13 research outputs found

    Abnormal auditory ERP N100 in children with dyslexia: comparison with their control siblings

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    <p>Abstract</p> <p>Background</p> <p>Recent research has implicated deficits of the working memory (WM) and attention in dyslexia. The N100 component of event-related potentials (ERP) is thought to reflect attention and working memory operation. However, previous studies showed controversial results concerning the N100 in dyslexia. Variability in this issue may be the result of inappropriate match up of the control sample, which is usually based exclusively on age and gender.</p> <p>Methods</p> <p>In order to address this question the present study aimed at investigating the auditory N100 component elicited during a WM test in 38 dyslexic children in comparison to those of 19 unaffected sibling controls. Both groups met the criteria of the International Classification of Diseases (ICD-10). ERP were evoked by two stimuli, a low (500 Hz) and a high (3000 Hz) frequency tone indicating forward and reverse digit span respectively.</p> <p>Results</p> <p>As compared to their sibling controls, dyslexic children exhibited significantly reduced N100 amplitudes induced by both reverse and forward digit span at Fp1, F3, Fp2, Fz, C4, Cz and F4 and at Fp1, F3, C5, C3, Fz, F4, C6, P4 and Fp2 leads respectively. Memory performance of the dyslexics group was not significantly lower than that of the controls. However, enhanced memory performance in the control group is associated with increased N100 amplitude induced by high frequency stimuli at the C5, C3, C6 and P4 leads and increased N100 amplitude induced by low frequency stimuli at the P4 lead.</p> <p>Conclusion</p> <p>The present findings are in support of the notion of weakened capture of auditory attention in dyslexia, allowing for a possible impairment in the dynamics that link attention with short memory, suggested by the anchoring-deficit hypothesis.</p

    Intergenerational transmission of parenting: findings from a UK longitudinal study.

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    BACKGROUND: The quality of parenting is associated with a wide range of child and adult outcomes, and there is evidence to suggest that some aspects of parenting show patterns of intergenerational transmission. This study aimed to determine whether such intergenerational transmission occurs in mothers and fathers in a UK birth cohort. METHODS: The study sample consisted of 146 mothers and 146 fathers who were recruited from maternity wards in England and followed up for 24 months ['Generation 2' (G2)]. Perceptions of their own parenting [by 'Generation1' (G1)] were assessed from G2 parents at 12 months using the Parental Bonding Instrument (PBI). G2 parents were filmed interacting with their 'Generation 3' (G3) children at 24 months. RESULTS: We found that G1 mothers' 'affection' was associated with positive parenting behaviour in the G2 fathers ('positive responsiveness' β = 0.19, P = 0.04 and 'cognitive stimulation' β = 0.26, P < 0.01). G1 mothers' 'control' was associated with negative parenting behaviour in G2 mothers (decreased 'engagement' β = -0.19, P = 0.04), and negative parenting behaviour in G2 fathers (increased 'control' β = 0.18, P = 0.05). None of the G1 fathers' parenting variables were significantly associated with G2 parenting. CONCLUSIONS: There is evidence of intergenerational transmission of parenting behaviour in this highly educated UK cohort, with reported parenting of grandmothers associated with observed parenting in both mothers and fathers. No association was seen with reported parenting of grandfathers. This raises the possibility that parenting interventions may have benefits that are realised across generations

    Hsf-1 affects podocyte markers NPHS1, NPHS2 and WT1 in a transgenic mouse model of TTRVal30Met-related amyloidosis

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    Introduction: Familial amyloid polyneuropathy is characterized by transthyretin (TTR) deposition in various tissues, including the kidneys. While deposition induces organ dysfunction, renal involvement in TTR-related amyloidosis could manifest from proteinuria to end-stage kidney failure. As proteinuria is considered result of glomerular filtration barrier injury we investigated whether TTR deposition affects either glomerular basement membrane (GBM) or podocytes. Materials and methods: Immunohistochemistry, immunoblot and gene expression studies for nephrin, podocin and WT1 were run on renal tissue from human-TTRV30M transgenic mice hemizygous or homozygous for heat shock factor one (Hsf-1). Transmission electron microscopy was used for evaluation of podocyte foot process width (PFW) and GBM thickness in Hsf-1 hemizygous mice with or without TTRV30M or amyloid deposition. Results: Glomeruli of hsf-1 hemizygous transgenic mice showed lower nephrin and podocin protein levels but an increased podocyte number when compared to Hsf-1 homozygous transgenic mice. Nephrin, podocin and WT1 gene expression levels were unaffected by the Hsf-1 carrier status. TTRV30M deposition was associated with increased PFW and GBM thickness. Conclusions: Under the effect of Hsf-1 hemizygosity, TTRV30M deposition has deleterious effects on GBM thickness, PFW and slit diaphragm composition, without affecting nephrin and podocin gene expression

    Human TTRV30M localization within podocytes in a transgenic mouse model of transthyretin related amyloidosis: does the environment play a role?

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    Transthyretin related amyloidosis is a nosological entity that leads to disability, diminished quality of life, all stages of chronic kidney disease and eventually death. Podocytes are polarized, highly differentiated epithelial cells important for proper nephron function. In the present study we investigated whether deposited TTRVal30Met (TTRV30M) molecules could be localized within podocytes in situ under the effect of different housing conditions (i.e. specific pathogen free [SPF] vs. non-SPF). Murine renal glomeruli from human TTRV30M (hTTRV30M) transgenic mice were examined via direct and indirect immunofluorescence techniques for the presence of hTTRV30M, murine serum amyloid P, activated caspase-3 and NPHS1. Association strength and amount of colocalization for NPHS1-hTTRV30M, NPHS1-activated caspase-3, hTTRV30M-murine serum amyloid P were estimated. Localization of hTTRV30M in podocytes was demonstrated by immuno-electron microscopy. Renal hTTRV30M gene and NPHS1 gene expression levels were estimated. Non-SPF transgenic mice showed increased glomerular hTTRV30M deposition compared to their SPF counterparts. Furthermore increased podocytic localization of hTTRV30M was noticed in non-SPF mice. Glomerular caspase-3 activation was increased only in the non SPF housing conditions. Podocytic caspase-3 activation was increased in SPF and in non-SPF transgenic mice when compared to non transgenic controls. Environmental conditions influence glomerular deposition and podocytic localization of hTTRV30M. In this context increased caspase-3 activation occurred
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