Amplification of computational power by the multiplication of bacteria exploring microfluidic networks encoding mathematical problems. [PDF]
Sudalaiyadum Perumal A +12 more
europepmc +1 more source
Partial inhibition of focal adhesion kinase (FAK) can paradoxically promote tumor growth, rather than simply producing a weaker antitumor effect than that observed with strong FAK suppression. In breast cancer and melanoma models, targeting p110δ PI3K, particularly in macrophages, counteracted these tumor‐promoting effects, highlighting the importance ...
Lydia Xenou +4 more
wiley +1 more source
The limits of scaling in aggregation-driven patterning of cell collectives
Zhao ML +4 more
europepmc +1 more source
Smartphone-based Structure-from-Motion for the remote assessment of trunk rotation in spine deformity. [PDF]
Suresh S +9 more
europepmc +1 more source
Unraveling the epigenetic code in cancer cell–tumor microenvironment crosstalk
Epigenetic regulation is a key driver of cancer development and progression. Diverse epigenetic alterations in cancer cells and components of the tumor microenvironment (TME) orchestrate their communication through multiple mechanisms. We discuss how the epigenetic code coordinates bidirectional cancer cell–TME crosstalk to promote cancer progression ...
Ji Hoon Park, Mi‐Young Kim
wiley +1 more source
Dipteran flight diversity is shaped by aerodynamic constraints, scaling, and evolutionary trade-offs. [PDF]
Le Roy C +3 more
europepmc +1 more source
Arginine methylation can be viewed as a persistence‐prone post‐translational modification regulated by a network of PRMTs. Competitive and compensatory interactions among PRMTs can redistribute methylation across substrate pools shaped by sequence, structural, spatial, and environmental layers, reinforcing RNA‐processing, chromatin, and signaling ...
So Hyun Kwon, Ji Min Lee
wiley +1 more source
Response to two letters on omega-3 supplementation and cognitive decline. [PDF]
Liao ZB, Wang YR.
europepmc +1 more source
Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer
Cancer cells' high translational demand creates opportunities to therapeutically target ribosome function. Ribosome stalling and collisions activate ZAKα and the ribotoxic stress response (RSR), which can trigger rapid, p53‐independent apoptosis in cancer.
Anastassiya Kim +7 more
wiley +1 more source
Strategies for pediatric dose derivation from population pharmacokinetic models. [PDF]
Krause A, Cellière G.
europepmc +1 more source

