Engineering of human brain organoids with a functional vascular-like system.

Human cortical organoids (hCOs), derived from human embryonic stem cells (hESCs), provide a platform to study human brain development and diseases in complex three-dimensional tissue. However, current hCOs lack microvasculature, resulting in limited oxygen and nutrient delivery to the inner-most parts of hCOs. We engineered hESCs to ectopically express human ETS variant 2 (ETV2). ETV2-expressing cells in hCOs contributed to forming a complex vascular-like network in hCOs. Importantly, the presence of vasculature-like structures resulted in enhanced functional maturation of organoids. We found that vascularized hCOs (vhCOs) acquired several blood-brain barrier characteristics, including an increase in the expression of tight junctions, nutrient transporters and trans-endothelial electrical resistance. Finally, ETV2-induced endothelium supported the formation of perfused blood vessels in vivo. These vhCOs form vasculature-like structures that resemble the vasculature in early prenatal brain, and they present a robust model to study brain disease in vitro.

[Endovascular repair of an iliac artery aneurysm after endovascular aneurysm repair with handmade iliac branch device: a case report].

An involved internal iliac artery is usually embolized when performing endovascular aneurysm repair for aortoiliac or isolated iliac artery aneurysm.This can lead to complications such as buttock claudication,colon ischaemia and erectile dysfunction.Iliac branch device (IBD) is an endograft designed specifically for iliac bifurcation to preserve internal iliac flow. It was performed with high technical success rates and encouraging mid-term patency. Here we report a case of right iliac aneurysm developed 3 years after endovascular aneurysm repair for an aortoiliac aneurysm, with the patient's left internal artery been sacrificed then. Using a handmade IBD, we excluded the aneurysm without occlusion of the ipsilateral internal iliac artery or any type of endoleak. Both the design and deployment of this IBD are distinctive that we would like to share our experience with all the colleagues.

[Endovascular treatment of a rare type of aortic arch aneurysm derived from the fourth aortic arch].

OBJECTIVE: To report a rare type of aortic arch aneurysm. METHODS: Three cases of aortic arch aneurysm derived from the fourth aortic arch were retrospectively analyzed. The pathogenesis and treatment of this type of aortic arch aneurysm were investigated. RESULTS: Most of the aneurysm body was located in the Z2 zone, which was the stem from the fourth aortic arch in the embryonic development period. All of the 3 cases could not be explained by common etiology. We speculated that the cause might be developmental anomaly of the fourth aortic arch. All the 3 aortic arch aneurysms were totally excluded with a covered stent. The technical success rate was 100%. Endoleak of type I was seen in one case, which was resolved in a later open surgery. During the follow-up, no type of complications was found. CONCLUSION: To the best of our knowledge, this is the first report of this type of aortic arch aneurysm. The cause may be developmental anomaly of the fourth aortic arch. Endovascular treatment of this type of aortic arch aneurysm is feasible.

[Diagnosis and surgical treatment results of angio-Behçet syndrome: an analysis of 26 patients].

OBJECTIVE: To analyze the diagnosis and surgical treatment results of angio-Behçet syndrome. METHODS: The clinical data of pre-operation diagnosis, surgical treatment methods and prospective efficacy of 26 patients who were diagnosed as Behçet syndrome between January 2003 and April 2011 was analyzed retrospectively. There were 23 male and 3 female patients, aging from 20 to 76 years with a mean of (37 ± 6) years. Among them, 3 patients showed the clinical symptoms as arterial stenosis or occlusion, 9 patients had aneurysm, 13 patients had phlebitis or phlebothrombosis. One patient had both aneurysm and venous thrombosis. Totally 11 patients had experienced 22 cases surgical treatment including interventional therapy for 8 cases, open operation for 13 cases and hybrid operation for 1 case. RESULTS: Twenty-two patients (84.6%) were followed up from 3 months to 96 months after various surgical treatment methods. The average follow-up periond was 39.3 months. Totally, perioperative mortality was 1/11 after surgical treatment. Healing rates were 7/8 and 8/13, recurrence rates were 5/8 and 7/8 in patients with interventional therapy compared with that of experiencing open surgery respectively. CONCLUSIONS: Behçet syndrome patients combined with various vascular lesions should be thought of angio-Behçet syndrome. Choosing correct surgical treatment according to patient's condition and timing of pathological changes are the keys of gaining satisfactory results.

Excessive adventitial stress drives inflammation-mediated fibrosis in hypertensive aortic remodelling in mice.

Hypertension induces significant aortic remodelling, often adaptive but sometimes not. To identify immuno-mechanical mechanisms responsible for differential remodelling, we studied thoracic aortas from 129S6/SvEvTac and C57BL/6 J mice before and after continuous 14-day angiotensin II infusion, which elevated blood pressure similarly in both strains. Histological and biomechanical assessments of excised vessels were similar at baseline, suggesting a common homeostatic set-point for mean wall stress. Histology further revealed near mechano-adaptive remodelling of the hypertensive 129S6/SvEvTac aortas, but a grossly maladaptive remodelling of C57BL/6 J aortas. Bulk RNA sequencing suggested that increased smooth muscle contractile processes promoted mechano-adaptation of 129S6/SvEvTac aortas while immune processes prevented adaptation of C57BL/6 J aortas. Functional studies confirmed an increased vasoconstrictive capacity of the former while immunohistochemistry demonstrated marked increases in inflammatory cells in the latter. We then used multiple computational biomechanical models to test the hypothesis that excessive adventitial wall stress correlates with inflammatory cell infiltration. These models consistently predicted that increased vasoconstriction against an increased pressure coupled with modest deposition of new matrix thickens the wall appropriately, restoring wall stress towards homeostatic consistent with adaptive remodelling. By contrast, insufficient vasoconstriction permits high wall stresses and exuberant inflammation-driven matrix deposition, especially in the adventitia, reflecting compromised homeostasis and gross maladaptation.