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[PMID]:28827114
[Au] Autor:Chakraborty S; Uddin A; Choudhury MN
[Ad] Endereço:Assam University, Biotechnology, Dargakona, 788011 Silchar, Assam, India. Electronic address: supriyoch_2008@rediffmail.com.
[Ti] Título:Factors affecting the codon usage bias of SRY gene across mammals.
[So] Source:Gene;630:13-20, 2017 Sep 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Codon usage bias (CUB) is extensively found in a wide variety genomes and it is mostly affected by mutation pressure and natural selection. Analysis of CUB helps in studying the evolutionary features of a genome. The SRY gene plays an important role in male reproductive organ and a good candidate to study the evolutionary forces, since little work was reported earlier on this gene. We used bioinformatic methods to analyze the protein-coding sequences of SRY gene in 172 different mammalian species to understand the patterns of codon usage and the evolutionary forces acting on it. We found that the codon bias of SRY gene varies widely across mammals. Relative synonymous codon usage (RSCU) value revealed that the codons such as TCG, CCG, CAT, ATT, ACT, GCT, GTT, GCG, GGG and GGT were over-represented. Correspondence analysis indicated that the distribution of codons was more close to the axes indicating that compositional constraints might correlate to codon bias. Z-score analysis on RSCU values of codons identified a set of 11 codons viz. TCT, TTT, CTA, CTC, TAT, CAG, CGT, ATA, ACC, AAT and GTA which differed significantly at p<0.01 between 5% high and low gene expression datasets. Further, it was evident from the neutrality plot that GC12 was influenced by both mutation pressure and natural selection. From the study we concluded that natural selection played a dominant role, but mutational pressure played a minor role in the codon usage pattern of SRY gene across mammals.
[Mh] Termos MeSH primário: Códon/genética
Genes sry
Seleção Genética
[Mh] Termos MeSH secundário: Animais
Viés
Códon/metabolismo
Evolução Molecular
Mamíferos/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Codon)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170823
[St] Status:MEDLINE


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[PMID]:28186606
[Au] Autor:Li H; Zhang K; Gao M; Zhang H; Wang Y; Zhang Y; Liu Y; Gai Z
[Ad] Endereço:Department of Genetic Metabolic Endocrinology, Qilu Children's Hospital of Shandong University, Jinan, Shandong 250022, China. liuyi-ly@126.com; gaizhongtao@sina.com.
[Ti] Título:[Analysis of genetic etiology of a female with 47,XXY syndrome].
[So] Source:Zhonghua Yi Xue Yi Chuan Xue Za Zhi;34(1):102-105, 2017 Feb 10.
[Is] ISSN:1003-9406
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: To explore the genetic cause of a female case with intellectual development disorder. METHODS: G banding karyotyping was performed for the patient. Following DNA extraction, the coding sequence of SRY gene was amplified with PCR and subjected to Sanger sequencing. qPCR was used to detect the copy numbers of the SRY gene. RESULTS: The karyotype of the patient was 47,XXY. PCR and qPCR analyses of the SRY gene showed a large deletion with null copy number. CONCLUSION: The female phenotype of the patient is probably due to deletion of the SRY gene on the Y chromosome. This is the first report of 47,XXY female case with deletion of the SRY gene in China.
[Mh] Termos MeSH primário: Cromossomos Humanos Y/genética
Genes sry/genética
Deficiência Intelectual/genética
Síndrome de Klinefelter/genética
Deleção de Sequência
[Mh] Termos MeSH secundário: Sequência de Bases
Bandeamento Cromossômico
Feminino
Seres Humanos
Cariótipo
Cariotipagem
Masculino
Reação em Cadeia da Polimerase
Literatura de Revisão como Assunto
Análise de Sequência de DNA/métodos
Homologia de Sequência do Ácido Nucleico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170629
[Lr] Data última revisão:
170629
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170211
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1003-9406.2017.01.024


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[PMID]:28083978
[Au] Autor:A Soliman N; Abd-Allah SH; Hussein S; Alaa Eldeen M
[Ad] Endereço:Zoology Department, Physiology Section, Faculty of Science, Zagazig University, Egypt.
[Ti] Título:Factors enhancing the migration and the homing of mesenchymal stem cells in experimentally induced cardiotoxicity in rats.
[So] Source:IUBMB Life;69(3):162-169, 2017 Mar.
[Is] ISSN:1521-6551
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Doxorubicin is an effective anti-neoplastic drug but its use is limited by its cardiotoxicity. Administration of mesenchymal stem cells (MSCs) for the management of cardiotoxicity was with poor myocardial homing capacity. With the aim of developing novel techniques to improve the migration of MSCs, we tested whether valproate and electric fields (EFs) direct the migration of MSCs towards the damaged myocardium. The study included five groups of female albino rats. The first group included 10 healthy rats as normal control group. The remaining 40 female rats received doxorubicin for induction of acute cardiotoxicity. Four rats were sacrificed for histopathological confirmation of cardiotoxicity. The remaining rats were equally divided into subsequent four groups. The second group included nine rats that did not receive further treatment (positive control group). The third group included nine rats which received intravenous bone marrow derived mesenchymal stem cells (BM-MSCs) after cardiotoxicity induction. The fourth group included nine rats which received BM-MSCs plus sodium valporate after cardiotoxicity induction. The fifth group included nine rats which received BM-MSCs plus sodium valporate after cardiotoxicity induction and were exposed to an electrical stimulation (ES). Blood samples were taken from all groups at the end of the study to estimate creatine kinase-MB (CK-MB), aspartate transaminase (AST) and lactate dehydrogenase (LDH). Heart tissues from all rats were used for RNA extraction for assessment of sry gene expression. Homing was tested by PKH26 fluorescence in myocardial tissue sections and by sry gene expression. The best biochemical and histopathological improvement in cardiotoxicity was demonstrated in group 5 (rats that received ES and valporate with MSCs). We concluded that EFs and sodium valproate enhance homing ability of MSCs towards the damaged myocardium in doxorubicin induced carditoxicity model. © 2017 IUBMB Life, 69(3):162-169, 2017.
[Mh] Termos MeSH primário: Antibióticos Antineoplásicos/efeitos adversos
Movimento Celular
Doxorrubicina/efeitos adversos
Transplante de Células-Tronco Mesenquimais
Células Mesenquimais Estromais/fisiologia
[Mh] Termos MeSH secundário: Animais
Cardiotoxicidade/patologia
Cardiotoxicidade/terapia
Células Cultivadas
Creatina Quinase Forma MB/metabolismo
Feminino
Expressão Gênica
Genes sry
L-Lactato Desidrogenase/metabolismo
Masculino
Miocárdio/enzimologia
Miocárdio/patologia
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibiotics, Antineoplastic); 80168379AG (Doxorubicin); EC 1.1.1.27 (L-Lactate Dehydrogenase); EC 2.7.3.2 (Creatine Kinase, MB Form)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170114
[St] Status:MEDLINE
[do] DOI:10.1002/iub.1600


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[PMID]:27804859
[Au] Autor:Merone J; Nwogu O; Redington JM; Uversky VN
[Ad] Endereço:Department of Molecular Medicine, Morsani College of Medicine, University of South Florida, Tampa, Florida 33612, FL. United States.
[Ti] Título:Intrinsic Disorder in Male Sex Determination: Disorderedness of Proteins from the Sry Transcriptional Network.
[So] Source:Curr Protein Pept Sci;18(5):482-514, 2017.
[Is] ISSN:1875-5550
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Sex differentiation is a complex process where sexually indifferent embryo progressively acquires male or female characteristics via tightly controlled, perfectly timed, and sophisticatedly intertwined chain of events. This process is controlled and regulated by a set of specific proteins, with one of the first steps in sex differentiation being the activation of the Y-chromosomal Sry gene (sexdetermining region Y) in males that acts as a switch from undifferentiated gonad somatic cells to testis development. There are several key players in this process, which constitute the Sry transcriptional network, and collective action of which governs testis determination. Although it is accepted now that many proteins engaged in signal transduction as well as regulation and control of various biological processes are intrinsically disordered (i.e., do not have unique structure and remain unstructured, or incompletely structured, under physiological conditions), the roles and profusion of intrinsic disorder in proteins involved in the male sex determination have not been accessed as of yet. The goal of this study is to cover this gap by analyzing some key players of the Sry transcriptional network. To this end, we employed a broad set of computational tools for intrinsic disorder analysis and conducted intensive literature search in order to gain information on the structural peculiarities of the Sry networkrelated proteins, their intrinsic disorder predispositions, and the roles of intrinsic disorder in their functions.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica no Desenvolvimento
Genes sry
Proteínas Intrinsicamente Desordenadas/química
Processamento de Proteína Pós-Traducional
Processos de Determinação Sexual
Fatores de Transcrição/química
[Mh] Termos MeSH secundário: Animais
Embrião de Mamíferos
Redes Reguladoras de Genes
Seres Humanos
Proteínas Intrinsicamente Desordenadas/genética
Proteínas Intrinsicamente Desordenadas/metabolismo
Masculino
Camundongos
Mapeamento de Interação de Proteínas
Testículo/citologia
Testículo/crescimento & desenvolvimento
Testículo/metabolismo
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Intrinsically Disordered Proteins); 0 (Transcription Factors)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161103
[St] Status:MEDLINE
[do] DOI:10.2174/1389203717666161028150244


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[PMID]:27715460
[Au] Autor:Soleymani B; Hafezian SH; Mianji GR; Mansouri K; Chaharaein B; Tajehmiri A; Sharifi Tabar M; Mostafaie A
[Ad] Endereço:a Medical Biology Research Center , Kermanshah University of Medical Sciences , Kermanshah , Iran.
[Ti] Título:Bovine Sex Determining Region Y: Cloning, Optimized Expression, and Purification.
[So] Source:Anim Biotechnol;28(1):44-52, 2017 Jan 02.
[Is] ISSN:1532-2378
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Sex determining region Y gene (SRY) is located on Y chromosome and encodes a protein with 229 amino acids. In this study, ORF region of SRY with a length of 690 bp was synthesized using PCR and ligated to pET28a (+), then transformed in E.coli DH5α. E.coli BL21 (DE3) strain was chosen to express recombinant bovine SRY protein. A set of optimization steps was taken including different concentrations of IPTG, glucose, and temperatures at differed incubation times after the induction. Results showed that temperature points and different concentrations of IPTG and glucose had a significant effect (p < 0.01) on total protein and recombinant bovine SRY. After purification, various temperatures and concentrations of IPTG showed meaningful effects (p < 0.01) on the solubility of expressed recombinant SRY. Highest soluble rSRY protein amount was achieved where 0.5 mM IPTG and 0.5% glucose was used at 20°C during induction. In the absence of glucose, the highest amount of soluble recombinant SRY levels were achieved at the concentrations of 0.8 mM of IPTG at 28°C, 20°C, and 1.5 mM IPTG at 37°C during induction for 16, 24, and 8 hours, respectively. Regarding the results obtained in this study, it could be stated that by decreasing temperature and inducer concentration, soluble bovine SRY protein expression increases.
[Mh] Termos MeSH primário: Bovinos/genética
Genes sry/genética
Proteína da Região Y Determinante do Sexo/genética
Cromossomo Y/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Sequência de Bases
Clonagem Molecular
Escherichia coli/genética
Escherichia coli/metabolismo
Expressão Gênica
Masculino
Fases de Leitura Aberta/genética
Domínios Proteicos
Proteínas Recombinantes
Análise de Sequência de DNA/veterinária
Proteína da Região Y Determinante do Sexo/isolamento & purificação
Proteína da Região Y Determinante do Sexo/metabolismo
Solubilidade
Temperatura Ambiente
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Recombinant Proteins); 0 (Sex-Determining Region Y Protein)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170124
[Lr] Data última revisão:
170124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161008
[St] Status:MEDLINE
[do] DOI:10.1080/10495398.2016.1198796


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[PMID]:27711951
[Au] Autor:Chauhan V; Jyotsna VP; Jain V; Khadgawat R; Dada R
[Ad] Endereço:Department of Endocrinology and Metabolism, All India Institute of Medical Sciences, New Delhi, India.
[Ti] Título:Novel Heterozygous Genetic Variants in Patients with 46,XY Gonadal Dysgenesis.
[So] Source:Horm Metab Res;49(1):36-42, 2017 Jan.
[Is] ISSN:1439-4286
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:46,XY gonadal dysgenesis (GD) constitutes a rare group of disorders characterized by the presence of dysfunctional testes in genotypic males. The molecular etiology is not known in about 2 thirds of instances. The aim of this study was to identify the genetic cause in patients with 46,XY gonadal dysgenesis. Based on clinical, cytogenetic, and biochemical screening, 10 patients with 46,XY GD were recruited. Direct sequencing of , , , , , genes was carried out for molecular analysis. Among 10 patients, 5 were diagnosed with complete gonadal dysgenesis (CGD), 3 with partial gonadal dysgenesis (PGD), and 3 with testicular agenesis. Molecular analysis revealed 12 heterozygous genetic changes, 4 of which were novel. One (c.416T>A) was observed in evolutionary conserved region of gene in a patient with CGD and was found to be probably damaging on in silico analysis. Other 3 were identified in gene (c.990+22 C>A, c.1387+1403T>A and p.131P), but their association with gonadal dysgenesis is not evident from our study. These genetic changes were absent in parents and 50 healthy control samples, which were also studied. With targeted sequencing approach, a molecular diagnosis was made in only one patient with 46,XY GD. The application of new genomic technologies is required for the precise evaluation of these rare genetic defects.
[Mh] Termos MeSH primário: Disgenesia Gonadal 46 XY/genética
Heterozigoto
Mutação
[Mh] Termos MeSH secundário: Adolescente
Adulto
Criança
Pré-Escolar
Receptor Nuclear Órfão DAX-1/genética
Análise Mutacional de DNA/métodos
Feminino
Genes sry
Proteínas Hedgehog/genética
Seres Humanos
Lactente
Masculino
Fatores de Transcrição SOX9/genética
Fator Esteroidogênico 1/genética
Fatores de Transcrição/genética
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DAX-1 Orphan Nuclear Receptor); 0 (DHH protein, human); 0 (DMRT1 protein); 0 (Hedgehog Proteins); 0 (NR0B1 protein, human); 0 (NR5A1 protein, human); 0 (SOX9 Transcription Factor); 0 (SOX9 protein, human); 0 (Steroidogenic Factor 1); 0 (Transcription Factors)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170327
[Lr] Data última revisão:
170327
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161007
[St] Status:MEDLINE
[do] DOI:10.1055/s-0042-114778


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[PMID]:28033659
[Au] Autor:Gunes SO; Metin Mahmutoglu A; Agarwal A
[Ad] Endereço:Department of Medical Biology, Faculty of Medicine, Ondokuz Mayis University, Samsun, Turkey.
[Ti] Título:Genetic and epigenetic effects in sex determination.
[So] Source:Birth Defects Res C Embryo Today;108(4):321-336, 2016 Dec.
[Is] ISSN:1542-9768
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sex determination is a complex and dynamic process with multiple genetic and environmental causes, in which germ and somatic cells receive various sex-specific features. During the fifth week of fetal life, the bipotential embryonic gonad starts to develop in humans. In the bipotential gonadal tissue, certain cell groups start to differentiate to form the ovaries or testes. Despite considerable efforts and advances in identifying the mechanisms playing a role in sex determination and differentiation, the underlying mechanisms of the exact functions of many genes, gene-gene interactions, and epigenetic modifications that are involved in different stages of this cascade are not completely understood. This review aims at discussing current data on the genetic effects via genes and epigenetic mechanisms that affect the regulation of sex determination. Birth Defects Research (Part C) 108:321-336, 2016. © 2016 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Processos de Determinação Sexual/genética
Diferenciação Sexual/genética
[Mh] Termos MeSH secundário: Epigenômica
Feminino
Genes sry/genética
Gônadas/fisiologia
Seres Humanos
Masculino
Fatores de Transcrição SOXE/genética
Análise para Determinação do Sexo/métodos
Fatores de Transcrição/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (SOXE Transcription Factors); 0 (Transcription Factors)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170823
[Lr] Data última revisão:
170823
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161230
[St] Status:MEDLINE
[do] DOI:10.1002/bdrc.21146


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[PMID]:27806792
[Au] Autor:Qin XY; Dong WK; Wang W; Dong ZY; Xiao Y; Lu WL; Wang DF
[Ad] Endereço:Department of Pediatrics, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, China.
[Ti] Título:[Analysis of clinical features and related genes variation in five patients with 46, XX male syndrome].
[So] Source:Zhonghua Er Ke Za Zhi;54(11):840-843, 2016 Nov 02.
[Is] ISSN:0578-1310
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To explore the clinical manifestations and molecular features of 46, XX male syndrome. The clinical and molecular data of five 46, XX male syndrome cases treated in the Department of Pediatrics of Shanghai Ruijin Hospital form August 2010 to August 2014 were retrospectively analyzed. The five patients were all sociopsychologically males and came to hospital respectively for short stature, ambiguous genitalia or gynecomastia. They were all below the normal male's average height, and their karyotype was all 46, XX. One case in five was verified as sex determining region of Y chromosome (SRY gene) positive revealed no abnormality in their external genitalia. He had short stature since childhood, whose SRY gene fragments were shown by FISH transferred to the ends of X chromosome. Three cases in four were SRY gene negative with ambiguous genitalia of cryptorchidism and testicular dysplasia to different degrees. The copy number variations of SOX9 gene was found in one case, the loss of heterozygosity area in DHH gene of one case. Another SRY gene negative patient who had normal male external genitalia, came to the hospital due to puberty gynecomastia, that of SOX9 gene and its upstream gene both increased. The main clinical characteristics of 46, XX male syndrome are male phenotype, 46, XX karyotype, gonad of testis or ovotestis and no uterus. In addition, short stature, ambiguous genitalia or gynecomastia can be one reason for hospital visits. SRY gene translocation, SOX9 gene and its upstream gene copy number increase all can lead to 46, XX male syndrome. The cause of some may play an important role in 46, XX male syndrome, but has not yet been determined.
[Mh] Termos MeSH primário: Transtornos Testiculares 46, XX do Desenvolvimento Sexual/genética
Genes sry
[Mh] Termos MeSH secundário: Transtornos Testiculares 46, XX do Desenvolvimento Sexual/patologia
Criança
China
Variações do Número de Cópias de DNA
Transtornos do Desenvolvimento Sexual
Feminino
Seres Humanos
Cariotipagem
Masculino
Testículo
Translocação Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170515
[Lr] Data última revisão:
170515
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161104
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0578-1310.2016.11.010


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[PMID]:27654689
[Au] Autor:Deeney S; Powers KN; Crombleholme TM
[Ad] Endereço:Laboratory for Fetal and Regenerative Biology, Department of Surgery, University of Colorado School of Medicine, and Division of Pediatric General, Thoracic and Fetal Surgery, Colorado Children's Hospital, Aurora, Colorado.
[Ti] Título:A comparison of sexing methods in fetal mice.
[So] Source:Lab Anim (NY);45(10):380-4, 2016 Sep 21.
[Is] ISSN:1548-4475
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Accurate mouse sexing is vital when conducting research examining sexual dimorphisms. Late fetal and newborn mouse pups are more immature than many previously described sexing methods allow. This study compares the sexing accuracy of a newly described internal gonad sexing method to a recently described peritoneal pigmentation sexing method in embryonic day 20 C57BL/6J mouse pups, using Sry genotyping to confirm the sex. The internal gonad sexing method was found to be highly accurate, while the peritoneal pigmentation method was slightly less accurate. Therefore, while Sry genotyping remains the gold standard, immediate and less expensive sexing methods can be performed accurately as early as the late fetal period in C57BL/6J mice.
[Mh] Termos MeSH primário: Camundongos Endogâmicos C57BL/anatomia & histologia
[Mh] Termos MeSH secundário: Animais
Embrião de Mamíferos/anatomia & histologia
Feminino
Genes sry
Genitália/anatomia & histologia
Genitália/embriologia
Técnicas de Genotipagem/veterinária
Masculino
Camundongos Endogâmicos C57BL/embriologia
Camundongos Endogâmicos C57BL/genética
Pigmentação
Reprodutibilidade dos Testes
Caracteres Sexuais
Análise para Determinação do Sexo/métodos
Análise para Determinação do Sexo/veterinária
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160923
[St] Status:MEDLINE
[do] DOI:10.1038/laban.1105


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[PMID]:27518446
[Au] Autor:Pienkowska-Schelling A; Handler J; Neuhauser S; Schelling C
[Ad] Endereço:Institut für Genetik, Vetsuisse-Fakultät Bern, Universität Bern.
[Ti] Título:[A case of 63,X/64,XX mosaicism in a subfertile pony mare].
[Ti] Título:Ein Fall von 63,X/64,XX Mosaizismus bei einer subfertilen Ponystute..
[So] Source:Schweiz Arch Tierheilkd;158(4):266-8, 2016 Apr.
[Is] ISSN:0036-7281
[Cp] País de publicação:Switzerland
[La] Idioma:ger
[Ab] Resumo:INTRODUCTION: The present case report describes a 6-year old subfertile pony mare, which became pregnant after the eleventh artificial insemination. The examination of the ovaries and the uterus did not reveal any abnormal clinical findings and the mare showed a regular oestrous cycle. Based on cytogenetic and molecular genetic analyses it became possible to elucidate the observed subfertility. The mosaic karyotype of the mare consisted of 63,X (20%) and 64,XX (80%) cells. A PCR analysis failed to amplify sequences from the equine SRY gene. The observed classic 63,X/64,XX mosaicism is a plausible explanation for the subfertility of the mare.
[Mh] Termos MeSH primário: Cavalos/genética
Infertilidade Feminina/veterinária
Mosaicismo/veterinária
Cromossomo X/genética
[Mh] Termos MeSH secundário: Animais
Feminino
Genes sry/genética
Infertilidade Feminina/genética
Inseminação Artificial/veterinária
Cariótipo
Reação em Cadeia da Polimerase/veterinária
Gravidez
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161217
[Lr] Data última revisão:
161217
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160813
[St] Status:MEDLINE
[do] DOI:10.17236/sat00059



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