Database : MEDLINE
Search on : digeorge and syndrome [Words]
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[PMID]: 29520614
[Au] Autor:Mannarelli D; Pauletti C; Accinni T; Carlone L; Frascarelli M; Lattanzi GM; Currà A; Fattapposta F
[Ad] Address:Department of Neurology and Psychiatry, Sapienza University of Rome, Viale dell'Università 30, 00185, Rome, Italy. daniela.mannarelli@uniroma1.it.
[Ti] Title:Attentional functioning in individuals with 22q11 deletion syndrome: insight from ERPs.
[So] Source:J Neural Transm (Vienna);, 2018 Mar 08.
[Is] ISSN:1435-1463
[Cp] Country of publication:Austria
[La] Language:eng
[Ab] Abstract:The 22q11 deletion syndrome (22q11DS), or DiGeorge syndrome (DG), is one of the most common genetic deletion syndromes. DG also carries a high risk for psychiatric disorders, with learning disabilities frequently being reported. Impairments in specific cognitive domains, such as executive functioning and attention, have also been described. The aim of this study was to investigate attentional functioning in a group of subjects with DG using ERPs, and in particular the P300 and CNV components. We studied ten patients with DG and ten healthy subjects that performed a P300 Novelty task and a CNV motor task. P3b amplitude was significantly lower in patients than in controls, while P3b latency was comparable in patients and controls. The P3a parameters were similar in both groups. All CNV amplitudes were significantly lower in DG patients than in controls. DG patients displayed slower reaction times in the CNV motor task than healthy subjects. These results point to a cognitive dysfunction related above all to executive attentional processing in DG patients. In particular, a specific difficulty emerged in selective attention and in the ability to orient and to sustain the anticipatory attention required for an executive motor response.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1007/s00702-018-1873-5

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[PMID]: 29520463
[Au] Autor:Mercer-Rosa L; Elci OU; Pinto NM; Tanel RE; Goldmuntz E
[Ad] Address:Division of Cardiology, Department of Pediatrics, The Children's Hospital of Philadelphia and Perelman School of Medicine at the University of Pennsylvania, 34th and Civic Center Blvd, Suite 8NW35, Philadelphia, PA, 19104, USA. mercerrosal@email.chop.edu.
[Ti] Title:22q11.2 Deletion Status and Perioperative Outcomes for Tetralogy of Fallot with Pulmonary Atresia and Multiple Aortopulmonary Collateral Vessels.
[So] Source:Pediatr Cardiol;, 2018 Mar 08.
[Is] ISSN:1432-1971
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Deletion of 22q11.2 (del22q11) is associated with adverse outcomes in patients with tetralogy of Fallot (TOF). We sought to investigate its contribution to perioperative outcome in patients with a severe form of TOF characterized by pulmonary atresia (PA) or severe pulmonary stenosis (PS) and major aortopulmonary collateral arteries (MAPCAS). We conducted a retrospective review of patients with TOF/MAPCAS who underwent staged surgical reconstruction between 1995 and 2006. Groups were compared according to 22q11.2 deletion status using t-tests or the Wilcoxon Rank sum test. We included 26 subjects, 24 of whom survived the initial operation. Of those, 21 subjects had known deletion status and constitute the group for this analysis [15 with no deletion present (ND) and 6 del22q11 subjects]. There was no difference with respect to occurrence of palliative procedure prior to initial operation, or to timing of closure of the ventricular septal defect (VSD). Other than higher prevalence of prematurity (50%) in the del22q11 group versus no prematurity in the ND, the groups were comparable in terms of pre-operative characteristics. The intra- and post-operative course outcomes (length of cardiopulmonary bypass, use of vasopressors, duration of intensive care and length of hospital stay, tube-feeding) were also comparable. Although the del22q11 had longer mechanical ventilation than the ND, this difference was not significant [68 h (range 4-251) vs. 45 h (range 3-1005), p = 0.81]. In this detailed comparison of a small patient cohort, 22q11.2 deletion syndrome was not associated with adverse perioperative outcomes in patients with TOF, PA, and MAPCAS when compared to those without 22q11.2 deletion syndrome. These results are relevant to prenatal and neonatal pre-operative counseling and planning.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1007/s00246-018-1840-9

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[PMID]: 29465581
[Au] Autor:Shi H; Wang Z
[Ad] Address:Key Laboratory of Thrombosis and Hemostasis of Ministry of Health, Jiangsu Institute of Hematology, The First Affiliated Hospital of Soochow University.
[Ti] Title:Atypical microdeletion in 22q11 deletion syndrome reveals new candidate causative genes: A case report and literature review.
[So] Source:Medicine (Baltimore);97(8):e9936, 2018 Feb.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:RATIONALE: 22q11 deletion syndrome, the most common chromosomal microdeletion disease, is caused by megabase-sized deletions on chromosome 22q11.2. It is characterized by a wide spectrum of congenital anomalies in velopharyngeal and facial, cardiac, genitourinary, vertebroskeletal, respiratory, digestive, and central nervous systems. Phenotype-genotype studies have revealed several causative genes that regulate the development of the third and fourth pharyngeal arches in human. However, the exact pathogenesis of this syndrome remains unknown. Herein, we report a case of 22q11 deletion syndrome with an atypical microdeletion of 125 kb. PATIENT CONCERNS: A 15-year-old Chinese girl presented with symptoms of facial dysmorphia, cardiac defects, velopharyngeal insufficiency, splenomegaly, immunodeficiency, and thrombocytopenia. DIAGNOSES: Microarray analysis revealed a 22q11.23 deletion of 125 kb (chromosome 22: 24276973-24402263), suggesting the diagnosis of 22q11 deletion syndrome. The haploinsufficient genes included GSTT2B, GSTT2, DDTL, DDT, GSTTP1, LOC391322, GSTT1, and GSTTP2. INTERVENTIONS: The patient was administrated glucocorticoids and calcium supplements. OUTCOMES: No epistaxis or petechiae episode occurred during the follow-up; her platelet count ranged between 60 × 10 and 80 × 10/L. LESSONS: Although none of the previous reported causative genes were affected in the patient, her clinical manifestations were typical of 22q11 deletion syndrome, apart from her progressive splenomegaly. This case indicated 8 new candidate pathogenic genes for 22q11 deletion syndrome. Given that the loss of these genes was sufficient to induce 22q11DS defects, whether these genes directly influence the pathogenesis of 22q11DS or through interactions with known hotspot mutations is worthy of research.
[Mh] MeSH terms primary: DiGeorge Syndrome/genetics
[Mh] MeSH terms secundary: Adolescent
Chromosome Deletion
Chromosomes, Human, Pair 22/genetics
Female
Humans
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180302
[Lr] Last revision date:180302
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:180222
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009936

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[PMID]: 29281626
[Au] Autor:Lin JR; Zhang Q; Cai Y; Morrow BE; Zhang ZD
[Ad] Address:Department of Genetics, Albert Einstein College of Medicine, Bronx, New York, United States of America.
[Ti] Title:Integrated rare variant-based risk gene prioritization in disease case-control sequencing studies.
[So] Source:PLoS Genet;13(12):e1007142, 2017 12.
[Is] ISSN:1553-7404
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Rare variants of major effect play an important role in human complex diseases and can be discovered by sequencing-based genome-wide association studies. Here, we introduce an integrated approach that combines the rare variant association test with gene network and phenotype information to identify risk genes implicated by rare variants for human complex diseases. Our data integration method follows a 'discovery-driven' strategy without relying on prior knowledge about the disease and thus maintains the unbiased character of genome-wide association studies. Simulations reveal that our method can outperform a widely-used rare variant association test method by 2 to 3 times. In a case study of a small disease cohort, we uncovered putative risk genes and the corresponding rare variants that may act as genetic modifiers of congenital heart disease in 22q11.2 deletion syndrome patients. These variants were missed by a conventional approach that relied on the rare variant association test alone.
[Mh] MeSH terms primary: Genetic Predisposition to Disease
Genetic Variation
Genome-Wide Association Study/methods
Sequence Analysis, DNA/methods
[Mh] MeSH terms secundary: Case-Control Studies
Computer Simulation
Data Interpretation, Statistical
DiGeorge Syndrome/genetics
Humans
Phenotype
Risk Factors
Sequence Analysis, DNA/statistics & numerical data
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1802
[Cu] Class update date: 180227
[Lr] Last revision date:180227
[Js] Journal subset:IM
[Da] Date of entry for processing:171228
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1007142

  5 / 2441 MEDLINE  
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[PMID]: 29455205
[Au] Autor:Bahamat AA; Assidi M; Lary SA; Almughamsi MM; Peer Zada AA; Chaudhary A; Abuzenadah A; Abu-Elmagd M; Al-Qahtani M
[Ad] Address:Center of Excellence in Genomic Medicine Research, King Abdulaziz University, Jeddah, Kingdom of Saudi Arabia.
[Ti] Title:Use of Array Comparative Genomic Hybridization for the Diagnosis of DiGeorge Syndrome in Saudi Arabian Population.
[So] Source:Cytogenet Genome Res;, 2018 Feb 17.
[Is] ISSN:1424-859X
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:DiGeorge syndrome (DGS) is a genetic disorder known as a clinically variable syndrome with over 180 associated phenotypic features. It is caused by a common human deletion in the 22q11.2 chromosomal region and currently is affecting approximately 1 in 4,000 individuals. Despite the prevalence of inherited diseases mainly due to consanguineous marriages, the current diagnosis of DGS in Saudi Arabia is mainly based on conventional high-resolution chromosome banding (karyotyping) and FISH techniques. However, advanced genome-wide studies for detecting microdeletions or duplications across the whole genome are needed. The aim of this study is to implement and use aCGH technology in clinical diagnosis of the 22q11.2 deletion in Saudi Arabian DGS patients and to confirm its effectiveness compared to conventional FISH and chromosome banding techniques. Thirty suspected DGS patients were assessed for chromosome 22q11.2 deletion using high-resolution G-banding, FISH, and aCGH. The aCGH results were compared with those obtained by the other 2 cytogenetic techniques. G-banding detected the 22q11.2 deletion in only 1 patient in the cohort. Moreover, it detected additional chromosomal aberrations in 3 other patients. Using FISH, allowed for detection of the 22q11.2 deletion in 2 out of 30 patients. Interestingly, the use of aCGH technique showed deletions in the chromosome 22q11.2 region in 8 patients, indicating a 4-fold increase in diagnostic detection capacity compared to FISH. Our results show the effectiveness of aCGH to overcome the limitations of FISH and G-banding in terms of diagnostic yield and allow whole genome screening and detection of a larger number of deletions and/or duplications in Saudi Arabian DGS patients. Except for balanced translocations and inversions, our data demonstrate the suitability of aCGH in the diagnostics of submicroscopic deletion syndromes such as DGS and most chromosomal aberrations or complex abnormalities scattered throughout the human genome. Our results recommend the implementation of aCGH in clinical genomic testing in Saudi Arabia to improve the diagnostic capabilities of health services while maintaining the use of conventional cytogenetic techniques for subsequent validation or for specific and known aberrations whenever required.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180218
[Lr] Last revision date:180218
[St] Status:Publisher
[do] DOI:10.1159/000487094

  6 / 2441 MEDLINE  
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[PMID]: 29449075
[Au] Autor:Broda CR; Cabrera AG; Rossano JW; Jefferies JL; Towbin JA; Chin C; Shamszad P
[Ad] Address:Department of Pediatrics, Lillie Frank Abercrombie Section of Pediatric and Congenital Cardiology, Baylor College of Medicine/Texas Children's Hospital, Houston, Texas, USA.
[Ti] Title:Cardiac transplantation in children with Down syndrome, Turner syndrome, and other chromosomal anomalies: A multi-institutional outcomes analysis.
[So] Source:J Heart Lung Transplant;, 2018 Jan 31.
[Is] ISSN:1557-3117
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: The purpose of this study was to describe the prevalence, characteristics, and outcomes in pediatric patients with chromosomal anomalies (CA) undergoing orthotopic heart transplantation (OHT). METHODS: A query of the database of the Pediatric Health Information System, a large administrative and billing database of 43 tertiary children's hospitals, was performed for the Years 2004 to 2016. Pediatric patients who received OHT were analyzed based on presence and type of CA. CA analyzed included: Down syndrome (DS); Turner syndrome (TS)/gonadal dysgenesis; conditions due to anomaly of unspecified chromosome; autosomal deletion; microdeletion; and autosomal anomaly. Healthcare-associated charge analysis during hospitalization for OHT and survival after OHT were assessed. RESULTS: A total of 3,080 hospitalizations were identified in which OHTs were performed. Of these OHTs, 64 (2.1%) were performed in patients with a concomitant diagnosis of CA. The presence of CA did not confer a higher risk of in-hospital mortality after OHT (odds ratio 1.2 [0.5 to 3.2], p = 0.651). Differences in in-hospital mortality between different types of CA, including DS and TS, did not reach statistical significance. Survival at 1-year post-OHT was similar in patients with CA compared to those without CA (p = 0.248). Length of stay after OHT was longer in patients with CA: 76 (interquartile range [IQR] 76 to 142 days vs 49 [IQR 21 to 98] days) (p < 0.001), respectively. Overall adjusted hospital charges were significantly higher in the CA group: $1.2 million (IQR $740,000 to $2.2 million) vs $792,000 (IQR $425,000 to $1.5 million] (p < 0.001), respectively. CONCLUSIONS: CA is present in ~2% of pediatric patients undergoing OHT. The presence of CA was not associated with increased mortality in pediatric patients undergoing OHT. Limitations of this study include the small number of patients available for analysis and a likely highly selective cohort of patients with CA.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180216
[Lr] Last revision date:180216
[St] Status:Publisher

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[PMID]: 29334651
[Au] Autor:Wang J; Zhang Y; Guo Z; Li R; Xue X; Sun Z; Niu R
[Ad] Address:Shanxi Key Laboratory of Ecological Animal Science and Environmental Veterinary Medicine, College of Animal Science and Veterinary Medicine, Shanxi Agricultural University, Taigu, Shanxi, 030801, China.
[Ti] Title:Effects of perinatal fluoride exposure on the expressions of miR-124 and miR-132 in hippocampus of mouse pups.
[So] Source:Chemosphere;197:117-122, 2018 Apr.
[Is] ISSN:1879-1298
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:To investigate the effects of perinatal fluoride exposure on learning and memory ability of mouse offspring, ICR female mice were received different doses of sodium fluoride (0, 25, 50, 100 mg/L NaF) from pregnant day 7 to lactational day 21. Pups were exposed to fluoride through the cord blood and breast milk. Open field test showed that compared to the control group, perinatal fluoride exposure significantly decreased the number of entries into the center zone in 100 mg/L NaF group. In the eight-arm maze test, the number of working memory errors, reference memory errors, and the total arm entries were significantly increased in fluoride treatment groups, compared to the control group. Additionally, 100 mg/L NaF significantly elevated the expression levels of miR-124, miR-132, and DiGeorge syndrome chromosomal region 8 (DGCR8) in hippocampus of mouse pups at postnatal day (PND) 21. Contrarily, methyl CpG binding protein 2 (MeCP2) were dramatically reduced in 50 and 100 mg/L NaF groups, while cAMP-response element binding protein (CREB) mRNA level was significantly decreased in all fluoride groups. These findings suggested that the impairment of learning and memory in mouse offspring induced by perinatal fluoride exposure may partly result from the enhanced miR-124 and miR-132 and the alterations of their target genes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180213
[Lr] Last revision date:180213
[St] Status:In-Process

  8 / 2441 MEDLINE  
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[PMID]: 29331595
[Au] Autor:Weinberger R; Weisman O; Guri Y; Harel T; Weizman A; Gothelf D
[Ad] Address:Sackler Faculty of Medicine, Tel Aviv University, Israel.
[Ti] Title:The interaction between neurocognitive functioning, subthreshold psychotic symptoms and pharmacotherapy in 22q11.2 deletion syndrome: A longitudinal comparative study.
[So] Source:Eur Psychiatry;48:20-26, 2018 Feb.
[Is] ISSN:1778-3585
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:BACKGROUND: The 22q11.2 deletion syndrome (22q11DS) is the most common genetic syndrome associated with schizophrenia. The goal of this study was to evaluate longitudinally the interaction between neurocognitive functioning, the presence of subthreshold psychotic symptoms (SPS) and conversion to psychosis in individuals with 22q11DS. In addition, we attempted to identify the specific neurocognitive domains that predict the longitudinal evolution of positive and negative SPS, as well as the effect of psychiatric medications on 22q11DS psychiatric and cognitive developmental trajectories. METHODS: Forty-four participants with 22q11DS, 19 with Williams syndrome (WS) and 30 typically developing (TD) controls, age range 12-35years, were assessed at two time points (15.2±2.1months apart). Evaluation included the Structured Interview for Prodromal Symptoms (SIPS), structured psychiatric evaluation and the Penn Computerized Neurocognitive Battery (CNB). RESULTS: 22q11DS individuals with SPS had a yearly conversion rate to psychotic disorders of 8.8%, compared to none in both WS and TD controls. Baseline levels of negative SPS were associated with global neurocognitive performance (GNP), executive function and social cognition deficits, in individuals with 22q11DS, but not in WS. Deficits in GNP predicted negative SPS in 22q11DS and the emergence or persistence of negative SPS. 22q11DS individuals treated with psychiatric medications showed significant improvement in GNP score between baseline and follow-up assessments, an improvement that was not seen in untreated 22q11DS. CONCLUSIONS: Our results highlight the time-dependent interplay among positive and negative SPS symptoms, neurocognition and pharmacotherapy in the prediction of the evolution of psychosis in 22q11DS.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180211
[Lr] Last revision date:180211
[St] Status:In-Data-Review

  9 / 2441 MEDLINE  
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[PMID]: 29362439
[Au] Autor:Zou Y; Chen Z; Jennings BL; Zhao G; Gu Q; Bhattacharya A; Cui Y; Yu B; Malik KU; Yue J
[Ad] Address:Department of Cardiology, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, P.R. China.
[Ti] Title:Deletion of DGCR8 in VSMCs of adult mice results in loss of vascular reactivity, reduced blood pressure and neointima formation.
[So] Source:Sci Rep;8(1):1468, 2018 Jan 23.
[Is] ISSN:2045-2322
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:DiGeorge syndrome chromosomal region 8 (DGCR8), a double-stranded-RNA-binding protein, participates in the miRNA biogenesis pathway and contributes to miRNA maturation by interacting with the RNAase III enzyme Drosha in cell nuclei. To investigate the role of DGCR8 in vascular smooth muscle cells (VSMCs) at the postnatal stages, we generated tamoxifen-inducible VSMC specific knockout (iKO) mice by crossing DGCR8 with VSMC specific tamoxifen-inducible Cre transgenic mice SMA-Cre-ER . DGCR8iKO mice display reduced body weight one month following tamoxifen treatment and died around 3 months. Blood pressure and vascular reactivity were significantly reduced in DGCR8iKO mice compared to control. Furthermore, loss of DGCR8 in VSMCs inhibited cell proliferation, migration and neointima formation. VSMC differentiation marker genes, including SMA and SM22, were downregulated in DGCR8 iKO mice. The majority of miRNAs were downregulated in DGCR8iKO mice. Disruption of the DGCR8-mediated miRNA biogenesis pathway attenuated multiple signaling pathways including ERK1/2 and AKT. Our results demonstrate that the DGCR8-mediated miRNA pathway is required for maintaining blood pressure, vascular reactivity and vascular wall remodeling at the postnatal stages.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180208
[Lr] Last revision date:180208
[St] Status:In-Data-Review
[do] DOI:10.1038/s41598-018-19660-z

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[PMID]: 29347911
[Au] Autor:Ward NJ; Green D; Higgins J; Dalmay T; Münsterberg A; Moxon S; Wheeler GN
[Ad] Address:School of Biological Sciences, University of East Anglia, Norwich Research Park, Norwich, NR4 7TJ, UK.
[Ti] Title:microRNAs associated with early neural crest development in Xenopus laevis.
[So] Source:BMC Genomics;19(1):59, 2018 01 18.
[Is] ISSN:1471-2164
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: The neural crest (NC) is a class of transitory stem cell-like cells unique to vertebrate embryos. NC cells arise within the dorsal neural tube where they undergo an epithelial to mesenchymal transition in order to migrate and differentiate throughout the developing embryo. The derivative cell types give rise to multiple tissues, including the craniofacial skeleton, peripheral nervous system and skin pigment cells. Several well-studied gene regulatory networks underpin NC development, which when disrupted can lead to various neurocristopathies such as craniofrontonasal dysplasia, DiGeorge syndrome and some forms of cancer. Small RNAs, such as microRNAs (miRNAs) are non-coding RNA molecules important in post-transcriptional gene silencing and critical for cellular regulation of gene expression. RESULTS: To uncover novel small RNAs in NC development we used high definition adapters and next generation sequencing of libraries derived from ectodermal explants of Xenopus laevis embryos induced to form neural and NC tissue. Ectodermal and blastula animal pole (blastula) stage tissues were also sequenced. We show that miR-427 is highly abundant in all four tissue types though in an isoform specific manner and we define a set of 11 miRNAs that are enriched in the NC. In addition, we show miR-301a and miR-338 are highly expressed in both the NC and blastula suggesting a role for these miRNAs in maintaining the stem cell-like phenotype of NC cells. CONCLUSION: We have characterised the miRNAs expressed in Xenopus embryonic explants treated to form ectoderm, neural or NC tissue. This has identified novel tissue specific miRNAs and highlighted differential expression of miR-427 isoforms.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1801
[Cu] Class update date: 180207
[Lr] Last revision date:180207
[St] Status:In-Process
[do] DOI:10.1186/s12864-018-4436-0


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