Complex networks emerging in natural and human-made systems tend to assume small-world structure. Is there a common mechanism underlying their self-organisation? Our computational simulations show that network diffusion (traffic flow or information transfer) steers network evolution towards emergence of complex network structures. The emergence is effectuated through adaptive rewiring: progressive adaptation of structure to use, creating short-cuts where network diffusion is intensive while annihilating underused connections. With adaptive rewiring as the engine of universal small-worldness, overall diffusion rate tunes the systems' adaptation, biasing local or global connectivity patterns. Whereas the former leads to modularity, the latter provides a preferential attachment regime. As the latter sets in, the resulting small-world structures undergo a critical shift from modular (decentralised) to centralised ones. At the transition point, network structure is hierarchical, balancing modularity and centrality - a characteristic feature found in, for instance, the human brain.
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http://dx.doi.org/10.1038/s41598-017-12589-9 | DOI Listing |
Cancer Sci
December 2024
Division of Molecular Therapeutics, Aichi Cancer Center Research Institute, Nagoya, Japan.
KRAS was long deemed undruggable until the discovery of the switch-II pocket facilitated the development of specific KRAS inhibitors. Despite their introduction into clinical practice, resistance mechanisms can limit their effectiveness. Initially, tumors rely on mutant KRAS, but as they progress, they may shift to alternative pathways, resulting in intrinsic resistance.
View Article and Find Full Text PDFCogn Neurodyn
December 2024
Center for Research, SRM Institute of Science and Technology, Ramapuram, Chennai, 600089 India.
This study delves into the examination of a network of adaptive synapse neurons characterized by a small-world network topology connected through electromagnetic flux and infused with randomness. First, this research extensively explores the existence of the global multi-stability of a single adaptive synapse-based neuron model with magnetic flux. The non-autonomous neuron model exhibits periodically switchable equilibrium states that are strongly related to the transitions between stable and unstable points in every whole periodic cycle, leading to the creation of global multi-stability.
View Article and Find Full Text PDFNPJ Syst Biol Appl
December 2024
Department of Developmental Biology and Genetics, Indian Institute of Science, Bengaluru, 560012, India.
Dysregulated pH is now recognised as a hallmark of cancer. Recent evidence has revealed that the endosomal pH regulator Na/H exchanger NHE9 is upregulated in colorectal cancer to impose a pseudo-starvation state associated with invasion, highlighting an underexplored mechanistic link between adaptive endosomal reprogramming and malignant transformation. In this study, we use a model that quantitatively captures the dynamics of the core regulatory network governing epithelial mesenchymal plasticity.
View Article and Find Full Text PDFCancer Metab
December 2024
Department of Medicine, School of Medicine, University of Louisville, Louisville, KY, 40202, USA.
Background: The efficacy of tyrosine kinase inhibitors (TKIs) targeting the EGFR is limited due to the persistence of drug-tolerant cell populations, leading to therapy resistance. Non-genetic mechanisms, such as metabolic rewiring, play a significant role in driving lung cancer cells into the drug-tolerant state, allowing them to persist under continuous drug treatment.
Methods: Our study employed a comprehensive approach to examine the impact of the glycolytic regulator 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase (PFKFB3) on the adaptivity of lung cancer cells to EGFR TKI therapies.
Cancers (Basel)
December 2024
Division of Molecular Psychoimmunology, Institute for Genetic Medicine, Hokkaido University, Sapporo 060-0818, Japan.
Cancer has long been believed to be a genetic disease caused by the accumulation of mutations in key genes involved in cellular processes. However, recent advances in sequencing technology have demonstrated that cells with cancer driver mutations are also present in normal tissues in response to aging, environmental damage, and chronic inflammation, suggesting that not only intrinsic factors within cancer cells, but also environmental alterations are important key factors in cancer development and progression. Pancreatic cancer tissue is mostly comprised of stromal cells and immune cells.
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