ORCID Profile
0000-0001-8222-0186
Current Organisations
World Health Organization
,
Universidade Federal do Pampa - Campus Uruguaiana
,
Retired
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Publisher: Springer Science and Business Media LLC
Date: 02-10-2013
Publisher: Cold Spring Harbor Laboratory
Date: 13-10-2023
Publisher: Springer Science and Business Media LLC
Date: 04-08-2011
Publisher: Public Library of Science (PLoS)
Date: 16-07-2008
Publisher: Oxford University Press (OUP)
Date: 12-2004
DOI: 10.1016/J.TRSTMH.2004.03.010
Abstract: Several studies suggest that in in iduals with substantial previous exposure to malaria, co-infection with multiple clones of Plasmodium falciparum can protect against subsequent clinical malaria attacks. Other studies, mainly of in iduals with little previous exposure, found the converse relationship. To test whether acquisition of such cross-protection tracks the acquisition of clinical immunity in general, 610 Tanzanian children aged 0-6 years were enrolled in a nine-month prospective study of the risk of morbidity in relation to parasitological status and merozoite surface protein 2 genotypes on enrolment. Prevalence of parasitaemia and multiplicity of infection increased with age. In the first year of life, the incidence of clinical malaria was almost three times higher in children with parasites at baseline than in those without. In older children, baseline P. falciparum infections appeared to protect against both parasitaemic and non-parasitaemic fever episodes. In children aged less than three years, baseline multiple infection tended to be associated with higher prospective risk of clinical malaria than single infection while in children aged more than three years the converse was found, but these effects were not statistically significant. These results provide further evidence that relationships between asymptomatic malaria infections and clinical malaria change with cumulative exposure.
Publisher: Springer Science and Business Media LLC
Date: 11-2003
DOI: 10.1038/NRG1206
Publisher: CSIRO Publishing
Date: 2017
DOI: 10.1071/RD16310
Abstract: Mercury is a ubiquitous environmental pollutant and mercury contamination and toxicity are serious hazards to human health. Some studies have shown that mercury impairs male reproductive function, but less is known about its effects following exposure at low doses and the possible mechanisms underlying its toxicity. Herein we show that exposure of rats to mercury chloride for 30 days (first dose 4.6 µg kg–1, subsequent doses 0.07 µg kg–1 day–1) resulted in mean (± s.e.m.) blood mercury concentrations of 6.8 ± 0.3 ng mL–1, similar to that found in human blood after occupational exposure or released from removal of amalgam fillings. Even at these low concentrations, mercury was deposited in reproductive organs (testis, epididymis and prostate), impaired sperm membrane integrity, reduced the number of mature spermatozoa and, in the testes, promoted disorganisation, empty spaces and loss of germinal epithelium. Mercury increased levels of reactive oxygen species and the expression of glutathione peroxidase (GPx) 1 and GPx4. These results suggest that the toxic effects of mercury on the male reproductive system are due to its accumulation in reproductive organs and that the glutathione system is its potential target. The data also suggest, for the first time, a possible role of the selenoproteins GPx1 and GPx4 in the reproductive toxicity of mercury chloride.
Publisher: Elsevier BV
Date: 04-2016
Location: United States of America
Location: No location found
No related grants have been discovered for David Schellenberg.