Publications by authors named "J G Stathopoulos"

Objective: Many studies have compared outcomes following anterior and posterior cervical fusion, yet the differences in the impacts of perioperative complications on outcomes have not been well studied. This study aimed to assess the differences in the effects of 30-day perioperative complications on patient-reported outcome measures (PROMs) after multilevel anterior versus posterior cervical fusion.

Methods: Adult patients who underwent anterior or posterior cervical fusion at three or more levels between 2014 and 2020 were analyzed.

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Purpose Of Review: Left ventricular (LV) hypertrophy (LVH) is a well recognized target organ adaptation to longstanding uncontrolled hypertension and other cardiovascular risk factors. It is also a strong and independent predictor of many cardiovascular disorders.

Recent Findings: This focused review explores the current concepts in screening, diagnosis, prevention, and treatment of LVH in patients with hypertension.

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Objectives: In the absence of sample validity testing, a healthcare provider may fail to identify a patient's adulteration of their urine sample. This study compared different methods for specific gravity (SG), pH, TECO™ Drug Adulteration Test Strip (dipstick) and oxidant assay to explain the differences and also make an informative decision on method selection.

Methods: Creatinine, SG and pH measurements are essential in sample validity testing.

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Lowering of prion protein (PrP) expression in the brain is a genetically validated therapeutic hypothesis in prion disease. We recently showed that antisense oligonucleotide (ASO)-mediated PrP suppression extends survival and delays disease onset in intracerebrally prion-infected mice in both prophylactic and delayed dosing paradigms. Here, we examine the efficacy of this therapeutic approach across diverse paradigms, varying the dose and dosing regimen, prion strain, treatment timepoint, and examining symptomatic, survival, and biomarker readouts.

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Prion disease is a fatal, incurable neurodegenerative disease of humans and other mammals caused by conversion of cellular prion protein (PrP; PrPC) into a self-propagating neurotoxic conformer (prions; PrPSc). Strong genetic proofs of concept support lowering PrP expression as a therapeutic strategy. Antisense oligonucleotides (ASOs) can provide a practical route to lowering one target mRNA in the brain, but their development for prion disease has been hindered by three unresolved questions from prior work: uncertainty about mechanism of action, unclear potential for efficacy against established prion infection, and poor tolerability of drug delivery by osmotic pumps.

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