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Biomedical subjects

B Xie

Publications and source records attributed to B Xie.

104 records · Page 6Linked to original sources
PubMed1993

Antioxidant properties of fractions and polyphenol constituents from green, oolong and black teas.

Green, oolong and black teas were extracted with water, and then the water extracts were extracted separately with three types of solvent, chloroform, ethyl acetate and butanol, to obtain eight fractions. Major flavanol was extracted by EtOAc, while most of the alkaloid was in the chloroform fraction. Thearubigin was greatest in the butanol fraction, and most of the amino acid remained in the water fraction. All fractions were systematically analyzed by UV spectrophotometer and reverse phase HPLC for those important components existing in green tea, oolong tea, and black tea. The pure compounds of (-)-epicatechin (EC), (-)-epicatechin gallate (ECG), (-)-epigallocatechin (EGC), (-)-epigallocatechin gallate (EGCG), free theaflavin, theaflavin monogallate-A, theaflavin monogallate-B, and theaflavin digallate were separated by LH-20 chromatography and reverse phase HPLC. All fractions and pure compounds were assayed for antioxidant activity and lipoxygenase inhibition activity. Flavanol showed very strong antioxidant activity and lipoxygenase inhibition.

Antioxidants↗
PubMed1992

Identification of a processed pseudogene related to the functional gene encoding the GM2 activator protein: localization of the pseudogene to human chromosome 3 and the functional gene to human chromosome 5.

The GM2 activator protein is an essential substrate cofactor for the hydrolysis of GM2 ganglioside by lysosomal beta-hexosaminidase A (EC 3.2.1.52). There have been conflicting reports as to the chromosomal localization of the gene encoding the activator. We demonstrate here that these conflicts were caused by the presence of a previously unidentified processed activator-pseudogene on chromosome 3, and we confirm a previous ELISA-based localization of the functional activator gene to chromosome 5. Our data indicate that the functional activator locus can still be considered a candidate site for defects causing some forms of spinal muscular atrophy.

Animals↗
PubMed1992

A Cys138-to-Arg substitution in the GM2 activator protein is associated with the AB variant form of GM2 gangliosidosis.

The AB-variant form of GM2 gangliosidosis is an inherited lysosomal storage disease. Biochemical data have linked its cause to the lack of a functional GM2 activator protein (activator). In the present study we identify a mutation in the gene encoding the activator protein of an AB-variant patient. These data represent direct evidence that the disease in the patient described here is a result of mutations at the Activator gene locus. A T412----C transition was found in the homozygous form in cDNA and genomic DNA from the patient. This nucleotide change would result in the substitution of Cys138 by an Arg residue in the activator protein. Whereas the patient's fibroblasts produce apparently normal levels of activator mRNA, they lack a functional activator protein. Transfection of either a construct containing the normal activator cDNA, pAct1, or a cDNA construct containing the T----C transition caused COS-1 cells to transcribe high levels of activator mRNA. Lysates from cells transfected with pAct1 produced an elevated level of both pro- and mature forms of the activator protein, with an accompanying 11-fold enhancement in the ability of purified hexosaminidase A to hydrolyze GM2 ganglioside. However, lysates from cells transfected with the mutant cDNA construct contained only low levels of the pro-activator protein, which failed to enhance hexosaminidase A activity significantly above the endogenous level of mock transfected COS cells. We conclude that the T412----C transition in the GM2 Activator gene of the patient is responsible for the disease phenotype.

Base Sequence↗
PubMed1991

Cyclic adenosine 3',5'-monophosphate suppresses interleukin 1-induced synthesis of matrix metalloproteinases but not of tissue inhibitor of metalloproteinases in human uterine cervical fibroblasts.

Interleukin 1 (IL-1) mediates many cellular functions, but the signal transduction mechanisms of its actions are not clearly understood. Here, we have examined the exact participation of cAMP in the IL-1-induced production of the precursors of matrix metalloproteinase (MMPs) and their specific inhibitor, tissue inhibitor of metalloproteinases (TIMP) in human uterine cervical fibroblasts. IL-1 significantly augmented the production of proMMP-1 (vertebrate procollagenase), proMMP-3 (prostromelysin), and TIMP without detectable changes in the intracellular level of cAMP. Dibutyryl cAMP (Bt2cAMP) and the cAMP elevating agent (forskolin) did not replace IL-1 as MMP inducers. On the contrary, the IL-1-mediated induction of proMMP-1 and proMMP-3 was significantly suppressed by treatment of the cells with Bt2cAMP, forskolin, or theophylline. The suppressive effect of Bt2cAMP on the IL-1-induced production of proMMP-1 and -3 was not due to the inhibition of zymogen secretion, but resulted from the decrease in the steady-state levels of proMMP-1 and proMMP-3 mRNAs. In contrast, Bt2cAMP slightly enhanced the IL-1-induced production of TIMP. The synthesis of proMMP-2 (72-kDa progelatinase/type IV procollagenase) was not altered by IL-1 and/or Bt2cAMP. These results suggest, first, that induction of proMMP-1 and -3 synthesis may share similar transduction pathways but they are distinct from those for proMMP-2 and TIMP synthesis and, second, that cAMP does not function as a second messenger in the MMPs' induction upon IL-1 stimulation in human uterine cervical fibroblasts. Thus, it is further suggested that the system that increases the intracellular cAMP level may be involved in negative regulation of proMMP-1 and -3 production.

Animals↗
PubMed1991

Isolation and expression of a full-length cDNA encoding the human GM2 activator protein.

We report the construction of a cDNA clone encoding a functional GM2-activator protein. The sequence of the complete 5' end of the coding region was determined by direct nucleotide sequencing of a fragment generated by multiple RACE PCR procedures from Hela cell cDNA. Specific oligonucleotides were synthesized from these data which allowed us to produce a PCR fragment that contained the complete coding sequence of the protein. This was then cloned into a mammalian expression vector. The ability of purified hexosaminidase A (beta-N-acetylhexosaminidase, EC 3.2.1.52) to hydrolyse labeled GM2 ganglioside was enhanced 10-fold more by the addition in the assay mix of lysate from transfected COS-1 cells than by the addition of identical amounts of lysate from mock transfected cells. Direct sequencing of PCR fragments from two sources also identified three polymorphisms.

Amino Acid Sequence↗
PubMed1991

Human glucocorticoid receptor gene promotor-homologous down regulation.

To study the regulation of the human glucocorticoid receptor (hGR), we characterized the promoter region by primer extension, S1 nuclease mapping and by DNA sequencing. We found that the promoter is extremely G + C rich (72% GC content) and contains a "TAATA" and a "CAT" box, eight "GGGCGG", three "CCGCCC" and two "CACCC" motifs and a motif similar to the glucocorticoid responsive element (GRE) which included two interchanged nucleotides "TCTTGT". In contrast to other steroid receptor genes, exon I or GHGR contains the major part of the 5' non-coding sequences of hGR mRNA while exon II contains coding sequences for the first 394 amino acid residues of the A/B region of hGR. The major transcriptional start site was found to be 134 bp upstream of the ATG initiation codon. Transfection of HeLa cells with plasmids containing various deletions of GHGR promoter fused to a promoterless CAT vector suggested the region between -470 and -1030, at the 5' end of the mRNA start site, to contain sequences required for down regulation by hormone.

Amino Acid Sequence↗
PubMed1991

[Role of nucleus parabrachialis medialis in the "renzhong" induced pressor response in rabbits].

Experiments were performed on 18 rabbits, bivagotomized, gallamine triethiodide immobilized and artificially ventilated. The effects of electrical stimulation of "renzhong" (Du 26) area and NPBM, separately and simultaneously, on arterial blood pressure and heart rate were observed before and after electrolytic or chemical lesion of NPBM. Electrical stimulation of "renzhong" area or NPBM, separately could elicit an increase in arterial blood pressure; when both "renzhong" and NPBM were stimulated, the pressor response to NPBM stimulation could affect that of "renzhong" area's. But after electrolytic or chemical lesion of NPBM, stimulation of NPBM could no longer elicit pressor response. On the other hand, the pressor response induced by electrical stimulation of "renzhong" area decreased obviously, after lesion of NPBM or transection of brain stem between NPBM and Nucleus trigemini principalis. These results suggest that NPBM might take part in the pressor response of "renzhong" area stimulation.

Acupuncture Points↗
PubMed1991

[Role of rostral ventrolateral medulla in the "renzhong" induced pressor response in rabbits].

Experiments were performed on 14 rabbits locally anesthetized with procaine. Both vagus nerves were cut. The animals were immobilized with gallamine trithiodide and maintained by artificial ventilation. The effects of electrical stimulation of "Renzhong" area on arterial blood pressure and heart rate were observed before and after microinjection of kainic acid (KA) into rostral ventrolateral medulla (RVL). Electrical stimulation of "Renzhong" area could elicit a very marked increase in arterial blood pressure, before microinjection of KA into RVL. Bilateral microinjection of KA (0.5 microgram, an excitotoxin) into RVL could essentially abolish the pressor effect of stimulation of "Renzhong" area. However, bilateral microinjection of NS into RVL showed no effects on the pressor effect of stimulation of "Renzhong" area. These results suggest that RVL plays a key role in the pressor effect of "Renzhong" area stimulation.

Acupuncture Points↗
PubMed1991

[A study on the serum biochemistry in carrier detection of Duchenne muscular dystrophy].

The serum levels of creatine kinase, creatine kinase isoenzyme (MB), lactate dehydrogenase, pyruvate kinase and myoglobin were studied in 85 carriers of Duchenne muscular dystrophy and 125 normal female controls. The results showed that the best single test for carrier detection was myoglobin or creatine kinase, the combination of multiple tests could increase the effectiveness of carrier detection, in which the best and most rational tests to use in combination were creatine kinase, lactate dehydrogenase and myoglobin.

Adolescent↗
PubMedDate not supplied

PEARLS: program for energetic analysis of receptor-ligand system.

Analysis of the energetics of small molecule ligand-protein, ligand-nucleic acid, and protein-nucleic acid interactions facilitates the quantitative understanding of molecular interactions that regulate the function and conformation of proteins. It has also been extensively used for ranking potential new ligands in virtual drug screening. We developed a Web-based software, PEARLS (Program for Energetic Analysis of Ligand-Receptor Systems), for computing interaction energies of ligand-protein, ligand-nucleic acid, protein-nucleic acid, and ligand-protein-nucleic acid complexes from their 3D structures. AMBER molecular force field, Morse potential, and empirical energy functions are used to compute the van der Waals, electrostatic, hydrogen bond, metal-ligand bonding, and water-mediated hydrogen bond energies between the binding molecules. The change in the solvation free energy of molecular binding is estimated by using an empirical solvation free energy model. Contribution from ligand conformational entropy change is also estimated by a simple model. The computed free energy for a number of PDB ligand-receptor complexes were studied and compared to experimental binding affinity. A substantial degree of correlation between the computed free energy and experimental binding affinity was found, which suggests that PEARLS may be useful in facilitating energetic analysis of ligand-protein, ligand-nucleic acid, and protein-nucleic acid interactions. PEARLS can be accessed at http://ang.cz3.nus.edu.sg/cgi-bin/prog/rune.pl.

Computer Simulation↗
PubMedDate not supplied

Management of mobile right atrial thrombi: a therapeutic dilemma.

BACKGROUND: Mobile right atrial thrombus is an uncommon finding on two-dimensional (2D) echocardiography. Therapeutic alternatives include systemic heparinization, systemic or local thrombolysis, and surgical removal. We report our clinical experience in six patients over a 3-year period (6000 echocardiograms) at a tertiary care referral center. METHODS: There were four men and two women with a mean age of 63 years (range: 47 to 73 years). Indications for echocardiography consisted of progressive dyspnea and chest pain in five patients and syncope with chest pain in one patient. RESULTS: All were observed to have a mobile thrombus in the right atrium. Ventilation perfusion (V/Q) scanning confirmed V/Q mismatch in all patients. Subsequent echocardiography (minutes to 1 day later) in three patients demonstrated absence of the thrombus suggesting pulmonary embolization. One patient died during transesophageal echocardiography (TEE) and autopsy confirmed a large pulmonary embolization in the main pulmonary artery. Treatment consisted of heparinization in 3 patients, systemic thrombolysis in 1 patient, and surgical removal of the thrombus in 1 patient. At surgery, a long serpiginous thrombus was seen in the right atrium, tethered to a fenestrated eustachian valve. There were 3 deaths: 1 patient treated with heparin; 1 patient treated with thrombolysis; and 1 during TEE. Two of the three patients treated with heparin and one patient undergoing surgical removal survived hospitalization. CONCLUSIONS: Mobile thrombus in the right atrium is an unusual echocardiographic finding. It portends a poor prognosis with death due to pulmonary embolism.

Aged↗