A metabolic network diagram illustrating the pathophysiological pathways of the Dampness-Heat Jaundice Syndrome (DHJS) model. The illustration is centered on a 'DHJS Rat' and the 'Alimentary system' (liver and gallbladder), with four octagonal 'Main pathway' boxes representing Carbohydrate, Lipid, Amino Acid, and Other Metabolism Disorders. Radiating from these nodes are numerous 'Sub-pathway' dashed boxes containing specific KEGG-based metabolic pathways, including Steroid Hormone Biosynthesis, Primary Bile Acid Biosynthesis, and Glycerophospholipid Metabolism. Key metabolites mentioned include bilirubin, cholic acid, corticosterone, and LysoPC. The diagram highlights 'Pathologic changes' such as Oxidative Stress and Hepatic Injury, indicated by thick purple arrows. Clinical biomarkers including TBil, TBA, ̳̳γ-GT, ALT, and MDA are shown with upward gray arrows, signifying elevation in the diseased state. This integrative map demonstrates the complex biochemical dysregulation across multiple systems associated with hepatic injury and bile secretion disorders.

A detailed pathophysiology diagram illustrating the metabolic pathway of heme degradation and its systemic physiological implications. The central panel displays the biochemical conversion of Heme to Biliverdin-IXα by the rate-limiting enzyme Heme Oxygenase-1 (requiring NADPH and 3O2), which releases carbon monoxide (CO) and ferrous iron (Fe II). Subsequently, Biliverdin-IXα is reduced to Bilirubin-IXα by Biliverdin Reductase using NADP(H). The diagram maps the downstream outcomes of these byproducts: CO is linked to vascular regulation, mitochondrial preservation, and immunomodulation through signaling molecules like p38 MAPK, NF-κB, and sGC. The 'Labile Iron Pool' is shown bifurcating into protective Ferritin sequestration or detrimental free radical catalysis. Bilirubin is associated with cellular and systemic antioxidant effects before undergoing hepatic conjugation via UDP-glucuronyl transferase for biliary excretion. Additionally, a 'Free Heme Pool' is noted for its role in TLR4-mediated inflammatory responses and endothelial injury. This clinical illustration serves as a comprehensive guide for medical students and researchers studying oxidative stress, heme metabolism, and cytoprotective mechanisms.

A detailed metabolic signaling pathway diagram illustrating the enzymatic catabolism of heme and its clinical implications. The diagram begins with Heme-b (central iron coordinated in a tetrapyrrole ring), which can contribute to hemoproteins or induce pro-inflammatory/pro-oxidant effects during cellular injury. The primary pathway shows heme oxygenase (inducible HO-1 and constitutive HO-2) catalyzing the conversion of heme to Biliverdin-IX̑ in the presence of 3O2, NADPH, and NADPH: Cytochrome p-450 Reductase. This reaction releases Carbon Monoxide (CO), which exerts anti-apoptotic and anti-inflammatory effects (protecting against IRI, ALI, and AKI), and Ferrous Iron (Fe-II), which can act as a pro-oxidant or trigger Ferritin for cytoprotection. Biliverdin-IX̑ is subsequently reduced to Bilirubin-IX̑ via NAD(P)H: Biliverdin Reductase. Both biliverdin and bilirubin are shown with their molecular structures and are associated with antioxidant, immunomodulatory, and lipid-regulating effects, offering protection in cardiovascular and metabolic disorders. This infographic serves as a comprehensive visual for cellular biochemistry and the cytoprotective roles of the HO system.

Clinical photograph of a neonate undergoing a non-invasive screening for neonatal jaundice (hyperbilirubinemia) using a Bili-ruler. The image shows a healthcare provider holding a rectangular, transparent-sleeved Bili-ruler against the infant's face. The ruler features a standardized color progression strip with six numbered patches (1–6). Each color patch increases in yellow intensity and contains a central circular aperture (hole). These apertures allow the clinician to compare the underlying skin tone directly against the calibrated reference colors to estimate bilirubin levels. The neonate demonstrates visible icterus (yellowish discoloration) of the skin and sclera. This diagnostic tool is designed as a low-cost, point-of-care alternative to electronic transcutaneous bilirubinometers (TcB) and serum testing, following the principle of cephalocaudal progression of jaundice. It is used in clinical settings to determine the need for further laboratory testing, phototherapy, or management of physiological and pathological jaundice.