What this platform knows, and how well it knows it.

Every constant in every model appears below with its value, its units, and an honest account of where it came from. The values are imported from the model code rather than retyped, and a test fails the build if a model gains a parameter that is not documented here — so this page cannot quietly drift away from what the simulations actually compute with.

Just over half of these parameters are educational estimates. That is the honest position for a teaching model of this scope, and it is the reason the platform reports directions and magnitudes rather than predictions. Select a class above to filter the tables.

Closed-loop circulation

app/hemodynamics/model.ts

Three compliant compartments exchanging a conserved blood volume, with Sunagawa ventricular-arterial coupling, a Guyton venous-return law, and a proportional baroreflex.

Symbol	Quantity	Value	Units	Provenance	Source
`Ees0`	End-systolic elastance	2.3	mmHg/mL	measured	Suga & Sagawa; human resting values cluster at 2–3 mmHg/mL
`V0`	ESPVR volume intercept	5	mL	estimated	Chosen inside the reported 0–20 mL range for the unstressed volume intercept
`alpha`	EDPVR scale	1.1	mmHg	fitted	Exponential end-diastolic relation fitted to a normal human filling curve
`beta`	EDPVR exponent	0.021	1/mL	fitted	Same fit; sets the stiffness of the passive chamber
`V0d`	EDPVR volume intercept	30	mL	estimated	Volume at which passive filling pressure reaches zero
`Cart`	Arterial compliance	1.6	mL/mmHg	measured	Total systemic arterial compliance in healthy adults, 1.3–2.0 mL/mmHg
`Cven`	Systemic venous compliance	90	mL/mmHg	measured	Venous compliance is roughly 30–50× arterial; reported 80–200 mL/mmHg
`Ccp`	Cardiopulmonary compliance	35	mL/mmHg	estimated	Lumped heart-plus-pulmonary compartment; set so resting filling pressure lands near 5.5 mmHg
`Ra0`	Arteriolar resistance	17.3	Wood units	measured	Total systemic resistance ≈ 18 Wood units (about 1450 dyn·s·cm⁻⁵), split here into arteriolar and venous components
`Rvr`	Venous return resistance	1.05	Wood units	fitted	Guyton's resistance to venous return; set so venous return equals 5 L/min at the resting gradient
`ITP0`	Resting intrathoracic pressure	-4	mmHg	measured	End-expiratory intrathoracic pressure, −3 to −5 mmHg
`HR0`	Intrinsic heart rate	70	bpm	estimated	Resting adult rate before reflex adjustment
`MAPset`	Baroreflex set point	93	mmHg	estimated	Normal mean arterial pressure; the reflex operating point
`gHR`	Chronotropic reflex gain	0.85	bpm per mmHg	estimated	Open-loop baroreflex gains of 0.5–1.5 bpm/mmHg are reported in humans
`gR`	Vasomotor reflex gain	0.6	fraction at full error	estimated	Chosen to give a physiological pressure response; not separately measured
`gEes`	Inotropic reflex gain	0.35	fraction at full error	estimated	Chosen to give a physiological pressure response
`gVeno`	Venoconstriction reflex gain	260	mL recruited at full error	estimated	Reflex mobilisation of unstressed venous volume; order of magnitude only
`tauHR`	Chronotropic time constant	2	s	measured	Vagal heart-rate responses settle within a few seconds
`tauR`	Vasomotor time constant	6	s	measured	Sympathetic vascular responses develop over 5–15 s
`tauEes`	Inotropic time constant	3.5	s	estimated	Intermediate between the vagal and vasomotor arms
`tauVeno`	Venoconstriction time constant	8	s	estimated	Slowest reflex effector in the model
`tauFill`	Diastolic filling time constant	90	ms	estimated	Sets how incompletely the ventricle fills when diastole is short

Molecule-to-chamber bridge

app/molecular/multiscale-model.ts

Maps myofilament activation onto ventricular mechanics using the same constitutive relations as the circulation model, so the two cannot drift apart.

Symbol	Quantity	Value	Units	Provenance	Source
`Ees0`	Reference end-systolic elastance	2.3	mmHg/mL	measured	Shared with the circulation model
`V0`	ESPVR volume intercept	5	mL	estimated	Shared with the circulation model
`V0d`	EDPVR volume intercept	30	mL	estimated	Shared with the circulation model
`alpha`	EDPVR scale	1.1	mmHg	fitted	Shared with the circulation model
`beta`	EDPVR exponent	0.021	1/mL	fitted	Shared with the circulation model
`EDV0`	Reference end-diastolic volume	115	mL	measured	Normal adult left ventricular end-diastolic volume, 100–140 mL
`SVR0`	Reference systemic resistance	18.35	Wood units	measured	Matches Ra0 + Rvr in the circulation model
`Cart`	Arterial compliance	1.6	mL/mmHg	measured	Shared with the circulation model
`Pven`	Downstream venous pressure	2	mmHg	estimated	Offset that makes the bridge's reference pressure agree with the circulation model
`tauFill`	Diastolic filling time constant	90	ms	estimated	Shared with the circulation model
`elastanceExponent`	Activation-to-elastance exponent	0.9	dimensionless	illustrative	Sublinear because elastance saturates as cross-bridges are already recruited; the exponent itself is not measured

Reference myofilament

app/disease-lab/disease-model.ts

The calcium transient and force-calcium relation of the reference cardiomyocyte. Every variant is expressed as a change to these.

Symbol	Quantity	Value	Units	Provenance	Source
`calciumAmplitude`	Peak systolic calcium increment	0.95	µM	measured	Intact ventricular myocytes reach roughly 1 µM at the peak of the transient
`diastolicCalcium`	Diastolic calcium	0.1	µM	measured	Resting cytosolic calcium, 80–150 nM
`calciumKd`	Half-activating calcium	1.65	µM	measured	pCa50 5.78; measured cardiac force-pCa relations cluster at 5.6–5.9
`hill`	Hill coefficient	3.2	dimensionless	measured	Cardiac force-pCa Hill coefficients of 3–7 are reported; a lumped thin-filament cooperativity, not a site count
`calciumRise`	Calcium release time constant	0.022	s	measured	The systolic calcium transient rises within tens of milliseconds
`calciumDecay`	Calcium removal time constant	0.185	s	measured	Human ventricular calcium decay time constants of 150–250 ms
`forceActivation`	Force redevelopment time constant	0.022	s	estimated	Chosen so force follows calcium with a physiological lag
`forceRelaxation`	Force relaxation time constant	0.062	s	estimated	Set so the reference relaxation half-time lands near 120 ms
`myosinAvailability`	Recruitable myosin fraction	1	relative	illustrative	Reference value of 1 by definition; variants shift it
`stiffness`	Passive chamber stiffness	1	relative	illustrative	Reference value of 1 by definition
`preload`	Filling relative to reference	1	relative	illustrative	Reference value of 1 by definition; variants shift it to represent chamber remodelling
`leakAmplitude`	Diastolic SR calcium leak	0	µM	illustrative	Zero in the reference myofilament; the RyR2 variant raises it. Sized so the diastolic excursion stays in the 0.15–0.30 µM range
`energeticFactor`	Energetic cost multiplier	1	relative	illustrative	Reference value of 1 by definition; scales the tension-time integral into a demand index
`stressTrigger`	Adrenergic leak sensitivity	0.03	dimensionless	illustrative	A heuristic index, not a measured quantity
`arrhythmiaBias`	Baseline arrhythmic substrate	0.04	0–1 index	illustrative	A heuristic index with no electrophysiology behind it

Vascular K_ATP channel

app/pathways/katp-model.ts

Nucleotide gating of the Kir6.1/SUR2B channel and its consequences for smooth-muscle membrane potential and arteriolar calibre.

Symbol	Quantity	Value	Units	Provenance	Source
`atpKi`	ATP half-inhibition	90	µM	estimated	Kir6.1-containing channels are markedly less ATP-sensitive than Kir6.2; chosen inside the reported range
`atpHill`	ATP Hill coefficient	1.2	dimensionless	estimated	Shallow inhibition consistent with reported ATP dose-responses
`adpKa`	MgADP half-activation	180	µM	estimated	Placed inside the free MgADP range spanned between perfusion and ischaemia
`adpHill`	MgADP Hill coefficient	1.5	dimensionless	estimated	Cooperative nucleotide activation at the SUR nucleotide-binding domains
`basalOpen`	Nucleotide-independent opening	0.02	fraction	measured	Near zero: the vascular channel requires Mg-nucleotides to open (Sung et al., PNAS 2021)
`maxOpen`	Maximum open probability	0.85	fraction	estimated	Ceiling on single-channel open probability
`eK`	Potassium reversal potential	-85	mV	measured	Nernst potential for potassium at physiological gradients
`vDepolarised`	Potential without K_ATP	-32	mV	estimated	Where the myocyte would sit on its other background currents alone
`gBackground`	Background conductance	1	relative	illustrative	Normalised to 1; every other conductance in the module is expressed against it
`gKatpMax`	K_ATP conductance reserve	120	relative to background	estimated	Large because channel density is high; opening a few percent clamps the membrane near E_K
`vHalf`	L-type activation midpoint	-34	mV	measured	Smooth-muscle L-type window current activates over −40 to −20 mV
`vSlope`	L-type activation slope	7	mV	measured	Boltzmann slope factors of 6–9 mV are reported
`toneFloor`	Voltage-independent tone	0.2	fraction	estimated	Stretch- and agonist-driven calcium entry that persists when the cell is hyperpolarised
`toneCeiling`	Voltage-dependent tone ceiling	1.25	relative	illustrative	Bounds the Boltzmann so a few millivolts of depolarisation cannot triple tone
`referenceConstriction`	Resting arteriolar constriction	0.3	fraction of maximum radius	estimated	Resistance arterioles hold substantial resting tone
`fixedResistanceFraction`	Non-arteriolar resistance	0.35	fraction	estimated	Conduit vessels, capillaries and venules in series, which do not dilate

JAK-STAT signalling

app/pathways/jakstat-model.ts

STAT nucleocytoplasmic cycling on the topology of Swameye et al. (PNAS 2003), with a SOCS feedback arm added as an educational extension.

Symbol	Quantity	Value	Units	Provenance	Source
`k1`	STAT phosphorylation	0.42	/min per unit receptor	estimated	Chosen to reproduce the published time to peak phosphorylation; NOT the value fitted in Swameye et al.
`k2`	pSTAT dimerisation	1.6	/min per unit	estimated	Second-order dimerisation; chosen for the published timescale
`k3`	Nuclear import	0.28	/min	estimated	Chosen so the nuclear signal peaks in the published window
`k4`	Nuclear export	0.16	/min	estimated	The published fit cannot identify the export rate independently; this is an educational value
`tau`	Nuclear residence delay	6	min	estimated	The delay in the published cycling model; its effect on cytoplasmic pSTAT is small
`kOn`	Receptor activation	0.55	/min per unit ligand	estimated	Educational estimate
`kOff`	Receptor deactivation	0.09	/min	estimated	Educational estimate
`basalActivation`	Ligand-independent activation	0	/min	illustrative	Zero in the reference pathway; the JAK2 V617F variant raises it
`socsSynthesis`	SOCS synthesis	0.075	/min	estimated	Part of the educational feedback extension, not the fitted model
`socsThreshold`	SOCS transcription threshold	0.22	nuclear STAT units	estimated	Educational extension
`socsDegradation`	SOCS degradation	0.021	/min	estimated	Educational extension; sets how long adaptation persists
`socsPotency`	SOCS receptor inhibition	0.35	SOCS units	estimated	Educational extension
`statTotal`	Total STAT pool	1	relative	illustrative	Normalised to 1
`receptorTotal`	Total receptor pool	1	relative	illustrative	Normalised to 1

Complement alternative pathway

app/pathways/complement-model.ts

A self-amplifying convertase loop on one unit of surface, opposed by factor H, CD55, CD46 with factor I, and CD59. On-surface complement kinetics vary by orders of magnitude with surface chemistry, so every rate here is an educational estimate chosen to reproduce the published qualitative behaviour.

Symbol	Quantity	Value	Units	Provenance	Source
`tickover`	Spontaneous C3 hydrolysis	3.50e-4	/min	estimated	Sized so an untouched host surface turns over only a percent or two of plasma C3 across the window
`formation`	Convertase assembly	4.3	/min per unit C3b	estimated	Set so the loop sits just below instability on a fully regulated cell — the defining property of the real system
`catalysis`	C3 cleavage by convertase	2.1	/min	estimated	The amplification step; chosen with formation to place the instability threshold
`deposition`	Nascent C3b reaching the surface	0.3	fraction	estimated	Most nascent C3b hydrolyses in the fluid phase before it can bind; the surviving fraction is surface-dependent
`decayIntrinsic`	Spontaneous convertase decay	0.35	/min	measured	The C3bBb convertase has an intrinsic half-life of roughly 90 seconds
`decayCd55`	CD55 decay acceleration	2.2	/min at full density	estimated	Erythrocytes lean on CD55, which is why PNH is a red-cell disease
`decayFactorH`	Factor H decay acceleration	2	/min at full docking	estimated	Glomerular endothelium leans on factor H, which is why CFH variants present as renal thrombotic microangiopathy
`inactivation`	Factor I cleavage of C3b	0.62	/min per unit cofactor	estimated	Competes directly against the loop for the same C3b; this rate decides the module's whole behaviour
`c5Density`	C3b density for half-maximal C5 convertase	0.035	fraction coverage	estimated	Low, because the C5 convertase needs one more C3b placed locally rather than global coverage
`c5Cleavage`	C5 cleavage rate	0.9	/min	estimated	Educational estimate
`macAssembly`	MAC assembly from C5b	0.8	/min	estimated	Educational estimate
`cd59Potency`	CD59 pore inhibition	0.94	fraction blocked	estimated	CD59 is a highly effective terminal inhibitor; near-complete at full density
`lysisThreshold`	MAC density for half-maximal lysis	0.045	fraction coverage	illustrative	Maps pore density onto a cell-population outcome; not a measured quantity
`opsonicThreshold`	Opsonin density for half-maximal clearance	0.12	fraction coverage	illustrative	Macrophage recognition is cooperative; the threshold itself is chosen, not measured
`shedding`	Loss of surface-bound fragments	0.012	/min	illustrative	Membrane turnover and macrophage nibbling; without it a healthy cell slowly acquires a coat it would never carry

Cited variant evidence

app/disease-lab/disease-model.ts

The disease laboratory’s variants and the evidence behind each parameter shift. Directions come from these sources; the magnitudes are educational estimates chosen to be visible.

Gene	Variant	Phenotype	Evidence	Source
`TNNT2`	p.Arg92Gln · R92Q	Hypertrophic cardiomyopathy	direct functional evidence	Human R92Q cardiomyocyte study ↗
`MYBPC3`	loss-of-function class	Hypertrophic cardiomyopathy	class-level evidence	MYBPC3 functional review ↗
`TNNT2`	p.Lys210del · ΔK210	Dilated cardiomyopathy	direct functional evidence	ΔK210 calcium-desensitization study ↗
`RYR2`	p.Arg4496Cys · R4496C	Catecholaminergic polymorphic VT	direct functional evidence	R4496C calcium-wave study ↗

Standing limitations

No model here is calibrated for patient-specific prediction. They reproduce the direction and the rough magnitude of a response, which is what a teaching model should do.
The circulation model lumps both ventricles and the pulmonary bed into a single cardiopulmonary compartment, and its arterial waveform is a drawn template rather than a solved pressure trace.
The myofilament model has no cross-bridge state variable and no length-dependent activation: sarcomere length is reported as a consequence of chamber volume, not as a cause of force.
Molecular-dynamics trajectories offered elsewhere in the platform are far too short to support claims about binding affinity, conformational populations, or variant pathogenicity.
Nothing here may be used for diagnosis, variant classification, prognosis, or treatment selection.