Search PubMed⌕ Search

Biomedical subjects

Hui Xiao

Publications and source records attributed to Hui Xiao.

29 records · Page 2Linked to original sources
PubMed2004

A molecular phylogeny of eurytomid wasps inferred from DNA sequence data of 28S, 18S, 16S, and COI genes.

Using partial DNA sequence data from nuclear 28S and 18S genes and mitochondrial 16S and COI genes, we reconstructed a phylogeny of the family Eurytomidae. Both maximum parsimony and Bayesian methods were employed. The analysis revealed a significant incongruence between the mitochondrial genes and the nuclear genes, and we chose the results from the nuclear genes as our preferred hypothesis. Our phylogeny suggested that the family Eurytomidae is not a monophyletic group; neither are the genera Eurytoma and Bruchophagus. The monophyly of genera Sycophila and Plutarchia was well supported, as was the close association of the genera Aiolomorphus, Tenuipetiolus, Bephratelloides, and Phylloxeroxenus. Our phylogeny also revealed an anticipated pattern, in which species groups from the genera Eurytoma and Bruchophagus are often more closely related to other small genera than to other species groups of the same genus. Subsequent taxonomic revisions include elevating the subfamily Rileyinae to a family status and the divisions of the genera Eurytoma and Bruchophagus.

Animals↗
PubMed2004

DeltaNp73beta is active in transactivation and growth suppression.

p73, a p53 family protein, shares significant sequence homolog and functional similarity with p53. However, unlike p53, p73 has at least seven alternatively spliced isoforms with different carboxyl termini (p73alpha-eta). Moreover, the p73 gene can be transcribed from a cryptic promoter located in intron 3, producing seven more proteins (DeltaNp73alpha-eta). DeltaNp73, which does not contain the N-terminal activation domain in p73, has been thought to be transcriptionally inactive and dominant negative over p53 or p73. To systemically analyze the activity of the DeltaN variant, we generated stable cell lines, which inducibly express DeltaNp73alpha, DeltaNp73beta, and various DeltaNp73beta mutants by using the tetracycline-inducible expression system. Surprisingly, we found that DeltaNp73beta is indeed active in inducing cell cycle arrest and apoptosis. Importantly, we found that, when DeltaNp73beta is expressed at a physiologically relevant level, it is capable of suppressing cell growth. We then demonstrated that these DeltaNp73beta activities are not cell type specific. We showed that the 13 unique residues at the N terminus are required for DeltaNp73beta to suppress cell growth. We also found that, among the 13 residues, residues 6 to 10 are critical to DeltaNp73beta function. Furthermore, we found that DeltaNp73beta is capable of inducing some p53 target genes, albeit to a lesser extent than does p73beta. Finally, we found that the 13 unique residues, together with the N-terminal PXXP motifs, constitute a novel activation domain. Like DeltaNp73beta, DeltaNp73gamma is active in transactivation. However, unlike DeltaNp73beta, DeltaNp73alpha is inactive in suppressing cell growth. Our data, together with others' previous findings, suggest that DeltaNp73beta may have distinct functions under certain cellular circumstances.

Alternative Splicing↗
PubMed2003

Role of elastin in pathologic calcification of xenograft heart valves.

Bioprosthetic heart valves fabricated from glutaraldehyde crosslinked porcine aortic valves often fail because of calcific degeneration. Calcification occurs in both cusp and aortic wall portions of bioprosthetic heart valves. The purpose of this study was to discern the role of different aortic wall components in the calcification process. Thus, we selectively extracted cells and other extracellular matrix proteins from porcine aorta using trypsin/DNase/RNase, cyanogen bromide (CNBr), and sodium hydroxide (NaOH) treatments and subdermally implanted these pretreated aortas in young rats. Total DNA and phospholipid data showed complete removal of cells by CNBr and NaOH treatments, whereas trypsin/DNase/RNase treatment was effective in removing DNA but not phospholipids. As shown by amino acid data and Masson's trichrome staining, collagen was removed in CNBr and NaOH treatments. Control fresh porcine aorta calcified significantly after 21 days of implantation (Ca 26.4 +/- 2.4 microg/mg). Removal of cells and collagen from the aorta by CNBr treatment did not lead to a statistically significant reduction in aortic calcification (Ca 20.8 +/- 3.0 microg/mg). Moreover, partial degradation of elastin fibers caused by NaOH (during extraction) and trypsin treatment (after implantation) of the aorta significantly increased elastin-oriented calcification (Ca 94.4 +/- 9.3 and 58.4 +/- 4.6 microg/mg, respectively). Our results indicate that the elastin component of the aorta may undergo independent calcification irrespective of devitalized cell-mediated calcification observed in glutaraldehyde crosslinked aortas. Our results also demonstrate the importance of studying elastin-oriented calcification in decellularized elastin-rich aortic matrices currently used in tissue-engineering applications.

Amino Acids↗
PubMed2003

Tip60 is a co-repressor for STAT3.

Tip60 (Tat-interactive protein, 60 kDa), a cellular protein with intrinsic histone acetyltransferase activity, is involved in DNA damage repair and apoptosis. Recent studies have suggested that Tip60 acts either as a co-activator or a co-repressor to modulate transcription. In this study, we demonstrate that Tip60 represses reporter gene expression when it is fused to the Gal4 DNA binding domain. We also show that Tip60 associates with histone deacetylase 7 (HDAC7) through its N-terminal zinc finger-containing region and that HDAC7 activity is required for the repressive effect of Tip60. Because endogenous Tip60 interacts with STAT3, we hypothesized that Tip60 might complex with STAT3 and HDAC7 and modulate STAT3-mediated trans-activation. Consistent with this hypothesis, the overexpression of Tip60 represses STAT3-driven reporter gene expression, which can be further potentiated by the co-transfection of HDAC7. Furthermore, interleukin-9-induced c-myc expression, which depends on STAT3 activity, is abrogated by exogenous expression of Tip60. This is the first demonstration of which Tip60 represses STAT3 activity in part through the recruitment of HDAC7.

Acetyltransferases↗
PubMed2003

Indirect assessment of small hydrophobic ligand binding to a model protein using a combination of ESI MS and HDX/ESI MS.

Direct mass spectrometric characterization of interactions between proteins and small hydrophobic ligands often poses a serious problem due to the complex instability in the gas phase. We have developed a method that probes the efficacy of ligand-protein interactions indirectly by monitoring changes in protein flexibility. The latter is assessed quantitatively using a combination of charge state distribution analysis and amide hydrogen exchange under both native and mildly denaturing conditions. The method was used to evaluate binding of a model protein cellular retinoic acid binding protein I to its natural ligand all-trans retinoic acid (RA), isomers 13-cis- and 9-cis-RA, and retinol, yielding the following order of ligand affinities: All-trans RA > 9-cis RA > 13-cis RA, with no detectable binding of retinol. This order is in agreement with the results of earlier fluorimetric titration studies. Furthermore, binding energy of the protein to each of retinoic acid isomers was determined based on the measured hydrogen exchange kinetics data acquired under native conditions.

Apoproteins↗
PubMed2003

Experimental study on therapeutic effect of in vivo expression of Cell I-Hep II recombinant polypeptide of fibronectin on murine H22 hepatocellular carcinoma.

AIM: To investigate the inhibitory effect of in vivo expression of expressing plasmid pCH510 of recombinant fibronectin polypeptide (CH50) on hepatocellular carcinoma and the improved therapeutic effect of pCH510 in combination with chemotherapeutic agents and Hsp70-H22 hepatocarcinoma antigen peptide on tumor. METHODS: Mice were inoculated with H22 hepatocarcinoma cells. The chemotactic effect of the expression of plasmid pCH510 on immunocytes was observed after in vivo transfection, tissue slicing and HE staining. Inhibitory effect of transfection with pCH510 on murine tumor originated from different inoculative doses was observed. The inhibitory effect of immediate transfection with pCH510 after chemotherapy on tumor was compared with that of transfection 5 days after chemotherapy. The change of function and amount of mouse peritoneal macrophages and the peripheral blood immunocytes resulted from administration of chemotherapeutic agents were detected. The peptides mixture was prepared from H22 hepatocarcinoma cells. pCH510 + Hsp70-H22 antigen peptides were injected into tumor-bearing mice with or without chemotherapy, to observe the inhibitory effects on tumor. RESULTS: At the tumor tissue site injected with pCH510, there were a great number of immunocytes which mainly were macrophages, lymphocytes and neutrophils. Transfection of plasmid pCH510 inhibited significantly the murine tumor induced by different inoculative doses. The inhibitory effect was negatively correlated with the inoculative dose. The therapeutic effect was not improved by immediate transfection with pCH510 after chemotherapy, but was significantly improved by transfection with pCH510 5 days after chemotherapy. Chemotherapeutic agent decreased the number of immunocytes and suppressed their activation in vivo. After injection of drug, the amount of immunocytes was the lowest from d 1 to d 3 and returned to normal level on the 10(th) day. Transfection with plasmid pCH510 alone could inhibit tumor induced by the inoculation with 10(4) H22 cells. The tumor originated from the inoculation with 10(5) H22 cells was inhibited by pCH510+Hsp70-H22 antigen peptides and that from the inoculation with 10(6) H22 cells was inhibited by pCH510+Hsp70-H22 antigen peptides in combination with chemotherapeutic agents. CONCLUSION: In vivo expression of pCH510 recruits immune cells, inhibits tumor growth, and enhances the efficacy of chemotherapy. But the proper timing of combining chemotherapy with pCH510 must be taken into great account. The synergism of pCH510 and Hsp70-H22 peptides can improve the efficacy, which could be further enhanced if they are used following chemotherapy. Chemotherapeutic agent + pCH510 + Hsp70-H22 peptides is a promising therapeutic approach of combination treatment of tumor.

Animals↗
PubMed2003

[The linear dimensions of human body measurements of Chinese male pilots in standing posture].

OBJECTIVE: To provide the latest anthropometric data of Chinese male pilots on a large scale. METHOD: 94 linear dimensions of human body measurements were defined, of which there are 42 fundamental items and 52 recommended items. The computer databanks were programmed, in which the subprograms were preset for data checking such as extreme value examination, logical judgement for data relationship, and measuring-remeasuring difference test. All workers were well trained before pilot measurements. 1739 male pilots from China Air Force was measured for the 42 fundamental items, and of which 904 pilots were measured for the 52 recommended items. RESULT: Mean, standard deviation, the maximum value, the minimal value, and the 5th, 50th, 95th percentile data of all the 94 items were given. The quality of the data was stable and reliable. CONCLUSION: All data of the 94 linear dimensions of human body measurements were valid and reliable with high precision.

Adult↗
PubMed2003

Epstein-Barr virus encoded latent membrane protein 1 induces TRAF1 expression to promote anti-apoptosis activity via NF-kappaB signaling pathway in nasopharyngeal carcinoma.

OBJECTIVES: To identify whether Epstein-Barr virus (EBV) encoded latent membrane protein 1 (LMP1) can induce tumor necrosis factor receptor-associated factor 1 (TRAF1) expression and promote its anti-apoptosis activity via the NF-kappaB signaling pathway, and assess that LMP1 suppresses apoptosis in nasopharyngeal carcinoma (NPC). METHODS: A stable transfected cell line HNE2-LMP1 was established by introducing LMP1 cDNA into HNE2 cells. Transactivation of TRAF1 was determined by luciferase reporter assay, while expression of TRAF1 mRNA was detected by RT-PCR and expression of TRAF1 protein and caspase 3 by Western blot analysis. Apoptosis activity was observed through fluorescence staining. RESULTS: LMP1 induced TRAF1 expression in NPC cells and caused a decrease in apoptosis. This induction could be blocked by antisense LMP1. Moreover, LMP1-mediated induction of a TRAF1 promoter-driven reporter gene was significantly impaired when the kappaB site kappaB1 or kappaB5 was disrupted, whereas mutation of kappaB3 had only a minor effect on LMP1 dependent up-regulation of the reporter gene. CONCLUSION: LMP1 induces TRAF1 expression and promotes its anti-apoptosis activity via the NF-kappaB signaling pathway, which may be one of the mechanisms that LMP1 uses to suppress apoptosis in NPC cells.

Apoptosis↗
PubMed2002

Specificity of interleukin-2 receptor gamma chain superfamily cytokines is mediated by insulin receptor substrate-dependent pathway.

Interleukins 9 (IL-9) and 4 are cytokines within the IL-2 receptor gamma chain (IL-2R gamma) superfamily that possess similar and unique biological functions. The signaling mechanisms, which may determine cytokine specificity and redundancy, are not well understood. IRS proteins are tyrosine-phosphorylated following IL-9 and IL-4 stimulation, a process in part mediated by JAK tyrosine kinases (Yin, T. G., Keller, S. R., Quelle, F. W., Witthuhn, B. A., Tsang, M. L., Lienhard, G. E., Ihle, J. N., and Yang, Y. C. (1995) J. Biol. Chem. 270, 20497--20502). In the present study, we used 32D cells stably transfected with insulin receptor (32D(IR)), which do not express any IRS proteins, as a model system to study the requirement of different structural domains of IRS proteins in IL-9- and IL-4-mediated functions. Overexpression of IRS-1 and IRS-2, but not IRS-4, induced proliferation of 32D(IR) cells in response to IL-9. The pleckstrin homology (PH) domain of IRS proteins is required for IRS-mediated proliferation stimulated by IL-9. The phosphotyrosine binding and Shc and IRS-1 NPXY binding domains are interchangeable for IRS to transduce the proliferative effect of IL-4. Therefore, the PH domain plays different roles in coupling IRS proteins to activated IL-9 and IL-4 receptors. The role of IRS proteins in determining cytokine specificity was corroborated by their ability to interact with different downstream signaling molecules. Although phosphatidylinositol 3' -kinase (PI3K) and Grb-2 interact with tyrosine-phosphorylated IRS proteins, Shp-2 only binds to IRS proteins following IL-4, but not IL-9, stimulation. Although PI3K activity is necessary for the IRS-1/2-mediated proliferative effect of IL-9 and IL-4, Akt activation is only required for cell proliferation induced by IL-4, but not IL-9. These data suggest that IRS-dependent signaling pathways work by recruiting different signaling molecules to determine specificity of IL-2R gamma superfamily cytokines.

Adaptor Proteins, Signal Transducing↗
PubMedDate not supplied

Involvement of matrix metalloproteinases and tenascin-C in elastin calcification.

Elastin degeneration and calcification occur in many cardiovascular diseases, including medial arterial elastocalcinosis, atherosclerosis, and bioprosthetic heart valve mineralization. In the present study, we tested the hypothesis that the onset and progression of elastin-oriented calcification is associated with matrix remodeling and elastin degradation events. We studied whether aluminum ions inhibit elastin calcification by reducing elastin degradation and altering remodeling events. Subdermal implantation of pure elastin in juvenile rats resulted in a time-dependent calcification of elastin, reaching high levels 21 days after implantation. In situ hybridization showed that elastin calcification was associated with an up-regulation of matrix metalloproteinase (MMP) mRNA expression, specifically MMP-9 and MMP-2. Gelatin zymography demonstrated increased MMP-9 and MMP-2 enzyme activities in early stages of elastin calcification. Calcified elastin displayed a time-dependent pattern of tenascin-C (TN-C) and alkaline phosphatase (AP) expression. Pretreatment of pure elastin with aluminum ions prior to implantation resulted in complete inhibition of elastin calcification. Aluminum ion binding to elastin was found to protect elastin against MMP-mediated degradation in vitro. Noncalcified, explanted aluminum-pretreated elastin exhibited reduced activities of MMPs. TN-C expression in elastin implants exhibited a time-dependent pattern that was also affected by pretreatment of elastin with aluminum ions. In conclusion, elastin calcification is accompanied by matrix remodeling events, and the efficacy of aluminum pretreatment in inhibiting elastin calcification may be related in part to its effects on elastin remodeling.

Alkaline Phosphatase↗