Database : MEDLINE
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[PMID]: 29506490
[Au] Autor:López M; García-Oguiza A; Armstrong J; García-Cobaleda I; García-Miñaur S; Santos-Simarro F; Seidel V; Domínguez-Garrido E
[Ad] Address:Molecular Diagnostic Unit, Fundación Rioja Salud, Logroño, La Rioja, Spain.
[Ti] Title:Rubinstein-Taybi 2 associated to novel EP300 mutations: deepening the clinical and genetic spectrum.
[So] Source:BMC Med Genet;19(1):36, 2018 Mar 05.
[Is] ISSN:1471-2350
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Rubinstein-Taybi syndrome (RSTS) is a rare autosomal dominant neurodevelopmental disorder characterized by broad thumbs and halluces. RSTS is caused by mutations in CREBBP and in EP300 genes in 50-60% and 8%, respectively. Up to now, 76 RSTS-EP300 patients have been described. We present the clinical and molecular characterization of a cohort of RSTS patients carrying EP300 mutations. METHODS: Patients were selected from a cohort of 72 individuals suspected of RSTS after being negative in CREBBP study. MLPA and panel-based NGS EP300 were performed. RESULTS: Eight patients were found to carry EP300 mutations. Phenotypic characteristics included: intellectual disability (generally mild), postnatal growth retardation, infant feeding problems, psychomotor and language delay and typical facial dysmorphisms (microcephaly, downslanting palpebral fissures, columella below the alae nasi, and prominent nose). Broad thumbs and/or halluces were common, but angulated thumbs were only found in two patients. We identified across the gene novel mutations, including large deletion, frameshift mutations, nonsense, missense and splicing alterations, confirming de novo origin in all but one (the mother, possibly underdiagnosed, has short and broad thumbs and had learning difficulties). CONCLUSIONS: The clinical evaluation of our patients corroborates that clinical features in EP300 are less marked than in CREBBP patients although it is difficult to establish a genotype-phenotype correlation although. It is remarkable that these findings are observed in a RSTS-diagnosed cohort; some patients harbouring EP300 mutations could present a different phenotype. Broadening the knowledge about EP300-RSTS phenotype may contribute to improve the management of patients and the counselling to the families.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1186/s12881-018-0548-2

  2 / 8463 MEDLINE  
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[PMID]: 29386359
[Au] Autor:Platt DJ; Smith AM; Arora N; Diamond MS; Coyne CB; Miner JJ
[Ad] Address:Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, MO 63110, USA.
[Ti] Title:Zika virus-related neurotropic flaviviruses infect human placental explants and cause fetal demise in mice.
[So] Source:Sci Transl Med;10(426), 2018 Jan 31.
[Is] ISSN:1946-6242
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Although Zika virus (ZIKV) infection in pregnant women can cause placental damage, intrauterine growth restriction, microcephaly, and fetal demise, these disease manifestations only became apparent in the context of a large epidemic in the Americas. We hypothesized that ZIKV is not unique among arboviruses in its ability to cause congenital infection. To evaluate this, we tested the capacity of four emerging arboviruses [West Nile virus (WNV), Powassan virus (POWV), chikungunya virus (CHIKV), and Mayaro virus (MAYV)] from related (flavivirus) and unrelated (alphavirus) genera to infect the placenta and fetus in immunocompetent, wild-type mice. Although all four viruses caused placental infection, only infection with the neurotropic flaviviruses (WNV and POWV) resulted in fetal demise. WNV and POWV also replicated efficiently in second-trimester human maternal (decidua) and fetal (chorionic villi and fetal membrane) explants, whereas CHIKV and MAYV replicated less efficiently. In mice, RNA in situ hybridization and histopathological analysis revealed that WNV infected the placenta and fetal central nervous system, causing injury to the developing brain. In comparison, CHIKV and MAYV did not cause substantive placental or fetal damage despite evidence of vertical transmission. On the basis of the susceptibility of human maternal and fetal tissue explants and pathogenesis experiments in immunocompetent mice, other emerging neurotropic flaviviruses may share with ZIKV the capacity for transplacental transmission, as well as subsequent infection and injury to the developing fetus.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review

  3 / 8463 MEDLINE  
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[PMID]: 29365063
[Au] Autor:Fry AE; Fawcett KA; Zelnik N; Yuan H; Thompson BAN; Shemer-Meiri L; Cushion TD; Mugalaasi H; Sims D; Stoodley N; Chung SK; Rees MI; Patel CV; Brueton LA; Layet V; Giuliano F; Kerr MP; Banne E; Meiner V; Lerman-Sagie T; Helbig KL; Kofman LH; Knight KM; Chen W; Kannan V; Hu C; Kusumoto H; Zhang J; Swanger SA; Shaulsky GH; Mirzaa GM; Muir AM; Mefford HC; Dobyns WB; Mackenzie AB; Mullins JGL; Lemke JR; Bahi-Buisson N; Traynelis SF; Iago HF; Pilz DT
[Ad] Address:Institute of Medical Genetics, University Hospital of Wales, Cardiff CF14 4XW, UK.
[Ti] Title:De novo mutations in GRIN1 cause extensive bilateral polymicrogyria.
[So] Source:Brain;, 2018 Jan 22.
[Is] ISSN:1460-2156
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Polymicrogyria is a malformation of cortical development. The aetiology of polymicrogyria remains poorly understood. Using whole-exome sequencing we found de novo heterozygous missense GRIN1 mutations in 2 of 57 parent-offspring trios with polymicrogyria. We found nine further de novo missense GRIN1 mutations in additional cortical malformation patients. Shared features in the patients were extensive bilateral polymicrogyria associated with severe developmental delay, postnatal microcephaly, cortical visual impairment and intractable epilepsy. GRIN1 encodes GluN1, the essential subunit of the N-methyl-d-aspartate receptor. The polymicrogyria-associated GRIN1 mutations tended to cluster in the S2 region (part of the ligand-binding domain of GluN1) or the adjacent M3 helix. These regions are rarely mutated in the normal population or in GRIN1 patients without polymicrogyria. Using two-electrode and whole-cell voltage-clamp analysis, we showed that the polymicrogyria-associated GRIN1 mutations significantly alter the in vitro activity of the receptor. Three of the mutations increased agonist potency while one reduced proton inhibition of the receptor. These results are striking because previous GRIN1 mutations have generally caused loss of function, and because N-methyl-d-aspartate receptor agonists have been used for many years to generate animal models of polymicrogyria. Overall, our results expand the phenotypic spectrum associated with GRIN1 mutations and highlight the important role of N-methyl-d-aspartate receptor signalling in the pathogenesis of polymicrogyria.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1093/brain/awx358

  4 / 8463 MEDLINE  
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[PMID]: 29501613
[Au] Autor:Tassano E; Uccella S; Giacomini T; Severino M; Siri L; Gherzi M; Celle ME; Porta S; Gimelli G; Ronchetto P
[Ad] Address:Laboratory of Cytogenetics, Istituto Giannina Gaslini, Genoa, Italy. Electronic address: eli.tassano@gmail.com.
[Ti] Title:3q29 microduplication syndrome: Description of two new cases and delineation of the minimal critical region.
[So] Source:Eur J Med Genet;, 2018 Mar 01.
[Is] ISSN:1878-0849
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Heterogeneous clinical and neuropsychological features, such as intellectual disability, developmental and language delay, hypotonia, and, to a lesser extent, microcephaly that is present in about the half of the reported patients, characterize the 3q29 microduplication syndrome with usually a milder phenotype compared with the corresponding 3q29 microdeletion syndrome. The duplications described so far range from 2.3 Mb to 1.6 Mb, spanning from TFRC to BDH1 genes. Here we report on two patients with overlapping interstitial duplications of the 3q29 region differing in size. Patient 1 harboured a common-seized 3q29 microduplication spanning ∼1.6 Mb, while patient 2 carried a very small 3q29 microduplication of 448.8 Kb encompassing only two genes, DLG1 and BDH1. Both patients presented clinical characteristics similar to those reported in the literature in 3q29 microduplication syndrome. Interestingly, heterotopic gray matter nodules were found along the right lateral ventricle on brain MRI in patient 1, thus expanding the neuroradiological phenotype in 3q29 microduplication syndrome, while patient 2 allowed us to define with more precision the smallest region of overlap (SRO). Gene content analysis of the duplicated region suggests that gain-of-dosage of DLG1 and BDH1 may be a good candidate for the main clinical features of this syndrome.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 8463 MEDLINE  
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[PMID]: 29343805
[Au] Autor:Makrythanasis P; Maroofian R; Stray-Pedersen A; Musaev D; Zaki MS; Mahmoud IG; Selim L; Elbadawy A; Jhangiani SN; Coban Akdemir ZH; Gambin T; Sorte HS; Heiberg A; McEvoy-Venneri J; James KN; Stanley V; Belandres D; Guipponi M; Santoni FA; Ahangari N; Tara F; Doosti M; Iwaszkiewicz J; Zoete V; Backe PH; Hamamy H; Gleeson JG; Lupski JR; Karimiani EG; Antonarakis SE
[Ad] Address:Department of Genetic Medicine and Development, University of Geneva, Geneva, Switzerland.
[Ti] Title:Biallelic variants in KIF14 cause intellectual disability with microcephaly.
[So] Source:Eur J Hum Genet;26(3):330-339, 2018 Mar.
[Is] ISSN:1476-5438
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Kinesin proteins are critical for various cellular functions such as intracellular transport and cell division, and many members of the family have been linked to monogenic disorders and cancer. We report eight individuals with intellectual disability and microcephaly from four unrelated families with parental consanguinity. In the affected individuals of each family, homozygosity for likely pathogenic variants in KIF14 were detected; two loss-of-function (p.Asn83Ilefs*3 and p.Ser1478fs), and two missense substitutions (p.Ser841Phe and p.Gly459Arg). KIF14 is a mitotic motor protein that is required for spindle localization of the mitotic citron rho-interacting kinase, CIT, also mutated in microcephaly. Our results demonstrate the involvement of KIF14 in development and reveal a wide phenotypic variability ranging from fetal lethality to moderate developmental delay and microcephaly.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review
[do] DOI:10.1038/s41431-017-0088-9

  6 / 8463 MEDLINE  
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[PMID]: 29030319
[Au] Autor:Dutta S; Celestine MJ; Khanal S; Huddleston A; Simms C; Arca JF; Mitra A; Heller L; Kraj PJ; Ledizet M; Anderson JF; Neelakanta G; Holder AA; Sultana H
[Ad] Address:Department of Biological Sciences, Old Dominion University, Norfolk, VA, USA.
[Ti] Title:Coordination of different ligands to copper(II) and cobalt(III) metal centers enhances Zika virus and dengue virus loads in both arthropod cells and human keratinocytes.
[So] Source:Biochim Biophys Acta;1862(1):40-50, 2018 01.
[Is] ISSN:0006-3002
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Trace elements such as copper and cobalt have been associated with virus-host interactions. However, studies to show the effect of conjugation of copper(II) or cobalt(III) metal centers to thiosemicarbazone ligand(s) derived from either food additives or mosquito repellent such as 2-acetylethiazole or citral, respectively, on Zika virus (ZIKV) or dengue virus (serotype 2; DENV2) infections have not been explored. In this study, we show that four compounds comprising of thiosemicarbazone ligand derived from 2-acetylethiazole viz., (E)-N-ethyl-2-[1-(thiazol-2-yl)ethylidene]hydrazinecarbothioamide (acetylethTSC) (compound 1), a copper(II) complex with acetylethTSC as a ligand (compound 2), a thiosemicarbazone ligand-derived from citral (compound 3) and a cobalt(III) complex with a citral-thiosemicarbazone ligand (compound 4) increased DENV2 and ZIKV replication in both mosquito C6/36 cells and human keratinocytes (HaCaT cells). Treatment of both cell lines with compounds 2 or 4 showed increased dengue viral titers at all three tested doses. Enhanced dengue viral plaque formation was also noted at the tested dose of 100µM, suggesting higher production of infectious viral particles. Treatment with the compounds 2 or 4 enhanced ZIKV and DENV2 RNA levels in HeLa cell line and primary cultures of mouse bone marrow derived dendritic cells. Also, pre- or post treatments with conjugated compounds 2 or 4 showed higher loads of ZIKV or DENV2 envelope (E) protein in HaCaT cells. No changes in loads of E-protein were found in ZIKV-infected C6/36 cells, when compounds were treated after infection. In addition, we tested bis(1,10-phenanthroline)copper(II) chloride ([Cu(phen) ]Cl , (compound 5) and tris(1,10-phenanthroline)cobalt(III) chloride ([Co(phen) ]Cl , (compound 6) that also showed enhanced DENV2 loads. Also, we found that copper(II) chloride dehydrate (CuCl ·2H O) or cobalt(II) chloride hexahydrate (CoCl ·6H O) alone had no effects as "free" cations. Taken together, these findings suggest that use of Cu(II) or Co(III) conjugation to organic compounds, in insect repellents and/or food additives could enhance DENV2/ZIKV loads in human cells and perhaps induce pathogenesis in infected individuals or individuals pre-exposed to such conjugated complexes. IMPORTANCE: Mosquito-borne diseases are of great concern to the mankind. Use of chemicals/repellents against mosquito bites and transmission of microbes has been the topic of interest for many years. Here, we show that thiosemicarbazone ligand(s) derived from 2-acetylethiazole or citral or 1,10-phenanthroline upon conjugation with copper(II) or cobalt(III) metal centers enhances dengue virus (serotype 2; DENV2) and/or Zika virus (ZIKV) infections in mosquito, mouse and human cells. Enhanced ZIKV/DENV2 capsid mRNA or envelope protein loads were evident in mosquito cells and human keratinocytes, when treated with compounds before/after infections. Also, treatment with copper(II) or cobalt(III) conjugated compounds increased viral titers and number of plaque formations. These studies suggest that conjugation of compounds in repellents/essential oils/natural products/food additives with copper(II) or cobalt(III) metal centers may not be safe, especially in tropical and subtropical places, where several dengue infection cases and deaths are reported annually or in places with increased ZIKV caused microcephaly.
[Mh] MeSH terms primary: Cobalt
Coordination Complexes
Copper
Dengue Virus/metabolism
Keratinocytes/virology
Viral Load/drug effects
Zika Virus/metabolism
[Mh] MeSH terms secundary: Animals
Cercopithecus aethiops
Cobalt/chemistry
Cobalt/pharmacology
Coordination Complexes/chemistry
Coordination Complexes/pharmacology
Copper/chemistry
Copper/pharmacology
Culicidae
HeLa Cells
Humans
Keratinocytes/metabolism
Keratinocytes/pathology
Vero Cells
Viral Envelope Proteins
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Name of substance:0 (Coordination Complexes); 0 (Viral Envelope Proteins); 3G0H8C9362 (Cobalt); 789U1901C5 (Copper)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:171015
[St] Status:MEDLINE

  7 / 8463 MEDLINE  
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[PMID]: 29518772
[Au] Autor:Çakmakli S; Çankaya T; Gürsoy S; Koç A; Kirbiyik Ö; Kiliçarslan ÖA; Özer E; Erçal D; Bozkaya ÖG
[Ad] Address:Department of Medical Genetics, Faculty of Medicine, Dokuz Eylul University, Izmir, Turkey.
[Ti] Title:Two Cases with Ring Chromosome 13 at either End of the Phenotypic Spectrum.
[So] Source:Cytogenet Genome Res;, 2018 Mar 09.
[Is] ISSN:1424-859X
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:Ring chromosome 13 is a rare genetic condition with an incidence of 1/58,000 in live births. Major clinical features of patients with ring chromosome 13 include growth and developmental retardation, microcephaly, facial dysmorphism, ambiguous genitalia, anal atresia, eye malformations, retinoblastoma, and hand, foot, and toe abnormalities. The severity of the phenotype depends on the amount of genetic material lost during ring chromosome formation. Here, we report 2 cases with ring chromosome 13 at either end of the phenotypic spectrum.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1159/000486775

  8 / 8463 MEDLINE  
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[PMID]: 29518228
[Au] Autor:He Z; Chen J; An S; Dong X; Yu J; Zhang S; Wu Y; Li G; Zhang Y; Wu J; Zhu X; Li M
[Ad] Address:School of Public Health, Sun Yat-sen University, Guangzhou, China.
[Ti] Title:The NLRP3 inflammasome activation mediates Zika virus associated inflammation.
[So] Source:J Infect Dis;, 2018 Mar 06.
[Is] ISSN:1537-6613
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Zika virus (ZIKV) is a mosquito-borne virus that has been identified as a cause of several severe disease manifestations, including congenital microcephaly and Guillain-Barré syndrome, meningoencephalitis and myelitis. Previous studies showed that ZIKV-infected patients exhibited elevated plasma levels of interleukin-1ß (IL-1ß), indicating that ZIKV may activate inflammasomes. However, the molecular basis for its viral pathogenesis remains poorly understood. In this current study, we found that ZIKV infection caused severe inflammatory pathological changes and promoted IL-1ß production in vitro as well as in vivo. We here demonstrate that the maturation and secretion of IL-1ß during ZIKV infection was mediated by NLRP3 inflammasome activation, and that ZIKV nonstructural protein 5 (NS5) facilitated the assembly of the NLRP3 inflammasome complex, leading to IL-1ß activation through interacting with NLRP3 and inducing reactive oxygen species (ROS) production. Collectively, our data identify NLRP3 inflammasome-derived IL-1ß production as a critical feature of the inflammation during ZIKV infection. These findings offer new insights into inflammasome-mediated diseases and may provide new therapeutic options for ZIKV-associated diseases.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1093/infdis/jiy129

  9 / 8463 MEDLINE  
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[PMID]: 29518067
[Au] Autor:Hall V; Walker WL; Lindsey NP; Lehman JA; Kolsin J; Landry K; Rabe IB; Hills SL; Fischer M; Staples JE; Gould CV; Martin SW
[Ti] Title:Update: Noncongenital Zika Virus Disease Cases - 50 U.S. States and the District of Columbia, 2016.
[So] Source:MMWR Morb Mortal Wkly Rep;67(9):265-269, 2018 Mar 09.
[Is] ISSN:1545-861X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Zika virus is a flavivirus primarily transmitted to humans by Aedes aegypti mosquitoes (1). Zika virus infections also have been documented through intrauterine transmission resulting in congenital infection; intrapartum transmission from a viremic mother to her newborn; sexual transmission; blood transfusion; and laboratory exposure (1-3). Most Zika virus infections are asymptomatic or result in mild clinical illness, characterized by acute onset of fever, maculopapular rash, arthralgia, or nonpurulent conjunctivitis; Guillain-Barré syndrome, meningoencephalitis, and severe thrombocytopenia rarely have been associated with Zika virus infection (1). However, congenital Zika virus infection can result in fetal loss, microcephaly, and other birth defects (1,2). In 2016, a total of 5,168 noncongenital Zika virus disease cases were reported from U.S. states and the District of Columbia. Most cases (4,897, 95%) were in travelers returning from Zika virus-affected areas. A total of 224 (4%) cases were acquired through presumed local mosquitoborne transmission, and 47 (1%) were acquired by other routes. It is important that providers in the United States continue to test symptomatic patients who live in or recently traveled to areas with ongoing Zika virus transmission or had unprotected sex with someone who lives in or traveled to those areas. All pregnant women and their partners should take measures to prevent Zika virus infection during pregnancy. A list of affected areas and specific recommendations on how to prevent Zika virus infection during pregnancy are available at https://www.cdc.gov/pregnancy/zika/protect-yourself.html.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Process
[do] DOI:10.15585/mmwr.mm6709a1

  10 / 8463 MEDLINE  
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[PMID]: 29504900
[Au] Autor:Marakhonov AV; Konovalov FA; Makaov AK; Vasilyeva TA; Kadyshev VV; Galkina VA; Dadali EL; Kutsev SI; Zinchenko RA
[Ad] Address:Research Centre for Medical Genetics, Moscow, Russia. marakhonov@generesearch.ru.
[Ti] Title:Primary microcephaly case from the Karachay-Cherkess Republic poses an additional support for microcephaly and Seckel syndrome spectrum disorders.
[So] Source:BMC Med Genomics;11(Suppl 1):8, 2018 Feb 13.
[Is] ISSN:1755-8794
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Primary microcephaly represents an example of clinically and genetically heterogeneous condition. Here we describe a case of primary microcephaly from the Karachay-Cherkess Republic, which was initially diagnosed with Seckel syndrome. CASE PRESENTATION: Clinical exome sequencing of the proband revealed a novel homozygous single nucleotide deletion in ASPM gene, c.1386delC, resulting in preterm termination codon. Population screening reveals allele frequency to be less than 0.005. Mutations in this gene were not previously associated with Seckel syndrome. CONCLUSIONS: Our case represents an additional support for the clinical continuum between Seckel Syndrome and primary microcephaly.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1186/s12920-018-0326-1


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