Biomedical subjects

Hong Xu

Publications and source records attributed to Hong Xu.

At least 37 records · Page 2Linked to original sources

PubMed2006

Differentiation of Dendrobium species used as "Huangcao Shihu" by rDNA ITS sequence analysis.

The genus Dendrobium Sw. is composed of 74 species and two varieties in China, and 32 species carry the name "Huangcao Shihu" on the herbal medicine market, making the identification of the origin of "Huangcao Shihu" difficult for consumers. Here, the ITS regions were sequenced and evaluated to differentiate the 18 Dendrobium species used as "Huangcao Shihu". Diversity in DNA sequences among various species was found with the inter-specific sequence divergence ranging from 3.2% to 37.9% in ITS1 and 5.0% to 26.6% in ITS2. Moreover, the variations within species were very low, ranging in sequence divergence from 0 to 3.0% in ITS1 and 0 to 4.0% in ITS2. Therefore, these species could be easily distinguished at the DNA level. Furthermore, based on the divergent ITS regions, five pairs of species-specific primers were designed and used for the rapid PCR identification of five Dendrobium species listed in the Chinese Pharmacopoeia.

DNA, Plant↗

PubMed2006

Differential effects of oxidative stress on hepatic endothelial and Kupffer cell eicosanoid release in response to endothelin-1.

OBJECTIVE: The vasoconstrictor endothelin-1 can induce vasomodulators release like nitric oxide in the liver. Here the authors explored whether endothelin-1 can stimulate endothelial and Kupffer cells release of other vasomodulators under normal and stress conditions. METHODS: Cells were cultured for 24 h and treated with H2O2 (25 microM) for 6 h and subsequently with endothelin-1 (10 nM) for 10 min. Eicosanoid release was assessed in the media by enzyme immunoassay. RESULTS: Endothelin-1 mediated cPLA2 phosphorylation and increased prostaglandin (PG) I2, PGE2 and thromboxane A2 (TXA2) release in endothelial cells while it only increased TXA2 in Kupffer cells. H2O2 significantly increased PGI2, PGE2 and TXA2 in endothelial cells through an upregulation of cyclooxygenase-2, thromboxane synthase A2, and phosphorylation of cPLA2. Endothelin-1-induced PGI2, PGE2, and TXA2 release in endothelial cells were inhibited by H2O2 correlating with the absence of further cPLA2 phosphorylation. In Kupffer cells, H2O2 only increased TXA2 synthesis and further endothelin-1 stimulation of TXA2 was possible through a higher increase in cPLA2. CONCLUSION: These results indicate that under normal conditions endothelial cells play a pivotal role in liver microcirculation regulation. Oxidative stress not only disrupts the basal balance of vasomodulators in the liver but also affects endothelin-1-induced effects in both Kupffer cells and endothelial cells.

Animals↗

PubMed2006

Flt3-ligand-mobilized peripheral blood, but not Flt3-ligand-expanded bone marrow, facilitating cells promote establishment of chimerism and tolerance.

Facilitating cells (CD8+/TCR-) (FCs) enhance engraftment of limiting numbers of hematopoietic stem cells (HSCs). The primary component of FCs is precursor-plasmacytoid dendritic cells (p-preDCs), a tolerogenic cell expanded by Flt3-ligand (FL). In this study, we evaluated the function and composition of FL-expanded FCs. FL treatment resulted in a significant increase of FCs in bone marrow (BM) and peripheral blood (PB). When FL-expanded FCs were transplanted with c-Kit+/Sca-1+/Lin- (KSL) cells into allogeneic recipients, BM-FCs exhibited significantly impaired function whereas PB-FCs were potently functional. A significant upregulation of P-selectin expression and downregulation of VCAM-1 (vascular cell adhesion molecule 1) were present on FL-expanded PB-FCs compared with FL BM-FCs. Stromal cell-derived factor-1 (SDF-1), and CXCR4 transcripts were significantly increased in FL PB-FCs and decreased in FL BM-FCs. Supernatant from FL PB-FCs primed HSC migration to SDF-1, confirming production of the protein product. The FL PB-FCs contained a predominance of p-preDCs and natural killer (NK)-FCs, and NK-FCs were lacking in FL BM-FCs. The impaired function for BM-FCs was restored within 5 days after cessation of treatment. Taken together, these data suggest that FCs may enhance HSC homing and migration via the SDF-1/CXCR4 axis and adhesion molecule modulation. These findings may have implications in development of strategies for retaining function of ex vivo manipulated FCs and HSCs.

Animals↗

PubMed2006

[Association of single nucleotide polymorphisms and haplotypes in DNA repair gene XRCC1 with susceptibility of breast cancer].

OBJECTIVE: To examine the contribution of the three most common single nucleotide polymorphisms (SNPs) in XRCC1 gene, C26304T, G27466A and G28152A, to susceptibility of breast cancer in Chinese Han population. METHODS: In this population-based case control study, 84 cases with breast cancer and 252 controls, matched to the cases in terms of habitation and age (5 years), were genotyped for the XRCC1 C26304T, G27466A and G28152A polymorphisms by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) methods. The haplotype distribution was estimated and compared by EH linkage software 1. 2. RESULT: The distribution of basic characteristics, such as age, alcohol drinking, the family history of malignancy in first and second relatives except cigarette smoking, were not significantly different between cases and controls. However, the percentage of ever or current smokers was significantly higher in cases (7.1%) than that in controls (2.0%). The distributions of allelotype and genotype of C26304T, G27466A and G28152A polymorphisms were also not significantly different between cases and controls. There was no significant association between the risk of breast cancer and these three SNPs of XRCC1 gene. The genetic linkage disequilibrium existed in these three polymorphic sites both in cases and controls, in which the CGG, CGA, CAG and TGG haplotypes were the most common. There was also no significant association of XRCC1 haplotype with risk of breast cancer. CONCLUSION: XRCC1 C26304T, G27466A and G28152A SNPs may not be associated with the susceptibility of breast cancer. The CGG, CGA, CAG and TGG haplotypes might be the most common haplotypes in Chinese Han population.

Adult↗

PubMed2006

[Association between genetic polymorphisms of metabolic enzymes and susceptibility of colorectal cancer].

OBJECTIVE: To investigate the association between CYP1A1, GSTM1, T1, UGT1A7 polymorphisms and colorectal cancer risk. METHODS: A case-control study of 140 patients with cancers and 343 health controls was conducted to investigate the role of CYP1A1, GSTM1, T1, UGT1A7 polymorphisms in colorectal cancer. Gene-gene interactions among CYP1A1, GSTM1, T1, UGT1A7 polymorphisms were detected by case-control study and case-only study. Genotypes of four genes polymorphisms were analyzed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and unconditional logistic regression was adopted to analyze the data. RESULTS: The CC, TC and CC genotypes of CYP1A1 T6235C significantly decreased the colorectal cancer risk as compared to TT genotype (OR = 0.493, 95% CI: 0.254-0.956, OR = 0.638, 95% CI: 0.427-0.952). GSTM1 and GSTT1 null genotype had no significant association with the increased risk of colorectal cancer while the mutant variants of UGT1A7 might increase the risk of colorectal cancer significantly (OR = 2.501, 95% CI: 1.456-4.296). The CORvalue for the gene-gene interactions between CYP1A1 variant and the null genotype of GSTT1, GSTM1-deleted and GSTT1-deleted genotype in the case-only design were 2.617 (95% CI: 1.015-6.752) and 3.935 (95% CI: 1.323-11.706), respectively. There was no significant interaction between CYP1A1 and GSTM1, CYP1A1 and UGT1A7. CONCLUSION: This study suggests that CYP1A1 and UGT1A7 variants might be associated with colorectal cancer. CYP1A1 and GSTM1 might interact on GSTT1 to influence the risk of colorectal cancer.

Cohort Studies↗

PubMed2006

[Development of methods for detection of H5N1 from human clinical specimens].

BACKGROUND: To establish a method for H5N1 RNA detection and laboratory diagnosis of suspected human avian influenza (H5N1) virus infected cases. METHODS: The typing and sub-typing primers were designed according to M and H5 and N1 gene respectively, and the RT-PCR and real-time PCR were developed using these primers. RESULTS: The RT-PCR and real-time PCR could be used for H5N1 detection specifically, and there was no cross reaction with other influenza subtypes such as H1 and H3. The sensitivity for RT-PCR and real-time PCR was 1 TCID50 and 0.01 TCID50 respectively. Thirteen laboratory confirmed human H5N1 cases were detected from 42 suspected cases by using these methods. CONCLUSION: The established RT-PCR and real-time PCR methods can be used for laboratory detection of suspected human H5N1 cases.

Animals↗

PubMed2006

[Study on structures of blattela germanica allergen, Bla g 2 expressed by eukaryotic and prokaryotic vectors using fluorescence and CD spectra].

The recombinant allergen, Bla g 2, was expressed by prokaryotic vector E. coli and eukaryotic vector P. Pastoris. The different structures and configurations of the Bla g 2 from E. coli and P. Pastoris were studied by fluorescence and circular dichroism. The secondary structures of Bla g 2 in solution, and the composition besides the type of its tertiary structure were proposed. These studies help understand the differences between prokaryotic and eukaryotic expression systems, reveal the relationship between the structure and the function of Bla g 2, and improve the production of this significant allergen.

Allergens↗

PubMed2005

Coordination frameworks constructed from bipyridyl piperazine and MCl2 (M = Co, Ni, Zn): structural characterization and optical properties.

Three metal-organic polymers, [CoCl2(bpfp)]n 1, {[NiCl2(bpfp)2](H2O)3}n 2 and [ZnCl2(bpfp)]n 3 (bpfp = N,N'-bis(3-pyridylformyl)piperazine), are formed by the self-assembly of the flexible bpfp with MCl2 (M = Co, Ni, Zn), respectively. X-Ray single-crystal structural analysis reveals that polymer 1 exhibits a novel grid network, in which the grid is composed of segments of bpfp and cobalt ions. Polymer 2 consists of 2D rhombohedral grids, the dimensions of the grid are 15.782 x 12.434 A2 and the diagonal-to-diagonal distances are 13.186 x 25.169 A2. In polymer 3, infinite wavelike chains are extended to 2D supramolecular arrays via C-H...Cl hydrogen bonds. The third-order nonlinear optical (NLO) behaviors of 1-3 and bpfp were investigated in dilute DMF solution by Z-scan measurement. The results show that 1, 2 and 3 exhibit good third-order NLO properties, which are quite different from bpfp that shows weak NLO behavior. This paper demonstrates that metal ions can strongly influence the crystal structures and third-order NLO properties of polymers.

2,2'-Dipyridyl↗

PubMed2005

Differences in apolipoprotein E3/3 and E4/4 allele-specific gene expression in hippocampus in Alzheimer disease.

Apolipoprotein E4 (APOE4) allele is a major risk factor for late-onset familial and sporadic Alzheimer disease (AD). The mechanism of action of APOE in the etiology of AD remains unclear. Using gene expression (microarray) analysis of human hippocampus from APOE3/3 AD and APOE4/4 AD cases, we found different gene transcription patterns between APOE4/4 and APOE3/3 AD cases. The expression of APOE4/4 alleles, in comparison to APOE3/3, is associated with upregulation of multiple gene transcripts encoding cell growth suppresser or arrest, signal transduction, myelinogenesis, cell adhesion and migration, heavy metal metabolism and detoxification. Whereas the APOE4 gene expression is associated with downregulation of gene transcripts involved in mitochondrial oxidative phosphorylation and energy metabolism, synaptic vesicle docking and fusing, and synaptic plasticity compared to APOE3. These mechanisms may contribute increased risk for AD and for cognitive dysfunction in AD patients who carry the APOE4 allele(s).

Aged↗

PubMed2005

Histone H3 tail positioning and acetylation by the c-Myb but not the v-Myb DNA-binding SANT domain.

The c-Myb transcription factor coordinates proliferation and differentiation of hematopoietic precursor cells. Myb has three consecutive N-terminal SANT-type repeat domains (R1, R2, R3), two of which (R2, R3) form the DNA-binding domain (DBD). Three amino acid substitutions in R2 alter the way Myb regulates genes and determine the leukemogenicity of the retrovirally transduced v-Myb oncogene. The molecular mechanism of how these mutations unleash the leukemogenic potential of Myb is unknown. Here we demonstrate that the c-Myb-DBD binds to the N-terminal histone tails of H3 and H3.3. C-Myb binding facilitates histone tail acetylation, which is mandatory during activation of prevalent differentiation genes in conjunction with CCAAT enhancer-binding proteins (C/EBP). Leukemogenic mutations in v-Myb eliminate the interaction with H3 and acetylation of H3 tails and abolish activation of endogenous differentiation genes. In primary v-myb-transformed myeloblasts, pharmacologic enhancement of H3 acetylation restored activation of differentiation genes and induced cell differentiation. Our data link a novel chromatin function of c-Myb with lineage-specific expression of differentiation genes and relate the loss of this function with the leukemic conversion of Myb.

Acetylation↗

PubMed2005

Biophysical studies of a ruthenium(II) polypyridyl complex binding to DNA and RNA prove that nucleic acid structure has significant effects on binding behaviors.

The interactions of a metal complex [Ru(phen)(2)PMIP](2+) {Ru=ruthenium, phen=1,10-phenanthroline, PMIP=2-(4-methylphenyl)imidazo[4,5-f]1,10-phenanthroline} with yeast tRNA and calf thymus DNA (CT DNA) have been investigated comparatively by UV-vis spectroscopy, fluorescence spectroscopy, viscosity measurements, isothermal titration calorimetry (ITC), as well as equilibrium dialysis and circular dichroism (CD). Spectroscopic studies together with ITC and viscosity measurements indicate that both binding modes of the Ru(II) polypyridyl complex to yeast tRNA and CT DNA are intercalation and yeast tRNA binding of the complex is stronger than CT DNA binding. ITC experiments show that the interaction of the complex with yeast tRNA is driven by a moderately favorable enthalpy decrease in combination with a moderately favorable entropy increase, while the binding of the complex to CT DNA is driven by a large favorable enthalpy decrease with a less favorable entropy increase. The results from equilibrium dialysis and CD suggest that both interactions are enantioselective and the Delta enantiomer of the complex may bind more favorably to both yeast tRNA and CT DNA than the Lambda enantiomer does, and that the complex is a better candidate for an enantioselective binder to yeast tRNA than to CT DNA. Taken together, these results indicate that the structures of nucleic acids have significant effects on the binding behaviors of metal complexes.

Base Sequence↗

PubMed2005

SNPselector: a web tool for selecting SNPs for genetic association studies.

SUMMARY: Single nucleotide polymorphisms (SNPs) are commonly used for association studies to find genes responsible for complex genetic diseases. With the recent advance of SNP technology, researchers are able to assay thousands of SNPs in a single experiment. But the process of manually choosing thousands of genotyping SNPs for tens or hundreds of genes is time consuming. We have developed a web-based program, SNPselector, to automate the process. SNPselector takes a list of gene names or a list of genomic regions as input and searches the Ensembl genes or genomic regions for available SNPs. It prioritizes these SNPs on their tagging for linkage disequilibrium, SNP allele frequencies and source, function, regulatory potential and repeat status. SNPselector outputs result in compressed Excel spreadsheet files for review by the user. AVAILABILITY: SNPselector is freely available at http://primer.duhs.duke.edu/

Algorithms↗

PubMed2005

NK cells play a critical role in the regulation of class I-deficient hemopoietic stem cell engraftment: evidence for NK tolerance correlates with receptor editing.

The role that NK cells play in the rejection of hemopoietic stem cell (HSC) and tolerance induction has remained controversial. In this study, we examined whether NK cells play a direct role in the rejection of HSC. Purified HSC from MHC class II-deficient mice engrafted readily in congenic mice, while HSC from class I-deficient donors (beta(2)-microglobulin(-/-) (beta(2)m(-/-))) failed to engraft. Recipient mice lacking CD8(+), CD4(+), or T cells also rejected HSC from class I-deficient donors, pointing directly to NK cells as the effector in rejection of HSC. Recipients, deficient in or depleted of NK cells, engrafted readily with beta(2)m(-/-) HSC. Expression of the activating Ly-49D and inhibitory Ly-49G2 receptors on recipient NK cells was significantly decreased in these beta(2)m(-/-)-->B6 chimeras, and the proportion of donor NK cells expressing Ly-49D was also significantly decreased. Notably, beta(2)m(-/-) chimeras accepted beta(2)m(-/-) HSC in second transplants, demonstrating that NK cells in the chimeras had been tolerized to beta(2)m(-/-). Taken together, our data demonstrate that NK cells play a direct role in the regulation of HSC engraftment, and down-regulation and/or deletion of specific NK subsets in mixed chimeras can contribute to the induction of NK cell tolerance in vivo. Moreover, our data show that bone marrow-derived elements significantly contribute to NK cell development and tolerance.

Animals↗

PubMed2005

Antitumor activity of a fusion of esophageal carcinoma cells with dendritic cells derived from cord blood.

The aim of this experiment was to develop a cytotoxic cancer vaccine (EC109-DC) prepared by fusions of esophageal carcinoma cells with dendritic cells derived from cord blood and to study the biological characteristics and resultant induction of antitumor immunity. CD34+ hematopoietic stem cells were isolated from cord blood using a CD34+ Progenitor Cell Isolation Kit by magnetic cell sorting system (MACS). CD34+ cells were incubated with rhGM-CSF, rhTNF-alpha and rhSCF for 2 weeks as DC (dendritic cells), and then by PEG-3600 to fuse with an esophageal carcinoma cell line. Selection with MACS marked with HLA-DR MicroBeads generated EC109-DC. Phenotypes and proliferation were analyzed by flow cytometry and cell culture in vitro. The lymphocyte proliferation reaction and CTL cytotoxicity were examined by MTT assay. The EC109-DC cells could proliferate slowly in vitro and highly expressed CD80, CD83 and CD86. The lymphocyte proliferation reaction and specific cytotoxicity against EC109 induced by EC109-DC cells were significantly higher than in control groups (p < 0.05). EC109-DC cells obtained by PEG fusion acquired the immuno-stimulating phenotype and could significantly stimulate the lymphocyte proliferation reaction and CTL activity. The results of this research provide the basis for materials to develop the DC-based vaccine against esophageal carcinoma.

Animals↗

PubMed2005

p53 mediates cellular dysfunction and behavioral abnormalities in Huntington's disease.

We present evidence for a specific role of p53 in the mitochondria-associated cellular dysfunction and behavioral abnormalities of Huntington's disease (HD). Mutant huntingtin (mHtt) with expanded polyglutamine (polyQ) binds to p53 and upregulates levels of nuclear p53 as well as p53 transcriptional activity in neuronal cultures. The augmentation is specific, as it occurs with mHtt but not mutant ataxin-1 with expanded polyQ. p53 levels are also increased in the brains of mHtt transgenic (mHtt-Tg) mice and HD patients. Perturbation of p53 by pifithrin-alpha, RNA interference, or genetic deletion prevents mitochondrial membrane depolarization and cytotoxicity in HD cells, as well as the decreased respiratory complex IV activity of mHtt-Tg mice. Genetic deletion of p53 suppresses neurodegeneration in mHtt-Tg flies and neurobehavioral abnormalities of mHtt-Tg mice. Our findings suggest that p53 links nuclear and mitochondrial pathologies characteristic of HD.

Animals↗

PubMed2005

The (CA)n polymorphism of the TNFR2 gene is associated with peak bone density in Chinese nuclear families.

Low peak bone density (PBD) in adulthood is an important determinant of osteoporotic fracture (OF) in the elderly. The tumor necrosis factor receptor 2 (TNFR2) gene has been considered as an important candidate gene for PBD due to its important role in bone turnover. In this study, we recruited a total of 1,263 subjects from 402 Chinese nuclear families composed of both parents and at least one daughter, and tested the association of the (CA)(n) polymorphism in intron 4 of the TNFR2 gene with PBD using a more contemporary quantitative transmission disequilibrium test (QTDT). Significant within-family association was detected between the CA16 allele and bone mineral density (BMD) at the lumbar spine with the P-value of 0.005 after permutations, which is still significant after correction for multiple testing. Some evidence of total-family association between the CA16 allele and lumbar spine BMD was found (P=0.021), although the significant level did not reach the empirical threshold (P< or =0.007). About 3.14% of lumbar spine BMD variation can be explained by the CA16 allele. In summary, our results suggest that the TNFR2 gene may play an important role in determining lumbar spine BMD variation in Chinese women.

Bone Density↗

PubMed2005

[A pilot study of spectrum of gene expression of acute leukemia].

OBJECTIVE: To investigate the gene expression of acute leukemia so as to study the pathogenesis of leukemia. METHODS: Five ml of bone marrow was collected from 22 patients with leukemia, 15 males and 7 females, aged 15-86, 17 with acute myelocytic leukemia, 4 with acute lymphocytic leukemia, and 1 with AHL. Mononuclear cells were isolated. Total RNA was extracted and mRNA was purified. DNA microarray technique with 12 848 genes was used to analyze the gene expression profiles. RESULTS: The predicted 45 genes were enormously expressed in 21 patients with acute leukemia, which were consistent with the ALL and AML classification standards reported by Golub and others. 7 genes which were overexpressed in multiple-resistant cell line K562-n/VCR were also overexpressed in 6 cases of refractory acute leukemia. Further analysis showed that 31 genes were upregulated in AML (M(4)-M(6)) and ALL but downregulated in AML (M(1)-M(3)). CONCLUSION: This results support the standard Golub has put forward. The reason that adult patients with ALL and subtypes of AML (M(4)-M(6)) have poorer prognosis in comparison with AMLM(1)-M(3) is attributed to alterations in gene expression. Primary drug resistance may be the major characteristics of refractory leukemia. Analysis of gene expression profile in acute leukemia is significant for classification and prognosis.

Adolescent↗

PubMed2005

Hyperphosphorylation of the BARD1 tumor suppressor in mitotic cells.

Although the BRCA1 tumor suppressor has been implicated in a number of cellular processes, it plays an especially important role in the DNA damage response as a regulator of cell cycle checkpoints and DNA repair pathways. In vivo, BRCA1 exists as a heterodimer with the BARD1 protein, and many of its biological functions are mediated by the BRCA1-BARD1 complex. Here, we show that BARD1 is phosphorylated in a cell cycle-dependent manner and that the hyperphosphorylated forms of BARD1 predominate during M phase. By mobility shift analysis and mass spectrometry, we have identified seven sites of mitotic phosphorylation within BARD1. All sites exist within either an SP or TP sequence, and two sites resemble the consensus motif recognized by cyclin-dependent kinases. To examine the functional consequences of BARD1 phosphorylation, we used a gene targeting knock-in approach to generate isogenic cell lines that express either wild-type or mutant forms of the BARD1 polypeptide. Analysis of these lines in clonogenic survival assays revealed that cells bearing phosphorylation site mutations are hypersensitive to mitomycin C, a genotoxic agent that induces interstrand DNA cross-links. These results implicate BARD1 phosphorylation in the cellular response to DNA damage.

Cell Cycle↗