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  • 1
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    Large recurrent microdeletions associated with schizophrenia (2008)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2008-08-01
    Beschreibung: Reduced fecundity, associated with severe mental disorders, places negative selection pressure on risk alleles and may explain, in part, why common variants have not been found that confer risk of disorders such as autism, schizophrenia and mental retardation. Thus, rare variants may account for a larger fraction of the overall genetic risk than previously assumed. In contrast to rare single nucleotide mutations, rare copy number variations (CNVs) can be detected using genome-wide single nucleotide polymorphism arrays. This has led to the identification of CNVs associated with mental retardation and autism. In a genome-wide search for CNVs associating with schizophrenia, we used a population-based sample to identify de novo CNVs by analysing 9,878 transmissions from parents to offspring. The 66 de novo CNVs identified were tested for association in a sample of 1,433 schizophrenia cases and 33,250 controls. Three deletions at 1q21.1, 15q11.2 and 15q13.3 showing nominal association with schizophrenia in the first sample (phase I) were followed up in a second sample of 3,285 cases and 7,951 controls (phase II). All three deletions significantly associate with schizophrenia and related psychoses in the combined sample. The identification of these rare, recurrent risk variants, having occurred independently in multiple founders and being subject to negative selection, is important in itself. CNV analysis may also point the way to the identification of additional and more prevalent risk variants in genes and pathways involved in schizophrenia.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2687075/" 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/PMC2687075/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stefansson, Hreinn -- Rujescu, Dan -- Cichon, Sven -- Pietilainen, Olli P H -- Ingason, Andres -- Steinberg, Stacy -- Fossdal, Ragnheidur -- Sigurdsson, Engilbert -- Sigmundsson, Thordur -- Buizer-Voskamp, Jacobine E -- Hansen, Thomas -- Jakobsen, Klaus D -- Muglia, Pierandrea -- Francks, Clyde -- Matthews, Paul M -- Gylfason, Arnaldur -- Halldorsson, Bjarni V -- Gudbjartsson, Daniel -- Thorgeirsson, Thorgeir E -- Sigurdsson, Asgeir -- Jonasdottir, Adalbjorg -- Jonasdottir, Aslaug -- Bjornsson, Asgeir -- Mattiasdottir, Sigurborg -- Blondal, Thorarinn -- Haraldsson, Magnus -- Magnusdottir, Brynja B -- Giegling, Ina -- Moller, Hans-Jurgen -- Hartmann, Annette -- Shianna, Kevin V -- Ge, Dongliang -- Need, Anna C -- Crombie, Caroline -- Fraser, Gillian -- Walker, Nicholas -- Lonnqvist, Jouko -- Suvisaari, Jaana -- Tuulio-Henriksson, Annamarie -- Paunio, Tiina -- Toulopoulou, Timi -- Bramon, Elvira -- Di Forti, Marta -- Murray, Robin -- Ruggeri, Mirella -- Vassos, Evangelos -- Tosato, Sarah -- Walshe, Muriel -- Li, Tao -- Vasilescu, Catalina -- Muhleisen, Thomas W -- Wang, August G -- Ullum, Henrik -- Djurovic, Srdjan -- Melle, Ingrid -- Olesen, Jes -- Kiemeney, Lambertus A -- Franke, Barbara -- GROUP -- Sabatti, Chiara -- Freimer, Nelson B -- Gulcher, Jeffrey R -- Thorsteinsdottir, Unnur -- Kong, Augustine -- Andreassen, Ole A -- Ophoff, Roel A -- Georgi, Alexander -- Rietschel, Marcella -- Werge, Thomas -- Petursson, Hannes -- Goldstein, David B -- Nothen, Markus M -- Peltonen, Leena -- Collier, David A -- St Clair, David -- Stefansson, Kari -- 089061/Wellcome Trust/United Kingdom -- G0901310/Medical Research Council/United Kingdom -- PDA/02/06/016/Department of Health/United Kingdom -- R01 MH078075/MH/NIMH NIH HHS/ -- R01MH71425-01A1/MH/NIMH NIH HHS/ -- England -- Nature. 2008 Sep 11;455(7210):232-6. doi: 10.1038/nature07229.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CNS Division, deCODE genetics, Sturlugata 8, IS-101 Reykjavik, Iceland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18668039" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): China ; Chromosomes, Human, Pair 1/genetics ; Chromosomes, Human, Pair 15/genetics ; Europe ; Gene Dosage/genetics ; Genetic Predisposition to Disease/*genetics ; Genome, Human/genetics ; Genotype ; Humans ; Loss of Heterozygosity ; Models, Genetic ; Polymorphism, Single Nucleotide/genetics ; Psychotic Disorders/genetics ; Schizophrenia/*genetics ; Sequence Deletion/*genetics
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    Common variants conferring risk of schizophrenia (2009)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2009-07-03
    Beschreibung: Schizophrenia is a complex disorder, caused by both genetic and environmental factors and their interactions. Research on pathogenesis has traditionally focused on neurotransmitter systems in the brain, particularly those involving dopamine. Schizophrenia has been considered a separate disease for over a century, but in the absence of clear biological markers, diagnosis has historically been based on signs and symptoms. A fundamental message emerging from genome-wide association studies of copy number variations (CNVs) associated with the disease is that its genetic basis does not necessarily conform to classical nosological disease boundaries. Certain CNVs confer not only high relative risk of schizophrenia but also of other psychiatric disorders. The structural variations associated with schizophrenia can involve several genes and the phenotypic syndromes, or the 'genomic disorders', have not yet been characterized. Single nucleotide polymorphism (SNP)-based genome-wide association studies with the potential to implicate individual genes in complex diseases may reveal underlying biological pathways. Here we combined SNP data from several large genome-wide scans and followed up the most significant association signals. We found significant association with several markers spanning the major histocompatibility complex (MHC) region on chromosome 6p21.3-22.1, a marker located upstream of the neurogranin gene (NRGN) on 11q24.2 and a marker in intron four of transcription factor 4 (TCF4) on 18q21.2. Our findings implicating the MHC region are consistent with an immune component to schizophrenia risk, whereas the association with NRGN and TCF4 points to perturbation of pathways involved in brain development, memory and cognition.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3077530/" 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/PMC3077530/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stefansson, Hreinn -- Ophoff, Roel A -- Steinberg, Stacy -- Andreassen, Ole A -- Cichon, Sven -- Rujescu, Dan -- Werge, Thomas -- Pietilainen, Olli P H -- Mors, Ole -- Mortensen, Preben B -- Sigurdsson, Engilbert -- Gustafsson, Omar -- Nyegaard, Mette -- Tuulio-Henriksson, Annamari -- Ingason, Andres -- Hansen, Thomas -- Suvisaari, Jaana -- Lonnqvist, Jouko -- Paunio, Tiina -- Borglum, Anders D -- Hartmann, Annette -- Fink-Jensen, Anders -- Nordentoft, Merete -- Hougaard, David -- Norgaard-Pedersen, Bent -- Bottcher, Yvonne -- Olesen, Jes -- Breuer, Rene -- Moller, Hans-Jurgen -- Giegling, Ina -- Rasmussen, Henrik B -- Timm, Sally -- Mattheisen, Manuel -- Bitter, Istvan -- Rethelyi, Janos M -- Magnusdottir, Brynja B -- Sigmundsson, Thordur -- Olason, Pall -- Masson, Gisli -- Gulcher, Jeffrey R -- Haraldsson, Magnus -- Fossdal, Ragnheidur -- Thorgeirsson, Thorgeir E -- Thorsteinsdottir, Unnur -- Ruggeri, Mirella -- Tosato, Sarah -- Franke, Barbara -- Strengman, Eric -- Kiemeney, Lambertus A -- Genetic Risk and Outcome in Psychosis (GROUP) -- Melle, Ingrid -- Djurovic, Srdjan -- Abramova, Lilia -- Kaleda, Vasily -- Sanjuan, Julio -- de Frutos, Rosa -- Bramon, Elvira -- Vassos, Evangelos -- Fraser, Gillian -- Ettinger, Ulrich -- Picchioni, Marco -- Walker, Nicholas -- Toulopoulou, Timi -- Need, Anna C -- Ge, Dongliang -- Yoon, Joeng Lim -- Shianna, Kevin V -- Freimer, Nelson B -- Cantor, Rita M -- Murray, Robin -- Kong, Augustine -- Golimbet, Vera -- Carracedo, Angel -- Arango, Celso -- Costas, Javier -- Jonsson, Erik G -- Terenius, Lars -- Agartz, Ingrid -- Petursson, Hannes -- Nothen, Markus M -- Rietschel, Marcella -- Matthews, Paul M -- Muglia, Pierandrea -- Peltonen, Leena -- St Clair, David -- Goldstein, David B -- Stefansson, Kari -- Collier, David A -- 089061/Wellcome Trust/United Kingdom -- 1R01HL087679-01/HL/NHLBI NIH HHS/ -- PDA/02/06/016/Department of Health/United Kingdom -- R01 MH078075/MH/NIMH NIH HHS/ -- England -- Nature. 2009 Aug 6;460(7256):744-7. doi: 10.1038/nature08186. Epub 2009 Jul 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉deCODE genetics, Sturlugata 8, IS-101 Reykjavik, Iceland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19571808" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; Chromosomes, Human, Pair 11/genetics ; Chromosomes, Human, Pair 18/genetics ; Chromosomes, Human, Pair 6/genetics ; DNA-Binding Proteins/genetics ; Genetic Markers/genetics ; Genetic Predisposition to Disease/*genetics ; Genome, Human/genetics ; Genome-Wide Association Study ; Genotype ; Humans ; Major Histocompatibility Complex/genetics ; Neurogranin/genetics ; Polymorphism, Single Nucleotide/*genetics ; Schizophrenia/*genetics/immunology ; Transcription Factors/genetics
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Rate of de novo mutations and the importance of father's age to disease risk (2012)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2012-08-24
    Beschreibung: Mutations generate sequence diversity and provide a substrate for selection. The rate of de novo mutations is therefore of major importance to evolution. Here we conduct a study of genome-wide mutation rates by sequencing the entire genomes of 78 Icelandic parent-offspring trios at high coverage. We show that in our samples, with an average father's age of 29.7, the average de novo mutation rate is 1.20 x 10(-8) per nucleotide per generation. Most notably, the diversity in mutation rate of single nucleotide polymorphisms is dominated by the age of the father at conception of the child. The effect is an increase of about two mutations per year. An exponential model estimates paternal mutations doubling every 16.5 years. After accounting for random Poisson variation, father's age is estimated to explain nearly all of the remaining variation in the de novo mutation counts. These observations shed light on the importance of the father's age on the risk of diseases such as schizophrenia and autism.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3548427/" 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/PMC3548427/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kong, Augustine -- Frigge, Michael L -- Masson, Gisli -- Besenbacher, Soren -- Sulem, Patrick -- Magnusson, Gisli -- Gudjonsson, Sigurjon A -- Sigurdsson, Asgeir -- Jonasdottir, Aslaug -- Jonasdottir, Adalbjorg -- Wong, Wendy S W -- Sigurdsson, Gunnar -- Walters, G Bragi -- Steinberg, Stacy -- Helgason, Hannes -- Thorleifsson, Gudmar -- Gudbjartsson, Daniel F -- Helgason, Agnar -- Magnusson, Olafur Th -- Thorsteinsdottir, Unnur -- Stefansson, Kari -- MH071425/MH/NIMH NIH HHS/ -- R01 MH071425/MH/NIMH NIH HHS/ -- England -- Nature. 2012 Aug 23;488(7412):471-5. doi: 10.1038/nature11396.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉deCODE Genetics, Sturlugata 8, 101 Reykjavik, Iceland. kong@decode.is〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22914163" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adult ; Autistic Disorder/epidemiology/etiology/*genetics ; Chromosomes, Human/genetics ; Female ; *Genetic Predisposition to Disease ; Genome, Human/genetics ; Humans ; Iceland/epidemiology ; Male ; Middle Aged ; Mothers ; *Mutation Rate ; Ovum/metabolism ; *Paternal Age ; Pedigree ; Polymorphism, Single Nucleotide/genetics ; Risk Factors ; Schizophrenia/epidemiology/etiology/*genetics ; Selection, Genetic/genetics ; Sequence Analysis, DNA ; Spermatozoa/metabolism ; Young Adult
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
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    CNVs conferring risk of autism or schizophrenia affect cognition in controls (2013)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2013-12-20
    Beschreibung: In a small fraction of patients with schizophrenia or autism, alleles of copy-number variants (CNVs) in their genomes are probably the strongest factors contributing to the pathogenesis of the disease. These CNVs may provide an entry point for investigations into the mechanisms of brain function and dysfunction alike. They are not fully penetrant and offer an opportunity to study their effects separate from that of manifest disease. Here we show in an Icelandic sample that a few of the CNVs clearly alter fecundity (measured as the number of children by age 45). Furthermore, we use various tests of cognitive function to demonstrate that control subjects carrying the CNVs perform at a level that is between that of schizophrenia patients and population controls. The CNVs do not all affect the same cognitive domains, hence the cognitive deficits that drive or accompany the pathogenesis vary from one CNV to another. Controls carrying the chromosome 15q11.2 deletion between breakpoints 1 and 2 (15q11.2(BP1-BP2) deletion) have a history of dyslexia and dyscalculia, even after adjusting for IQ in the analysis, and the CNV only confers modest effects on other cognitive traits. The 15q11.2(BP1-BP2) deletion affects brain structure in a pattern consistent with both that observed during first-episode psychosis in schizophrenia and that of structural correlates in dyslexia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stefansson, Hreinn -- Meyer-Lindenberg, Andreas -- Steinberg, Stacy -- Magnusdottir, Brynja -- Morgen, Katrin -- Arnarsdottir, Sunna -- Bjornsdottir, Gyda -- Walters, G Bragi -- Jonsdottir, Gudrun A -- Doyle, Orla M -- Tost, Heike -- Grimm, Oliver -- Kristjansdottir, Solveig -- Snorrason, Heimir -- Davidsdottir, Solveig R -- Gudmundsson, Larus J -- Jonsson, Gudbjorn F -- Stefansdottir, Berglind -- Helgadottir, Isafold -- Haraldsson, Magnus -- Jonsdottir, Birna -- Thygesen, Johan H -- Schwarz, Adam J -- Didriksen, Michael -- Stensbol, Tine B -- Brammer, Michael -- Kapur, Shitij -- Halldorsson, Jonas G -- Hreidarsson, Stefan -- Saemundsen, Evald -- Sigurdsson, Engilbert -- Stefansson, Kari -- G0701748/Medical Research Council/United Kingdom -- England -- Nature. 2014 Jan 16;505(7483):361-6. doi: 10.1038/nature12818. Epub 2013 Dec 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] deCODE genetics/Amgen, Sturlugata 8, IS-101 Reykjavik, Iceland [2]. ; 1] Central Institute of Mental Health, University of Heidelberg Medical Faculty Mannheim, 68159 Mannheim, Germany [2]. ; deCODE genetics/Amgen, Sturlugata 8, IS-101 Reykjavik, Iceland. ; Landspitali, Department of Psychiatry, National University Hospital, IS-101 Reykjavik, Iceland. ; Central Institute of Mental Health, University of Heidelberg Medical Faculty Mannheim, 68159 Mannheim, Germany. ; 1] deCODE genetics/Amgen, Sturlugata 8, IS-101 Reykjavik, Iceland [2] Landspitali, Department of Psychiatry, National University Hospital, IS-101 Reykjavik, Iceland. ; Institute of Psychiatry, King's College, 16 De Crespigny Park, London SE5 8AF, UK. ; 1] Landspitali, Department of Psychiatry, National University Hospital, IS-101 Reykjavik, Iceland [2] University of Iceland, Faculty of Medicine, University of Iceland, IS-101 Reykjavik, Iceland. ; Rontgen Domus, Egilsgotu 3, IS-101 Reykjavik, Iceland. ; Mental Health Centre Sct. Hans, Copenhagen University Hospital, Research Institute of Biological Psychiatry, Boserupvej 2, DK-4000 Roskilde, Denmark. ; Tailored Therapeutics, Lilly Research Laboratories, Eli Lilly and Company, Lilly Corporate Center DC 1940, Indianapolis, Indiana 46285, USA. ; H. Lundbeck A/S, Ottiliavej 9, DK-2500 Valby, Denmark. ; University of Iceland, Faculty of Medicine, University of Iceland, IS-101 Reykjavik, Iceland. ; The State Diagnostic and Counselling Centre, Digranesvegur 5, IS-200 Kopavogur, Iceland. ; 1] University of Iceland, Faculty of Medicine, University of Iceland, IS-101 Reykjavik, Iceland [2] The State Diagnostic and Counselling Centre, Digranesvegur 5, IS-200 Kopavogur, Iceland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24352232" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adolescent ; Adult ; Aged ; Autistic Disorder/*genetics ; Brain/abnormalities/anatomy & histology/metabolism ; Case-Control Studies ; Chromosome Deletion ; Chromosomes, Human/genetics ; Chromosomes, Human, Pair 15/genetics ; Cognition/*physiology ; DNA Copy Number Variations/*genetics ; Dyslexia/genetics ; Female ; Fertility/genetics ; *Genetic Predisposition to Disease ; Heterozygote ; Humans ; Iceland ; Learning Disorders/genetics ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Neuropsychological Tests ; Phenotype ; Schizophrenia/*genetics ; Young Adult
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
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    A mutation in APP protects against Alzheimer's disease and age-related cognitive decline (2012)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2012-07-18
    Beschreibung: The prevalence of dementia in the Western world in people over the age of 60 has been estimated to be greater than 5%, about two-thirds of which are due to Alzheimer's disease. The age-specific prevalence of Alzheimer's disease nearly doubles every 5 years after age 65, leading to a prevalence of greater than 25% in those over the age of 90 (ref. 3). Here, to search for low-frequency variants in the amyloid-beta precursor protein (APP) gene with a significant effect on the risk of Alzheimer's disease, we studied coding variants in APP in a set of whole-genome sequence data from 1,795 Icelanders. We found a coding mutation (A673T) in the APP gene that protects against Alzheimer's disease and cognitive decline in the elderly without Alzheimer's disease. This substitution is adjacent to the aspartyl protease beta-site in APP, and results in an approximately 40% reduction in the formation of amyloidogenic peptides in vitro. The strong protective effect of the A673T substitution against Alzheimer's disease provides proof of principle for the hypothesis that reducing the beta-cleavage of APP may protect against the disease. Furthermore, as the A673T allele also protects against cognitive decline in the elderly without Alzheimer's disease, the two may be mediated through the same or similar mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jonsson, Thorlakur -- Atwal, Jasvinder K -- Steinberg, Stacy -- Snaedal, Jon -- Jonsson, Palmi V -- Bjornsson, Sigurbjorn -- Stefansson, Hreinn -- Sulem, Patrick -- Gudbjartsson, Daniel -- Maloney, Janice -- Hoyte, Kwame -- Gustafson, Amy -- Liu, Yichin -- Lu, Yanmei -- Bhangale, Tushar -- Graham, Robert R -- Huttenlocher, Johanna -- Bjornsdottir, Gyda -- Andreassen, Ole A -- Jonsson, Erik G -- Palotie, Aarno -- Behrens, Timothy W -- Magnusson, Olafur T -- Kong, Augustine -- Thorsteinsdottir, Unnur -- Watts, Ryan J -- Stefansson, Kari -- HL-102924/HL/NHLBI NIH HHS/ -- HL-102925/HL/NHLBI NIH HHS/ -- HL-102926/HL/NHLBI NIH HHS/ -- HL-103010/HL/NHLBI NIH HHS/ -- England -- Nature. 2012 Aug 2;488(7409):96-9. doi: 10.1038/nature11283.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉deCODE genetics, Sturlugata 8, 101 Reykjavik, Iceland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22801501" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Aging/*genetics ; Alleles ; Alzheimer Disease/*genetics/pathology/physiopathology/prevention & control ; Amyloid Precursor Protein Secretases/metabolism ; Amyloid beta-Protein Precursor/chemistry/*genetics/*metabolism ; Aspartic Acid Endopeptidases/metabolism ; Cognition/physiology ; Cognition Disorders/*genetics/*physiopathology/prevention & control ; Genetic Predisposition to Disease ; HEK293 Cells ; Humans ; Mutation/*genetics ; Plaque, Amyloid/genetics/metabolism
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
    Digitale Medien
    Digitale Medien
    Diapause induction in the codling moth, Cydia pomonella: effect of prediapause temperatures (1992)
    Springer
    Entomologia experimentalis et applicata 62 (1992), S. 131-137 
    Details
    ISSN: 1570-7458
    Schlagwort(e): Cydia pomonella ; codling moth ; diapause induction ; critical photoperiod ; prediapause temperature
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Biologie
    Notizen: Abstract The effect of four prediapause temperatures (18, 22, 26 and 30°C) on the photoperiodic response of the codling moth, Cydia pomonella (L.), was studied under controlled conditions. The highest rates of diapause were recorded, for all day-lengths, at temperatures of 22 and 26°C while relatively lower rates of diapause were elicited at 18 and 30°C. The same trend was demonstrated by projecting the values of the critical photoperiod which induces 50% diapause (=CPhP50) over the prediapause temperature. The change in diapause incidence as a function of photoperiod, at all prediapause temperatures, exhibited a response characteristic of long-day insects, i.e. high rates of diapause at short days (12–13.5 h) and a decrease in diapause incidence at long days (14–15 h). The results for temperatures 22, 26 and 30°C support the view that lower prediapause temperatures enhance diapause induction, at a give photoperiod, while higher temperatures tend to avert or diminish the process. On the other hand, the low rates of diapause obtained at 18°C contradict this view. Nevertheless, high correlation was found between the laboratory evidence and field data, indicating the adaptability of the Israeli codling moth to subtropical climate.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00345484
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  • 7
    Digitale Medien
    Digitale Medien
    Diapause induction in the codling moth, Cydia pomonella: effect of larval diet (1992)
    Springer
    Entomologia experimentalis et applicata 62 (1992), S. 269-275 
    Details
    ISSN: 1570-7458
    Schlagwort(e): Cydia pomonella ; codling moth ; diapause induction ; photoperiod ; larval diet
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Biologie
    Notizen: Abstract The effect of larval diet on diapause induction in the Israeli strain of the codling moth, Cydia pomonella (L.), was studied in a field trial using intact apple fruits of two varieties: ‘Ana’ (early-ripening, in the end of June) and ‘Granny Smith’ (late-ripening, in October). Diapause incidence increased as fruit age (determined as days from fruit-set) progressed. These results corroborate former studies on other strains of the codling moth, where excised fruits were used. The combination of 80-day-old, fully ripe, ‘Ana’ fruit treatment with the longest days of the year, yielded 38% diapause. This result demonstrates that mature fruit (inducing diapause) cannot completely override the effect of long day (averting diapause), but does confirm that larval diet modifies the photoperiodic induction of diapause in the codling moth.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00353446
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