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Biomedical subjects

Q Meng

Publications and source records attributed to Q Meng.

At least 91 records · Page 5Linked to original sources

Increases in eotaxin-positive cells in induced sputum from atopic asthmatic subjects after inhalational allergen challenge.

BACKGROUND: Eosinophils are believed to be critical proinflammatory cells in airway mucosal damage in asthma. Eotaxin is a C-C chemokine with selective activity for eosinophils and basophils. Previous studies have shown increased expression of eotaxin in the airways of asthmatics at baseline. We aimed to investigate eotaxin expression during the late-phase reaction to allergen inhalation in atopic asthmatics. METHODS: Sputum induction was performed before and 24 h after inhalational allergen challenge in atopic asthmatics, and eotaxin protein was detected immunocytochemically. RESULTS: Thirteen patients with a mean decrease in forced expiratory volume in 1 s of 28% (+/-1.5) during the early asthmatic reaction, and 39% (+/-4.7) during the late asthmatic reaction produced sufficient sputum for study. The percentage of eosinophils in sputum was increased 24 h after allergen challenge (P<0.004), and eosinophil percentages in sputum after challenge correlated with the magnitude of the late-phase reaction (r=0.56, P=0.05). The percentage of eotaxin-positive cells increased from 12.6% (range 2-43.8) to 24.3% (8.1-47.1, P<0.005). Allergen-induced increases in eotaxin-positive cells correlated with increases in eosinophils (r=0.63, P<0.01). CONCLUSIONS: These findings suggest that eotaxin may contribute to allergen-induced recruitment of eosinophils to the airway in asthmatic subjects.

Adult↗

Experimental therapy of a platelet-activating factor antagonist (ginkgolide B) on photochemically induced thrombotic cerebral ischaemia in tree shrews.

1. The aim of the present study was to investigate the effects of a platelet-activating factor (PAF) antagonist (ginkgolide B; GB) on brain oedema, ion homeostasis, monoamine neurotransmitter disturbances in ischaemic penumbra and the neuroprotective mechanisms of the PAF antagonist. 2. Photochemically induced thrombotic cerebral ischaemia in tree shrews was used as the experimental model and changes in histopathology and the content of monoamine neurotransmitters (measured by a spectrofluorometer), water content (measured by a specific gravimetric method), sodium and calcium (measured by an atomic absorption spectrophotometer) in the penumbra were observed. 3. Results show that content of noradrenaline (NA), dopamine (DA) and 5-hydroxytryptamine (5-HT) decreased in the penumbra, while 5-HT metabolite 5-hydroxyindole-3-acetic acid, sodium, calcium and water contents increased markedly (P < 0.01) after photochemical reaction. 4. In tree shrews treated with GB (5 mg/kg, i.v.) 6 h after photochemical reaction, cortical NA, DA and 5-HT contents recovered to control levels and water and calcium contents decreased significantly (P < 0.01). 5. The results suggest that PAF may play an important role in inducing calcium overload, brain oedema and secondary brain damage in penumbra and that GB produces its neuroprotective effects by inhibiting the pathological manifestation of PAF.

Animals↗

Ultraviolet radiation down-regulates expression of the cell-cycle inhibitor p21WAF1/CIP1 in human cancer cells independently of p53.

PURPOSE: To investigate the regulation of G1 cyclin-dependent kinase inhibitor p21WAF1/CIP1 by ultraviolet (UV) radiation in human carcinoma cells. MATERIALS AND METHODS: Human cancer cell lines were irradiated with UV-C (254 nm) radiation, and their responses were characterized by Western blotting, Northern blotting, semi-quantitative RT-PCR analysis, trypan blue staining and flow cytometric cell cycle analysis. RESULTS: At 24 h after UV irradiation, p21 expression was down-regulated in various cancer cell types (breast, prostrate, cervix, colon, glioma, squamous cancers), independently of their p53 genetic and functional status. UV-mediated down-regulation of p21 was dose- and time-dependent, was observed at the protein and mRNA levels, and did not correlate with cytotoxicity. Reduction of p21 protein levels required about 4 and 1 h, respectively, in MCF-7 and MDA-MB-231 breast cancer cells; some of the UV-induced decreases in p21 levels in these cell lines was due to enhanced proteasomal degradation. Despite decreased p21 levels, UV-irradiated breast cancer cells with wild-type p53 (MCF-7) retained the capacity for G1 cell-cycle arrest, whereas UV-treated cells with mutant p53 (MDA-MB-231) accumulated in S phase, suggesting a p53-dependent G1 checkpoint in MCF-7. UV treatment caused other alterations in cell-cycle regulatory, DNA repair and tumour suppressor genes, as described in this report. CONCLUSIONS: In contrast to X-rays, UV causes down-regulation of the cell-cycle inhibitor p21 in tumour cells. It is postulated that this may be an adaptation to promote the growth and survival of transformed cells.

BRCA2 Protein↗

Fermentation substrate and dilution rate interact to affect microbial growth and efficiency.

The effect of dilution rate (D) on carbohydrate, fibrous and nonfibrous, and protein fermentation by ruminal microorganisms was studied using a single-effluent continuous-culture system. The diets of fibrous carbohydrate, nonfibrous carbohydrate, or protein were formulated with soybean hulls (FC), ground corn (NFC), or isolated soy protein (PR) as the primary ingredient, respectively. Six dilution rates (.025, .050, .075, .10, .15, and .20/h of fermenter volume) were used. Digestibilities of DM, OM, and CP for the three diets and of NDF and ADF for the FC diet decreased (P<.001) as D increased, although the response of the digestibility to D varied with diet. Increasing D resulted in an increase in pH (P<.001) and a decrease (P<.001) in ammonia concentration. Daily volatile fatty acid production increased (quadratic; P<.01) for the FC and NFC diets, but decreased (quadratic; P<.001) for the PR diet. Increasing D quadratically increased (P<.001) the molar percentage of acetate and propionate, but quadratically decreased (P<.001) butyrate and valerate for the FC and NFC diets. For the PR diet, the molar percentage of propionate and valerate increased (quadratic; P<.01), whereas acetate and butyrate decreased (linear; P<.001) in response to increasing D. Molar percentage of isobutyrate and isovalerate decreased (P<.01) with increasing D for all three diets. As D increased, daily microbial N production showed quadratic responses with maximum values achieved at .126, .143, and .187/h D for the FC, NFC, and PR diet, respectively. There was a positive correlation between microbial growth efficiency (MOEFF) and D. A quadratic model fit the data of MOEFF as affected by D, and maximum MOEFF of 37.3, 59.6, and 71.4 g of bacterial N/kg OM truly fermented were calculated to be achieved at .177, .314, and .207/h D for the FC, NFC, and PR diet, respectively. Dilution rate significantly influenced the ruminal microbial fermentation of fibrous and nonfibrous carbohydrates and proteins, and was positively related to microbial yield and growth efficiency. In addition, microbial nitrogen composition, and therefore efficiency, was affected by substrate fermented.

Animal Feed↗

Effect of WT1 gene expression on cell growth and proliferation in myeloid leukemia cell lines.

OBJECTIVE: To investigate the effects and mechanism of Wilms' tumor (WT1) antisense oligonucleotides (AS-oligomers) on proliferation and apoptosis in myeloid leukemia cell lines. METHODS: K562 and HL-60 cells were cultured in presence of WT1 oligomers. Both cell lines express WT1 gene with no p53 protein expression. Cells growth, apoptosis and expression of WT1, bcl-2 genes were analysed using 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenylmetrazolium bromide (MTT) colorimetric assay, flow cytometry and reverse transcription-polymerase chain reaction (RT-PCR) methods. RESULTS: WT1 antisense oligonucleotides inhibited cellular proliferation of K562 cells and the effect was concentration-dependent. When cultured at concentration of 200 micrograms/ml oligomers, growth inhibition was 46.2% for antisense oligonucleotide cultivated group and 28.1% for sense oligonucleotide cultured group (P = 0.008) respectively. WT1 antisense oligonucleotide can induce apoptosis of K562 and HL-60 cells. Percentages of apoptotic cells in antisense oligonucleotide and sense oligonucleotide treated groups were 30.88% versus 13.62% for K562 cells and 40.15% versus 4.23% for HL-60 cells. However the growth of HL-60 cells and expression of bcl-2 gene were unaffected. CONCLUSIONS: The WT1 gene is related with proliferation and apoptosis of leukemic cells. Effect of anti-apoptosis may be independent of the cellular p53 status and bcl-2 expression. WT1 gene may play an important role in leukemogenesis.

Apoptosis↗

Evi-1 and MDS1-Evi-1 genes in pathogenesis of myelodysplastic syndromes and post-MDS acute myeloid leukemia.

OBJECTIVE: To investigate expression of Evi-1 and MDS1-Evi-1 genes in myelodysplastic syndromes (MDS) and post-MDS acute myeloid leukemia (post-MDS AML), and its role in pathogenesis or progression of MDS and post-MDS AML. METHODS: Expression of Evi-1 and MDS1-Evi-1 genes was examined in 31 MDS, 11 post-MDS AML, and 34 de novo AML patients by a semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: Evi-1 expression was not detected in bone marrow samples of 8 normal controls, but low MDS1-Evi-1 expression levels (MDS1-Evi-1/GAPDH < 0.1) were detected in 3 of the 8 controls. Evi-1 RNA was expressed in 1 of 8 RA, 8 of 13 RAEB and 6 of 9 RAEB-T patients, and the percentage of Evi-1 expression in RAEB(T) patients was higher than that in RA (P < 0.05). MDS1-Evi-1 expression was detected in 5 of 8 RA, 9 of 13 RAEB and 5 of 9 RAEB-T patients, and MDS1-Evi-1 expression levels (MDS1-Evi-1/GAPDH > 0.1) were markedly higher than those in the controls. Evi-1 expression was gradually increased in 4 of 5 RAEB-T patients with transformation from MDS to AML. The percentages of Evi-1 and MDS1-Evi-1 expression in post-MDS AML patients were significantly (P < 0.01 and P < 0.05 respectively) higher than those in de novo AML. The colonies of hematopoietic progenitor cells were decreased in Evi-1 and MDS1-Evi-1-positive MDS patients as compared with those in Evi-1 and MDS1-Evi-1-negative patients. CONCLUSION: Abnormal expression of the Evi-1 gene and overexpression of MDS1-Evi-1 gene may play a role in the pathogenesis or progression of MDS and post-MDS AML.

Adult↗

BRCA1 as a potential human prostate tumor suppressor: modulation of proliferation, damage responses and expression of cell regulatory proteins.

In addition to breast and ovarian cancer in women, recent evidence suggests that germ-line mutations of the breast cancer susceptibility gene-1 (BRCA1) also confer an increased life-time risk for prostate cancer in male probands. However, it is not known if and how BRCA1 functions in prostate cancer. We stably expressed wild-type (wt) and tumor-associated mutant BRCA1 transgenes in DU-145, a human prostate cancer cell line with low endogenous expression of BRCA1. As compared with parental cells and vector transfected clones, wtBRCA1 clones exhibited: (1) a slightly decreased proliferation rate (doubling time = 25 h as compared with 22 h for control cells); (2) a (3-6)-fold increase in sensitivity to chemotherapy drugs (adriamycin, camptothecin, and taxol); (3) increased susceptibility to drug-induced apoptosis; (4) reduced repair of single-strand DNA strand breaks; and (5) alterations in expression of key cellular regulatory proteins (including BRCA2, p300, Mdm-2, p21(WAF1/CIP1), Bcl-2 and Bax). Clones transfected with the 5677insA breast cancer-associated mutant BRCA1 (insBRCA1) displayed a similar phenotype to wtBRCA1 clones, except that insBRCA1 clones had a significantly decreased proliferation rate (doubling time = 42 h). On the other hand, cells transfected with with 185delAG mutant BRCA1 showed no obvious phenotype as compared with parental or vector transfected cells. These findings suggest that BRCA1 may function as a human prostate tumor suppressor by virtue of its ability to modulate proliferation and various components of the cellular damage response. They also suggest several potential target gene products for a BRCA1 prostate tumor suppressor function.

Antineoplastic Agents↗

IL-4- and IL-5-positive T lymphocytes, eosinophils, and mast cells in allergen-induced late-phase cutaneous reactions in atopic subjects.

It has previously been shown that cells mRNA+ for T(H2)-type cytokines (IL-4 and IL-5) infiltrate the site of allergen-induced cutaneous late-phase reactions (LPR) in atopic subjects. In this study we have used the same experimental model to identify the cell source of both IL-4 and IL-5 mRNA and protein product. Allergen-induced LPRs were provoked in the skin of atopic individuals and the sites microscopically examined at 6, 24, and 48 hours. Using single in situ hybridization and immunohistochemistry, we first showed that the numbers of IL-4 and IL-5 mRNA and protein product positive cells peaked at 24 hours. This coincided with the magnitude of the LPR. By double in situ hybridization/immunohistochemistry, we then established (in 24-hour biopsy specimens) that the percentage of CD3+ T lymphocytes, EG2+ eosinophils, and tryptase-positive mast cells that were either IL-4 or IL-5 mRNA+ was 19%, 24%, and 5% and 19%, 20%, and 5%, respectively. Conversely, the percentage of EG2+ and tryptase-positive cells that were IL-4 or IL-5 protein product positive were 62% and 53% and 72% and 29%, respectively. IL-4 and IL-5 protein did not colocalize to CD3+ cells. CD68+ macrophages were negative in both in situ hybridization and immunohistochemistry. With eosinophils we obtained direct evidence of time-dependent stimulus-induced IL-4 and IL-5 mRNA transcription by semiquantitative reverse transcription-polymerase chain reaction of cells incubated with either IgG- or sIgA-coated particles in vitro. Taken together, these experiments suggest that eosinophils, mast cells, and T cells all contribute in variable degrees to the expression of IL-4 and IL-5 in human cutaneous LPR. The failure to colocalize IL-4/IL-5 protein (as opposed to mRNA) to CD3+ cells is attributed to the inability of T lymphocytes to store and concentrate sufficient intracellular amounts of these cytokines to produce positive immunostaining.

Adult↗

High-affinity immunoglobulin E receptor (Fc epsilon RI)-bearing eosinophils, mast cells, macrophages and Langerhans' cells in allergen-induced late-phase cutaneous reactions in atopic subjects.

We have used in situ hybridization (ISH) and immunohistochemistry (IHC) to investigate the kinetics of the expression for Fc epsilon RI mRNA (alpha-, beta- and gamma-chains), the alpha-chain protein product, as well as the phenotype of the mRNA- or protein-positive cells in allergen-induced late-phase skin reactions in atopic subjects. Compared with diluent controls, there were significant increases in the total number of mRNA+ cells for the alpha-, beta- and gamma-chains for Fc epsilon RI at all time-points (6, 24 and 48 hr) after allergen challenge (P < 0.01). By double IHC/ISH significant increases in alpha-, beta- and gamma-chain mRNA+ macrophages, eosinophils, mast cells and CD1a+ cells were also observed after allergen challenge (P < 0.05). The distribution of Fc epsilon RI subunit (alpha-, beta-, or gamma-chain) mRNA+ co-localization was CD68+ macrophages (42-47%), EG2+ eosinophils (33-39%), tryptase+ mast cells (5-11%) and CD1a+ Langerhans' cells (2-4%). Using single IHC, significant increases in the total number of Fc epsilon RI protein+ cells (P < 0.01) were observed 24 and 48 hr after allergen challenge. Double IHC showed that the distribution of Fc epsilon RI+ cells was tryptase+ mast cells (33%), CD68+ macrophages (36%), EG2+ eosinophils (20%), CD1a+ Langerhans' cells (4%) and unidentified cells (7%), at the 24-hr allergen-challenged sites. These observations suggest that the cutaneous late-phase reaction in man is associated with up-regulation of Fc epsilon RI on eosinophils, macrophages, mast cells and Langerhans' cells.

Allergens↗

Comparison of the mutagenic potency of 1,3-butadiene at the hprt locus of T-lymphocytes following inhalation exposure of female B6C3F1 mice and F344 rats.

1,3-Butadiene (BD) is an indirect alkylating agent that has greater cancer potency in the mouse than in the rat. The purpose of the present study was to compare the mutagenic potency of BD at the hprt locus of T-lymphocytes of exposed mice and rats and to determine whether mutations induced in this marker gene can be used as a quantitative indicator for species differences in susceptibility to cancer. To this end, experiments were conducted to define the effects of exposure duration and the time elapsed after exposures on the frequency of hprt mutations (Mf) in T-cells from female B6C3F1 mice and F344 rats of similar age (4-5 weeks) when exposed to BD by inhalation. The accumulation of hprt mutations in T-cells from thymus was assessed in animals necropsied 2 weeks after exposure to 0 or 1250 ppm BD for 1 or 2 weeks, while the time course for the appearance of hprt mutant T-cells (i.e., the phenotypic expression and cell migration) in thymus and spleen was evaluated in animals necropsied at weekly/biweekly intervals up to 10 weeks after exposure for 2 weeks. At necropsy, T-cells were isolated from thymus and spleen and cultured in the presence of IL-2, concanavalin A, and 6-thioguanine (Walker and Skopek, Mutat. Res., 288, 151-162, 1993). BD exposures of 1 and 2 weeks led to mutagenic effects in mouse thymus, with the average Mfs being 3- and 5-fold greater than background values, respectively. In rat thymus, there was only a 1.7-fold increase in Mfs after 2 weeks of BD exposure. In the mutant expression experiment, hprt Mfs in thymus and spleen of both species increased for several weeks post-exposure and then declined. Hprt Mfs in thymus reached maximum levels at 2 weeks post-exposure in mice (Mfs = 11.3 +/- 2.4 x 10(-6)) and at 3 weeks post-exposure in rats (4.9 +/- 1.2 x 10(-6)), while hprt Mfs in spleen reached peak levels at 5 weeks post-exposure in mice (19.7 +/- 1.9 x 10(-6)) and 4 weeks post-exposure in rats (10.1 +/- 1.8 x 10(-6)). Background Mfs for mouse and rat thymus and spleen ranged from 1.6 +/- 0.3 x 10(-6) to 3.0 +/- 1.1 x 10(-6). Statistical analyses of the hprt Mf data for spleen demonstrated that, under these exposure conditions, the mutagenic potency of BD (represented by the difference in the areas under the phenotypic expression curves of treated versus control animals) was 5-fold greater in mice than in rats. The magnitude of the species differences in mutagenic potency, observed after 2 weeks of BD exposure, resembles the species differences in metabolism more closely than the species differences in cancer potency.

Animals↗

Increased expression of high affinity IgE (FcepsilonRI) receptor-alpha chain mRNA and protein-bearing eosinophils in human allergen-induced atopic asthma.

FcepsilonRI receptors play an important role in allergen-induced mediator release and antigen presentation by mast cells, basophils, and monocyte/macrophages in atopic disorders. The expression of FcepsilonRI by tissue eosinophils in atopic asthma after allergen challenge has not been established. For this reason we attempted to identify mRNA and protein product + FcepsilonRIalpha eosinophils in cytospins made from bronchoalveolar lavage (BAL) from atopic asthmatics (n = 9) and nonatopic normal subjects (n = 4) 24 h after segmental challenge with allergen or diluent. Messenger RNA for FcepsilonRIalpha was determined using in situ hybridization and FcepsilonRIalpha protein expression by immunocytochemistry using a mouse monoclonal antibody 22E7. Colocalization of FcepsilonRIalpha receptors to eosinophils was performed using chromotrope 2R. When compared with a control challenge, segmental challenge with Dermatophagoides pteronyssinus induced significant BAL eosinophilia (p = 0.007). The total number of BAL FcepsilonRIalpha mRNA and protein-positive cells also increased in asthmatics, median values 2 (0.7-7.2) and 11.5 (0.6-65.0) x 10(6) cells (p = 0.02) and 0 (0-0.3 x 10(6)) and 3.1 x 10(6) (0.45 - 162.5 x 10(6)) cells (p = 0.007), respectively, for mRNA and protein. Net increases in FcepsilonRIalpha+ cells correlated with the net increases in BAL eosinophils (r = 0.98, p = 0.0001 for mRNA and r = 0.72, p = 0.02 for protein). Colocalization studies with chromotrope 2R revealed that only 4% of FcepsilonRIalpha+ cells were eosinophils after control challenge and, in contrast, 85 to 95% of FcepsilonRIalpha+ cells were eosinophils after allergen. There were no differences in the numbers of FcepsilonRIalpha+ cells or eosinophils in normal control subjects. Our results demonstrated that local endobronchial allergen provocation in atopic asthmatics results in increased synthesis and expression of FcepsilonRIalpha predominantly on BAL eosinophils.

Adult↗

Lectin-like activity of Escherichia coli K88, Salmonella choleraesuis, and Bifidobacteria pseudolongum of porcine gastrointestinal origin.

The lectin-like activity of Escherichia coli K88, Salmonella choleraesuis, and Bifidobacteria pseudolongum of porcine gastrointestinal origin was studied by hemagglutination (HA) and HA inhibition assays. Although all the bacterial strains were able to agglutinate Porcine and Lagomorpna erythrocytes, much higher HA titers were consistently observed for B. pseudolongum than for E. coli K88 or S. choleraesuis. Proteinaceous components and glycoproteins were responsible for the HA of E. coli K88 and B. pseudolongum, respectively, because a remarkable reduction of HA titers occurred due to treatment of E. coli K88 with protease or trypsin and of B. pseudolongum with protease and periodate. Hemagglutination of E. coli K88, S. choleraesuis, and B. pseudolongum was strongly inhibited by galactosyl residue-containing glycoproteins, including porcine and bovine mucin, thyroglobulin, and fetuin. Some sugars, including lactose, galactose, xylose, and xylooligosaccharide (XOS), at a relatively high concentration (47 to 92 mg/mL) also exhibited an inhibitory activity for the HA of B. pseudolongum. This result, combined with the enhanced HA activity of the three bacterial strains by modification of Lagomorpna erythrocytes with neuraminidase, indicated that galactosyl residue-containing glycoproteins mediated the HA of E. coli K88, S. choleraesuis, and B. pseudolongum. Our study demonstrated that proteinaceous or glycoproteinaceous lectin-like substances that recognize galactosyl residue-containing molecules, especially intestinal mucin, exist on the surface of E. coli K88, S. choleraesuis, and B. pseudolongum.

Animals↗

[Determination of tryptophan in human serum by high-performance liquid chromatography].

In this paper a high-performance liquid chromatographic(HPLC) method has been developed to determine the concentration of tryptophan(Trp) in human serum. Serum sample was precipitated with trichloroacetic acid solution(0.6 mol.L-1) to remove protein and centrifuged and assayed by HPLC. The operating conditions were NOVA-PAK C18 column(3.9 mm x 150 mm), KH2PO4(0.1 mol.L-1) mobile phase with flow rate of 0.7 ml.min-1, and detective wave-length at 295 nm. The linear range was 1.223-2447.381 mumol.L-1. The detection limit was 0.612 mumol.L-1. The average recovery was 96.3%. Intra-assay CV is less than 4% and inter-assay less than 5%. The concentration of Trp in normal adult serum was 46.603 +/- 5.108 mumol.L-1. The detection time of serum Trp was within 5 min. The results suggest that this method is simple, fast, accurate, and convenient.

Adult↗

[Detection of TT virus infection and clinical investigation in patients with liver diseases].

104 serum samples from patients with liver diseases were detected for TTV DNA by nested-PCR method. The results showed that 25 of 104(24%) were positive for TTV DNA. Among 104 samples, 48%(12/42) were positive for nonA-E and G 19% (4/12) were positive for hepatitis A 25% (8/32) were positive hepatitis B 11.1% (1/9) was positive hepatitis C 4 of 6(66.7%) fulminant hepatitis cases were detected positive for TTV DNA. The partial gene of two TTV isolates from the patients were cloned and sequenced. The sequence analysis shows that there is 98.4% nucleotide identity between AB008394(from Japan) and one isolate from the patient (TTVEC023). The results suggest that TTV is associated with acute, chronic and fulminant hepatitis. TTV infection would be the important cause of non A-E and G hepatitis.

Adolescent↗

[An observation on antiviral effect of IFN--alpha N1 (Wellferon) in patients with chronic hepatitis B].

In order to observe the antiviral effect of IFN-alpha N1(Wellferon, British Glaxowellcome Company) on CHB, each 50 cases of CHB were selected as the therapy group and the control group. The patients in the therapy group were administrated with 3MU of IFN-alpha N1 once a day for one week, and then 3MU of IFN-alpha N1 three times weekly for 11-23 weeks, whereas the patients in the control group did not receive any antiviral treatment. At 3 months, the serum alanine transaminsae(ALT) was decreased to normal level in 84%(42/50) cases of the therapy group, while only in 46% (23/50) cases of the control group (P < 0.01). The negative seroconversion rate of HBeAg was 56.7% (17/30) and 10.8% (4/37), of HBV DNA was 36.4%(12/33) and 5.9% (1/17) in therapy and control groups respectively. There was obvious difference in two groups. The results suggest that IFN-alpha N1 is satisfying antiviral drug for CHB patients or patients non-responsive to other IFNs.

Adult↗

[Detection of GBV-C/HGV infection in patients with liver diseases].

The aim of this article is to study the prevalence of GBV-C/HGV in patients with liver diseases and the clinical features in patients with (GBV-C/HGV infection. The serum samples were obtained from 169 patients with liver diseases in You An Hospital). Serum GBV-C/HGV RNA was detected by reverse transcription nested polymerase chain reaction (RT-nPCR) using two primer pairs of 5' untranslated region (5' UTR) of HGV. Serum anti-HGV was detected by ELISA simultaneously. The partial GBV-C/HGV genome isolated from one patient was cloned into T vectors and sequenced by dideoxy-mediated chain termination methods. Among 169 patients with various liver diseases, the GBV-C/HGV RNA positive rate was 9.5% (16/169), including 11.1% (1/9) of AHA, 4.1% (3/73) of CHB, 16.2% (6/37) of CHC, 13.3% (2/15) of AH(nonA-E) 12.5% (1/8) of CH(nonA-E) 15.4% (2/13) of LC and 33.3% (1/3) of SH cases. Of 29 patients having a history of surgical operation and transfusion, 9(31.0%) was positive for GBV-C/HGV RNA, which was remarkably higher than those cases without surgical operation and transfusion. The sequence analysis showed that there was 89.14%-98.91% nucleotide identity between our isolate and published GBV-C/HGV isolates. The results also suggested that infection rate of GBV-C/HGV was around 9.5% in patients from Beijing region, patients with GBV-C/HGV infection might show various clinical features and GBV-C/HGV might not be the major cause of hepatitis nonA-E.

5' Untranslated Regions↗