[Experience of Sun's procedure for chronic type B dissection with aortic arch involvement].

Objective: To study the surgical treatment of chronic type B dissection with aortic arch involvement using Sun's procedure. Methods: Between February 2009 and December 2015, 29 patients [20 males, 9 females, with a mean age of (41±12) years, range 24-64 years] with type B dissection with aortic arch involvement underwent Sun's procedure. Sixteen patient had a history of hypertension. Marfan syndrome was observed in 9 cases, coronary artery disease in 3 cases, mitral regurgitation in 3 patients, cerebrovascular disease in one patient. Twenty-two patients suffered proximal aortic arch disease, 4 cases experienced history of aortic root procedure and 2 subjects had history of pregnancy. Four patients had aortic arch malformation. Results: One case suffered from massive cerebral infarction after surgery and died in another hospital. Concomitant procedures included mitral valve replacement in 3 cases, coronary artery bypass grafting in 3 patients, reconstruction of the right aberrant subclavian artery in one patient. Ventilator support exceeding 24 hours obseved in 2 patients. One of them recieved continuous renal replacement therapy and recovered before discharge. Spinal cord injury was obseved in one case, brain infarction in one patient and pericardial drainage in one case. Two patients required tracheotomy. During 12-94 (43±23) months' follow-up, thoracoabdominal aortic replacment was performed in 4 patients, thoracic endovascular aortic repair (TEVAR) in 2 subjects and repair of perivalvular leakage in one patient. Conclusions: Sun's procedure obtained satisfactory results in patients with chronic type B dissection with aortic arch involvement. Concomitant repair of proximal aortic arch lesions and distal type B dissection can be adopted using Sun's procedure.

Cell surface activation of the erythropoietin receptor by Friend spleen focus-forming virus gp55.

The leukemogenic membrane glycoprotein gp55, encoded by Friend spleen focus-forming virus (SFFV), induces erythroid cell proliferation through its interaction with the erythropoietin receptor (EPO-R). There are two forms of gp55 in SFFV-infected cells: an intracellular form (more than 95% of the total protein), which is localized within the endoplasmic reticulum (ER) membranes, and a cell surface form (about 3 to 5%). Because both forms of the viral proteins bind to EPO-R, it is not clear whether the viral protein induces mitogenesis intracellularly or at the cell surface. To address this question, we constructed an EPO-R mutant that contained a 6-amino-acid (DEKKMP) C-terminus ER retention signal. Biochemical and functional analyses with this mutant indicated that it was completely retained in the ER and not expressed at the cell surface. Further analysis showed that the mutant, like the wild-type EPO-R, interacted with SFFV gp55. However, this apparent intracellular interaction between the two proteins failed to induce growth factor-independent proliferation of Ba/F3 cells. Furthermore, spontaneous variants of the ER-retained EPO-R selected on the basis of their ability to induce cell proliferation when coexpressed with gp55 were exclusively expressed at the cell surface. Thus, our results support the hypothesis that the mitogenic activation of the EPO-R by gp55 requires the interaction of the two proteins at the cell surface.