Project description:Lead Exposure and Human Brain Evolution: A 2-Million-Year Perspective This study reveals that lead exposure was pervasive throughout human evolution, not just a modern phenomenon. Researchers analyzed 51 fossil teeth from multiple hominid species spanning 2+ million years across three continents, finding lead exposure evidence in 73% of specimens using advanced laser ablation mass spectrometry. The team then used human brain organoids carrying either modern or archaic (Neanderthal-like) variants of the NOVA1 gene to test lead's neurological impacts. They discovered that the archaic variant showed greater vulnerability to lead-induced disruption of FOXP2 expression—a gene crucial for speech and language development. This suggests environmental lead exposure may have created evolutionary pressure favoring the modern human NOVA1 variant, potentially giving our species advantages in communication and social cohesion. The research challenges established paradigms about both environmental toxin history and human evolution, proposing that gene-environment interactions with neurotoxins helped shape our species' cognitive development over millions of years.
Project description:This study examines the relationship between sleep apnea and glucose metabolism. Physiological studies have demonstrated that 5 days of exposure to intermittent hypoxia (similar to what occurs with sleep apnea) leads to significant improvements in glucose tolerance. Therefore, this study investigates the hypothesis that intermittent hypoxia may lead to upregulation of some novel peptide(s) that have a powerful glucose lowering action.
Project description:In this study we analyzed the effects of lead-exposure up hippocampal gene expression in males and females exposed to 0ppm, 250ppm and 750ppm lead during two different developmental periods, perinatal (in utero through to weaning at PND21) and postnatal (PND0-PND45), across three strains (Fischer, Long Evans and Sprague Dawley). All tissue was taken at PND 55. We used affymetrix Rat Gene 1.0ST arrays to obtain global gene expression data from each animal, with a group size of 4 for all conditions (Total number of Arrays = 119) Gene expression was profiled in the hippocampus of rats at no lead exposure (0ppm), 250ppm and 750 ppm lead exposure levels during perinatal and postnatal developmental periods of both males and females of three strains of rat (Fischer, Long Evans and Sprague Dawley).
Project description:Lead exposure causes a variety of health effects, especially in children, that may include cognitive and behavioural problems. This study explores the mechanisms associated with this relationship by assessing alterations in gene expression of C57BL/6J pups treated with 50mg/kg lead compared to controls. In addition this study also analyzed brain gene expression differences in Metallothionein I and II (Mt-I and Mt-II) knockout mice treated with lead.
Project description:Quantifying impact of lead on cytokine production and gene expression in PBMCs Cells were treated with 10mkM lead acetate for one day, washed and grown in RPMI for the second day. Lead acetate was not added to matching control cells.
Project description:Lead exposure causes a variety of health effects, especially in children, that may include cognitive and behavioural problems. This study explores the mechanisms associated with this relationship by assessing alterations in gene expression of C57BL/6J pups treated with 50mg/kg lead compared to controls. In addition this study also analyzed brain gene expression differences in Metallothionein I and II (Mt-I and Mt-II) knockout mice treated with lead. Pups of three genotypes (C57BL/6J, Mt-KO with a C57BL/6J background and Heterozygote Mt-KO) were injected with lead acetate during synaptogenesis and weight-matched controls were injected with saline at the same time points. Whole brains were harvested and RNA extracted and pooled from 5 pups and hybridized to Mouse Genome 430 2.0 Arrays. In total 6 arrays were used, one for each genotype and treatment.
Project description:In this study we analyzed the effects of lead-exposure up hippocampal gene expression in males and females exposed to 0ppm, 250ppm and 750ppm lead during two different developmental periods, perinatal (in utero through to weaning at PND21) and postnatal (PND0-PND45), across three strains (Fischer, Long Evans and Sprague Dawley). All tissue was taken at PND 55. We used affymetrix Rat Gene 1.0ST arrays to obtain global gene expression data from each animal, with a group size of 4 for all conditions (Total number of Arrays = 119)
Project description:The purpose of this study was to clarify the possible mechanism of common carp brain injury after exposure to lead through transcriptome analysis. Transcriptome analysis showed that 2141 differentially expressed genes were identified. Among these, 502 genes were up-regulated and 1639 genes were down-regulated. Meanwhile, GO enrichment analysis showed Transport, biological_process, DNA-templated (regulation of transcription) and signal transduction contained the most differential genes in the biological process. Furthermore, KEGG pathway enrichment analysis showed Ion channels, GnRH signaling pathway, cell adhesion molecules, Wnt signaling pathway, and calcium signaling pathway were significantly enriched. In addition, 10 differentially expressed genes were selected for qRT-PCR detection, and the results demonstrated that the selected genes exhibited the same trends with the RNA-Seq results, which indicates the transcriptome sequencing data is reliable. In conclusion, the above results provide a theoretical basis for clarifying the relationship between lead exposure and brain injury in common carp and for further studying of the genes related to lead poisoning.