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Nitric oxide
Pathway / Endothelial activation & erosion

Nitric oxide

metabolite

Nitric oxide produced by endothelial cells regulates vasodilation and suppresses platelet adhesion; reduced bioavailability reflects endothelial dysfunction and predisposes to thrombosis.

Pathway placement
Cascade stepEndothelial activation & erosion
Confidencehigh
RationaleEndothelial signaling and dysfunction marker; inhibits platelet activation.
Also acts inPlatelet activation, Vascular inflammation
Druggability
Not assessed (no mapped human gene target).

Type I vs Type II discrimination

ScoresShared / rises in both
R — rupture / Type-I
67
C — confounder / Type-II
56
A — assay feasibility
42
E — evidence strength
38
T1DI (composite)
9
Specificity differential (R−C)+11.1
Confounder panel (Type-II drivers)
1sepsis / systemic inflammationmag 2
2anemia / acute blood lossmag 2
3hypovolemia / dehydrationn/a
4tachyarrhythmiamag 1
5hypoxemia / respiratory failuremag 2
6hypertensive emergencymag 2
7high-demand / peri-operative stressmag 1
Coverage: 6/7 confounders with evidence
Tier: deep-scored (abstract-extracted) · 12 supporting references. See the discrimination table for all markers.

Assay & specimen

Class-level default (no specific cleared assay)— generic method inferred from analyte class; confirm against a specific product insert before use.
Specimen
Serum, plasma or urine
Collection tube
Serum separator (gold/red-top, SST) · Lithium heparin (green-top) · Sterile urine container
Method / principle
LC-MS/MS (targeted metabolomics) or enzymatic colorimetric where available
Reagent / substrate
Stable-isotope-labeled internal standard (MS); or enzyme-coupled Trinder reagent
Platform
LC-MS/MS; some automated chemistry
Turnaround · availability
Send-out / research · Specialized / research

Literature evidence(22)

Clinical trials(3)