Reverse geometry shoulder replacement for proximal humeral metastases

The management of skeletal metastases can be challenging for the orthopaedic surgeon. They represent a significant source of pain and disability for cancer patients, adding to the morbidity of their condition. Treatment is directed at the alleviation of symptoms and the restoration of function. Metastatic involvement of the proximal humerus can be especially debilitating, having the potential to cause severe pain and loss of function. We present a report of three such cases where reverse geometry proximal shoulder replacement was used to provide a pain free functional range of movement in patients with concomitant rotator cuff disease. In all cases, significant symptomatic relief was achieved postoperatively with preservation of upper limb function. No surgical complications were noted. It is our belief that this novel surgical strategy provides a valuable and effective option for the management of proximal humeral metastatic disease in the rotator cuff deficient patient.     

茶碱减少肺泡间隔厚度以改善高氧暴露新生大鼠肺发育的研究(英文)

目的明确高氧暴露新生大鼠肺组织的肺泡间隔增厚是否由肺泡间隔细胞凋亡抑制引起,进一步研究茶碱是否可以通过减少肺泡间隔厚度改善高氧暴露新生大鼠的肺发育。方法建立新生SD大鼠高氧暴露(85%O2)肺损伤模型,将新生大鼠随机分为3组。①新生大鼠每日注射生理盐水并予高氧暴露;②新生大鼠每日注射生理盐水并置正常空气中;③新生大鼠注射茶碱20 mg/(kg.d)并予高氧暴露。并运用TUNEL法检测肺泡间隔中的凋亡细胞,用免疫组织化学技术检测肺泡间隔中的肌成纤维细胞。结果高氧暴露7 d的新生大鼠肺组织肺泡间隔增厚,肺泡间隔细胞凋亡减少,肺泡间隔肌成纤维细胞数量增加;而茶碱可以使高氧暴露后新生大鼠肺组织肺泡间隔细胞变薄,肺泡间隔细胞凋亡增加,肺泡间隔肌成纤维细胞减少。结论茶碱可以通过减少肺泡间隔厚度,减少肺泡间隔内的肌成纤维细胞数量,进而改善高氧暴露新生大鼠的肺发育。增加肺泡间隔细胞凋亡可能是茶碱的作用机制之一。肌成纤维细胞作为一种重要的间质细胞,可能在高氧引起的肺泡间隔细胞凋亡异常及肺泡间隔增厚等变化中起重要作用。[临床儿科杂志,2010,28(12):1101-1107]     

Double-stranded RNA induces sickle erythrocyte adherence to endothelium: a potential role for viral infection in vaso-occlusive pain episodes in sickle cell anemia

Vaso-occlusive pain episodes in sickle cell anemia are hypothesized to be precipitated by adherence of sickle erythrocytes to vascular endothelium in the microcirculation. Febrile episodes, thought to be viral in etiology, are frequently associated with vaso-occlusion; however, a direct link between viral infection and vascular occlusion has not yet been established. Many pathogenic viruses contain double- stranded RNA or replicate through double-stranded RNA intermediates. Double-stranded RNA has been shown to induce vascular cell adhesion molecule-1 (VCAM-1) protein expression on endothelial cells. Recently, a new adhesion pathway has been described between VCAM-1 expressed on cytokine stimulated endothelium and the alpha 4 beta 1 integrin complex expressed on sickle reticulocytes. Based on these observations, the hypothesis was developed that viral infection, through double-stranded RNA intermediates, increases endothelial VCAM-1 expression leading to sickle erythrocyte adhesion to endothelium via an alpha 4 beta 1-VCAM-1- -dependent mechanism. In support of this hypothesis, endothelial cells exposed to the synthetic double-stranded RNA poly(I:C) or the RNA virus parainfluenza 1 (Sendai virus) express increased levels of VCAM-1 and support increased sickle erythrocyte adherence under continuous flow at 1.0 dyne/cm2 shear stress as compared with unstimulated endothelium. Blocking antibodies directed against either VCAM-1 on the endothelium or alpha 4 beta 1 on sickle erythrocytes inhibit nearly all of the increased sickle cell adherence caused by poly(I:C) or Sendai virus. These results support the hypothesis that viruses, through double- stranded RNA elements, can induce sickle erythrocyte adherence to endothelium through alpha 4 beta 1-VCAM-1--mediated adhesion and provide a potential link between viral infection and microvascular occlusion precipitating sickle cell pain episodes.