Search PubMed⌕ Search

Biomedical subjects

Ying Huang

Publications and source records attributed to Ying Huang.

At least 127 records · Page 7Linked to original sources
PubMed2005

[Multivariate prognostic analysis for patients with unresectable esophageal carcinoma after concurrent chemoradiotherapy].

BACKGROUND & OBJECTIVE: Concurrent chemoradiotherapy is recommended as standard treatment for unresectable esophageal carcinoma now. This study was to analyze the prognostic factors of unresectable esophageal carcinoma after concurrent chemoradiotherapy. METHODS: A total of 132 unresectable esophageal carcinoma patients received concurrent chemoradiotherapy from Jan. 1996 to Dec. 2003 in our hospital. All patients received chemotherapy at the beginning of radiotherapy, and when the radiation dose escalated to 40 Gy. Total dose of irradiation was 60-70 Gy. Gender, age, disease course, focus location, swallow embarrassment, weight loss, Karnofsky's performance status (KPS) score, family history, hemoglobin (HB) before therapy, X-ray type, pathologic grade, focus length, TNM stage, irradiation method and technology, irradiation dose, radiotherapy interval, short-term effect, esophagus perforation, esophagus haemorrhage, and retreatment methods were used as analysis factors for Cox regression univariate and multivariate analyses. RESULTS: Univariate analysis showed that diseases course, focus location, weight loss, M stage, short-term effect, esophagus perforation, esophagus haemorrhage, and retreatment methods were prognostic factors of these patients. Multivariate analysis showed that M stage [P=0.014, odds ratio (OR)=2.515], short-term effect (P < 0.001, OR=2.181), esophagus perforation (P=0.022, OR=3.266), and retreatment methods (P=0.026, OR=1.142) were independent prognostic factors. CONCLUSION: The main prognostic factors of the patients with unresectable esophageal carcinoma treated with concurrent chemoradiotherapy are M stage, short-term effect, esophagus perforation, and retreatment methods.

Adult↗
PubMed2005

[Simultaneous determination of cimaterol, clenbuterol and salbutamol in feeds by capillary zone electrophoresis].

A method for simultaneous determination of cimaterol, clenbuterol and salbutamol in feeds was developed by capillary zone electrophoresis. The effects of the experimental conditions on the separation and determination of cimaterol, clenbuterol and salbutamol have been examined. Under the optimum conditions, all three compounds were completely separated in 8 min. The linear range of cimaterol, clenbuterol and salbutamol was 0.1-1.0 mg/L, and the detection limits (S/N = 3) were 0.02, 0.03 and 0.02 mg/L, respectively. The developed method has been used for the determination of spiked feed samples. The recoveries of cimaterol, clenbuterol and salbutamol were 89%-103%, 86%-91% and 83%-87%, respectively. The relative standard deviations for cimaterol, clenbuterol and salbutamol were 3.8%-4.3%, 3.6%-5.0% and 4.0%-5.6%, respectively. The proposed method is a sensitive, fast and simple method for the determination of cimaterol, clenbuterol and salbutamol in feeds.

Albuterol↗
PubMed2005

[Clinical application of acupuncture for treatment of heroin withdrawal syndrome].

OBJECTIVE: To make technical standard of acupuncture manipulation for acupuncture treatment of heroin withdrawal syndrome. METHODS: Two hundred and twenty cases of heroin withdrawal syndrome were randomly divided into an acupuncture group of 111 cases and a control group of 109 cases. They were respectively treated with acupuncture and oral administration of lofexidine hydrochloride, and their therapeutic effects were observed. RESULTS: The heroin dependence (acute stage) were effectively withdrawn in the two groups. The treatment group in change of total scores for withdrawal symptoms before and after treatment, the total scores for withdrawal symptoms at the 4th and 5th days, treatment of insomnia and the score for self-Hamilton Anxiety Scale and the score after at the 4th day was superior to the control group (P < 0.05, P < 0.01, P < 0.001). CONCLUSION: Acupuncture has a satisfactory, rapid, safe and reliable clinical therapeutic effect.

Acupuncture Therapy↗
PubMed2005

[A method of HPRE synthesis via transcription by T7 RNA polymerase in vitro].

OBJECTIVE: To synthesize highly pure HBV post-transcriptional regulatory element (HPRE) via transcription in vitro by T7 RNA polymerase. METHODS: HPRE gene was amplified by PCR from a template containing HBV complete genomic DNA and cloned into plasmid pGEM-11zf. The cloned DNA sequence was transcribed by T7 RNA polymerase. RESULTS: The construction of HPRE gene recombinant plasmid and production of HPRE via transcription in vitro was successful. CONCLUSION: In vitro transcription by T7 RNA polymerase can be used to synthesize highly pure HPRE.

DNA-Directed DNA Polymerase↗
PubMed2005

[Intratympanic dexamethasone injections for intractable Meniere's disease].

OBJECTIVE: To investigate the efficacy of intratympanic dexamethasone injections (IDI) and intermittent pressure (IP) for 13 patients with intractable Meniere's disease (MD). METHOD: Dexamethasone (5 g/L) was injected into the middle ear. The injection was repeated the next day and weekly for 3 weeks. Together with tympanic intermittent pressure (IP). RESULT: The 13 patients was followed up for 2-5 years. Complete relief vertigo was maintained in 9 cases,improved in 3 cases. The injection was repeated in 1 patient with recurrent vertigo and total control of vertigo was obtained. Tinnitus disappeared in 5 cases, reduced in 3 case, unchanged in 5 cases. Hearing was improved in 9 cases, unchanged in 4 cases. CONCLUSION: IDI and IP are effective for intractable MD. The benefits of IDI and IP are easy application for doctors and reasonable cost which can be accepted by patients easily.

Adult↗
PubMed2005

Hypoxia-simulating agents and selective stimulation of arsenic trioxide-induced growth arrest and cell differentiation in acute promyelocytic leukemic cells.

BACKGROUND AND OBJECTIVES: We recently reported that hypoxia-mimetic agents cobalt chloride (CoCl2 CoCl2 ) and desferrioxamine (DFO) could induce differentiation of acute myeloid leukemic (AML) cells. Here, we investigate whether these two agents influence the in vitro differentiation-inducing effect of arsenic trioxide (As2O3) on AML cells, an effective drug for the treatment of acute promyelocytic leukemia (APL) that is a unique subtype of AML with a specific fusion protein, PML-RARalpha. DESIGN AND METHODS: The APL cell line NB4 and non-APL promonocytic leukemic cell line U937 were treated with As2O3 (0.5 microM) combined with CoCl2 (50 microM) or DFO (10 microM). The U937/PR9 subclone, whose expression of PML-RARalpha protein can be induced by Zn2+, was also investigated. Cellular differentiation was evaluated by morphological criteria and myeloid differentiation-related antigens and marker gene expression. The hypoxia-inducible factor-1alpha (HIF-1alpha) mRNA and protein were detected, respectively, by semi-quantitative/real-time quantitative reverse transcription polymerase chain reaction and immunoblots. PML-RARalpha protein was also analyzed. RESULTS: CoCl2 and DFO potentiated the growth-inhibiting and differentiation-inducing effects of low-dose As2O3, the latter enhancing CoCl2 and DFO-induced accumulation of HIF-1alpha protein in NB4 cells but not in U937 cells. These two hypoxia-mimetic agents also accelerated As2O3-induced modulation and degradation of PML-RARalpha protein in NB4 cells. Furthermore, inducible expression of the fusion gene restored the co-operative effects of As2O3 and CoCl2/DFO on U937/PR9 cells in terms of growth arrest, differentiation induction and HIF-1alpha protein accumulation. INTERPRETATION AND CONCLUSIONS: Mimicked hypoxia enhanced As2O3-induced differentiation, in which HIF-1alpha and PML/RARalpha proteins played an important role. These data provide new insights into the understanding of the mechanisms of the action of As2O3 in the treatment of patients with APL.

Antineoplastic Agents↗
PubMed2005

[Study on population diversity and antimicrobial activity of actinomycete from acidic soil in Xizang area].

156 actinomycetes were isolated from 10 soil samples collected in Tibet by the method of DDC(dispersion and differential centrifugation). The isolates were assigned to 32 different groups on the basis of their morphological characters and colors of substrate mycelium, aerial hyphae and pigment. The result of cell-wall DAP on 65 representative strains selected from these groups was that 9 strains were different from Streptomyces. The analysis of ARDRA and 16S rDNA sequeces showed that the isolates belonged to the genus Streptomyces and five different rare actinomycete genera respectively. Antimicrobial activity of the representative strains was also tested, with the result that 38.5% isolates were positive.

Actinobacteria↗
PubMed2005

[The promoter activity of the DNA sequence corresponding to HCV 5'UTR in HepG2].

OBJECTIVE: To study the promoter activity in HepG2 cells of the DNA sequence corresponding to the HCV 5'UTR. METHODS: Plasmids, 5'UTR-Luc(+) and 5'UTR-Luc(-) carrying the forward and reverse DNA sequences corresponding to the HCV 5'UTR respectively were constructed, and subsequently transfected into HepaG2 cells. The luciferase activity and the mRNA of the luciferase gene were then detected. The 5'UTR sequence was cloned into a GFP vector to make 5'UTR-EGFP, and then the GFP expression was confirmed by fluorescence microscopy. RESULTS: 5'UTR-Luc(+) had an obvious luciferase activity whereas 5'UTR-Luc(-) had nearly no luciferase activity. The former had a high level of luciferase mRNA while the latter could not be detected. An intense green fluorescence expression was observed in the cells transfected with the plasmid of 5'UTR-EGFP. CONCLUSION: The forward DNA sequence corresponding to HCV 5'-UTR had an obvious promoter activity in hepG2 cells. It may play an important role in the replication of HCV.

5' Untranslated Regions↗
PubMed2005

[Expression of HoxA10 in acute leukemia and its significance].

To investigate the expression of HoxA(10) mRNA in acute leukemia patients and its significance, HoxA(10) level was detected by reverse transcription polymerase chain reaction (RT-PCR) in 50 patients with acute leukemias, 7 healthy volunteers and 3 patients with ITP (idiopathic thrombocytopenic purpura). The regularity of the expression of HoxA(10) gene in acute leukemia and the relationship between HoxA(10) level and the prognosis of leukemia was explored. The results showed that HoxA(10) was expressed in all types of acute myelogenous leukemia; HoxA(10) message was also observed in acute lymphoblastic leukemia patients and part of control groups. 3 normal donors were found not to express HoxA(10). The level of HoxA(10) mRNA of acute myelogenous leukemia patients was significantly higher than that of acute lymphoblastic leukemia patients and controls (P < 0.01). HoxA(10) gene appeared to be more strongly expressed in AML-M(1) and -M(2) subtypes than in AML-M(4) and -M(5) subtypes, and the gene was notable high expressed in acute promyelocytic leukemia. The number of blast and promyeloid cells in the bone marrow was positive related with the level of HoxA (r = 0.635, P < 0.01). The level of HoxA(10) of 9 non-responsive patients was higher than that of 8 remission patients, but there was no significant difference between them (P = 0.258). HoxA(10) was overexpressed in acute myelogenous leukemia. It is concluded that HoxA(10) is a major transcription factor regulating hematopoiesis and a mark to differentiate lymphoid leukemia and myelogenous leukemia, but not a specific gene of cancer. The level of HoxA(10) is related with load of leukemic cells and curative effect, and can affect occurrence and development of leukemia in combination with many cytokines, HoxA(10) may facilitate the leukemia progression with another cofactors.

Adolescent↗
PubMed2004

Estradiol acutely attenuates glutamate-induced calcium overload in primarily cultured rat hippocampal neurons through a membrane receptor-dependent mechanism.

Increasing lines of evidence indicate that estrogen acts as a neuroprotective agent through a nongenomic mechanism. We tested the hypothesis that 17beta-estradiol could rapidly attenuate glutamate-induced calcium (Ca2+) overload in rat primary hippocampal neurons via a membrane receptor-dependent mechanism. The bulk cytosolic intracellular Ca2+ level was measured in neurons with fluorescent Ca2+ probe fluo3. Preexposure of primary cultured hippocampal neurons to 17beta-estradiol for 3 min attenuated intracellular Ca2+ increase induced by glutamate in a concentration-dependent manner. The action of 17beta-estradiol was reversible after washout. Administration of membrane-impermeable 17beta-estradiol conjugated to bovine serum albumin (E2-BSA) produced the same effect, suggesting possible involvement of cell membrane receptors. ICI 182,780, a specific estrogen receptor (ER) antagonist, blocked the neuronal response to 17beta-estradiol and estradiol BSA, indicating a role of specific ERs. The present study demonstrates that 17beta-estradiol acutely reduces glutamate-stimulated intracellular Ca2+ increase via ERs probably on the cell surface of the hippocampal neurons.

Aniline Compounds↗
PubMed2004

Tumor suppressor RASSF1A is a microtubule-binding protein that stabilizes microtubules and induces G2/M arrest.

RASSF1A is a putative tumor suppressor gene that is inactivated in a variety of human tumors. Expression of exogenous RASSF1A has been shown to inhibit tumor growth in vitro and in animals. However, the molecular mechanisms by which RASSF1A mediates its tumor suppressive effects remain to be elucidated. Here, we report that RASSF1A is a microtubule-binding protein that interacts with and stabilizes microtubules. We have identified the RASSF1A region harboring a basic domain that appears to mediate the interactions between RASSF1A and microtubules. The basic domain-containing RASSF1C isoform also interacts with and stabilizes microtubules. We further show that in addition to G1 arrest, RASSF1A promotes growth arrest in the G2/M phase of the cell cycle and endogenous RASSF1A also interacts with microtubules. Based on our results, we propose that RASSF1A may mediate its tumor suppressive effects by inducing growth arrest in the G1 and G2/M phases. Together, these results provide important new insights into the molecular mechanisms by which this novel tumor suppressor mediates its biological effects.

Amino Acid Sequence↗
PubMed2004

Papillary and follicular thyroid carcinomas show distinctly different microarray expression profiles and can be distinguished by a minimum of five genes.

PURPOSE: We have previously conducted independent microarray expression analyses of the two most common types of nonmedullary thyroid carcinoma, namely papillary thyroid carcinoma (PTC) and follicular thyroid carcinoma (FTC). In this study, we sought to combine our data sets to shed light on the similarities and differences between these tumor types. MATERIALS AND METHODS: Microarray data from six PTCs, nine FTCs, and 13 normal thyroid samples were normalized to remove interlaboratory variability and then analyzed by unsupervised clustering, t test, and by comparison of absolute and change calls. Expression changes in four genes not previously implicated in thyroid carcinogenesis were verified by reverse transcriptase polymerase chain reaction on these same samples, together with eight additional FTC tumors. RESULTS: PTCs showed two distinct groups of genes that were either over- or underexpressed compared with normal thyroid, whereas the predominant changes in FTCs were of decreased expression. Five genes could collectively distinguish the two tumor types. PTCs showed overexpression of CITED1, claudin-10 (CLDN10), and insulin-like growth factor binding protein 6 (IGFBP6) but showed no change in expression of caveolin-1 (CAV1) or -2 (CAV2); conversely, FTCs did not express CLDN10 and had decreased expression of IGFBP6 and/or CAV1 and CAV2. CONCLUSION: PTC and FTC show distinctive microarray expression profiles, suggesting that either they have different molecular origins or they diverge distinctly from a common origin. Furthermore, if verified in a larger series of tumors, these genes could, in combination with known tumor-specific chromosome translocations, form the basis of a valuable diagnostic tool.

Adenocarcinoma, Follicular↗
PubMed2004

Protein kinase Cdelta mediates retinoic acid and phorbol myristate acetate-induced phospholipid scramblase 1 gene expression: its role in leukemic cell differentiation.

Although phospholipid scramblase 1 (PLSCR1) was originally identified based on its capacity to promote transbilayer movement of membrane phospholipids, subsequent studies also provided evidence for its role in cell proliferation, maturation, and apoptosis. In this report, we investigate the potential role of PLSCR1 in leukemic cell differentiation. We show that all-trans retinoic acid (ATRA), an effective differentiation-inducing agent of acute promyelocytic leukemic (APL) cells, can elevate PLSCR1 expression in ATRA-sensitive APL cells NB4 and HL60, but not in maturation-resistant NB4-LR1 cells. ATRA- and phorbol 12-myristate 13-acetate (PMA)-induced monocytic differentiation is accompanied by increased PLSCR1 expression, whereas only a slight or no elevation of PLSCR1 expression is observed in U937 cells differentiated with dimethyl sulfoxide (DMSO), sodium butyrate, or vitamin D3. Cell differentiation with ATRA and PMA, but not with vitamin D3 or DMSO, results in phosphorylation of protein kinase Cdelta (PKCdelta), and the PKCdelta-specific inhibitor rottlerin nearly eliminates the ATRA- and PMA-induced expression of PLSCR1, while ectopic expression of a constitutively active form of PKCdelta directly increases PLSCR1 expression. Finally, decreasing PLSCR1 expression with small interfering RNA inhibits ATRA/PMA-induced differentiation. Taken together, these results suggest that as a protein induced upon PKCdelta activation, PLSCR1 is required for ATRA- and PMA-triggered leukemic cell differentiation.

Cell Differentiation↗
PubMed2004

The p53 paddy wagon: COP1, Pirh2 and MDM2 are found resisting apoptosis and growth arrest.

For years, the growth inhibitory effects of the tumor suppressor p53 were thought to be antagonized predominantly by the ubiquitin ligase, MDM2. It has long been established that MDM2 physically associates with p53 and targets this tumor suppressor for proteasomal degradation. In light of recent findings, it now appears that MDM2 may not be the only ubiquitin ligase that negatively controls p53 function. Two recently discovered proteins, Pirh2 and COP1, are also believed to facilitate p53 degradation via the ubiquitin-proteasome pathway. Both proteins are upregulated by p53 as well as genotoxic stress and each has been found to directly promote p53 ubiquitination and degradation. Future studies in this field will now face the challenge of elucidating the physiological significance of three molecules all apparently able to independently facilitate p53 degradation and abrogate its function.

Apoptosis↗
PubMed2004

Novel pearl-necklace porous CdS nanofiber templated by organogel.

A new cholesterol organogelator 4 was synthesized and its gelation property was evaluated. It was confirmed that 4 was an effective gelator for various organic solvents and could self-assemble into network fibers with a bilayer of folded conformation in some organic solvents. Moreover, organogelator 4 could act as a template for the synthesis of novel pearl-necklace porous CdS nanofibers. The transcription process of organogel fibers into CdS nanofibers was investigated, and it was found that Cd2+ ions were coated on the organogel fibers by the interaction with ester groups of 4, which might lead to the change of the arrangement of the organogelator and seemed to serve as nucleation sites for metalization. The further growth of CdS began with these nucleation sites along the organogel fibers. Meanwhile, parts of 4 free from organogel fibers have an effect on the formation of the CdS nanofibers consisting of the network and wormlike CdS particles.

Journal Article↗
PubMed2004

Membrane transporters and channels: role of the transportome in cancer chemosensitivity and chemoresistance.

Membrane transporters and channels (collectively the transportome) govern cellular influx and efflux of ions, nutrients, and drugs. We used oligonucleotide arrays to analyze gene expression of the transportome in 60 human cancer cell lines used by the National Cancer Institute for drug screening. Correlating gene expression with the potencies of 119 standard anticancer drugs identified known drug-transporter interactions and suggested novel ones. Folate, nucleoside, and amino acid transporters positively correlated with chemosensitivity to their respective drug substrates. We validated the positive correlation between SLC29A1 (nucleoside transporter ENT1) expression and potency of nucleoside analogues, azacytidine and inosine-glycodialdehyde. Application of an inhibitor of SLC29A1, nitrobenzylmercaptopurine ribonucleoside, significantly reduced the potency of these two drugs, indicating that SLC29A1 plays a role in cellular uptake. Three ABC efflux transporters (ABCB1, ABCC3, and ABCB5) showed significant negative correlations with multiple drugs, suggesting a mechanism of drug resistance. ABCB1 expression correlated negatively with potencies of 19 known ABCB1 substrates and with Baker's antifol and geldanamycin. Use of RNA interference reduced ABCB1 mRNA levels and concomitantly increased sensitivity to these two drugs, as expected for ABCB1 substrates. Similarly, specific silencing of ABCB5 by small interfering RNA increased sensitivity to several drugs in melanoma cells, implicating ABCB5 as a novel chemoresistance factor. Ion exchangers, ion channels, and subunits of proton and sodium pumps variably correlated with drug potency. This study identifies numerous potential drug-transporter relationships and supports a prominent role for membrane transport in determining chemosensitivity. Measurement of transporter gene expression may prove useful in predicting anticancer drug response.

ATP-Binding Cassette Transporters↗
PubMed2004

Proteasome inhibitor MG132 upregulates death receptor 5 and cooperates with Apo2L/TRAIL to induce apoptosis in Bax-proficient and -deficient cells.

Apo2L/TRAIL (tumor necrosis factor-related apoptosis inducing ligand (TRAIL), also known as Apo2L) is a potentially important anticancer agent awaiting clinical trials. Unfortunately, however, some cancer cells exhibit resistance to Apo2L/TRAIL, which could limit the use of this potentially promising anticancer agent. Although the molecular basis of the inherent or acquired resistance to Apo2L/TRAIL remains unclear, previous studies indicate that Bax deficiency can confer resistance to Apo2L/TRAIL. Proteasome inhibition is also emerging as a promising therapeutic strategy to manage human malignancies. Here, we report that proteasome inhibitor MG132 upregulates Apo2L/TRAIL death receptor 5 expression in both Bax-proficient and -deficient HCT116 cells. MG132 effectively cooperated with Apo2L/TRAIL to induce apoptosis in both Bax-proficient and -deficient cells that was coupled with caspases-8 and -3 activation and Bid cleavage. Although both agents in combination also induced cytochrome c and Smac release from mitochondria into cytosol and activated caspase-9 in Bax-proficient cells, their effects on these events were significantly diminished in Bax-deficient cells. These results suggest that Bax is not absolutely required for death receptor 5-dependent apoptotic signals and MG132 by upregulating DR5 effectively cooperates with Apo2L/TRAIL to overcome Bax deficiency-induced resistance to Apo2L/TRAIL. Our results have important clinical implications in that the use of Apo2L/TRAIL and proteasome inhibitors in combination could prove to be a novel therapeutic strategy to manage the Apo2L/TRAIL-resistant tumors.

Antineoplastic Agents↗