Relevant bibliographies by topics / Schlafen12

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Academic literature on the topic 'Schlafen12'

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Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Schlafen12"

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Chen, Jiaxing, and Leslie A. Kuhn. "Deciphering the three-domain architecture in schlafens and the structures and roles of human schlafen12 and serpinB12 in transcriptional regulation." Journal of Molecular Graphics and Modelling 90 (July 2019): 59–76. http://dx.doi.org/10.1016/j.jmgm.2019.04.003.

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Zhao, Liang, Brent Neumann, Kathleen Murphy, John Silke, and Thomas J. Gonda. "Lack of reproducible growth inhibition by Schlafen1 and Schlafen2 in vitro." Blood Cells, Molecules, and Diseases 41, no. 2 (2008): 188–93. http://dx.doi.org/10.1016/j.bcmd.2008.03.006.

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Kocziszky, Eva. "„ es wächst schlafend des Wortes Gewalt“. Schlafen und Wachen bei Hölderlin." Études Germaniques 293, no. 1 (2019): 55. http://dx.doi.org/10.3917/eger.293.0055.

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de la Casa-Esperón, Elena. "From mammals to viruses: the Schlafen genes in developmental, proliferative and immune processes." BioMolecular Concepts 2, no. 3 (2011): 159–69. http://dx.doi.org/10.1515/bmc.2011.018.

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AbstractThe Schlafen genes have been associated with proliferation control and with several differentiation processes, as well as with disparate phenotypes such as immune response, embryonic lethality and meiotic drive. They constitute a gene family with widespread distribution in mammals, where they are expressed in several tissues, predominantly those of the immune system. Moreover, horizontal transfer of these genes to orthopoxviruses suggests a role of the viral Schlafens in evasion to the host immune response. The expression and functional studies of this gene family will be reviewed under the prism of their evolution and diversification, the challenges they pose and the future avenues of research.
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Vomhof-DeKrey, Emilie E., Josey Umthun, and Marc D. Basson. "Loss of Schlafen3 influences the expression levels of Schlafen family members in ileum, thymus, and spleen tissue." PeerJ 8 (January 28, 2020): e8461. http://dx.doi.org/10.7717/peerj.8461.

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Background The Schlafen (Slfn) family proteins are important for regulation of cell growth, cell differentiation and cell cycle progression. We sought to distinguish Slfn family expression in Slfn3 knockout (KO) mice after RNA sequencing analysis of Slfn3KO vs. wildtype (WT) mice revealed varying expressions of Slfn family in ileal mucosa. Methods Quantitative PCR analysis of Slfn members was evaluated in ileal mucosa, thymus and spleen tissue since Slfn family members have roles in differentiating intestinal and immune cells. Results Ileal mucosa of Slfn3KO mice displayed a decrease in Slfn3, 4, 8 and 9 while Slfn1 and 5 increased in mRNA expression vs. WT mice. Thymic tissue had a Slfn9 increase and a Slfn4 decrease while splenic tissue had a Slfn8 and Slfn9 increase in Slfn3KO mice vs. WT mice. These differential expressions of Slfn members could indicate a feedback regulatory mechanism within the Slfn family. Indeed, MATCH™ tool from geneXplain predicted that all Slfn members have regions in their promoters for the Kruppel-like factor-6 transcription factor. In addition, NFAT related factors, ING4, ZNF333 and KLF4 are also predicted to bind in up to 6 of the 8 Slfn promoters. This study further describes a possible autoregulatory mechanism amongst the Slfn family members which could be important in how they regulate the differentiation of various cell types.
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Al-Marsoummi, Sarmad, Emilie E. Vomhof-DeKrey, and Marc D. Basson. "Schlafens: Emerging Proteins in Cancer Cell Biology." Cells 10, no. 9 (2021): 2238. http://dx.doi.org/10.3390/cells10092238.

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Schlafens (SLFN) are a family of genes widely expressed in mammals, including humans and rodents. These intriguing proteins play different roles in regulating cell proliferation, cell differentiation, immune cell growth and maturation, and inhibiting viral replication. The emerging evidence is implicating Schlafens in cancer biology and chemosensitivity. Although Schlafens share common domains and a high degree of homology, different Schlafens act differently. In particular, they show specific and occasionally opposing effects in some cancer types. This review will briefly summarize the history, structure, and non-malignant biological functions of Schlafens. The roles of human and mouse Schlafens in different cancer types will then be outlined. Finally, we will discuss the implication of Schlafens in the anti-tumor effect of interferons and the use of Schlafens as predictors of chemosensitivity.
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Shin, Soonim. "Eine Opposition gegen Autoritätssysteme des Marktes?" Soziologiemagazin 11, no. 2-2018 (2019): 47–61. http://dx.doi.org/10.3224/soz.v11i2.05.

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Der Soziologe Ulrich Beck hatte einmal die Konsument_innen als „schlafende Riesen“ (Beck 2009: 131) bezeichnet. In diesem Sinne schrieb die Journalistin Tanja Busse (2006, 2007), Konsument_innen könnten die Produktion bestimmen, wenn sie nur die Augen öffnen. Da die Konsument_innen aber schliefen, seien sie für Missstände der globalisierten Wirtschaft verantwortlich, nämlich für die Missachtung von Umwelt- und Sozialstandards – also etwa für Hühner in Käfigen oder für versklavte Näherinnen. Dieser Beitrag zeigt an einem Beispiel, dass Konsument_innen nicht – wie behauptet – auf dem Markt souverän sein können, dass sie also nicht einfach so in der Lage sind, die Produktion zu lenken und ihre gewünschten Produkte zu bekommen. Souverän sind eher die Produzent_innen als die Konsument_innen. Letztere schlafen nicht, wie der Vorwurf gegen sie lautet: Sie werden von den Produzent_innen einfach nicht ausreichend über die Produkte informiert. Im Beispiel geht es um die Schwierigkeiten bei der Einführung neuer Lebensmittel in den USA, nämlich von Fleisch und Milch von Weideland- oder Freilandrindern: Am Anfang gab es keine Nachfrage von Konsument_innen, auf die die Produzent_innen reagierten – es gab nur ein Angebot von kleinen Produzent_innen, die sich bei den Konsument_innen erst mühsam einen Markt schaffen mussten. Mit ihrer Graswurzel-Initiative, einer Bewegung von unten, halfen diese Produzent_innen vielen Konsument_innen dabei, ein alternatives Angebot an Fleisch und Milch zu bekommen.
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Hanelt, Lorenz, and Martin Gary. "Schlafende Kapazität." Versicherungswirtschaft 74, no. 6 (2019): 28–29. http://dx.doi.org/10.1007/s43239-019-0008-1.

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Yuan, Lisi, Yingjie Yu, Matthew A. Sanders, Adhip P. N. Majumdar, and Marc D. Basson. "Schlafen 3 induction by cyclic strain regulates intestinal epithelial differentiation." American Journal of Physiology-Gastrointestinal and Liver Physiology 298, no. 6 (2010): G994—G1003. http://dx.doi.org/10.1152/ajpgi.00517.2009.

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The intestinal epithelium is subjected to repetitive deformation during normal gut function by peristalsis and villous motility. In vitro, cyclic strain promotes intestinal epithelial proliferation and induces an absorptive phenotype characterized by increased dipeptidyl dipeptidase (DPPIV) expression. Schlafen 3 is a novel gene recently associated with cellular differentiation. We sought to evaluate whether Schlafen 3 mediates the effects of strain on the differentiation of intestinal epithelial cell (IEC)-6 in the absence or presence of cyclic strain. Strain increased Schlafen 3 mRNA and protein. In cells transfected with a control-nontargeting siRNA, strain increased DPPIV-specific activity. However, Schlafen 3 reduction by siRNA decreased basal DPPIV and prevented any stimulation of DPPIV activity by strain. Schlafen 3 reduction also prevented DPPIV induction by sodium butyrate (1 mM) or transforming growth factor (TGF)-β (0.1 ng/ml), two unrelated differentiating stimuli. However, Schlafen-3 reduction by siRNA did not prevent the mitogenic effect of strain or that of EGF. Blocking Src and phosphatidyl inositol (PI3)-kinase prevented strain induction of Schlafen 3, but Schlafen 3 induction required activation of p38 but not ERK. These results suggest that cyclic strain induces an absorptive phenotype characterized by increased DPPIV activity via Src-, p38-, and PI3-kinase-dependent induction of Schlafen 3 in rat IEC-6 cells on collagen, whereas Schlafen 3 may also be a key factor in the induction of intestinal epithelial differentiation by other stimuli such as sodium butyrate or TGF-β. The induction of Schlafen 3 or its human homologs may modulate intestinal epithelial differentiation and preserve the gut mucosa during normal gut function.
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Döser, Johannes. "Der schlafende Josef." PSYCHE 73, no. 12 (2019): 1036–39. http://dx.doi.org/10.21706/ps-73-12-1036.

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Dissertations / Theses on the topic "Schlafen12"

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Smutná, Katarína 1991. "Schlafen 12, a novel HIV restriction factor involved in latency." Doctoral thesis, Universitat Pompeu Fabra, 2019. http://hdl.handle.net/10803/666297.

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The process of HIV latency establishment and maintenance is not clearly understood. Homeostatic proliferation (HSP) is a major mechanism by which long-lived naive and memory CD4 T cells are maintained in vivo. HSP also contributes to the persistence of HIV latent reservoir. Furthermore, HIV-infected naive CD4 T cells cultured under HSP condition are refractory to reactivation, in contrast to TCR-activated memory CD4 T cells. This might be due to the suggested post-transcriptional block in naive HSP-cultured cells. Here we compared a transcriptomic signature of naive and memory CD4 T cells. Among differentially expressed genes that may influence HIV latency, we identified Schlafen 12 (SLFN12) as an interesting candidate for a potential HIV restriction factor. Our results showed that SLFN12 establishes post-transcriptional block in HIV infected cells and thus inhibits both, HIV production as well as its reactivation from latently infected cells. These findings may help to better understand the mechanisms underlying HIV latency and its reversal in HSP-maintained naive CD4 T cells. All together it might contribute to the design of novel HIV eradication strategies.
El proceso por el cual el virus de la Inmunodeficiencia Humana (VIH) establece y mantiene un estado de latencia no se conoce en su totalidad. La proliferación homeostática (HSP, de sus siglas en ingés “Homeostatic proliferation”) es uno de los mecanismos por el cual las células T CD4 “naive” y de memoria se mantienen in vivo. Además, HSP también contribuye al mantenimiento del reservorio de virus en forma latente. Además, las células T CD4 “naive” infectadas y cultivadas en condiciones de HSP no son capaces de reactivarse a diferencia de las células T CD4 de memoria activadas vía TCR. Estudios previos sugieren que esta observación se debe a un bloqueo post-transcripcional en células T “naive” cultivadas en condiciones de HSP. En esta tesis comparamos la perfil del transcriptoma de células T CD4 “naive” y de memoria. Entre los genes diferencialmente expresados que podrían participar en el proceso de latencia del VIH, identificamos Schlafen 12 (SLFN12) como un candidato interesante que podría ser un factor de restricción del virus. Los resultados de este trabajo muestran que SLFN12 establece un bloqueo post-transcripcional en células infectadas por VIH, y de esta forma inhibe tanto la producción del virus como su reactivación en células infectadas de forma latente. Estas observaciones pueden ser de gran ayuda para entender mejor los mecanismos subyacentes a la latencia del VIH así como su reactivación en células CD4 T “naive” mantenidas bajo condiciones de HSP. En su conjunto, estos resultados podrían contribuir al diseño de nuevas estrategias para erradicar el VIH.
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Hochedlinger, Michael. ""Der schlafende Riese". Das Österreichische Staatsarchiv, Abteilung Kriegsarchiv." Universität Potsdam, 2005. http://opus.kobv.de/ubp/volltexte/2008/2077/.

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Goodbody, Rory Eric. "Functional analysis of viral schlafen from camelpox virus." Thesis, Imperial College London, 2009. http://hdl.handle.net/10044/1/5378.

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This thesis concerns gene 176R from camelpox virus (CMLV) that encodes a protein known as viral schlafen (v-slfn). v-slfn has an N-terminal domain related to the p26 protein from baculovirus and a C-terminal domain related to mammalian schlafen proteins. A full length v-slfn is expressed by all sequenced orthopoxviruses except vaccinia virus (VACV) and variola virus. The baculovirus p26 proteins are poorly characterised, with no known function. In contrast, murine schlafen (m-slfn) proteins are upregulated in response to infection and the promoter for m-slfn2 has NF-κB and AP-1 binding sites. The prototypic slfn, m-slfn1, halts cellular proliferation by inhibition of cyclin D1 expression in vitro and both m-slfn1 and m-slfn8 reduce thymocyte proliferation in vivo. v-slfn is a predominantly cytoplasmic protein of 57 kDa that is expressed both early and late during CMLV infection. Expression of v-slfn reverses the growth arrest resulting from m-slfn1 expression, and this is a result of a reversal of the inhibition of cyclin D1 expression. This effect can be seen following overexpression of various transcription factors that upregulate cyclin D1 expression. Recombinant VACV expressing enhanced levels of v-slfn replicated and spread at a comparable rate to control viruses in vitro, but was less virulent than controls in the intranasal model of infection in vivo. A group of viruses based on VACV WR were constructed, which lack the gene fragments (B2R and B3R) corresponding to CMLV 176R. The undisrupted sequence for 176R was also re-inserted at this locus, resulting in a virus that expresses v-slfn from its natural promoter. In vitro characterisation showed no differences in replication or spread when compared to controls. Thus, v-slfn is an orthologue of mammalian slfn proteins, and may exert its effect by reversing their inhibition of cellular proliferation.
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Shair, Kathy Ho Yen. "Electromelia virus-host interactions : the viral growth factor and Schlafen proteins." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619967.

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Huber, Elisabeth [Verfasser], and Karl-Peter [Akademischer Betreuer] Hopfner. "The schlafen core domain: from structure to function / Elisabeth Huber ; Betreuer: Karl-Peter Hopfner." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2018. http://d-nb.info/1203544936/34.

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Geserick, Peter. "Identifikation der Slfn-(Schlafen)-Proteinfunktion und deren Bedeutung in der Zellzykluskontrolle und der T-Zellontogenie." [S.l. : s.n.], 2005. http://www.diss.fu-berlin.de/2005/6/index.html.

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Ferraioli, Domenico. "Assessment and relevance of the putative DNA/RNA helicase Schlafen-11 in ovarian and breast cancer." Thesis, Lyon, 2019. http://www.theses.fr/2019LYSE1324/document.

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Schlafen 11 (SLFN11) est une ADN/ARN hélicase décrite pour la première fois pour son rôle dans le développement et la différenciation des thymocytes chez la souris. Elle fait partie d'une famille de protéines présentant divers degrés d'homologie entre les espèces, mais qu’est présente de façon constante chez les mammifères. Le rôle de cette ADN/ARN hélicase, SLFN11, a été associé de façon causale à la sensibilité de réponse aux différents agents alkylants (agents endommageant l'ADN, les inhibiteurs de topo-isomérase I et II) dans le NCI-60. Dans la première étude, nous avons développé un protocole d’immunohistochimie (IHC) sur des biopsies paraffinées de carcinome séreux de l'ovaire de haut grade (HGSOC), afin de valider un anticorps (Ab) anti-SLFN11 et d’en déterminer l'expression. En IHC, nous avons testé et validé un Ab anti-SLFN11, en choisissant entre deux anti-SLFN11 Ab utilisés normalement pour le Western Blot. Premièrement, il a été développé dans une culture cellulaire (CCB) de HGSOC et, successivement, dans une série indépendante de micro-array (TMA) de HGSOC. Pour chaque cas, nous avons évalué soit le score d'intensité (IS) que le score de distribution (DS) en évaluant au moins 300 cellules. Un score histologique (HS) a été obtenu comme suit : HS=IS x DS. Successivement, nous avons appliqué notre protocole à une plus large série d'échantillons de HGSOC pour confirmer nos résultats préliminaires. Nous avons trouvé un anticorps fiable dans les séries CCB et TMA permettant de déterminer l'expression IHC de SLFN11. Ces résultats ont été confirmés dans notre plus large série de HGSOC. Brièvement, comme pour les séries indépendantes de TMA, nous avons constaté que la HS de l'expression de SLFN11 est présente dans environ 60%. En parallèle, le SLFN11 n'a pas été exprimé dans 40 % des cas qui, cliniquement, correspondent, dans environ 60 % de ces cas (16/27), aux patients résistant aux sels de platine. Une faible expression de SLFN11 en IHC pourrait être corrélée à la réponse à la chimiothérapie(CT) à base de platine. Dans la deuxième étude, nous étudions l’état transcriptionnel du SLFN11 dans le cancer du sein en effectuant une méta-analyse de plus de 7000 cas à partir de 35 étudies publiquement disponibles. Par l’analyse de corrélation, nous avons identifié 537 transcrits qui corrèle, au-delà du 95e percentile selon le coefficient de Pearson, avec l’expression de SLFN11. En particulier, voie l’analyse par “Gene Ontology” SLFN11 est lié au transcrits impliqués dans le système immunitaire : "réponse immunitaire", "l’activation lymphocytaire" et "l’activation des lymphocytes T". En outre, voie le “likehood lasso regression ”, nous avons signalé une très forte association entre le SLFN11 et les signatures immunitaires dans le cancer du sein. Enfin, grâce à la “multiple corresponded analysis ”, nous avons découvert un sous-groupe de patients, défini "SLFN11-Hot cluster", caractérisé par une expression élevé de SLFN11, récepteurs d'œstrogènes(ER) négatives, un phénotype basal, un jeune âge, une signature élevée de CD3D et de STAT1. En utilisant la "Cox proportional hazard regression", l’expression élevé de SLFN11, l’indice de prolifération élevé et le ER négative sont des paramètres indépendants lié à la survie sans maladie chez les patients soumises à la CT. Notre deuxième travail decrit un rôle spécifique pour le SLFN11 dans le cancer du sein probablement en relation avec la modulation du système immunitaire et une forte corrélation entre l’expression de SFLN11 et un sous-type moléculaire spécifique de cancer du sein (récepteurs négatifs aux œstrogènes, phénotype de type basal). Autres études devront être réalisées afin de: 1) mieux comprendre la fonction du SLFN11 dans les cellules cancéreuses, 2) valider un protocole IHC fiable et standardisé pour évaluer l’expression de SLFN11, 3) utiliser SFLN11 comme biomarqueur prédictif de réponse aux DDA et PARP inhibiteurs et 4) établir sa relation avec le système immunitaire
Schlafen 11 (SLFN11) is a putative DNA/RNA helicase, first described for its role in thymocyte development and differentiation in mouse models. SLFN11 is part of a family of proteins with various degree of homology across species, but intriguingly being consistently present only in vertebrates and especially in mammals. Recently, the role of this putative DNA/RNA helicase, SLFN11, was causally associated with sensitivity to DNA damaging agents, such as platinum salts, topoisomerase I and II inhibitors, and other alkylators in the NCI-60 panel of cancer cell lines. In the first study, we validate an anti-SLFN11 antibody in formalin-fixed paraffin-embedded (FFPE) high-grade serous ovarian carcinoma (HGSOC) samples, developing an immunohistochemistry (IHC) protocol in order to determinate the expression of SLFN11 in our series of HGSOC. Indeed, we tested and validated a reliable SLFN 11 antibody (Ab) in IHC choosing between two anti-SLFN11 Ab used normally for Western Blot (WB) in culture cell block (CCB) of ovarian carcinoma and in an independent series of HGSOCs tissue micro-array (TMA). For each case, we evaluated both the Intensity Score (IS) and the Distribution Score (DS) evaluating at least 300 cells. A Histological Score (HS)was obtained as follow: HS=IS x DS. Successively, we applied our protocol to a large case series of HGSOC samples to confirm our preliminary results. We found one antibody to be reliable in CCB and TMA series allowing to determinate clearly IHC expression of SLFN11. These results were confirmed in our large case series of FFPE HGSOC samples. Briefly, as for TMA independent series, we found that the HS for SLFN11 expression presents a normal distribution with a prevalent (≈ 60%) intermediate expression. Parallel SLFN11 was not expressed in practically 40% of cases that clinically corresponded to the platinum resistant patients in about 60% of cases (16/27). So, we believe that low IHC expression of SLFN 11 should be correlated to response to the platinum-based chemotherapy. In the second study, we investigate the transcriptional landscape of SLFN11 in breast cancer performing a gene expression microarray meta-analysis of more than 7000 cases from 35 publicly available data sets. By correlation analysis, we identified 537 transcripts in the top 95th percentile of Pearson’s coefficients with SLFN11 identifying “immune response”, “lymphocyte activation” and “T cell activation” as top Gene Ontology enriched processes. Furthermore, we reported very strong association of SLFN11 with immune signatures in breast cancer through penalized maximum likelihood lasso regression. Finally, through multiple corresponded analysis we discovered a subgroup of patients, defined “SLF11-hot cluster”, characterized by high SLFN11 levels, estrogen receptor(ER) negativity, basal-like phenotype, elevated CD3D, STAT1 signature, and young age. Using Cox proportional hazard regression, we characterized that SLFN11 high levels, high proliferation index, and ER negativity are independent parameters for longer disease-free interval in patients undergoing chemotherapy. We believe that our second work supports proof of concept that: i) A clear and specific role for SLFN11 in breast cancer, in likely connection with the immune system modulation in such disease entity, ii) a strong correlation between high SFLN 11 and specific molecular subtype of breast cancer (estrogen receptor negativity, basal-like phenotype). Further studies will be performed to confirm our hypothesis in order to: 1) better understand the function of SLFN 11 in cancer cell, 2) validate an easy, reliable and standardized IHC protocol to assessment SLFN11, 3) use SFLN11expression as a predictive biomarker of response to DDA and PARP inhibitors and 4) determinate the relationship with immune system
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Unbehaun, Axel. "Die vegetative Kontrolle der Herzfrequenz und ihre Koordination mit dem respiratorischen System untersucht im Schlafen und Wachen innerhalb der Pubertät: eine zeitreihenanalytische Studie /." [S.l.] : [s.n.], 1998. http://deposit.ddb.de/cgi-bin/dokserv?idn=956625053.

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Unbehaun, Axel. "Die vegetative Kontrolle der Herzfrequenz und ihre Koordination mit dem respiratorischen System untersucht im Schlafen und Wachen nnerhalb der Pubertaet: Eine zeitreihenanalytische Studie." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 1998. http://dx.doi.org/10.18452/14420.

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Die Atmung und das Herz-Kreislauf-System interagieren als zwei in Reihe angeordnete funktionelle Einheiten. Die gleichsinnige Kontrolle beider Systeme bildet die Grundlage homöostatischer Bedingungen im Organismus. Neurophysiologische Studien geben Hinweise auf die Existenz eines gemeinsamen neuronalen kardiorespiratorischen Netzwerkes, welches im ventrolateralen Teil der Medulla oblongata gelegen ist. Da zentrale Mechanismen der Regulation einer direkten Untersuchung nicht zugänglich sind, erweisen sich die linearen und nichtlinearen Verfahren der Zeitreihenanalyse als hilfreich, um Erkenntnisse von der Arbeitsweise des kardiorespiratorischen Kontrollsystems zu gewinnen. Grundlage der Studie bildet eine Datenbank polygraphischer Messungen (einschließlich EKG, thorakales und abdominales Respirogramm, Elektrookulogramm und Aktogramm), die an 42 gesunden Kindern, 11 Mädchen und 31 Knaben im Alter von 12 bis 15 Jahren erhoben wurde. Die Messungen erfolgten über 24 Stunden hinweg, während folgender Vigilanzstadien: ruhiger Wachzustand, REM- und nonREM-Schlaf. Die spektralen Charakteristika der Herzfrequenzvariabilität wurden berechnet, um die sympatho-vagale Einflußnahme auf den Nodus sinusoidalis kennzeichnen zu können. Die lineare Intensität der kardiorespiratorischen Beziehung wurde aus den Kohärenzspektren abgeleitet. Um nichtlineares Verhalten erfassen zu können, wurden der größte Lyapunov-Exponent und die Korrelationsdimension der Herzfrequenz, sowie die Korrelationsdimension des Atemsignals bestimmt. Die Analyse der Herzfrequenzvariabilität ergab für die Gesamtleistung die höchsten Werte innerhalb der REM-Phasen, im Wachzustand lagen diese deutlich niedriger und während des nonREM-Schlafes waren sie am kleinsten. Dieses Verhalten wurde im wesentlichen bestimmt von Änderungen der Spektralleistung im niederfrequenten Bereich. Die Komplexität der Herzfrequenz, die sich mit der Korrelationsdimension schätzen läßt, zeigte eine deutliche Abnahme im Schlaf. Dagegen erwies sich der Lyapunov-Exponent als weniger sensitiv bezüglich der Vigilanz. Die kardiorespiratorische Kohärenz ließ eine strenge Abhängigkeit vom Vigilanzstadium erkennen mit hohen Werten im nonREM-Schlaf und dem Minimum innerhalb der REM-Phasen. Im Gegensatz zur Komplexität der Herzfrequenz erreichte die Komplexität der Atmung die niedrigsten Werte in den REM-Phasen. Mit den Ergebnissen der Spektralanalyse lassen sich vigilanzstadienspezifische Einstellungen in der vegetativen Kontrolle der Herzfrequenz abgrenzen. Die nichtlinearen Verfahren offenbaren niederdimensionale deterministisch-chaotische Strukturen der Herzfrequenz. Die Zahl unabhängiger Mechanismen, die Anteil an der kardiorespiratorischen Regulation haben, ist im Wachzustand am größten. Diese Änderungen lassen das Gesamtsystem in Abhängigkeit von der Vigilanz verschiedene Arbeitspunkte einnehmen.
Breathing and blood flow interact as two, in series coupled units. To adapt heart beat and oxygen supply, a common coordination is required. Concluded from neurophysiological investigations, there is evidence for the existence of one cardiorespiratory network located in the ventrolateral part of the medulla. Since the physiological mechanisms inside the complex regulatory network are not readily accessible, linear and non-linear methods of time series analysis are a useful approach to investigate cardiorespiratory control. To study normal regulation, 42 healthy children, 11 girls and 31 boys (12-15 yr.), were investigated throughout 24 hours under different states of vigilance: wakefulness at rest, REM, and nonREM-sleep. All participants underwent polygraphic measurements, including ECG, thoracic and abdominal respirograms, electrooculogram, and actogram. To estimate the sympatho-vagal drive to the sinus node, the parameters of heart rate power spectra were calculated. The linear intensity of cardiorespiratory coupling was concluded from the coherence spectra. As to non-linear properties of heart rate, the largest Lyapunov exponents as well as the correlation dimension were determined. Similarly, the correlation dimension of the respiratory signals was evaluated. The total power of the heart rate spectrum was found to be greatest during REM, it decreased during wakefulness and was low in nonREM-sleep. These variations are mainly accounted for by low frequency power. The "complexity" of heart rate, as indicated by the correlation dimension, is diminished during sleep phases, whereas the Lyapunov exponents are less affected. The cardiorespiratory coherence is strongly modulated by vigilance with an increase during nonREM and lowest values during REM. The complexity of respiration was also affected by vigilance. A different behavior of heart rate complexity was found during REM-phases. Concluded from spectral analysis, a specific setting of autonomic heart rate regulation for each vigilance stage can be suggested. A low dimensional deterministic chaos is present in heart rate time series. More independent control loops were found to be active during wakefulness. Revealed by parameters of the non-linear dynamics, different stages of vigilance determine different operating points in the cardiorespiratory coordination.
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Geserick, Peter [Verfasser]. "Identifikation der Slfn-(Schlafen)-Proteinfunktion und deren Bedeutung in der Zellzykluskontrolle und der T-Zellontogenie / vorgelegt von Peter Geserick." 2005. http://d-nb.info/973449462/34.

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Books on the topic "Schlafen12"

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Huber, Thomas. Bilder schlafen. Salon, 1998.

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Martin, Marko. Schlafende Hunde: Erzählungen. Eichborn, 2009.

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Schlafende Hunde: Erzählungen. Eichborn, 2009.

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Katase, Kazuo. Kazuo Katase: Schlafende Sterne. Westfälischer Kunstverein, 1994.

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editor, Maass Sebastian 1981, ed. "Verräter schlafen nicht". Regin-Verlag, 2011.

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Überwachen und schlafen. Peter Lang, 2001.

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Kelman, Judith. Wenn engel schlafen. [Goldmann]1988., 1988.

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Thubron, Colin. Sibirien: Schlafende Erde - erwachendes Land. Droemer Knaur, 2003.

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Wittstock, Joachim. Keulenmann und schlafende Muse: Erfahrungsschritte. Hora, 2005.

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Hirshkowitz, Max. Besser schlafen für Dummies. 4th ed. John Wiley & Sons, 2012.

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Book chapters on the topic "Schlafen12"

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Däfler, Martin-Niels. "Schlafen." In Gib mir Geduld – aber flott! Springer Fachmedien Wiesbaden, 2018. http://dx.doi.org/10.1007/978-3-658-19730-8_26.

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Kahl-Scholz, Martina. "Schlafen." In Mensch! Erstaunliches über den Körper. Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-56155-3_6.

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Piehl, Jona. "Schlafen." In Gebrauchsanleitungen optimal gestalten. Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-642-56311-9_1.

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Stefan, Harald, Josef Eberl, Franz Allmer, et al. "Schlafen, beeinträchtigt." In POP® — PraxisOrientierte Pflegediagnostik. Springer Vienna, 2009. http://dx.doi.org/10.1007/978-3-211-79910-9_64.

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Gewalt, Wolfgang. "Schwimmen und Schlafen." In Wale und Delphine. Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-78205-3_4.

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Stefan, Harald, Josef Eberl, Franz Allmer, et al. "Schlafen, beeinträchtigt, Risiko." In POP® — PraxisOrientierte Pflegediagnostik. Springer Vienna, 2009. http://dx.doi.org/10.1007/978-3-211-79910-9_63.

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Birbaumer, N., and R. F. Schmidt. "Wachen, Aufmerksamkeit und Schlafen." In Physiologie des Menschen. Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-09334-4_7.

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Birbaumer, N., and R. F. Schmidt. "Wachen, Aufmerksamkeit und Schlafen." In Physiologie des Menschen. Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-662-09346-7_7.

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Birbaumer, N., and R. F. Schmidt. "Wachen, Aufmerksamkeit und Schlafen." In Springer-Lehrbuch. Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22217-1_16.

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Birbaumer, N., and R. F. Schmidt. "Wachen, Aufmerksamkeit und Schlafen." In Springer-Lehrbuch. Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-662-22216-4_16.

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Conference papers on the topic "Schlafen12"

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Fertsch, S., A. Wolter, B. Munder, et al. "Kann Lipofilling schlafende Brustkrebszellen aktivieren?" In 39. Jahrestagung der Deutschen Gesellschaft für Senologie. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1687962.

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Gürgan, S., K. Bosse, B. Böer, et al. "Zufallsbefund bei prophylaktischer Operation- „der schlafende Hund“." In Wissenschaftliche Abstracts zur 40. Jahrestagung der Deutschen Gesellschaft für Senologie e.V. (DGS) Interdisziplinär. Kommunikativ. Digital. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1730163.

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Pommier, Yves, and Junko Murai. "Abstract IA19: PARP trapping and Schlafen 11." In Abstracts: AACR Special Conference on DNA Repair: Tumor Development and Therapeutic Response; November 2-5, 2016; Montreal, QC, Canada. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1557-3125.dnarepair16-ia19.

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Pommier, Yves G., and Junko Murai. "Abstract IA21: PARP trapping and Schlafen 11 to kill cancer cells." In Abstracts: AACR International Conference held in cooperation with the Latin American Cooperative Oncology Group (LACOG) on Translational Cancer Medicine; May 4-6, 2017; São Paulo, Brazil. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.tcm17-ia21.

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Murai, Junko, Rozenn Josse, James H. Doroshow, and Yves Pommier. "Abstract 1718: Schlafen 11 (SLFN11) is a critical determinant of cellular sensitivity to PARP inhibitors." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1718.

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Zoppoli, Gabriele, Marie Regairaz, Elisabetta Leo, William C. Reinhold, and Yves Pommier. "Abstract 4693: The putative DNA/RNA Helicase Schlafen-11 sensitizes cancer cells to topoisomerase I inhibitors." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4693.

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Schwartz, Anthony L., Sukhbir Kaur, Sai-Wen Tang, Yves Pommier, and David D. Roberts. "Abstract 3054: CD47 signaling regulates a DNA damage response pathway by suppressing the expression of Schlafen-11 (SLFN11)." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3054.

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Oh, Phil-Sun, Vaishali B. Patel, Matthew A. Sanders, et al. "Abstract 5203: Schlafen-3 decreases cancer stem cell marker expression and autocrine/ juxtacrine signaling in FOLFOX-resistant colon cancer cells." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-5203.

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Murai, Junko, and Yves Pommier. "Abstract B64: Schlafen 11 (SLFN11) irreversibly blocks cell cycle recovery independently of ATR following replicative damage by poly(ADPribose) polymerase inhibitors." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-b64.

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Marzi, Laetitia, Ludmila Szabova, Zoe Weaver Ohler, et al. "Abstract 365: Indotecan (LMP400), indimitecan (LMP776) and LMP744, a new class of non-camptothecin topoisomerase I inhibitors selective for schlafen11-positive and BRCA-deficient cells that synergize with olaparib." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-365.

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