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[PMID]: 25707986
[Au] Autor:Moser VC; Phillips PM; McDaniel KL
[Ad] Address:Toxicity Assessment Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development, US Environmental Protection Agency, Research Triangle Park, NC, United States. Electronic address: Moser.ginger@epa.gov.
[Ti] Title:Assessment of biochemical and behavioral effects of carbaryl and methomyl in Brown-Norway rats from preweaning to senescence.
[So] Source:Toxicology;331:1-13, 2015 May 4.
[Is] ISSN:1879-3185
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:Factors impacting life stage-specific sensitivity to chemicals include toxicokinetic and toxicodynamic changes. To evaluate age-related differences in the biochemical and behavioral impacts of two typical N-methyl carbamate pesticides, we systematically compared their dose-response and time-course in preweanling (postnatal day, PND, 18) and adult male Brown Norway rats (n=9-10/dose or time) ranging from adolescence to senescence (1, 4, 12, 24mo). Carbaryl was administered orally at 3, 7.5, 15, or 22.5mg/kg and data were collected at 40min after dosing, or else given at 3 or 15mg/kg and data collected at 30, 60, 120, and 240min. Methomyl was studied only in adult and senescent rat (4, 12, 24mo) in terms of dose-response (0.25. 0.6, 1.25, 2.5mg/kg) and time-course (1.25mg/kg at 30, 60, 120, 240min). Motor activity as well as brain and erythrocyte (RBC) cholinesterase (ChE) activity were measured in the same animals. In the carbaryl dose-response, PND18 rats were the most sensitive to the brain ChE-inhibiting effects of carbaryl, but 12- and 24-mo rats showed more motor activity depression even at similar levels of brain ChE inhibition. We have previously reported that brain ChE inhibition, but not motor activity effects, closely tracked carbaryl tissue levels. There were no age-related differences in methomyl-induced ChE inhibition across doses, but greater motor activity depression was again observed in the 12- and 24-mo rats. Carbaryl time-course data showed that motor activity depression reached a maximum later, and recovered slower, in the 12- and 24-mo rats compared to the younger ages; slowest recovery and maximal effects were seen in the 24-mo rats. Acetylcholinesterase sensitivity (concentration-inhibition curves) was measured in vitro using control tissues from each age. Inhibitory concentrations of carbaryl were somewhat lower in PND18, 12-, and 24-mo tissues compared to 1- and 4-mo, but there were no differences with methomyl-treated tissues. Thus, in the dose-response and time-course, there were dissociations between brain ChE inhibition and the magnitude as well as recovery of motor activity changes. The explanation for this dissociation is unclear, and is likely due to early development followed by aging-related decline in both kinetic parameters and neurological responsiveness.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1504
[Js] Journal subset:IM
[St] Status:In-Data-Review

  2 / 1274577 MEDLINE  
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[PMID]: 25698507
[Au] Autor:Kikuchihara Y; Abe H; Tanaka T; Kato M; Wang L; Ikarashi Y; Yoshida T; Shibutani M
[Ad] Address:Laboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology, 3-5-8 Saiwai-cho, Fuchu-shi, Tokyo 183-8509, Japan. Electronic address: 50009155010@st.tuat.ac.jp....
[Ti] Title:Relationship between brain accumulation of manganese and aberration of hippocampal adult neurogenesis after oral exposure to manganese chloride in mice.
[So] Source:Toxicology;331:24-34, 2015 May 4.
[Is] ISSN:1879-3185
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:We previously found persistent aberration of hippocampal adult neurogenesis, along with brain manganese (Mn) accumulation, in mouse offspring after developmental exposure to 800-ppm dietary Mn. Reduction of parvalbumin (Pvalb)(+) γ-aminobutyric acid (GABA)-ergic interneurons in the hilus of the dentate gyrus along with promoter region hypermethylation are thought to be responsible for this aberrant neurogenesis. The present study was conducted to examine the relationship between the induction of aberrant neurogenesis and brain Mn accumulation after oral Mn exposure as well as the responsible mechanism in young adult animals. We used two groups of mice with 28- or 56-day exposure periods to oral MnCl2·xH2O at 800ppm as Mn, a dose sufficient to lead to aberrant neurogenesis after developmental exposure. A third group of mice received intravenous injections of Mn at 5-mg/kg body weight once weekly for 28 days. The 28-day oral Mn exposure did not cause aberrations in neurogenesis. In contrast, 56-day oral exposure caused aberrations in neurogenesis suggestive of reductions in type 2b and type 3 progenitor cells and immature granule cells in the dentate subgranular zone. Brain Mn accumulation in 56-day exposed cases, as well as in directly Mn-injected cases occurred in parallel with reduction of Pvalb(+) GABAergic interneurons in the dentate hilus, suggesting that this may be responsible for aberrant neurogenesis. For reduction of Pvalb(+) interneurons, suppression of brain-derived neurotrophic factor-mediated signaling of mature granule cells may occur via suppression of c-Fos-mediated neuronal plasticity due to direct Mn-toxicity rather than promoter region hypermethylation of Pvalb.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1504
[Js] Journal subset:IM
[St] Status:In-Data-Review

  3 / 1274577 MEDLINE  
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[PMID]: 25899937
[Au] Autor:Rubinstein ML
[Ti] Title:Scanning the brain for answers about effectiveness of graphic warning labels.
[So] Source:Tob Control;24(3):211-2, 2015 May.
[Is] ISSN:1468-3318
[Cp] Country of publication:England
[La] Language:eng
[Pt] Publication type:EDITORIAL
[Em] Entry month:1504
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1136/tobaccocontrol-2014-052205

  4 / 1274577 MEDLINE  
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[PMID]: 25564288
[Au] Autor:Wang AL; Lowen SB; Romer D; Giorno M; Langleben DD
[Ad] Address:Annenberg Public Policy Center, University of Pennsylvania, Philadelphia, Pennsylvania, USA....
[Ti] Title:Emotional reaction facilitates the brain and behavioural impact of graphic cigarette warning labels in smokers.
[So] Source:Tob Control;24(3):225-32, 2015 May.
[Is] ISSN:1468-3318
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Warning labels on cigarette packages are an important venue for information about the hazards of smoking. The 2009 US Family Smoking Prevention and Tobacco Control Act mandated replacing the current text-only labels with graphic warning labels. However, labels proposed by the Food and Drug Administration (FDA) were challenged in court by the tobacco companies, who argued successfully that the proposed labels needlessly encroached on their right to free speech, in part because they included images of high emotional salience that indiscriminately frightened rather than informed consumers. METHODS: We used functional MRI to examine the effects of graphic warning labels' emotional salience on smokers' brain activity and cognition. Twenty-four smokers viewed a random sequence of blocks of graphic warning labels that have been rated high or low on an 'emotional reaction' scale in previous research. RESULTS: We found that labels rated high on emotional reaction were better remembered, associated with reduction in the urge to smoke, and produced greater brain response in the amygdala, hippocampi, inferior frontal gyri and the insulae. CONCLUSIONS: Recognition memory and craving are, respectively, correlates of effectiveness of addiction-related public health communications and interventions, and amygdala activation facilitates the encoding of emotional memories. Thus, our results suggest that emotional reaction to graphic warning labels contributes to their public health impact and may be an integral part of the neural mechanisms underlying their effectiveness. Given the urgency of the debate about the constitutional risks and public health benefits of graphic warning labels, these preliminary findings warrant consideration while longitudinal clinical studies are underway.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1504
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1136/tobaccocontrol-2014-051993

  5 / 1274577 MEDLINE  
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[PMID]: 25546608
[Au] Autor:Haobam R; Tripathy D; Kaidery NA; Mohanakumar KP
[Ad] Address:1 Division of Cell Biology & Physiology, Laboratory of Clinical and Experimental Neuroscience, CSIR-Indian Institute of Chemical Biology , Jadavpur, Kolkata, India .
[Ti] Title:Embryonic stem cells derived neuron transplantation recovery in models of parkinsonism in relation to severity of the disorder in rats.
[So] Source:Rejuvenation Res;18(2):173-84, 2015 Apr.
[Is] ISSN:1557-8577
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:6-Hydroxydopamine (6-OHDA)- and 1-methyl-4-phenylpyridinium (MPP(+))-induced hemi-parkinsonism was investigated in relation to the severity of the disorder in terms of behavioral disability and nigral neuronal loss and recovery regarding the number of stem cell-derived neurons transplanted in the striatum. Intra-median forebrain bundle infusion of the parkinsonian neurotoxins and intra-striatal transplantation of differentiated embryonic stem cells (ESCs) were carried out by rat brain stereotaxic surgery. The severity of the disease was determined using the number of amphetamine- or apomorphine-induced rotations, striatal dopamine levels as estimated by high-performance liquid chromatography (HPLC)-electrochemistry, and the number of surviving tyrosine hydroxylase immunoreactive dopaminergic neurons in the substantia nigra pars compacta. Rats that received unilateral infusion of 6-OHDA or MPP(+) responded with dose-dependent, unilateral bias in turning behavior when amphetamine or apomorphine was administered. Rotational asymmetry in both models correlated significantly well with the loss in the number of nigral dopaminergic neurons and striatal dopamine depletion. Transplantation of 2×10(5) differentiated murine ESCs revealed remarkably similar kinds of recovery in both animal models. The survival of the grafted dopaminergic cells in the striatum was better in animals with low-severity parkinsonism, but poor in the animals with severe parkinsonism. Amphetamine-induced rotational recovery correlated positively with an increasing number of cells transplanted in animals with uniform nigral neuronal lesion. These results suggest that disease severity is an important factor for determining the number of cells to be transplanted in parkinsonian rats for desirable recovery, which may be true in clinical conditions too.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1504
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1089/rej.2014.1626

  6 / 1274577 MEDLINE  
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[PMID]: 25482164
[Au] Autor:Hou XQ; Zhang L; Yang C; Rong CP; He WQ; Zhang CX; Li S; Su RY; Chang X; Qin JH; Chen YB; Xian SX; Wang Q
[Ad] Address:1 DME Center, Institute of Clinical Pharmacology, Guangzhou University of Chinese Medicine , Guangzhou, China .
[Ti] Title:Alleviating effects of bushen-yizhi formula on ibotenic Acid-induced cholinergic impairments in rat.
[So] Source:Rejuvenation Res;18(2):111-27, 2015 Apr.
[Is] ISSN:1557-8577
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:This study explored the curative effect and underlying mechanisms of a traditional Chinese medicine compound prescription, Bushen-Yizhi formula (BSYZ), in ibotenic acid (IBO)-induced rats. Morris water maze and novel object recognition tests showed that BSYZ significantly improved spatial and object memory. Brain immunohistochemistry staining showed that BSYZ significantly up-regulated expression of choline acetyltransferase (ChAT) and nerve growth factor (NGF) in the hippocampus and cortex. The protein tyrosine kinase high-affinity receptor TrkA was slightly increased in the hippocampus and cortex, and significantly enhanced in the nucleus basalis of Meynert (NBM) after BSYZ intervention. The immunoreactivity of the p75 low-affinity receptor in BSYZ-treated rats was significantly strengthened in the cortex. Similar expression trends of nerve growth factor (NGF), TrkA, and p75 mRNA were observed in the hippocampus and cortex. Additionally, BSYZ reversed IBO-induced disorders of acetylcholine (ACh) levels, ChAT, and cholinesterase (ChE) in the cortex, which was consistent with the changes in mRNA levels of ChAT and acetylcholinesterase (AChE). Expression of ChAT and AChE proteins and mRNA in the hippocampus was up-regulated, whereas the apoptosis-relative protein cleaved caspase-3 was decreased after administration of BSYZ. Moreover, changes in cell death were confirmed by histological morphology. Thus, the results indicated that the BSYZ formula could ameliorate memory impairments in IBO-induced rats, and it exerted its therapeutic action probably by modulating cholinergic pathways, NGF signaling, and anti-apoptosis. Overall, it is suggested that the BSYZ formula might be a potential therapeutic approach for the treatment of Alzheimer's disease (AD) and other cholinergic impairment-related diseases.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1504
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1089/rej.2014.1603

  7 / 1274577 MEDLINE  
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[PMID]: 25848050
[Au] Autor:Bilek E; Ruf M; Schäfer A; Akdeniz C; Calhoun VD; Schmahl C; Demanuele C; Tost H; Kirsch P; Meyer-Lindenberg A
[Ad] Address:Departments of Psychiatry and Psychotherapy....
[Ti] Title:Information flow between interacting human brains: Identification, validation, and relationship to social expertise.
[So] Source:Proc Natl Acad Sci U S A;112(16):5207-12, 2015 Apr 21.
[Is] ISSN:1091-6490
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Social interactions are fundamental for human behavior, but the quantification of their neural underpinnings remains challenging. Here, we used hyperscanning functional MRI (fMRI) to study information flow between brains of human dyads during real-time social interaction in a joint attention paradigm. In a hardware setup enabling immersive audiovisual interaction of subjects in linked fMRI scanners, we characterize cross-brain connectivity components that are unique to interacting individuals, identifying information flow between the sender's and receiver's temporoparietal junction. We replicate these findings in an independent sample and validate our methods by demonstrating that cross-brain connectivity relates to a key real-world measure of social behavior. Together, our findings support a central role of human-specific cortical areas in the brain dynamics of dyadic interactions and provide an approach for the noninvasive examination of the neural basis of healthy and disturbed human social behavior with minimal a priori assumptions.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1504
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1073/pnas.1421831112

  8 / 1274577 MEDLINE  
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[PMID]: 25848046
[Au] Autor:Polley S; Louzada S; Forni D; Sironi M; Balaskas T; Hains DS; Yang F; Hollox EJ
[Ad] Address:Department of Genetics, University of Leicester, Leicester LE1 7RH, United Kingdom;...
[Ti] Title:Evolution of the rapidly mutating human salivary agglutinin gene (DMBT1) and population subsistence strategy.
[So] Source:Proc Natl Acad Sci U S A;112(16):5105-10, 2015 Apr 21.
[Is] ISSN:1091-6490
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The dietary change resulting from the domestication of plant and animal species and development of agriculture at different locations across the world was one of the most significant changes in human evolution. An increase in dietary carbohydrates caused an increase in dental caries following the development of agriculture, mediated by the cariogenic oral bacterium Streptococcus mutans. Salivary agglutinin [SAG, encoded by the deleted in malignant brain tumors 1 (DMBT1) gene] is an innate immune receptor glycoprotein that binds a variety of bacteria and viruses, and mediates attachment of S. mutans to hydroxyapatite on the surface of the tooth. In this study we show that multiallelic copy number variation (CNV) within DMBT1 is extensive across all populations and is predicted to result in between 7-20 scavenger-receptor cysteine-rich (SRCR) domains within each SAG molecule. Direct observation of de novo mutation in multigeneration families suggests these CNVs have a very high mutation rate for a protein-coding locus, with a mutation rate of up to 5% per gamete. Given that the SRCR domains bind S. mutans and hydroxyapatite in the tooth, we investigated the association of sequence diversity at the SAG-binding gene of S. mutans, and DMBT1 CNV. Furthermore, we show that DMBT1 CNV is also associated with a history of agriculture across global populations, suggesting that dietary change as a result of agriculture has shaped the pattern of CNV at DMBT1, and that the DMBT1-S. mutans interaction is a promising model of host-pathogen-culture coevolution in humans.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1504
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1073/pnas.1416531112

  9 / 1274577 MEDLINE  
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[PMID]: 25848027
[Au] Autor:Barrio JR; Small GW; Wong KP; Huang SC; Liu J; Merrill DA; Giza CC; Fitzsimmons RP; Omalu B; Bailes J; Kepe V
[Ad] Address:Departments of Molecular and Medical Pharmacology, jbarrio@mednet.ucla.edu vkepe@mednet.ucla.edu....
[Ti] Title:In vivo characterization of chronic traumatic encephalopathy using [F-18]FDDNP PET brain imaging.
[So] Source:Proc Natl Acad Sci U S A;112(16):E2039-47, 2015 Apr 21.
[Is] ISSN:1091-6490
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Chronic traumatic encephalopathy (CTE) is an acquired primary tauopathy with a variety of cognitive, behavioral, and motor symptoms linked to cumulative brain damage sustained from single, episodic, or repetitive traumatic brain injury (TBI). No definitive clinical diagnosis for this condition exists. In this work, we used [F-18]FDDNP PET to detect brain patterns of neuropathology distribution in retired professional American football players with suspected CTE (n = 14) and compared results with those of cognitively intact controls (n = 28) and patients with Alzheimer's dementia (AD) (n = 24), a disease that has been cognitively associated with CTE. [F-18]FDDNP PET imaging results in the retired players suggested the presence of neuropathological patterns consistent with models of concussion wherein brainstem white matter tracts undergo early axonal damage and cumulative axonal injuries along subcortical, limbic, and cortical brain circuitries supporting mood, emotions, and behavior. This deposition pattern is distinctively different from the progressive pattern of neuropathology [paired helical filament (PHF)-tau and amyloid-ß] in AD, which typically begins in the medial temporal lobe progressing along the cortical default mode network, with no or minimal involvement of subcortical structures. This particular [F-18]FDDNP PET imaging pattern in cases of suspected CTE also is primarily consistent with PHF-tau distribution observed at autopsy in subjects with a history of mild TBI and autopsy-confirmed diagnosis of CTE.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1504
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1073/pnas.1409952112

  10 / 1274577 MEDLINE  
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[PMID]: 25848016
[Au] Autor:Mandel-Brehm C; Salogiannis J; Dhamne SC; Rotenberg A; Greenberg ME
[Ad] Address:Department of Neurobiology, and....
[Ti] Title:Seizure-like activity in a juvenile Angelman syndrome mouse model is attenuated by reducing Arc expression.
[So] Source:Proc Natl Acad Sci U S A;112(16):5129-34, 2015 Apr 21.
[Is] ISSN:1091-6490
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Angelman syndrome (AS) is a neurodevelopmental disorder arising from loss-of-function mutations in the maternally inherited copy of the UBE3A gene, and is characterized by an absence of speech, excessive laughter, cognitive delay, motor deficits, and seizures. Despite the fact that the symptoms of AS occur in early childhood, behavioral characterization of AS mouse models has focused primarily on adult phenotypes. In this report we describe juvenile behaviors in AS mice that are strain-independent and clinically relevant. We find that young AS mice, compared with their wild-type littermates, produce an increased number of ultrasonic vocalizations. In addition, young AS mice have defects in motor coordination, as well as abnormal brain activity that results in an enhanced seizure-like response to an audiogenic challenge. The enhanced seizure-like activity, but not the increased ultrasonic vocalizations or motor deficits, is rescued in juvenile AS mice by genetically reducing the expression level of the activity-regulated cytoskeleton-associated protein, Arc. These findings suggest that therapeutic interventions that reduce the level of Arc expression have the potential to reverse the seizures associated with AS. In addition, the identification of aberrant behaviors in young AS mice may provide clues regarding the neural circuit defects that occur in AS and ultimately allow new approaches for treating this disorder.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1504
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1073/pnas.1504809112


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