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  • 1
    Publication Date: 2011-06-24
    Description: More than half of the world's population now lives in cities, making the creation of a healthy urban environment a major policy priority. Cities have both health risks and benefits, but mental health is negatively affected: mood and anxiety disorders are more prevalent in city dwellers and the incidence of schizophrenia is strongly increased in people born and raised in cities. Although these findings have been widely attributed to the urban social environment, the neural processes that could mediate such associations are unknown. Here we show, using functional magnetic resonance imaging in three independent experiments, that urban upbringing and city living have dissociable impacts on social evaluative stress processing in humans. Current city living was associated with increased amygdala activity, whereas urban upbringing affected the perigenual anterior cingulate cortex, a key region for regulation of amygdala activity, negative affect and stress. These findings were regionally and behaviourally specific, as no other brain structures were affected and no urbanicity effect was seen during control experiments invoking cognitive processing without stress. Our results identify distinct neural mechanisms for an established environmental risk factor, link the urban environment for the first time to social stress processing, suggest that brain regions differ in vulnerability to this risk factor across the lifespan, and indicate that experimental interrogation of epidemiological associations is a promising strategy in social neuroscience.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lederbogen, Florian -- Kirsch, Peter -- Haddad, Leila -- Streit, Fabian -- Tost, Heike -- Schuch, Philipp -- Wust, Stefan -- Pruessner, Jens C -- Rietschel, Marcella -- Deuschle, Michael -- Meyer-Lindenberg, Andreas -- England -- Nature. 2011 Jun 22;474(7352):498-501. doi: 10.1038/nature10190.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Central Institute of Mental Health, University of Heidelberg/Medical Faculty Mannheim, 68159 Mannheim, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21697947" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/*physiology ; Anxiety Disorders/epidemiology ; *Cities/epidemiology ; Gyrus Cinguli/*physiology ; Humans ; Hydrocortisone/blood ; *Life Style ; Magnetic Resonance Imaging ; Mental Health/statistics & numerical data ; Models, Neurological ; Mood Disorders/epidemiology ; Rural Health/statistics & numerical data ; Sample Size ; Schizophrenia/epidemiology ; Stress, Psychological/blood/epidemiology/*physiopathology ; Time Factors ; Urban Health/statistics & numerical data ; Urbanization
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2014-08-19
    Description: Necroptosis has emerged as an important pathway of programmed cell death in embryonic development, tissue homeostasis, immunity and inflammation. RIPK1 is implicated in inflammatory and cell death signalling and its kinase activity is believed to drive RIPK3-mediated necroptosis. Here we show that kinase-independent scaffolding RIPK1 functions regulate homeostasis and prevent inflammation in barrier tissues by inhibiting epithelial cell apoptosis and necroptosis. Intestinal epithelial cell (IEC)-specific RIPK1 knockout caused IEC apoptosis, villus atrophy, loss of goblet and Paneth cells and premature death in mice. This pathology developed independently of the microbiota and of MyD88 signalling but was partly rescued by TNFR1 (also known as TNFRSF1A) deficiency. Epithelial FADD ablation inhibited IEC apoptosis and prevented the premature death of mice with IEC-specific RIPK1 knockout. However, mice lacking both RIPK1 and FADD in IECs displayed RIPK3-dependent IEC necroptosis, Paneth cell loss and focal erosive inflammatory lesions in the colon. Moreover, a RIPK1 kinase inactive knock-in delayed but did not prevent inflammation caused by FADD deficiency in IECs or keratinocytes, showing that RIPK3-dependent necroptosis of FADD-deficient epithelial cells only partly requires RIPK1 kinase activity. Epidermis-specific RIPK1 knockout triggered keratinocyte apoptosis and necroptosis and caused severe skin inflammation that was prevented by RIPK3 but not FADD deficiency. These findings revealed that RIPK1 inhibits RIPK3-mediated necroptosis in keratinocytes in vivo and identified necroptosis as a more potent trigger of inflammation compared with apoptosis. Therefore, RIPK1 is a master regulator of epithelial cell survival, homeostasis and inflammation in the intestine and the skin.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4206266/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4206266/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dannappel, Marius -- Vlantis, Katerina -- Kumari, Snehlata -- Polykratis, Apostolos -- Kim, Chun -- Wachsmuth, Laurens -- Eftychi, Christina -- Lin, Juan -- Corona, Teresa -- Hermance, Nicole -- Zelic, Matija -- Kirsch, Petra -- Basic, Marijana -- Bleich, Andre -- Kelliher, Michelle -- Pasparakis, Manolis -- R01 AI075118/AI/NIAID NIH HHS/ -- R01AI075118/AI/NIAID NIH HHS/ -- T32 AI095213/AI/NIAID NIH HHS/ -- England -- Nature. 2014 Sep 4;513(7516):90-4. doi: 10.1038/nature13608. Epub 2014 Aug 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Institute for Genetics, Centre for Molecular Medicine (CMMC), and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, 50931 Cologne, Germany [2]. ; Institute for Genetics, Centre for Molecular Medicine (CMMC), and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, 50931 Cologne, Germany. ; Department of Cancer Biology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA. ; Tierforschungszentrum, University of Ulm, Albert-Einstein-Allee 11, D-89081 Ulm, Germany. ; Institute for Laboratory Animal Science, Hannover Medical School, D-30625 Hannover, Germany. ; 1] Department of Cancer Biology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA [2].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25132550" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Caspase 8/metabolism ; Cell Survival ; Epithelial Cells/*cytology/metabolism/*pathology ; Fas-Associated Death Domain Protein/deficiency/metabolism ; Female ; *Homeostasis ; Inflammation/metabolism/pathology ; Intestines/cytology/metabolism/pathology ; Keratinocytes/metabolism/pathology ; Male ; Mice ; Mice, Knockout ; Myeloid Differentiation Factor 88/metabolism ; *Necrosis ; Paneth Cells/metabolism/pathology ; Receptor-Interacting Protein Serine-Threonine ; Kinases/deficiency/genetics/*metabolism ; Receptors, Tumor Necrosis Factor, Type I/deficiency/metabolism ; Skin/cytology/metabolism/pathology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2013-08-13
    Description: Epileptic encephalopathies are a devastating group of severe childhood epilepsy disorders for which the cause is often unknown. Here we report a screen for de novo mutations in patients with two classical epileptic encephalopathies: infantile spasms (n = 149) and Lennox-Gastaut syndrome (n = 115). We sequenced the exomes of 264 probands, and their parents, and confirmed 329 de novo mutations. A likelihood analysis showed a significant excess of de novo mutations in the approximately 4,000 genes that are the most intolerant to functional genetic variation in the human population (P = 2.9 x 10(-3)). Among these are GABRB3, with de novo mutations in four patients, and ALG13, with the same de novo mutation in two patients; both genes show clear statistical evidence of association with epileptic encephalopathy. Given the relevant site-specific mutation rates, the probabilities of these outcomes occurring by chance are P = 4.1 x 10(-10) and P = 7.8 x 10(-12), respectively. Other genes with de novo mutations in this cohort include CACNA1A, CHD2, FLNA, GABRA1, GRIN1, GRIN2B, HNRNPU, IQSEC2, MTOR and NEDD4L. Finally, we show that the de novo mutations observed are enriched in specific gene sets including genes regulated by the fragile X protein (P 〈 10(-8)), as has been reported previously for autism spectrum disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3773011/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3773011/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Epi4K Consortium -- Epilepsy Phenome/Genome Project -- Allen, Andrew S -- Berkovic, Samuel F -- Cossette, Patrick -- Delanty, Norman -- Dlugos, Dennis -- Eichler, Evan E -- Epstein, Michael P -- Glauser, Tracy -- Goldstein, David B -- Han, Yujun -- Heinzen, Erin L -- Hitomi, Yuki -- Howell, Katherine B -- Johnson, Michael R -- Kuzniecky, Ruben -- Lowenstein, Daniel H -- Lu, Yi-Fan -- Madou, Maura R Z -- Marson, Anthony G -- Mefford, Heather C -- Esmaeeli Nieh, Sahar -- O'Brien, Terence J -- Ottman, Ruth -- Petrovski, Slave -- Poduri, Annapurna -- Ruzzo, Elizabeth K -- Scheffer, Ingrid E -- Sherr, Elliott H -- Yuskaitis, Christopher J -- Abou-Khalil, Bassel -- Alldredge, Brian K -- Bautista, Jocelyn F -- Boro, Alex -- Cascino, Gregory D -- Consalvo, Damian -- Crumrine, Patricia -- Devinsky, Orrin -- Fiol, Miguel -- Fountain, Nathan B -- French, Jacqueline -- Friedman, Daniel -- Geller, Eric B -- Glynn, Simon -- Haut, Sheryl R -- Hayward, Jean -- Helmers, Sandra L -- Joshi, Sucheta -- Kanner, Andres -- Kirsch, Heidi E -- Knowlton, Robert C -- Kossoff, Eric H -- Kuperman, Rachel -- McGuire, Shannon M -- Motika, Paul V -- Novotny, Edward J -- Paolicchi, Juliann M -- Parent, Jack M -- Park, Kristen -- Shellhaas, Renee A -- Shih, Jerry J -- Singh, Rani -- Sirven, Joseph -- Smith, Michael C -- Sullivan, Joseph -- Lin Thio, Liu -- Venkat, Anu -- Vining, Eileen P G -- Von Allmen, Gretchen K -- Weisenberg, Judith L -- Widdess-Walsh, Peter -- Winawer, Melodie R -- 1RC2NS070342/NS/NINDS NIH HHS/ -- NS053998/NS/NINDS NIH HHS/ -- NS077274/NS/NINDS NIH HHS/ -- NS077276/NS/NINDS NIH HHS/ -- NS077303/NS/NINDS NIH HHS/ -- NS077364/NS/NINDS NIH HHS/ -- R56AI098588/AI/NIAID NIH HHS/ -- U01 NS053998/NS/NINDS NIH HHS/ -- U01 NS077274/NS/NINDS NIH HHS/ -- U01 NS077276/NS/NINDS NIH HHS/ -- U01 NS077303/NS/NINDS NIH HHS/ -- U01 NS077364/NS/NINDS NIH HHS/ -- U01AI067854/AI/NIAID NIH HHS/ -- UL1 TR000005/TR/NCATS NIH HHS/ -- England -- Nature. 2013 Sep 12;501(7466):217-21. doi: 10.1038/nature12439. Epub 2013 Aug 11.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23934111" target="_blank"〉PubMed〈/a〉
    Keywords: Child Development Disorders, Pervasive ; Cohort Studies ; Exome/genetics ; Female ; Fragile X Mental Retardation Protein/metabolism ; Genetic Predisposition to Disease/genetics ; Humans ; Infant ; Intellectual Disability/*genetics/physiopathology ; Lennox Gastaut Syndrome ; Male ; Mutation/*genetics ; Mutation Rate ; N-Acetylglucosaminyltransferases/genetics ; Probability ; Receptors, GABA-A/genetics ; Spasms, Infantile/*genetics/physiopathology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2018-09-11
    Description: An integrated genomic analysis of anaplastic meningioma identifies prognostic molecular signatures An integrated genomic analysis of anaplastic meningioma identifies prognostic molecular signatures, Published online: 10 September 2018; doi:10.1038/s41598-018-31659-0 An integrated genomic analysis of anaplastic meningioma identifies prognostic molecular signatures
    Electronic ISSN: 2045-2322
    Topics: Natural Sciences in General
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  • 5
    Publication Date: 2011-08-02
    Description: Intestinal immune homeostasis depends on a tightly regulated cross talk between commensal bacteria, mucosal immune cells and intestinal epithelial cells (IECs). Epithelial barrier disruption is considered to be a potential cause of inflammatory bowel disease; however, the mechanisms regulating intestinal epithelial integrity are poorly understood. Here we show that mice with IEC-specific knockout of FADD (FADD(IEC-KO)), an adaptor protein required for death-receptor-induced apoptosis, spontaneously developed epithelial cell necrosis, loss of Paneth cells, enteritis and severe erosive colitis. Genetic deficiency in RIP3, a critical regulator of programmed necrosis, prevented the development of spontaneous pathology in both the small intestine and colon of FADD(IEC-KO) mice, demonstrating that intestinal inflammation is triggered by RIP3-dependent death of FADD-deficient IECs. Epithelial-specific inhibition of CYLD, a deubiquitinase that regulates cellular necrosis, prevented colitis development in FADD(IEC-KO) but not in NEMO(IEC-KO) mice, showing that different mechanisms mediated death of colonic epithelial cells in these two models. In FADD(IEC-KO) mice, TNF deficiency ameliorated colon inflammation, whereas MYD88 deficiency and also elimination of the microbiota prevented colon inflammation, indicating that bacteria-mediated Toll-like-receptor signalling drives colitis by inducing the expression of TNF and other cytokines. However, neither CYLD, TNF or MYD88 deficiency nor elimination of the microbiota could prevent Paneth cell loss and enteritis in FADD(IEC-KO) mice, showing that different mechanisms drive RIP3-dependent necrosis of FADD-deficient IECs in the small and large bowel. Therefore, by inhibiting RIP3-mediated IEC necrosis, FADD preserves epithelial barrier integrity and antibacterial defence, maintains homeostasis and prevents chronic intestinal inflammation. Collectively, these results show that mechanisms preventing RIP3-mediated epithelial cell death are critical for the maintenance of intestinal homeostasis and indicate that programmed necrosis of IECs might be implicated in the pathogenesis of inflammatory bowel disease, in which Paneth cell and barrier defects are thought to contribute to intestinal inflammation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Welz, Patrick-Simon -- Wullaert, Andy -- Vlantis, Katerina -- Kondylis, Vangelis -- Fernandez-Majada, Vanesa -- Ermolaeva, Maria -- Kirsch, Petra -- Sterner-Kock, Anja -- van Loo, Geert -- Pasparakis, Manolis -- England -- Nature. 2011 Jul 31;477(7364):330-4. doi: 10.1038/nature10273.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genetics, Centre for Molecular Medicine, University of Cologne, Zulpicher Str. 47a, 50674 Cologne, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21804564" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Chronic Disease ; Colitis/enzymology/metabolism/*pathology ; Colon/enzymology/metabolism/*pathology ; Cysteine Endopeptidases/metabolism ; Enteritis/enzymology/metabolism/*pathology ; Epithelial Cells/enzymology/metabolism/*pathology ; Fas-Associated Death Domain Protein/deficiency/*metabolism ; Inflammatory Bowel Diseases/enzymology/metabolism/pathology ; Intracellular Signaling Peptides and Proteins/deficiency/metabolism ; Metagenome/physiology ; Mice ; Myeloid Differentiation Factor 88/deficiency/metabolism ; Necrosis ; Paneth Cells/pathology ; Receptor-Interacting Protein Serine-Threonine Kinases/*antagonists & ; inhibitors/*metabolism ; Signal Transduction ; Tumor Necrosis Factors/deficiency
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2014-09-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kirsch, Joachim -- Scholer, Hans -- England -- Nature. 2014 Sep 11;513(7517):172. doi: 10.1038/513172a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Heidelberg, Germany. ; Max Planck Institute for Molecular Biomedicine, Munster, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25209789" target="_blank"〉PubMed〈/a〉
    Keywords: Humans ; Pluripotent Stem Cells ; *Retraction of Publication as Topic ; Science/*standards ; Scientific Misconduct
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2018-10-16
    Description: SMC3 protein levels impact on karyotype and outcome in acute myeloid leukemia SMC3 protein levels impact on karyotype and outcome in acute myeloid leukemia, Published online: 15 October 2018; doi:10.1038/s41375-018-0287-6 SMC3 protein levels impact on karyotype and outcome in acute myeloid leukemia
    Print ISSN: 0887-6924
    Electronic ISSN: 1476-5551
    Topics: Medicine
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