1,721,350 research outputs found
Contributions to the understanding of Soviet Taylorism from October to NEP (1917-1929)
Full text linkFil: Sgrazzutti, Jorge. Universidad Nacional de Rosario. Facultad de Humanidades y Artes; ArgentinaFil: Oliva, Antonio. Universidad Nacional de Rosario. Facultad de Humanidades y Artes; Argentin
La Revolución Rusa en el país de los zares. Impactos y problemas
Full text linkFil: Sgrazzutti, Jorge. Universidad Nacional de Rosario; Argentina
Fil: Oliva, Antonio. Universidad Nacional de Rosario; Argentin
Editorial: Genetics of sudden unexplained death in children and young adults: state of the art, testing and implications for translational research, public health and forensic pathology
Full text linkEditorial: Genetics of sudden unexplained death in children and young adults: state of the art, testing and implications for translational research, public health and forensic patholog
Genetic predisposition and cellular basis for ischemia-induced ST-segment changes and arrhythmias.
No full textVentricular tachycardia and fibrillation (VT/VF) complicating Brugada syndrome, a genetic disorder linked to SCN5A mutations, and VF complicating acute myocardial infarction (AMI) have both been linked to phase 2 reentry. Because of these mechanistic similarities in arrhythmogenesis, we examined the contribution of SCN5A mutations to VT/VF complicating AMI. Nineteen consecutive patients developing VF during AMI were enrolled. Wild-type (WT) and mutant SCN5A genes were co-expressed with SCN1B in TSA201 cells and studied using whole-cell patch-clamp techniques. One missense mutation (G400A) in SCN5A was detected in a conserved region among the cohort of 19 patients. A H558R polymorphism was detected on the same allele. Unlike the other 18 patients who each developed 1-2 VF episodes during acute MI, the mutation carrier developed six episodes of VT/VF within the first 12 hours. All VT/VF episodes were associated with ST segment changes and were initiated by short-coupled extrasystoles. We describe the first sodium channel mutation to be associated with the development of an arrhythmic storm during acute ischemia. These findings suggest that a loss of function in SCN5A may predispose to ischemia induced arrhythmic storm. These results could be very useful for forensic implications regarding genetic screening in relatives
Progression of electroanatomic substrate and electric storm recurrence in a patient with Brugada syndrome
No full textIn December 2011, a 39-year-old man resuscitated from out-of-hospital cardiac arrest caused by ventricular fibrillation received the diagnosis of Brugada syndrome on the basis of a spontaneous Brugada type 1 ECG pattern (Figure 1A). Before implantation of a cardioverter-defibrillator, the patient, after providing written informed consent, underwent a 3-dimensional electroanatomic mapping of the right ventricle (RV) as part of a clinical research study approved by ethics committee of our institution. A localized low-voltage area with delayed and fragmented potentials was evident in both bipolar and unipolar voltage maps in the anterior RV outflow tract. The patient was discharged with no antiarrhythmic medication and was free of arrhythmic events at implantable cardioverter-defibrillator interrogation for 1 year
Negative autopsy and sudden cardiac death
No full textForensic medicine defines the unexplained sudden death as a death with a non-conclusive diagnosis after autopsy. Molecular diagnosis is being progressively incorporated in forensics, mainly due to improvement in genetics. New genetic technologies may help to identify the genetic cause of death, despite clinical interpretation of genetic data remains the current challenge. The identification of an inheritable defect responsible for arrhythmogenic syndromes could help to adopt preventive measures in family members, many of them asymptomatic but at risk of sudden death. This multidisciplinary translational research requires a specialized team
Genetic causes of sudden infant death syndrome: a postmortem investigation not to be missed
No full textSudden cardiac deaths in infancy have always been assumed to be caused by genetic defects in ion channels, given its lack of structural abnormalities. Nevertheless, it is possible that some of the variants listed as putative pathogenic mutations may be innocuous functionally. Therein lies the difficulty in determining the “actionableness” of these rare, nonfunctionally characterized genetic variants when the probability of pathogenicity for that given variant is not 100%. Believe it or not, together with the preliminary hypotheses raised by Harris et al regarding possible novel respiratory viral infections as causes of SIDS, we still do need to account the putative role of HCM genetic variants in SIDS, which lead us a new scenario in diagnosis and prevention of this lethal entity
Same-session multiple procedures in office-based surgery: A warning for the growing and dangerous field of office surgery
No full textNo abstract availabl
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