RESUMO
OBJECTIVE: To visualize and describe collaborative electronic health record (EHR) usage for hospitalized patients with heart failure. MATERIALS AND METHODS: We identified records of patients with heart failure and all associated healthcare provider record usage through queries of the Northwestern Medicine Enterprise Data Warehouse. We constructed a network by equating access and updates of a patient's EHR to a provider-patient interaction. We then considered shared patient record access as the basis for a second network that we termed the provider collaboration network. We calculated network statistics, the modularity of provider interactions, and provider cliques. RESULTS: We identified 548 patient records accessed by 5113 healthcare providers in 2012. The provider collaboration network had 1504 nodes and 83 998 edges. We identified 7 major provider collaboration modules. Average clique size was 87.9 providers. We used a graph database to demonstrate an ad hoc query of our provider-patient network. DISCUSSION: Our analysis suggests a large number of healthcare providers across a wide variety of professions access records of patients with heart failure during their hospital stay. This shared record access tends to take place not only in a pairwise manner but also among large groups of providers. CONCLUSION: EHRs encode valuable interactions, implicitly or explicitly, between patients and providers. Network analysis provided strong evidence of multidisciplinary record access of patients with heart failure across teams of 100+ providers. Further investigation may lead to clearer understanding of how record access information can be used to strategically guide care coordination for patients hospitalized for heart failure.
Assuntos
Apresentação de Dados , Registros Eletrônicos de Saúde/estatística & dados numéricos , Insuficiência Cardíaca , Reconhecimento Automatizado de Padrão , Mineração de Dados , Pessoal de Saúde , Hospitalização , Humanos , Interface Usuário-ComputadorRESUMO
Plasma lipoprotein(a) (Lp[a]) level is an independent risk factor of cardiovascular disease that is under strong genetic control. We conducted a genome-wide association study of plasma Lp(a) in 386 members of a founder population that adheres to a communal lifestyle, proscribes cigarette smoking, and prepares and eats meals communally. We identified associations with 77 single nucleotide polymorphisms (SNPs) spanning 12.5 Mb on chromosome 6q26-q27 that met criteria for genome-wide significance (P Assuntos
Cromossomos Humanos Par 6/genética
, Estudo de Associação Genômica Ampla
, Lipoproteína(a)
, Isoformas de Proteínas
, Animais
, Mapeamento Cromossômico
, Elementos Facilitadores Genéticos
, Predisposição Genética para Doença
, Genótipo
, Humanos
, Kringles/genética
, Desequilíbrio de Ligação
, Lipoproteína(a)/sangue
, Lipoproteína(a)/genética
, Polimorfismo de Nucleotídeo Único
, Isoformas de Proteínas/sangue
, Isoformas de Proteínas/genética
, Religião
, South Dakota
, População Branca/genética
RESUMO
BACKGROUND: Evolutionarily conserved sequences likely have biological function. METHODS: To determine whether variation in conserved sequences in non-coding DNA contributes to risk for human disease, we studied six conserved non-coding elements in the Th2 cytokine cluster on human chromosome 5q31 in a large Hutterite pedigree and in samples of outbred European American and African American asthma cases and controls. RESULTS: Among six conserved non-coding elements (> 100 bp, > 70% identity; human-mouse comparison), we identified one single nucleotide polymorphism (SNP) in each of two conserved elements and six SNPs in the flanking regions of three conserved elements. We genotyped our samples for four of these SNPs and an additional three SNPs each in the IL13 and IL4 genes. While there was only modest evidence for association with single SNPs in the Hutterite and European American samples (P < 0.05), there were highly significant associations in European Americans between asthma and haplotypes comprised of SNPs in the IL4 gene (P < 0.001), including a SNP in a conserved non-coding element. Furthermore, variation in the IL13 gene was strongly associated with total IgE (P = 0.00022) and allergic sensitization to mold allergens (P = 0.00076) in the Hutterites, and more modestly associated with sensitization to molds in the European Americans and African Americans (P < 0.01). CONCLUSION: These results indicate that there is overall little variation in the conserved non-coding elements on 5q31, but variation in IL4 and IL13, including possibly one SNP in a conserved element, influence asthma and atopic phenotypes in diverse populations.
Assuntos
Asma/genética , Cromossomos Humanos Par 5/genética , Interleucina-13/genética , Interleucina-4/genética , Hipersensibilidade Respiratória/genética , Sequência Conservada/genética , Predisposição Genética para Doença/genética , Testes Genéticos/métodos , Variação Genética/genética , Heterozigoto , Humanos , Linhagem , Polimorfismo de Nucleotídeo Único/genética , Análise de Sequência de DNARESUMO
The establishment of ICOS as an important regulator of Th2 development and effector function makes the ICOS locus an attractive candidate for Th2-mediated diseases, such as asthma and allergy. In evaluation of this candidate locus in humans, we identified 11 variants and determined that two in the putative promoter region are significantly associated with allergic sensitization and serum IgE levels. In addition, cultures of activated PBMCs from individuals homozygous for the associated polymorphisms produced increased levels of the Th2 cytokines, IL-4, IL-5, and IL-13, as well as TNF-alpha compared with controls. One of the polymorphisms, -1413G/A, demonstrated differential NF-kappaB binding in mobility shift analysis, suggesting that this polymorphism has functional consequences. Overall, these data demonstrate that ICOS is a susceptibility gene for allergic sensitization, perhaps through the promotion of Th2 differentiation.
