Results 131 to 140 of about 2,220,924 (260)
Integrating Artificial Intelligence and Point-of-Care Ultrasound Within the Clinical-Scientific Method: A Framework for Safer, Smarter Medicine. [PDF]
Izquierdo-Pretel G.
europepmc +1 more source
Perspective: Dimensions of the scientific method. [PDF]
Voit EO.
europepmc +1 more source
Finding novel vulnerabilities of hypomorphic BRCA1 alleles
Synthetic lethality screens performed to identify novel vulnerabilities often model complete gene loss, thereby overlooking patient‐derived hypomorphic mutations. In this study, we have performed genome‐wide CRISPR screens on BRCA1 hypomorphic mutations, showing BRCA1I26A behaves like wild‐type, while BRCA1R1699Q mimics deficiency. Furthermore, we have
Anne Schreuder +10 more
wiley +1 more source
Irreversibility in quantum mechanics
R. C. Bishop, A. Bohm, M. Gadella
doaj +1 more source
Keeping AI in medicine and radiology within the framework of scientific method: measuring to close the epistemic gap. [PDF]
Pesapane F, Sardanelli F.
europepmc +1 more source
Big data: the end of the scientific method? [PDF]
Succi S, Coveney PV.
europepmc +1 more source
Many patients with urothelial cancer do not benefit from treatment with pembrolizumab, while at risk of severe side effects. Changes in the levels of circulating tumor DNA early during treatment, measured by a simple and affordable assay that can be easily implemented in the clinic, can be used as a prognostic tool to identify these patients.
Youssra Salhi +14 more
wiley +1 more source
MITF maintains genome stability in nonmelanocyte lineages
MITF is essential for melanocyte survival and acts as an oncogene in 10%–20% of melanomas. We show that MITF depletion causes genome instability in nonmelanocytic cells, leading to LATS2‐mediated P53 activation, cell cycle arrest, and apoptosis. This study highlights the role of MITF as a genome maintenance factor beyond the melanocyte lineage. Created
Drifa H. Gudmundsdottir +13 more
wiley +1 more source
The novel styrylquinazolinone‐based molecule W1B effectively suppresses glioblastoma by inhibiting IGF1R and EGFR. In high‐glucose microenvironments driving tumor resistance, W1B acts synergistically with the EGFR inhibitor dacomitinib. This combination safely blocks compensatory survival signaling in zebrafish xenograft models. Showcasing promising in
Patryk Rurka +9 more
wiley +1 more source

