Create accountLogin

Recent searches

No recent searches

Search options

Only available when logged in.
mastodon.gamedev.place is one of the many independent Mastodon servers you can use to participate in the fediverse.
Mastodon server focused on game development and related topics.

Administered by:

Server stats:

5.1K
active users

mastodon.gamedev.place: AboutProfiles directoryPrivacy policy

Mastodon: AboutGet the appKeyboard shortcutsView source codev4.3.7

#cell

56 posts7 participants0 posts today
Public
Rxiv mechanobio

📰 "Effective interface forces to model boundary effects in a finite-size metamaterial through the reduced relaxed micromorphic model"
arxiv.org/abs/2504.21697 #Physics.App-Ph #Forces #Cell

arXiv logo
arXiv.orgEffective interface forces to model boundary effects in a finite-size metamaterial through the reduced relaxed micromorphic modelWe use the reduced relaxed micromorphic model (RRMM) to capture the effective "bulk" dynamical response of finite size metamaterial specimens made out of a Labyrinthine unit cell. We show that for small finite-size specimens, boundary effects can play a major role, so that the RRMM needs an enrichment to capture the metamaterial's bulk response, as well as the boundary effects. A benchmark test is introduced to show that different metamaterial/ homogeneous material interfaces can drive completely different responses even if the bulk metamaterial remains the same. We show with no remaining doubts that the concept of "interface forces" must necessarily be introduced if one wants to model finite-size metamaterials in a homogenized framework.
Public
Rxiv mechanobio

📰 "Glucagon and insulin production in pancreatic cells modeled using Petri nets and Boolean networks"
arxiv.org/abs/2504.21578 #Q-Bio.Cb #Dynamics #Cs.Cl #Cell

arXiv logo
arXiv.orgGlucagon and insulin production in pancreatic cells modeled using Petri nets and Boolean networksDiabetes is a civilization chronic disease characterized by a constant elevated concentration of glucose in the blood. Many processes are involved in the glucose regulation, and their interactions are very complex. To better understand those processes we set ourselves a goal to create a Petri net model of the glucose regulation in the whole body. So far we have managed to create a model of glycolysis and synthesis of glucose in the liver, and the general overview models of the glucose regulation in a healthy and diabetic person. In this paper we introduce Petri nets models of insulin secretion in beta cell of the pancreas, and glucagon in the pancreas alpha cells. Those two hormones have mutually opposite effects: insulin preventing hyperglycemia, and glucagon preventing hypoglycemia. Understanding the mechanisms of insulin and glucagon secretion constitutes the basis for understanding diabetes. We also present a model in which both processes occur together, depending on the blood glucose level. The dynamics of each model is analysed. Additionally, we transform the overall insulin and glucagon secretion system to a Boolean network, following standard transformation rules.
Public
Rxiv mechanobio

📰 "Crystal structures of Kif2A complexed with WDR5 reveal the structural plasticity of WIN-S7 sites"
doi.org/doi:10.3724/abbs.20250
pubmed.ncbi.nlm.nih.gov/403025
#CellDivision #Cell

SciEngineCrystal structures of Kif2A complexed with WDR5 reveal the structural plasticity of WIN-S7 sites<p indent="0mm">Chromosome congression and spindle assembly are essential for genomic stability and proper cell division, with deficiencies in these processes linked to tumorigenesis. WD repeat-containing protein 5 (WDR5), a core component of the mixed lineage leukemia (MLL) methyltransferase complex, directly binds to kinesin family member 2A (Kif2A) to regulate these mitotic events. Despite the importance of this interaction, its structural basis for Kif2A recognition by WDR5 remains unclear. Here, we determine the crystal structure of WDR5 in complex with a Kif2A-derived peptide (residues 114–122) at a resolution of <sc>1.85 Å.</sc> Structural analysis reveals that Kif2A engages both the WIN and S7 sites of WDR5 via Arg117 and Ser121, with Ser121 forming hydrogen bonds with WDR5 Tyr191 and Lys259, driving Tyr191 rotation and opening the S7 pocket. Additional structures of WDR5 complexed with truncated or mutated Kif2A peptides and a WDR5 Y191F variant highlight the dynamic nature of Tyr191. Notably, anti-WDR5 compounds exhibit a similar binding mode at the WDR5 WIN-S7 site. The results of mutagenesis combined with isothermal titration calorimetry (ITC) assays underscore the critical roles of Arg117 and Ser121 in mediating the binding of Kif2A to WDR5. In summary, our findings provide atomic-level insights into the molecular mechanisms underlying the non-canonical mitotic function of the MLL/WDR5 complex and highlight WIN-S7 sites as promising therapeutic targets for diseases associated with chromosomal instability, such as cancers.</p>
Public
Rxiv mechanobio

📰 "DLCM: a versatile multi-level solver for heterogeneous multicellular systems"
arxiv.org/abs/2504.20565 #Q-Bio.Pe #Dynamics #Q-Bio.Qm #Cell

arXiv logo
arXiv.orgDLCM: a versatile multi-level solver for heterogeneous multicellular systemsComputational modeling of multicellular systems may aid in untangling cellular dynamics and emergent properties of biological cell populations. A key challenge is to balance the level of model detail and the computational efficiency, while using physically interpretable parameters to facilitate meaningful comparisons with biological data. For this purpose, we present the DLCM-solver (discrete Laplacian cell mechanics), a flexible and efficient computational solver for spatial and stochastic simulations of populations of cells, developed from first principle to support mechanistic investigations. The solver has been designed as a module in URDME, the unstructured reaction-diffusion master equation open software framework, to allow for the integration of intra-cellular models with extra-cellular features handled by the DLCM. The solver manages discrete cells on a fixed lattice and reaction-transport events in a continuous-time Markov chain. Space-continuous micro-environment quantities such as pressure and chemical substances are supported by the framework, permitting a variety of modeling choices concerning chemotaxis, mechanotaxis, nutrient-driven cell growth and death, among others. An essential and novel feature of the DLCM-solver is the coupling of cellular pressure to the curvature of the cell populations by elliptic projection onto the computational grid, with which we can include effects from surface tension between populations. We demonstrate the flexibility of the framework by implementing benchmark problems of cell sorting, cellular signaling, tumor growth, and chemotaxis models. We additionally formally analyze the computational complexity and show that it is theoretically optimal for systems based on pressure-driven cell migration. In summary, the solver balances efficiency and a relatively fine resolution, while supporting a high level of interpretability.
ExploreLive feeds
About