An obvious increase in the gate leakage current has been commonly observed in GaN HEMTs, after Plasma-enhanced chemical vapor deposition (PECVD) SiN passivation has been observed to obviously increase. This paper presents an Al/SiN stack layer passivation structure. The high gate leakage current in GaN HEMTs caused by the PECVD SiN passivation is distinctly reduced by 2 to 3 orders of magnitude by introducing a thin Al layer. It is mainly attributed to the Al layer blocking and minimizing the damage for the (Al)GaN surface in the build-up of the luminance process of PECVD SiN and then reducing the surface trap density. TEM mapping and SRIM software simulation reveal that neither damage nor inter-diffusion is demonstrated at the Al/AlGaN interface, where a continuous crystalline region is observed. The moderate current collapse suppression and 32.8% improvement in V_BR are achieved in GaN HEMTs with Al/SiN passivation.

Background. Dapagliflozin, a sodium glucose transporter protein‐2 (SGLT‐2) inhibitor, reduces the risk for cardiovascular diseases. However, the influence of dapagliflozin on nondissecting abdominal aortic aneurysms (AAAs) remains unclear. Methods. AAAs were created in male C57BL/6 mice via intra‐aortic porcine pancreatic elastase (PPE) infusion. Mice were daily treated with dapagliflozin (1 or 5 mg/kg body weight) or an equal volume of vehicle through oral gavage beginning one day prior to PPE infusion for 14 days. To investigate its translational value, dapagliflozin or vehicle was also administered to mice with existing AAAs in another cohort. Aortic diameters were measured prior to (day 0 for baseline) and 14 days after PPE infusion. After sacrifice, mice aortae were collected, and following histological analyses were performed. Results. Dapagliflozin treatment significantly reduced aneurysmal aortic expansion following PPE infusion as compared to vehicle treatment especially at 5 mg/kg body weight (approximately 21% and 33% decreases in 1 and 5 mg/kg treatment groups, respectively). The dose‐dependent attenuation of AAAs by dapagliflozin was also confirmed on histological analyses. Dapagliflozin remarkably reduced aortic accumulation of macrophages, CD4⁺ T cells, and B cells particularly following dapagliflozin treatment at 5 mg/kg. Dapagliflozin treatment also markedly attenuated medial SMC loss. Though the difference was not significant, dapagliflozin treatment tended to attenuate CD8⁺ T cells and elastin degradation. Dapagliflozin treatment at 5 mg/kg caused a 53% reduction in neovessel density. Furthermore, dapagliflozin treatment mitigated further progress of existing AAAs. Conclusion. Dapagliflozin treatment ameliorated PPE‐induced AAAs by inhibiting aortic leukocytes infiltration and angiogenesis.

Background: Interleukin‐19 is an immunosuppressive cytokine produced by immune and nonimmune cells, but its role in abdominal aortic aneurysm (AAA) pathogenesis is not known. This study aimed to investigate interleukin‐19 expression in, and influences on, the formation and progression of experimental AAAs. Methods and Results: Human specimens were obtained at aneurysm repair surgery or from transplant donors. Experimental AAAs were created in 10‐ to 12‐week‐old male mice via intra‐aortic elastase infusion. Influence and potential mechanisms of interleukin‐19 treatment on AAAs were assessed via ultrasonography, histopathology, flow cytometry, and gene expression profiling. Immunohistochemistry revealed augmented interleukin‐19 expression in both human and experimental AAAs. In mice, interleukin‐19 treatment before AAA initiation via elastase infusion suppressed aneurysm formation and progression, with attenuation of medial elastin degradation, smooth‐muscle depletion, leukocyte infiltration, neoangiogenesis, and matrix metalloproteinase 2 and 9 expression. Initiation of interleukin‐19 treatment after AAA creation limited further aneurysmal degeneration. In additional experiments, interleukin‐19 treatment inhibited murine macrophage recruitment following intraperitoneal thioglycolate injection. In classically or alternatively activated macrophages in vitro, interleukin‐19 downregulated mRNA expression of inducible nitric oxide synthase, chemokine C‐C motif ligand 2, and metalloproteinases 2 and 9 without apparent effect on cytokine‐expressing helper or cytotoxic T‐cell differentiation, nor regulatory T cellularity, in the aneurysmal aorta or spleen of interleukin‐19–treated mice. Interleukin‐19 also suppressed AAAs created via angiotensin II infusion in hyperlipidemic mice. Conclusions: Based on human evidence and experimental modeling observations, interleukin‐19 may influence the development and progression of AAAs.

Intimal hyperplasia (IH) is a negative vascular remodeling after arterial injury. IH occasionally occurs in elastase‐induced abdominal aortic aneurysm (AAA) mouse models. This study aims to clarify the incidence and histological characteristics of IH in aneurysmal mice. A retrospective study was conducted by including 42 male elastase‐induced mouse AAA models. The IH incidence, aortic diameters with or without IH, and hyperplasia lesional features of mice were analyzed. Among 42 elastase‐induced AAA mouse models, 10 mice developed mild IH (24%) and severe IH was found in only 2 mice (5%). The outer diameters of the AAA segments in mice with and without IH did not show significant difference. Both mild and severe IH lesions show strong smooth muscle cell positive staining, but endothelial cells were occasionally observed in severe IH lesions. There was obvious macrophage infiltration in the IH lesions of the AAA mouse models, especially in mice with severe IH. However, only a lower numbers of T cells and B cells were found in the IH lesion. Local cell‐secreted matrix metalloproteinases (MMP) 2 was highly expressed in all IH lesions, but MMP9 was only overexpressed in severe lesions. In conclusion, this study is the first to demonstrate the occurrence of aneurysmal IH and its histological characteristics in an elastase‐induced mouse AAA model. This will help researchers better understand this model, and optimize it for use in AAA‐related research.

Aim: Compared with the C57BL/6N substrain, the C57BL/6J substrain is more susceptible to the angiotensin II (Ang II)-induced development of dissected abdominal aortic aneurysms (AAAs). The aim of this study was to elucidate whether the widely used C57BL/6N mouse substrain is as susceptible as the C57BL/6J mouse substrain to porcine pancreatic elastase (PPE) infusion-induced experimental nondissected AAA development.Methods: Experimental nondissected AAAs were induced in C57BL/6J and C57BL/6N mice via transient aortic luminal infusion of PPE. On Day 0 (baseline) and Day 14 after PPE infusion, the abdominal aortic diameter was directly measured. Aortic aneurysmal segment samples were collected, and histopathological analysis was performed.Results: On Day 14 after PPE infusion, aortic diameters were significantly increased in both mouse substrains (from approximately 0.51 to 1.24 mm in C57BL/6J mice and from 0.51 to 1.18 mm in C57BL/6N mice). The increase in diameter of all the mice exceeded 50% and met the criteria for AAA model establishment (143% and 135% in C57BL/6J mice and C57BL/6N mice, respectively). PPE infusion also induced obvious local aortic wall macrophage and T-cell infiltration, elastin degradation, smooth muscle cell depletion and high metallopeptidase (MMP)-2 and MMP-9 expression levels in C57BL/6N mice, but these differences were not significant compared with those in C57BL/6J mice. However, PPE infusion led to the recruitment of more B cells and the sprouting of more neovessels at the aneurysmal lesion site in C57BL/6J mice than in C57BL/6N mice.Conclusion: The C57BL/6N mouse substrain is suitable for establishing a model of AAA via elastase infusion.

Objective: Type I interferon receptor signaling contributes to several autoimmune and vascular diseases such as lupus, atherosclerosis and stroke. The purpose of this study was to assess the influence of type I interferon receptor deficiency on the formation and progression of experimental abdominal aortic aneurysms (AAAs). Methods: AAAs were induced in type I interferon receptor subunit 1 (IFNAR1)-deficient and wild type control male mice via intra-infrarenal aortic infusion of porcine pancreatic elastase. Immunostaining for IFNAR1 was evaluated in experimental and clinical aneurysmal abdominal aortae. The initiation and progression of experimental AAAs were assessed via ultrasound imaging prior to (day 0) and days 3, 7 and 14 following elastase infusion. Aneurysmal histopathology was analyzed at sacrifice. Results: Increased aortic medial and adventitial IFNAR1 expression was present in both clinical AAAs harvested at surgery and experimental AAAs. Following AAA induction, wild type mice experienced progressive, time-dependent infrarenal aortic enlargement. This progression was substantially attenuated in IFNAR1-deficient mice. On histological analyses, medial elastin degradation, smooth muscle cell depletion, leukocyte accumulation and neoangiogenesis were markedly diminished in IFNAR1-deficient mice in comparison to wild type mice. Conclusion: IFNAR1 deficiency limited experimental AAA progression in response to intra-aortic elastase infusion. Combined with clinical observations, these results suggest an important role for IFNAR1 activity in AAA pathogenesis.