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Articles 1 - 2 of 2
Full-Text Articles in Pharmaceutical Preparations
Digoxin Toxicity And Acute Renal Failure In A 75 Year-Old Female, Daniel Zaayenga, Andrew Caravello, Nicholas Tomasello
Digoxin Toxicity And Acute Renal Failure In A 75 Year-Old Female, Daniel Zaayenga, Andrew Caravello, Nicholas Tomasello
Rowan-Virtua Research Day
Digoxin toxicity can present with varying manifestations. While pathognomonic symptoms such as xanthopsia (object appearing yellow) are a board favorite it is not a required finding and is in fact not seen with most patients. Rather digoxin toxicity presents with more non-specific symptoms such as GI distress (anorexia, N/V) neurological distress (lethargy, fatigue, delirium, confusion, disorientation, weakness. EKG findings are varied and include premature ventricular contractions, bradycardia, atrial tachyarrhythmias with AV block, ventricular bigeminy, junctional rhythms, various degrees of AV nodal blockade, ventricular tachycardia, and ventricular fibrillation. Although rarely seen, digoxin is one of the only causes of bidirectional ventricular …
Targeting Ribosome Assembly Factors Selectively Protects P53 Positive Cells From Chemotherapeutic Agents, Russell T. Sapio, Anastasiya Nezdyur, Matthew Krevetski, Leonid Anikin, Vincent J. Manna, N. Minkovsky, Dimitri G Pestov
Targeting Ribosome Assembly Factors Selectively Protects P53 Positive Cells From Chemotherapeutic Agents, Russell T. Sapio, Anastasiya Nezdyur, Matthew Krevetski, Leonid Anikin, Vincent J. Manna, N. Minkovsky, Dimitri G Pestov
Rowan-Virtua School of Osteopathic Medicine Faculty Scholarship
Many chemotherapeutic agents act in a nondiscriminatory fashion, targeting both cancerous and noncancerous cells in Sphase and Mphase. One approach to reduce the toxic side effects in normal tissue is to exploit the differences in p53 functionality between cancerous and noncancerous cells. For example, activating p53 signaling by nongenotoxic means can transiently arrest noncancerous p53 positive cells in G1 phase and protect them from the cytotoxic effects of chemotherapeutic drugs. However, since most cancerous cells have faulty p53 signaling, they will proceed to cycle, and continue to be affected by the drug. In this study we asked if this G1‐phase …