De Prophet Error Rate; UP = Unique Peptides. Functional assignment of protein identifications was predicted manually using The Institute for Genomic Research Comprehensive Microbial Resource (JCVI-CMR) (http://cmr.jcvi.org/tigr-scripts/CMR/ GenomePage.cgi?org = ntlm01). Significantly different protein abundances (G-test; p#0.05) are indicated with shading and their common names are shown. (DOC)AcknowledgmentsWe thank Edwin Lowe of the University of Tasmania Central Science Laboratory for in-house method development and processing of MudPIT samples.Author ContributionsConceived and designed the experiments: RN JB TR. Performed the experiments: RN. Analyzed the data: RN MB. Contributed reagents/ materials/analysis tools: JB TR MB. Wrote the paper: RN MB.Alkaline Induced Anaerobiosis in L. monocytogenes
Perfluorinated compounds (PFCs) are persistent, bioaccumulative toxicants. Widespread human exposures to PFCs, including in fetuses, is well documented [1,2]. Among these compounds, Perfluorooctane sulfonate (PFOS) is the most intensively studied member of PFC family, and is daily used in clothing, carpets, textiles, upholstery, paper, packaging and cleaning products [3]. In recent years, researchers have reported PFCs contamination in river, tap and bottled water in Japan, the US, Europe and in developing countries such as Thailand, Malaysia and Vietnam. The accumulation of PFOS in mammals is mainly in the liver and serum, as well as in the brain up to as high as 32 of the serum concentration [4]. For PFOS might cross the placenta barrier [5,6] and blood-brain barrier [7], some previous studies have focused on the developmental neurotoxicity induced by PFOS [8,9,10]. Additionally, Johansson et al. found that neonatal exposure of mice to PFOS altered the expression of proteins critical for normal brain development and Anlotinib chemical information caused neurobehavioral defects, which persists into adulthood life [11,12].A study based on 4,943 mother-child pairs has looked into the relationship between PFOS serum concentration of both child and mother in paired Vasopressin supplier samples over a wide range of the child’s age (1?19 years) and found PFOS concentration tended to be higher in children than in their mothers. Since this difference persisted until they were at least 19 years of age for PFOS [13], it is also important to explore the neurotoxicity of PFOS in adults. The effects of PFOS on adult brain and its potential mechanism remains unclear. It is reported that PFOS exposure cause a deficit in spatial memory in adult male mice [14] without disturbing motor and sensory function, general activity and exploratory behavior. All these indicate that PFOS probably causes deficits in some brain areas such as hippocampus, which is structure directly responsible for the acquisition and the retention of spatial memory and especially vulnerable to damage [15]. The purpose of this study is to determine the neurotoxicity of PFOS treatment and the potential mechanism in adult mice. Herein, the water maze study is utilized to assess impairments in spatial learning and memory after exposure to PFOS for three months. The apoptosis profile of hippocampal cells as well as the levels of glutamate, gamma-aminobutyric acid (GABA), dopamineNeurotoxicity of PFOS in Adult Mice(DA), 3,4-dihydrophenylacetic acid (DOPAC), and homovanillic acid (HVA) are evaluated (Figure S1. and Figure S2). By twodimensional fluorescence difference in gel electrophoresis (2DDIGE) and western blotting analysis, the target pr.De Prophet Error Rate; UP = Unique Peptides. Functional assignment of protein identifications was predicted manually using The Institute for Genomic Research Comprehensive Microbial Resource (JCVI-CMR) (http://cmr.jcvi.org/tigr-scripts/CMR/ GenomePage.cgi?org = ntlm01). Significantly different protein abundances (G-test; p#0.05) are indicated with shading and their common names are shown. (DOC)AcknowledgmentsWe thank Edwin Lowe of the University of Tasmania Central Science Laboratory for in-house method development and processing of MudPIT samples.Author ContributionsConceived and designed the experiments: RN JB TR. Performed the experiments: RN. Analyzed the data: RN MB. Contributed reagents/ materials/analysis tools: JB TR MB. Wrote the paper: RN MB.Alkaline Induced Anaerobiosis in L. monocytogenes
Perfluorinated compounds (PFCs) are persistent, bioaccumulative toxicants. Widespread human exposures to PFCs, including in fetuses, is well documented [1,2]. Among these compounds, Perfluorooctane sulfonate (PFOS) is the most intensively studied member of PFC family, and is daily used in clothing, carpets, textiles, upholstery, paper, packaging and cleaning products [3]. In recent years, researchers have reported PFCs contamination in river, tap and bottled water in Japan, the US, Europe and in developing countries such as Thailand, Malaysia and Vietnam. The accumulation of PFOS in mammals is mainly in the liver and serum, as well as in the brain up to as high as 32 of the serum concentration [4]. For PFOS might cross the placenta barrier [5,6] and blood-brain barrier [7], some previous studies have focused on the developmental neurotoxicity induced by PFOS [8,9,10]. Additionally, Johansson et al. found that neonatal exposure of mice to PFOS altered the expression of proteins critical for normal brain development and caused neurobehavioral defects, which persists into adulthood life [11,12].A study based on 4,943 mother-child pairs has looked into the relationship between PFOS serum concentration of both child and mother in paired samples over a wide range of the child’s age (1?19 years) and found PFOS concentration tended to be higher in children than in their mothers. Since this difference persisted until they were at least 19 years of age for PFOS [13], it is also important to explore the neurotoxicity of PFOS in adults. The effects of PFOS on adult brain and its potential mechanism remains unclear. It is reported that PFOS exposure cause a deficit in spatial memory in adult male mice [14] without disturbing motor and sensory function, general activity and exploratory behavior. All these indicate that PFOS probably causes deficits in some brain areas such as hippocampus, which is structure directly responsible for the acquisition and the retention of spatial memory and especially vulnerable to damage [15]. The purpose of this study is to determine the neurotoxicity of PFOS treatment and the potential mechanism in adult mice. Herein, the water maze study is utilized to assess impairments in spatial learning and memory after exposure to PFOS for three months. The apoptosis profile of hippocampal cells as well as the levels of glutamate, gamma-aminobutyric acid (GABA), dopamineNeurotoxicity of PFOS in Adult Mice(DA), 3,4-dihydrophenylacetic acid (DOPAC), and homovanillic acid (HVA) are evaluated (Figure S1. and Figure S2). By twodimensional fluorescence difference in gel electrophoresis (2DDIGE) and western blotting analysis, the target pr.
