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With the advent of digital healthcare without borders, enormous amounts of health information are captured and computerized. As healthcare quality largely depends on the reliability of given health information, personal health records should be accessible according to patients’ mobility, even as they travel or migrate to other countries. However, since all the health information is scattered in multiple places, it is an onerous task to carry it whenever people move to other countries. To effectively and efficiently utilize health information, interoperability, which is the ability of various healthcare information technologies to exchange, to interpret, and to use data, is needed. Hence, building a robust transnational health information infrastructure with clear interoperability guidelines considering heterogeneous aspects is necessary. For this purpose, this study proposes a Transnational Health Record framework, which enables access to personal health records anywhere. We review related literature and define level-specific interoperability guidelines, business processes, and requirements for the Transnational Health Record system framework.

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Macrophages play an important role in the host defense mechanism. In response to infection, macrophages activate a genetic program of pro-inflammatory response to kill any invading pathogen, and initiate an adaptive immune response. We have identified RUVBL2 - an ATP-binding protein belonging to the AAA+ (ATPase associated with diverse cellular activities) superfamily of ATPases - as a novel regulator in pro-inflammatory response of macrophages. Gene knockdown of Ruvbl2, or pharmacological inhibition of RUVBL1/2 activity, compromises type-2 nitric oxide synthase (Nos2) gene expression, nitric oxide production and anti-bacterial activity of mouse macrophages in response to lipopolysaccharides (LPS). RUVBL1/2 inhibitor similarly inhibits pro-inflammatory response in human monocytes, suggesting functional conservation of RUVBL1/2 in humans. Transcriptome analysis further revealed that major LPS-induced pro-inflammatory pathways in macrophages are regulated in a RUVBL1/2-dependent manner. Furthermore, RUVBL1/2 inhibition significantly reduced the level of histone H3K4me3 at the promoter region of Nos2 and Il6, two prototypical pro-inflammatory genes, and diminished the recruitment of NF-kappaB to the corresponding enhancers. Our study reveals RUVBL1/2 as an integral component of macrophage pro-inflammatory responses through epigenetic regulations, and the therapeutic potentials of RUVBL1/2 inhibitors in the treatment of diseases caused by aberrant activation of pro-inflammatory pathways.