For the VP organs to run as one body, each package must import a sibling's result across a named seam rather than re-derive it. This page is the integumentary package's labelled seam record: it adds no new mechanism, exposes the one internal cross-target coupling (a pigment-loss lesion removes the melanin screen and raises the oncology hazard), and declares what it inherits and hands off.
For the VP organ packages to assemble as one body without any package re-deriving another's owned quantity, each interface is a named seam under a single-source-of-truth rule. This page is the integumentary package's complete labelled seam record — adding no new mechanism and no new constant. It inherits the dermal-perfusion magnitude (circulatory), organ identity and measured γ (DNA) and the R19 substrate; it exposes the one internal cross-target coupling — a melanocyte-target lesion that removes the melanin screen raises the shared oncology hazard, re-exported verbatim from the verified pathology layer [V] Simulation-verified [L] Cited anchor, absolute relative risk open [O] Open (obstacle stated); and it declares its hand-offs (gene-lesion → disease_wp, immune / rheumatology seams, out-of-class infections) as contracts, not yet live wiring. Two runs hash identically and the core-battery hash stays fixed.
One body needs labelled seams, not one big model
The whole VP programme is a family of organ packages that must eventually run as one body without any package secretly re-deriving another's result. The discipline that makes that safe is the single source of truth (SSOT): each quantity is owned by exactly one package, and every other package that needs it imports it across a named seam rather than re-computing it. This page is the integumentary package's complete, labelled seam record — it adds no new mechanism and no new constant; it only states, in one machine-readable place, what the package imports, what cross-target coupling it exposes, and what it hands off. The same record is emitted as reports/seam_manifest.json for the one-body runner.
| Seam class | Meaning | Count | Live? |
|---|---|---|---|
| Inherited-in | read-only inputs vendored from a sibling, never re-derived here | 3 | yes (vendored) |
| Internal-live | a cross-target coupling computed live in this package, now exposed as a labelled output | 1 | yes |
| Declared-out | contracts to sibling packages — declared, not yet live wiring | 6 | no (declared) |
The exposed coupling: a pigment lesion raises the cancer hazard
The one genuinely internal cross-target coupling in this package — the thing ยง5.3 asks to surface — is that a melanocyte-target (T3) lesion which removes the melanin screen raises the shared oncology-kernel hazard. It is already computed inside the pathology layer; here it is exposed verbatim (the numbers below are re-exported from the verified pathology functions, not recomputed, so the seam output provably is the internal link surfaced). Removing the screen with an albinism-type lesion raises the squamous-cell-carcinoma cumulative hazard to a relative risk of about 2.58× versus pigmented skin (incidence relative risk about 2.24×), and removes the screen that normally blunts a sunburn, raising the melanoma burst relative risk to about 10.59×. That the lesion's delivered-ultraviolet attenuation is exactly 1.00 (no screen at all) is the mechanistic reason.
The coupling is causal, not a correlate: restoring an exogenous screen (sunscreen) brings the squamous hazard back down to about 1.13× — the screen is the lever (yes). This is the seam the one-body runner needs in order to let a pigment-target lesion modify a cancer-target rate without either target re-deriving the other.
What the package imports (inherited-in seams)
These are the read-only inputs the package vendors from a sibling and never re-derives. Each is owned elsewhere and carried in under inherited/.
| From package | Imported quantity | Consumed by | Note |
|---|---|---|---|
| Circulatory | dermal-perfusion magnitude (cited) | T9 vasomotor | the vasomotor layer adds only the reactivity dynamics and leaves the perfusion magnitude an inherited citation |
| DNA (gene-clock) | organ identity + emergence order + measured master-gene γ | every target | identity and order live in DNA; γ is measured, read-only, never fitted, vendored and re-vendored on change |
| Substrate | the R19 bistable switch (with spinodal / barrier / dwell) | every target + layer | the one shared primitive, vendored once |
What the package hands off (declared-out seams)
These are the entities that belong to a sibling package by etiology class — a single defining gene, an immune effector, or a pathogen — not to this jamming-class package. They are declared contracts, not yet live wiring: the integration harness that would import the sibling's parameters does not exist yet, so each is named honestly with the in-package dynamics-side back-pointer it will connect to once the harness is built. Naming them is what keeps every disease where its mechanism actually lives.
| Seam target | Owned there | Dynamics side here | Status |
|---|---|---|---|
Gene-lesion → disease_wp | single-gene rare genodermatoses (ichthyoses, ectodermal dysplasias, oculocutaneous albinism, xeroderma pigmentosum, hereditary cancer syndromes, other genodermatoses) | the matching T-target trajectory (T1+T4, T5, T3→oncology, oncology, T8…) | declared |
| Immune-hematologic | urticaria / angioedema (mast-cell / histamine) | — not a skin jamming-class target | declared |
| Immune-effector | lichen planus / inflammatory dermatoses | — needs an immune-effector seam | declared |
| Rheumatology | the fixed digital ischemia of secondary Raynaud (connective-tissue disease) | T9 covers primary reversible Raynaud | declared |
| Immune-effector | rosacea inflammatory chemistry beyond the LL-37 / Demodex flag | T9 carries the vasomotor reactivity + the amplifier flag | declared |
| Out-of-class | cutaneous infections (impetigo, cellulitis, dermatophytosis, herpes, warts) | — not an R19-dynamics failure at all | out-of-class |
Grades and reproducibility
The exposed coupling is a simulation-verified cross-target shape [V] Simulation-verified — a pigment lesion raises the cancer hazard, and the screen is the causal lever — resting on cited epidemiology [L] Cited anchor; the absolute relative-risk magnitude is open [O] Open (obstacle stated), inheriting the oncology obstacle (a population baseline rate plus an absolute dose calibration). The inherited and declared seams carry the owning package's grade. This layer introduces no new constant: every number on this page is re-exported from the pathology layer, and the rest are declarations.
The seam manifest is deterministic on its own terms: two independent runs hash to an identical SHA-256, separate from the core battery and every disease layer. Crucially, this layer only reads the disease layers — it never alters them, and it never imports the core battery — so the core T1–T5+oncology result hash is unchanged at 1fb59f556e01… and the pathology hash is unchanged at 0a4404ccde65….