Physical activity and sudden cardiac death in elders--a Croatian study

The paper deals with the sudden cardiac death in elders due to physical activity in Croatia and to compare it to other population groups who practice physical activity. The data are a part of a retrospective study dealing with 59 sudden death due to physical activity in men in Croatia: from January 1, 1988 to December 31, 2008. Fifteen aged 65 to 82 years were recreationally engaged in physical activity: six in swimming, four in tennis, one in driving a bicycle, one in jogging, two in bowling and one died during sexual act. Only one had symptoms of pectoral angina, two suffered from arterial hypertension, and two had congestive heart failure. Eleven were without symptoms before exercise. At forensic autopsy, fourteen had coronary heart disease, seven had critical coronary artery stenosis, three had occluded left descendens anterior coronary artery and four critical coronary stenosis, four had a recent myocardial infarctions, and eleven had myocardial scars due to previous myocardial infarctions. Twelve of them had left ventricular hypertrophy: 15-25 mm. In Croatia, about 7per cent of the entire male population undertake recreational physical activity, while 13 per cent of them are elders. A sudden cardiac death due to recreational physical activity in elders reached 1.71/100 000 yearly, in the entire male population engaged in recreational physical exercise: 0.75/100 000 (p = 0.05730), in the total male population aged 15-40 engaged in sports and recreational physical exercise: 0.57/100.0000 (p = 0.00387), in young athletes: 0.15/100 000 (p = 0.00000). Medical examination of all elderly persons has to be done before starting of recreational physical activity: by clinical examination, searching for risk factors for atherosclerosis, performing ECG at rest, stress ECG, and echocardiography and to repeat the medical examination at least once a year Physical activity should start with a warm-up period and with a gradually increasing load, and usually not to exceed 6-7 metabolic equivalents (METs).     

Induced cell injury and cell death as a cause of congenital malformations in rats

Summary Enbryopathy has been produced by inhibition of histiotrophic nutrition in the rat using a number of agents which prevent this process. The experiments were carried outin vitro at various stages of development before the inception of a chorio allantoic placenta. Dose-dependent effects on the embryo were demonstrated using the acid bisazo dye Trypan Blue, which inhibits endocytosis, and an enzyme inhibitor of bacterial origin known as leupeptin which inhibits cathepsin B, H and L. Homogenates of rat kidney and placenta also produced congenital defects; the concommitant electron microscopical changes in the yolk sac suggest that these effects too are due to alterations in the availability or quality of histiotroph.     

Mammalian cells: Damage in late replicating DNA as the most efficient cause of reproductive death

Chinese hamster cells were synchronized by mitotic shake off, labeled in the first S period with ¹²⁵IUdR, cooled to 4 °C in the G2 stage and then stored up to 4 days to accumulate damage due to ¹²⁵I disintegrations in cell DNA. There was a large difference in the efficiency of induction of reproductive death when damage accumulated in the DNA, which replicated in the second half of the DNA synthesis period, was compared with damage accumulated in the DNA, which replicated in the first half of the DNA synthesis period. Damage accumulated in the late replicated DNA appears to be the most critical. This result suggests that the mammalian cell nucleus is not homogeneous with respect to the damaging events leading to reproductive death and may stress the importance for cell survival of the integrity of the late-replicating, heterochromatic DNA near the nucleus membrane.     

Turner syndrome morphology and morphometrics: Cardiac hypoplasia as a cause of midgestation death

BACKGROUND: A female fetus with massive truncal-limb hydrops and large, loculated, nuchal hygromas in midgestation is highly likely to have Turner syndrome. This phenotype is recognized to be usually lethal, with only more mildly affected fetuses surviving to term birth. METHODS: The morphology and morphometrics of 117 midgestation fetuses with phenotypic Turner syndrome were analyzed. RESULTS: More than 90% of fetuses with phenotypic Turner syndrome were found to have heart weights below the 2.5 centile, as well as lung hypoplasia and restricted limb growth for brain weight standards, although brain weight was only mildly reduced for gestational age. In contrast, subnormal heart weight was much less common among fetuses with other etiologies of hydrops, hygromas, or pleural effusions. CONCLUSIONS: We hypothesize that myocardial hypoplasia is a primary defect in Turner syndrome, and it leads to or is a major contributor to the phenotypic features that end in midgestational death.     

Spontaneous rupture of the spleen as a cause of death of a patient with uremia

A case of spontaneous rupture of the spleen in young patient with uremia treated with hemodialyses is presented. A course of the disease was acute with severe shock leading to patient's death. Possible edema of the spleen and subcapsular hematomas related to the uremic coagulopathy and the use of heparin during hemodialyses may be the factors predisposing to the rupture of the spleen.     

Starvation induced cell death in autophagy-defective yeast mutants is caused by mitochondria dysfunction

Autophagy is a highly-conserved cellular degradation and recycling system that is essential for cell survival during nutrient starvation. The loss of viability had been used as an initial screen to identify autophagy-defective (atg) mutants of the yeast Saccharomyces cerevisiae, but the mechanism of cell death in these mutants has remained unclear. When cells grown in a rich medium were transferred to a synthetic nitrogen starvation media, secreted metabolites lowered the extracellular pH below 3.0 and autophagy-defective mutants mostly died. We found that buffering of the starvation medium dramatically restored the viability of atg mutants. In response to starvation, wild-type (WT) cells were able to upregulate components of the respiratory pathway and ROS (reactive oxygen species) scavenging enzymes, but atg mutants lacked this synthetic capacity. Consequently, autophagy-defective mutants accumulated the high level of ROS, leading to deficient respiratory function, resulting in the loss of mitochondria DNA (mtDNA). We also showed that mtDNA deficient cells are subject to cell death under low pH starvation conditions. Taken together, under starvation conditions non-selective autophagy, rather than mitophagy, plays an essential role in preventing ROS accumulation, and thus in maintaining mitochondria function. The failure of response to starvation is the major cause of cell death in atg mutants.     

Eosinophilic bronchitis-like lesion as the cause of death in a Macaca mulatta: a first case report

BACKGROUND: Eosinophilic bronchitis is a recently described, relatively benign condition in humans that is characterized by a corticosteroid-responsive chronic cough and sputum eosinophilia without the abnormalities of airway function seen in asthma. The exact cause of this condition is currently unknown, however has been associated with various occupational exposures in humans. It has also been reported to progress to irreversible airway obstruction. This disease has been reported in dogs and horses, but not in non-human primates. METHODS: Gross examination of an otherwise healthy 13-year-old, colony-born Macaca mulatta, which died of severe non-responsive respiratory distress revealed that the lungs were markedly inflated and moist. RESULTS: Hematoxylin and eosin-stained sections from the lungs contained widespread accumulation of eosinophils, sloughed epithelial cells, and mucus centered around bronchioles and adjacent airways. There was no evidence of mast cell infiltration of peribronchiolar smooth muscle, goblet cell hyperplasia, or basement membrane thickening. CONCLUSIONS: This ruled out recurrent episodes as would be expected in asthma, favoring the diagnosis of an eosinophilic bronchitis-like lesion. We report a first case of eosinophilic bronchitis-like features in a M. mulatta.