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Biomedical subjects

H Xiao

Publications and source records attributed to H Xiao.

At least 19 recordsLinked to original sources
PubMed2006

Increased glycophorin A somatic cell variant frequency in arsenic-exposed patients of Guizhou, China.

Exposure to arsenic through domestic burning arsenic-containing coal causes various tumors in a population of Guizhou, China. The glycophorin A (GPA) assay is a human mutation assay detecting somatic variation in erythrocytes expressing the MN blood type, and was used to assess genotoxicity of arsenic-exposed patients. Peripheral blood was collected from 18 adult healthy subjects and 40 arsenic-exposed patients in heparin-treated tubes. Erythrocytes were isolated, fixed in formalin and immuno-labeled with fluorescent antibodies against GPA, followed by flow cytometry analysis. Arsenic exposure increased the variant frequency (expressed as the number of variant red cells per 10(6) erythrocytes): NN, 3.7 in healthy subjects versus 21.2 in arsenic-exposed patients; N phi, 12.6 versus 33.1; MM, 13.1 versus 110; and M phi, 5.2 versus 20.3. The total GPA variant frequency was increased about five-fold (34.7 in healthy subjects versus 185 in arsenosis patients). Furthermore, the variant frequency was significantly higher in skin tumor-bearing patients: NN, 19.4 in arsenic-exposed non-tumor patients versus 31.5 in tumor-bearing patients; N phi, 29.5 versus 54.5; MM, 102 versus 159; M phi, 15.9 versus 45.1. Total GPA variant frequency in arsenic-exposed patients bearing skin tumors was significantly increased compared to patients without skin tumors (167 versus 290). The relationship between arsenic exposure history and GPA variant frequency was less evident. These data demonstrate that arsenic exposure is associated with mutations at the GPA locus, an effect exaggerated in patients bearing arsenic-induced skin tumors. The variant frequency of GPA could be a useful biomarker for arsenic exposure and arsenic carcinogenesis.

Adult↗
PubMed2006

Temporal recruitment of CCAAT/enhancer-binding proteins to early and late adipogenic promoters in vivo.

The CCAAT/enhancer-binding protein (C/EBP) family of transcriptional regulators is critically important for the activation of adipogenic genes during differentiation. The C/EBPbeta and delta isoforms are rapidly induced upon adipocyte differentiation and are responsible for activating the adipogenic regulators C/EBPalpha and peroxisome proliferator activated receptor (PPAR)gamma2, which together activate the majority of genes expressed in differentiating adipocytes. However, mitosis is required following the induction of adipogenesis, and the activation of C/EBPalpha and PPARgamma2 gene expression is delayed until cell division is underway. Previous studies have used electromobility shift assays to suggest that this delay is due, at least in part, to a delay between the induction of C/EBPbeta protein levels and the acquisition of DNA binding capacity by C/EBPbeta. Here we used in vivo chromatin immunoprecipitation analysis of the C/EBPalpha, PPARgamma2, resistin, adiponectin, and leptin promoters to examine the kinetics of C/EBP protein binding to adipogenic genes in differentiating cells. In contrast to prior studies, we determined that C/EBPbeta and delta were bound to endogenous regulatory sequences controlling the expression of these genes within 1-4 h of adipogenic induction. These results indicated that C/EBPbeta and delta bind not only to genes that are induced early in the adipogenic process but also to genes that are induced much later during differentiation, without a delay between induction of C/EBP protein levels and DNA binding by these proteins. We also showed that each of the genes examined undergoes a transition in vivo from early occupancy by C/EBPbeta and delta to occupancy by C/EBPalpha at times that correlate with the induction of C/EBPalpha protein levels, demonstrating the generality of the transition during adipogenesis and indicating that the binding of specific C/EBP isoforms does not correlate with timing of expression from each gene. We have concluded that C/EBP family members bind to adipogenic genes in vivo in a manner that follows the induction of C/EBP protein synthesis.

3T3-L1 Cells↗
PubMed2005

Highly pathogenic H5N1 influenza virus infection in migratory birds.

H5N1 avian influenza virus (AIV) has emerged as a pathogenic entity for a variety of species, including humans, in recent years. Here we report an outbreak among migratory birds on Lake Qinghaihu, China, in May and June 2005, in which more than a thousand birds were affected. Pancreatic necrosis and abnormal neurological symptoms were the major clinical features. Sequencing of the complete genomes of four H5N1 AIV strains revealed them to be reassortants related to a peregrine falcon isolate from Hong Kong and to have known highly pathogenic characteristics. Experimental animal infections reproduced typical highly pathogenic AIV infection symptoms and pathology.

Amino Acid Sequence↗
PubMed2005

Variability of G1 gene of hantaviruses occurring in the Hubei Province, P.R. China from 1985 to 2000.

We studied variability of G1 gene of hantaviruses occurring in the Hubei province, P.R. China. Serum samples were collected from 229 patients with hemorrhagic fever with renal syndromes (HFRS) during 1985--1989 and 1996--2000 and were tested by RT-PCR for the presence of Hantaan and Seoul viruses (HTNVs, SEOVs) and by restriction fragment length polymorphism (RFLP) analysis for the respective pattern. Out of 229 sera 166 (72.5%) were hantavirus-positive by RT-PCR, including 124 from 1985--1989 and 42 from 1996--2000, with HTNVs in majority (80.1%) and SEOVs in minority (19.9%). By RFLP analysis, four types of RFLP pattern were recognized. In the 133 HTNV isolates the A pattern was most predominant (62.5%), while the remaining patterns B, C, and D were present in minority. This kind of the RFLP pattern distribution was observed regardless the year of virus isolation. In contrast, only one type of RFLP pattern was obtained from 33 SEOVs, but this was different from that of R22 virus. Our results indicate that temporal factor, represented by years 1985--2000 seems to be too short to affect markedly the genetic makeup of the hantaviruses investigated.

Adolescent↗
PubMed2005

Effect of cordycepin on Hantaan virus 76-118 infection of primary human embryonic pulmonary fibroblasts--characterization of apoptotic effects.

The cDNA microarray technique was used to study gene epression in human embryonic pulmonary fibroblasts (HEPF) infected with Hantaan virus (HTNV) under the influence of cordycepin (Cor), an inhibitor of post-transcriptional pre-mRNA polyadenylation. Four apoptotic genes, the insulin-like growth factor binding protein 1, NFkB inhibitor alpha, caspase-3 and NFkB1 were up-regulated in both infected and uninfected Cor-treated cells and two cell cycle-associated genes, CDC-like kinase and beta-induced transforming growth factor were up-regulated in Cor-untreated cells but down-regulated in Cor-treated cells. Cell morphology examination, quantitative RT-PCR, and immunofluorescence (IF) test suggested that following the Cor treatment the HTNV infection took place, but late viral gene expression was slightly reduced. Three parameters, namely caspase-3 activity, annexin V binding, and cell cycle were used to detect apoptosis. The results suggested that the induction of apoptosis in HEPF by HTNV started at 6 hrs post infection (p.i.). Following the Cor treatment, however, the caspase-3 activity began to increase at 24 hrs p.i. Thus it is suggested that inhibition of de novo late viral protein synthesis by Cor changes the apoptosis pathway and cell cycle by delaying caspase-3 gene expression and by up/down-regulating of expression of other apoptotic and cell cycle-associated genes. This implicates that HTNV can induce apoptosis in HEPF even without de novo viral protein synthesis and with a reduced and slowed viral maturation.

Animals↗
PubMed2004

Generation of a polyclonal antibody specifically against the p33(ING1b) tumor suppressor.

The p33(ING1b) tumor suppressor protein plays a prominent role in cellular stress responses including cell cycle arrest, DNA repair, apoptosis, and chromatin remodeling. As the main product of the inhibitor of growth 1 (ING1) gene, p33(ING1b) is the most intensively studied protein of the ING family. So far, most ING1 antibodies have been raised against full-length proteins. Since all ING1 isoforms share an identical carboxyl-terminus, and commercially available ING1 antibodies often lack specificity, we sought to develop a polyclonal antibody capable of specifically recognizing the p33(ING1b) protein. Here, we describe the development and characterization of the p33(ING1b)-specific antibody.

Amino Acid Sequence↗
PubMed2004

Serological characterization of a hantavirus from Hubei, China.

Hantavirus HV114, isolated from urine of a patient during epidemic of hemorrhagic fever with renal syndrome (HFRS) in China, was subjected to a detailed serological characterization using enzyme-linked immunosorbent assay (ELISA), neutralization test and indirect immunofluorescence antibody assay (IFA). It has been found that HV114 is antigenically similar to the hantavirus A9 strain isolated in China and to the Hantaan 76-118 virus (HTNV 76-118), but different from the hantaviruses isolated from Apodemus agrarius in the region endemic for HFRS.

Animals↗
PubMed2002

Destabilisation of oil-water emulsions and separation by dissolved air flotation.

The roles of aluminium and ferric sulphates as destabilising agents for oil-water emulsions that have been stabilised by a non-ionic surfactant (Span 20) are investigated in terms of oil removal. The effects of coagulant dose, pH, and the duration and intensity of both slow and fast mixing are considered. Electrokinetic measurements indicate that oil droplets have a negative zeta potential that is weakly dependent on pH. The chosen coagulants are shown to be effective in reducing the zeta potential of the oil droplets, and charge reversal was observed for aluminium sulphate. Oil removals up to 99.3% at pH 8 and 99.94% at pH 7 are seen for aluminium sulphate and ferric sulphate respectively. Rapid mixing times of around 120 s and flocculation times ranging from 15 to 20 min appear to be optimal for the DAF separation. It is concluded that relatively low average mixing speeds for coagulation and flocculation are essential for efficient operation.

Air↗
PubMed2001

Histone tails modulate nucleosome mobility and regulate ATP-dependent nucleosome sliding by NURF.

Nucleosome Remodeling Factor (NURF) is an ATP-dependent nucleosome remodeling complex that alters chromatin structure by catalyzing nucleosome sliding, thereby exposing DNA sequences previously associated with nucleosomes. We systematically studied how the unstructured N-terminal residues of core histones (the N-terminal histone tails) influence nucleosome sliding. We used bacterially expressed Drosophila histones to reconstitute hybrid nucleosomes lacking one or more histone N-terminal tails. Unexpectedly, we found that removal of the N-terminal tail of histone H2B promoted uncatalyzed nucleosome sliding during native gel electrophoresis. Uncatalyzed nucleosome mobility was enhanced by additional removal of other histone tails but was not affected by hyperacetylation of core histones by p300. In addition, we found that the N-terminal tail of the histone H4 is specifically required for ATP-dependent catalysis of nucleosome sliding by NURF. Alanine scanning mutagenesis demonstrated that H4 residues 16-KRHR-19 are critical for the induction of nucleosome mobility, revealing a histone tail motif that regulates NURF activity. An exchange of histone tails between H4 and H3 impaired NURF-induced sliding of the mutant nucleosome, indicating that the location of the KRHR motif in relation to global nucleosome structure is functionally important. Our results provide functions for the N-terminal histone tails in regulating the mobility of nucleosomes.

Adenosine Triphosphate↗
PubMed2001

Restoration of decreased N-methyl-d-asparate receptor activity by brain-derived neurotrophic factor in the cultured hippocampal neurons: involvement of cAMP.

Brain-derived neurotrophic factor (BDNF) may play an important role in the modulation of N-methyl-d-asparate (NMDA) receptor function. To elucidate the underlying mechanisms, whole-cell patch-clamp recording was used to assess the effect of BDNF on the responses of cultured hippocampal neurons to the glutamate receptor agonist NMDA. We found that peak amplitude of NMDA-evoked currents in cultured hippocampal pyramidal neurons at Day 18 in vitro decreased significantly compared to that of NMDA currents at Day 10 or 14. Interestingly, NMDA-evoked currents were greatly enhanced by BDNF (50 ng/ml) in cultured neurons at Day 18, but not at Day 10 or 14. Treatment with Rp-cAMP abolished the potentiating effects of BDNF on NMDA current. Elevating the amount of cytosolic cAMP by preincubation with forskolin or Sp-cAMP also enhanced NMDA currents as effectively as BDNF in 18-day-old hippocampal neurons. Measurement of the cellular content of cAMP by RIA indicated that cultured hippocampal neurons showed decreased basal cAMP levels at the time NMDA currents were decreased and BDNF increased the decreased cAMP levels. Taken together, these results suggest that BDNF may restore decreased NMDA receptor activity in cultured hippocampal neurons by the cAMP pathway.

Animals↗
PubMed2001

Cables enhances cdk2 tyrosine 15 phosphorylation by Wee1, inhibits cell growth, and is lost in many human colon and squamous cancers.

Cyclin-dependent kinase 2 (cdk2) is a small serine/threonine kinase that regulates cell cycle progression. Cdk2 activity is tightly controlled by several mechanisms, including phosphorylation and dephosphorylation events. Cables is a recently described novel cdk-interacting protein. In proliferating cells, Cables was predominantly localized in the nucleus by cell fractionation and immunostaining. Expression of Cables in HeLa cells inhibited cell growth and colony formation. Cables enhanced cdk2 tyrosine 15 phosphorylation by the Wee1 protein kinase, an inhibitory phosphorylation, which led to decreased cdk2 kinase activity. The gene encoding Cables is located on human chromosome 18q11-12, a site that is frequently lost in squamous, colon, and pancreas cancers. We found that Cables was strongly expressed in normal human epithelial cells including squamous and glandular mucosa. Breast and pancreatic cancers show strong Cables expression; however, loss of Cables expression was found in approximately 50-60% of primary colon and head and neck cancer specimens. Lack of Cables expression was associated with loss of heterozygosity on chromosome 18q11. The data provide evidence for a Cables-mediated interplay between cdk2 and Wee1 that leads to inhibition of cell growth. Conversely, loss of Cables may cause uncontrolled cell growth and enhance tumor formation.

Animals↗
PubMed2001

Suppression of gene amplification and chromosomal DNA integration by the DNA mismatch repair system.

Mismatch repair (MMR)-deficient cells are shown to produce >15-fold more methotrexate-resistant colonies than MMR normal cells. The increased resistance to methotrexate is primarily due to gene amplification since all the resistant clones contain double-minute chromosomes and increased copy numbers of the DHFR gene. In addition, integration of linearized or retroviral DNAs into chromosomes is also significantly elevated in MMR-deficient cells. These results suggest that in addition to microsatellite instability and homeologous recombination, MMR is also involved in suppression of other genome instabilities such as gene amplification and chromosomal DNA integration.

Adaptor Proteins, Signal Transducing↗
PubMed2001

[Tissue tropism of novel nonenveloped DNA virus in experimentally infected rhesus monkey].

OBJECTIVE: To investigate the tissue tropism of transfusion transmitted virus (TTV), a novel nonenveloped DNA virus, in experimentally infected Rhesus monkey. METHODS: Filtrate of feces of one patient with TTV infection was fed into the stomachs of ten Rhesus monkeys. Five (?) monkeys were killed during viremia and their tissues were collected to be examined for the presence of replicative virus DNA by in situ hybridization, dot blot hybridization with antisense probe and hybridization/nuclease protection assay. RESULTS: The virus contents (density of electrophoretic band) in the liver, PBMC, and serum of three infected monkeys 50.1%, 31.0%, and 18.9% respectively; the relative proportion was 2.65;1.64;1.00. TTV was detected in liver, spleen, stomach, small intestine and its lymph nodes, PBMC, colon, and serum; however, viral plus-chain, a putative replicative intermediate, was found only in liver, spleen, small intestine, and lymphoid cells. CONCLUSION: Transfusion transmitted virus is hepato-, spleno-, and lymphoid cell-tropic, and may has multiple routes of transmission.

Animals↗
PubMed2001

[The transcription and expression of IL-18 gene in HBV infectors].

OBJECTIVE: To evaluate the possible roles of interleukin 18 (IL-18) in hepatitis B virus (HBV) infection. METHODS: Peripheral blood lymphocytes from 3 groups of HBV infectors (including 15 asymptomatic carriers, 30 patients with chronic hepatitis, 12 patients with fulminant hepatitis) and 10 blood donors (as normal controls) were analyzed. The transcription and expression of IL-18 in PBMC were assessed by semi-quantitive reverse transcription polymerase chain reaction and flow cytometry. RESULTS: (1) There were significant differences in the transcription and expression levels of IL-18 between each group of HBV infectors. Interestingly, it was highest in fulminant hepatitis group, and lowest in asymptomatic carrier group. However there was no significant difference between chronic hepatitis and normal controls. The severity of disease was accompanied with the elevation of IL-18 production. (2) The severity degree of liver inflammation in chronic hepatitis was ccompanied with the elevation of IL-18 production. (3) The transcription and expression of IL-18 in chronic hepatitis B correlated with serum ALT positively (r = 0.54, P < 0.01; r = 0.63, P < 0.01). (4) There was a positive correlation in transcription and expression of IL-18 in each group of HBV infectors (asymptomatic carrier r = 0.980, P < 0.001; chronic hepatitis r = 0.910, P < 0.001; fulminant hepatitis r = 0.975, P < 0.001). CONCLUSION: IL-18 may take part in the host immunity against HBV,and relate to the inflammation degree of liver.

Female↗
PubMed2001

Inhibition of extracellular signal-regulated kinase (ERK) mediates cell cycle phase independent apoptosis in vinblastine-treated ML-1 cells.

Chemotherapeutic agents induce alterations in intracellular signal transduction cascades that culminate in the initiation of the apoptotic program. Here, the relationship between the mitogen-activated protein kinase (MAPK) response and apoptosis in ML-1 cells treated with vinblastine and paclitaxel was investigated. We show that these compounds elicit different effects on MAPKs with vinblastine, but not paclitaxel, increasing both c-Jun-NH2-terminal kinase (JNK) and p38 activity. However, vinblastine and paclitaxel both induced apoptosis with similar kinetics, suggesting that increased JNK and p38 activity is not required for apoptosis that is induced by microtubule interfering agents. Strikingly, the abrogation of extracellular signal-regulated kinase (ERK)-signaling by the MAPK/ERK kinase (MEK)1/2 inhibitor PD098059 in combination with vinblastine robustly induced apoptosis in ML-1 cells at a rate much faster than treatment with vinblastine alone and occurred at all phases of the cell cycle. This apoptotic induction was attributed to JNK activation because: (a) non-JNK-activating concentrations of vinblastine failed to increase apoptosis in the presence of PD098059; (b) apoptosis induced by paclitaxel, which did not activate JNK, was not potentiated by PD098059; and (c) transduction of an inhibitor of JNK activity partially suppressed both JNK activity and apoptosis induced by vinblastine plus PD098059. Additionally, we found that the activation of JNK by vinblastine occurred upstream of effector caspase activation because treatment with a pan-specific caspase inhibitor (valine-alanine-aspartate-fluoromethylketone) resulted in complete abrogation of apoptosis with no effect on MAPK signaling. Taken together, these data suggest that inhibition of the MEK-->ERK signal transduction cascade alleviates cell cycle dependence for vinblastine-induced apoptosis by a mechanism that requires JNK activation.

Antineoplastic Agents, Phytogenic↗
PubMed2001

Buthus martensi Karsch agonist of skeletal-muscle RyR-1, a scorpion active polypeptide: antinociceptive effect on rat peripheral nervous system and spinal cord, and inhibition of voltage-gated Na(+) currents in dorsal root ganglion neurons.

The antinociceptive effect and potential antinociceptive mechanism of Buthus martensi Karsch agonist of skeletal-muscle RyR-1 (BmK AS-1), a scorpion venom derived neurotoxic polypeptide, have been investigated in rats. The results show that: (a) the withdrawal latency to rat plantar radiant heat was increased significantly by 100 and 150% after intrathecal injection of 0.6 and 1.2 microg doses; (b) C components of rat nociceptive flexion reflex were reduced to 72, 50 and 29% after intraplantar injection of 5, 10 and 20 microg doses; (c) both central (spinal cord) and peripheral antinociceptive effects of BmK AS-1 could not be reversed by naloxone; (d) tetrodotoxin-resistant (TTX-R) Na(+) current was depressed to 83.87+/-1.64, 64.73+/-5.43 and 15.85+/-17.63%, and tetrodotoxin-sensitive (TTX-S) Na(+) current was depressed to about 81.27+/-2.5, 49.08+/-8.09 and 9.03+/-12.34% with 0.2, 1.0 and 10 microg/ml BmK AS-1 measured using patch clamp recording in rat small dorsal root ganglion (DRG) neurons, respectively. The results indicate that BmK AS-1 may be a new component with potent antinociceptive activity mediated by modulating TTX-S and TTX-R Na(+) channels.

Animals↗