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Biomedical subjects

E Mera

Publications and source records attributed to E Mera.

7 recordsLinked to original sources
PubMed1998

Risk factors for childhood burn injuries: a case-control study from Greece.

During a 12-month period 239 children who presented with a burn injury at the Emergency Department of a teaching children's hospital in Athens, with city-wide coverage, and 239 gender- and age-matched controls with minor non-injury ailments were interviewed. The questionnaire covered sociodemographic characteristics of the children and their families, information allowing the construction of a burn avoidance index in their homes and items from the Achenback scale that were synthesized into a child activity score. The data were analyzed through conditional logistic regression. In general, socio-demographic variables were not of overwhelming importance, although some of the findings indicate that supervision lapses and barefoot walking of gypsy children increase the risk of burn injuries. The kitchen in an inherently high risk place for injuries and the powerful inverse association of the burn avoidance index with burn injury risk points towards steps that could be easily taken and impart substantial protection. There was no evidence in this study of burn injury proneness or that hyperactivity of the child increased the risk of burn injury; indeed, the results point in the opposite direction. Our results strongly support the view that childhood burn injuries are largely environmentally conditioned and, accordingly, easily preventable.

Burns↗
PubMed1998

Diet during pregnancy in relation to birthweight in healthy singletons.

We have investigated the relationship between consumption of food groups and intake of energy-generating macronutrients on the one hand, and birthweight on the other among apparently healthy singleton, term babies. Three hundred and sixty-eight women who delivered in six maternity clinics in two Greek cities during specified days over an 8-month period completed a 190-item, interviewer-administered, validated, semiquantitative food frequency questionnaire. Study participants also provided information on sociodemographic, reproductive and lifestyle variables. Data were analysed using multiple regression modelling. Nutritional variables were energy-adjusted, and non-nutritional correlates of birthweight were accounted for. The analysis revealed most of the established non-nutritional associations of birthweight -- an indication of study validity. Among food groups, meat and meat products and fish and sea food were suggestively associated with increased birthweight (two tailed P-values 0.08 and 0.16, respectively). Among energy-generating nutrients, monounsaturated fat was positively associated with birthweight and significantly so in several of the models. We consider our findings are considered as compatible with hypotheses linking fish and meat intake to fetal growth and as indicative of a positive association between intake of monounsaturated fat and birthweight.

Adult↗
PubMed1997

Aplastic anemia in a young coke plant worker.

The objective of this study was to make a contribution to the debate on the cause-effect relationship between low-dose exposure to benzene and onset of hemopathies. We report the case of a coke plant worker suffering from aplastic anemia. Before being hired at the coke plant, he underwent a medical examination including a blood cell count: no disease or abnormalities of the blood crasis were found. For 3 years the patient was then exposed to gas containing-as measured in environmental investigation carried out at the coke plant-concentrations of benzene lower than TLV-TWA ACGIH (measured values 21-109 micrograms/m3). In the absence from the patient's history of any exposure to other myelotoxic agents and of any earlier pathology causing aplastic anemia, we assume there is a relationship between exposure to low levels of benzene and onset of the disease. However, it is very important to consider that exposure to low levels of benzene could promote myelotoxic reactions when the working environment contains other substances that may act synergistically or compete for the same metabolism sites, or when carcinogenic substances are present in the working environment.

Adult↗
PubMedDate not supplied

Cimetidine prevents and partially reverses CCl4-induced liver cirrhosis.

Liver injury produced by CCl4 depends on its metabolism by the liver cytochrome P450 enzyme system to a highly reactive intermediate (CCl3.). Cimetidine impairs cytochrome P450 and stimulates regenerative processes acting on DNA synthesis. This work was performed to investigate whether cimetidine may prevent CCl4-induced liver cirrhosis. Male Wistar rats were used: animals in group 1 received CCl4 (0.04 g per 100 g, i.p.) three times a week for 8 weeks; group 2 was treated with CCl4 plus cimetidine (120 mg kg-1, p.o.) three times a week for 8 weeks; group 3 received CCl4 for 8 weeks and then cimetidine for 4 weeks. Alkaline phosphatase, gamma-glutamyl transpeptidase (gamma-GTP) and alanine aminotransferase (ALT) activities, as well as protein and bilirubin, were measured in serum; collagen and lipoperoxidation were quantified in liver. Intoxication with CCl4 increased (P < 0.05) serum activities of alkaline phosphatase, gamma-GTP and ALT, and bilirubin concentration; liver collagen and lipoperoxidation were also increased. Cimetidine treatment prevented or reverted the increases in the three enzyme activities and in bilirubin content and the fall in proteins. It is worth noting that cimetidine co-treatment completely prevented both the increase in collagen content and the lipid peroxidation. The protective effect of cimetidine can be attributed to a reduction in cytochrome P450. However, it could also stimulate regenerative processes.

Alanine Transaminase↗