Long-chain acyl-CoA synthetase (ACSL) family members include five different ACSL isoforms, each encoded by a separate gene and have multiple spliced variants. ACSLs on endoplasmic reticulum and mitochondrial outer membrance catalyze fatty acids with chain lengths from 12 to 20 carbon atoms to form acyl-CoAs, which are lipid metabolic intermediates and involved in fatty acid metabolism, membrane modifications and various physiological processes. Gain- or loss-of-function studies have shown that the expression of individual ACSL isoforms can alter the distribution and amount of intracellular fatty acids. Changes in the types and amounts of fatty acids, in turn, can alter the expression of intracellular ACSLs. ACSL family members affect not only the proliferation of normal cells, but the proliferation of malignant tumor cells. They also regulate cell apoptosis through different signaling pathways and molecular mechanisms. ACSL members have individual functions in fatty acid metabolism in different types of cells depending on substrate preferences, subcellular location and tissue specificity, thus contributing to liver diseases and metabolic diseases, such as fatty liver disease, obesity, atherosclerosis and diabetes. They are also linked to neurological disorders and other diseases. However, the mechanisms are unclear. This review addresses new findings in the classification and properties of ACSLs and the fatty acid metabolism-associated effects of ACSLs in diseases.

Porcine aortas may prove to be useful ex-vivo models in the study of aortic dissection haemodynamics. These models are reproducible and may be used in the study of complex haemodynamic forces during the development and propagation of TBAD. Our three porcine models give a potential possibility in helping clinicians isolate and analyse complex haemodynamical factors in the development, propagation and prognosis of TBAD.

Aortic remodeling after TEVAR in chronic dissection is a continuous process. There were no significant differences between chronic dissections and aneurysms in all volumetric parameters. Treating chronic dissections early, before aneurysm formation, did not appear to have a morphologic advantage.

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CD19 chimeric antigen receptor (CAR) T cell therapy has shown impressive results in treating acute lymphoblastic leukemia (B-ALL), chronic lymphoblastic leukemia (B-CLL), and B-cell non-Hodgkin lymphoma (B-NHL) over the past few years. Meanwhile, the cytokine release syndrome (CRS), which could be moderate or even life-threatening, has emerged as the most significant adverse effect in the clinical course of this novel targeting immunotherapy. In this systematic review, we analyzed the incidence of severe CRS in 19 clinical trials selected from studies published between 2010 and 2017. The pooled severe CRS proportion was 29.3% (95% confidence interval [CI] 12.3-49.1%) in B-ALL, 38.8% (95%CI 12.9-67.6%) in B-CLL, and 19.8% (95%CI 4.2-40.8%) in B-NHL. In the univariate meta regression analysis, the proliferation of CD19-CAR-T cell in vivo was correlated with the severe CRS. Specifically, total infusion cell dose contributed to the severe CRS occurring in B-ALL patients but not in B-CLL or B-NHL patients. Tumor burden was strongly associated with the severity of CRS in B-ALL. Besides, post-HSCT CD19 CAR-T cell infusion represented lower severe CRS incidence. Further investigations into the risk factors of CRS in B-CLL and B-NHL are needed.

Aortic dissection is a dangerous pathological condition where blood intrudes into the layers of the arterial walls, creating an artificial channel (false lumen). In the absence of thrombosis or surgical intervention, blood will enter the false lumen through the proximal tear, and join the true lumen again through a distal tear. Rupture of the weakened outer wall will result in extremely high mortality rates. Type B thoracic aortic dissection (TAD), occurring along the descending aorta, can be repaired surgically by the deployment of an endovascular stent graft, concealing the proximal entry tear. Blood might still flow into the false lumen (FL) through the distal tear. The domain of such flow should be minimized, as complete thrombosis of the FL is generally believed to be more beneficial for the patient. The dependence on the area ratios of the lumens and size of these tears is studied by computational fluid dynamics

Horseshoe kidney may cause technical and access problems during open aortic aneurysm repair. The aim of this study is to report two cases from our institution and to review the world's literature on successful endovascular infrarenal aneurysm repair in patients with horseshoe kidneys. A retrospective review of a prospectively entered departmental computerized database was performed for the two patients from our institution. Articles were searched electronically from PubMed and Medline, using the terms 'horseshoe kidney' and 'aneurysm'. Endovascular cases were reviewed from the world's literature. In addition to the two patients from our institution, there were 19 patients with infrarenal aneurysms and horseshoe kidneys in published literature who underwent successful endovascular aneurysm repair. The occlusion of lower-pole or accessory renal arteries does not seem to cause significant endoleak or renal impairment in the long run. In conclusion, our experience and current literature seem to suggest that endovascular repair of infrarenal aortic aneurysms for patients with horseshoe kidneys is safe. Renal impairment will depend on the area of kidney perfused by the accessory renal arteries. The endovascular treatment option is less invasive than open repair, and circumvents the problem of difficult exposure, especially in those patients with significant co-morbidity.

Purpose: The aim of this study was to investigate the role of miR-33-5p in abdominal aortic aneurysm progression, which regulated adenosine triphosphate-binding cassette transporter A1 (ABCA1)-mediated cholesterol efflux and lipid accumulation in THP-1 macrophage-derived foam cells through the PI3K/Akt pathway. Methods: Quantitative reverse transcription polymerase chain reaction was used to evaluate the expression level of miR-33-5p and ABCA1 mRNA in abdominal aortic aneurysm patient and normal person tissues. The relationship between miR-33-5p and ABCA1 was examined by dual luciferase report assay. High-performance liquid chromatography was used to evaluate the levels of cholesterol contents. Cholesterol efflux detection was performed by liquid scintillator. The expression of inflammatory cytokines was detected by quantitative reverse transcription polymerase chain reaction. Western blot was applied to determine the expression levels of ABCA1, PI3K (p-PI3K), and Akt (p-Akt). Results: The quantitative reverse transcription polymerase chain reaction analysis results revealed miR-33-5p overexpression in abdominal aortic aneurysm tissues, but the expression level of ABCA1 was lower in abdominal aortic aneurysm tissues than non-abdominal aortic aneurysm tissues. Subsequently, the dual luciferase report gene assay confirmed that ABCA1 was a target of miR-33-5p, and miR-33-5p-negative regulated ABCA1 expression. Moreover, the expression levels of p-PI3K, p-Akt, and ABCA1 were decreased in THP-1 cell transferred with ABCA1 siRNA, but knockdown of miR-33-5p had an opposite effect. Furthermore, knockdown of miR-33-5p decreased the expression of MMP-2, MMP-9, TNF-α, total cellular cholesterol, and promoted cholesterol efflux in THP-1-derived foam cells. Importantly, LY294002 (PI3K inhibitor) or si-ABCA1 completely inhibited the stimulatory effects of miR-33-5p inhibitor. Conclusion: This study has found that knockdown of miR-33-5p induced ABCA1 expression and promoted inflammatory cytokines and cholesterol efflux likely via activating the PI3K/Akt signaling pathway.