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"Pathological physiology"
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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
Premature ejaculation: an update on definition and pathophysiology
Premature ejaculation (PE) is the most common male sexual dysfunction, which represents a diagnostic as well as a therapeutic challenge for physicians. However, no universally accepted definition is currently available for PE. As a result, physicians continue to diagnose patients with PE according to major guidelines set by the professional societies. These guidelines either recommend the use of validated questionnaires or patient-reported outcomes. Recent efforts directed toward classifying PE may help provide a better understanding of the prevalence and risk factors of this disorder. While the exact etiology of PE has not been clearly elucidated, several risk factors have been strongly reported in the literature. Clearly, to understand the revised definition of PE, its etiology and pathophysiology is necessary to improve the clinical management of this medical condition and form the basis of future research in this regard. In this review, we highlight the past and current definitions of PE and present an appraisal on the classifications and theories suggested for the etiopathogenesis of PE.
Journal Article
Thrombotic microangiopathies: a general approach to diagnosis and management
Thrombotic thrombocytopenic purpura is broadly defined as a thrombotic microangiopathy occurring in the context of severe ADAMTS13 deficiency (< 10%).7 ADAMTS13 is a normal enzyme in plasma that cleaves large forms of the coagulation protein von Willebrand factor into smaller functional subunits. The acquired form of TTP is thought to be due to an autoantibody against ADAMTS13, and the inherited form is due to a genetic deficiency of ADAMTS13. In 1996, Furlan and colleagues28 and Tsai29 independently found that patients with TTP had unusually large von Willebrand factor multimers in their plasma and that this was due to a reduction in the levels of the cleaving enzyme. Large von Willebrand factor multimers bind to platelets and form plateletrich fibrin strands, which leads to intravascular hemolysis and ischemic tissue injury. Tsai and [Lian EC]10 and Furlan and colleagues11 subsequently identified inhibitory antibodies as the cause for acquired disease. In 2001, the von Willebrand factor cleaving enzyme was identified as ADAMTS13 based on kindred studies involving patients with the congenital form of TTP called Upshaw-Schulman syndrome.8 Congenital TTP often presents in childhood but can manifest for the first time after a \"second hit\" later in life; for women, this can occur during or immediately after pregnancy.8,9 ADAMTS13 testing has no role in the initial management of thrombotic microangiopathy. Severely reduced levels of ADAMTS13 are consistent with the diagnosis of TTP and can distinguish TTP from atypical HUS; however, results of ADAMTS13 testing should not be used to guide initial treatment. If TTP is suspected, plasma exchange should be instituted regardless of the results of ADAMTS13 testing.
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