The outcomes of carbon dioxide digital subtraction angiography for percutaneous transluminal balloon angioplasty of access circuits and venous routes in hemodialysis patients.

The outcomes of carbon dioxide digital subtraction angiography (CO2-DSA) for performing percutaneous transluminal balloon angioplasty (balloon PTA) in hemodialysis patients has not been fully clarified. The purpose was to compare the outcomes of balloon PTA of hemodialysis shunts in terms of vessel patency between patients treated using CO2-DSA and conventional digital subtraction angiography using iodine contrast medium (C-DSA).We retrospectively evaluated 76 patients (38 males and 38 females, mean age: 65.0 ±â€Š14.0 years). They were under hemodialysis and treated with balloon PTA using CO2-DSA or C-DSA at our institution between 2009 and 2016. Mean duration of the follow-up period was 25.59 ±â€Š21.45 months. We compared the patency rates obtained after CO2-DSA-based balloon PTA with those after C-DSA-based balloon PTA. Secondary patency, which was defined as the duration of patency after all further endovascular interventions until surgical repair, was considered as the endpoint in this study.Overall, 19 and 57 patients underwent CO2-DSA- and C-DSA-based balloon PTA, respectively. CO2-DSA- and C-DSA-based balloon PTA produced clinical success rates of 100% and 96.5%, respectively. Blood vessel injury occurred in one patient who underwent C-DSA-based balloon PTA. No major complications occurred in CO2 group. At 24 months, the post-PTA secondary patency rates of CO2-DSA- and C-DSA-based balloon PTA were 94.1% and 93.9%, respectively (P = .9594).CO2-DSA is safe for hemodialysis patients. Compared with C-DSA, CO2-DSA-based balloon PTA produces have a similar secondary patency rate.

CD8+ T cells specific for a malaria cytoplasmic antigen form clusters around infected hepatocytes and are protective at the liver stage of infection.

Following Anopheles mosquito-mediated introduction into a human host, Plasmodium parasites infect hepatocytes and undergo intensive replication. Accumulating evidence indicates that CD8(+) T cells induced by immunization with attenuated Plasmodium sporozoites can confer sterile immunity at the liver stage of infection; however, the mechanisms underlying this protection are not clearly understood. To address this, we generated recombinant Plasmodium berghei ANKA expressing a fusion protein of an ovalbumin epitope and green fluorescent protein in the cytoplasm of the parasite. We have shown that the ovalbumin epitope is presented by infected liver cells in a manner dependent on a transporter associated with antigen processing and becomes a target of specific CD8(+) T cells from the T cell receptor transgenic mouse line OT-I, leading to protection at the liver stage of Plasmodium infection. We visualized the interaction between OT-I cells and infected hepatocytes by intravital imaging using two-photon microscopy. OT-I cells formed clusters around infected hepatocytes, leading to the elimination of the intrahepatic parasites and subsequent formation of large clusters of OT-I cells in the liver. Gamma interferon expressed in CD8(+) T cells was dispensable for this protective response. Additionally, we found that polyclonal ovalbumin-specific memory CD8(+) T cells induced by de novo immunization were able to confer sterile protection, although the threshold frequency of the protection was relatively high. These studies revealed a novel mechanism of specific CD8(+) T cell-mediated protective immunity and demonstrated that proteins expressed in the cytoplasm of Plasmodium parasites can become targets of specific CD8(+) T cells during liver-stage infection.