例RF钉断裂，5例Harrington上钩脱落，6例棍断裂，其余患者内固定稳固，脊髓，马尾神经恢复，除35例仍为A级外，余脊髓神经功能恢复1-3个级别。结论 各种不同内固定可保持或增强脊柱的稳定，胸腰段脊柱脊髓损伤的外科治疗应根据骨折类型，脊髓及马尾神经损伤程度选择手术入路及内固定材料。     

经皮穿刺髓核成形术治疗腰椎间盘突出症初步临床报道

目的　寻求一种简单、安全、有效、微创的椎间盘突出症治疗方法。方法　对 1 6例腰椎间盘突出症采用经皮穿刺髓核成形术 (Nucleoplasty)治疗 ,并对其疗效进行观察分析。 结果　全部患者经二周至一个月短期随访 ,症状均有不同程度改善 ,疗效优良率为 93 8% ,有效率为 1 0 0 %。未发现明显并发症。结论　髓核成形术是一种先进、安全、有效的椎间盘突出微创手术 ,具有操作简单、安全、微创、疗效佳、恢复快、无需住院等优点。     

Klinische Erfahrungen mit der Knorpel-Knochen-Transplantation

The treatment of deep cartilage defects in load-bearing joints is a problem that still has no satisfactory solution. Full-thickness defects of the articular cartilage rarely heal spontaneously, usually leaving damage that can lead to early arthrosis. Techniques currently available for the treatment of chondral defects include abrasion, drilling, micro-fracturing, transplantation of tissue autografts and allografts, and cell transplantation. Osteochondral autograft transplantation is currently the only surgical cartilage repair technique known to lead to the formation of genuine hyaline articular cartilage and its retention at least in the medium term. The Draenert method, in which a water-cooled diamond bone-cutting system is used, is an effective procedure for resurfacing the joints affected by localised cartilaginous defects, even when there is also severe bone loss. Donor-side morbidity can be kept to a minimum by filling the defect caused by harvesting with a press-fit cylinder of cancellous bone covered with periosteum for protection.     

De-novo expression of vascular ecto-5′-nucleotidase and down-regulation of glomerular ecto-ATPase in experimental chronic renal transplant failure

Ischemic injury plays an important role in chronic renal transplant failure (CRTF). Down-regulation of ecto-adenosine triphosphatase (ATPase) in combination with up-regulation of ecto-5'-nucleotidase is a hallmark of ischemic injury. We studied the expression of renal ecto-5'-nucleotidase and ecto-ATPase in experimental renal transplantation. Fisher 344-to-Lewis allografted rats were either treated with an angiotensin-converting enzyme inhibitor (ACEi) or left untreated. Lewis-to-Lewis syngrafted rats served as controls. Untreated allografted rats developed proteinuria, glomerulosclerosis, and mild intimal hyperplasia. ACEi completely prevented focal and segmental glomerulosclerosis (FGS) and proteinuria, but significantly enhanced intimal hyperplasia. Untreated allografted rats revealed marked vascular ecto-5'-nucleotidase activity, which increased with ACEi. Vascular ecto-5'-nucleotidase activity was absent in syngrafted animals. Ecto-5'-nucleotidase activity correlated well with intimal hyperplasia. Glomerular ecto-ATPase expression was significantly reduced in untreated allografted rats compared to syngrafted rats and correlated well with the extent of FGS. ACEi prevented reduction in glomerular ecto-ATPase. We found de-novo expression of ecto-5'-nucleotidase at sites of renal intimal hyperplasia. Glomerular ecto-ATPase expression was markedly reduced in allografted rats and was prevented by ACEi. These enzyme expression patterns suggest local ischemic damage in experimental CRTF.