Oncologic outcome of CO2 laser surgery for glottic carcinoma.
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Adult↗
Biomedical subjects
Xiao-hong Chen
Publications and source records attributed to Xiao-hong Chen.
Inactivation of the tumor suppressor Krüppel-like factor 6 (KLF6) by mutation or decreased expression in hepatocellular carcinomas.
BACKGROUND AND AIM: The Krüppel-like transcription factor KLF6 is a novel tumor-suppressor gene. It was inactivated in human prostate cancer and other tumors tissue, as the result of frequent mutation and loss of heterozygosity (LOH). However, there is no data reporting the levels of KLF6 both mRNA and protein in hepatocellular carcinomas (HCCs). We therefore detected mutations and expression of KLF6 in HCC tissues and further observed the effect of it on cell growth in HCC cell lines. METHODS: We analyzed the exon-2 of KLF6 gene by direct DNA sequencing, and detected the expression of KLF6 by RT-PCR and Western blot in 23 HCC tissues and corresponding nontumorous tissues. Loss of growth suppressive effect of the HCC-derived KLF6 mutant was characterized by in vitro growth curves plotted, flow cytometry and Western blotting. RESULTS: KLF6 mutations were found in 2 of 23 HCC tissues and one of mutations was missense. Expression of KLF6 mRNA or protein was down-regulated in 8 (34.7%) or 9 (39.1%) of 23 HCC tissues. Wild-type KLF6 (wtKLF6) inhibited cellular proliferation and prolonged G1-S transition by inducing the expression of p21WAF1 following stable transfection into cultured HepG2 cells, but tumor-derived KLF6 mutant (mKLF6) had no effects. CONCLUSION: Our findings suggest that KLF6 may be involved in pathogenesis of HCC.
Blotting, Western↗
[Mutations of the tumor suppressor Kruppel-like factor 6 (KLF6) gene in hepatocellular carcinoma and its effect of growth suppression on human hepatocellular carcinoma cell line HepG2].
OBJECTIVE: To explore the mutated KLF6 gene in hepatocellular carcinoma (HCC) and to characterize its behavior in human hepatocellular carcinoma cell line HepG2. METHODS: We analyzed the DNA isolated from 23 hepatocellular carcinoma tissues and their adjacent nontumor tissues by polymerase chain reaction (PCR). Direct sequencing was used to establish the incidence of mutation in exon2 of the KLF6 gene. Loss of growth suppressive function of the HCC-derived KLF6 mutants was characterized by in vitro analyzing alteration of cell cycle and MTT assay. Expression of p21WAF1, a possible downstream gene of KLF6, was detected in human hepatocellular carcinoma cell line HepG2 transiently transfected with KLF6 genes. RESULTS: Mutations of KLF6 were found in 2 of the 23 (8.7%) hepatocellular carcinomas. The two mutations were located in the transactivation domain and one of them resulted in single amino acid substitution of TGG (W) by GGG (G) at codon 162. Unlike the wild-type KLF6, cancer-derived KLF6 mutants neither suppressed growth nor induced p21WAF1 following transfection into culture cells. CONCLUSIONS: Mutations of the KLF6 gene may play a role in the pathogenesis of HCC, but are not the dominating mechanism resulting in inactivation of KLF6 functions. KLF6 suppresses hepatocellular carcinoma cell proliferation partly through upregulating expression of the p21WAF1 gene.
Base Sequence↗
Construction and characterization of a cDNA library from human liver tissue with chronic hepatitis B.
OBJECTIVE: To construct a cDNA library from human liver tissue with chronic hepatitis B and check its quality for investigating the expression level of liver tissue infected by hepatitis B virus. This will then be used to find the relevant genes and interesting proteins associated with the development of hepatitis B. METHODS: The total RNA from liver tissue with chronic hepatitis B was extracted and the mRNA was purified using TRIZOL method. Switching mechanism at 5' end of the RNA transcript (SMART) technique and CDS III/3' primer were used for first-strand cDNA synthesis. Long distance polymerase chain reaction (LD PCR) was then used to synthesize the double-strand cDNA that was then digested by Sfi I and fractionated by CHROMA SPIN-400 column. The longer than 0.4 kb cDNAs were collected and ligated to lambdaTriplEx2 vector. Then lambda phage packaging reaction and library amplification were performed. The qualities of both unamplified and amplified cDNA libraries were strictly checked by conventional titer determination. Fourteen plaques were randomly picked and tested using PCR with universal primers derived from the sequence flanking the vector. RESULTS: The titers of unamplifed and amplified libraries were 1.94 x 10(6) pfu/ml and 1.49 x 10(9) pfu/ml respectively. The percentages of recombinants from both libraries were 98.15% in unamplified library and 98.76% in amplified library. The lengths of the inserts were 1.23 kb in average, 1-2 kb in 64.29%, and 0.5-1.0 kb in 35.71%. CONCLUSION: A high quality cDNA library from human liver tissue with chronic hepatitis B was successfully constructed.
DNA, Complementary↗
[Construction and characterization of a cDNA library from human liver tissue of cirrhosis].
OBJECTIVE: To construct a cDNA library from human liver tissue of cirrhosis. METHODS: The total RNA from human liver tissue of cirrhosis was extracted using Trizol method, and the mRNA was purified using mRNA purification kit. SMART technique and CDSIII/3' primer were used for first-strand cDNA synthesis. Long distance PCR was then used to synthesize the double-strand cDNA that was then digested by proteinase K and Sfi I, and was fractionated by CHOMA SPIN-400 column. The cDNA fragments longer than 0.4 kb were collected and ligated to lambdaTripl Ex2 vector. Then lambda-phage packaging reaction and library amplification were performed. The qualities of both unamplified and amplified cDNA libraries was strictly checked by conventional titer determination. Eleven plaques were randomly picked and tested using PCR with universal primers derived from the sequence flanking the vector. RESULTS: The titers of unamplifed and amplified libraries were 1.03 x 10(6) pfu/ml and 1.36 x 10(9) pfu/ml respectively. The percentages of recombinants from both libraries were 97.24 % in unamplified library and 99.02 % in amplified library. The lengths of the inserts were 1.02 kb in average (36.36 % 1 approximately equals 2 kb and 63.64 % 0.5 approximately equals 1.0 kb). CONCLUSION: A high quality cDNA library from human liver tissue of cirrhosis was constructed successfully, which can be used for screening and cloning new special genes associated with the occurrence of cirrhosis.
DNA, Complementary↗
[Association of genetic polymorphisms in glutathione S-transferases M1 with hepatitis beta-related hepatocellular carcinoma].
OBJECTIVE: To investigate the association of genetic polymorphisms in glutathione S-transferases(GST) M1 with hepatitis beta-related hepatocellular carcinoma (HCC). METHODS: Genomic DNA was isolated from peripheral blood of HBsAg carriers, including 91 cases of HCC, 58 liver cirrhosis(LC), 63 chronic hepatitis B(CHB), and 134 normal controls. GSTM1 genotypes were detected by multiplex PCR. RESULTS: The null genotype of GSTM1 was significantly frequent in patients with HCC compared with controls (P<0.05), but there were no significant differences in frequency of GSTM1 null genotype among patients with liver cirrhosis, chronic hepatitis B and normal controls. Subjects carrying null genotypes of GSTM1 had higher risk of developing HCC compared with those carrying positive genotype (OR=1.81.95% CI=1.05 approximately equals 3.12). CONCLUSION: The GSTM1-null genotype may be associated with an increased risk of HCC, but not of CHB and LC.
Adult↗
[Inhibitory effect of ginkgolide B on angiogenesis in chronic inflammation].
AIM: To investigate the inhibitory effect of ginkgolide B on angiogenesis in chronic inflammation and the possible mechanisms. METHODS: The murine chronic granulomatous air pouch model was used to observe the anti-angiogenesis effect of ginkgolide B. The vascular index was determined by colorimetry of carminic acid, and angiogenesis was observed by histology method. The interleukin-1beta (IL-1beta) levels in mice serum and in supernatants of U937 cell culture stimulated by phorbol 12-myristate 13-acetate (PMA) were detected by radioimmunoassay (RIA). The tumor necrosis factor-alpha (TNF-alpha) levels in mice serum and in supernatant of U937 cell culture were measured by cytotoxicity bioassay. The mRNA expression of IL-1beta and TNF-alpha of U937 cell culture was investigated by RT-PCR. RESULTS: Oral administration of ginkgolide B 25 and 100 mg x kg(-1) was shown to significantly inhibit the vascular index of murine chronic granulomatous air pouch model with the inhibitory rate of 22.52% and 25.29%, respectively. This result was supported by histological observation. Concomitantly, the IL-1beta levels in mice serums were also significantly decreased with the inhibitory rate of 50.61% and 58.66%; so were the TNF-alpha levels with the inhibitory rate of 28.91% and 52.41%. Ginkgolide B at concentration of 1 x 10(-5) to 1 x 10(-8) mol x L(-1) could also reduce both the IL-1beta and TNF-alpha contents in the supernatants of U937 cell culture stimulated by PMA, but the scopes of changes were much different. For IL-1beta the IC50 was 1.93 x 10(-8) mol x L(-1), while ginkgolide B at concentration of 1 x 10(-5) mol x L(-1) only decreased the release of TNF-alpha by 25.99%. Furthermore, ginkgolide B at concentrations of 1 x 10(-5) to 1 x 10(-7) mol x L(-1) was shown to significantly inhibit TNF-alpha mRNA expression of U937 cells; and at concentrations of 1 x 10(-5) and 1 x 10(-6) mol x L(-1) could inhibit IL-1beta mRNA expression. CONCLUSION: Ginkgolide B was shown to significantly inhibit angiogenesis of the murine chronic granulomatous air pouch model, reduce the IL-1beta and TNF-alpha levels in mice serums, and significantly inhibit IL-1beta and TNF-alpha mRNA expression and protein secretion in supernatants of U937 cell culture. It was suggested that reduction of proangiogenic cytokines IL-1beta and TNF-alpha secretion may contribute to the anti-angiogenesis effect of ginkgolide B in the murine chronic granulomatous air pouch model.
Animals↗
Ginsenoside-Ro enhances cell proliferation and modulates Th1/Th2 cytokines production in murine splenocytes.
AIM: To study the effects of ginsenoside-Ro on cell proliferation and cytokine production in murine splenocytes. METHODS: The effect of ginsenoside-Ro on murine splenocytes proliferation was studied using [3H] thymidine incorporation assay. Effects of ginsenoside-Ro on the production of cytokines interleukin-2 (IL-2), interferon-gamma (IFN-gamma) and interleukin-4 (IL-4) from murine splenocytes were detected by ELISA method. Effects of ginsenoside-Ro on mRNA level of Th1 cytokine IFN-gamma and Th2 cytokine IL-4 were evaluated by reverse transcription polymerase chain reaction (RT-PCR) analysis. RESULTS: Ginsenoside-Ro showed no mitogenic effect on unstimulated murine splenocytes. It enhanced the proliferation of Con A-induced murine splenocytes and the production of IL-2 at concentrations of 1-10 micromol x L(-1). Moreover, ginsenoside-Ro increased the production and expression of Th2 cytokine IL-4 and decreased the production and expression of Th1 cytokine IFN-gamma in Con A-induced murine splenocytes at concentrations of 2-10 micromol x L(-1). CONCLUSION: Ginsenoside-Ro showed immunomodulatory effects by regulating the production and expression of Th1/Th2 cytokines in murine splenocytes.
Animals↗
[Determination of trace Pb in whole blood by Zeeman-GFAAS].
The determination method for trace Pb in whole blood was studied, which was diluted by 0.5% HNO3. In the measurement, Zeeman-GFAAS was used and the relative condition was discussed. This method shows that the detection limit was 10.0 pg, the relative standard deviation of standards (RSD) was 0.36%-1.8%, the relative standard deviation of samples (RSD) was 1.4%-2.3%, and the recovery rate was 96.0%-101.7%. The concurrent interference was low. This method is simple and rapid. It is an ideal method to determine trace Pb in whole blood.
Algorithms↗
[Proof of solid state cathodoluminescence by using brightness waveform].
Three different inorganic-organic hetero-junctions (A: ITO/SiO2/Alq3/Al, B: ITO/Alq3/SiO2/Al and C: ITO/SiO2/Alq3/SiO2/Al) were fabricated. The emission can be observed only under positive bias in devices A and B, but under both biases in device C according to their brightness waveforms. With increasing voltage, the increase in blue emission in devices B and C is faster than that in green emission. This is because that the recombination of hot electrons and holes, i.e., electron-hole pairs, produced blue emission in devices B and C, and the recombination of electrons injected from Al with the accumulated holes, which are excited by hot electrons, produced green emission in device A. Hence, the emissions of the devices are attributed to not only the recombination of electrons and accumulated holes, but also the cathodoluminescence-like (CL-like) emission.
English Abstract↗
[Up-regulation of transcription factors GATA-1 and GATA-2 induced by Panax notoginosides in hematopoietic cells].
OBJECTIVE: To observe the role of Panax notoginosides (PNS) in up-regulation of GATA family transcription factors, and explore intracellular signal pathway of PNS in the proliferation of hematopoietic cells. METHODS: Human bone marrow cells were incubated with different concentrations of PNS for colony-forming assay. Human cell lines HL-60, K562, CHRF-288 and Meg-01 were incubated with PNS (10 mg/L) for 14 days. The cell nuclear proteins were extracted and analyzed by Western blot with antibodies against GATA-1, GATA-2. Electrophoretic mobility shift assay (EMSA) and antibody gel supershift assay was performed using (32)P labeled GATA consensus oligonucleotide which contains binding site for GATA transcription factors. RESULTS: PNS could promote the proliferation of CFU-GM and CFU-E and induce the expression of GATA-1, GATA-2. The nuclear proteins of both GATA-1 and GATA-2 in K562, CHRF-288 and Meg-01 cells treated by PNS were increased by (1.5 - 2.8) and (2.0 - 3.1)-fold over untreated cells respectively. GATA binding activity initiated by PNS was apparently elevated to form higher density band of GATA-DNA complex. While there was no detectable change in HL-60 cells before and after PNS treatment. The predominant GATA binding complex was mainly attributable to both GATA-1 and GATA-2 proteins being in phosphorylated status. CONCLUSION: PNS can induce the synthesis of transcription factors GATA-1 and GATA-2 and enhance their DNA binding activity, which could play a role in the up-regulation of the expression genes related to proliferation and differentiation in hematopoietic cells.
Blotting, Western↗
Imrecoxib: a novel and selective cyclooxygenase 2 inhibitor with anti-inflammatory effect.
AIM: To investigate the inhibitory effect of imrecoxib, a synthetic compound of completely new structure, on cyclooxygenase 1 (COX-1) and 2 (COX-2) and its anti-inflammatory effect in vivo. METHODS: The inhibitory effects of imrecoxib on cyclooxygenase 1 and 2 were studied using whole cell assay with murine peritoneal macrophages induced by calcimycin and LPS. The inhibitory effects of imrecoxib on mRNA level of COX-1 and COX-2 in human macrophage cell line U937 were detected by reverse transcription polymerase chain reaction (RT-PCR) analysis. Effects of imrecoxib on acute and chronic inflammation were evaluated in rat carrageenan induced edema model and rat adjuvant-induced arthritis model, respectively. RESULTS: Imrecoxib was found to inhibit COX-1 and COX-2 with IC50 value of 115+/-28 nmol/L and 18+/-4 nmol/L, respectively. Imrecoxib was shown to selectively and dose-dependently inhibit COX-2 mRNA level. Imrecoxib effectively inhibited carrageenan-induced acute inflammation at the doses of 5, 10, and 20 mg/kg i.g. and adjuvant-induced chronic inflammation at the doses of 10 and 20 mg/kg/d i.g. CONCLUSION: Imrecoxib is a novel and moderately selective COX-2 inhibitor that possesses anti-inflammatory effect by inhibition of COX-2 mRNA expression.
Animals↗
Immunoenhancing activity of protopanaxatriol-type ginsenoside-F3 in murine spleen cells.
AIM: To investigate the immunoenhancing activity of ginsenoside-F3 in murine spleen cells and explore its mechanism. METHODS: The enhancing effect of ginsenoside-F3 on murine spleen cell proliferation was studied using [3H]thymidine incorporation assay. Effects of ginsenoside-F3 on the production of type 1 cytokines IL-2, IFN-gamma, and type 2 cytokines IL-4 and IL-10 from murine spleen cells were detected by ELISA method. Effects of ginsenoside-F3 on mRNA level of cytokines IL-4, IFN-gamma, and transcription factors T-bet and GATA-3 were evaluated by RT-PCR analysis. Effect of ginsenoside-F3 on NF-kappaB DNA binding activity in murine spleen cells was investigated by electrophoretic mobility shift assays (EMSA). RESULTS: Ginsenoside-F3 at 0.1-100 micromol/L not only promoted the murine spleen cell proliferation, but also increased the production of IL-2 and IFN-gamma, while decreased the production of IL-4 and IL-10 from murine spleen cells with the maximal effect at 10 micromol/L. RT-PCR analysis displayed that ginsenoside-F3 enhanced the IFN-gamma and T-bet gene expression and decreased IL-4 and GATA-3 gene expression. EMSA experiment showed that ginsenoside-F3 10 micromol/L enhanced the NF-kappaB DNA binding activity induced by ConA in murine spleen cells. CONCLUSION: Ginsenoside-F3 has immunoenhancing activity by regulating production and gene expression of type 1 cytokines and type 2 cytokines in murine spleen cells.
Animals↗
[Effectiveness of recombinant adenovirus p53 injection on laryngeal cancer: phase I clinical trial and follow up].
OBJECTIVE: To evaluate the efficacy and toxicity of recombinant adenovirus p53 injection (SBN-1) in patients with laryngeal cancer. METHODS: Twelve cases with laryngeal cancer, 11 males and 1 female, aged 59.5 +/- 12.4 years, were randomly divided into three groups of 4 patients. The patients received intratumor injection of SBN-1 at the dosage of 1 x 10(10)VP, 1 x 10(11)VP, or 1 x 10(12)VP once every other day for 2 courses of treatment with 5 times of injection as one course of treatment. Two days after the injection the patients were operated on. After the operation SBN-1 of the same doses was injected around the tumor bed. The patients were followed up for more than 3 years by correspondence and out-patient department examinations. ELISA was used to detect the serum anti-adenoviral IgG and IgM, and interleukin-2 receptor (IL-2R). Immunohistochemistry was used to examine the expression of p53 protein in the tumor tissues. Flow cytometry was used to examine the T cell subgroup. The symptoms and side effects were observed. RESULTS: One patient in the 10(12)VP group presented self-limited fever (38.2-38.6 degrees C) and no other abnormality was observed after the SBN-1 injection. Specific antibody to SBN-1 turned from negative to positive two or three weeks after the first injection. P53 protein expression was significantly enhanced in tumors after injection of SBN-1. The serum level of IL-2R was 750 +/- 401 pg/ml before treatment and 552 +/- 203 pg/ml after treatment. The numbers of CD3, CD4, and CD8 were 66 +/- 10, 41 +/- 15, and 32 +/- 10 respectively before the treatment and were 67 +/- 9, 43 +/- 8, and 34 +/- 16 respectively after treatment, and the CD4/CD8 ratio was 1.4 +/- 0.6 before the treatment and was 1.6 +/- 0.9 after treatment. The abnormality in SIL-2R level and the disorder of T cell subgroup were improved in 2 cases. Followed up for over 3 years showed that all cases still lived free of cancer. CONCLUSION: Safe and effective on laryngeal cancer without obvious adverse events, local injection of SBN-1 is a promising treatment.
Adenoviridae↗
[The emission of rare earth complex Eu(asprin)3phen].
Two kinds of electroluminescent devices were fabricated by doping the rare earth complex Eu(asprin)3phen into polymer PVK: (1) ITO/PVK:RE/LiF/Al; (2) ITO/PVK:RE/PBD/LiF/Al. A great difference in the EL spectrum was found between the two kinds of devices. In device (2) the intensity of 594 nm was rather weak compared with that of 614 nm. The spectrum was consistent with the photoluminescence (PL) spectrum under the state of thin film. But in device (1), the peak emission of 594 nm was comparable to that of 614 nm. Preliminary discuss on this phenomenon was made; in device (1), the recombination region was close to the metal cathode, effect of metal cathode on the electroluminescence of the rare earth complex caused the changes of the EL emission which was quite different from the TL emission. The phenomenon was not observed in device (2) whose recombination region was far from the cathode because an electron-transport layer was inserted.
Chelating Agents↗
A case of bullous morphea reported in mainland China.
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Adult↗
[Two mechanisms of the color-tunable organic electroluminescence by the voltage applied].
Two devices structures of ITO/PVK: Rubrene/Al and ITO/Alq3:MN-PPV/Al were developed. Their characters of photoluminescence and electroluminscence were studied. The result showed that there were great difference between the photoluminescence and electroluminscence at a doping ratio of 2 wt% in ITO/PVK: Rubrene/Al. It is concluded that energy transfer in these dye-doped devices occurred by Förster energy transfer processes. And the trap effect of electrons of Rubrene on holes of PVK resulted in different combination probability of PVK excitation in photoluminescence and electroluminescence. At the same time, the two EL devices were color-tunable when the bias voltage was increased. The mechanisms which cause color variation are different. In the first device, it indicates that the energy transfer process from PVK to Rubrene is not complete. The combination probability of PVK excitation which does not contribute to the emission of Rubrene is increased when the bias voltage increases. But in the second device, there are many micro-interfaces due to the phase-separation just like the interface in a double layer device. The tunneling interface barriers of carriers is the main cause of color variation in the second device.
English Abstract↗
High-performance liquid chromatography coupled with electrospray ionization tandem mass spectrometry for the determination of flocoumafen and brodifacoum in whole blood.
A high-performance liquid chromatographic-tandem mass spectrometric (HPLC-MS-MS) assay was developed and validated to determine quantitatively flocoumafen and brodifacoum in whole blood using warfarin as an internal standard (IS). Liquid-liquid extraction, using ethyl acetate, was used to isolate flocoumafen, brodifacoum and the IS from the biological matrix. Detection was performed on a mass spectrometer by negative electrospray ionization (ESI) in multiple reaction monitoring (MRM) mode. The calibration curves were linear (r(2) > 0.998) in the concentration range of 0.1-100.0 ng ml(-1) with a lower limit of quantification of 0.05 ng ml(-1) for flocoumafen, and 0.1 ng ml(-1) for brodifacoum in whole blood. Intra-day and inter-day relative standard deviations (RSDs) were less than 8.0% and 10.8%, respectively. Recoveries of flocoumafen and brodifacoum ranged from 78.0% to 83.7%. This assay can be used to determine trace flocoumafen and brodifacoum in whole blood to investigate suspected poisoning of human and animals.
4-Hydroxycoumarins↗