Институционализация памяти: научно-организационные формы и практики изучения Великой Отечественной войны в советской и постсоветской историографии

Статья подготовлена в рамках проекта «Великая Отечественная война в пространстве исторической памяти Юга России» Подпрограммы фундаментальных исследований «Проблемы социально-экономического и этнополитического развития южного макрорегиона» Программы Президиума РАН «Фундаментальные проблемы пространственного развития Российской Федерации: междисциплинарный синтез» на 2009–2011 гг

Health-related quality of life and mental health problems after a disaster: Are chronically ill survivors more vulnerable to health problems?

Studies have shown that the chronically ill are at higher risk for reduced health-related quality of life (HRQL) and for mental health problems. A combination with traumatic events might increase this risk. This longitudinal study among 1216 survivors of a disaster examines whether chronically ill survivors had a different course of HRQL and mental health problems compared to survivors without chronic diseases. HRQL and mental health problems were measured 3 weeks, 18 months and 4 years post-disaster. Data on pre-disaster chronic diseases was obtained from the electronic medical records of general practitioners. Random coefficient analyses showed significant interaction effects for social functioning, bodily pain and emotional role limitations at T2 only. Chronically ill survivors did not consistently have a different course of general health, physical role limitations, and mental health problems. In conclusion, chronic diseases were not an important risk factor for impaired HRQL and mental health problems among survivors

Erythropoietin induces neovascularization and improves cardiac function in rats with heart failure after myocardial infarction

ObjectivesWe assessed the effects of erythropoietin (EPO) treatment in a rat model of post-myocardial infarction (MI) heart failure.BackgroundErythropoietin, traditionally known as a hematopoietic hormone, has been linked to neovascularization. Whereas administration of EPO acutely after MI reduces infarct size and improves cardiac function, its role in the failing heart is unknown.MethodsRats underwent coronary ligation or sham surgery. Rats with MI were randomly assigned to: untreated (MI), a single bolus of EPO immediately after MI induction (MI-EPO-early), EPO treatment immediately after MI and once every three weeks (MI-EPO-early+late), and EPO treatment starting three weeks after induction of MI, once every three weeks (MI-EPO-late). After nine weeks, hemodynamics, infarct size, myosin heavy chain (MHC) isoforms, myocyte hypertrophy, and capillary density were measured.ResultsErythropoietin treatment started immediately after MI (MI-EPO-early and MI-EPO-early+late) resulted in a 23% to 30% reduction in infarct size (p < 0.01) and, accordingly, hemodynamic improvement. Erythropoietin treatment, started three weeks after MI (MI-EPO-late), did not affect infarct size, but resulted in an improved cardiac performance, reflected by a 34% reduction in left ventricular end-diastolic pressure (p < 0.01), and 46% decrease in atrial natriuretic peptide levels (p < 0.05). The improved cardiac function was accompanied by an increased capillary density (p < 0.01), an increased capillary-to-myocyte ratio (p < 0.05), and a partial reversal of beta-MHC (p < 0.05) in all treated groups.ConclusionsIn addition to its effect on infarct size reduction, EPO treatment improves cardiac function in a rat model of post-MI heart failure. This observation may be explained by neovascularization, associated with an increased alpha-MHC expression

Cardiomyocyte hypocontractility and reduced myofibril density in end-stage pediatric cardiomyopathy

Dilated cardiomyopathy amongst children (pediatric cardiomyopathy, pediatric CM) is associated with a high morbidity and mortality. Because little is known about the pathophysiology of pediatric CM, treatment is largely based on adult heart failure therapy. The reason for high morbidity and mortality is largely unknown as well as data on cellular pathomechanisms is limited. Here, we assessed cardiomyocyte contractility and protein expression to define cellular pathomechanisms in pediatric CM. Explanted heart tissue of 11 pediatric CM patients and 18 controls was studied. Contractility was measured in single membrane-permeabilized cardiomyocytes and protein expression was assessed with gel electrophoresis and western blot analysis. We observed increased Ca2+-sensitivity of myofilaments which was due to hypophosphorylation of cardiac troponin I, a feature commonly observed in adult DCM. We also found a significantly reduced maximal force generating capacity of pediatric CM cardiomyocytes, as well as a reduced passive force development over a range of sarcomere lengths. Myofibril density was reduced in pediatric CM compared to controls. Correction of maximal force and passive force for myofibril density normalized forces in pediatric CM cardiomyocytes to control values. This implies that the hypocontractility was caused by the reduction in myofibril density. Unlike in adult DCM we did not find an increase in compliant titin isoform expression in end-stage pediatric CM. The limited ability of pediatric CM patients to maintain myofibril density might have contributed to their early disease onset and severity