Phase response curves (PRCs) are widely used in circadian clocks, neuroscience, and heart physiology. They quantify the response of an oscillator to pulse-like perturbations. Phase response curves provide valuable information on the properties of oscillators and their synchronization. This chapter discusses biological self-sustained oscillators (circadian clock, physiological rhythms, etc.) in the context of nonlinear dynamics theory. Coupled oscillators can synchronize with different frequency ratios, can generate toroidal dynamics (superposition of independent frequencies), and may lead to deterministic chaos. These nonlinear phenomena can be analyzed with the aid of a phase transition curve, which is intimately related to the phase response curve. For illustration purposes, this chapter discusses a model of circadian oscillations based on a delayed negative feedback. In a second part, the chapter provides a step-by-step recipe to measure phase response curves. It discusses specifications of this recipe for circadian rhythms, heart rhythms, neuronal spikes, central pattern generators, and insect communication. Finally, it stresses the predictive power of measured phase response curves. PRCs can be used to quantify the coupling strength of oscillations, to classify oscillator types, and to predict the complex dynamics of periodically driven oscillations.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/S0076-6879(08)03801-9 | DOI Listing |
Sci Rep
January 2025
Department of Genetics, The University of Alabama at Birmingham, Birmingham, AL, USA.
Nowadays, chemotherapy and immunotherapy remain the major treatment strategies for Triple-Negative Breast Cancer (TNBC). Identifying biomarkers to pre-select and subclassify TNBC patients with distinct chemotherapy responses is essential. In the current study, we performed an unbiased Reverse Phase Protein Array (RPPA) on TNBC cells treated with chemotherapy compounds and found a leading significant increase of phosphor-AURKA/B/C, AURKA, AURKB, and PLK1, which fall into the mitotic kinase group.
View Article and Find Full Text PDFNat Med
January 2025
Vall d'Hebron Hospital Campus and Vall d'Hebron Institute of Oncology (VHIO), University of Vic - Central University of Catalonia, Barcelona, Spain.
Encorafenib + cetuximab (EC) is approved for previously treated BRAF V600E-mutant metastatic colorectal cancer (mCRC) based on the BEACON phase 3 study. Historically, first-line treatment of BRAF V600E-mutant mCRC with chemotherapy regimens has had limited efficacy. The phase 3 BREAKWATER study investigated EC+mFOLFOX6 versus standard of care (SOC) in patients with previously untreated BRAF V600E mCRC.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Medical Biology, Albert Szent-Györgyi Medical School, University of Szeged, Somogyi u. 4, Szeged, 6720, Hungary.
In our research, we performed temporal transcriptomic profiling of host cells infected with Equid alphaherpesvirus 1 (EHV-1) by utilizing direct cDNA sequencing based on nanopore MinION technology. The sequencing reads were harnessed for transcript quantification at various time points. Viral infection-induced differential gene expression was identified through the edgeR package.
View Article and Find Full Text PDFSci Rep
January 2025
Institute of Animal Reproduction and Food Research, Polish Academy of Sciences in Olsztyn, 10-748, Olsztyn, Poland.
Mares with endometrosis exhibit histological changes not only in the endometrium but also in the myometrium that suggest possible functional impairment. The molecular background of these changes is not well understood. We hypothesize that the transcriptomic profile of the mare myometrium varies depending on the degree of endometrosis in mares.
View Article and Find Full Text PDFNat Commun
January 2025
Robson DNA Science Centre, Charbonneau Cancer Institute, Department of Biochemistry & Molecular Biology, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
To tolerate oxidative stress, cells enable DNA repair responses often sensitive to poly(ADP-ribose) (PAR) polymerase 1 and 2 (PARP1/2) inhibition-an intervention effective against cancers lacking BRCA1/2. Here, we demonstrate that mutating the CHD6 chromatin remodeler sensitizes cells to PARP1/2 inhibitors in a manner distinct from BRCA1, and that CHD6 recruitment to DNA damage requires cooperation between PAR- and DNA-binding domains essential for nucleosome sliding activity. CHD6 displays direct PAR-binding, interacts with PARP-1 and other PAR-associated proteins, and combined DNA- and PAR-binding loss eliminates CHD6 relocalization to DNA damage.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!