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[PMID]:28455345
[Au] Autor:Wang D; Tosevska A; Heiß EH; Ladurner A; Mölzer C; Wallner M; Bulmer A; Wagner KH; Dirsch VM; Atanasov AG
[Ad] Endereço:Department of Pharmacognosy, University of Vienna, Austria.
[Ti] Título:Bilirubin Decreases Macrophage Cholesterol Efflux and ATP-Binding Cassette Transporter A1 Protein Expression.
[So] Source:J Am Heart Assoc;6(5), 2017 Apr 28.
[Is] ISSN:2047-9980
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Mild but chronically elevated circulating unconjugated bilirubin is associated with reduced total and low-density lipoprotein cholesterol concentration, which is associated with reduced cardiovascular disease risk. We aimed to investigate whether unconjugated bilirubin influences macrophage cholesterol efflux, as a potential mechanism for the altered circulating lipoprotein concentrations observed in hyperbilirubinemic individuals. METHODS AND RESULTS: Cholesterol efflux from THP-1 macrophages was assessed using plasma obtained from normo- and hyperbilirubinemic (Gilbert syndrome) humans (n=60 per group) or (heterozygote/homozygote Gunn) rats (n=20 per group) as an acceptor. Hyperbilirubinemic plasma from patients with Gilbert syndrome and Gunn rats induced significantly reduced cholesterol efflux compared with normobilirubinemic plasma. Unconjugated bilirubin (3-17.1 µmol/L) exogenously added to plasma- or apolipoprotein A1-supplemented media also decreased macrophage cholesterol efflux in a concentration- and time-dependent manner. We also showed reduced protein expression of the ATP-binding cassette transporter A1 (ABCA1), a transmembrane cholesterol transporter involved in apolipoprotein A1-mediated cholesterol efflux, in THP-1 macrophages treated with unconjugated bilirubin and in peripheral blood mononuclear cells obtained from hyperbilirubinemic individuals. Furthermore, we demonstrated that bilirubin accelerates the degradation rate of the ABCA1 protein in THP-1 macrophages. CONCLUSIONS: Cholesterol efflux from THP-1 macrophages is decreased in the presence of plasma obtained from humans and rats with mild hyperbilirubinemia. A direct effect of unconjugated bilirubin on cholesterol efflux was demonstrated and is associated with decreased ABCA1 protein expression. These data improve our knowledge concerning bilirubin's impact on cholesterol transport and represent an important advancement in our understanding of bilirubin's role in cardiovascular disease.
[Mh] Termos MeSH primário: Transportador 1 de Cassete de Ligação de ATP/metabolismo
Bilirrubina/sangue
Colesterol/sangue
Doença de Gilbert/sangue
Macrófagos/metabolismo
[Mh] Termos MeSH secundário: Animais
Apolipoproteína A-I/sangue
Estudos de Casos e Controles
Modelos Animais de Doenças
Regulação para Baixo
Feminino
Doença de Gilbert/diagnóstico
Doença de Gilbert/genética
Seres Humanos
Modelos Lineares
Masculino
Proteólise
Ratos Gunn
Ratos Wistar
Células THP-1
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ABCA1 protein, human); 0 (APOA1 protein, human); 0 (ATP Binding Cassette Transporter 1); 0 (Apolipoprotein A-I); 97C5T2UQ7J (Cholesterol); RFM9X3LJ49 (Bilirubin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE


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[PMID]:29091567
[Au] Autor:Rencic J; Zhou M; Hsu G; Dhaliwal G
[Ad] Endereço:From the Department of Medicine, Tufts Medical Center, Boston (J.R., M.Z.); and the Department of Medicine, University of California, San Francisco, and the Medical Service, San Francisco Veterans Affairs Medical Center - both in San Francisco (G.H., G.D.).
[Ti] Título:Circling Back for the Diagnosis.
[So] Source:N Engl J Med;377(18):1778-1784, 2017 Nov 02.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Colecistite Aguda/diagnóstico
Hiperbilirrubinemia/etiologia
Esferocitose Hereditária/diagnóstico
[Mh] Termos MeSH secundário: Dor Abdominal/etiologia
Adulto
Colecistite Aguda/etiologia
Diagnóstico Diferencial
Vesícula Biliar/diagnóstico por imagem
Doença de Gilbert/complicações
Anticorpos Anti-Hepatite B/sangue
Seres Humanos
L-Lactato Desidrogenase/sangue
Masculino
Hepatopatia Gordurosa não Alcoólica/complicações
Obesidade/complicações
Esferocitose Hereditária/complicações
Vômito/etiologia
[Pt] Tipo de publicação:CASE REPORTS; CLINICAL CONFERENCE; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hepatitis B Antibodies); EC 1.1.1.27 (L-Lactate Dehydrogenase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171102
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMcps1701742


  3 / 796 MEDLINE  
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[PMID]:28338110
[Au] Autor:Radoi VE; Ursu RI; Poenaru E; Arsene C; Bohiltea CL; Bohiltea R
[Ad] Endereço:Synevo Romania, Central Laboratory, Medical Genetics Department; Department of Medical Genetics; Carol Davila University of Medicine and Pharmacy, Faculty of General Medicine Bucharest, Romania.
[Ti] Título:Frequency of the UGT1A1*28 Polymorphism in a Romanian Cohort of Gilbert Syndrome Individuals.
[So] Source:J Gastrointestin Liver Dis;26(1):25-28, 2017 Mar.
[Is] ISSN:1842-1121
[Cp] País de publicação:Romania
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND AIMS: Gilbert syndrome (GS) is characterized by unconjugated hyperbilirubinemia without liver disease or overt hemolysis and it is found in 3-10% of the general population. Inherited hyperbilirubinaemia is attributable to a reduced UGT1A1 activity. The UGT1A1 promoter (TA) repeats variants are documented of being involved in abnormally elevated bilirubin levels. The aim of the present study is to analyze the impact of UGT1A1 promoter variants on bilirubin levels in Romanian patients clinically supected with GS. METHODS: The study group included 897 subjects: 292 GS patients and 605 healthy controls. Genomic DNA was extracted from the peripheral blood leukocytes. All individuals were screened for the presence of the (TA) insertion in the TATA box region of UGT1A1 gene by PCR amplification. This case-control study was conducted at the Department of Medical Genetics, Synevo, Romania. RESULTS: UGT1A1*28 (7TA) revealed the highest frequency (61.87%) of all individuals, while the UGT1A1*1 (6TA) allele was found in 36.79%. We identified two other variants of the UGT1A1 gene, depending on the number of TA repeats in the promoter: 5TA (0.61%) and 8TA (0.72%). The (TA)7/7 homozygous genotype was identified in 32.33% of all individuals, while the (TA)6/7 heterozygous genotype was the most prevalent (57.64%). The wild type (TA)6/6 was identified in 7.36% of the whole cohort. CONCLUSIONS: Because other polymorphisms have been associated with GS, the absence of the UGT1A1*28 allele does not rule out this condition. The results suggest that in the Romanian population there is a strong correlation between the UGT1A1*28 polymorphism and hyperbilirubinemia in patients with GS.
[Mh] Termos MeSH primário: Doença de Gilbert/genética
Glucuronosiltransferase/genética
Polimorfismo Genético
[Mh] Termos MeSH secundário: Adolescente
Adulto
Distribuição por Idade
Idoso
Estudos de Casos e Controles
Criança
Pré-Escolar
Feminino
Frequência do Gene
Genótipo
Seres Humanos
Lactente
Masculino
Meia-Idade
Regiões Promotoras Genéticas/genética
Romênia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.4.1.- (UGT1A1 enzyme); EC 2.4.1.17 (Glucuronosyltransferase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170325
[St] Status:MEDLINE
[do] DOI:10.15403/jgld.2014.1121.261.ugt


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[PMID]:28321066
[Au] Autor:Aiso M; Yagi M; Tanaka A; Miura K; Miura R; Arizumi T; Takamori Y; Nakahara S; Maruo Y; Takikawa H
[Ad] Endereço:Department of Medicine, Teikyo University School of Medicine, Japan.
[Ti] Título:Gilbert Syndrome with Concomitant Hereditary Spherocytosis Presenting with Moderate Unconjugated Hyperbilirubinemia.
[So] Source:Intern Med;56(6):661-664, 2017.
[Is] ISSN:1349-7235
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:We experienced a case of a 19-year-old man with Gilbert syndrome with concomitant hereditary spherocytosis. The patient presented with moderate unconjugated hyperbilirubinemia, and inherited etiology was strongly suspected. The diagnosis of Gilbert syndrome was confirmed by the genetic analysis of the UGT1A1 gene, demonstrating UGT1A1*28 and compound heterozygote UGT1A1*6. In addition, since the laboratory findings and imaging studies revealed lysemia as well as gallstone and splenomegaly, a diagnosis of hereditary spherocytosis was made as a comorbidity. Both Gilbert syndrome and hereditary spherocytosis are hereditary diseases with a high frequency, and the hyperbilirubinemia may be exacerbated when these two diseases are concomitant.
[Mh] Termos MeSH primário: Doença de Gilbert/complicações
Doença de Gilbert/genética
Glucuronosiltransferase/genética
Hiperbilirrubinemia/complicações
Esferocitose Hereditária/complicações
[Mh] Termos MeSH secundário: Cálculos Biliares/complicações
Seres Humanos
Masculino
Esplenomegalia/complicações
Adulto Jovem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.4.1.- (UGT1A1 enzyme); EC 2.4.1.17 (Glucuronosyltransferase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170516
[Lr] Data última revisão:
170516
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE
[do] DOI:10.2169/internalmedicine.56.7362


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[PMID]:28296739
[Au] Autor:de Souza MM; Vaisberg VV; Abreu RM; Ferreira AS; daSilvaFerreira C; Nasser PD; Paschoale HS; Carrilho FJ; Ono SK
[Ad] Endereço:Department of Gastroenterology, University of São Paulo School of Medicine, São Paulo, Brazil.
[Ti] Título:UGT1A1*28 relationship with abnormal total bilirubin levels in chronic hepatitis C patients: Outcomes from a case-control study.
[So] Source:Medicine (Baltimore);96(11):e6306, 2017 Mar.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Gilbert syndrome (GS) is a frequent benign clinical condition, marked by intermittent unconjugated hyperbilirubinemia, mostly due to the polymorphism uridine diphosphate-glucuronosyltransferase 1A1*28 (UGT1A1*28). Hyperbilirubinemia has been reported in a GS patient undergoing hepatitis C treatment, and other UGT isoforms polymorphisms have been linked to worse outcomes in viral hepatitis. Yet, little is known to GS contributions' to the liver disease scenario. Our aim was to assess UGT1A1 genotypes' frequency in chronic hepatitis C (CHC) patients and correlate with total bilirubin (TB). This is a case-control study in a large tertiary medical center. Cases were CHC patients confirmed by hepatitis C virus (HCV)-polymerase chain reaction. Exclusion criteria were hepatitis B virus or human immunodeficiency virus (HIV) coinfection. Control were healthy blood donors. UGT1A1 promoter region gene genotyping was performed, and bilirubin serum levels were available for HCV patients. Genotypes and alleles frequencies were similar in case (n = 585; P = 0.101) and control groups (n = 313; P = 0.795). Total bilirubin increase was noticed according to thymine-adenine repeats in genotypes (P < 0.001), and the TB greater than 1 mg/dL group had more UGT1A1*28 subjects than in the group with TB values <1 mg/dL (18.3 vs 5.3; P < 0.001). Bilirubin levels are linked to the studied polymorphisms, and this is the first time that these findings are reported in a chronic liver disease sample. Among patients with increased TB levels, the frequency of UGT1A1*28 is higher than those with normal TB. Personalized care should be considered to GS, regarding either abnormal bilirubin levels or drug metabolism.
[Mh] Termos MeSH primário: Bilirrubina/sangue
Glucuronosiltransferase/genética
Hepatite C Crônica/sangue
[Mh] Termos MeSH secundário: Adulto
Idoso
Estudos de Casos e Controles
Feminino
Doença de Gilbert/genética
Hepatite C Crônica/genética
Seres Humanos
Masculino
Meia-Idade
Regiões Promotoras Genéticas
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
EC 2.4.1.- (UGT1A1 enzyme); EC 2.4.1.17 (Glucuronosyltransferase); RFM9X3LJ49 (Bilirubin)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170403
[Lr] Data última revisão:
170403
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170316
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000006306


  6 / 796 MEDLINE  
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[PMID]:28100328
[Au] Autor:Yuan XY; He XL; Zou H; Zou RY
[Ad] Endereço:Department of Pediatric Hematology and Oncology, Hunan People's Hospital, Changsha 410005, China. hexiangl@163.com.
[Ti] Título:[Repeated yellowing of the skin and sclera for 2 years].
[So] Source:Zhongguo Dang Dai Er Ke Za Zhi;19(1):77-80, 2017 Jan.
[Is] ISSN:1008-8830
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:A two-year-old girl was admitted due to repeated yellowing of the skin and sclera for 2 years and had no other specific symptoms or signs. The use of phenobarbital could relieve the symptoms of jaundice. Multiple examinations showed increased indirect bilirubin levels, and the results of aminotransferases and liver imaging were normal. There was no evidence of hemolysis. The analysis of UGT1A1 gene in her family found that this child had double homozygous mutation of c.211G>A(G71R) and c.1456T>G(Y486D), which had been reported as the pathogenic mutation for Gilbert syndrome. Her parents carried double heterozygous mutation of G71R and Y486D and had no symptom of jaundice. The child was diagnosed as having Gilbert syndrome. It is concluded that as for patients with unconjugated hyperbilirubinemia which cannot be explained by liver damage and hemolysis, their family history should be investigated in detail and gene analysis should be performed as early as possible, in order to identify congenital bilirubin metabolic disorders.
[Mh] Termos MeSH primário: Doença de Gilbert/diagnóstico
Glucuronosiltransferase/genética
Mutação
[Mh] Termos MeSH secundário: Pré-Escolar
Feminino
Seres Humanos
Esclera/patologia
Pele/patologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.4.1.- (UGT1A1 enzyme); EC 2.4.1.17 (Glucuronosyltransferase)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170120
[St] Status:MEDLINE


  7 / 796 MEDLINE  
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[PMID]:28096081
[Au] Autor:Hinds TD; Hosick PA; Chen S; Tukey RH; Hankins MW; Nestor-Kalinoski A; Stec DE
[Ad] Endereço:Department of Physiology and Pharmacology, University of Toledo College of Medicine, Toledo, Ohio.
[Ti] Título:Mice with hyperbilirubinemia due to Gilbert's syndrome polymorphism are resistant to hepatic steatosis by decreased serine 73 phosphorylation of PPARα.
[So] Source:Am J Physiol Endocrinol Metab;312(4):E244-E252, 2017 Apr 01.
[Is] ISSN:1522-1555
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Gilbert's syndrome in humans is derived from a polymorphism (TA repeat) in the hepatic gene that results in decreased conjugation and increased levels of unconjugated bilirubin. Recently, we have shown that bilirubin binds directly to the fat-burning nuclear peroxisome proliferator-activated receptor-α (PPARα). Additionally, we have shown that serine 73 phosphorylation [Ser(P) ] of PPARα decreases activity by reducing its protein levels and transcriptional activity. The aim of this study was to determine whether humanized mice with the Gilbert's polymorphism (HuUGT*28) have increased PPARα activation and reduced hepatic fat accumulation. To determine whether humanized mice with Gilbert's mutation (HuUGT*28) have reduced hepatic lipids, we placed them and C57BL/6J control mice on a high-fat (60%) diet for 36 wk. Body weights, fat and lean mass, and fasting blood glucose and insulin levels were measured every 6 wk throughout the investigation. At the end of the study, hepatic lipid content was measured and PPARα regulated genes as well as immunostaining of Ser(P) PPARα from liver sections. The HuUGT*28 mice had increased serum bilirubin, lean body mass, decreased fat mass, and hepatic lipid content as well as lower serum glucose and insulin levels. Also, the HuUGT*28 mice had reduced Ser(P) PPARα immunostaining in livers and increased PPARα transcriptional activity compared with controls. A chronic but mild endogenous increase in unconjugated hyperbiliubinemia protects against hepatic steatosis through a reduction in Ser(P) PPARα, causing an increase in PPARα transcriptional activity.
[Mh] Termos MeSH primário: Fígado Gorduroso/genética
Doença de Gilbert/genética
Hiperbilirrubinemia/genética
PPAR alfa/metabolismo
[Mh] Termos MeSH secundário: Tecido Adiposo/metabolismo
Adiposidade/genética
Animais
Glicemia/metabolismo
Peso Corporal/genética
Fígado Gorduroso/metabolismo
Doença de Gilbert/metabolismo
Hiperbilirrubinemia/metabolismo
Insulina/sangue
Fígado/metabolismo
Masculino
Camundongos
Atividade Motora/fisiologia
Consumo de Oxigênio/fisiologia
Fosforilação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Insulin); 0 (PPAR alpha)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170119
[St] Status:MEDLINE
[do] DOI:10.1152/ajpendo.00396.2016


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[PMID]:27943244
[Au] Autor:Chiddarwar AS; D'Silva SZ; Colah RB; Ghosh K; Mukherjee MB
[Ad] Endereço:National Institute of Immunohaematology (ICMR), K.E.M Hospital Campus, Mumbai, India.
[Ti] Título:Genetic Variations in Bilirubin Metabolism Genes and Their Association with Unconjugated Hyperbilirubinemia in Adults.
[So] Source:Ann Hum Genet;81(1):11-19, 2017 Jan.
[Is] ISSN:1469-1809
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The present study was undertaken to investigate the genotype and allele frequencies of the variants in the four bilirubin metabolism genes (UGT1A1, OATP2, HMOX1, and BLVRA) and their association with hyperbilirubinemia. MATERIAL AND METHODS: Genotyping of 17 genetic variants was performed in 115 adults with hyperbilirubinemia and 150 controls by PCR-RFLP, GeneScan analysis, and direct DNA sequencing. RESULTS: Genetic polymorphisms of the UGT1A1 promoter, specifically the T-3279G phenobarbital-responsive enhancer module and (TA)7 dinucleotide repeat, as well as the intron and coding region variants of the OATP2, HMOX1, and BLVRA genes, were significantly higher among the cases than the controls. Further, nearly 82% of the cases showed the presence of significantly four or more variants as compared to 37% of the controls (P < 0.0001) and the mean total serum bilirubin levels also increased according to the number of variants co-expressed. CONCLUSIONS: This study demonstrates that polymorphisms in the bilirubin metabolism genes had a significant effect on bilirubin levels and could be genetic risk factors for hyperbilirubinemia.
[Mh] Termos MeSH primário: Doença de Gilbert/genética
Glucuronosiltransferase/genética
Heme Oxigenase-1/genética
Oxirredutases atuantes sobre Doadores de Grupo CH-CH/genética
Membro 1b1 da Família de Transportadores de Ânion Orgânico Carreador de Soluto/genética
[Mh] Termos MeSH secundário: Adulto
Estudos de Casos e Controles
Feminino
Frequência do Gene
Estudos de Associação Genética
Predisposição Genética para Doença
Seres Humanos
Desequilíbrio de Ligação
Masculino
Redes e Vias Metabólicas
Meia-Idade
Polimorfismo Genético
Regiões Promotoras Genéticas
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Solute Carrier Organic Anion Transporter Family Member 1b1); EC 1.14.14.18 (HMOX1 protein, human); EC 1.14.14.18 (Heme Oxygenase-1); EC 1.3.- (Oxidoreductases Acting on CH-CH Group Donors); EC 1.3.1.24 (biliverdin reductase); EC 2.4.1.- (UGT1A1 enzyme); EC 2.4.1.17 (Glucuronosyltransferase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170530
[Lr] Data última revisão:
170530
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161213
[St] Status:MEDLINE
[do] DOI:10.1111/ahg.12179


  9 / 796 MEDLINE  
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[PMID]:27251332
[Au] Autor:Bergua A; Hohberger B
[Ad] Endereço:Augenklinik am Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Schwabachanlage 6, 91054, Erlangen, Deutschland. antonio.bergua@uk-erlangen.de.
[Ti] Título:[Unilateral conjunctival chemosis with edematous facial involvement].
[Ti] Título:Einseitige Bindehautchemosis mit ödematöser Gesichtsbeteiligung..
[So] Source:Ophthalmologe;114(2):167-169, 2017 Feb.
[Is] ISSN:1433-0423
[Cp] País de publicação:Germany
[La] Idioma:ger
[Mh] Termos MeSH primário: Doenças da Túnica Conjuntiva/diagnóstico
Doenças da Túnica Conjuntiva/patologia
Edema/diagnóstico
Edema/patologia
Face/patologia
Doença de Gilbert/diagnóstico
Doença de Gilbert/patologia
[Mh] Termos MeSH secundário: Adulto
Diagnóstico Diferencial
Seres Humanos
Masculino
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171014
[Lr] Data última revisão:
171014
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160603
[St] Status:MEDLINE
[do] DOI:10.1007/s00347-016-0284-y


  10 / 796 MEDLINE  
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[PMID]:27978934
[Au] Autor:Sun L; Zhang L; Li M; Teng XY; Qi LM; Zhou XG; Lang ZW; Wang P
[Ad] Endereço:Department of Pathology, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China.
[Ti] Título:[The analysis of UGT1A1 gene mutations in hereditary unconjugated hyperbilirubinemia].
[So] Source:Zhonghua Gan Zang Bing Za Zhi;24(11):863-866, 2016 Nov 20.
[Is] ISSN:1007-3418
[Cp] País de publicação:China
[La] Idioma:chi
[Mh] Termos MeSH primário: Síndrome de Crigler-Najjar
Glucuronosiltransferase/genética
Mutação
[Mh] Termos MeSH secundário: Bilirrubina
Síndrome de Crigler-Najjar/genética
Feminino
Doença de Gilbert
Seres Humanos
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.4.1.- (UGT1A1 enzyme); EC 2.4.1.17 (Glucuronosyltransferase); RFM9X3LJ49 (Bilirubin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170904
[Lr] Data última revisão:
170904
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161217
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1007-3418.2016.11.013



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