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"Physiology, Pathological"
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Ischemia/Reperfusion Injury following Acute Myocardial Infarction: A Critical Issue for Clinicians and Forensic Pathologists
Acute myocardial infarction (AMI) is a leading cause of morbidity and mortality. Reperfusion strategies are the current standard therapy for AMI. However, they may result in paradoxical cardiomyocyte dysfunction, known as ischemic reperfusion injury (IRI). Different forms of IRI are recognized, of which only the first two are reversible: reperfusion-induced arrhythmias, myocardial stunning, microvascular obstruction, and lethal myocardial reperfusion injury. Sudden death is the most common pattern for ischemia-induced lethal ventricular arrhythmias during AMI. The exact mechanisms of IRI are not fully known. Molecular, cellular, and tissue alterations such as cell death, inflammation, neurohumoral activation, and oxidative stress are considered to be of paramount importance in IRI. However, comprehension of the exact pathophysiological mechanisms remains a challenge for clinicians. Furthermore, myocardial IRI is a critical issue also for forensic pathologists since sudden death may occur despite timely reperfusion following AMI, that is one of the most frequently litigated areas of cardiology practice. In this paper we explore the literature regarding the pathophysiology of myocardial IRI, focusing on the possible role of the calpain system, oxidative-nitrosative stress, and matrix metalloproteinases and aiming to foster knowledge of IRI pathophysiology also in terms of medicolegal understanding of sudden deaths following AMI.
Journal Article
A Selective Inhibitor of eIF2α Dephosphorylation Protects Cells from ER Stress
Most protein phosphatases have little intrinsic substrate specificity, making selective pharmacological inhibition of specific dephosphorylation reactions a challenging problem. In a screen for small molecules that protect cells from endoplasmic reticulum (ER) stress, we identified salubrinal, a selective inhibitor of cellular complexes that dephosphorylate eukaryotic translation initiation factor 2 subunit α (eIF2α). Salubrinal also blocks eIF2α dephosphorylation mediated by a herpes simplex virus protein and inhibits viral replication. These results suggest that selective chemical inhibitors of eIF2α dephosphorylation may be useful in diseases involving ER stress or viral infection. More broadly, salubrinal demonstrates the feasibility of selective pharmacological targeting of cellular dephosphorylation events.
Journal Article
Haschek and Rousseaux's handbook of toxicologic pathology
Haschek and Rousseaux's Handbook of Toxicologic Pathology is a key reference on the integration of structure and functional changes in tissues associated with the response to pharmaceuticals, chemicals and biologics.The 3e has been expanded by a full volume, and covers aspects of safety assessment not discussed in the 2e.
eBook
Effect of Anodal Transcranial Direct Current Stimulation on Autism: A Randomized Double-Blind Crossover Trial
The aim of this study was to evaluate the Childhood Autism Rating Scale (CARS), Autism Treatment Evaluation Checklist (ATEC), and Children’s Global Assessment Scale (CGAS) after anodal transcranial direct current stimulation (tDCS) in individuals with autism. Twenty patients with autism received 5 consecutive days of both sham and active tDCS stimulation (1 mA) in a randomized double-blind crossover trial over the left dorsolateral prefrontal cortex (F3) for 20 minutes in different orders. Measures of CARS, ATEC, and CGAS were administered before treatment and at 7 days posttreatment. The result showed statistical decrease in CARS score (P<0.001). ATEC total was decreased from 67.25 to 58 (P<0.001). CGAS was increased at 7 days posttreatment (P=0.042). Our study suggests that anodal tDCS over the F3 may be a useful clinical tool in autism.
Journal Article
Scalp thickening and folding in a pubertal boy
THE CASE: A 16-year-old boy with developmental delay and intellectual disability developed dramatic chronic wrinkling of his scalp over a year ago.The lesions were persistent but not symptomatic.What's the diagnosis? CUTIS VERTICIS GYRATA
Journal Article
