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  • 1
    Language: English
    In: Behavioural Brain Research, 01 October 2012, Vol.234(2), pp.212-222
    Description: ► N-back task performance assessed in paired and single players using fNIRS. ► Paired players revealed significant increase in cortical between-brain connectivity. ► Paired players revealed significant larger cortical hemodynamic responses. ► Paired players showed no increase in behavioral performance. ► Findings designate fNIRS as suitable tool for monitoring between-brain connectivity. The present study aimed to step into two-person neuroscience by investigating the hemodynamic correlates of between-brain connectivity during joint task performance. To test this approach, wireless functional near-infrared spectroscopy (fNIRS) was used to record brain signals during performance of a dual n-back task simultaneously in paired players as compared to single players. Evaluating functional connectivity between the paired players’ brains using wavelet transform coherence (WTC) analysis revealed (1) a significant increase in between-brain coherence during joint task performance as compared to baseline condition. These patterns were observed in two frequency bands, i.e. in the heart rate (HR) frequency and in low-frequency oscillations (LFOs). (2) Averaged hemodynamic responses revealed larger responses in total hemoglobin concentration changes [tHb] for the paired players as compared to the single players; in addition, within the paired players groups joint task performance revealed larger changes in [tHb] as compared to a rest period and to a baseline condition. (3) No increase in behavioral performance was found in the paired players as compared to the single players. Our findings designate fNIRS as suitable tool for monitoring interpersonal performances between two subjects. The results show that two-person performance leads to relevant and significant effects, which are detectable using between-brain connectivity analysis. Using this approach can provide additional insight into interpersonal activation patterns not detectable using typical one-person experiments. Our study demonstrates the potential of simultaneously assessing cerebral hemodynamic responses for various two-person experimental paradigms and research areas where interpersonal performances are involved.
    Keywords: Two-Person Neuroscience ; Functional Near-Infrared Spectroscopy (Fnirs) ; Functional Connectivity ; Wavelet Transform Coherence (Wtc) ; Heart Rate Frequency ; Low-Frequency Oscillations (Lfos) ; Prefrontal Cortex ; Anatomy & Physiology
    ISSN: 0166-4328
    E-ISSN: 0166-4328
    E-ISSN: 18727549
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  • 2
    In: Critical Care Medicine, 2015, Vol.43(11), pp.2354-2359
    Description: OBJECTIVES:: To assess the success of electrical cardioversion for the treatment of new-onset atrial fibrillation in critically ill patients and to evaluate the stability of sinus rhythm in responders during the subsequent 24 hours. DESIGN:: Retrospective study. SETTING:: Twelve-bed cardiosurgical ICU at a university hospital. PATIENTS:: Seventy-two consecutive patients with postoperative new-onset atrial fibrillation (〈 7 d of duration) treated by electrical cardioversion. INTERVENTIONS:: Electrical cardioversion using synchronized biphasic shocks. MEASUREMENTS AND MAIN RESULTS:: During 144 electrical cardioversions, 209 shocks were delivered to 72 patients. Maximal energy (200 J) was used in 85% of shocks. Electrical cardioversion immediately restored sinus rhythm in 102 sessions (71%). Pretreatment with amiodarone did not increase the success rates. During the follow-up, the percentages of sinus rhythm decreased from 43% after 1 hour to 23% after 24 hours. However, at ICU discharge, 54 patients (75%) were in sinus rhythm. Of the 54 patients in sinus rhythm, only 18 (33%) converted to sinus rhythm after repeated cardioversions, whereas the remaining 36 (66%) did so spontaneously or with amiodarone. CONCLUSIONS:: Biphasic electrical cardioversion in cardiosurgical ICU patients was immediately successful in restoring sinus rhythm in 71% of sessions. However, early relapse of atrial fibrillation was common in the 24-hour follow-up. At ICU discharge, the majority of patients were in sinus rhythm, but the efficacy of repetitive electrical cardioversion in restoring sinus rhythm was disappointing.
    Keywords: Medicine;
    ISSN: 0090-3493
    E-ISSN: 15300293
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  • 3
    Language: English
    In: Cancer Research, 04/15/2013, Vol.73(8 Supplement), pp.2017-2017
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
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  • 4
    Language: English
    In: Bock, Christoph, Eleni M. Tomazou, Arie B. Brinkman, Fabian Müller, Femke Simmer, Hongcang Gu, Natalie Jäger, Andreas Gnirke, Hendrik G. Stunnenberg, and Alexander Meissner. 2010. “Quantitative Comparison of Genome-Wide DNA Methylation Mapping Technologies.” Nature Biotechnology 28 (10): 1106–1114.
    Description: DNA methylation plays a key role in regulating eukaryotic gene expression. Although mitotically heritable and stable over time, patterns of DNA methylation frequently change in response to cell differentiation, disease and environmental influences. Several methods have been developed to map DNA methylation on a genomic scale. Here, we benchmark four of these approaches by analyzing two human embryonic stem cell lines derived from genetically unrelated embryos and a matched pair of colon tumor and adjacent normal colon tissue obtained from the same donor. Our analysis reveals that methylated DNA immunoprecipitation sequencing (MeDIP-seq), methylated DNA capture by affinity purification (MethylCap-seq), reduced representation bisulfite sequencing (RRBS) and the Infinium HumanMethylation27 assay all produce accurate DNA methylation data. However, these methods differ in their ability to detect differentially methylated regions between pairs of samples. We highlight strengths and weaknesses of the four methods and give practical recommendations for the design of epigenomic case-control studies.
    Keywords: DNA Methylation -- Genetics ; Genome, Human -- Genetics ; Sequence Analysis, DNA -- Methods;
    ISSN: 1087-0156
    ISSN: 1546-1696
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  • 5
    In: Nature, 2014, Vol.510(7506), p.537
    Description: Epigenetic alterations, that is, disruption of DNA methylation and chromatin architecture, are now acknowledged as a universal feature of tumorigenesis. Medulloblastoma, a clinically challenging, malignant childhood brain tumour, is no exception. Despite much progress from recent genomics studies, with recurrent changes identified in each of the four distinct tumour subgroups (WNT-pathway-activated, SHH-pathway-activated, and the less-well-characterized Group 3 and Group 4), many cases still lack an obvious genetic driver. Here we present whole-genome bisulphite-sequencing data from thirty-four human and five murine tumours plus eight human and three murine normal controls, augmented with matched whole-genome, RNA and chromatin immunoprecipitation sequencing data. This comprehensive data set allowed us to decipher several features underlying the interplay between the genome, epigenome and transcriptome, and its effects on medulloblastoma pathophysiology. Most notable were highly prevalent regions of hypomethylation correlating with increased gene expression, extending tens of kilobases downstream of transcription start sites. Focal regions of low methylation linked to transcription-factor-binding sites shed light on differential transcriptional networks between subgroups, whereas increased methylation due to re-normalization of repressed chromatin in DNA methylation valleys was positively correlated with gene expression. Large, partially methylated domains affecting up to one-third of the genome showed increased mutation rates and gene silencing in a subgroup-specific fashion. Epigenetic alterations also affected novel medulloblastoma candidate genes (for example, LIN28B), resulting in alternative promoter usage and/or differential messenger RNA/microRNA expression. Analysis of mouse medulloblastoma and precursor-cell methylation demonstrated a somatic origin for many alterations. Our data provide insights into the epigenetic regulation of transcription and genome organization in medulloblastoma pathogenesis, which are probably also of importance in a wider developmental and disease context.
    Keywords: Gene Expression Regulation, Neoplastic ; Gene Silencing ; DNA Methylation -- Genetics ; Medulloblastoma -- Genetics ; Sequence Analysis, DNA -- Methods;
    ISSN: 0028-0836
    E-ISSN: 1476-4687
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  • 6
    Language: English
    In: Pugh, Trevor J., Shyamal Dilhan Weeraratne, Tenley C. Archer, Daniel A. Pomeranz Krummel, Daniel Auclair, James Bochicchio, Mauricio O. Carneiro, et al. 2012. Medulloblastoma exome sequencing uncovers subtype-specific somatic mutations. Nature 488(7409): 106-110.
    Description: Medulloblastomas are the most common malignant brain tumors in children1. Identifying and understanding the genetic events that drive these tumors is critical for the development of more effective diagnostic, prognostic and therapeutic strategies. Recently, our group and others described distinct molecular subtypes of medulloblastoma based on transcriptional and copy number profiles2–5. Here, we utilized whole exome hybrid capture and deep sequencing to identify somatic mutations across the coding regions of 92 primary medulloblastoma/normal pairs. Overall, medulloblastomas exhibit low mutation rates consistent with other pediatric tumors, with a median of 0.35 non-silent mutations per megabase. We identified twelve genes mutated at statistically significant frequencies, including previously known mutated genes in medulloblastoma such as CTNNB1, PTCH1, MLL2, SMARCA4 and TP53. Recurrent somatic mutations were identified in an RNA helicase gene, DDX3X, often concurrent with CTNNB1 mutations, and in the nuclear co-repressor (N-CoR) complex genes GPS2, BCOR, and LDB1, novel findings in medulloblastoma. We show that mutant DDX3X potentiates transactivation of a TCF promoter and enhances cell viability in combination with mutant but not wild type beta-catenin. Together, our study reveals the alteration of Wnt, Hedgehog, histone methyltransferase and now N-CoR pathways across medulloblastomas and within specific subtypes of this disease, and nominates the RNA helicase DDX3X as a component of pathogenic beta-catenin signaling in medulloblastoma.
    Keywords: Article;
    ISSN: 0028-0836
    E-ISSN: 14764687
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  • 7
  • 8
    In: Nature, 2012, Vol.482(7384), p.226
    Description: Glioblastoma multiforme (GBM) is a lethal brain tumour in adults and children. However, DNA copy number and gene expression signatures indicate differences between adult and paediatric cases (1-4). To explore the genetic events underlying this distinction, we sequenced the exomes of 48 paediatric GBM samples. Somatic mutations in the H3.3-ATRX-DAXX chromatin remodelling pathway were identified in 44% of tumours (21/48). Recurrent mutations in H3F3A, which encodes the replication-independent histone 3 variant H3.3, were observed in 31% of tumours, and led to amino acid substitutions at two critical positions within the histone tail (K27M, G34R/G34V) involved in key regulatory post-translational modifications. Mutations in ATRX([alpha]-thalassaemia/mental retardation syndrome X-linked) (5) and DAXX (death-domain associated protein), encoding two subunits of a chromatin remodelling complex required for H3.3 incorporation at pericentric heterochromatin and telomeres (6,7), were identified in 31% of samples overall, and in 100% of tumours harbouring a G34R or G34V H3.3 mutation. Somatic TP53 mutations were identified in 54% of all cases, and in 86% of samples with H3F3A and/or ATRX mutations. Screening of a large cohort of gliomas of various grades and histologies (n = 784) showed H3F3A mutations to be specific to GBM and highly prevalent in children and young adults. Furthermore, the presence of H3F3A/ATRX-DAXX/TP53 mutations was strongly associated with alternative lengthening of telomeres and specific gene expression profiles. This is, to our knowledge, the first report to highlight recurrent mutations in a regulatory histone in humans, and our data suggest that defects of the chromatin architecture underlie paediatric and young adult GBM pathogenesis.
    Keywords: Gene Mutation -- Research ; Dna -- Research ; Dna -- Physiological Aspects ; Glioblastomas -- Genetic Aspects ; Glioblastomas -- Research ; Tumor Proteins -- Physiological Aspects ; Tumor Proteins -- Research;
    ISSN: 0028-0836
    E-ISSN: 14764687
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