3,203 research outputs found
pook (n)
No full textpook n...their hats 'd be,you know _ had a kind o' notches,see; they kind o' stick up - little pook like that,see. (ie cone-shaped object? cf _pook_ of hay etc)YesJ. D. A. WIDDOWSON JAN 1973DNE-cit OKUsed I and SupUsed I and Sup2Used IA modified version of the slip contents is used in the DNE
pook (n); pooks (n.pl.)
No full textpook n....we'd get up .... there would be the large hay mows. We didn't call 'em mows or piles of hay. We call 'em pooks of hay.And we'd get behind the pooks o' hay an' we'd imitate the lady....YesDNE-citJ. D. A. WIDDOWSON JUL 1974Used I and SupUsed I and Sup1Used
Epigenetic-based therapies for Friedreich ataxia
No full textThis article has been made available through the Brunel Open Access Publishing Fund.Friedreich ataxia (FRDA) is a lethal autosomal recessive neurodegenerative disorder caused primarily by a homozygous GAA repeat expansion mutation within the first intron of the FXN gene, leading to inhibition of FXN transcription and thus reduced frataxin protein expression. Recent studies have shown that epigenetic marks, comprising chemical modifications of DNA and histones, are associated with FXN gene silencing. Such epigenetic marks can be reversed, making them suitable targets for epigenetic-based therapy. Furthermore, since FRDA is caused by insufficient, but functional, frataxin protein, epigenetic-based transcriptional re-activation of the FXN gene is an attractive therapeutic option. In this review we summarize our current understanding of the epigenetic basis of FXN gene silencing and we discuss current epigenetic-based FRDA therapeutic strategies. © 2014 Sandi, Sandi, Anjomani Virmouni, Al-Mahdawi and Pook
Software Management 2012: Nachhaltiges Software Management
No full textBrandt-Pook H, Fleer A, Spitta T, Wattenberg M, eds. Software Management 2012: Nachhaltiges Software Management. Lecture Notes in Informatics (LNI). 2012;P-209
Software Management 2006: Beratung in der Softwareentwicklung: Modelle - Methoden - Best Practices
No full textBrandt-Pook H, Simonsmeier W, Spitta T, Gesellschaft für Informatik. Fachausschuss Management der Anwendungsentwicklung und Wartung, eds. Software Management 2006: Beratung in der Softwareentwicklung: Modelle - Methoden - Best Practices. LNI, Edition Proceedings. 2006;P-98:142
The emerging role of 5-hydroxymethylcytosine in neurodegenerative diseases
No full textCopyright © 2014 Al-Mahdawi, Anjomani Virmouni and Pook. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.This article has been made available through the Brunel Open Access Publishing Fund.DNA methylation primarily occurs within human cells as a 5-methylcytosine (5mC) modification of the cytosine bases in CpG dinucleotides. 5mC has proven to be an important epigenetic mark that is involved in the control of gene transcription for processes such as development and differentiation. However, recent studies have identified an alternative modification, 5-hydroxymethylcytosine (5hmC), which is formed by oxidation of 5mC by ten-eleven translocation (TET) enzymes. The overall levels of 5hmC in the mammalian genome are approximately 10% of 5mC levels, although higher levels have been detected in tissues of the central nervous system (CNS). The functions of 5hmC are not yet fully known, but evidence suggests that 5hmC may be both an intermediate product during the removal of 5mC by passive or active demethylation processes and also an epigenetic modification in its own right, regulating chromatin or transcriptional factors involved in processes such as neurodevelopment or environmental stress response. This review highlights our current understanding of the role that 5hmC plays in neurodegenerative diseases, including Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), fragile X-associated tremor/ataxia syndrome (FXTAS), Friedreich ataxia (FRDA), Huntington's disease (HD), and Parkinson's disease (PD).Sara Anjomani Virmouni was supported by funding to Mark A. Pook from the Friedreich’s Ataxia Research Alliance(FARA)
DNA methylation and trinucleotide repeat expansion diseases
No full textCopyright @ 2012 InTechThis article has been made available through the Brunel Open Access Publishing Fund.This article is made available through the Brunel Open Access Publishing Fund
Entwicklung und Betrieb eines Campus-Management-Systems - Aspekte zur Nachhaltigkeit am Beispiel TISS
No full textGrechenig T, Spitta T, Suppersberger M, Kleinert W, Kier C, Pöll M. Entwicklung und Betrieb eines Campus-Management-Systems - Aspekte zur Nachhaltigkeit am Beispiel TISS. In: Brandt-Pook H, Gesellschaft für Informatik. Fachausschuss Management der Anwendungsentwicklung und Wartung, eds. Software Management 2012. LNI. Vol P-209. Bonn: GI e.V.; 2012: 135-152
Frataxin deficiency increases cyclooxygenase 2 and prostaglandins in cell and animal models of Friedreich's ataxia
No full text© The Author 2014. Published by Oxford University Press
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.An inherited deficiency of the mitochondrial protein frataxin causes Friedreich's ataxia (FRDA); the mechanism by which this deficiency triggers neuro- and cardio-degeneration is unclear. Microarrays of neural tissue of animal models of the disease showed decreases in antioxidant genes, and increases in inflammatory genes. Cyclooxygenase (COX)-derived oxylipins are important mediators of inflammation. We measured oxylipin levels using tandem mass spectrometry and ELISAs in multiple cell and animal models of FRDA. Mass spectrometry revealed increases in concentrations of prostaglandins, thromboxane B2, 15-HETE and 11-HETE in cerebellar samples of knockin knockout mice. One possible explanation for the elevated oxylipins is that frataxin deficiency results in increased COX activity. While constitutive COX1 was unchanged, inducible COX2 expression was elevated over 1.35-fold (P < 0.05) in two Friedreich's mouse models and Friedreich's lymphocytes. Consistent with higher COX2 expression, its activity was also increased by 58% over controls. COX2 expression is driven by multiple transcription factors, including activator protein 1 and cAMP response element-binding protein, both of which were elevated over 1.52-fold in cerebella. Taken together, the results support the hypothesis that reduced expression of frataxin leads to elevation of COX2-mediated oxylipin synthesis stimulated by increases in transcription factors that respond to increased reactive oxygen species. These findings support a neuroinflammatory mechanism in FRDA, which has both pathomechanistic and therapeutic implications.The study was supported by NIH grants NS077777, EY012245 and AG025532 to G.A.C., and USDA-ARS Intramural Projects 5306-51530-019-00D and 1 U24 DK097154-01 to J.W.N. Funding to pay the Open Access publication charges for this article was provided by the NIH
Supplemental Material for Pook et al., 2019
No full textFile S1: Additional method section on setting a target-coverage.File S2: Additional method section on the graphical representation of haplotype blocks.File S3: Additional method section - toy example for calculation of bEHH.Table S1: Proportion of variance explained between the full SNP-dataset (X), a SNP-subset (Xs) and the block dataset (Z). For comparability the number of parameters in Xs and Z were chosen equally using traditionally heritability estimation as in de los Campos (2017).Table S2: Influence of the window size on the haplotype library for chromosome 1 in the PE DH-lines.Table S3: Influence of the weighting of block length (wl) and number of haplotypes (wn) on the haplotype library for chromosome 1 in the PE DH-lines.Table S4: Influence of using the extended-block-identification on the haplotype library in dependency of the parameter t of the extended-block-identification-step for chromosome 1 in the PE DH-lines.Figure S1: Dataset for the toy example used in File S3.Figure S2: Comparison of the block structure and an bifurcation plot (Sabeti et al., 2002, Gautier and Vitalis, 2012) according SNP 10'000 on chromosome 1 in the KE DH-lines. Figure S3: Comparision of the block structure for MCMB=1'000 (A), MCMB=5'000 (B), MCMB=20'000 (C) for the first 20'000 SNPs of chromosome 1 in the KE DH-lines.</div
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