Digital transformation in healthcare - architectures of present and future information technologies.

Healthcare providers all over the world are faced with a single challenge: the need to improve patient outcomes while containing costs. Drivers include an increasing demand for chronic disease management for an aging population, technological advancements and empowered patients taking control of their health experience. The digital transformation in healthcare, through the creation of a rich health data foundation and integration of technologies like the Internet of Things (IoT), advanced analytics, Machine Learning (ML) and Artificial Intelligence (AI), is recognized as a key component to tackle these challenges. It can lead to improvements in diagnostics, prevention and patient therapy, ultimately empowering care givers to use an evidence-based approach to improve clinical decisions. Real-time interactions allow a physician to monitor a patient 'live', instead of interactions once every few weeks. Operational intelligence ensures efficient utilization of healthcare resources and services provided, thereby optimizing costs. However, procedure-based payments, legacy systems, disparate data sources with the limited adoption of data standards, technical debt, data security and privacy concerns impede the efficient usage of health information to maximize value creation for all healthcare stakeholders. This has led to a highly-regulated, constrained industry. Ultimately, the goal is to improve quality of life and saving people's lives through the creation of the intelligent healthcare provider, fully enabled to deliver value-based healthcare and a seamless patient experience. Information technologies that enable this goal must be extensible, safe, reliable and affordable, and tailored to the digitalization maturity-level of the individual organization.

Fibroblast growth factor-2 requires glial-cell-line-derived neurotrophic factor for exerting its neuroprotective actions on glutamate-lesioned hippocampal neurons.

FGF-2 is a potent neurotrophic factor for several populations of CNS neurons and has been shown to protect hippocampal neurons from glutamate-induced cell death in vitro and in vivo. Mechanisms underlying the neurotrophic and protective actions of FGF-2 have been resolved only in part. Using glutamate-treated cultured hippocampal neurons we show that FGF-2 shares its neuroprotective capacity with GDNF. Hippocampal neurons express glial-cell-line-derived neurotrophic factor (GDNF), its receptors c-Ret and the lipid-anchored GDNF family receptor-alpha1 (GFRalpha-1), and the FGF receptor 1 (FGFR I). Neutralizing antibodies to GDNF abolish the neuroprotective effect of FGF-2. In support of the notion that GDNF is required to permit the protective effects of FGF-2 we find that FGF-2 up-regulates GDNF and GFRalpha-1 in hippocampal neurons. Furthermore, FGF-2-induced GDNF causes enhanced phosphorylation of c-Ret and the signaling components Akt and Erk. A putative downstream target of FGF-2 and GDNF are bcl-2 gene family members, whose mRNAs are differentially up-regulated by the two factors. Together, these data suggest that GDNF is an important protective factor for glutamate-lesioned hippocampal neurons and an essential mediator of the neuroprotective actions of FGF-2.