A bile pigment that is a degradation product of HEME.
A condition characterized by an abnormal increase of BILIRUBIN in the blood, which may result in JAUNDICE. Bilirubin, a breakdown product of HEME, is normally excreted in the BILE or further catabolized before excretion in the urine.
Yellow discoloration of the SKIN; MUCOUS MEMBRANE; and SCLERA in the NEWBORN. It is a sign of NEONATAL HYPERBILIRUBINEMIA. Most cases are transient self-limiting (PHYSIOLOGICAL NEONATAL JAUNDICE) occurring in the first week of life, but some can be a sign of pathological disorders, particularly LIVER DISEASES.
Mutant strain of Rattus norvegicus which is used as a disease model of kernicterus.
Linear TETRAPYRROLES that give a characteristic color to BILE including: BILIRUBIN; BILIVERDIN; and bilicyanin.
A term used pathologically to describe BILIRUBIN staining of the BASAL GANGLIA; BRAIN STEM; and CEREBELLUM and clinically to describe a syndrome associated with HYPERBILIRUBINEMIA. Clinical features include athetosis, MUSCLE SPASTICITY or hypotonia, impaired vertical gaze, and DEAFNESS. Nonconjugated bilirubin enters the brain and acts as a neurotoxin, often in association with conditions that impair the BLOOD-BRAIN BARRIER (e.g., SEPSIS). This condition occurs primarily in neonates (INFANT, NEWBORN), but may rarely occur in adults. (Menkes, Textbook of Child Neurology, 5th ed, p613)
A clinical manifestation of HYPERBILIRUBINEMIA, characterized by the yellowish staining of the SKIN; MUCOUS MEMBRANE; and SCLERA. Clinical jaundice usually is a sign of LIVER dysfunction.
Accumulation of BILIRUBIN, a breakdown product of HEME PROTEINS, in the BLOOD during the first weeks of life. This may lead to NEONATAL JAUNDICE. The excess bilirubin may exist in the unconjugated (indirect) or the conjugated (direct) form. The condition may be self-limiting (PHYSIOLOGICAL NEONATAL JAUNDICE) or pathological with toxic levels of bilirubin.
Inborn errors of bilirubin metabolism resulting in excessive amounts of bilirubin in the circulating blood, either because of increased bilirubin production or because of delayed clearance of bilirubin from the blood.
A family of enzymes accepting a wide range of substrates, including phenols, alcohols, amines, and fatty acids. They function as drug-metabolizing enzymes that catalyze the conjugation of UDPglucuronic acid to a variety of endogenous and exogenous compounds. EC 2.4.1.17.
Diazonium compounds are organic derivatives containing the general formula R-N2+X-, where R represents an aryl or alkyl group, and X- is an anion such as bromide or chloride, formed by the reaction of amines with nitrous acid in an acidic medium.
1,3,6,7-Tetramethyl-4,5-dicarboxyethyl-2,8-divinylbilenone. Biosynthesized from hemoglobin as a precursor of bilirubin. Occurs in the bile of AMPHIBIANS and of birds, but not in normal human bile or serum.
A familial form of congenital hyperbilirubinemia transmitted as an autosomal recessive trait. It is characterized by icterus and brain damage caused by a glucuronyl transferase deficiency in the liver and faulty bilirubin conjugation.
A benign familial disorder, transmitted as an autosomal dominant trait. It is characterized by low-grade chronic hyperbilirubinemia with considerable daily fluctuations of the bilirubin level.
Treatment of disease by exposure to light, especially by variously concentrated light rays or specific wavelengths.
An emulsifying agent produced in the LIVER and secreted into the DUODENUM. Its composition includes BILE ACIDS AND SALTS; CHOLESTEROL; and ELECTROLYTES. It aids DIGESTION of fats in the duodenum.
A major protein in the BLOOD. It is important in maintaining the colloidal osmotic pressure and transporting large organic molecules.
Derivatives of GLUCURONIC ACID. Included under this heading are a broad variety of acid forms, salts, esters, and amides that include the 6-carboxy glucose structure.
Azo compounds are organic compounds characterized by the presence of one or more azo groups, -N=N-, linking two aromatic rings, which can impart various colors and are used in dyes, pharmaceuticals, and chemical research.
Blood tests that are used to evaluate how well a patient's liver is working and also to help diagnose liver conditions.
A subclass of enzymes which includes all dehydrogenases acting on carbon-carbon bonds. This enzyme group includes all the enzymes that introduce double bonds into substrates by direct dehydrogenation of carbon-carbon single bonds.
Impairment of bile flow due to obstruction in small bile ducts (INTRAHEPATIC CHOLESTASIS) or obstruction in large bile ducts (EXTRAHEPATIC CHOLESTASIS).
Method of analyzing chemicals using automation.
Aminobenzenesulfonic acids. Organic acids that are used in the manufacture of dyes and organic chemicals and as reagents.
A mixed function oxidase enzyme which during hemoglobin catabolism catalyzes the degradation of heme to ferrous iron, carbon monoxide and biliverdin in the presence of molecular oxygen and reduced NADPH. The enzyme is induced by metals, particularly cobalt. EC 1.14.99.3.
A phenolphthalein that is used as a diagnostic aid in hepatic function determination.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
A colorless compound formed in the intestines by the reduction of bilirubin. Some is excreted in the feces where it is oxidized to urobilin. Some is reabsorbed and re-excreted in the bile as bilirubin. At times, it is re-excreted in the urine, where it may be later oxidized to urobilin.
The art or process of comparing photometrically the relative intensities of the light in different parts of the spectrum.
An infant during the first month after birth.
Enzymes of the transferase class that catalyze the conversion of L-aspartate and 2-ketoglutarate to oxaloacetate and L-glutamate. EC 2.6.1.1.
A ubiquitous stress-responsive enzyme that catalyzes the oxidative cleavage of HEME to yield IRON; CARBON MONOXIDE; and BILIVERDIN.
An enzyme that catalyzes the conversion of L-alanine and 2-oxoglutarate to pyruvate and L-glutamate. (From Enzyme Nomenclature, 1992) EC 2.6.1.2.
Pathological processes of the LIVER.
A commonly used laboratory solvent. It was previously used as an anesthetic, but was banned from use in the U.S. due to its suspected carcinogenicity.
The identification of selected parameters in newborn infants by various tests, examinations, or other procedures. Screening may be performed by clinical or laboratory measures. A screening test is designed to sort out healthy neonates (INFANT, NEWBORN) from those not well, but the screening test is not intended as a diagnostic device, rather instead as epidemiologic.
A nucleoside diphosphate sugar which serves as a source of glucuronic acid for polysaccharide biosynthesis. It may also be epimerized to UDP iduronic acid, which donates iduronic acid to polysaccharides. In animals, UDP glucuronic acid is used for formation of many glucosiduronides with various aglycones.
Substances used for the detection, identification, analysis, etc. of chemical, biological, or pathologic processes or conditions. Indicators are substances that change in physical appearance, e.g., color, at or approaching the endpoint of a chemical titration, e.g., on the passage between acidity and alkalinity. Reagents are substances used for the detection or determination of another substance by chemical or microscopical means, especially analysis. Types of reagents are precipitants, solvents, oxidizers, reducers, fluxes, and colorimetric reagents. (From Grant & Hackh's Chemical Dictionary, 5th ed, p301, p499)

Phospholipid hydroperoxide cysteine peroxidase activity of human serum albumin. (1/2289)

Human serum albumin (HSA) reduced the phospholipid hydroperoxide, 1-palmitoyl-2-(13-hydroperoxy-cis-9, trans-11-octadecadienoyl)-l-3-phosphatidylcholine (PLPC-OOH) to the corresponding hydroxy-derivative with a high apparent affinity (Km=9. 23+/-0.95 microM). Removal of bound lipid during purification increased this activity. At physiological concentration, HSA reduced the phospholipid hydroperoxide in the absence of a cofactor. However, in the presence of a cofactor (reductant), the rate of the reaction was increased. All of the major aminothiols in plasma could act as reductants, the best being the most abundant, cysteine (Km=600+/-80 microM). For every nanomole of PLPC-OOH reduced by HSA, 1.26 nmol of cystine was formed, indicating a reaction stoichiometry of 1 mol PLPC-OOH to 2 mol cysteine. We used chemical modification to determine which amino acid residues on HSA were responsible for the activity. Oxidation of thiol group(s) by N-ethylmaleimide led to a reduction in the rate of activity, whereas reduction of thiols by either dithiothreitol or the angiotensin-converting enzyme inhibitor, captopril, increased the activity. Both N-ethylmaleimide-modified HSA and dithiothreitol-treated HSA exhibited increased apparent affinities for PLPC-OOH. For a range of preparations of albumin with different modifications, the activity on PLPC-OOH was dependent on the amount of free thiol groups on the albumin (correlation coefficient=0.91). Patients with lowered albumin concentrations after septic shock showed lowered total plasma thiol concentrations and decreased phospholipid hydroperoxide cysteine peroxidase (PHCPx) activities. These results therefore show for the first time that HSA exhibits PHCPx activity, and that the majority of the activity depends on the presence of reduced thiol group(s) on the albumin.  (+info)

Bilirubin, formed by activation of heme oxygenase-2, protects neurons against oxidative stress injury. (2/2289)

Heme oxygenase (HO) catalyzes the conversion of heme to carbon monoxide, iron, and biliverdin, which is immediately reduced to bilirubin (BR). Two HO active isozymes exist: HO1, an inducible heat shock protein, and HO2, which is constitutive and highly concentrated in neurons. We demonstrate a neuroprotective role for BR formed from HO2. Neurotoxicity elicited by hydrogen peroxide in hippocampal and cortical neuronal cultures is prevented by the phorbol ester, phorbol 12-myristate 13-acetate (PMA) via stimulation of protein kinase C. We observe phosphorylation of HO2 through the protein kinase C pathway with enhancement of HO2 catalytic activity and accumulation of BR in neuronal cultures. The neuroprotective effects of PMA are prevented by the HO inhibitor tin protoporphyrin IX and in cultures from mice with deletion of HO2 gene. Moreover, BR, an antioxidant, is neuroprotective at nanomolar concentrations.  (+info)

Genomic structure of the canalicular multispecific organic anion-transporter gene (MRP2/cMOAT) and mutations in the ATP-binding-cassette region in Dubin-Johnson syndrome. (3/2289)

Dubin-Johnson syndrome (DJS) is an autosomal recessive disease characterized by conjugated hyperbilirubinemia. Previous studies of the defects in the human canalicular multispecific organic anion transporter gene (MRP2/cMOAT) in patients with DJS have suggested that the gene defects are responsible for DJS. In this study, we determined the exon/intron structure of the human MRP2/cMOAT gene and further characterized mutations in patients with DJS. The human MRP2/cMOAT gene contains 32 exons, and it has a structure that is highly conserved with that of another ATP-binding-cassette gene, that for a multidrug resistance-associated protein. We then identified three mutations, including two novel ones. All mutations identified to date are in the cytoplasmic domain, which includes the two ATP-binding cassettes and the linker region, or adjacent putative transmembrane domain. Our results confirm that MRP2/cMOAT is the gene responsible for DJS. The finding that mutations are concentrated in the first ATP-binding-cassette domain strongly suggests that a disruption of this region is a critical route to loss of function.  (+info)

Soccer players under regular training show oxidative stress but an improved plasma antioxidant status. (4/2289)

Physical activity is known to induce oxidative stress in individuals subjected to intense exercise. In this study, we investigated the lipoprotein profile and the plasma antioxidant status in a group of soccer players engaged in a regular training programme. As was expected for aerobic exercise, high-density lipoprotein-cholesterol (HDL-C) and HDL3-C levels were significantly increased in the sportsmen (P<0.05). Total plasma antioxidant capacity was 25% higher in sportsmen than in controls (P<0.005). Accordingly, plasma hydrosoluble antioxidant levels (ascorbic acid and uric acid) were found to be significantly elevated in the soccer players (P<0.005). In addition, these subjects showed high concentrations of alpha-tocopherol in plasma compared with controls (P<0.005). Furthermore, an increase in plasma superoxide dismutase activity was also observed in relation to exercise (P<0.01). The elevation in plasma activities of antioxidant enzymes and the higher levels of free radical scavengers of low molecular mass may compensate the oxidative stress caused by physical activity. High levels of high-density lipoprotein in plasma may offer additional protection by inhibiting low-density lipoprotein oxidation and thus liposoluble antioxidant consumption. Therefore, soccer players under regular training show an improved plasma antioxidant status in comparison to sedentary controls.  (+info)

Functional heterogeneity of UDP-glucuronosyltransferase as indicated by its differential development and inducibility by glucocorticoids. Demonstration of two groups within the enzyme's activity towards twelve substrates. (5/2289)

1. UDP-glucuronosyltransferase activity towards 12 substrates has been assessed in rat liver during the perinatal period. 2. Between days 16 and 20 of gestation, enzyme activities towards the substrates 2-aminophenol, 2-aminobenzoate, 4-nitrophenol, 1-naphthol, 4-methylumbelliferone and 5-hydroxytryptamine (the 'late foetal' group) surge to reach adult values, while activities towards bilirubin, testosterone, beta-oestradiol, morphine, phenolphthalein, and chloramphenicol (the 'neonatal' group) remain negligible or at less than 10% of adult values. 3. By the second postnatal day, enzyme activities towards the neonatal group have attained, or approached adult values. 4. Dexamethasone precociously stimulates in 17-day foetal liver in utero transferase activities in the late foetal, but not the neonatal group. A similar inductive pattern is found for 15-day foetal liver in organ culture. 5. It is suggested that foetal glucocorticoids, whose synthesis markedly increases between days 16 and 20 of gestation, are responsibile for triggering the simultaneous surge of all the hepatic UDP-glucuronosyltransferase activities in the late foetal group. The neonatal group of activities apparently require a different or additional stimulus for their appearance. 6. The relationship of these two groups of transferase activities to other similar groups observed during induction by xenobiotics and enzyme purification is discussed.  (+info)

Role of bilirubin overproduction in revealing Gilbert's syndrome: is dyserythropoiesis an important factor? (6/2289)

Gilbert's syndrome was diagnosed in 37 patients with unconjugated hyperbilirubinaemia without overt haemolysis or structural liver abnormality, who had a marked reduction in hepatic bilirubin UDP-glucuronosyltransferase activity (B-GTA) (as compared with that of 23 normal subjects). No significant correlation existed in these patients between serum bilirubin level and the values of B-GTA, thus suggesting that factors other than a low B-GTA must influence the degree of hyperbilirubinaemia in Gilbert's syndrome. Studies of 51Cr erythrocyte survival and 59Fe kinetics in 10 unselected patients demonstrated slight haemolysis in eight, whereas mild ineffective erythropoiesis was suggested in all from a low 24-hour incorporation of radioactive iron into circulating red cells. This overproduction of bilirubin resulting from mild haemolysis and perhaps dyserythropoiesis might reflect only an extreme degree of the normal situation. It certainly contributes to the hyperbilirubinaemia of Gilbert's syndrome and may play a major role in the manifestation of this condition.  (+info)

Unconjugated bilirubin exhibits spontaneous diffusion through model lipid bilayers and native hepatocyte membranes. (7/2289)

The liver is responsible for the clearance and metabolism of unconjugated bilirubin, the hydrophobic end-product of heme catabolism. Although several putative bilirubin transporters have been described, it has been alternatively proposed that bilirubin enters the hepatocyte by passive diffusion through the plasma membrane. In order to elucidate the mechanism of bilirubin uptake, we measured the rate of bilirubin transmembrane diffusion (flip-flop) using stopped-flow fluorescence techniques. Unconjugated bilirubin rapidly diffuses through model phosphatidylcholine vesicles, with a first-order rate constant of 5.3 s-1 (t(1)/(2) = 130 ms). The flip-flop rate is independent of membrane cholesterol content, phospholipid acyl saturation, and lipid packing, consistent with thermodynamic analyses demonstrating minimal steric constraint to bilirubin transmembrane diffusion. The coincident decrease in pH of the entrapped vesicle volume supports a mechanism whereby the bilirubin molecule crosses the lipid bilayer as the uncharged diacid. Transport of bilirubin by native rat hepatocyte membranes exhibits kinetics comparable with that in model vesicles, suggesting that unconjugated bilirubin crosses cellular membranes by passive diffusion through the hydrophobic lipid core. In contrast, there is no demonstrable flip-flop of bilirubin diglucuronide or bilirubin ditaurate in phospholipid vesicles, yet these compounds rapidly traverse isolated rat hepatocyte membranes, confirming the presence of a facilitated uptake system(s) for hydrophilic bilirubin conjugates.  (+info)

Auxiliary partial orthotopic liver transplantation for Crigler-Najjar syndrome type I. (8/2289)

OBJECTIVE: To determine if auxiliary partial orthotopic liver transplantation (APOLT) has the long-term potential to correct the underlying abnormality in Crigler-Najjar syndrome type 1 (CNS1) without the need for total liver replacement. BACKGROUND: Orthotopic liver transplantation has been used successfully to replace the defective enzyme in CNS1. Experimental studies have shown that only 1% to 2% of the normal hepatocyte mass is needed for bilirubin conjugation. If APOLT corrects the underlying metabolic abnormality, it has the advantage of preserving the native liver, which would serve as a "safety net" should the graft fail, and there is the potential for gene therapy in the future with possible withdrawal of immunosuppression. METHODS: Seven APOLT procedures were performed in six recipients with CNS1. Median age at transplantation was 10.5 years. Six transplants were performed as a left auxiliary liver transplant, and one was performed as a right auxiliary liver transplant. Median serum bilirubin level at transplantation was 320 micromol/L. All patients required 12 to 16 hours of phototherapy daily before the transplant to maintain serum bilirubin levels between 250 and 350 micromol/L. RESULTS: Median serum bilirubin level was 50 micromol/L at day 5 after the transplant and 23 micromol/L at a median follow-up of 32 months. In four children, early severe acute rejection developed, requiring conversion to tacrolimus; one underwent a second transplant for chronic rejection and graft atrophy but died from lymphoproliferative disease 6 months after the second transplant. CONCLUSIONS: This report shows that APOLT is technically feasible and provides adequate hepatocyte mass to correct the underlying metabolic abnormality in CNS1.  (+info)

Bilirubin is a yellowish pigment that is produced by the liver when it breaks down old red blood cells. It is a normal byproduct of hemoglobin metabolism and is usually conjugated (made water-soluble) in the liver before being excreted through the bile into the digestive system. Elevated levels of bilirubin can cause jaundice, a yellowing of the skin and eyes. Increased bilirubin levels may indicate liver disease or other medical conditions such as gallstones or hemolysis. It is also measured to assess liver function and to help diagnose various liver disorders.

Hyperbilirubinemia is a medical condition characterized by an excessively high level of bilirubin in the bloodstream. Bilirubin is a yellowish pigment produced by the liver when it breaks down old red blood cells. Normally, bilirubin is conjugated (made water-soluble) in the liver and then excreted through the bile into the digestive system. However, if there is a problem with the liver's ability to process or excrete bilirubin, it can build up in the blood, leading to hyperbilirubinemia.

Hyperbilirubinemia can be classified as either unconjugated or conjugated, depending on whether the bilirubin is in its direct (conjugated) or indirect (unconjugated) form. Unconjugated hyperbilirubinemia can occur due to increased production of bilirubin (such as in hemolytic anemia), decreased uptake of bilirubin by the liver, or impaired conjugation of bilirubin in the liver. Conjugated hyperbilirubinemia, on the other hand, is usually caused by a problem with the excretion of conjugated bilirubin into the bile, such as in cholestatic liver diseases like hepatitis or cirrhosis.

Symptoms of hyperbilirubinemia can include jaundice (yellowing of the skin and eyes), dark urine, light-colored stools, itching, and fatigue. Treatment depends on the underlying cause of the condition and may involve medications, dietary changes, or surgery.

Neonatal jaundice is a medical condition characterized by the yellowing of a newborn baby's skin and eyes due to an excess of bilirubin in the blood. Bilirubin is a yellowish substance produced by the normal breakdown of red blood cells, which are then processed by the liver and excreted through the bile. In neonatal jaundice, the liver is not yet fully developed and cannot process bilirubin quickly enough, leading to its accumulation in the body.

Neonatal jaundice typically appears within the first 2-4 days of life and can range from mild to severe. Mild cases may resolve on their own without treatment, while more severe cases may require medical intervention such as phototherapy or a blood transfusion. Risk factors for neonatal jaundice include prematurity, bruising during birth, blood type incompatibility between mother and baby, and certain genetic disorders.

It is important to monitor newborns closely for signs of jaundice and seek medical attention if concerned, as untreated neonatal jaundice can lead to serious complications such as brain damage or hearing loss.

I'm sorry for any confusion, but "Rats, Gunn" is not a recognized medical term or phrase. It appears to be a nonsensical expression without specific meaning in the context of medicine or healthcare. If you have any questions about medical terminology or concepts, I would be happy to try and help answer those for you!

Bile pigments are the yellow-brown colored end products of hemoglobin breakdown in the liver. Hemoglobin is a protein found in red blood cells that carries oxygen throughout the body. When these cells are broken down, heme (the non-protein part of hemoglobin) is converted into biliverdin, which is then converted into bilirubin. Bilirubin is further metabolized and excreted by the liver as a component of bile, a digestive fluid that helps break down fats in the small intestine.

Under normal conditions, the liver effectively removes and excretes bilirubin from the body through the bile ducts into the small intestine. However, when there is an overproduction of bilirubin or a problem with its elimination, it can accumulate in the blood, leading to jaundice (yellowing of the skin and eyes) and other symptoms associated with liver dysfunction.

In summary, bile pigments are the waste products formed during the breakdown of hemoglobin, primarily consisting of bilirubin, which is eliminated from the body via the liver and bile ducts.

Kernicterus is a severe form of brain damage caused by high levels of bilirubin, a yellow pigment that forms when red blood cells break down. It's most commonly seen in newborns, particularly those with a condition called ABO or Rh incompatibility, where the baby's blood type is different from the mother's. This can lead to an increased breakdown of the baby's red blood cells and a buildup of bilirubin.

In kernicterus, the bilirubin reaches such high levels that it becomes toxic and can damage the brain, particularly areas like the basal ganglia and brainstem. This can result in symptoms such as severe jaundice (a yellowing of the skin and eyes), lethargy, high-pitched crying, poor feeding, and eventually seizures, hearing loss, and developmental delays.

Kernicterus is preventable with timely treatment, which may include phototherapy (using light to break down bilirubin) or exchange transfusion (replacing the baby's blood with fresh donor blood). If you suspect your newborn has jaundice or if their skin appears yellow, it's important to seek medical attention immediately.

Jaundice is a medical condition characterized by the yellowing of the skin, sclera (whites of the eyes), and mucous membranes due to an excess of bilirubin in the bloodstream. Bilirubin is a yellow-orange pigment produced when hemoglobin from red blood cells is broken down. Normally, bilirubin is processed by the liver and excreted through bile into the digestive system. However, if there's an issue with bilirubin metabolism or elimination, it can accumulate in the body, leading to jaundice.

Jaundice can be a symptom of various underlying conditions, such as liver diseases (hepatitis, cirrhosis), gallbladder issues (gallstones, tumors), or blood disorders (hemolysis). It is essential to consult a healthcare professional if jaundice is observed, as it may indicate a severe health problem requiring prompt medical attention.

Neonatal hyperbilirubinemia is a condition characterized by an excessively high level of bilirubin in the blood of newborn infants. Bilirubin is a yellowish pigment produced by the normal breakdown of red blood cells. Normally, bilirubin is processed by the liver and excreted through the bile into the digestive system. However, in neonatal hyperbilirubinemia, the liver may be unable to process bilirubin quickly enough, leading to its accumulation in the bloodstream. This can cause the skin and eyes of the newborn to appear yellow, a condition known as jaundice.

Neonatal hyperbilirubinemia is relatively common and usually resolves on its own within a few days or weeks. However, if bilirubin levels become too high, they can cause brain damage (kernicterus) in severe cases. Treatment may include phototherapy to help break down bilirubin, exchange transfusions, or other interventions to support liver function and reduce bilirubin levels.

Hyperbilirubinemia is a condition characterized by an excess of bilirubin in the blood. Bilirubin is a yellowish substance produced by the liver when it breaks down old red blood cells. Normally, bilirubin is processed by the liver and excreted through the bile ducts and into the digestive system. However, if there is a problem with the liver or the bile ducts, bilirubin can build up in the blood, causing hyperbilirubinemia.

Hereditary hyperbilirubinemia refers to forms of the condition that are caused by genetic mutations. There are several types of hereditary hyperbilirubinemia, including:

1. Dubin-Johnson syndrome: This is a rare autosomal recessive disorder characterized by chronic conjugated hyperbilirubinemia and a dark brownish-black pigmentation of the liver. It is caused by mutations in the MRP2 gene, which provides instructions for making a protein that helps to remove bilirubin from the liver cells into the bile ducts.

2. Rotor syndrome: This is another rare autosomal recessive disorder characterized by chronic conjugated hyperbilirubinemia. It is caused by mutations in the SLCO1B1 and SLCO1B3 genes, which provide instructions for making proteins that help to transport bilirubin into the liver cells.

3. Crigler-Najjar syndrome: This is a rare autosomal recessive disorder characterized by severe unconjugated hyperbilirubinemia. It is caused by mutations in the UGT1A1 gene, which provides instructions for making an enzyme that helps to conjugate bilirubin in the liver.

4. Gilbert syndrome: This is a common autosomal recessive disorder characterized by mild unconjugated hyperbilirubinemia. It is caused by mutations in the UGT1A1 gene, but to a lesser degree than Crigler-Najjar syndrome.

In general, hereditary hyperbilirubinemias are managed with close monitoring of bilirubin levels and may require treatment with phototherapy or exchange transfusion in severe cases. In some cases, liver transplantation may be necessary.

Glucuronosyltransferase (UDP-glucuronosyltransferase) is an enzyme belonging to the family of glycosyltransferases. It plays a crucial role in the process of biotransformation and detoxification of various endogenous and exogenous substances, including drugs, hormones, and environmental toxins, in the liver and other organs.

The enzyme functions by transferring a glucuronic acid moiety from a donor molecule, uridine diphosphate glucuronic acid (UDP-GlcUA), to an acceptor molecule, which can be a variety of hydrophobic compounds. This reaction results in the formation of a more water-soluble glucuronide conjugate, facilitating the excretion of the substrate through urine or bile.

There are multiple isoforms of glucuronosyltransferase, classified into two main families: UGT1 and UGT2. These isoforms exhibit different substrate specificities and tissue distributions, allowing for a wide range of compounds to be metabolized through the glucuronidation pathway.

In summary, Glucuronosyltransferase is an essential enzyme in the detoxification process, facilitating the elimination of various substances from the body by conjugating them with a glucuronic acid moiety.

Diazonium compounds are a class of organic compounds that contain the functional group -N=N+E-, where E- represents a halide ion or an organic cation. They are typically prepared by treating an aromatic primary amine with nitrous acid (HNO2) in an acidic medium, which results in the formation of a diazonium ion.

The general reaction can be represented as follows:

R-NH2 + HNO2 + HX → R-N=N+X- + 2H2O

where R represents the aromatic ring and X- is a halide ion (Cl-, Br-, or I-).

Diazonium compounds are important intermediates in organic synthesis, particularly in the preparation of azo dyes and other colored compounds. They are also useful for introducing functional groups into aromatic rings through various chemical reactions such as sandmeyer reaction, gattermann reaction etc. However, diazonium salts are generally unstable and can decompose explosively if heated or subjected to strong shock or friction. Therefore, they must be handled with care.

Biliverdine is a greenish pigment that is a byproduct of the breakdown of heme, which is a component of hemoglobin in red blood cells. It is formed when bilirubin, another byproduct of heme degradation, is reduced in the liver. Biliverdine is then converted back to bilirubin and excreted from the body as part of bile.

Elevated levels of biliverdine in the blood can indicate liver dysfunction or other medical conditions that affect the breakdown of heme. It may also be present in high concentrations in certain types of hemolytic anemia, where there is excessive destruction of red blood cells and subsequent release of large amounts of heme into the circulation.

Crigler-Najjar Syndrome is a rare inherited genetic disorder that affects the metabolism of bilirubin, a yellow pigment produced when hemoglobin breaks down. This condition is characterized by high levels of unconjugated bilirubin in the blood, which can lead to jaundice, kernicterus, and neurological damage if left untreated.

There are two types of Crigler-Najjar Syndrome: Type I and Type II.

Type I is the more severe form, and it is caused by a mutation in the UGT1A1 gene, which encodes for an enzyme responsible for conjugating bilirubin. People with this type of Crigler-Najjar Syndrome have little to no functional enzyme activity, leading to very high levels of unconjugated bilirubin in the blood. This form is usually diagnosed in infancy and requires regular phototherapy or a liver transplant to prevent neurological damage.

Type II is a milder form of the disorder, caused by a mutation that results in reduced enzyme activity but not complete loss of function. People with this type of Crigler-Najjar Syndrome usually have milder symptoms and may not require regular phototherapy or a liver transplant, although they may still be at risk for neurological damage if their bilirubin levels become too high.

Both types of Crigler-Najjar Syndrome are inherited in an autosomal recessive manner, meaning that an individual must inherit two copies of the mutated gene (one from each parent) to develop the condition.

Gilbert's disease, also known as Gilbert's syndrome, is a common and mild condition characterized by **intermittent** elevations in bilirubin levels in the bloodstream without any evidence of liver damage or disease. Bilirubin is a yellowish pigment that forms when hemoglobin breaks down. Normally, it gets processed in the liver and excreted through bile.

In Gilbert's disease, there is an impaired ability to conjugate bilirubin due to a deficiency or dysfunction of the enzyme UDP-glucuronosyltransferase 1A1 (UGT1A1), which is responsible for the glucuronidation process. This results in mild unconjugated hyperbilirubinemia, where bilirubin levels may rise and cause mild jaundice, particularly during times of fasting, illness, stress, or dehydration.

Gilbert's disease is typically an incidental finding, as it usually does not cause any significant symptoms or complications. It is often discovered during routine blood tests when bilirubin levels are found to be slightly elevated. The condition is usually harmless and does not require specific treatment, but avoiding triggers like fasting or dehydration may help minimize the occurrence of jaundice.

Phototherapy is a medical treatment that involves the use of light to manage or improve certain conditions. It can be delivered in various forms, such as natural light exposure or artificial light sources, including lasers, light-emitting diodes (LEDs), or fluorescent lamps. The wavelength and intensity of light are carefully controlled to achieve specific therapeutic effects.

Phototherapy is most commonly used for newborns with jaundice to help break down bilirubin in the skin, reducing its levels in the bloodstream. This type of phototherapy is called bilirubin lights or bili lights.

In dermatology, phototherapy can be applied to treat various skin conditions like psoriasis, eczema, vitiligo, and acne. Narrowband ultraviolet B (UVB) therapy, PUVA (psoralen plus UVA), and blue or red light therapies are some examples of dermatological phototherapies.

Phototherapy can also be used to alleviate symptoms of seasonal affective disorder (SAD) and other mood disorders by exposing patients to bright artificial light, which helps regulate their circadian rhythms and improve their mood. This form of phototherapy is called light therapy or bright light therapy.

It's essential to consult a healthcare professional before starting any phototherapy treatment, as inappropriate use can lead to adverse effects.

Bile is a digestive fluid that is produced by the liver and stored in the gallbladder. It plays an essential role in the digestion and absorption of fats and fat-soluble vitamins in the small intestine. Bile consists of bile salts, bilirubin, cholesterol, phospholipids, electrolytes, and water.

Bile salts are amphipathic molecules that help to emulsify fats into smaller droplets, increasing their surface area and allowing for more efficient digestion by enzymes such as lipase. Bilirubin is a breakdown product of hemoglobin from red blood cells and gives bile its characteristic greenish-brown color.

Bile is released into the small intestine in response to food, particularly fats, entering the digestive tract. It helps to break down large fat molecules into smaller ones that can be absorbed through the walls of the intestines and transported to other parts of the body for energy or storage.

Serum albumin is the most abundant protein in human blood plasma, synthesized by the liver. It plays a crucial role in maintaining the oncotic pressure or colloid osmotic pressure of blood, which helps to regulate the fluid balance between the intravascular and extravascular spaces.

Serum albumin has a molecular weight of around 66 kDa and is composed of a single polypeptide chain. It contains several binding sites for various endogenous and exogenous substances, such as bilirubin, fatty acids, hormones, and drugs, facilitating their transport throughout the body. Additionally, albumin possesses antioxidant properties, protecting against oxidative damage.

Albumin levels in the blood are often used as a clinical indicator of liver function, nutritional status, and overall health. Low serum albumin levels may suggest liver disease, malnutrition, inflammation, or kidney dysfunction.

Glucuronates are not a medical term per se, but they refer to salts or esters of glucuronic acid, a organic compound that is a derivative of glucose. In the context of medical and biological sciences, glucuronidation is a common detoxification process in which glucuronic acid is conjugated to a wide variety of molecules, including drugs, hormones, and environmental toxins, to make them more water-soluble and facilitate their excretion from the body through urine or bile.

The process of glucuronidation is catalyzed by enzymes called UDP-glucuronosyltransferases (UGTs), which are found in various tissues, including the liver, intestines, and kidneys. The resulting glucuronides can be excreted directly or further metabolized before excretion.

Therefore, "glucuronates" can refer to the chemical compounds that result from this process of conjugation with glucuronic acid, as well as the therapeutic potential of enhancing or inhibiting glucuronidation for various clinical applications.

Azo compounds are organic compounds characterized by the presence of one or more azo groups (-N=N-) in their molecular structure. The term "azo" is derived from the Greek word "azō," meaning "to boil" or "to sparkle," which refers to the brightly colored nature of many azo compounds.

These compounds are synthesized by the reaction between aromatic amines and nitrous acid or its derivatives, resulting in the formation of diazonium salts, which then react with another aromatic compound containing an active methylene group to form azo compounds.

Azo compounds have diverse applications across various industries, including dyes, pigments, pharmaceuticals, and agrochemicals. They are known for their vibrant colors, making them widely used as colorants in textiles, leather, paper, and food products. In addition, some azo compounds exhibit unique chemical properties, such as solubility, stability, and reactivity, which make them valuable intermediates in the synthesis of various organic compounds.

However, certain azo compounds have been found to pose health risks due to their potential carcinogenicity and mutagenicity. As a result, regulations have been imposed on their use in consumer products, particularly those intended for oral consumption or direct skin contact.

Liver function tests (LFTs) are a group of blood tests that are used to assess the functioning and health of the liver. These tests measure the levels of various enzymes, proteins, and waste products that are produced or metabolized by the liver. Some common LFTs include:

1. Alanine aminotransferase (ALT): An enzyme found primarily in the liver, ALT is released into the bloodstream in response to liver cell damage. Elevated levels of ALT may indicate liver injury or disease.
2. Aspartate aminotransferase (AST): Another enzyme found in various tissues, including the liver, heart, and muscles. Like ALT, AST is released into the bloodstream following tissue damage. High AST levels can be a sign of liver damage or other medical conditions.
3. Alkaline phosphatase (ALP): An enzyme found in several organs, including the liver, bile ducts, and bones. Elevated ALP levels may indicate a blockage in the bile ducts, liver disease, or bone disorders.
4. Gamma-glutamyl transferase (GGT): An enzyme found mainly in the liver, pancreas, and biliary system. Increased GGT levels can suggest liver disease, alcohol consumption, or the use of certain medications.
5. Bilirubin: A yellowish pigment produced when hemoglobin from red blood cells is broken down. Bilirubin is processed by the liver and excreted through bile. High bilirubin levels can indicate liver dysfunction, bile duct obstruction, or certain types of anemia.
6. Albumin: A protein produced by the liver that helps maintain fluid balance in the body and transports various substances in the blood. Low albumin levels may suggest liver damage, malnutrition, or kidney disease.
7. Total protein: A measure of all proteins present in the blood, including albumin and other types of proteins produced by the liver. Decreased total protein levels can indicate liver dysfunction or other medical conditions.

These tests are often ordered together as part of a routine health checkup or when evaluating symptoms related to liver function or disease. The results should be interpreted in conjunction with clinical findings, medical history, and other diagnostic tests.

Oxidoreductases acting on CH-CH group donors are a class of enzymes within the larger group of oxidoreductases, which are responsible for catalyzing oxidation-reduction reactions. Specifically, this subclass of enzymes acts upon donors containing a carbon-carbon (CH-CH) bond, where one atom or group of atoms is oxidized and another is reduced during the reaction process. These enzymes play crucial roles in various metabolic pathways, including the breakdown and synthesis of carbohydrates, lipids, and amino acids.

The reactions catalyzed by these enzymes involve the transfer of electrons and hydrogen atoms between the donor and an acceptor molecule. This process often results in the formation or cleavage of carbon-carbon bonds, making them essential for numerous biological processes. The systematic name for this class of enzymes is typically structured as "donor:acceptor oxidoreductase," where donor and acceptor represent the molecules involved in the electron transfer process.

Examples of enzymes that fall under this category include:

1. Aldehyde dehydrogenases (EC 1.2.1.3): These enzymes catalyze the oxidation of aldehydes to carboxylic acids, using NAD+ as an electron acceptor.
2. Dihydrodiol dehydrogenase (EC 1.3.1.14): This enzyme is responsible for the oxidation of dihydrodiols to catechols in the biodegradation of aromatic compounds.
3. Succinate dehydrogenase (EC 1.3.5.1): A key enzyme in the citric acid cycle, succinate dehydrogenase catalyzes the oxidation of succinate to fumarate and reduces FAD to FADH2.
4. Xylose reductase (EC 1.1.1.307): This enzyme is involved in the metabolism of pentoses, where it reduces xylose to xylitol using NADPH as a cofactor.

Cholestasis is a medical condition characterized by the interruption or reduction of bile flow from the liver to the small intestine. Bile is a digestive fluid produced by the liver that helps in the breakdown and absorption of fats. When the flow of bile is blocked or reduced, it can lead to an accumulation of bile components, such as bilirubin, in the blood, which can cause jaundice, itching, and other symptoms.

Cholestasis can be caused by various factors, including liver diseases (such as hepatitis, cirrhosis, or cancer), gallstones, alcohol abuse, certain medications, pregnancy, and genetic disorders. Depending on the underlying cause, cholestasis may be acute or chronic, and it can range from mild to severe in its symptoms and consequences. Treatment for cholestasis typically involves addressing the underlying cause and managing the symptoms with supportive care.

"Autoanalysis" is not a term that is widely used in the medical field. However, in psychology and psychotherapy, "autoanalysis" refers to the process of self-analysis or self-examination, where an individual analyzes their own thoughts, feelings, behaviors, and experiences to gain insight into their unconscious mind and understand their motivations, conflicts, and emotional patterns.

Self-analysis can involve various techniques such as introspection, journaling, meditation, dream analysis, and reflection on past experiences. While autoanalysis can be a useful tool for personal growth and self-awareness, it is generally considered less reliable and comprehensive than professional psychotherapy or psychoanalysis, which involves a trained therapist or analyst who can provide objective feedback, interpretation, and guidance.

I'm sorry for any confusion, but "Sulfanilic Acids" is not a recognized medical term or a specific medical condition. Sulfanilic acid is a chemical compound with the formula H2SO3NCH2COOH. It is used in various industrial applications such as dye and drug synthesis, but it is not a term that would be commonly used in medical contexts.

If you have any questions related to medical topics or conditions, I'd be happy to help! Please provide more information so I can give you a relevant and accurate response.

Sulfobromophthalein (BSP or bromsulphthalein) is not typically defined in a medical dictionary as it is a chemical compound. However, I can provide you with some information about its use in a medical context:

Sulfobromophthalein is a chemical compound primarily used for liver function tests. It is a dye that is injected into the patient's bloodstream, and then its clearance rate from the blood is measured to evaluate liver function. A healthy liver should quickly remove the dye from the blood and excrete it through the bile ducts into the digestive system. If the liver is not functioning properly, the clearance of sulfobromophthalein will be slower, leading to higher levels of the dye remaining in the bloodstream over time.

The test using sulfobromophthalein has largely been replaced by more modern and specific liver function tests; however, it was once widely used for assessing overall liver health and diagnosing conditions such as hepatitis, cirrhosis, and liver damage due to various causes.

The liver is a large, solid organ located in the upper right portion of the abdomen, beneath the diaphragm and above the stomach. It plays a vital role in several bodily functions, including:

1. Metabolism: The liver helps to metabolize carbohydrates, fats, and proteins from the food we eat into energy and nutrients that our bodies can use.
2. Detoxification: The liver detoxifies harmful substances in the body by breaking them down into less toxic forms or excreting them through bile.
3. Synthesis: The liver synthesizes important proteins, such as albumin and clotting factors, that are necessary for proper bodily function.
4. Storage: The liver stores glucose, vitamins, and minerals that can be released when the body needs them.
5. Bile production: The liver produces bile, a digestive juice that helps to break down fats in the small intestine.
6. Immune function: The liver plays a role in the immune system by filtering out bacteria and other harmful substances from the blood.

Overall, the liver is an essential organ that plays a critical role in maintaining overall health and well-being.

Urobilinogen is a colorless or slightly yellowish compound that is formed in the intestines as a byproduct of the breakdown of bilirubin, which is a waste product produced from the breakdown of old red blood cells. Some urobilinogen gets reabsorbed into the bloodstream and is carried to the liver, where it is converted back into bilirubin. The rest is excreted in the stool, giving it its normal brown color.

Abnormally high levels of urobilinogen in the urine can be a sign of certain medical conditions, such as liver disease or hemolytic anemia, which can cause increased breakdown of red blood cells and therefore increased production of bilirubin and urobilinogen. Low levels of urobilinogen in the urine can also be significant, as they may indicate a problem with the liver's ability to reabsorb or metabolize urobilinogen.

It is important to note that urobilinogen testing is not typically used as a standalone diagnostic tool, but rather as one piece of information to be considered in conjunction with other test results and clinical findings.

Spectrophotometry is a technical analytical method used in the field of medicine and science to measure the amount of light absorbed or transmitted by a substance at specific wavelengths. This technique involves the use of a spectrophotometer, an instrument that measures the intensity of light as it passes through a sample.

In medical applications, spectrophotometry is often used in laboratory settings to analyze various biological samples such as blood, urine, and tissues. For example, it can be used to measure the concentration of specific chemicals or compounds in a sample by measuring the amount of light that is absorbed or transmitted at specific wavelengths.

In addition, spectrophotometry can also be used to assess the properties of biological tissues, such as their optical density and thickness. This information can be useful in the diagnosis and treatment of various medical conditions, including skin disorders, eye diseases, and cancer.

Overall, spectrophotometry is a valuable tool for medical professionals and researchers seeking to understand the composition and properties of various biological samples and tissues.

A newborn infant is a baby who is within the first 28 days of life. This period is also referred to as the neonatal period. Newborns require specialized care and attention due to their immature bodily systems and increased vulnerability to various health issues. They are closely monitored for signs of well-being, growth, and development during this critical time.

Aspartate aminotransferases (ASTs) are a group of enzymes found in various tissues throughout the body, including the heart, liver, and muscles. They play a crucial role in the metabolic process of transferring amino groups between different molecules.

In medical terms, AST is often used as a blood test to measure the level of this enzyme in the serum. Elevated levels of AST can indicate damage or injury to tissues that contain this enzyme, such as the liver or heart. For example, liver disease, including hepatitis and cirrhosis, can cause elevated AST levels due to damage to liver cells. Similarly, heart attacks can also result in increased AST levels due to damage to heart muscle tissue.

It is important to note that an AST test alone cannot diagnose a specific medical condition, but it can provide valuable information when used in conjunction with other diagnostic tests and clinical evaluation.

Heme Oxygenase-1 (HO-1) is an inducible enzyme that catalyzes the degradation of heme into biliverdin, iron, and carbon monoxide. It is a rate-limiting enzyme in the oxidative degradation of heme. HO-1 is known to play a crucial role in cellular defense against oxidative stress and inflammation. It is primarily located in the microsomes of many tissues, including the spleen, liver, and brain. Induction of HO-1 has been shown to have cytoprotective effects, while deficiency in HO-1 has been associated with several pathological conditions, such as vascular diseases, neurodegenerative disorders, and cancer.

Alanine transaminase (ALT) is a type of enzyme found primarily in the cells of the liver and, to a lesser extent, in the cells of other tissues such as the heart, muscles, and kidneys. Its primary function is to catalyze the reversible transfer of an amino group from alanine to another alpha-keto acid, usually pyruvate, to form pyruvate and another amino acid, usually glutamate. This process is known as the transamination reaction.

When liver cells are damaged or destroyed due to various reasons such as hepatitis, alcohol abuse, nonalcoholic fatty liver disease, or drug-induced liver injury, ALT is released into the bloodstream. Therefore, measuring the level of ALT in the blood is a useful diagnostic tool for evaluating liver function and detecting liver damage. Normal ALT levels vary depending on the laboratory, but typically range from 7 to 56 units per liter (U/L) for men and 6 to 45 U/L for women. Elevated ALT levels may indicate liver injury or disease, although other factors such as muscle damage or heart disease can also cause elevations in ALT.

Liver diseases refer to a wide range of conditions that affect the normal functioning of the liver. The liver is a vital organ responsible for various critical functions such as detoxification, protein synthesis, and production of biochemicals necessary for digestion.

Liver diseases can be categorized into acute and chronic forms. Acute liver disease comes on rapidly and can be caused by factors like viral infections (hepatitis A, B, C, D, E), drug-induced liver injury, or exposure to toxic substances. Chronic liver disease develops slowly over time, often due to long-term exposure to harmful agents or inherent disorders of the liver.

Common examples of liver diseases include hepatitis, cirrhosis (scarring of the liver tissue), fatty liver disease, alcoholic liver disease, autoimmune liver diseases, genetic/hereditary liver disorders (like Wilson's disease and hemochromatosis), and liver cancers. Symptoms may vary widely depending on the type and stage of the disease but could include jaundice, abdominal pain, fatigue, loss of appetite, nausea, and weight loss.

Early diagnosis and treatment are essential to prevent progression and potential complications associated with liver diseases.

Chloroform is a volatile, clear, and nonflammable liquid with a mild, sweet, and aromatic odor. Its chemical formula is CHCl3, consisting of one carbon atom, one hydrogen atom, and three chlorine atoms. Chloroform is a trihalomethane, which means it contains three halogens (chlorine) in its molecular structure.

In the medical field, chloroform has been historically used as an inhaled general anesthetic agent due to its ability to produce unconsciousness and insensibility to pain quickly. However, its use as a surgical anesthetic has largely been abandoned because of several safety concerns, including its potential to cause cardiac arrhythmias, liver and kidney damage, and a condition called "chloroform hepatopathy" with prolonged or repeated exposure.

Currently, chloroform is not used as a therapeutic agent in medicine but may still be encountered in laboratory settings for various research purposes. It's also possible to find traces of chloroform in drinking water due to its formation during the disinfection process using chlorine-based compounds.

Neonatal screening is a medical procedure in which specific tests are performed on newborn babies within the first few days of life to detect certain congenital or inherited disorders that are not otherwise clinically apparent at birth. These conditions, if left untreated, can lead to serious health problems, developmental delays, or even death.

The primary goal of neonatal screening is to identify affected infants early so that appropriate treatment and management can be initiated as soon as possible, thereby improving their overall prognosis and quality of life. Commonly screened conditions include phenylketonuria (PKU), congenital hypothyroidism, galactosemia, maple syrup urine disease, sickle cell disease, cystic fibrosis, and hearing loss, among others.

Neonatal screening typically involves collecting a small blood sample from the infant's heel (heel stick) or through a dried blood spot card, which is then analyzed using various biochemical, enzymatic, or genetic tests. In some cases, additional tests such as hearing screenings and pulse oximetry for critical congenital heart disease may also be performed.

It's important to note that neonatal screening is not a diagnostic tool but rather an initial step in identifying infants who may be at risk of certain conditions. Positive screening results should always be confirmed with additional diagnostic tests before any treatment decisions are made.

Uridine Diphosphate Glucuronic Acid (UDP-Glucuronic Acid) is not a medical term per se, but rather a biochemical term. It is a compound that plays an essential role in the detoxification process in the liver. UDP-Glucuronic Acid is a nucleotide sugar derivative that combines with toxins, drugs, and other substances to form glucuronides, which are then excreted through urine or bile. This process is known as glucuronidation, and it helps make the substances more water-soluble and easier for the body to eliminate.

Indicators and reagents are terms commonly used in the field of clinical chemistry and laboratory medicine. Here are their definitions:

1. Indicator: An indicator is a substance that changes its color or other physical properties in response to a chemical change, such as a change in pH, oxidation-reduction potential, or the presence of a particular ion or molecule. Indicators are often used in laboratory tests to monitor or signal the progress of a reaction or to indicate the end point of a titration. A familiar example is the use of phenolphthalein as a pH indicator in acid-base titrations, which turns pink in basic solutions and colorless in acidic solutions.

2. Reagent: A reagent is a substance that is added to a system (such as a sample or a reaction mixture) to bring about a chemical reaction, test for the presence or absence of a particular component, or measure the concentration of a specific analyte. Reagents are typically chemicals with well-defined and consistent properties, allowing them to be used reliably in analytical procedures. Examples of reagents include enzymes, antibodies, dyes, metal ions, and organic compounds. In laboratory settings, reagents are often prepared and standardized according to strict protocols to ensure their quality and performance in diagnostic tests and research applications.

"Bilirubin: The Test , Bilirubin Test: Total bilirubin; TBIL; Neonatal bilirubin; Direct bilirubin; Conjugated bilirubin; ... δ bilirubin = total bilirubin - (unconjugated bilirubin + conjugated bilirubin) The half-life of delta bilirubin is equivalent ... Direct bilirubin = Conjugated bilirubin + delta bilirubin In the liver, bilirubin is conjugated with glucuronic acid by the ... Total bilirubin = direct bilirubin + indirect bilirubin Elevation of both alanine aminotransferase (ALT) and bilirubin is more ...
... is a water-soluble reaction intermediate over the process of conjugation of indirect bilirubin. Bilirubin ... In this case, total serum bilirubin increases while the ratio of direct bilirubin to indirect bilirubin remains 96 to 4 as up ... not bilirubin. If it is the liver that cannot effectively transfer the indirect bilirubin into bilirubin glucuronide and ... insoluble bilirubin. This form of bilirubin also is referred to as indirect-reacting or unconjugated bilirubin. Dubin-Johnson ...
Bilirubin di-glucuronide is a conjugated form of bilirubin formed in bilirubin metabolism. The hydrophilic character of ... Bilirubin mono-glucuronide Chowdhury, J. R.; Chowdhury, N. R.; Wu, G.; Shouval, R.; Arias, I. M. (1981). "Bilirubin mono- and ... 2007-08-29). "Modulation of sinusoidal and canalicular elimination of bilirubin-glucuronides by rifampicin and other ... bilirubin diglucuronide enables it to be water-soluble. It is pumped across the hepatic canalicular membrane into the bile by ...
The systematic name of this enzyme class is bilirubin:oxygen oxidoreductase. This enzyme is also called bilirubin oxidase M-1. ... In enzymology, a bilirubin oxidase, BOD or BOx, (EC 1.3.3.5) is an enzyme encoded by a gene in various organisms that catalyzes ... Two structures of bilirubin oxidase from the ascomycete Myrothecium verrucaria have been deposited in the Protein Data Bank ( ... July 2010). "X-ray analysis of bilirubin oxidase from Myrothecium verrucaria at 2.3 A resolution using a twinned crystal". Acta ...
... bilirubin-glucuronoside, and two products, bilirubin and bilirubin-bisglucuronoside. This enzyme belongs to the family of ... The systematic name of this enzyme class is bilirubin-glucuronoside:bilirubin-glucuronoside D-glucuronosyltransferase. Other ... bilirubin + bilirubin-bisglucuronoside Hence, this enzyme has one substrate, ... In enzymology, a bilirubin-glucuronoside glucuronosyltransferase (EC 2.4.1.95) is an enzyme that catalyzes the chemical ...
"Bilirubin". American Chemical Society. Retrieved 2021-05-28. "Community Awards". Harvard-MIT Health Sciences and Technology. ... London and colleagues demonstrated that hemoglobin is the endogenous source of bilirubin, an important event in the fields of ...
The resulting bilirubin contains the suffix IXα to identify the composition of its structure by indicating its parent molecule ... "Bilirubin". American Chemical Society. Retrieved 2021-10-19. Heme+Oxygenase at the U.S. National Library of Medicine Medical ... Watson C (1977). "Historical Review of Bilirubin Chemistry". In Berk P (ed.). Chemistry and Physiology of Bile Pigments. p. 5. ... Biliverdin IXα undergoes biotransformation via biliverdin reductase to form bilirubin IXα. Bilins play important roles across ...
... some bilirubin glucuronide is converted back to bilirubin via bacterial enzymes in the terminal ileum. This bilirubin is ... which rapidly reduces to free bilirubin. Bilirubin binds tightly to plasma proteins (especially albumin) in the blood stream ... Bile pigment Bilirubin Biliverdin Heme Urobilin Boron W, Boulpaep E. Medical Physiology: A cellular and molecular approach, ... ISBN 1-4160-2328-3 Kay IT, Weimer M, Watson CJ (1963). "The formation in vitro of stercobilin from bilirubin" Journal of ...
Kalakonda, Aditya; John, Savio (2018-10-27). "Physiology, Bilirubin". NCBI Bookshelf. PMID 29261920. Retrieved 2019-05-04. ...
Jaundice is caused by hyperbilirubinemia, or abnormally high levels of bilirubin in the blood. Bilirubin is usually bound to ... However, in neonatal jaundice, the concentration of bilirubin overwhelms that of albumin and some of the bilirubin remains ... Normally bilirubin would not be able to diffuse across the blood-brain barrier, but in infants, the barrier is immature and has ... Bilirubin is toxic as it prevents the phosphorylation of many proteins, including synapsin I which binds vesicles in the ...
... high bilirubin levels; distorted sense of taste, headache, and dizziness; high blood pressure; distorted sense of hearing, ...
... and serum bilirubin. The expected pattern on hemoglobin electrophoresis in people with beta-thalassemia is an increased level ...
The release of heme leads to the production of bilirubin and depletion of plasma proteins, such as albumin, haptoglobin, and ... "Bilirubin and hemolytic anemia". eClinpath. Retrieved 2019-05-08. "Thrombotic Microangiopathy (TMA)". UNC Kidney Center. ... and release unconjugated bilirubin into the blood plasma circulation. Typically, the spleen destroys mildly abnormal red blood ... "Total bilirubin in athletes, determination of reference range". Biology of Sport. 34 (1): 45-48. doi:10.5114/biolsport. ...
"Bilirubin and hemolytic anemia". eClinpath. Retrieved 2019-05-08. Online Mendelian Inheritance in Man (OMIM): Orthosatic ... Morgan WT, Muller-Eberhard U, Lamola AA (January 1978). "Interaction of rabbit hemopexin with bilirubin". Biochimica et ...
... and bilirubin have been shown to be potent scavengers of hydroperoxyl radicals. They have also been shown to inhibit ... In bruises, its breakdown into bilirubin leads to a yellowish color. Biliverdin has been found in excess in the blood of humans ... Bilirubin Heme Stercobilin Tetrapyrrole Urobilin Boron W, Boulpaep E. Medical Physiology: a cellular and molecular approach, ... Some studies have found that people with higher concentration levels of bilirubin and biliverdin in their bodies have a lower ...
"Bilirubin and hemolytic anemia". eClinpath. Retrieved 2019-05-08. Schaer, D. J.; Buehler, P. W.; Alayash, A. I.; Belcher, J. D ...
Bilirubin is almost universally elevated. Alkaline phosphatase is often elevated in pregnancy due to production from the ...
The other major final product of heme degradation is bilirubin. Increased levels of this chemical are detected in the blood if ... Intestines metabolise bilirubin into urobilinogen. Urobilinogen leaves the body in faeces, in a pigment called stercobilin. ... When the porphyrin ring is broken up, the fragments are normally secreted as a yellow pigment called bilirubin, which is ... In hemolysis (accelerated breakdown of red blood cells), associated jaundice is caused by the hemoglobin metabolite bilirubin, ...
Bilirubin is its major pigment. Bile acts partly as a surfactant which lowers the surface tension between either two liquids or ... This is why it is sometimes known as the 'graveyard of red blood cells'. A product of this digestion is the pigment bilirubin, ... If there is too much cholesterol or bilirubin in the bile, or if the gallbladder does not empty properly the systems can fail. ... This is how gallstones form when a small piece of calcium gets coated with either cholesterol or bilirubin and the bile ...
75 IU/mL Bilirubin level > 0.01 mg/dL ALP > 2 IU/L Peritoneal washing Rosen 2009, p. 22 Rosen 2009, p. 422-4 Tintinalli JE, ...
Mutations in this gene cause serious problems for bilirubin metabolism; each syndrome can be caused by one or many mutations, ... Phenobarbital treatment does not help to lower bilirubin level, because it only increases the amount of mutated UGT1A1 enzyme, ... Kadakol A, Ghosh SS, Sappal BS, Sharma G, Chowdhury JR, Chowdhury NR (2000). "Genetic lesions of bilirubin uridine- ... In this case phenobarbital treatment helps to lower bilirubin lever by more than 30%. Hyperbilirubinemia, familial transient ...
Bilirubin absorbs light at wavelengths between 450 and 460 nm. Spectrophotometry can also detect the presence of oxyhemoglobin ... May 2008). "Revised National Guidelines for Analysis of Cerebrospinal Fluid for Bilirubin in Suspected Subarachnoid Haemorrhage ... Florkowski, Christopher; Ungerer, Jacobus; Southby, Sandi; George, Peter (17 December 2004). "CSF Bilirubin Measurement for ... and therefore no bilirubin is present. After the cerebrospinal fluid is obtained, a variety of its parameters can be checked, ...
Ma J.S.; Yan F.; Wang C.Q.; An J.Y. (1989). "Hypocrellin-A sensitized photooxidation of bilirubin". Photochemistry and ...
ZZ, ZE, EE and EZ are the four structural isomers of bilirubin. ZZ is the stable, more insoluble form. Other forms are ... Lumirubin is a structural isomer of bilirubin, which is formed during phototherapy used to treat neonatal jaundice. This polar ... "The Effects of Bilirubin and Lumirubin on Metabolic and Oxidative Stress Markers". Frontiers in Pharmacology. 12: 567001. doi: ... and its effects are considered less toxic than those of bilirubin. Lumirubin is excreted into bile or urine. ...
Total bilirubin more than 331.5 μmol/L (19.5 mg/dL) (hyperbilirubinemia). Direct bilirubin more than 34 μmol/L (2.0 mg/dL). The ... Further inhibition of bilirubin conjugation leads to increased levels of bilirubin in the blood. However, these results have ... ISBN 8180562107, 9788180562105 McDonagh, A. F. (2007). "Movement of Bilirubin and Bilirubin Conjugates Across the Placenta". ... with a rapid rise of serum bilirubin up to 255 μmol/L (15 mg/dL). Phase two - bilirubin levels decline to about 34 μmol/L (2 mg ...
... is among the few plants which have been verified to contain the pigment bilirubin, which is usually found in ... "Animal Pigment Bilirubin Discovered in Plants". Journal of the American Chemical Society. 131 (8): 2830. doi:10.1021/ja809065g ...
... bile serves also as the route of excretion for bilirubin, a byproduct of red blood cells recycled by the liver. Bilirubin ... The two main pigments of bile are bilirubin, which is yellow, and its oxidised form biliverdin, which is green. When mixed, ... The blockage of bile might cause a buildup of bilirubin in the bloodstream which can result in jaundice. There are several ... In the human liver, bile is composed of 97-98% water, 0.7% bile salts, 0.2% bilirubin, 0.51% fats (cholesterol, fatty acids, ...
Bilimetrix developed the first point-of-care device for measuring bilirubin in newborns. Early detection of harmful bilirubin ... a bilirubin-induced neurological condition. Since very early in his career, Tiribelli was fascinated by bilirubin. Expanding ... Claudio Tiribelli (born 6 October 1946) is an Italian hepatologist best known for his studies on bilirubin and Kernicterus, ... "claudio tiribelli bilirubin - Search Results - PubMed". PubMed. Retrieved 11 August 2021. Bellentani, Stefano; Saccoccio, ...
Methodist Hospital of Brooklyn - New York - 1967-1981 Developed a new method for measuring the bilirubin content of amniotic ... doi:10.1016/0010-7824(70)90019-3. Mallikarjuneswara VR, Clemetson CA, Carr JJ (1 March 1970). "Determination of bilirubin in ...
MacGill M (July 24, 2018). "High bilirubin levels: Meaning, symptoms, and tests". Medical News Today. Retrieved 2018-10-21. ... Increased levels of Bilirubin, causing skin and white parts of the eyes to turn yellow Inhibits urinary nitrous oxide ...

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