Edward B Thorp

Nov 18, 2024 | nature.com | Coraline Borowczyk |Minna Kaikkonen |William Tressel |James B. Stein |Edward B Thorp |Emmanuel L. Gautier | +3 more

AbstractMetabolic dysregulation, including perturbed glutamine–glutamate homeostasis, is common among patients with cardiovascular diseases, but the underlying mechanisms remain largely unknown. Using the human MESA cohort, here we show that plasma glutamine–glutamate ratio is an independent risk factor for carotid plaque progression.

May 29, 2024 | digitalcommons.library.tmc.edu | Matthew DeBerge |Rajesh chaudhary |Samantha Schroth |Edward B Thorp

AbstractImmune cell function among the myocardium, now more than ever, is appreciated to regulate cardiac function and pathophysiology. This is the case for both innate immunity, which includes neutrophils, monocytes, dendritic cells, and macrophages, as well as adaptive immunity, which includes T cells and B cells.

Jan 12, 2024 | edwardthorp.medium.com | Edward B Thorp

You hear a lot of outlandish salaries being offered in tech. They exist, but it’s definitely tunnel vision. It’s the sort of stories that spread on social media. Like Netflix’s $800,000 engineering post and the $300,000 prompt engineering salary you’ve seen thrown around. But that’s all sensationalism.

Oct 17, 2023 | mdpi.com | Danish Saleh |Samantha Schroth |Edward B Thorp |Matthew J. Feinstein

1. Introduction 1.1. Cardiovascular Disease, Heart Failure, and InflammationCardiovascular diseases comprise the leading cause of death in the United States [1]. Heart failure encompasses an array of pathophysiologic processes culminating in myocardial pump dysfunction and circulatory failure.

Sep 15, 2023 | jci.org | Edward B Thorp

AbstractInterest in cardioimmunology has reached new heights as the experimental cardiology field works to tap the unrealized potential of immunotherapy for clinical care. Within this space is the cardiac macrophage, a key modulator of cardiac function in health and disease. After a myocardial infarction, myeloid macrophages both protect and harm the heart. To varying degrees, such outcomes are a function of myeloid ontogeny and heterogeneity, as well as functional cellular plasticity.