Distinct Genetic Risk Based on Association of MET in Families With Co-occurring Autism and Gastrointestinal Conditions
In addition to the core behavioral symptoms of autism spectrum disorder, many patients present with complex medical conditions including gastrointestinal dysfunction. A functional variant in the promoter of the gene encoding the MET receptor tyrosine kinase is associated with autism spectrum disorde...
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| Veröffentlicht in: | Pediatrics (Evanston) 2009-03, Vol.123 (3), p.1018-1024 |
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| creator | Campbell, Daniel B Buie, Timothy M Winter, Harland Bauman, Margaret Sutcliffe, James S Perrin, James M Levitt, Pat |
| description | In addition to the core behavioral symptoms of autism spectrum disorder, many patients present with complex medical conditions including gastrointestinal dysfunction. A functional variant in the promoter of the gene encoding the MET receptor tyrosine kinase is associated with autism spectrum disorder, and MET protein expression is decreased in the temporal cortex of subjects with autism spectrum disorder. MET is a pleiotropic receptor that functions in both brain development and gastrointestinal repair. On the basis of these functions, we hypothesized that association of the autism spectrum disorder-associated MET promoter variant may be enriched in a subset of individuals with co-occurring autism spectrum disorder and gastrointestinal conditions.
Subjects were 918 individuals from 214 Autism Genetics Resource Exchange families with a complete medical history including gastrointestinal condition report. Genotypes at the autism spectrum disorder-associated MET promoter variant rs1858830 were determined. Family-based association test and chi(2) analyses were used to determine the association of MET rs1858830 alleles with autism spectrum disorder and the presence of gastrointestinal conditions.
In the entire 214-family sample, the MET rs1858830 C allele was associated with both autism spectrum disorder and gastrointestinal conditions. Stratification by the presence of gastrointestinal conditions revealed that the MET C allele was associated with both autism spectrum disorder and gastrointestinal conditions in 118 families containing at least 1 child with co-occurring autism spectrum disorder and gastrointestinal conditions. In contrast, there was no association of the MET polymorphism with autism spectrum disorder in the 96 families lacking a child with co-occurring autism spectrum disorder and gastrointestinal conditions. chi(2) analyses of MET rs1858830 genotypes indicated over-representation of the C allele in individuals with co-occurring autism spectrum disorder and gastrointestinal conditions compared with non-autism spectrum disorder siblings, parents, and unrelated controls.
These results suggest that disrupted MET signaling may contribute to increased risk for autism spectrum disorder that includes familial gastrointestinal dysfunction. |
| doi_str_mv | 10.1542/peds.2008-0819 |
| format | Article |
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Subjects were 918 individuals from 214 Autism Genetics Resource Exchange families with a complete medical history including gastrointestinal condition report. Genotypes at the autism spectrum disorder-associated MET promoter variant rs1858830 were determined. Family-based association test and chi(2) analyses were used to determine the association of MET rs1858830 alleles with autism spectrum disorder and the presence of gastrointestinal conditions.
In the entire 214-family sample, the MET rs1858830 C allele was associated with both autism spectrum disorder and gastrointestinal conditions. Stratification by the presence of gastrointestinal conditions revealed that the MET C allele was associated with both autism spectrum disorder and gastrointestinal conditions in 118 families containing at least 1 child with co-occurring autism spectrum disorder and gastrointestinal conditions. In contrast, there was no association of the MET polymorphism with autism spectrum disorder in the 96 families lacking a child with co-occurring autism spectrum disorder and gastrointestinal conditions. chi(2) analyses of MET rs1858830 genotypes indicated over-representation of the C allele in individuals with co-occurring autism spectrum disorder and gastrointestinal conditions compared with non-autism spectrum disorder siblings, parents, and unrelated controls.
These results suggest that disrupted MET signaling may contribute to increased risk for autism spectrum disorder that includes familial gastrointestinal dysfunction.</description><identifier>ISSN: 0031-4005</identifier><identifier>EISSN: 1098-4275</identifier><identifier>DOI: 10.1542/peds.2008-0819</identifier><identifier>PMID: 19255034</identifier><identifier>CODEN: PEDIAU</identifier><language>eng</language><publisher>Elk Grove Village, IL: Am Acad Pediatrics</publisher><subject>Alleles ; Autism ; Autistic Disorder - genetics ; Biological and medical sciences ; Child ; Child clinical studies ; Comorbidity ; Developmental disorders ; Digestive system ; Female ; Gastrointestinal diseases ; Gastrointestinal Diseases - genetics ; Gene expression ; General aspects ; Genetic aspects ; Genetic Predisposition to Disease - genetics ; Genotype ; Genotype & phenotype ; Humans ; Infantile autism ; Kinases ; Linkage Disequilibrium ; Male ; Medical sciences ; Pediatrics ; Phenotype ; Polymorphism ; Promoter Regions, Genetic - genetics ; Proto-Oncogene Proteins - genetics ; Proto-Oncogene Proteins c-met ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; Receptors, Growth Factor - genetics ; Risk Factors ; Signal Transduction - genetics</subject><ispartof>Pediatrics (Evanston), 2009-03, Vol.123 (3), p.1018-1024</ispartof><rights>2009 INIST-CNRS</rights><rights>COPYRIGHT 2009 American Academy of Pediatrics</rights><rights>Copyright American Academy of Pediatrics Mar 2009</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c428t-e2671bd05a4344d726c97eca61c7e374ee889907644fd94156726389fa25a9c83</citedby><cites>FETCH-LOGICAL-c428t-e2671bd05a4344d726c97eca61c7e374ee889907644fd94156726389fa25a9c83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27929,27930</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21189785$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19255034$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Campbell, Daniel B</creatorcontrib><creatorcontrib>Buie, Timothy M</creatorcontrib><creatorcontrib>Winter, Harland</creatorcontrib><creatorcontrib>Bauman, Margaret</creatorcontrib><creatorcontrib>Sutcliffe, James S</creatorcontrib><creatorcontrib>Perrin, James M</creatorcontrib><creatorcontrib>Levitt, Pat</creatorcontrib><title>Distinct Genetic Risk Based on Association of MET in Families With Co-occurring Autism and Gastrointestinal Conditions</title><title>Pediatrics (Evanston)</title><addtitle>Pediatrics</addtitle><description>In addition to the core behavioral symptoms of autism spectrum disorder, many patients present with complex medical conditions including gastrointestinal dysfunction. A functional variant in the promoter of the gene encoding the MET receptor tyrosine kinase is associated with autism spectrum disorder, and MET protein expression is decreased in the temporal cortex of subjects with autism spectrum disorder. MET is a pleiotropic receptor that functions in both brain development and gastrointestinal repair. On the basis of these functions, we hypothesized that association of the autism spectrum disorder-associated MET promoter variant may be enriched in a subset of individuals with co-occurring autism spectrum disorder and gastrointestinal conditions.
Subjects were 918 individuals from 214 Autism Genetics Resource Exchange families with a complete medical history including gastrointestinal condition report. Genotypes at the autism spectrum disorder-associated MET promoter variant rs1858830 were determined. Family-based association test and chi(2) analyses were used to determine the association of MET rs1858830 alleles with autism spectrum disorder and the presence of gastrointestinal conditions.
In the entire 214-family sample, the MET rs1858830 C allele was associated with both autism spectrum disorder and gastrointestinal conditions. Stratification by the presence of gastrointestinal conditions revealed that the MET C allele was associated with both autism spectrum disorder and gastrointestinal conditions in 118 families containing at least 1 child with co-occurring autism spectrum disorder and gastrointestinal conditions. In contrast, there was no association of the MET polymorphism with autism spectrum disorder in the 96 families lacking a child with co-occurring autism spectrum disorder and gastrointestinal conditions. chi(2) analyses of MET rs1858830 genotypes indicated over-representation of the C allele in individuals with co-occurring autism spectrum disorder and gastrointestinal conditions compared with non-autism spectrum disorder siblings, parents, and unrelated controls.
These results suggest that disrupted MET signaling may contribute to increased risk for autism spectrum disorder that includes familial gastrointestinal dysfunction.</description><subject>Alleles</subject><subject>Autism</subject><subject>Autistic Disorder - genetics</subject><subject>Biological and medical sciences</subject><subject>Child</subject><subject>Child clinical studies</subject><subject>Comorbidity</subject><subject>Developmental disorders</subject><subject>Digestive system</subject><subject>Female</subject><subject>Gastrointestinal diseases</subject><subject>Gastrointestinal Diseases - genetics</subject><subject>Gene expression</subject><subject>General aspects</subject><subject>Genetic aspects</subject><subject>Genetic Predisposition to Disease - genetics</subject><subject>Genotype</subject><subject>Genotype & phenotype</subject><subject>Humans</subject><subject>Infantile autism</subject><subject>Kinases</subject><subject>Linkage Disequilibrium</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Pediatrics</subject><subject>Phenotype</subject><subject>Polymorphism</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Proto-Oncogene Proteins c-met</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. Psychiatry</subject><subject>Receptors, Growth Factor - genetics</subject><subject>Risk Factors</subject><subject>Signal Transduction - genetics</subject><issn>0031-4005</issn><issn>1098-4275</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkU1vEzEQhi0EoqFw5YgsJLhtanvttX0MoQ1IRZVQEUfL9XoTl42derx8_Hu8SgSIk-fweOadeRB6ScmSCs4uDr6HJSNENURR_QgtKNGq4UyKx2hBSEsbTog4Q88A7gkhXEj2FJ1RzYQgLV-g7-8DlBBdwRsffQkOfw7wDb-z4HucIl4BJBdsCbVOA_50eYtDxFd2H8bgAX8NZYfXqUnOTTmHuMWrqQTYYxt7vLFQcgqx-HmEHSsY-zC3gufoyWBH8C9O7zn6cnV5u_7QXN9sPq5X143jTJXGs07Su54Iy1vOe8k6p6V3tqNO-lZy75XSmsiO86HXnIquIq3Sg2XCaqfac_T22PeQ08NUc5h9AOfH0UafJjBdp2sHpiv4-j_wPk25hgbDmKo3ZFRWqDlCWzt6U6-W6m4_i0vj6Lfe1OTrG7OiuuuoqHYqvzzyLieA7AdzyGFv8y9DiZn1mVmfmfWZWV_98OqUYrrb-_4vfvJVgTcnwIKz45BtdAH-cIxSpaUSlbs4cruw3f0I2c-TqsYcHPxTUtaatoahqv0NXZCyCg</recordid><startdate>20090301</startdate><enddate>20090301</enddate><creator>Campbell, Daniel B</creator><creator>Buie, Timothy M</creator><creator>Winter, Harland</creator><creator>Bauman, Margaret</creator><creator>Sutcliffe, James S</creator><creator>Perrin, James M</creator><creator>Levitt, Pat</creator><general>Am Acad Pediatrics</general><general>American Academy of Pediatrics</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TS</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>NAPCQ</scope><scope>U9A</scope><scope>7X8</scope></search><sort><creationdate>20090301</creationdate><title>Distinct Genetic Risk Based on Association of MET in Families With Co-occurring Autism and Gastrointestinal Conditions</title><author>Campbell, Daniel B ; Buie, Timothy M ; Winter, Harland ; Bauman, Margaret ; Sutcliffe, James S ; Perrin, James M ; Levitt, Pat</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c428t-e2671bd05a4344d726c97eca61c7e374ee889907644fd94156726389fa25a9c83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Alleles</topic><topic>Autism</topic><topic>Autistic Disorder - genetics</topic><topic>Biological and medical sciences</topic><topic>Child</topic><topic>Child clinical studies</topic><topic>Comorbidity</topic><topic>Developmental disorders</topic><topic>Digestive system</topic><topic>Female</topic><topic>Gastrointestinal diseases</topic><topic>Gastrointestinal Diseases - genetics</topic><topic>Gene expression</topic><topic>General aspects</topic><topic>Genetic aspects</topic><topic>Genetic Predisposition to Disease - genetics</topic><topic>Genotype</topic><topic>Genotype & phenotype</topic><topic>Humans</topic><topic>Infantile autism</topic><topic>Kinases</topic><topic>Linkage Disequilibrium</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Pediatrics</topic><topic>Phenotype</topic><topic>Polymorphism</topic><topic>Promoter Regions, Genetic - genetics</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Proto-Oncogene Proteins c-met</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopathology. Psychiatry</topic><topic>Receptors, Growth Factor - genetics</topic><topic>Risk Factors</topic><topic>Signal Transduction - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Campbell, Daniel B</creatorcontrib><creatorcontrib>Buie, Timothy M</creatorcontrib><creatorcontrib>Winter, Harland</creatorcontrib><creatorcontrib>Bauman, Margaret</creatorcontrib><creatorcontrib>Sutcliffe, James S</creatorcontrib><creatorcontrib>Perrin, James M</creatorcontrib><creatorcontrib>Levitt, Pat</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Physical Education Index</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Pediatrics (Evanston)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Campbell, Daniel B</au><au>Buie, Timothy M</au><au>Winter, Harland</au><au>Bauman, Margaret</au><au>Sutcliffe, James S</au><au>Perrin, James M</au><au>Levitt, Pat</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Distinct Genetic Risk Based on Association of MET in Families With Co-occurring Autism and Gastrointestinal Conditions</atitle><jtitle>Pediatrics (Evanston)</jtitle><addtitle>Pediatrics</addtitle><date>2009-03-01</date><risdate>2009</risdate><volume>123</volume><issue>3</issue><spage>1018</spage><epage>1024</epage><pages>1018-1024</pages><issn>0031-4005</issn><eissn>1098-4275</eissn><coden>PEDIAU</coden><abstract>In addition to the core behavioral symptoms of autism spectrum disorder, many patients present with complex medical conditions including gastrointestinal dysfunction. A functional variant in the promoter of the gene encoding the MET receptor tyrosine kinase is associated with autism spectrum disorder, and MET protein expression is decreased in the temporal cortex of subjects with autism spectrum disorder. MET is a pleiotropic receptor that functions in both brain development and gastrointestinal repair. On the basis of these functions, we hypothesized that association of the autism spectrum disorder-associated MET promoter variant may be enriched in a subset of individuals with co-occurring autism spectrum disorder and gastrointestinal conditions.
Subjects were 918 individuals from 214 Autism Genetics Resource Exchange families with a complete medical history including gastrointestinal condition report. Genotypes at the autism spectrum disorder-associated MET promoter variant rs1858830 were determined. Family-based association test and chi(2) analyses were used to determine the association of MET rs1858830 alleles with autism spectrum disorder and the presence of gastrointestinal conditions.
In the entire 214-family sample, the MET rs1858830 C allele was associated with both autism spectrum disorder and gastrointestinal conditions. Stratification by the presence of gastrointestinal conditions revealed that the MET C allele was associated with both autism spectrum disorder and gastrointestinal conditions in 118 families containing at least 1 child with co-occurring autism spectrum disorder and gastrointestinal conditions. In contrast, there was no association of the MET polymorphism with autism spectrum disorder in the 96 families lacking a child with co-occurring autism spectrum disorder and gastrointestinal conditions. chi(2) analyses of MET rs1858830 genotypes indicated over-representation of the C allele in individuals with co-occurring autism spectrum disorder and gastrointestinal conditions compared with non-autism spectrum disorder siblings, parents, and unrelated controls.
These results suggest that disrupted MET signaling may contribute to increased risk for autism spectrum disorder that includes familial gastrointestinal dysfunction.</abstract><cop>Elk Grove Village, IL</cop><pub>Am Acad Pediatrics</pub><pmid>19255034</pmid><doi>10.1542/peds.2008-0819</doi><tpages>7</tpages></addata></record> |
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| subjects | Alleles Autism Autistic Disorder - genetics Biological and medical sciences Child Child clinical studies Comorbidity Developmental disorders Digestive system Female Gastrointestinal diseases Gastrointestinal Diseases - genetics Gene expression General aspects Genetic aspects Genetic Predisposition to Disease - genetics Genotype Genotype & phenotype Humans Infantile autism Kinases Linkage Disequilibrium Male Medical sciences Pediatrics Phenotype Polymorphism Promoter Regions, Genetic - genetics Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins c-met Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Receptors, Growth Factor - genetics Risk Factors Signal Transduction - genetics |
| title | Distinct Genetic Risk Based on Association of MET in Families With Co-occurring Autism and Gastrointestinal Conditions |
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