V-Model: a new perspective for EHR-based phenotyping

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited.Abstract Background Narrative resources in electronic health records make clinical phenotyping study difficult to achieve. If a narrative patient history can be represented in a timeline, this would greatly enhance the efficiency of information-based studies. However, current timeline representations have limitations in visualizing narrative events. In this paper, we propose a temporal model named the V-Model which visualizes clinical narratives into a timeline. Methods We developed the V-Model which models temporal clinical events in v-like graphical structure. It visualizes patient history on a timeline in an intuitive way. For the design, the representation, reasoning, and visualization (readability) aspects were considered. Furthermore, the unique graphical notation helps to find hidden patterns of a specific patient group. For evaluation, we verified our distinctive solutions, and surveyed usability. The experiments were carried out between the V-Model and a conventional timeline model group. Eighty medical students and physicians participated in this evaluation. Results The V-Model was proven to be superior in representing narrative medical events, provide sufficient information for temporal reasoning, and outperform in readability compared to a conventional timeline model. The usability of the V-Model was assessed as positive. Conclusions The V-Model successfully resolves visualization issues of clinical documents, and provides better usability compared to a conventional timeline model

Influence of Solute Size on Membrane Fouling during Polysaccharide Enrichment Using Dense Polymeric UF Membrane: Measurements and Mechanisms

Fouling mechanisms associated with membrane-based polysaccharide enrichment were determined using a dense ultrafiltration (UF) membrane. Dextran with different molecular weights (MWs) was used as a surrogate for polysaccharides. The influence of dextran MW on fouling mechanisms was quantified using the Hermia model. Flux data obtained with different dextran MWs and filtration cycles were plotted to quantify the more appropriate fouling mechanisms among complete pore blocking, standard pore blocking, intermediate pore blocking, and cake filtration. For 100,000 Da dextran, all four mechanisms contributed to the initial fouling. As the filtration progressed, the dominant fouling mechanism appeared to be cake filtration with a regression coefficient (R2) of approximately 0.9519. For 10,000 Da, the R2 value for cake filtration was about 0.8767 in the initial filtration. Then, the R2 value gradually decreased as the filtration progressed. For 6000 Da, the R2 values of the four mechanisms were very low in the initial filtration. However, as the filtration progressed, the R2 value for cake filtration reached 0.9057. These results clearly show that the fouling mechanism of dense UF membranes during polysaccharide enrichment can be quantified. In addition, it was confirmed that the dominant fouling mechanism can change with the size of the polysaccharide and the duration of filtration

Chronic expression of interferon-gamma leads to murine autoimmune cholangitis with a female predominance

In most autoimmune diseases the serologic hallmarks of disease precede clinical pathology by years. Therefore, the use of animal models in defining early disease events becomes critical. We took advantage of a “designer” mouse with dysregulation of interferon gamma (IFNγ) characterized by prolonged and chronic expression of IFNγ through deletion of the IFNγ 3′-untranslated region adenylate uridylate-rich element (ARE). The ARE-Del-/- mice develop primary biliary cholangitis (PBC) with a female predominance that mimics human PBC that is characterized by up-regulation of total bile acids, spontaneous production of anti-mitochondrial antibodies, and portal duct inflammation. Transfer of CD4 T cells from ARE-Del-/- to B6/Rag1-/- mice induced moderate portal inflammation and parenchymal inflammation, and RNA sequencing of liver gene expression revealed that up-regulated genes potentially define early stages of cholangitis. Interestingly, up-regulated genes specifically overlap with the gene expression signature of biliary epithelial cells in PBC, implying that IFNγ may play a pathogenic role in biliary epithelial cells in the initiation stage of PBC. Moreover, differentially expressed genes in female mice have stronger type 1 and type 2 IFN signaling and lymphocyte-mediated immune responses and thus may drive the female bias of the disease. Conclusion: Changes in IFNγ expression are critical for the pathogenesis of PBC. (Hepatology 2016;64:1189-1201)