Open Surgical Repair of Abdominal Aortic Aneurysms Maintains a Pivotal Role in the Endovascular Era.

Since the advent of endovascular aortic repair (EVAR) nearly three decades ago, there has been a paradigm shift in the treatment of the abdominal aortic aneurysm (AAA) to favor EVAR due to its reduced operative mortality, less invasive nature, and faster recovery times. However, more recently there has been an accumulation of data from large meta-analyses and randomized clinical trials revealing that EVAR has no survival benefit after approximately 2 years and is associated with substantially higher rates of reintervention and aneurysm rupture in the long term. These findings call into question the durability of EVAR compared with open aortic repair and emphasize the need for surgeons to remain competent with open aortic surgery in the modern era.

Exome sequencing reveals a novel COL2A1 mutation implicated in multiple epiphyseal dysplasia.

Mutations in the COMP, COL9A1, COL9A2, COL9A3, MATN3, and SLC26A2 genes cause approximately 70% of multiple epiphyseal dysplasia (MED) cases. The genetic changes involved in the etiology of the remaining cases are still unknown, suggesting that other genes contribute to MED development. Our goal was to identify a mutation causing an autosomal dominant form of MED in a large multigenerational family.

Insulin-like growth factor-1 increases synthesis of collagen type I via induction of the mRNA-binding protein LARP6 expression and binding to the 5' stem-loop of COL1a1 and COL1a2 mRNA.

Collagen content in atherosclerotic plaque is a hallmark of plaque stability. Our earlier studies showed that insulin-like growth factor-1 (IGF-1) increases collagen content in atherosclerotic plaques of Apoe(-/-) mice. To identify mechanisms we investigated the effect of IGF-1 on the la ribonucleoprotein domain family member 6 (LARP6).

Differential requirement for nitric oxide in IGF-1-induced anti-apoptotic, anti-oxidant and anti-atherosclerotic effects.

We have shown previously that insulin like-growth factor I (IGF-1) suppressed atherosclerosis in Apoe(-/-) mice and activated endothelial nitric oxide (NO) synthase. To determine whether IGF-1-induced atheroprotection depends on NO, IGF-1- or saline-infused mice were treated with l-NAME, the pan-NO synthase inhibitor or with d-NAME (control). IGF-1 reduced atherosclerosis in both the d-NAME and l-NAME groups suggesting that IGF-1's anti-atherogenic effect was NO-independent.

The effect of nebivolol versus metoprolol succinate extended release on asymmetric dimethylarginine in hypertension.

This study sought to determine if metoprolol succinate ER (MET), and nebivolol (NEB), a β1-AR with increased bioavailability of nitric oxide (NO), would have differing effects on plasma asymmetric dimethylarginine concentration in hypertensives. It was hypothesized that NEB, a β1-AR antagonist and β3-AR agonist with NO-releasing properties, and MET, only a β1-AR antagonist, would have different effects on plasma asymmetric dimethylarginine (ADMA) concentration. Forty-one hypertensive subjects randomly received either 50 mg of MET (n = 19) or 5 mg of NEB (n = 22) for 4 weeks followed by 100 mg MET and 10 mg NEB for 4 weeks.