Hepatic levels of UDP-glucuronic acid (UDP-GA), UDP-glucose, NAD + , and total adenine nucleotides (TAN) and activities of UDP-glucuronyltransferase (UDP-GT) and UDP-glucose dehydrogenase were measured on Day 4.
Anti-HbcAg. Antibody to hepatitis B core proteins.. The hepatitis B core protein is manufactured in the hepatocyte nucleus and then released into the cytoplasm where it is coated with HBsAg to make the complete virus. AntiHBsAg is initially synthesized whole the B virus is actively replicating and thus, anti-HbcAg and HBsAg together are markers for continued infectivity. Anti-HBAg (HBcAb) and HBsAb together indicate recovery from hepatitis B and immunity against reinfection.
Candida leads to brain fog because having systemic candidiasis means you're constantly drinking alcohol, as yeasts convert sugars into alcohol. This also congests the liver, another major co-factor in brain fog. If the liver, the filter for blood, is congested, it cannot take toxins out of the bloodstream fast enough. These toxins will pass the blood-brain barrier of the brain and deplete the brain of oxygen and glycogen.
Accumulating evidence indicates that mutations in the human UGT1 gene locus abolish hepatic bilirubin UDP-glucuronosyltransferase activity and cause the subsequent accumulation of bilirubin to toxic levels in patients with Crigler-Najjar type 1 (CN-I). Genetic and biochemical criteria are required to link CN-I with mutations in UGT1. Here we present analysis of mutations at the UGT1 locus in three individuals that were clinically diagnosed with CN-I (two related and one unrelated). Each patient carries a single base substitution that alters conserved residues in the transferase enzyme molecule, serine to phenylalanine at codon 376 and glycine to glutamic acid at codon 309. Each was homozygous for the defect as demonstrated by sequencing and RFLPs. Mutant cDNAs, constructed by site-directed mutagenesis, inserted into expression vectors, and transfected into COS-1 cells, supported the synthesis of the bilirubin transferase protein but only cells transfected with the wild-type cDNA expressed bilirubin UDP-glucuronosyltransferase activity. The data provide conclusive evidence that alterations at Gly 309 and Ser 376 are the genetic basis for CN-I in these families. These results suggest that the two codons, located in conserved regions of the molecule, are part of the active site of the bilirubin enzyme.
Synthesis in vitro with UDP-glucuronic acid, UDP-glucose or UDP-xylose as the sugar donor led exclusively to the formation of monoconjugated bilirubin-IX alpha.
Glucose – glycogen normally 4% liver weight (60-70 g). A 70-kg man uses roughly 12 g gluc/hr. Serum glucose rarely depressed in liver disease unless it is far advanced and imminently fatal.
Globulins: Many types. Immunoglobulins synthesized by plasma cells; alpha and beta by hepatocyte and intestinal mucosal cells. Electrophoresis separates globulins into components; gamma increased diffusely in hepatocellular diseases, cirrhosis, and particularly in autoimmune chronic hepatitis.
Microbial virulence is generally considered to be multifactorial with infection resulting from the sum of several globally regulated virulence factors. Estrogen may serve as a signal for global virulence induction in Candida albicans. Nonsteroidal estrogens and estrogen receptor antagonists may therefore have interesting effects on yeast and their virulence factors. Growth of C. albicans was monitored by viable plate counts at timed intervals after inoculation into yeast nitrogen broth plus glucose. To determine if increased growth of yeast in the presence of estradiol was due to tyrosine kinase-mediated signaling, we measured growth in the presence of genistein, estradiol or genistein plus estradiol and compared these conditions to controls, which were not supplemented with either compound. Unexpectedly, genistein stimulated growth of C. albicans. In addition, genistein was found to increase the rate of germination (possibly reflecting release from G(0) into G(1) cell cycle phase) and also increased Hsp90 expression, demonstrated by a dot blot technique which employed a commercial primary antibody detected with chemiluminescence with horseradish peroxidase-labeled secondary antibody. These biological effects may be attributable to genistein's activity as a phytoestrogen. In contrast, nafoxidine suppressed growth of Candida and mildly diminished Hsp90 expression. This study raises the possibility of receptor cross-talk between estrogen and isoflavinoid compounds, and antiestrogens which may affect the same signaling system, though separate targets for each compound were not ruled out.
Very often a most serious acute reaction after the infusion (1 to 3 hours later) is noted consisting of fever, shaking chills, hypotension, anorexia, nausea, vomiting, headache, dyspnea, and tachypnea. This reaction sometimes subsides with later applications of the drug and may in part be due to histamine liberation. An increase in prostaglandin-synthesis may also play a role. Often the most difficult decision has to be made, whether the fever is disease- or drug-related. In order to decrease the likelihood and severity of the symptoms, initial doses should be low and increased slowly. The liposomal preperation obviously has a lower incidence of the syndrome. Acetaminophen, pethidine, diphenhydramine and/or hydrocortisone have all be used to treat or prevent the syndrome, but the prophylactic use of these drugs should be limited.
In humans, more than 18 functional UGTs have been isolated, and several have demonstrated significant reactivity toward estrogens and their metabolites, catecholestrogens (14, 15, 16, 17, 18, 19, 20, 21) . UGT1A1 is thought to play a major role in the metabolism of estradiol (E2) because a Crigler-Najjar patient deficient in UGT1A1 had a 70% decrease in the hepatic glucuronidation of E2 compared with liver microsomes from healthy subjects (18) . UGT1A1 also catalyzes the glucuronidation of hydroxylated metabolites of E2 and estrone (17)... A common variant in the UGT1A1 gene, designated as UGT1A1*28 [A(TA)7TAA], is known to decrease the level of gene expression (30 , 31) . Variability in the expression of the UGT1A1 protein resulting from this polymorphism may lead to important differences in estrogen biotransformation.
Catechol estrogens are major estrogen metabolites in mammals and are the most potent naturally occurring inhibitors of catechol-amine metabolism. These estrogen compounds have been implicated in carcinogenic activity and the 4/2-hydroxyestradiol concentration has been shown to be elevated in neoplastic human mammary tissue compared to normal human breast tissue. Three human liver UDP-glucuronosyltransferases, UGT2B7, UGT1A1, and UGT1A3, have been shown to catalyze the glucuronidation of catechol estrogens and lead to their enhanced elimination via urine or bile.