Comparison of Eversion Carotid Endarterectomy and Patch Carotid Endarterectomy: A Retrospective Study of 6 Years of Experience.

BACKGROUND The aim of this study was to compare early and long-term results of eversion carotid endarterectomy (e-CEA) and patch carotid endarterectomy (p-CEA). MATERIAL AND METHODS In a retrospective study, we collected data on 441 patients who underwent CEA (e-CEA=211 vs. p-CEA=230) between October 2009 and October 2015 at our institute. Economic costs, postoperative hospital days, use of shunts and antibiotics, early (30-day) complications, long-term restenosis, and mortality rates were compared between groups during 4 to 76 months of follow-up. RESULTS Patients in the p-CEA group had a significantly higher percentage of antibiotic use (58.3% vs. 27%, respectively; P0.05). Long-term complication, including stroke or heart attack, recurrent stenosis rate, and mortality rate, showed no difference between the 2 groups (all P>0.05). Kaplan-Meier analysis shows that the recurrent stenosis-free and survival rates were not significantly different between the 2 groups (P=0.867, P=0.177, respectively). CONCLUSIONS The adverse event rates of perioperative and long-term follow-up showed no significant difference between the e-CEA and p-CEA groups. Both e-CEA and p-CEA are effective for carotid artery stenosis.

Differential regulation of T and B lymphocytes by PD-1 and SOCS-1 signaling in hepatitis C virus-associated non-Hodgkin's lymphoma.

HCV infection is associated with immune dysregulation and B cell Non-Hodgkins lymphoma (HCV-NHL). We have previously shown in vitro that HCV core protein differentially regulates T and B cell functions through two negative signaling pathways, programmed death-1 (PD-1) and suppressor of cytokine signaling-1 (SOCS-1). In this report, we performed a detailed immunologic analysis of T and B cell functions in the setting of HCV-NHL. We observed that T cells isolated from patients with HCV-NHL exhibited an exhausted phenotype including decreased expression of viral-specific and non-specific activation markers; whereas B cells exhibited an activated phenotype including over-expression of cell activation markers and immunoglobulins compared to healthy subjects. Individuals with HCV alone or NHL alone exhibited abnormal T and B cell phenotypes, but to a lesser extent compared to HCV-NHL. This differential activation of T and B lymphocytes was inversely associated with the expression of PD-1 and SOCS-1. Interestingly, blocking PD-1 during TCR activation inhibited SOCS-1 gene expression, suggesting that these regulatory pathways are linked in T cells. Importantly, blocking PD-1 also restored the impaired T cell functions observed in the setting of HCV-NHL. These results support a coordinated mechanism by which HCV might cause immune dysregulation that is associated to HCV-NHL.

PD-1 modulates regulatory T cells and suppresses T-cell responses in HCV-associated lymphoma.

T regulatory (T(R)) cells suppress T-cell responses that are critical in the development of chronic viral infection and associated malignancies. Programmed death-1 (PD-1) also has a pivotal role in regulation of T-cell functions during chronic viral infection. To examine the role of PD-1 pathway in regulating T(R)-cell functions that inhibit T-cell responses during virus-associated malignancy, T(R) cells were investigated in the setting of hepatitis C virus-associated lymphoma (HCV-L), non-HCV-associated lymphoma (non-HCV-L), HCV infection alone and healthy subjects (HS). Relatively high numbers of CD4(+)CD25(+) and CD8(+)CD25(+) T(R) cells, as well as high levels of PD-1 expressions on these T(R) cells were found in the peripheral blood of subjects with HCV-L compared with those from non-HCV-L or HCV alone or HS. T(R) cells from the HCV-L subjects were capable of suppressing the autogeneic lymphocyte response, and depletion of T(R) cells in peripheral blood mononuclear cells from HCV-L improved T-cell proliferation. Additionally, the suppressed T-cell activation and proliferation in HCV-L was partially restored by blocking the PD-1 pathway ex vivo, resulting in both a reduction in T(R)-cell number and the ability of T(R) to suppress the activity of effector T cells. This study suggests that the PD-1 pathway is involved in regulating T(R) cells that suppress T-cell functions in the setting of HCV-associated B-cell lymphoma.