Background: Sarcopenia has been proposed as a prognostic factor for various diseases. Patients with critical limb ischemia (CLI) have a very poor prognosis, but sarcopenia has not been reported as a prognostic factor for CLI patients. If sarcopenia is associated with the prognosis of CLI patients, it could help select the treatment plan. Therefore, we examined whether sarcopenia is a prognostic factor for CLI patients. Methods: We performed a retrospective study of CLI patients diagnosed with Fontaine III or IV peripheral artery disease who underwent preoperative computed tomography imaging and revascularization between January 2002 and December 2009. The presence of sarcopenia was defined as skeletal muscle area of <114.0 cm 2 for men or <89.8 cm 2 for women using transverse computed tomography scans at the third lumbar vertebra. We compared the 5-year survival rate and clinical characteristics between patients with or without sarcopenia. We also screened possible prognostic factors for overall survival using hazard ratios (HRs) with 95% confidence intervals (CIs). Results: Of 64 eligible patients, 28 patients had sarcopenia and 36 did not. There were significant differences in age, skeletal muscle area, body mass index, and the presence of smoking, cerebrovascular disease, and hemodialysis between patients with and without sarcopenia (all P < .05). The 5-year survival rate was significantly lower in patients with sarcopenia (23.5% vs 77.5%, P [ .001). Prognostic factors for overall survival were the presence of sarcopenia (HR, 3.22; 95% CI, 1.24-9.11; P [ .02), requirement for hemodialysis (HR, 4.30; 95% CI, 1.60-12.2; P [ .004), and postoperative complications (HR, 5.02; 95% CI, 1.90-13.7; P [ .001). Conclusions: Our results suggest that sarcopenia is a prognostic factor for CLI patients. Exercise and nutritional interventions focusing on improving sarcopenia might be useful treatment options for CLI patients.

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Objective: Arteriovenous fistulae (AVF) are the preferred vascular access for hemodialysis, but the primary success rate of AVF remains poor. Successful AVF maturation requires vascular wall thickening and outward remodeling. A key factor determining successful AVF maturation is inflammation that is characterized by accumulation of both T-cells and macrophages. We have previously shown that anti-inflammatory (M2) macrophages are critically important for vascular wall thickening during venous remodeling; therefore, regulation of macrophage accumulation may be an important mechanism promoting AVF maturation. Since CD4+ T-cells such as T-helper type 1 cells, T-helper type 2 cells, and regulatory T-cells can induce macrophage migration, proliferation, and polarization, we hypothesized that CD4+ T-cells regulate macrophage accumulation to promote AVF maturation. Approach and Results: In a mouse aortocaval fistula model, T-cells temporally precede macrophages in the remodeling AVF wall. CsA (cyclosporine A; 5 mg/kg, sq, daily) or vehicle (5% dimethyl sulfoxide) was administered to inhibit T-cell function during venous remodeling. CsA reduced the numbers of T-helper type 1 cells, T-helper type 2, and regulatory T-cells cells, as well as M1- and M2-macrophage accumulation in the wall of the remodeling fistula; these effects were associated with reduced vascular wall thickening and increased outward remodeling in wild-type mice. However, these effects were eliminated in nude mice, showing that the effects of CsA on macrophage accumulation and adaptive venous remodeling are T-cell-dependent. Conclusions: T-cells regulate macrophage accumulation in the maturing venous wall to control adaptive remodeling. Regulation of T-cells during AVF maturation may be a strategy that can improve AVF maturation.

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Sarcopenia is a risk factor for worse cardiovascular event-free survival, and SAPT and statin therapy reduced this risk for patients with CLI. Furthermore, SAPT but not dual antiplatelet therapy increased cardiovascular event-free survival in patients with sarcopenia.

We report a case of acute type B aortic dissection with the complication of bowel ischemia and abdominal stent graft compression treated by emergency thoracic aortic stent grafting after endovascular aneurysm repair (EVAR) for abdominal aortic aneurysm (AAA). A 69-year-old male was admitted to our hospital for sudden thoraco-abdominal pain. He had past treatment history of EVAR for AAA half a year ago. A computed tomography (CT) showed acute type B aortic dissection, and conservative treatment was initially performed. Three days after occurrence of aortic dissection, worsened abdominal pain and melena were observed. CT showed that the true lumen and abdominal stent graft was compressed by the false lumen. Emergency thoracic endovascular repair (TEVAR) was performed to close the entry tear. After the operation, the image views and the symptoms were improved. The state was still stable 6 months later. TEVAR for acute type B aortic dissection can become one of the effective treatments.

Ecotropic murine leukemia virus (MuLV) infection is initiated by the interaction between the surface glycoprotein (SU) of the virus and its cell-surface receptor mCAT-1. We investigated the SU-receptor interaction by using a naturally occurring soluble SU which was encoded by the envelope (env) gene of a defective endogenous MuLV, Fv-4 r . Binding of the SU to mCAT-1-positive mouse cells was completed by 1 min at 37°C. The SU could not bind to mouse cells that were persistently infected by ecotropic MuLVs (but not amphotropic or dualtropic MuLVs) or transfected with wild-type ecotropic env genes or a mutant env gene which can express only precursor Env protein that is restricted to retention in the endoplasmic reticulum. These cells were also resistant to superinfection by ecotropic MuLVs. Thus, superinfection resistance correlated with the lack of SU-binding capacity. After binding to the cells, the SU appeared to undergo some conformational changes within 1 min in a temperature-dependent manner. This was suggested by the different properties of two monoclonal antibodies (MAbs) reactive with the same C-terminal half of the Fv-4 r SU domain, including a proline-rich motif which was shown to be important for conformation of the SU and interaction between the SU and the transmembrane protein. One MAb reacting with the soluble SU bound to cells was dissociated by a temperature shift from 4 to 37°C. Such dissociation was not observed in cells synthesizing the SU or when another MAb was used, indicating that the dissociation was not due to a temperature-dependent release of the MAb but to possible conformational changes in the SU.At the initial step of virus infection, a virion binds to a specific cell-surface receptor. The receptor binding protein of a virion is the envelope glycoprotein of enveloped viruses or the capsid protein of nonenveloped viruses. After binding, the virion penetrates the cell by crossing the plasma membrane either by fusion between the viral and cellular membranes in enveloped viruses or by lysis or permeabilization of the cellular membrane in nonenveloped viruses. There are two alternative pathways of virus entry: entry occurs either at the outer cell surface membrane or at the endosomal membrane after endocytosis of a virion. These pathways are often referred to as the pH-independent and pH-dependent entries. For viruses using a pH-dependent pathway, the acidification of the endosome is essential to the penetration step. The decreased pH induces conformational changes in the envelope or capsid proteins of a virus to create its active form for penetration (24, 37).Retroviruses have two envelope proteins, a surface glycoprotein (SU) and a transmembrane protein (TM), which are involved in receptor binding and fusion between a virus and a cell. The TM is anchored in the lipid bilayer of the virion. The complex of the SU and TM is held together by disulfide bonds and noncovalent interactions. Most retroviruses use a pH-independent entry pathway, with the exception of ecotropic murine leukemia vi...