Summary Background For patients with end-stage renal disease who are not candidates for fistula, dialysis access grafts are the best option for chronic haemodialysis. However, polytetrafluoroethylene arteriovenous grafts are prone to thrombosis, infection, and intimal hyperplasia at the venous anastomosis. We developed and tested a bioengineered human acellular vessel as a potential solution to these limitations in dialysis access. Methods We did two single-arm phase 2 trials at six centres in the USA and Poland. We enrolled adults with end-stage renal disease. A novel bioengineered human acellular vessel was implanted into the arms of patients for haemodialysis access. Primary endpoints were safety (freedom from immune response or infection, aneurysm, or mechanical failure, and incidence of adverse events), and efficacy as assessed by primary, primary assisted, and secondary patencies at 6 months. All patients were followed up for at least 1 year, or had a censoring event. These trials are registered with ClinicalTrials.gov, NCT01744418 and NCT01840956. Findings Human acellular vessels were implanted into 60 patients. Mean follow-up was 16 months (SD 7·6). One vessel became infected during 82 patient-years of follow-up. The vessels had no dilatation and rarely had post-cannulation bleeding. At 6 months, 63% (95% CI 47–72) of patients had primary patency, 73% (57–81) had primary assisted patency, and 97% (85–98) had secondary patency, with most loss of primary patency because of thrombosis. At 12 months, 28% (17–40) had primary patency, 38% (26–51) had primary assisted patency, and 89% (74–93) had secondary patency. Interpretation Bioengineered human acellular vessels seem to provide safe and functional haemodialysis access, and warrant further study in randomised controlled trials. Funding Humacyte and US National Institutes of Health.

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mutant mice show compulsive behavior similar to trichotillomania, a human obsessive-compulsive-spectrum disorder. The only lineage-labeled cells in the brains of mice are microglia, suggesting that defective microglia caused the disorder. What is the source of the microglia? It has been posited that all microglia progenitors arise at embryonic day (E) 7.5 during yolk sac hematopoiesis, and colonize the brain at E9.5. In contrast, we show the presence of two microglia subpopulations: canonical, non- microglia and microglia. Unlike non- microglia, microglia progenitors appear to be generated during the second wave of yolk sac hematopoiesis, then detected in the aorto-gonad-mesonephros (AGM) and fetal liver, where they are greatly expanded, prior to infiltrating the E12.5 brain. Further, we demonstrate that hematopoietic progenitor cells taken from fetal liver are competent to give rise to microglia Although the two microglial subpopulations are very similar molecularly, and in their response to brain injury and participation in synaptic pruning, they show distinct brain distributions which might contribute to pathological specificity. Non- microglia significantly outnumber microglia, but they cannot compensate for the loss of function in microglia, suggesting further crucial differences between the two subpopulations.

Our study highlights how hybrid strategies incorporating surgical and endovascular approaches can be used successfully in treating patients with complex thoracic aortic aneurysms. This combined approach potentially expands the field of endovascular stent grafting and is an attractive solution for patients with poor cardiopulmonary reserves.

Treatment modality of CCA has largely evolved from operative to endovascular intervention at our institution. Treatment benefits of endovascular modality include shorter convalescent and less procedural-related complications. This evolution reflects the improvement of endovascular devices and increased utility of endovascular applications.

In access-challenged patients, a statistically significant reduction in HeRO-related bacteremia was noted compared with TDC literature. The device had similar function and patency compared with conventional arteriovenous graft literature.

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In patients presenting with rest pain and tissue loss who are treated with SFA percutaneous interventions, patency is negatively affected by compromised and poor runoffs in keeping with the bypass literature. More importantly, freedom from recurrent symptoms and limb salvage are incrementally curtailed as runoff scores worsen. These findings are consistent with the bypass literature.