Living scenes / Research microenvironments
One environment from the atlas, replayed with the model that runs behind it. Impose a gene state, introduce a treatment, and follow delivery and the cell’s response along a single timeline, with what the model computes kept distinct from what is carried only as context.
Experimental chamber / Executable spatial coupling
Unlike the uniform scene, this chamber calculates separate oxygen, nutrient and drug fields at thirteen locations. Each location then runs the existing cellular mechanism and redox models with its own local inputs. Explore where the treatment has access and where stress changes the response.
Start with the coupled defaults: environment first, molecule entry, then washout. Run the chamber and press Play to follow the computed response.
A matched component experiment: replay the same settings with aggregate transport hindrance set to zero. Zero means this model term is off, not that real tissue has no matrix.
Legacy mode: the drug boundary uses the same coefficient as matrix transport. Supply is the reservoir level; exchange is the rate coefficient. These are dimensionless assumptions, not measured perfusion or endothelial permeability.
Requires checkpoint feedback. A factor slows drug crossing between two neighboring locations in both directions; oxygen and nutrients keep their existing transport. Zero closes the edge; one leaves it open. This is an assumed partition, not measured anatomy or permeability.
Requires checkpoint feedback. When enabled, available intracellular drug supplies the legacy treatment mechanism (target occupancy replaces it when explicit paclitaxel binding is enabled); extracellular drug remains the delivery field. Rates are assumed per-substep fractions, shared by candidate and parent. Set sequestration above zero to hold some drug out of the mechanism and compare against an independent run without sequestration. Remobilization returns held drug to availability.
Requires cellular uptake and paclitaxel alone; candidates are not supported in this mode. Available drug can bind a finite target pool and detach. Computed occupancy replaces the exposure-to-target shortcut. Rates and capacity are assumptions.
At eight checkpoints, untreated local cycling and ROS pressure alter oxygen/nutrient consumption for the next interval. This makes the transport field respond to modeled cellular activity. Treatment effects do not yet change consumption; no disease growth is simulated.
Assumed activity from 0 (closed) to 1 (default), shared by all conditions and constant during the run. These change only the exploratory ID2 states, not injury or repair. They are not measured enzyme levels, gene knockouts or drug inhibition.
Set FA-core to zero to close modification routes. Set USP1 to zero to close reset routes. Rerun to calculate the consequences.
Compare identical exposure and mechanism assumptions with and without slower resolution of one injury proxy. This is not a gene knockout or a measured DNA-repair intervention.
A supported medicine or hypothetical candidate is compared with untreated cells at each checkpoint. Its modeled mechanism injury signal feeds a separate persistent cell history. Untreated, parent and candidate share the same transport fields; treatment does not alter the environment or predict clinical outcomes.
This E1 state machine remembers prior stress. It is separate from the production cell model and does not simulate mutations, cell division, measured repair kinetics or treatment-driven feedback.
Scientific limits: This is an uncalibrated one-dimensional lattice, not reconstructed Pancreatic (PDAC) tissue. The local sites are independent aggregate-cell evaluations, not individual cells. Transport can receive optional untreated metabolic feedback. Treatment effects do not change transport. There is no cell migration, vascular remodeling, mutation emergence or validated treatment response. The Atlas is shown for learning, not used to invent coefficients.
These components are mapped, but not all are executable. Select any actor to see exactly what the backend represents.
Tissue-specific Atlas components
Extracellular / stromal · context only
Stroma-rich architecture with collagen-dominated ECM; literature describes fractions up to roughly 80% in some tumors.
Question: How does matrix organization alter the accessible routes between a vessel and malignant cells?
Needed for execution: Human collagen/hyaluronan spatial distribution, pore architecture, diffusion and hydraulic transport.
Evidence: Erkan 2012; Tian 2019 (Atlas source set)
Vascular / interstitial interface · context only
The Atlas reports a large collapsed-vessel fraction and high pressure in an autochthonous murine model; human values are not interchangeable.
Question: Does the molecule fail before reaching the tumor cell?
Needed for execution: Human perfusion and spatial drug exposure, pressure and permeability with matched specimen context.
Evidence: Provenzano 2012; DuFort 2012 (Atlas source set)
Cellular / nuclear · context only
A modeled tumor-cell response can be tested for imposed KRAS activation, stress and the three implemented drug families.
Question: Which intracellular bottleneck limits a treatment after it arrives?
Needed for execution: Heterogeneous clone composition, validated mutation trajectories, spatially resolved cell-state observations.
Evidence: Backend qualitative mechanism registry; Atlas PDAC context
Atlas observation · location not yet resolved · context only
75–130 mmHg, mean ~99 mmHg in an autochthonous murine model; human tumor pressure was not measured in the sourced literature.
Question: Which physical component or molecular interaction does this observation constrain?
Needed for execution: Identify the relevant physical component, spatial/assay context, units, uncertainty and a validated mechanism-to-model mapping.
Evidence: Provenzano 2012 via DuFort 2012
Atlas observation · location not yet resolved · context only
About 75% of vessels in pancreatic tumors were described as collapsed.
Question: Which physical component or molecular interaction does this observation constrain?
Needed for execution: Identify the relevant physical component, spatial/assay context, units, uncertainty and a validated mechanism-to-model mapping.
Evidence: Provenzano 2012
Atlas observation · location not yet resolved · context only
Up to 3.8 kPa (~30 mmHg) at the center of murine tumors.
Question: Which physical component or molecular interaction does this observation constrain?
Needed for execution: Identify the relevant physical component, spatial/assay context, units, uncertainty and a validated mechanism-to-model mapping.
Evidence: Nia 2017
Atlas observation · location not yet resolved · context only
Reports describe stroma reaching up to ~80% of tumor volume with collagen dominating ECM protein.
Question: Which physical component or molecular interaction does this observation constrain?
Needed for execution: Identify the relevant physical component, spatial/assay context, units, uncertainty and a validated mechanism-to-model mapping.
Evidence: Erkan 2012; Tian 2019
These are the existing Atlas observations and, where available, curated tissue actors. They do not automatically contribute numerical forces, interactions or geometry to the backend replay.
Reference: high oxygen/nutrients, no alteration. Untreated and treated: identical stress and gene state. Reference differences do not isolate a single cause.
Choose a tissue, gene perturbation and treatment, then run the actual qualitative backend model to view the response over 12 iterations.
Research scene / Redox network
This second teaching network represents ROS pressure, glutathione reserve, GPX4-like lipid-peroxide removal, oxidative DNA stress and adaptive antioxidant response. It runs separately from the treatment model; the two outputs are not yet chemically coupled.
Run the scene to populate this mechanistic teaching network.
Molecular participants / DNA interstrand crosslink repair
Our current four-stage simulation uses abstract injury quantities. Here are some of the real molecular participants associated with replication-coupled interstrand crosslink repair. Select a stage, then an actor to learn what it does, how scientists study it, and what we would need before implementing its interactions.
Loading the evidence-linked actor map…
Living scene / Controlled disturbance
Give the same starting cell a temporary environmental disturbance, then restore its conditions. Compare four matched trajectories to separate the disturbance from a hypothetical recovery intervention. This tests memory of earlier injury, not the onset of a disease.
From demonstration to biological experiment
Use a species-appropriate ROS assay with controls for probe artifacts, localization and timing. A generic fluorescence signal is not a molecular species count.
Quantify reduced and oxidized glutathione (GSH/GSSG) and GPX4 activity in a defined cell system. Protein expression alone is not catalytic flux.
Measure lipid oxidation, oxidative DNA lesions and cell-cycle outcomes before, during and after washout, with matched controls and independent replicates.
Our current redox and cell-state values have no physical units or experimentally fitted rates. Their educational role is to reveal testable questions, not establish how a real patient or tissue responds.
All rates and states are qualitative hypotheses. The recovery support control represents no existing or proposed drug, and model steps are not real biological time.
Individual cells, real extracellular matrix, spatial transport, ROS/GSH/GPX4 chemistry, mutation emergence, tissue-specific disease trajectories, immune-cell interactions, and calibrated treatment effects are not yet implemented in this replay. The existing research chamber and component studies provide starting points—not completed physics.