'Pseudo' pseudoaneurysm following robotic assisted partial nephrectomy.

A 65-year-old female presented to clinic requesting follow up for a history of right robotic partial nephrectomy done at an outside institution 2 years prior. Initial pathology demonstrated a grade 2/4 3.4 cm clear cell renal cell carcinoma with negative margins.

Diffusion of Robotic Technology Into Urologic Practice has Led to Improved Resident Physician Robotic Skills.

Objective: To investigate whether propagation of robotic technology into urologic practice and training programs has improved baseline urology resident trainee robotic skills.

Design: Questionnaires were completed by each urology resident trainee participating in a training course and asked about access to robotic simulation, robot experience, and console time. Baseline resident trainee scores on the Mimic Robotic Simulator (Mimic Technologies, Inc.

Impact of Resident Involvement on Robot-Assisted Radical Prostatectomy Outcomes.

Objective: This study examines perioperative outcomes of resident involvement during various steps of robot-assisted radical prostatectomy (RARP).

Methods: The RARP procedure was divided into seven steps: bladder takedown (BTD), endopelvic fascia, bladder neck (BN), seminal vesicle/vas deferens, pedicle/nerve sparing, apex, and anastomosis. Three hundred seventy-two RARPs performed by a single surgeon were analyzed.

Urology residents experience comparable workload profiles when performing live porcine nephrectomies and robotic surgery virtual reality training modules.

In pursuit of improving the quality of residents' education, the Southeastern Section of the American Urological Association (SES AUA) hosts an annual robotic training course for its residents. The workshop involves performing a robotic live porcine nephrectomy as well as virtual reality robotic training modules. The aim of this study was to evaluate workload levels of urology residents when performing a live porcine nephrectomy and the virtual reality robotic surgery training modules employed during this workshop.

Differential effects of 24-hydroxycholesterol and 27-hydroxycholesterol on beta-amyloid precursor protein levels and processing in human neuroblastoma SH-SY5Y cells.

Background: Activation of the liver x receptors (LXRs) by exogenous ligands stimulates the degradation of beta-amyloid 1-42 (Abeta42), a peptide that plays a central role in the pathogenesis of Alzheimer's disease (AD). The oxidized cholesterol products (oxysterols), 24-hydroxycholesterol (24-OHC) and 27-hydroxycholesterol (27-OHC), are endogenous activators of LXRs. However, the mechanisms by which these oxysterols may modulate Abeta42 levels are not well known.

Differential effects of 24-hydroxycholesterol and 27-hydroxycholesterol on tyrosine hydroxylase and alpha-synuclein in human neuroblastoma SH-SY5Y cells.

Evidence suggests that environmental and dietary factors may contribute to the pathogenesis of Parkinson's disease (PD). High dietary intake of cholesterol is such a factor that has been shown to increase or decrease the risk of PD. However, because circulating cholesterol does not cross the blood-brain barrier, the mechanisms linking dietary cholesterol to the pathogenesis of PD remain to be understood.

Regulation of beta-amyloid levels in the brain of cholesterol-fed rabbit, a model system for sporadic Alzheimer's disease.

Accumulation of beta-amyloid (Abeta) peptide in the brain is a major hallmark of Alzheimer's disease (AD). Hypercholesterolemia is a risk factor for AD and has been shown by laboratory studies to cause Abeta accumulation. Abeta levels in the brain are governed by its generation from amyloid precursor protein by beta-secretase (BACE1), degradation by the insulin degrading enzyme (IDE), clearance from the brain by the low density lipoprotein receptor-related protein (LRP-1), and transport from circulation into the brain by receptor for advanced glycation end products (RAGE).

Hypercholesterolemia-induced Abeta accumulation in rabbit brain is associated with alteration in IGF-1 signaling.

Hypercholesterolemia increases levels of beta-amyloid (Abeta), a peptide that accumulates in Alzheimer's disease brains. Because cholesterol in the blood does not cross the blood brain barrier (BBB), the link between circulating cholesterol and Abeta accumulation is not understood. In contrast to cholesterol, the oxidized cholesterol metabolite 27-hydroxycholesterol can cross the BBB, potentially increasing Abeta levels.