Biomedical subjects

S Q Xia

Publications and source records attributed to S Q Xia.

6 recordsLinked to original sources

PubMed2004

Conjugation metabolism of acetaminophen and bilirubin in extrahepatic tissues of rats.

An anhepatic rat model was used to explore the extrahepatic conjugating metabolism of acetaminophen and serum bilirubin. The recovery of glucuronide- and sulfate-acetaminophen was 47.5% in normal control and 13.4% in model rats in the urine collected for 6 h after administration of acetaminophen 20 mg kg(-1). Following the increase of acetaminophen dose to 150 mg kg(-1), the recovery of urinary glucuronide-acetaminophen increased by 53.9% in normal control; but it decreased by 36.4% in model rats. In contrast to normal control, the pretreatment with phenobarbital did not affect acetaminophen and its metabolite levels in plasma and urine in model rats. After the establishment of anhepatic model the serum direct bilirubin rose dramatically. Urinary bilirubin test was positive in model rats, but not in normal control. No changes were observed in serum total bilirubin and ratio of direct/total bilirubin after the pretreatment with ranitidine or phenobarbital 50 mg kg (-1), i.p. for 5 days in model rats. The results indicate that the glucuronide- and sulfate-acetaminophen formed in the extrahepatic tissues of model rats is 28.2% of normal control, serum free bilirubin can be transformed into conjugated bilirubin in extrahepatic tissues, and the regulation mechanism of phase II conjugating enzymes is different between the hepatic and extrahepatic tissues.

Acetaminophen↗

PubMed2001

Simultaneous nitrogen and phosphorus removal under low dissolved oxygen conditions.

A full-scale test was operated by using low dissolved oxygen activated sludge process to enhance biological nitrogen and phosphorus removal. When the influent concentrations of CODcr, TN and TP varied in a range of 352.9 mg/L-1338.2 mg/L, 34.4 mg/L-96.3 mg/L, and 2.21 mg/L-24.0 mg/L, the average removal efficiencies were 94.9%, 86.7% and 93.0%, respectively. During the test period of two months, effluent means of CODcr, BOD5, NH3-N, TN and TP were below 50 mg/L, 25 mg/L, 10 mg/L and 1.0 mg/L, respectively. The low dissolved oxygen activated sludge process has a simple flow sheet, fewer facilities and high N and P removal efficiency. It is very convenient to retrofit the conventional activated sludge process with the above process.

Bioreactors↗

PubMed2000

Solid-phase synthesis of muramyl dipeptide (MDP) derivatives using a multipin method.

Solid-phase synthetic method of muramyl dipeptide derivatives is reported. A diverse library of muramyl dipeptides could be potentially synthesized by acylation, reductive alkylation, sulfonamide formation, urea formation, N-alkylation, amine addition, or component Ugi reactions based on this method for drug screening.

Acetylmuramyl-Alanyl-Isoglutamine↗

PubMed1999

Markers in the promoter region of interleukin-10 (IL-10) gene in myasthenia gravis: implications of diverse effects of IL-10 in the pathogenesis of the disease.

Interleukin-10 (IL-10) is an important pleiotropic cytokine with both anti-inflammatory and B lymphocyte stimulating functions. The expression of IL-10 is tightly controlled. A bi-allelic polymorphism and 2 CA repeat microsatellites located in the promoter region of IL-10 gene were analysed in Swedish myasthenia gravis (MG) patients and ethnically matched healthy individuals. The prevalence of a 'high secretor' phenotype of IL-10 (IL-10 1 G/G) was higher in IL-1beta TaqI polymorphism allele 2 positive healthy individuals ('high secretor' phenotype for IL-1beta) than in healthy individuals negative for this allele. No such balance was found in MG patients. In one of the microsatellites, IL10.R, allele 112 was associated with patients having normal thymic histology. No relation of IL10.R allele 112 to proinflammatory cytokine gene polymorphisms and serum IgG, IgM and autoantibodies against nicotinic acetylcholine receptor (nAchR-Ab) was found. In another microsatellite, IL10.G, allele 134 was associated with patients having higher level of nAchR-Ab in their circulation. Our results demonstrated novel genetic markers within IL-10 gene indicating different mechanisms for IL-10 involved in the disease.

Alleles↗

PubMed1998

Genetic association of Ctla-4 to myasthenia gravis with thymoma.

Cytotoxic T lymphocyte associated antigen-4 (CTLA-4) plays a pivotal role in downregulating both the cellular and the humoral response by suppressing ongoing responses of activated T cells. Our earlier study showed that genetic variations in interleukin-1 genes confer susceptibility to myasthenia gravis, especially in patients having the lowest risk from major histocompatibility complex genes. Here we describe an association of Ctla-4 gene to the disease with thymoma and a higher prevalence of CTLA-4 gene polymorphism allele 104 in patients positive for IL-1beta TaqI allele 2, an IL-1beta 'high secretor' phenotype. There was no association in patients with hyperplasia and normal thymic histology. These results further advocate that MG is a polygenetic disease and suggest that co-stimulators such as CTLA-4 and CD28 might have an important role in the pathogenesis of the disease.

Abatacept↗

PubMedDate not supplied

Phenacetin O-deethylation in extrahepatic tissues of rats.

Phenacetin O-deethylation is a marker reaction of CYP450 1A2 activity. The drug-metabolizing enzyme is constitutively expressed in liver. In this study, an in vivo rat model for assessment of extrahepatic metabolism was used to investigate phenacetin O-deethylation and the alterations in the disposition of phenacetin due to the loss of liver function. Rats were divided into the model and normal control groups. The model was established according to our previously described method. The concentrations of phenacetin and its major metabolites acetaminophen, glucuronate-acetaminophen and sulfate-acetaminophen in plasma and urine were determined by HPLC. 30 min after intravenous administration of 0.16% phenacetin 10 mg x kg(-1), plasma acetaminophen in the model group was only 3.6% of that in the control group (0.09+/-0.04 microg x mL(-1) vs 2.49+/-0.85 microg x mL(-1), n = 8). 30 min after intragastric injection of 0.4% phenacetin 30 mg x kg(-1), plasma acetaminophen formation was very slight, about 8.6% of plasma phenacetin in the model group (0.74+/-0.43 microg x mL(-1) acetaminophen vs 8.57+/-8.42 microg x mL(-1) phenacetin) and 6.8% in the control group (1.06+/-0.59 microg x mL(-1) acetaminophen vs 15.47+/-7.21 microg x mL(-1) phenacetin, n = 8); no significant differences were observed in plasma phenacetin, total acetaminophen and the ratio of acetaminophen to phenacetin between control and model groups. In the urine collected for 3 h after intravenous administration of 0.16% phenacetin 10 mg x kg(-1), the total recovery of acetaminophen (as free, glucuronate- and sulfate-acetaminophen ) in the model group was 4.6% of that in the control group (4.47+/-4.27 microg vs 96.63+/-8.50 microg, n = 6), but phenacetin recovery in the model group was 9 times higher than that in the control group (15.03+/-17.72 microg vs 1.66+/-0.50 microg). The results indicate that phenacetin O-deethylation in the extrahepatic tissues and the first-pass metabolism of the probe compound seem to be negligible in rats, but the renal excretion of phenacetin, as a compensation, dramatically increases in model rats.

Acetaminophen↗