Base de dados : MEDLINE
Pesquisa : C16.320 [Categoria DeCS]
Referências encontradas : 12779 [refinar]
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[PMID]:28457858
[Au] Autor:Srinivas M; Verselis VK; White TW
[Ad] Endereço:Department of Biological and Vision Sciences, SUNY College of Optometry, New York, NY 10036, USA.
[Ti] Título:Human diseases associated with connexin mutations.
[So] Source:Biochim Biophys Acta;1860(1):192-201, 2018 01.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Gap junctions and hemichannels comprised of connexins impact many cellular processes. Significant advances in our understanding of the functional role of these channels have been made by the identification of a host of genetic diseases caused by connexin mutations. Prominent features of connexin disorders are the inability of other connexins expressed in the same cell type to compensate for the mutated one, and the ability of connexin mutants to dominantly influence the activity of other wild-type connexins. Functional studies have begun to identify some of the underlying mechanisms whereby connexin channel mutation contributes to the disease state. Detailed mechanistic understanding of these functional differences will help to facilitate new pathophysiology driven therapies for the diverse array of connexin genetic disorders. This article is part of a Special Issue entitled: Gap Junction Proteins edited by Jean Claude Herve.
[Mh] Termos MeSH primário: Conexinas/genética
Conexinas/metabolismo
Doenças Genéticas Inatas
[Mh] Termos MeSH secundário: Doenças Genéticas Inatas/genética
Doenças Genéticas Inatas/metabolismo
Doenças Genéticas Inatas/patologia
Doenças Genéticas Inatas/terapia
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; REVIEW
[Nm] Nome de substância:
0 (Connexins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


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[PMID]:29305302
[Au] Autor:Bukowska B; Karwowski BT
[Ad] Endereço:Food Science Department, Faculty of Pharmacy, Medical University of Lodz, Muszynskiego 1, 90-151 Lodz, Poland. Electronic address: barbara.bukowska@umed.lodz.pl.
[Ti] Título:Actual state of knowledge in the field of diseases related with defective nucleotide excision repair.
[So] Source:Life Sci;195:6-18, 2018 Feb 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Xeroderma pigmentosum (XP), trichothiodystrophy (TTD) and Cockayne syndrome (CS) are rare genetic diseases characterized by a large range of clinical symptoms. However, they are all associated with defects in nucleotide excision repair (NER), the system responsible for removing bulky DNA lesions such as those generated by UV light: cyclobutane pyrimidine dimers (CPDs) and pyrimidine-pyrimidone photoproducts (6-4 PPs). Over the past years, detailed structural and biochemical information on NER-associated proteins has emerged. In the first part of the article we briefly present the main steps of the NER pathway with an emphasis on the precise role of certain proteins. Further, we focus on clinical manifestations of the disorders and describe the diagnostic procedures. Then we consider how current therapy and advanced technology could improve patients' quality of life. Although to date the discussed diseases remain incurable, effective sun protection, a well thought out diet, and holistic medical care provide longer life and better health. This review summarizes the current state of knowledge regarding the epidemiology of NER-associated diseases, their genetic background, clinical features, and treatment options.
[Mh] Termos MeSH primário: Reparo do DNA/genética
Reparo do DNA/fisiologia
Doenças Genéticas Inatas/genética
[Mh] Termos MeSH secundário: Animais
Síndrome de Cockayne/genética
Seres Humanos
Síndromes de Tricotiodistrofia/genética
Xeroderma Pigmentoso/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180107
[St] Status:MEDLINE


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[PMID]:29326244
[Au] Autor:Dunbar CE; High KA; Joung JK; Kohn DB; Ozawa K; Sadelain M
[Ad] Endereço:Hematology Branch, National Heart, Lung and Blood Institute, Bethesda, MD, USA. dunbarc@nhlbi.nih.gov m-sadelain@ski.mskcc.org.
[Ti] Título:Gene therapy comes of age.
[So] Source:Science;359(6372), 2018 01 12.
[Is] ISSN:1095-9203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:After almost 30 years of promise tempered by setbacks, gene therapies are rapidly becoming a critical component of the therapeutic armamentarium for a variety of inherited and acquired human diseases. Gene therapies for inherited immune disorders, hemophilia, eye and neurodegenerative disorders, and lymphoid cancers recently progressed to approved drug status in the United States and Europe, or are anticipated to receive approval in the near future. In this Review, we discuss milestones in the development of gene therapies, focusing on direct in vivo administration of viral vectors and adoptive transfer of genetically engineered T cells or hematopoietic stem cells. We also discuss emerging genome editing technologies that should further advance the scope and efficacy of gene therapy approaches.
[Mh] Termos MeSH primário: Terapia Genética
[Mh] Termos MeSH secundário: Animais
Edição de Genes
Técnicas de Transferência de Genes
Doenças Genéticas Inatas/terapia
Engenharia Genética
Terapia Genética/efeitos adversos
Vetores Genéticos
Doenças Hematológicas/terapia
Seres Humanos
Neoplasias/terapia
Doenças Neuromusculares/terapia
Pesquisa Médica Translacional
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180113
[St] Status:MEDLINE


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[PMID]:29255211
[Au] Autor:Schmidt RE; Grimbacher B; Witte T
[Ad] Endereço:Klinik für Immunologie und Rheumatologie, Medizinische Hochschule Hannover (MHH), Carl-Neuberg Straße 1, D-30625 Hannover, Germany.
[Ti] Título:Autoimmunity and primary immunodeficiency: two sides of the same coin?
[So] Source:Nat Rev Rheumatol;14(1):7-18, 2017 Dec 19.
[Is] ISSN:1759-4804
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Autoimmunity and immunodeficiency were previously considered to be mutually exclusive conditions; however, increased understanding of the complex immune regulatory and signalling mechanisms involved, coupled with the application of genetic analysis, is revealing the complex relationships between primary immunodeficiency syndromes and autoimmune diseases. Single-gene defects can cause rare diseases that predominantly present with autoimmune symptoms. Such genetic defects also predispose individuals to recurrent infections (a hallmark of immunodeficiency) and can cause primary immunodeficiencies, which can also lead to immune dysregulation and autoimmunity. Moreover, risk factors for polygenic rheumatic diseases often exist in the same genes as the mutations that give rise to primary immunodeficiency syndromes. In this Review, various primary immunodeficiency syndromes are presented, along with their pathogenetic mechanisms and relationship to autoimmune diseases, in an effort to increase awareness of immunodeficiencies that occur concurrently with autoimmune diseases and to highlight the need to initiate appropriate genetic tests. The growing knowledge of various genetically determined pathologic mechanisms in patients with immunodeficiencies who have autoimmune symptoms opens up new avenues for personalized molecular therapies that could potentially treat immunodeficiency and autoimmunity at the same time, and that could be further explored in the context of autoimmune rheumatic diseases.
[Mh] Termos MeSH primário: Doenças Autoimunes/imunologia
Autoimunidade/imunologia
Síndromes de Imunodeficiência/imunologia
Doenças Reumáticas/imunologia
[Mh] Termos MeSH secundário: Artrite Reumatoide/genética
Artrite Reumatoide/imunologia
Doenças Autoimunes/terapia
Autoimunidade/genética
Diagnóstico Diferencial
Doenças Genéticas Inatas/complicações
Doenças Genéticas Inatas/genética
Doenças Genéticas Inatas/imunologia
Predisposição Genética para Doença
Estudo de Associação Genômica Ampla/métodos
Seres Humanos
Síndromes de Imunodeficiência/genética
Síndromes de Imunodeficiência/terapia
Lúpus Eritematoso Sistêmico/genética
Lúpus Eritematoso Sistêmico/imunologia
Terapia de Alvo Molecular/métodos
Mutação
Doenças Raras/genética
Doenças Reumáticas/genética
Doenças Reumáticas/terapia
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171227
[Lr] Data última revisão:
171227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE
[do] DOI:10.1038/nrrheum.2017.198


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[PMID]:29190701
[Au] Autor:Hsieh AR; Chen DP; Chattopadhyay AS; Li YJ; Chang CC; Fann CSJ
[Ad] Endereço:Graduate Institute of Biostatistics, China Medical University, Taichung, Taiwan.
[Ti] Título:A non-threshold region-specific method for detecting rare variants in complex diseases.
[So] Source:PLoS One;12(11):e0188566, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A region-specific method, NTR (non-threshold rare) variant detection method, was developed-it does not use the threshold for defining rare variants and accounts for directions of effects. NTR also considers linkage disequilibrium within the region and accommodates common and rare variants simultaneously. NTR weighs variants according to minor allele frequency and odds ratio to combine the effects of common and rare variants on disease occurrence into a single score and provides a test statistic to assess the significance of the score. In the simulations, under different effect sizes, the power of NTR increased as the effect size increased, and the type I error of our method was controlled well. Moreover, NTR was compared with several other existing methods, including the combined multivariate and collapsing method (CMC), weighted sum statistic method (WSS), sequence kernel association test (SKAT), and its modification, SKAT-O. NTR yields comparable or better power in simulations, especially when the effects of linkage disequilibrium between variants were at least moderate. In an analysis of diabetic nephropathy data, NTR detected more confirmed disease-related genes than the other aforementioned methods. NTR can thus be used as a complementary tool to help in dissecting the etiology of complex diseases.
[Mh] Termos MeSH primário: Doenças Genéticas Inatas/genética
[Mh] Termos MeSH secundário: Estudos de Associação Genética
Seres Humanos
Desequilíbrio de Ligação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188566


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[PMID]:29192748
[Au] Autor:Hernán Martínez J; Mangual Garcia MM; Gutiérrez Acevedo M; Sánchez Cruz A; Laboy I; Rivera C; Mansilla P; Palermo Garofalo C; Lourdes Miranda M; Torres Rafael O
[Ti] Título:A middle aged woman with isolated ACTH deficiency associated with transient growth hormone deficiency.
[So] Source:Bol Asoc Med P R;108(1):3-6, 2016.
[Is] ISSN:0004-4849
[Cp] País de publicação:Puerto Rico
[La] Idioma:eng
[Ab] Resumo:Isolated ACTH deficiency (IAD) is a rare entity characterized by secondary adrenal insufficiency with low levels of serum cortisol, decreased production of ACTH, adequate secretion of other pituitary hormones and normal pituitary structure on radioimaging. The prevalence of IAD as a cause of secondary adrenal insufficiency has not been determined. Impairment of growth hormone (GH) secretion has been noted in 20 to 30% of patients with IAD which is normalized after glucocorticoid replacement. We report the case of a 50 years-old female with symptoms and laboratory results suggestive of adrenal insufficiency. Insulin tolerance test confirmed ACTH and growth hormone deficiency. The rest of the anterior pituitary hormones were normal. A pituitary MRI was unremarkable. Glucocorticoid replacement therapy started and eight months afterwards glucagon stimulation test revealed persistent ACTH deficiency but nor- mal growth hormone secretion. IAD can present with nonspecific symptoms and could be potentially fatal in an acute stressful period. Prompt recognition is essential to decrease morbidity and mortality.
[Mh] Termos MeSH primário: Hormônio Adrenocorticotrópico/deficiência
Doenças do Sistema Endócrino/complicações
Doenças Genéticas Inatas/complicações
Glucocorticoides/administração & dosagem
Hormônio do Crescimento Humano/deficiência
Hipoglicemia/complicações
Resistência à Insulina
[Mh] Termos MeSH secundário: Doenças do Sistema Endócrino/diagnóstico
Feminino
Doenças Genéticas Inatas/diagnóstico
Terapia de Reposição Hormonal/métodos
Seres Humanos
Hipoglicemia/diagnóstico
Meia-Idade
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucocorticoids); 12629-01-5 (Human Growth Hormone); 9002-60-2 (Adrenocorticotropic Hormone)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171214
[Lr] Data última revisão:
171214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE


  7 / 12779 MEDLINE  
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[PMID]:29095280
[Au] Autor:Zeng MF; Chen L; Ye HY; Gong W; Zhou LN; Li YM; Zhao XL
[Ad] Endereço:aDepartment of Endocrinology, Huashan Hospital North bDepartment of Endocrinology, Huashan Hospital, Fudan University, Shanghai, China.
[Ti] Título:Primary hypothyroidism and isolated ACTH deficiency induced by nivolumab therapy: Case report and review.
[So] Source:Medicine (Baltimore);96(44):e8426, 2017 Nov.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Nivolumab is a monoclonal IgG antibody blocking programmed death receptor-1 (PD1), leading to restoration of the natural T-cell-mediated immune response against the cancer cells. However, it also causes plenty of autoimmune-related adverse events, which often involves endocrine system. PATIENT CONCERNS: A 54-year-old male with renal clear cell carcinoma was treated with nivolumab intravenously. Routine monitoring showed elevated thyroid-stimulating hormone and low free thyroxine after the 6th administration of nivolumab. After the 12th administration, he developed general fatigue, recurrent hypoglycemia, and relative hypotension. Laboratory tests showed low sodium, low morning cortisol without correspondence increase of corticotrophin (ACTH). Other pituitary hormones were normal. MRI showed no space-occupying lesions, but heterogeneous enhancement of the pituitary gland. DIAGNOSES: Primary hypothyroidism and isolated ACTH deficiency. The etiologies were assumed to be nivolumab induced autoimmune lymphocytic thyroiditis and hypophysitis, respectively. INTERVENTIONS: Hormone replacements with levothyroxine and acetate cortisone were given orally. Nivolumab was adjusted to lower dose and longer interval. OUTCOMES: The patient felt good after adequate replacement. Nivolumab was returned to routine dose and interval six months later. And the metastasis was not obviously progressed during this time. LESSONS: The present report provides the first detailed presentation of combined hypothyroidism and isolated ACTH deficiency induced by nivolumab. Adrenal deficiency often develops insidiously. We suggest routine monitoring of fasting blood-glucose, blood pressure and serum sodium as well as thyroid function during nivolumab and other cancer immunotherapies. When unexpected fatigue, hypoglycemia, hypotension or hyponatremia appeared, adrenal deficiency should be taken into consideration.
[Mh] Termos MeSH primário: Hormônio Adrenocorticotrópico/deficiência
Anticorpos Monoclonais/efeitos adversos
Antineoplásicos/efeitos adversos
Carcinoma de Células Renais/tratamento farmacológico
Doenças do Sistema Endócrino/induzido quimicamente
Doenças Genéticas Inatas/induzido quimicamente
Hipoglicemia/induzido quimicamente
Hipotireoidismo/induzido quimicamente
Neoplasias Renais/tratamento farmacológico
[Mh] Termos MeSH secundário: Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antineoplastic Agents); 31YO63LBSN (nivolumab); 9002-60-2 (Adrenocorticotropic Hormone)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171103
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008426


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[PMID]:29029902
[Au] Autor:Wilder EG; Frieder J; Sulhan S; Michel P; Cizenski JD; Wright JM; Menter MA
[Ad] Endereço:Division of Dermatology, Baylor University Medical Center, Dallas, Texas.
[Ti] Título:Spectrum of orocutaneous disease associations: Genodermatoses and inflammatory conditions.
[So] Source:J Am Acad Dermatol;77(5):809-830, 2017 Nov.
[Is] ISSN:1097-6787
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The oral cavity and cutaneous organ systems share a close embryologic origin. Therefore, there are numerous dermatologic conditions presenting with concomitant oral findings of which the dermatologist must be aware. The second article in this continuing medical education series reviews inflammatory orocutaneous conditions and a number of genodermatoses. It is essential for dermatologists to be familiar with oral cavity manifestations associated with dermatologic diseases for prompt diagnosis, management, and appropriate referral to stomatology and dentistry.
[Mh] Termos MeSH primário: Doenças Genéticas Inatas/genética
Predisposição Genética para Doença/epidemiologia
Doenças da Boca/genética
Dermatopatias/genética
[Mh] Termos MeSH secundário: Doença de Darier/epidemiologia
Doença de Darier/genética
Doença de Darier/fisiopatologia
Educação Médica Continuada
Epiderme/patologia
Feminino
Doenças Genéticas Inatas/epidemiologia
Doenças Genéticas Inatas/fisiopatologia
Seres Humanos
Incidência
Masculino
Doenças da Boca/epidemiologia
Doenças da Boca/fisiopatologia
Mucosa Bucal/patologia
Prognóstico
Doenças Raras
Medição de Risco
Dermatopatias/epidemiologia
Dermatopatias/fisiopatologia
Neoplasias Cutâneas/epidemiologia
Neoplasias Cutâneas/genética
Neoplasias Cutâneas/fisiopatologia
Esclerose Tuberosa/epidemiologia
Esclerose Tuberosa/genética
Esclerose Tuberosa/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171015
[St] Status:MEDLINE


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[PMID]:28985496
[Au] Autor:Quinodoz M; Royer-Bertrand B; Cisarova K; Di Gioia SA; Superti-Furga A; Rivolta C
[Ad] Endereço:Department of Computational Biology, Unit of Medical Genetics, University of Lausanne, 1011 Lausanne, Switzerland.
[Ti] Título:DOMINO: Using Machine Learning to Predict Genes Associated with Dominant Disorders.
[So] Source:Am J Hum Genet;101(4):623-629, 2017 Oct 05.
[Is] ISSN:1537-6605
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In contrast to recessive conditions with biallelic inheritance, identification of dominant (monoallelic) mutations for Mendelian disorders is more difficult, because of the abundance of benign heterozygous variants that act as massive background noise (typically, in a 400:1 excess ratio). To reduce this overflow of false positives in next-generation sequencing (NGS) screens, we developed DOMINO, a tool assessing the likelihood for a gene to harbor dominant changes. Unlike commonly-used predictors of pathogenicity, DOMINO takes into consideration features that are the properties of genes, rather than of variants. It uses a machine-learning approach to extract discriminant information from a broad array of features (N = 432), including: genomic data, intra-, and interspecies conservation, gene expression, protein-protein interactions, protein structure, etc. DOMINO's iterative architecture includes a training process on 985 genes with well-established inheritance patterns for Mendelian conditions, and repeated cross-validation that optimizes its discriminant power. When validated on 99 newly-discovered genes with pathogenic mutations, the algorithm displays an excellent final performance, with an area under the curve (AUC) of 0.92. Furthermore, unsupervised analysis by DOMINO of real sets of NGS data from individuals with intellectual disability or epilepsy correctly recognizes known genes and predicts 9 new candidates, with very high confidence. In summary, DOMINO is a robust and reliable tool that can infer dominance of candidate genes with high sensitivity and specificity, making it a useful complement to any NGS pipeline dealing with the analysis of the morbid human genome.
[Mh] Termos MeSH primário: Genes Dominantes
Doenças Genéticas Inatas/genética
Sequenciamento de Nucleotídeos em Larga Escala/métodos
Aprendizado de Máquina
Mutação
Software
[Mh] Termos MeSH secundário: Bases de Dados Genéticas
Genoma Humano
Genômica
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171007
[St] Status:MEDLINE


  10 / 12779 MEDLINE  
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[PMID]:28981501
[Au] Autor:Paternoster L; Tilling K; Davey Smith G
[Ad] Endereço:Medical Research Council Integrative Epidemiology Unit, University of Bristol, Bristol, United Kingdom.
[Ti] Título:Genetic epidemiology and Mendelian randomization for informing disease therapeutics: Conceptual and methodological challenges.
[So] Source:PLoS Genet;13(10):e1006944, 2017 Oct.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The past decade has been proclaimed as a hugely successful era of gene discovery through the high yields of many genome-wide association studies (GWAS). However, much of the perceived benefit of such discoveries lies in the promise that the identification of genes that influence disease would directly translate into the identification of potential therapeutic targets, but this has yet to be realized at a level reflecting expectation. One reason for this, we suggest, is that GWAS, to date, have generally not focused on phenotypes that directly relate to the progression of disease and thus speak to disease treatment.
[Mh] Termos MeSH primário: Doença das Coronárias/genética
Doenças Genéticas Inatas/genética
Estudo de Associação Genômica Ampla
Análise da Randomização Mendeliana
[Mh] Termos MeSH secundário: Doença das Coronárias/epidemiologia
Doença das Coronárias/terapia
Progressão da Doença
Doenças Genéticas Inatas/epidemiologia
Doenças Genéticas Inatas/patologia
Doenças Genéticas Inatas/terapia
Predisposição Genética para Doença
Seres Humanos
Fenótipo
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171022
[Lr] Data última revisão:
171022
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171006
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1006944



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