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How a responsive reproduction factor is determinant in a prey-predator dynamics: A numerical and analytical study in a discrete-time model.
Chaos
January 2025
Physics Institute, University of São Paulo, 05508-090 São Paulo, SP, Brazil.
In this work, we investigate the dynamics of a discrete-time prey-predator model considering a prey reproductive response as a function of the predation risk, with the prey population growth factor governed by two parameters. The system can evolve toward scenarios of mutual or only of predators extinction, or species coexistence. We analytically show all different types of equilibrium points depending on the ranges of growth parameters.
View Article and Find Full Text PDFThe misalignment of incentives in academic publishing and implications for journal reform.
Proc Natl Acad Sci U S A
February 2025
Department of Data and Decision Science, Technion-Israel Institute of Technology, Haifa 3200003, Israel.
For most researchers, academic publishing serves two goals that are often misaligned-knowledge dissemination and establishing scientific credentials. While both goals can encourage research with significant depth and scope, the latter can also pressure scholars to maximize publication metrics. Commercial publishing companies have capitalized on the centrality of publishing to the scientific enterprises of knowledge dissemination and academic recognition to extract large profits from academia by leveraging unpaid services from reviewers, creating financial barriers to research dissemination, and imposing substantial fees for open access.
View Article and Find Full Text PDFIdentification of key regulators in pancreatic ductal adenocarcinoma using network theoretical approach.
PLoS One
January 2025
Department of Chemistry, Ashoka University, Sonipat, Haryana, India.
Pancreatic Ductal Adenocarcinoma (PDAC) is a devastating disease with poor clinical outcomes, which is mainly because of delayed disease detection, resistance to chemotherapy, and lack of specific targeted therapies. The disease's development involves complex interactions among immunological, genetic, and environmental factors, yet its molecular mechanism remains elusive. A major challenge in understanding PDAC etiology lies in unraveling the genetic profiling that governs the PDAC network.
View Article and Find Full Text PDFGoverned by the unfolded protein response (UPR), the ability to counteract endoplasmic reticulum (ER) stress is critical for maintaining cellular homeostasis under adverse conditions. Unresolved ER stress leads to cell death through mechanisms that are yet not completely known. To identify key UPR effectors involved in unresolved ER stress, we performed an ethyl methanesulfonate (EMS) suppressor screen on the Arabidopsis mutant, which is impaired in activating cytoprotective UPR pathways.
View Article and Find Full Text PDFDouble-strand breaks represent the most dangerous form of DNA damage, and in resting cells, these breaks are sealed via the non-homologous end joining (NHEJ) factor Ligase IV (LIG4). Excessive NHEJ may be genotoxic, necessitating multiple mechanisms to control NHEJ activity. However, a clear mechanism of transcriptional control for them has not yet been identified.
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