The use of parasites as bioindicators of pesticide exposure

Organisms used in risk assessment of pesticides must be the most sensitive ones to pesticides exposure. The aim of this study was to observe the effect of two commercial pesticide products (containing glyphosate and tolylfluanid) to larval stages of parasites Cooperia curticei, Ostertagia circumcincta, Haemonchus contortus and Trichostrongylus axei. There were two concentrations tested for each product vs. control group. Larvae (500 individuals/Petri dish) were incubated at 27 °C and observed daily for 42 days

Antioxidant Enzymes of Honeybee Larvae Exposed to Oxamyl

Oxamyl is a carbamate insecticide used to control a broad spectrum of insects. It can also affect non-targeted organisms when applied incorrectly. The world food production depends partially on honeybee pollination abilities and therefore it is directly linked to the health of bees. The success of the colony development depends, among other factors, on the health of the larvae. The first 6 days are crucial for their development. In this stage, the worker larvae grow exponentially and may be exposed to xenobiotics via their diet. In this study, we investigated the effect of oxamyl on honeybee larvae (Apis mellifera) by monitoring the changes in their antioxidant enzyme system. The activities of superoxide dismutase, catalase and glutathione-S-transferase were determined in the homogenates of in vitro reared honeybee larvae after their single dietary exposure to oxamyl at doses of 1.25, 2.5, 5, 10 and 20 µg a.i./larva (a. i.—active ingredient). The doses of oxamyl did not cause statistically significant changes in the activities of the enzymes. Even a slight activation of these enzymes protected the larvae from the adverse effects of the reactive oxygen species (ROS). Marked changes in both the enzyme activity and the content of lipid peroxidation products were observed at the oxamyl dose of 10 µg a. i./larva. This fact may indicate a potential oxidative damage to the larvae. These results allowed us to assume that the toxic effects of oxamyl involves not only the inhibition of acetylcholine esterase but is also associated with ROS production

Safe trapping of Cs in heat-treated zeolite matrices. Part. 2

Safe trapping of cesium was investigated by heat-treating at various temperatures a Slovakian clinoptilolite-rich tuff sample, previously subjected to exhaustive exchange with Cs(+). The influence of temperature on the process effectiveness was studied and the mechanism of Cs(+) immobilization explained. Treating the Cs-exchanged material, at 1000 degrees C results in zeolite breakdown and the formation of an amorphous, likely glassy, phase, which safely encapsulates the polluting cation, as it has been demonstrated by standard leaching tests. This study indicates that clinoptilolite-rich tuff is a good candidate for immobilization of cesium, taken up by ion exchange

Adenine nucleotide translocase family: Four isoforms for apoptosis modulation in cancer

Mitochondria have important functions in mammalian cells as the energy powerhouse and integrators of the mitochondrial pathway of apoptosis. The adenine nucleotide translocase (ANT) is a family of proteins involved in cell death pathways that perform distinctly opposite functions to regulate cell fate decisions. On the one hand, ANT catalyzes the adenosine triphosphate export from the mitochondrial matrix to the intermembrane space with the concomitant import of ADP from the intermembrane space to the matrix. On the other hand, during periods of stress, ANT could function as a lethal pore and trigger the process of mitochondrial membrane permeabilization, which leads irreversibly to cell death. In human, ANT is encoded by four homologous genes, whose expression is not only tissue specific, but also varies according to the pathophysiological state of the cell. Recent evidence revealed a differential role of the ANT isoforms in apoptosis and a deregulation of their expression in cancer. In this review, we introduce the current knowledge of ANT in apoptosis and cancer cells and propose a novel classification of ANT isoforms. © 2011 Macmillan Publishers Limited All rights reserved

Environmental and societal factors associated with COVID-19-related death in people with rheumatic disease: an observational study

Published by Elsevier Ltd.Background: Differences in the distribution of individual-level clinical risk factors across regions do not fully explain the observed global disparities in COVID-19 outcomes. We aimed to investigate the associations between environmental and societal factors and country-level variations in mortality attributed to COVID-19 among people with rheumatic disease globally. Methods: In this observational study, we derived individual-level data on adults (aged 18-99 years) with rheumatic disease and a confirmed status of their highest COVID-19 severity level from the COVID-19 Global Rheumatology Alliance (GRA) registry, collected between March 12, 2020, and Aug 27, 2021. Environmental and societal factors were obtained from publicly available sources. The primary endpoint was mortality attributed to COVID-19. We used a multivariable logistic regression to evaluate independent associations between environmental and societal factors and death, after controlling for individual-level risk factors. We used a series of nested mixed-effects models to establish whether environmental and societal factors sufficiently explained country-level variations in death. Findings: 14 044 patients from 23 countries were included in the analyses. 10 178 (72·5%) individuals were female and 3866 (27·5%) were male, with a mean age of 54·4 years (SD 15·6). Air pollution (odds ratio 1·10 per 10 μg/m3 [95% CI 1·01-1·17]; p=0·0105), proportion of the population aged 65 years or older (1·19 per 1% increase [1·10-1·30]; p<0·0001), and population mobility (1·03 per 1% increase in number of visits to grocery and pharmacy stores [1·02-1·05]; p<0·0001 and 1·02 per 1% increase in number of visits to workplaces [1·00-1·03]; p=0·032) were independently associated with higher odds of mortality. Number of hospital beds (0·94 per 1-unit increase per 1000 people [0·88-1·00]; p=0·046), human development index (0·65 per 0·1-unit increase [0·44-0·96]; p=0·032), government response stringency (0·83 per 10-unit increase in containment index [0·74-0·93]; p=0·0018), as well as follow-up time (0·78 per month [0·69-0·88]; p<0·0001) were independently associated with lower odds of mortality. These factors sufficiently explained country-level variations in death attributable to COVID-19 (intraclass correlation coefficient 1·2% [0·1-9·5]; p=0·14). Interpretation: Our findings highlight the importance of environmental and societal factors as potential explanations of the observed regional disparities in COVID-19 outcomes among people with rheumatic disease and lay foundation for a new research agenda to address these disparities.MAG is supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases (grant numbers K01 AR070585 and K24 AR074534 [JY]). KDW is supported by the Department of Veterans Affairs and the Rheumatology Research Foundation Scientist Development award. JAS is supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases (grant numbers K23 AR069688, R03 AR075886, L30 AR066953, P30 AR070253, and P30 AR072577), the Rheumatology Research Foundation (K Supplement Award and R Bridge Award), the Brigham Research Institute, and the R. Bruce and Joan M. Mickey Research Scholar Fund. NJP is supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases (T32-AR-007258). AD-G is supported by grants from the Centers for Disease Control and Prevention and the Rheumatology Research Foundation. RH was supported by the Justus-Liebig University Giessen Clinician Scientist Program in Biomedical Research to work on this registry. JY is supported by grants from the National Institutes of Health (K24 AR074534 and P30 AR070155).info:eu-repo/semantics/publishedVersio