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Y Xu

Publications and source records attributed to Y Xu.

At least 1,153 records · Page 64Linked to original sources
PubMed1993

[Purification and properties of beta-mannanases from alkalophilic Bacillus N16-5].

Three extracellular alkaline beta-mannanases from an alkalophilic Bacillus N16-5 were purified to electrophoretic homogeneity by (NH4)2SO4 precipitation, DEAE-Sephadex A-25 chromatography, hydroxyapatite chromatography and preparative electrophoresis. Molecular weights and pI values of the beta-mannanases (M-1, M-2 and M-3) were 51000, 38000 and 34700 by SDS-PAGE and 4.3, 2.5 and 2.5 by PAGEIEF, respectively. The optimum pH for enzyme catalysis were 9.0 for M-1 and 10.0 for M-2 and M-3, respectively. All of three enzymes were the most active at 70 degrees C. The activities of three enzymes were strongly inhibited by Ag1+, Hg2+ and Mn2+. Michaelis constants (Km) of the enzyme M-1, M-2 and M-3 for mannase from konjak were 2.9, 1.7 and 12.5 mg/ml, maximum velocities (Vmax) for the saccharide were 27500, 47500 and 15700 mumol.min-1.mg-1, respectively. Konjak was hydrolyzed by the enzyme M-1, and major components in digests were mono-, di-, tri- and tetra-saccharides.

Bacillus↗
PubMed1993

Effects of caffeine on cholinergic agonist- and K(+)-induced cytosolic Ca++ signals and secretion in porcine adrenal chromaffin cells.

A possible involvement of Ca(++)-induced Ca++ release mechanisms in muscarinic agonist-induced, extracellular Ca(++)-independent, catecholamine secretion in porcine adrenal chromaffin cells was examined. Caffeine was found to induce rapid increases in cytosolic Ca++ ([Ca++]in) in a ryanodine-sensitive manner. In addition, caffeine pretreatment inhibited methacholine (a selective muscarinic agonist)- and thapsigargin (thapsigargin depletes inositol 1,4,5-trisphosphate-sensitive Ca++ pools)-induced increases in [Ca++]in as well as methacholine-induced secretion. However, several lines of evidence suggest that Ca(++)-induced Ca++ release does not play a major role in methacholine-induced increases in [Ca++]in. Instead, the results are more compatible with the notion that Ins(1,4,5)P3 and caffeine activate Ca++ release from the same intracellular Ca++ pool, or that distinct Ca++ pools, if they exist, can equilibrate rapidly. Caffeine pretreatment was also observed to eliminate nicotinic responses but not elevated extracellular K(+)-induced responses, suggesting that caffeine blocks nicotinic receptor-channels.

Animals↗
PubMed1993

Simple obesity and obesity hyperlipemia treated with otoacupoint pellet pressure and body acupuncture.

161 cases of simple obesity with or without hyperlipemia were treated by pellet pressure on auricular acupoints plus body acupuncture for 3 months in a single-blind experiment. Patients on Capsulae Olei Oenothera Erythrosepalae were taken as positive controls. Body weight, circumference of chest, abdomen, arms and legs, the appetite, sleep, bowel movement, blood TC, TG and HDL-C were recorded for comparison. The results indicated that treatment in the auricular and body acupoint group was superior to treatment in the control group. In the acupoint group body weight dropped by an average of 5.04 kg in 84.55% of the patients, who also showed decreased appetite, blood TC and TG.

Acupuncture Points↗
PubMed1992

Probing the phosphocholine-binding site of human C-reactive protein by site-directed mutagenesis.

Human C-reactive protein (CRP) can activate the classical pathway of complement and function as an opsonin only when it is complexed to an appropriate ligand. Most known CRP ligands bind to the phosphocholine (PCh)-binding site of the protein. In the present study, we used oligonucleotide-directed site-specific mutagenesis to investigate structural determinants of the PCh-binding site of CRP. Eight mutant recombinant (r) CRP, Y40F; E42Q; Y40F, E42Q; K57Q; R58G; K57Q, R58G; W67K; and K57Q, R58G, W67K were constructed and expressed in COS cells. Wild-type and all mutant rCRP except for the W67K mutants bound to solid-phase PCh-substituted bovine serum albumin (PCh-BSA) with similar apparent avidities. However, W67K rCRP had decreased avidity for PCh-BSA and the triple mutant, K57Q, R58G, W67K, failed to bind PCh-BSA. Inhibition experiments using PCh and dAMP as inhibitors indicated that both Lys-57 and Arg-58 contribute to PCh binding. They also indicated that Trp-67 provides interactions with the choline group. The Y40F and E42Q mutants were found to have increased avidity for fibronectin compared to wild-type rCRP. We conclude that the residues Lys-57, Arg-58, and Trp-67 contribute to the structure of the PCh-binding site of human CRP. Residues Tyr-40 and Glu-42 do not appear to participate in the formation of the PCh-binding site of CRP, however, they may be located in the vicinity of the fibronectin-binding site of CRP.

Amino Acid Sequence↗
PubMed1992

Molecular cloning and functional expression of a brain-specific somatostatin receptor.

The PCR and conventional library screening were used to clone the brain-specific somatostatin receptor rSSTR-4 from a rat genomic library. The deduced amino acid sequence encodes a protein of 384 amino acids and displays structural and sequence homologies with members of the G protein-receptor superfamily. The amino acid sequence of rSSTR-4 is 60% and 48% identical to that of somatostatin receptors SSTR-1 and SSTR-2, respectively, two recently cloned subtypes. Competition curve analysis of the binding properties of the receptor transiently expressed in COS-1 cells revealed a higher apparent affinity for somatostatin 14 than for somatostatin 28. In contrast, the somatostatin analogs SMS 201-995, IM 4-28, and MK-678 failed to displace specific binding in transfected cells. These characteristics resemble the pharmacological binding properties of the previously described brain-specific somatostatin-receptor subtype. Examination of the tissue distribution of mRNA for rSSTR-4 revealed expression limited to various brain regions with highest levels in the cortex and hippocampus. Thus, based on the pharmacology and tissue localization of this receptor, we conclude that rSSTR-4 represents a brain-specific somatostatin receptor.

Amino Acid Sequence↗
PubMed1992

Inhibition of tobacco-specific nitrosamine-induced lung tumorigenesis in A/J mice by green tea and its major polyphenol as antioxidants.

In this study we examined the effects of green tea and its major components, (-)-epigallocatechin gallate (EGCG) and caffeine, on the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung tumorigenesis in A/J mice. We also studied the effects of green tea and EGCG on O6-methylguanine and 8-hydroxydeoxyguanosine (8-OH-dGuo) formation in lung tissues caused by NNK treatment. Mice were given 2% tea, 560 ppm EGCG, or 1120 ppm caffeine in drinking water for 13 weeks. During this time, NNK (11.65 mg/kg body weight) was administered by gavage three times weekly for 10 weeks from weeks 3 to 12. The bioassay was terminated 6 weeks after the last NNK treatment. Mice treated with NNK developed 22.5 lung adenomas per mouse, whereas NNK-treated mice that drank green tea or EGCG as drinking water developed only 12.2 (P less than 0.01) and 16.1 (P less than 0.05) tumors per mouse, respectively. Mice that drank green tea or caffeine solution showed lower body weight gains, although little difference in water and diet consumption was noted in these groups. While green tea and EGCG exerted little effect on the formation of O6-methylguanine, a critical DNA lesion in NNK lung tumorigenesis, both treatments suppressed the increase of 8-OH-dGuo levels in mouse lung DNA. The inhibition of 8-OH-dGuo formation in lung DNA by green tea and EGCG is consistent with their ability to inhibit lung tumorigenesis by NNK. Because 8-OH-dGuo is a DNA lesion caused by oxidative damage, these results suggest that the mechanism of inhibition by green tea and EGCG in NNK-induced lung tumorigenesis is due at least partly to their antioxidant properties.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1992

Simultaneous depletion of CD4+ and CD8+ T lymphocytes is required to reactivate chronic infection with Toxoplasma gondii.

C57BL/6 mice chronically infected with an avirulent strain (ME-49) of Toxoplasma gondii were used to study the mechanisms by which T lymphocytes and IFN-gamma prevent reactivation of latent infection. Infected animals were treated with mAb, either anti-CD8, anti-CD4, anti-CD4 plus anti-CD8, anti-IFN-gamma, or anti-CD4 plus anti-IFN-gamma and the mice followed for survival, histopathology, cyst numbers, and spleen cell cytokine responses. In agreement with previously published findings, treatment with anti-IFN-gamma antibodies fully reactivated the asymptomatic infection, inducing massive necrotic areas in the brain with the appearance of free tachyzoites and death of all animals within 2 wk. Mice treated with the combination of anti-CD4 plus anti-CD8 antibodies showed augmented pathology and mortality nearly identical to the anti-IFN-gamma- treated animals. In contrast, treatment with anti-CD4 or anti-CD8 mAb alone failed to result in significantly enhanced brain pathology or mortality. In additional experiments, full reactivation of infection was observed in mice treated with anti-CD4 plus anti-IFN-gamma indicating that CD4+ lymphocytes are not required for the pathology resulting from IFN-gamma neutralization. Cytokine measurements on parasite Ag-stimulated spleen cells from mAb-treated mice indicated that both CD4+ and CD8+ cells produce IFN-gamma whereas only CD4+ cells contribute to parasite Ag-induced IL-2 synthesis. Together, these results suggest that CD4+ and CD8+ lymphocytes act additively or synergistically to prevent reactivation of chronic T. gondii infection probably through the production of IFN-gamma.

Animals↗
PubMed1992

Wavelet-encoded MR imaging.

Wavelet encoding is presented and compared to phase encoding. In wavelet encoding a distribution of spins is excited by a slice selective RF pulse; for each repetition time the distribution excited has the profile of a wavelet at different scale and translation. The spin density can be reconstructed with an inverse wavelet transform. Wavelet encoding has three advantages over phase encoding: (1) there is no Gibb's ringing from partial volume effects, (2) the effective repetition time can be 36 times the repetition time for a 256 x 256 image, and (3) motion artifacts are local and dramatically reduced. Using wavelet encoding, a 256 x 256 T2-weighted projection image can be acquired in 33 s.

Artifacts↗
PubMed1992

Mapping of the SLA complex of miniature swine: mapping of the SLA gene complex by pulsed field gel electrophoresis.

The overall order of the regions of the swine major histocompatibility complex (MHC), the SLA complex, was determined by pulsed field gel electrophoresis (PFGE). It was found that the order of the regions is class II-class III-class I. A class I probe hybridized to a 420 kb Mlu I and a 420 kb Not I fragment as did a class III probe for C2. None of the class II probes hybridized to these fragments. Thus, linkage of class I to class III was shown. The class III C2, Bf, and C4 genes were found to residue in a 190 kb Not I fragment. Linkage of class III and class II genes was shown when both the class III C4 and the class II DR probes hybridized to the same 195 kb Sac II and 340 kb Not I fragments. The class I probe did not hybridize to these fragments. The order of the regions, class II-class III-class I, is similar to that of human MHC genes and may have been conserved in evolution so that coordinated expression of MHC genes could be achieved.

Animals↗
PubMed1992

Time-varying stiffness of human elbow joint during cyclic voluntary movement.

The objective of this study was to determine the extent to which subjects modulate their elbow joint mechanical properties during ongoing arm movement. Small pseudo-random force disturbances were applied to the wrist with an airjet actuator while subjects executed large (1 rad) elbow joint movements. Using a lumped parameter model of the muscle, tendon and proprioceptive feedback dynamics, a time-varying system identification technique was developed to analyze the phasic changes in the elbow joint's mechanical response. The mechanical properties were found to be time-varying, and well approximated by a quasi-linear second-order model. The stiffness of the arm was found to drop during movement. The arm was always underdamped, with the damping ratio changing during movement. Inertia estimates were constant and consistent with previous measurements. Overall, the moving arm was found to be very compliant, with a peak stiffness value less than the lowest value measured during posture, and a natural frequency of less than 3 Hz. Changing the speed of movement, or the load from gravity, changed the stiffness measured, but not in strict proportion to the change in net muscle torque.

Adult↗
PubMed1992

Effect of age and gender on in vivo ethanol elimination, hepatic alcohol dehydrogenase activity, and NAD+ availability in F344 rats.

It has been reported that aging strikingly decreases in vivo ethanol metabolism in F344 rats without major effects on hepatic alcohol dehydrogenase (ADH) activity. Because hepatic ADH activity is not always rate limiting in the oxidation of ethanol, we measured in vivo ethanol elimination rate (EER), hepatic ADH activity, and the hepatic-cytoplasmic and mitochondrial redox states after acute ethanol application in 2- and 12-month-old F344 rats of both sexes. In male, but not in female, animals EER decreased with age significantly, by 28% (P less than 0.01). The body-to-liver weight ratio was significantly increased in male (39.4 +/- 1.5 vs 46.5 +/- 2.0; P less than 0.05), but not in female, animals with age. Specific activity of ADH was not significantly changed by age, while the activity was significantly reduced with age in male, but not female, rats when related to body weight (5.1 +/- 0.4 vs 3.9 +/- 0.3 mumoles/100 g b.wt./min; P less than 0.05). The cytoplasmic, but not the mitochondrial (NAD+) to (NADH), ratio was significantly decreased with age in male livers (317 +/- 48 vs 793 +/- 128, P less than 0.05), while this was not the case in female livers. In summary, the data show a sex dependence of the effect of age on ethanol metabolism. The observed reduction in in vivo EER with age in male animals is due at least in part to an increased body-to-liver weight ratio, decreased hepatic ADH activity, and reduced availability of NAD+, the cofactor of the ADH reaction. The cause of this may be decreased transport of reducing equivalents through the mitochondrial membrane due to a lack of shuttle systems or a change in the physicochemical properties of the mitochondrial membrane, or decreased reutilization of NADH as NADPH resulting from a reduction of microsomal ethanol oxidation with age.

Aging↗