Chunnel debranching for hybrid repair of thoracoabdominal aortic aneurysm

Hybrid repair of a thoracoabdominal aortic aneurysm comprising thoracic endovascular aortic repair and total renovisceral debranching is a feasible alternative to open repair, especially for high-risk patients. However, transperitoneal debranching is a relatively complicated procedure that requires deep dissection around vital abdominal organs. Therefore, we developed a new debranching technique called Chunnel debranching, which was characterized by transaortic tunneling using a covered stent between the target artery and the prosthetic graft anastomosed on the aneurysmal wall using an inclusion technique. This procedure increases the feasibility of renovisceral debranching with fewer dissections than conventional transperitoneal debranching

Rare Diagnosis of a Multilobular Pulmonary Mass

CASE PRESENTATION: A 57-year-old woman was admitted to our hospital for an abnormal chest shadow found during routine chest radiography. She had no respiratory symptoms. Her medical history included dyslipidemia, and her surgical history included conization for cervical cancer at age 38 years. She was a social drinker and ex-smoker of approximately 10 cigarettes per day (from ages 20 to 30 years); she denied recreational drug use

Intravital imaging identifies the VEGF-TXA₂ axis as a critical promoter of PGE₂ secretion from tumor cells and immune evasion

がん細胞が免疫から逃れるメカニズムの解明 --がん細胞と血管内皮細胞との細胞間相互作用--. 京都大学プレスリリース. 2021-05-28.Prostaglandin E₂ (PGE₂) promotes tumor progression through evasion of anti-tumor immunity. In stark contrast to cyclooxygenase-dependent production of PGE₂, little is known whether or not PGE₂ secretion is regulated within tumor tissues. Here, we show that VEGF-dependent release of thromboxane A₂ (TXA₂) triggers Ca²⁺ transients in tumor cells, culminating in PGE₂ secretion and subsequent immune evasion in the early stages of tumorigenesis. Ca²⁺ transients caused cPLA2 activation and triggered the arachidonic acid cascade. Ca²⁺ transients were monitored as the surrogate marker of PGE₂ secretion. Intravital imaging of BrafV600E mouse melanoma cells revealed that the proportion of cells exhibiting Ca²⁺ transients is markedly higher in vivo than in vitro. The TXA₂ receptor was indispensable for the Ca²⁺ transients in vivo, high intra-tumoral PGE₂ concentration, and evasion of anti-tumor immunity. Notably, treatment with a vascular endothelial growth factor (VEGF) receptor antagonist and an anti-VEGF antibody rapidly suppressed Ca²⁺ transients and reduced TXA₂ and PGE₂ concentrations in tumor tissues. These results identify the VEGF-TXA₂ axis as a critical promoter of PGE₂-dependent tumor immune evasion, providing a molecular basis underlying the immunomodulatory effect of anti-VEGF therapies