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  • 1
    Language: English
    In: Neuroscience, May 17, 2012, Vol.210, p.168(11)
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.neuroscience.2012.03.002 Byline: K.E. Morrison (a), D.W. Curry (b), M.A. Cooper (a) Keywords: social defeat; dominance; stress; resilience; coping; conditioned defeat Abbreviations: AH, anterior hypothalamus; ANOVA, analysis of variance; BLA, basolateral amygdale; BNST, bed nucleus of the stria terminalis; dLS, dorsal lateral septum; dMeA, dorsal medial amygdale; GS, goat serum; IL, infralimbic cortex; LA, lateral amygdale; MPOA, medial preoptic area; PBS, phosphate buffered saline; PL, prelimbic cortex; PVN, paraventricular nucleus of the hypothalamus; vLS, ventral lateral septum; vMeA, ventral medial amygdale; VMHL, lateral ventromedial hypothalamus; vmPFC, ventromedial prefrontal cortex Abstract: Although exposure to social stress leads to increased depression-like and anxiety-like behavior, some individuals are more vulnerable than others to these stress-induced changes in behavior. Prior social experience is one factor that can modulate how individuals respond to stressful events. In this study, we investigated whether experience-dependent resistance to the behavioral consequences of social defeat was associated with a specific pattern of neural activation. We paired weight-matched male Syrian hamsters in daily aggressive encounters for 2 weeks, during which they formed a stable dominance relationship. We also included control animals that were exposed to an empty cage each day for 2 weeks. Twenty-four hours after the final pairing or empty cage exposure, half of the subjects were socially defeated in 3, 5-min encounters, whereas the others were not socially defeated. Twenty-four hours after social defeat, animals were tested for conditioned defeat in a 5-min social interaction test with a non-aggressive intruder. We collected brains after social defeat and processed the tissue for c-Fos immunoreactivity. We found that dominants were more likely than subordinates to counter-attack the resident aggressor during social defeat, and they showed less submissive and defensive behavior at conditioned defeat testing compared with subordinates. Also, social status was associated with distinct patterns of defeat-induced neural activation in select brain regions, including the amygdala, prefrontal cortex, hypothalamus, and lateral septum. Our results indicate that social status is an important form of prior experience that predicts both initial coping style and the degree of resistance to social defeat. Further, the differences in defeat-induced neural activation suggest possible brain regions that may control resistance to conditioned defeat in dominant individuals. Author Affiliation: (a) Department of Psychology, University of Tennessee, Knoxville, TN 37996, USA (b) Neuroscience Graduate Program, Emory University, Atlanta, GA 30322, USA Article History: Accepted 1 March 2012
    Keywords: Stress (Psychology) -- Analysis ; Stress (Psychology) -- Social Aspects ; Phosphates -- Analysis ; Phosphates -- Social Aspects ; Brain -- Analysis ; Brain -- Social Aspects ; Hamsters -- Analysis ; Hamsters -- Social Aspects ; Neurosciences -- Analysis ; Neurosciences -- Social Aspects
    ISSN: 0306-4522
    Source: Cengage Learning, Inc.
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  • 2
    Language: English
    In: Neuroscience, 04/2015, Vol.291, C, pp.1-14
    Description: •Stress resilience is an active process that involves distinct neural circuits.•Experience-dependent neural plasticity in key brain regions supports resilience.•Dominant hamsters show resistance to the effects of social defeat.•Neural plasticity in vmPFC circuits supports stress resistance in dominant hamsters. Humans and other animals show a remarkable capacity for resilience following traumatic, stressful events. Resilience is thought to be an active process related to coping with stress, although the cellular and molecular mechanisms that support active coping and stress resistance remain poorly understood. In this review, we focus on the neurobiological mechanisms by which environmental and social experiences promote stress resistance. In male Syrian hamsters, exposure to a brief social defeat stressor leads to increased avoidance of novel opponents, which we call conditioned defeat. Also, hamsters that have achieved dominant social status show reduced conditioned defeat as well as cellular and molecular changes in the neural circuits controlling the conditioned defeat response. We propose that experience-dependent neural plasticity occurs in the prelimbic (PL) cortex, infralimbic (IL) cortex, and ventral medial amygdala (vMeA) during the maintenance of dominance relationships, and that adaptations in these neural circuits support stress resistance in dominant individuals. Overall, behavioral treatments that promote success in competitive interactions may represent valuable interventions for instilling resilience.
    Keywords: Bdnf ; Bla ; Bnst ; Cck ; Cea ; CRF ; Drn ; Hpa ; 5-Ht ; Il ; Lab ; Lal ; Mea ; Nac ; Nmda ; Pl ; PTSD ; Sal ; Vmea ; Vmpfc ; Amygdala ; Dominance Relationships ; Infralimbic Cortex ; Medial Prefrontal Cortex ; Resilience ; Social Defeat;
    ISSN: 03064522
    E-ISSN: 18737544
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  • 3
    Language: English
    In: Neuroscience, 5/2012, Vol.210, C, pp.168-178
    Description: Although exposure to social stress leads to increased depression-like and anxiety-like behavior, some individuals are more vulnerable than others to these stress-induced changes in behavior. Prior social experience is one factor that can modulate how individuals respond to stressful events. In this study, we investigated whether experience-dependent resistance to the behavioral consequences of social defeat was associated with a specific pattern of neural activation. We paired weight-matched male Syrian hamsters in daily aggressive encounters for 2 weeks, during which they formed a stable dominance relationship. We also included control animals that were exposed to an empty cage each day for 2 weeks. Twenty-four hours after the final pairing or empty cage exposure, half of the subjects were socially defeated in 3, 5-min encounters, whereas the others were not socially defeated. Twenty-four hours after social defeat, animals were tested for conditioned defeat in a 5-min social interaction test with a non-aggressive intruder. We collected brains after social defeat and processed the tissue for c-Fos immunoreactivity. We found that dominants were more likely than subordinates to counter-attack the resident aggressor during social defeat, and they showed less submissive and defensive behavior at conditioned defeat testing compared with subordinates. Also, social status was associated with distinct patterns of defeat-induced neural activation in select brain regions, including the amygdala, prefrontal cortex, hypothalamus, and lateral septum. Our results indicate that social status is an important form of prior experience that predicts both initial coping style and the degree of resistance to social defeat. Further, the differences in defeat-induced neural activation suggest possible brain regions that may control resistance to conditioned defeat in dominant individuals. Highlights▶Dominant individuals show reduced conditioned defeat compared with subordinates. ▶Social status leads to modest differences in baseline neural activation. ▶Social status produces distinct patterns of defeat-induced neural activation. ▶Defeat-induced neural activation in the prefrontal cortex is linked to resilience.
    Keywords: Social Defeat ; Dominance ; Stress ; Resilience ; Coping ; Conditioned Defeat ; Ah ; Anova ; Bla ; Bnst ; Dls ; Dmea ; Gs ; Il ; La ; Mpoa ; PBS ; Pl ; Pvn ; Vls ; Vmea ; Vmhl ; Vmpfc;
    ISSN: 03064522
    E-ISSN: 18737544
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  • 4
    Language: English
    In: Neuroscience, April 4, 2014, Vol.264, p.17
    Description: To access, purchase, authenticate, or subscribe to the full-text of this article, please visit this link: http://dx.doi.org/10.1016/j.neuroscience.2013.11.014 Byline: K.E. Morrison [kmorr@vet.upenn.edu] (*), A.B. Rodgers, C.P. Morgan, T.L. Bale Key words puberty; adolescence; epigenetics; brain maturation; sex differences Highlights * Puberty is a critical period of brain development. * Puberty is a time of greater risk for neuropsychiatric disease. * Epigenectic mechanisms are involved in normal maturational processes. * Therefore, epigenetic mechanisms are a likely target for environmental perturbation. * This review discusses epigenetic processes in pubertal brain maturation. Abstract Puberty is a critical period of development during which the reemergence of gonadotropin-releasing hormone secretion from the hypothalamus triggers a cascade of hormone-dependent processes. Maturation of specific brain regions including the prefrontal cortex occurs during this window, but the complex mechanisms underlying these dynamic changes are not well understood. Particularly, the potential involvement of epigenetics in this programming has been under-examined. The epigenome is known to guide earlier stages of development, and it is similarly poised to regulate vital pubertal-driven brain maturation. Further, as epigenetic machinery is highly environmentally responsive, its involvement may also lend this period of growth to greater vulnerability to external insults, resulting in reprogramming and increased disease risk. Importantly, neuropsychiatric diseases commonly present in individuals during or immediately following puberty, and environmental perturbations including stress may precipitate disease onset by disrupting the normal trajectory of pubertal brain development via epigenetic mechanisms. In this review, we discuss epigenetic processes involved in pubertal brain maturation, the potential points of derailment, and the importance of future studies for understanding this dynamic developmental window and gaining a better understanding of neuropsychiatric disease risk. Abbreviations AVP, arginine vasopressin; BNST, bed nucleus of the stria terminalis; DNMT, DNA methyltransferase; ER[alpha], estrogen receptor alpha; ER[beta], estrogen receptor beta; GnRH, gonadotropin-releasing hormone; HDAC, histone deacetylase; HPA, hypothalamic--pituitary--adrenal; miRs, microRNAs; PFC, prefrontal cortex; PN, postnatal day Author Affiliation: Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, United States * Corresponding author. Address: Department of Animal Biology, University of Pennsylvania, 3800 Spruce Street, 201E Vet, Philadelphia, PA 19104, United States. Tel: +1-215-898-1368; fax: +1-215-573-5187. Article History: Accepted 6 November 2013 (miscellaneous) This article is part of a Special Issue entitled: Epigenetics in Brain Function.
    Keywords: Pituitary Hormones – Analysis ; Epigenetic Inheritance – Analysis ; Estrogens – Analysis ; Puberty – Analysis ; Methyltransferases – Analysis ; Adolescence – Analysis
    ISSN: 0306-4522
    E-ISSN: 18737544
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  • 5
    Language: English
    In: Journal of Neurology, Neurosurgery & Psychiatry November 2013, Vol.84(11), p.e2
    Description: Large scale genetic studies such as genome–wide association studies (GWAS) in Parkinson's disease (PD) have revealed genetic susceptibility factors and continue to offer new insights both into the genetics of sporadic disease and its pathogenesis, with the potential for identification of an at–risk population and novel therapeutic targets. However, the methodology importantly requires larger data sets for replication of novel findings.
    Keywords: Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke ; Parkinson'S Disease ; Stroke
    ISSN: 0022-3050
    ISSN: 00223050
    E-ISSN: 1468-330X
    E-ISSN: 1468330X
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  • 6
    Language: English
    In: Engineering Structures, 6/2012, Vol.39, C, pp.162-175
    Description: Highlights► The inclusion of steel fibres improves the deformation capacity of columns. ► Minimum shear reinforcement is required to improve effectiveness of steel fibres. ► Slenderness affects ductility if second-order effects are important. ► In general, EC-8 code is on the safe side for medium to high axial loads. ► In columns with steel fibres, EC-8 code predictions are conservative. The inclusion of ductility requirements is necessary to guarantee the safety design of any concrete structure subjected to unexpected and/or reversal loads. It is important to outline that plastic hinges may be developed in columns of reinforced concrete buildings, especially in column-foundation joints. The deformation capacity of the column depends on its slenderness. However, few experimental tests of normal and fibre-reinforced concrete columns in the range of medium slenderness (between 5 and 10) have been performed for the case of cyclic loading. This paper presents an experimental research study on the behaviour of slender columns subjected to combinations of constant axial and lateral cyclic loads. In order to study the behaviour of this type of element fourteen experimental tests were performed. The experimental results make it possible to calibrate numerical models, and to validate simplified methods. The following variables are studied: slenderness, axial load level, transverse reinforcement ratio, and volumetric steel-fibre ratio. The maximum load and deformation capacity of the columns are analyzed. It is interesting to note that the deformation capacity depends on the four test variables analyzed. Moreover, the inclusion of steel fibres into the concrete mixture increases the deformation capacity. The inclusion of a minimum transverse reinforcement is required in order to improve the effectiveness of the steel fibres. Thus, the column behaviour suffers moderate strength losses due to cyclic loads. Finally, slenderness influences the deformation capacity if second-order effects are important, the cross-section displays ductile behaviour, and the capacity of the materials is reached.
    Keywords: Slender Column ; Confined Concrete ; Reinforced Concrete ; Steel Fibre ; Ductility ; Energy Dissipation ; Strength ; Axial Load ; Cyclic Load;
    ISSN: 01410296
    E-ISSN: 18737323
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  • 7
    Language: English
    In: Water Science and Technology, 03/2003, Vol.47(6), pp.167-169
    Description: Water problems have a human dimension where the ideas, perceptions, values and life-styles of individuals in their different roles have an impact. A many-sided set of stakeholders is preferable in any decision process, with empowerment of those less able to make their views known.
    Keywords: Conferences ; Empowerment ; Stakeholders ; Perception ; Decision Making ; Synthesis ; Decision Making ; Synthesis ; Water Resources and Supplies ; Water Law and Institutions ; General ; Characteristics, Behavior and Fate;
    ISBN: 1843394383
    ISSN: 0273-1223
    E-ISSN: 1996-9732
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  • 8
    Language: English
    In: Neurochemistry International, 8/2011, Vol.59(1), pp.73-80
    Description: Highlights ► We use differentiated human SH-SY5Y cells exposed to paraquat or MPP + to mimic PD. ► We find increased expression of iron importers TfR1, DMT1+IRE, TfR2 and mitoferrin-2. ► TfR2 and mitoferrin-2 may be involved in transport of iron into mitochondria. ► These findings support mitochondrial iron deficiency driving neuronal iron uptake. Background Neuronal iron accumulation is thought to be relevant to the pathogenesis of Parkinson’s disease (PD), although the mechanism remains elusive. We hypothesized that neuronal iron uptake may be stimulated by functional mitochondrial iron deficiency. Objective To determine firstly whether the mitochondrial toxin, 1-methyl-4-phenylpyridinium iodide (MPP +), results in upregulation of iron-import proteins and transporters of iron into the mitochondria, and secondly whether similar changes in expression are induced by toxins with different mechanisms of action. Methods We used quantitative PCR and Western blotting to investigate expression of the iron importers, divalent metal transporter, transferrin receptor 1 and 2 (TfR1 and TfR2) and mitoferrin-2 and the iron exporter ferroportin in differentiated SH-SY5Y cells exposed to three different toxins relevant to PD, MPP +, paraquat (a free radical generator) and lactacystin (an inhibitor of the ubiquitin–proteasome system (UPS)). Results MPP + resulted in increased mRNA and protein levels of genes involved in cellular iron import and transport into the mitochondria. Similar changes occurred following exposure to paraquat, another inducer of oxidative stress. Lactacystin also resulted in increased TfR1 mRNA levels, although the other changes were not found. Conclusion Our results support the hypothesis of a functional mitochondrial iron deficit driving neuronal iron uptake but also suggest that differences exist in neuronal iron handling induced by different toxins.
    Keywords: Dcfda ; Dmt1 ; Fpn ; Ire ; Irp ; Mfrn2 ; Mpp + ; 6-Ohda ; PD ; Ros ; Tfr1 ; Tfr2 ; UPS ; Parkinson’s Disease ; Iron ; Transferrin Receptor ; Divalent Metal ; Transporter ; Mitoferrin ; Mpp +;
    ISSN: 01970186
    E-ISSN: 18729754
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  • 9
    Language: English
    In: Parkinsonism & Related Disorders, 04/2015, Vol.21(4), pp.394-397
    Description: BackgroundGTP cyclohydrolase I (GCH1) mutations are the commonest cause of Dopa-responsive dystonia (DRD). Clinical phenotypes can be broad, even within a single family. MethodsWe present clinical, genetic and functional imaging data on a British kindred in which affected subjects display phenotypes ranging from DRD to Parkinson's disease (PD). Twelve family members were studied. Clinical examination, dopamine transporter (DAT) imaging, and molecular genetic analysis of GCH1 and the commonest known familial PD-related genes were performed. ResultsWe have identified a novel missense variant, c.5A 〉 G, p.(Glu2Gly), within the GCH1 gene in affected family members displaying a range of phenotypes.Two affected subjects carrying this variant had abnormal DAT imaging. These two with abnormal DAT imaging had a PD phenotype, while the remaining three subjects with the novel GCH1 variant had normal DAT imaging and a DRD phenotype. ConclusionsWe propose that this GCH1 variant is pathogenic in this family and these findings suggest that similar mechanisms involving abnormal GTP cyclohydolase I may underlie both PD and DRD. GCH1 genetic testing should be considered in patients with PD and a family history of DRD. •We have identified a novel missense variant, c.5A 〉 G, p.(Glu2Gly), within the GCH1 gene in family with Dopa responsive dystonia (DRD) and parkinsonism.•Those with parkinsonism had abnormal DaTscans, indicating nigrostriatal neurodegeneration.•These findings suggest that similar mechanisms involving abnormal GTP cyclohydolase I may underlie both Parkinson's disease and Dopa responsive dystonia.
    Keywords: Parkinson'S Disease ; Dopa Responsive Dystonia ; Gch1 ; Spect Dat Imaging;
    ISSN: 13538020
    E-ISSN: 18735126
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  • 10
    Language: English
    In: Engineering Structures, June, 2012, Vol.39, p.162(14)
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.engstruct.2012.02.003 Byline: K.E. Caballero-Morrison, J.L. Bonet, Juan Navarro-Gregori, J.R. Marti-Vargas Keywords: Slender column; Confined concrete; Reinforced concrete; Steel fibre; Ductility; Energy dissipation; Strength; Axial load; Cyclic load Abstract: a* The inclusion of steel fibres improves the deformation capacity of columns. a* Minimum shear reinforcement is required to improve effectiveness of steel fibres. a* Slenderness affects ductility if second-order effects are important. a* In general, EC-8 code is on the safe side for medium to high axial loads. a* In columns with steel fibres, EC-8 code predictions are conservative. Author Affiliation: Instituto de Ciencia y Tecnologia del Hormigon, Universitat Politecnica de Valencia, Camino de Vera s/n, 46022 Valencia, Spain Article History: Received 25 June 2011; Revised 15 December 2011; Accepted 5 February 2012
    ISSN: 0141-0296
    Source: Cengage Learning, Inc.
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