WHO to collaborate with ReAct in fight against antibiotic resistance

sperm, brain tumours, Common drugs, diabetes, chronic wounds, magnetism, intestinal tumours, molecular scissors, disease, genetic, immune cells, drug development, Diabetes, Antibiotic, hydrogen generation, chronic obstructive pulmonary disease, malaria, photosynthesis, kidney failure, Brain tumours, mental health, blood cancer, cancer, dementia, cancer treatment, antibiotic resistance, blood vessel leakage, quantum simulations, atrial fibrillation, batteries, goiter treatment, terahertz radiation, organic materials , Guild of European Research Intensive Universities, gene copies, social anxiety, blue light screens, ‘Our hope is that these findings will make it possible to discover a way to selectively inhibit the TGF-beta signals that stimulate tumour development without knocking out the signals that inhibit tumour development, and that this can eventually be used in the fight against cancer,’ says Eleftheria Vasilaki, postdoctoral researcher at Ludwig Institute for Cancer Research at Uppsala University and lead author of the study. TGF-beta regulates cell growth and specialisation, in particular during foetal development. In the context of tumour development, TGF-beta has a complicated role. Initially, it inhibits tumour formation because it inhibits cell division and stimulates cell death. At a late stage of tumour development, however, TGF-beta stimulates proliferation and metastasis of tumour cells and thereby accelerates tumour formation. TGF-beta’s signalling mechanisms and role in tumour development have been studied at the Ludwig Institute for Cancer Research at Uppsala University for the past 30 years. Recent discoveries at the Institute, now published in the current study in Science Signaling, explain part of the mechanism by which TGF-beta switches from suppressing to enhancing tumour development. Uppsala researchers, in collaboration with a Japanese research team, discovered that TGF-beta along with the oncoprotein Ras, which is often activated in tumours, affects members of the p53 family. The p53 protein plays a key role in regulating tumour development and is often altered – mutated – in tumours. TGF-beta and Ras suppress the effect of mutated p53, thereby enhancing the effect of another member of the p53 family, namely delta-Np63, which in turn stimulates tumour development and metastasis.

The Uppsala University-based network ReAct recently presented a so-called Toolbox developed to guide actors in curbing antimicrobial resistance at a WHO regional workshop in Morocco. WHO has decided to promote the tool.

Last year, WHO adopted a Global Action Plan on Antibiotic Resistance, and later that year, the global network ReAct released a so-called Toolbox, with advice and checklists for actors that wish to take action against antibiotic resistance. Now, WHO has decided to recommend it to any member states that are in the process of implementing their own national action plans.

The meeting in Morocco was arranged by WHO EMRO (Eastern Mediterranean Regional Office), which includes 22 member states in the Middle East and Northern Africa. The participants are practicing medical workers and policymakers from a number of different organisations in the countries of the region. The main purpose of the meeting was to provide participants with tools for implementing their own national action plans, based on the action plan provided by WHO, in their respective countries.

‘We are very pleased that WHO will integrate the ReAct Toolbox in their work, and we are pleased to contribute to this workshop,’ said Anna Zorzet, Grant Manager and Coordinator, ReAct Europe.

The ReAct Toolbox is a web-based resource which gathers information, advice and checklists to be used in the fight against antibiotic resistance.