STAMINA: Bioinformatics Platform for Monitoring and Mitigating Pandemic Outbreaks

Data Availability Statement: All data driven applications used the our world in data COVID-19 datasets, complimented by proprietary datasets share by the STAMINA consortium.Copyright © 2022 by the authors. This paper presents the components and integrated outcome of a system that aims to achieve early detection, monitoring and mitigation of pandemic outbreaks. The architecture of the platform aims at providing a number of pandemic-response-related services, on a modular basis, that allows for the easy customization of the platform to address user’s needs per case. This customization is achieved through its ability to deploy only the necessary, loosely coupled services and tools for each case, and by providing a common authentication, data storage and data exchange infrastructure. This way, the platform can provide the necessary services without the burden of additional services that are not of use in the current deployment (e.g., predictive models for pathogens that are not endemic to the deployment area). All the decisions taken for the communication and integration of the tools that compose the platform adhere to this basic principle. The tools presented here as well as their integration is part of the project STAMINA.The paper presented is based on research undertaken as part of the European Commission-funded project STAMINA (Grant Agreement 883441)

Self-administration of methohexital, midazolam and ethanol: effects on the pituitary–adrenal axis in rhesus monkeys

There is disagreement in the literature with respect to how drugs of abuse affect the functioning of the hypothalamic–pituitary–adrenal (HPA) axis, and whether these changes in endocrine function may be related to the rewarding effects of these drugs.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/46363/1/213_2004_Article_1986.pd

Effect of Sodium Valproate On Naloxone-Stimulated Acth and Cortisol Release in Humans

1. Gamma-aminobutyric acid (GABA) and endogenous opioids each inhibit hypothalamic CRH secretion. In humans, the opioid antagonist, naloxone, stimulates the release of CRH, and so of ACTH and cortisol, while alprazolam, an indirect GABA(A) agonist, blocks naloxone-induced ACTH and cortisol secretion. Sodium valproate (SV) inhibits ACTH release in response to CRH, metyrapone and substance P. We hypothesized that, if this action is GABA(A)-mediated, SV should also inhibit naloxone-stimulated ACTH release