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Biomedical subjects

T Wang

Publications and source records attributed to T Wang.

At least 685 records · Page 38Linked to original sources
PubMed1991

Increased levels of monohydroxy metabolites of arachidonic acid and linoleic acid in LDL and aorta from atherosclerotic rabbits.

Lipid peroxidation results in the formation of peroxy and hydroperoxy metabolites of polyunsaturated fatty acids which can directly or indirectly affect many cellular processes. Lipid hydroperoxides are rapidly metabolized to the corresponding monohydroxy products by various cellular peroxidases. We have measured the amounts of monohydroxy metabolites of linoleic acid (18:2) and arachidonic acid (20:4) in lipids derived from aorta and LDL from rabbits fed a diet enriched in cholesterol and peanut oil for either 8 or 15 weeks. Increased amounts of the 9-hydroxy, and, to a lesser extent, the 13-hydroxy metabolite of 18:2 were observed in aorta and LDL from cholesterol-fed rabbits at both 8 and 15 weeks. The amounts of esterified 11-, 12- and 15-hydroxy metabolites of 20:4 in aortae from cholesterol-fed rabbits were similar to controls after 8 weeks, but about 3-fold higher after 15 weeks. These monohydroxy metabolites of 20:4 were also detected in LDL lipids in cholesterol-fed rabbits. The greater amounts of hydroxy-18:2 in the cholesterol-fed group could be explained by an approx. 2-4-fold increase in 18:2 in aorta and LDL. In contrast, the amounts of 20:4 in aortic lipids were lower in cholesterol-fed rabbits than in controls. Thus, the percentage of esterified 20:4 which had been oxidized to its 11, 12, and 15-hydroxylated metabolites was about 5-times higher in the cholesterol-fed group. Our results would be consistent with the hypothesis that increased amounts of peroxidized 18:2 and 20:4 in lipids could be involved in the development of atherosclerotic lesions in cholesterol-fed rabbits.

Animals↗
PubMed1991

Molecular basis of phenotypic heterogeneity in phenylketonuria.

BACKGROUND: Phenylketonuria is a metabolic disorder that results from a deficiency of the hepatic enzyme phenylalanine hydroxylase. Its clinical phenotype varies widely, and to date more than 10 mutations in the phenylalanine hydroxylase gene have been identified in persons with the disorder. We attempted to relate the clinical phenotype of patients to their genotype. METHODS: We studied 258 patients with phenylketonuria from Denmark and Germany for the presence of eight mutations previously found in patients from these countries. The in vitro activity of the enzymes associated with these mutations was determined by expression analysis in heterologous mammalian cells. The level of activity was then used to predict the in vivo level of phenylalanine hydroxylase activity in patients with various combinations of mutant phenylalanine hydroxylase alleles. RESULTS: The eight mutations involved 64 percent of all mutant phenylalanine hydroxylase alleles in the patients. Expression analysis showed that these mutant enzymes produced from 0 to 50 percent of normal enzyme activity. The predicted level of phenylalanine hydroxylase activity correlated strongly with the pretreatment serum level of phenylalanine (r = 0.91, P less than 0.001 in the Danish patients and r = 0.74, P less than 0.001 in the German patients), phenylalanine tolerance in the Danish patients (r = 0.84, P less than 0.001), and the serum phenylalanine level measured after standardized oral protein loading in the German patients (r = 0.84, P less than 0.001). CONCLUSIONS: Our results strongly support the hypothesis that there is a molecular basis for phenotypic heterogeneity in phenylketonuria. The establishment of genotype will therefore aid in the prediction of biochemical and clinical phenotypes in patients with this disease.

Alleles↗
PubMed1991

Founder effect of a prevalent phenylketonuria mutation in the Oriental population.

A missense mutation has been identified in the human phenylalanine hydroxylase [PAH; phenylalanine 4-monooxygenase; L-phenylalanine, tetrahydrobiopterin:oxygen oxidoreductase (4-hydroxylating), EC 1.14.16.1] gene in a Chinese patient with classic phenylketonuria (PKU). A G-to-C transition at the second base of codon 413 in exon 12 of the gene results in the substitution of Pro413 for Arg413 in the mutant protein. This mutation (R413P) results in negligible enzymatic activity when expressed in heterologous mammalian cells and is compatible with a classic PKU phenotype in the patient. Population genetic studies reveal that this mutation is tightly linked to restriction fragment length polymorphism haplotype 4, which is the predominant haplotype of the PAH locus in the Oriental population. It accounts for 13.8% of northern Chinese and 27% of Japanese PKU alleles, but it is rare in southern Chinese (2.2%) and is absent in the Caucasian population. The data demonstrate unambiguously that the mutation occurred after racial divergence of Orientals and Caucasians and suggest that the allele has spread throughout the Orient by a founder effect. Previous protein polymorphism studies in eastern Asia have led to the hypothesis that "northern Mongoloids" represented a founding population in Asia. Our results are compatible with this hypothesis in that the PKU mutation might have occurred in northern Mongoloids and subsequently spread to the Chinese and Japanese populations.

Asian People↗
PubMed1991

A prevalent missense mutation in Northern Europe associated with hyperphenylalaninaemia.

A missense mutation has been identified in the phenylalanine hydroxylase (PAH) gene of a Danish patient with hyperphenylalaninaemia (HPA). An A-to-G transition at the second base of codon 414 results in the substitution of Cys for Tyr in the mutant PAH protein. In in vitro expression studies, the Tyr414-to-Cys414 mutant construct produced a protein which exhibited a significant amount of normal PAH enzyme activity, which is consistent with both in vitro and in vivo measurements of PAH activity in HPA patients. Population genetic studies reveal that this mutation is present on 50% of mutant haplotype 4 chromosomes in the Danish population. Together with the previously reported codon 158 mutation, these two mutant alleles comprise over 90% of all mutant haplotype 4 chromosomes in the Northern European population. Thus, two allele-specific oligonucleotide probes can detect most mutant haplotype 4 chromosomes in Northern Europe.

Alleles↗
PubMed1991

Thrombospondin production and thrombospondin-mediated adhesion in U937 cells.

U937 cells have low levels of surface thrombospondin (TSP) under control conditions but express higher levels after treatment for 1 day with 100 nM phorbol myristate acetate (PMA). Increased surface expression is due, in part, to increased biosynthesis. Untreated U937 cells do not adhere to TSP-coated plastic culture dishes but adhere strongly to TSP after stimulation with PMA. Untreated U937 cells also adhere weakly to endothelial cell monolayers while PMA-treated U937 cells attach strongly to monolayers of rat pulmonary artery endothelial cells. Endothelial cell adhesion appears to be mediated, in part, by TSP since antibodies to TSP partially inhibit.

Animals↗
PubMed1991

Photocure bonding agent containing phosphoric methacrylate.

Effective photocure phosphoric methacrylate bonding agents which bonded a dental composite to tooth substrates were proposed. Methacryloyloxydecyl phosphoric acid (MDP) or 2-methacryloyloxyethyl phenyl phosphoric acid (Phenyl-P) was dissolved in triethyleneglycol dimethacrylate (TEGDMA) with camphorquinone (CQ) and N-phenylglycine (NPG). The combination of CQ and NPG was a good visible-light initiator for the polymerization. The highest bond strength was 5 MPa to dentin and 10 MPa to enamel when the adhesive contained Phenyl-P in TEGDMA. Dentin and enamel were recommended for demineralization with an aqueous mixture of 0.3 mol/L EDTA diammonium salt and 0.2 mol/L EDTA ammonium iron salt for generation of better bond strength.

Animals↗
PubMed1991

Phenylketonuria missense mutations in the Mediterranean.

Two missense mutations have been identified in the phenylalanine hydroxylase (PAH) genes of an Italian phenylketonuria (PKU) patient. Both mutations occurred in exon 7 of the PAH gene, resulting in the substitution of Trp for Arg at amino acid 252 (R252W) and of Leu for Pro (P281L) at amino acid 281 of the protein. Expression vectors containing either the normal human PAH cDNA or mutant cDNAs were constructed and transfected into cultured mammalian cells. Extracts from cells transfected with either mutant construct showed negligible enzyme activity and undetectable levels of immunoreactive PAH protein as compared to the normal construct. These results are compatible with the severe classical PKU phenotype observed in this patient. Population genetic studies in the Italian population revealed that both the R252W and the P281L mutations are in linkage disequilibrium with mutant restriction fragment length polymorphism (RFLP) haplotype 1, which is the most prevalent RFLP haplotype in this population. The R252W mutation is present in 10% and the P281L mutation is present in 20% of haplotype 1 mutant chromosomes. These mutations are both very rare among other European populations, suggesting a Mediterranean origin for these mutant chromosomes.

Base Sequence↗
PubMed1991

Missense mutations prevalent in Orientals with phenylketonuria: molecular characterization and clinical implications.

Two missense mutations in the phenylalanine hydroxylase (PAH) genes of Orientals with phenylketonuria (PKU) have been identified. A G-to-A transition in exon 7 of the gene results in the substitution of Gln243 for Arg243 (R243Q) and accounts for 18% of all PKU chromosomes among Chinese. An A-to-G transition in exon 6 of the gene results in the substitution of Cys204 for Tyr204 (Y204C) and identifies about 13 and 5% of all PKU chromosomes in the Chinese and Japanese populations, respectively. The R243Q construct produced less than 10% of normal PAH activity in in vitro expression analysis in a eukaryotic cell system, and patients homozygous for this substitution exhibit a severe clinical phenotype. These results are consistent with previous findings in this expression system. The Y204C construct, however, produced near normal levels of PAH enzyme activity and immunoreactivity in this in vitro expression system. Because this substitution is present only on PKU chromosomes, it is a valuable marker for identifying the corresponding mutant allele for carrier screening of PKU. With the characterization of these two substitutions, about 60% of PKU alleles in China can now be identified. The continuing search for additional PKU mutations will permit effective carrier screening and prenatal gene diagnosis of PKU in East Asia.

Alleles↗
PubMed1991

Major histocompatibility complex antigens and murine islet allograft survival.

Immunomodulation of rodent islets can significantly prolong allograft survival. We utilized a murine model of primary islet transplantation to study the relationship between allograft survival and the quantitative pretransplant expression of class I and II MHC antigens in freshly isolated CBA/J islets, and islets subjected to 37 degrees C tissue culture, brief culture at 7 degrees C, or exposure of the donor to lipopolysaccharide. Seven-day culture resulted in decreased class II expression, a tendency to decreased class I expression, and a significant prolongation of allograft survival. Brief culture at 7 degrees C resulted in increased class I expression, a trend to decreased class II expression, and no significant change in allograft survival. Donor pretreatment with LPS resulted in increased class I expression without significant change in class II expression and was correlated with prolongation of allograft survival. These studies demonstrate that an upregulation of MHC class I by in vitro or in vivo islet pretreatment is not associated with an acceleration of islet rejection. Reduction of class II was associated with delayed rejection. These results do not support a major role of the indirect pathway of antigen presentation in islet rejection in vivo. Certain protocols that alter the usual expression of class I and II on pancreatic islets are associated with alteration in the initiation and/or propagation of the normal cell-mediated rejection process, suggesting that the concept of pretransplant treatment should continue to be pursued.

Animals↗
PubMed1991

Macronuclei and micronuclei in Tetrahymena thermophila contain high-mobility-group-like chromosomal proteins containing a highly conserved eleven-amino-acid putative DNA-binding sequence.

HMG (high-mobility-group protein) B and HMG C are abundant nonhistone chromosomal proteins isolated from Tetrahymena thermophila macronuclei with solubilities, molecular weights, and amino acid compositions like those of vertebrate HMG proteins. Genomic clones encoding each of these proteins have been sequenced. Both are single-copy genes that encode single polyadenylated messages whose amounts are 10 to 15 times greater in growing cells than in starved, nongrowing cells. The derived amino acid sequences of HMG B and HMG C contain a highly conserved sequence, the HMG 1 box, found in vertebrate HMGs 1 and 2, and we speculate that this sequence may represent a novel, previously unrecognized DNA-binding motif in this class of chromosomal proteins. Like HMGs 1 and 2, HMGs B and C contain a high percentage of aromatic amino acids. However, the Tetrahymena HMGs are small, are associated with nucleosome core particles, and can be specifically extracted from macronuclei by elutive intercalation, properties associated with vertebrate HMGs 14 and 17, not HMGs 1 and 2. Thus, it appears that these Tetrahymena proteins have features in common with both of the major subgroups of higher eucaryotic HMG proteins. Surprisingly, a linker histone found exclusively in transcriptionally inactive micronuclei also has several HMG-like characteristics, including the ability to be specifically extracted from nuclei by elutive intercalation and the presence of the HMG 1 box. This finding suggests that at least in T. thermophila, proteins with HMG-like properties are not restricted to regions of transcriptionally active chromatin.

Amino Acid Sequence↗
PubMed1991

Gap junctions in the glandular epithelium of normal human endometrium.

Freeze-fracture replicas were used to study gap junctions in the glandular epithelium of the human endometrium. The junctions were found to be small both in number and size during the early and mid-proliferative phases of the cycle. In the late proliferative phase and later in the cycle, their number and size were significantly increased (p less than 0.05). In the late secretory phase, the gap junctions again showed a significant reduction both in number and size (p less than 0.05) in comparison with the mid-secretory phase. These findings suggest that the formation and growth of gap junctions might be induced by estrogens, and that they might play a role in the differentiation of the endometrial cells as well as in the coordination of their secretory function.

Adult↗
PubMed1991

Effect of 2-(methacryloxy)ethyl phenyl hydrogen phosphate on adhesion to dentin.

A variety of methacrylate-based materials has been developed with the capacity of adhering to dentin. This study investigated the effectiveness of 2-(methacryloxy)ethyl phenyl hydrogenphosphate (phenyl-P) for bonding 5% phenyl-P in methyl methacrylate (MMA) to dentinal surfaces. Polymerization of the phenyl-P/MMA monomer was initiated by partially oxidized tri-n-butyl borane catalyst (TBB). The mean tensile bond strength of 5% phenyl-P in MMA to dentin that was pre-treated with an aqueous solution of 10% citric acid/3% ferric chloride, abbreviated as 10-3, was found to be 10.5 MPa. Scanning electron microscope examination demonstrated the formation of a transitional or "hybrid" layer of resin-reinforced dentin, created by the intermingling and entanglement of polymerized resin with collagen bundles exposed by dentin pre-treatment with 10-3, an effective remover of the dentinal smear layer. This "hybrid" layer or zone was essential for high tensile bond strength to be attained. Phenyl-P was found to be effective in promoting monomer diffusion and impregnating monomer into demineralized dentinal surfaces. The formation of the "hybrid" layer of resin-reinforced dentin followed in situ resin polymerization initiated by partially oxidized tri-n-butyl borane (TBB). Ferric (Fe3+) ions deposited on dentinal surfaces from the 10-3 solution also acted to improve monomer diffusion and entanglement with demineralized dentin, and facilitated the formation of the "hybrid" layer/zone.

Acid Etching, Dental↗
PubMed1991

[An experimental study on acupoint neiguan-heart short reflex].

It is reported that the dichotomizing afferent fibers supply both the pericardium and the brachium in rat. This finding provides a possible morphological explanation for short reflex which transmits messages only through the connection of peripheral nerve dichotomization. The animals utilized in this study were 15 male or female wistar rats (235-360 g). Rats were anesthetized with 26% urethane (100mg/100g b. wt, i.p.) and then, acute myocardial ischemia (AMI) was produced by pituitrin (1.0-1.5 u/a rat, i.M.). Following anesthetization and AMI, The I lead of electrocardiogram (ECG) was recorded, the superficial electrical resistance and cutaneous temperature of the acupoint Neiguan and Zusali were measured. In order to break off the long reflex which invokes some effects through central nervous system, the dorsal roots were removed of spinal cord segments cervical 6) C6-thoracic 1(T1). In this condition, the AMI can decrease in superficial electrical resistance and cutaneous temperature of the acupoint Neiguan (P less than 0.01). Acupuncture at Neiguan can also influence the superficial electrical resistance of the acupoint Neiguan, improve in the ECG, increase in the heart rate, but acupuncture at Zusali has no these effects. It suggests that acupoint Neiguan and heart can be connected through a short reflex.

Acupuncture Points↗
PubMed1991

Mast cells in the chick digestive tract. I. Development.

Mast cells in the digestive tract of the developing chick embryo were studied with histochemistry and electron microscopy (EM). The cells appeared in the esophagus, proventriculus and small intestine on about the 13th day of incubation, whereas mast cells in the tongue appeared earlier. The staining properties and ultrastructure of the mast cells varied with development. In 13- and 15-day embryos, mast cells showed a pale metachromasia with toluidine blue, and stained blue with Alcian Blue-Safranin O (AB-S). In the 18-day embryo, mast cells stained a deep purple with toluidine blue. Stained with AB-S, most of the mast cell granules stained blue, but some red granules were also seen in a few cells. In the newly hatched chick, the cells stained a strong reddish purple with toluidine blue. Stained with AB-S, a few cells contained only blue or red granules, but most contained both. Observations with the EM revealed that the internal structure of the granules varied with the stage of embryonic development. The basis for the changes in staining properties and ultrastructure of the mast cell in the developing chick embryo were discussed.

Animals↗