Multi-Layer Repair Interfaces in Biological-Information Syntax: Neural, Immune, Cellular, and Genomic-Regulatory Coupling Conditions

This theoretical preprint introduces Repair_BI as a formal object for evaluating cross-layer repair-interface claims within biological-information syntax. The object is defined as Repair_BI = (N_L, I_L, C_L, G_L, T_L, Int_R, Obs_R, Fail_R), where neural signalling, immune or inflammatory modulation, cellular-state transition, genomic-regulatory response, tissue-level repair outcome, declared interface relations, observable classes, and failure conditions are assigned distinct formal status. The paper uses tissue repair and regeneration as a public interdomain test field. It examines repair-interface paths across adult wound repair, skin and muscle neuroimmune repair, denervated wound and nerve-derived macrophage pathways, fracture repair, liver regeneration, human and murine single-cell wound maps, axolotl limb regeneration, zebrafish heart regeneration, fetal scarless repair, and methodological limits in single-cell and regulatory-state interpretation. The central contribution is a weighted interdomain admissibility matrix that distinguishes perturbation-rich evidence, incomplete perturbation paths, single-cell or spatial regulatory maps, comparative-regeneration evidence, scaffold reviews, boundary cases, and methodological constraints. The paper then assigns operator-family readings—register, interval, pulse, silence, density, contour, transition, closure, and transposition—to the resulting repair-interface paths. The framework is classificatory. Its function is to determine when a cross-layer repair claim is supported, incomplete, restricted, comparative, hypothesis-only, method-bounded, or inadmissible. The paper thereby provides a public intermediate layer between biological-information grammar and later formal developments concerning higher-order biological syntax, repair interfaces, and interdomain biological-information analysis.