Research on design of hospital inspection information system and HIS interface / 中国医学装备

Objective:To develop an interface program between a hospital inspection information system and Hospital Information System(HIS). Such interface program not only guarantees the safety and independence of HIS, but achieves interoperability between HIS and other third-party system.Methods: The interface program between the inspection information system and HIS conforming to hospital demands is developed by using Visual Studio 2008 development platform and WebServices+XML technology.Results: The interface between the inspection information system and HIS operates stably, reliably and efficiently, avoiding manually input information errors, reducing the amount of registration work, and raising work efficiency.Conclusion:WebServices+XML technology is utilized to develop an interface characterized by safety, stability and reliable performance, realizing resource sharing among information systems in the hospital. Besides, the interface can be expanded in the future to adapt to other third-party system, achieving customization.

XCT790 inhibits rat vascular smooth muscle cells proliferation through down-regulating the expression of estrogen-related receptor alpha / 药学学报

Abnormal proliferation of vascular smooth muscle cells (VSMCs) plays an important role in several pathological processes of cardiovascular diseases. In this study, the effects of XCT790, a potent and selective inverse agonist of estrogen-related receptor alpha (ERRalpha), on rat VSMCs proliferation and related signal pathways were investigated. The proliferative activity of VSMCs was determined by CCK-8 assay. The mRNA levels of ERRalpha, PGC-1alpha, OPN and MCAD were assayed by RT-PCR. The protein levels of ERRalpha, ERK2 and p-ERK1/2 were evaluated by Western blotting. ELISA was used to assess the protein expression of VEGF. The results showed that XCT790 (5-20 micromol x L(-1)) inhibited rat VSMCs proliferation, and the expression of ERRalpha and its target genes, as well as p-ERK1/2, were also inhibited. XCT790 inhibited VSMCs proliferation in a dose-dependent manner at the dose range from 5 to 20 micromol x L(-1) and in a time-dependent manner at the dose range from 10 to 20 micromol x L(-1). These findings demonstrate that XCT790 inhibits rat VSMCs proliferation by down-regulating the gene level of ERRalpha and thus inhibiting the ERK signal pathway, suggesting that ERRalpha may be a novel potential target for therapeutic approaches to inhibit VSMCs proliferation, which plays an important role in several cardiovascular diseases.