ABSTRACT
Defining legislation for electronic prescription systems (EPS) is inherently challenging due to conflicting interests and requirements. The study aimed to develop a comprehensive EPS within the Czech healthcare framework, integrating legislative, process, and technical aspects to ensure security, user acceptability, and compliance with health regulations. A process modeling tool based on hierarchical state machines was employed to create a detailed process architecture for the EPS. Key participants, scenarios, and state transitions were identified and incorporated into a process model using the Craft.CASE based on the BORM methodology. The final process architecture model facilitated interdisciplinary communication and consensus-building among stakeholders, including healthcare professionals, IT specialists, and legislators. The model served as a foundation for the legislative framework and was included in the explanatory memorandum for the draft amendment to the Pharmaceuticals Act. The use of hierarchical state machines and process modeling tools in developing healthcare legislation effectively reduced misunderstandings and ensured precise implementation. This method can be applied to other complex legislative and system design projects, enhancing stakeholder communication and project success.
Subject(s)
Electronic Prescribing , Electronic Prescribing/standards , Czech Republic , HumansABSTRACT
Liver fibrosis is a reversible pathological process caused by chronic liver damage and a major risk factor for hepatocellular carcinoma (HCC). Hepatic stellate cell (HSC) activation is considered the main target for liver fibrosis therapy. However, the efficiency of this strategy is limited due to the complex microenvironment of liver fibrosis, including excessive extracellular matrix (ECM) deposition and hypoxia-induced imbalanced ECM metabolism. Herein, nilotinib (NIL)-loaded hyaluronic acid (HA)-coated Ag@Pt nanotriangular nanozymes (APNH NTs) were developed to inhibit HSCs activation and remodel the microenvironment of liver fibrosis. APNH NTs efficiently eliminated intrahepatic reactive oxygen species (ROS) due to their inherent superoxide dismutase (SOD) and catalase (CAT) activities, thereby downregulating the expression of NADPH oxidase-4 (NOX-4) and inhibiting HSCs activation. Simultaneously, the oxygen produced by the APNH NTs further alleviated the hypoxic microenvironment. Importantly, the released NIL promoted collagen depletion by suppressing the expression of tissue inhibitor of metalloproteinase-1 (TIMP-1), thus synergistically remodeling the microenvironment of liver fibrosis. Notably, an in vivo study in CCl4-induced mice revealed that APNH NTs exhibited significant antifibrogenic effects without obvious long-term toxicity. Taken together, the data from this work suggest that treatment with the synthesized APNH NTs provides an enlightening strategy for remodeling the microenvironment of liver fibrosis with boosted antifibrogenic activity.