Search PubMed⌕ Search

Biomedical subjects

Q Huang

Publications and source records attributed to Q Huang.

At least 91 records · Page 5Linked to original sources
PubMed2001

[The effect of Paeonol on erythrocyte deformability determined by micropipette aspiration technique].

OBJECTIVE: The effect of Paeonol (PAE) on erythorcyet(RBC) deformability was studied in order to provide experimental data for the application in clinic and the evaluation in pharmacological action. METHODS: Micropipette Aspiration Technique was used to determine the RBC deformation length. The method of calculation was also simplified and a new apparent deformation Index(ADI) was defined. RESULTS: PAE could increase the ADImin and ADImax and decrease Tmax significantly. CONCLUSION: PAE has the effect of deformational ability on RBC. Micropipette aspiration technique is a feasible method for determining the effect of traditional Chinese medicine on erythrocyte deformability.

Acetophenones↗
PubMed2001

[Study on the effects of increased iodized salt intake on the incidence of thyroid diseases].

OBJECTIVE: To study the annual incidence of thyroid diseases before and after the increase of iodized salt intake. METHOD: A total of 26,010 persons were examined from mid August to the end of December in 1999. RESULTS: 1. Three hundred and ten patients of thyroid diseases were identified from 1990 to July 1999. One hundred and eighty-three patients were diagnosed after iodine supplementation. 2. The constitution of thyroid diseases had changed significantly regarding the increase of hyperthyroidism, simple goiter and thyroid nodule. 3. Fifty-five patients with hyperthyroidism including 39 patients (70.91%) receiving iodine supplementation were diagnosed. The average annual incidence of hyperthyroidism after iodine supplementation was 36.87 per 100,000, a three-time increase as compared with that before iodine supplementation. The incidence of hyperthyroidism began to show a significant rise in 1996. The year with highest annual incidence was 1997, remaining at high level after supplying iodized salt. Since then the annual relative risk for hyperthyroidism had been increasing. CONCLUSION: The number of patients with thyroid diseases showed a significant increase after mass iodine supplement. At the same time, the spectrum of thyroid diseases had also changed. Iodized salt intake and the incidence of hyperthyroidism showed a significant correlation. However, the typical model of the change of disease patterns incidence needs further study.

Adult↗
PubMed2001

[Effect of transfected Cx43 gene on the gap junction intercellular communication and the human glioma cells proliferation].

OBJECTIVE: To investigate the role of connexin 43 (Cx43) gene in the gap junction intercellular communication (GJIC) and the development of glioma so as to demonstrate the feasibility of using Cx43cDNA as the target of gene therapy for gliomas. METHODS: TJ905 human glioblastoma cell line without Cx43 gene expression was transfected with Cx43cDNA mediated by lipofectamine. Northern blot, in situ hybridization and immunocytochemistry were used for examination of Cx43mRNA and its protein examination; MTT assay and silver colloid stain were used to detect cell proliferation. TUNEL method was used to determine the cell apoptosis. Scrape loading dye transfer (SLDT) was used to monitor GJIC. RESULTS: The TJ905 transfectants resulted in dramatic upregulation of Cx43mRNA and its protein, with the GJIC of transfected glioma cells restored. Clones with high Cx43 expression also showed reduced proliferation in vitro. However, the cell apoptosis did not increase following the transfection with Cx43 gene. CONCLUSION: These results indicate that Cx gene and gap junction intercellular communication are of crucial importance in malignant glioma cell growth and development. Cx43 gene may be a target for gene therapy of gliomas.

Blotting, Northern↗
PubMed2001

[Culture and identification of fetal human retinal photoreceptors].

OBJECTIVE: To investigate the methods of isolation and culture of fetal human retinal photoreceptors. METHODS: Fetal human retinal photoreceptors were obtained by enzyme gradation digestion, cultured in media conditioned by retinal pigment epithelial cells (RPE-CM), identified by morphologic observation and immunohistochemically stained with rod specific opsin 4D2 (Rho 4D2) antibody. The digested retinal tissues were tested by hematoxylin-eosin (HE) staining. RESULTS: Enzyme gradation digestion could obtain relatively pure retinal photoreceptors. These cells were stained positively for Rho 4D2 antibody, and survived in RPE-CM for a long time. CONCLUSION: Fetal human retinal photoreceptors obtained by enzyme gradation digestion can survive in RPE-CM for a long time and express rod specific opsin. This culture system will provide a source for human retinal photoreceptor transplantation and further studies of photoreceptors in vitro.

Cell Division↗
PubMed2001

[Preparation of green fluorescent protein retrovirus and its application in mediating gene transfer into retinal pigment epithelial cells].

OBJECTIVE: To determine whether human retinal pigment epithelial (RPE) cells can be infected by retrovirus and modified by retrovirus-mediated gene transfer. METHODS: Recombination retroviral vector pLNCX-GFP (green fluorescent protein, GFP) was generated by inserting 780 bp GFP cDNA fragment into the MCS site of pLNCX. pLNCX-GFP was transfected into ecotropic packaging cell line PhiX-Eco and amphotropic packaging cell line PhiX-Ampho and PA317. Retroviral titer was tested by counting GFP expression of NIH3T3 cells. Then RPE cells were infected by using GFP retrovirus-containing supernatant. RESULTS: GFP was expressed and retrovirus was produced upon pLNCX-GFP being transfected into packaging cell line. The GFP retrovirus was able to infect primary cultured human RPE cells and immortalized RPE cell line. CONCLUSION: The retrovirus can introduce a foreign gene into RPE cells efficiently, thereby it can be used as an important tool to deliver gene into RPE for therapy of fundus diseases.

Cells, Cultured↗
PubMed2001

[Using Hsp70 promoter to regulate target gene expression in tumor].

OBJECTIVE: To regulate gene expression in the desired tumor cells both in vitro and in vivo. METHODS: Heat inducible green fluorescent protein (GFP) expression plasmid and adenovirus were built by using different sizes of 5' end regulating sequence from human heat shock protein (Hsp) gene as promoter and GFP cDNA as report gene. GFP expression turned on by heating was observed in the cultured cells and the tumor grown in the dorsal skin window chamber. RESULTS: A 400 bp of Hsp gene 5' end regulating sequence can be activated by heating and it can drive report gene expression effectively both in vitro and in vivo. CONCLUSIONS: Heating can selectively induce gene expression in the targeted tumor. It provides an useful tool for cancer gene therapy because it possibly maximizes tumor cell killing and minimizes normal tissue damage.

Adenoviridae↗
PubMed2001

[The role of p38 MAPK in LPS induced ICAM-1 expression on endothelial cell].

OBJECTIVE: To study the role of p38 mitogen-activated protein kinase (MAPK) in lipopolysaccharide (LPS) induced expression of intercellular adhesion molecule-1 (ICAM-1) on human umbilical vein endothelial cell (HUVEC). METHODS: HUVEC was harvested and cultured before being divided into two groups, i,e. stimulating group (S) and priming group (P). In S group, the cultured endothelial cell was stimulated by LPS. In P group, endothelial cell was pre-treated with SB 203580 2 hours before LPS stimulation. The expressions of ICAM-1 mRNA and protein in HUVEC of two groups and their dose-effect relationship with stimulator and inhibitor were observed. Furthermore the p38 mRNA activity of HUVEC was detected. RESULTS: After LPS stimulation, ICAM-1 molecule on the surface of endothelium increased significantly at 8 to 36 hours. Cytoplasmic mRNA increased obviously at 2 hours. The activity of p38 MAPK increased at 15 min and reached peak value at 30 to 60 min after that HUVEC was stimulated by LPS. CONCLUSION: Inhibitor SB 203580 of p38 might significantly inhibit the inducing effect of LPS. LPS could regulate the expression of ICAM-1 gene and protein in HUVEC by activating p38 MAPK signal transduction passage.

Cells, Cultured↗
PubMed2000

KIAP, a novel member of the inhibitor of apoptosis protein family.

We have identified a novel human gene, kiap (kidney inhibitor of apoptosis protein) that encodes a single BIR domain and a RING zinc finger domain. kiap has been assigned to the q13.3 region of human chromosome 20 by fluorescent in situ hybridization analysis. Northern blot analysis indicates that KIAP is expressed mainly in placenta, lymph node and fetal kidney. In this report, we show that overexpression of KIAP blocks apoptosis induced by menadione or by overexpression of BAX. In addition, we show that overexpression of KIAP enhances apoptosis induced by etoposide, and, that KIAP fails to block apoptosis induced by overexpression of Fas. Thus, KIAP, a new member of the inhibitor of apoptosis protein (IAP) family, has pleiotropic effects on apoptosis induced by various stimuli.

Amino Acid Sequence↗
PubMed2000

Enhancement of radiotherapy by hyperthermia-regulated gene therapy.

PURPOSE: Interleukin 12 (IL-12) has shown strong antitumoral effects in numerous pre-clinical studies and appears to act synergistically with radiation in murine tumors. The major impediment to its clinical use has been its systemic toxicity. While using intratumorally injected viral gene therapy vectors encoding IL-12 reduces systemic side effects substantially, elevated systemic transgene levels are still observed because adenovirus can reach the circulation. Further restricting IL-12 expression in the tumor is therefore desirable in a combined radiation and adenovirus mediated cancer gene therapy regimen. METHODS AND MATERILAS: Hyperthermia-regulated gene therapy was tested in a nonimmunogenic B16.F10 melanoma line that is syngeneic with C57BL/6 mice. For hyperthermic gene therapy, an adenoviral vector coding for IL-12 under the control of the promoter of the human heat shock protein 70B (hsp70B) was used. One week after transplantation (at a 5-7 mm diameter), tumors were irradiated with 3 x 11 Gy (mo-we-fri). Adenovirus was injected at 3 x 10(8) pfu/tumor 24 h before the last radiation fraction or 3 days afterwards. Hyperthermia was performed 24 h later at 42.5 degrees C. Growth delay to reaching 3 times initial tumor volume was chosen as the biologic endpoint. IL-12 levels in tumor and serum were determined by using the enzyme-linked immunosorbant assay (ELISA). RESULTS: Adenovirus mediated intratumoral expression of IL-12 under the control of a heat inducible promoter in combination with hyperthermia is almost as effective as that under the control of a constitutive cytomegaly virus (CMV) promoter while systemic transgene levels are substantially reduced with the heat inducible promoter. The response to radiotherapy is improved considerably when combined with heat inducible gene therapy without apparent systemic toxicity. When used as a single dose, applying IL-12 gene therapy after completion of radiotherapy appears to be beneficial. CONCLUSIONS: Hyperthermia-regulated gene therapy in combination with radiation is feasible and therapeutically effective in murine tumors with no apparent systemic toxicity.

Adenoviridae↗
PubMed2000

Complete arterial revascularization in multivessel coronary artery disease with 2 conduits (skeletonized grafts and T grafts).

BACKGROUND: Complete arterial CABG is a surgical option to improve long-term results in the treatment of coronary artery disease (CAD). Harvesting of multiple arterial grafts is commonly associated with prolonged operating times and increased trauma. By use of new operative techniques (skeletonized grafts and the T-graft approach), CABG in multivessel CAD is now possible with only 2 grafts. We present our experience in the use of these techniques on a routine basis. METHODS AND RESULTS: Between March 1996 and September 1999, 490 patients (aged 61+/-9 years, 20% female) underwent complete arterial CABG. Left ventricular ejection fraction ranged from 15% to 85% (mean 59+/-15%). Triple-vessel disease was present in 88% of the patients. The incidence of diabetes mellitus was 32% (14% insulin dependent). Either both internal thoracic arteries (ITAs) (23%) or the left ITA and radial artery (77%) were used as conduits. In 85% of the patients, a T graft was created. Mean operating time was 198+/-46 minutes; bypass time, 82+/-25 minutes; and ischemic time, 58+/-22 minutes. Two to 7 (mean 4.1+/-0.9) anastomoses were performed per patient. Perioperative intra-aortic balloon pump was necessary in 12 patients (2.4%). The rate of perioperative myocardial infarction was 1.2%. Sternal complications occurred in 1. 0%, and in-hospital mortality was 2.2%. Postoperative coronary angiography in 172 patients (35%) documented excellent patency rates (left ITA 98.3%, right ITA 96.5%, and radial artery 96.6%). CONCLUSIONS: Complete arterial revascularization in multivessel CAD is possible with the use of only 2 grafts with good perioperative results. This approach allows for complete arterial CABG on a routine basis.

Adult↗
PubMed2000

Single-strand conformation polymorphism analysis to detect the p53 mutation in colon tumor samples by capillary electrophoresis.

The polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) technique is developed for the detection of point mutations in DNA samples, and is very useful in the research of tumors. The traditional SSCP was carried out with slab gel electrophoresis (SGE), but this is time-consuming and labor-intensive, particularly for clinical diagnoses. We have developed a capillary electrophoresis (CE) method for SSCP detection with a linear polyacrylamide gel solution as the sieving matrix. Twenty colon tumor samples were detected with SSCP-CE and the point mutation in exon 7 of the p53 gene was found in six of the samples. Based on the sequencing results, the accuracy of SSCP-CE was better than that of SSCP-SGE. We hope this rapid and convenient method could be applied in the clinical diagnosis of tumors soon.

Base Sequence↗
PubMed2000

Drosophila pro-apoptotic Bcl-2/Bax homologue reveals evolutionary conservation of cell death mechanisms.

Genetic analysis of programmed cell death in Drosophila reveals many similarities with mammals. Heretofore, a missing link in the fly has been the absence of any Bcl-2/Bax family members, proteins that function in mammals as regulators of mitochondrial cytochrome c release. A Drosophila homologue of the human killer protein Bok (DBok) was identified. The predicted structure of DBok is similar to pore-forming Bcl-2/Bax family members. DBok induces apoptosis in insect and human cells, which is suppressible by anti-apoptotic human Bcl-2 family proteins. A caspase inhibitor suppressed DBok-induced apoptosis but did not prevent DBok-induced cell death. Moreover, DBok targets mitochondria and triggers cytochrome c release through a caspase-independent mechanism. These characteristics of DBok reveal evolutionary conservation of cell death mechanisms in flies and humans.

Amino Acid Sequence↗
PubMed2000

Heat-induced gene expression as a novel targeted cancer gene therapy strategy.

One of the main advantages of gene therapy over traditional therapy is the potential to target the expression of therapeutic genes in desired cells or tissues. To achieve targeted gene expression, we experimented with a new approach based on the long-established phenomenon of the heat shock response. By using the green fluorescence protein as a reporter gene, it was demonstrated that expression of a heterologous gene with a heat shock protein 70 promoter could be elevated to 500-1000-fold over background by moderate hyperthermia (39 degrees C to 43 degrees C) in tissue cultured cells. The heat-induced green fluorescence protein expression was first detectable at 3 h after heating and reached a maximum at 18-24 h. The expression dropped back to baseline within 72 h. In addition, when cells were infected with adenovirus vectors containing the heat-inducible interleukin 12 or tumor necrosis factor alpha genes and then heated (42 degrees C, 30 min), expression was at least 13,600- or 6.8 x 10(5)-fold over background, respectively. Intralesion injection of the interleukin-12-carrying adenovirus vector in a mouse melanoma tumor model caused significant tumor growth delay only with hyperthermia treatment. Our results therefore support heat-induced gene expression as a feasible approach for targeted cancer gene therapy.

Adenoviridae↗
PubMed2000

[The roles of alpha B-crystallin during early phase of myocardial ischemic preconditioning in rats].

OBJECTIVE: This study designed to observe intracellular translocation of alpha B-crystallin, a small heat shock protein, and its possible implication during the early phase of myocardial ischemic preconditioning in isolated Langendorff rat hearts. Eighteen male Wistar rats(180-250 g) were randomly divided into three groups: 1. Control group(Ctrl) was perfused with K-H solution throughout the experiment; 2. ischemia-reperfusion group (I-R) experienced 30 min of global ischemia and 120 min of reperfusion and 3. preconditioning and ischemia-reperfusion group(PC + I-R) was preconditioned with three cycles of short myocardial ischemia(5 min each, separated by 5 min of reperfusion) prior to 30 min of ischemia and 120 min of reperfusion. It was showed that cytosolic soluble alpha B-crystallin rapidly translocated to insoluble intracellular structure after ischemic preconditioning, then gradually returned to soluble cytosol pool and almost completely recovered at about 60 min after preconditioning. In the meanwhile, ischemic preconditioning markedly alleviated subsequent myocardial ischemia-reperfusion injury, as indicated by the improvement of LVP, + dp/dt max, coronary flow, heart rate, CPK release and malondialdehyde(MDA) production. The results suggest that the intracellular translocation of alpha B-crystallin might be important for myocardial protection during the early phase of ischemic preconditioning.

Animals↗
PubMed2000

Photoactivated gamma-secretase inhibitors directed to the active site covalently label presenilin 1.

Cleavage of amyloid precursor protein (APP) by the beta- and gamma-secretases generates the amino and carboxy termini, respectively, of the A beta amyloidogenic peptides A beta40 and A beta42--the major constituents of the amyloid plaques in the brain parenchyma of Alzheimer's disease patients. There is evidence that the polytopic membrane-spanning proteins, presenilin 1 and 2 (PS1 and PS2), are important determinants of gamma-secretase activity: mutations in PS1 and PS2 that are associated with early-onset familial Alzheimer's disease increase the production of A beta42 (refs 4-6), the more amyloidogenic peptide; gamma-secretase activity is reduced in neuronal cultures derived from PS1-deficient mouse embryos; and directed mutagenesis of two conserved aspartates in transmembrane segments of PS1 inactivates the ability of gamma-secretase to catalyse processing of APP within its transmembrane domain. It is unknown, however, whether PS1 (which has little or no homology to any known aspartyl protease) is itself a transmembrane aspartyl protease or a gamma-secretase cofactor, or helps to colocalize gamma-secretase and APP. Here we report photoaffinity labelling of PS1 (and PS2) by potent gamma-secretase inhibitors that were designed to function as transition state analogue inhibitors directed to the active site of an aspartyl protease. This observation indicates that PS1 (and PS2) may contain the active site of gamma-secretase. Interestingly, the intact, single-chain form of wild-type PS1 is not labelled by an active-site-directed photoaffinity probe, suggesting that intact wild-type PS1 may be an aspartyl protease zymogen.

Alzheimer Disease↗
PubMed2000

Presenilin 1 is linked with gamma-secretase activity in the detergent solubilized state.

gamma-Secretase is a membrane-associated protease that cleaves within the transmembrane region of amyloid precursor protein to generate the C termini of the two Abeta peptide isoforms, Abeta40 and Abeta42. Here we report the detergent solubilization and partial characterization of gamma-secretase. The activity of solubilized gamma-secretase was measured with a recombinant substrate, C100Flag, consisting largely of the C-terminal fragment of amyloid precursor protein downstream of the beta-secretase cleavage site. Cleavage of C100Flag by gamma-secretase was detected by electrochemiluminescence using antibodies that specifically recognize the Abeta40 or Abeta42 termini. Incubation of C100Flag with HeLa cell membranes or detergent-solubilized HeLa cell membranes generates both the Abeta40 and Abeta42 termini. Recovery of catalytically competent, soluble gamma-secretase critically depends on the choice of detergent; CHAPSO (3-[(3-cholamidopropyl)dimethylammonio]-2-hydroxy-1-propanesulfonate) but not Triton X-100 is suitable. Solubilized gamma-secretase activity is inhibited by pepstatin and more potently by a novel aspartyl protease transition-state analog inhibitor that blocks formation of Abeta40 and Abeta42 in mammalian cells. Upon gel exclusion chromatography, solubilized gamma-secretase activity coelutes with presenilin 1 (PS1) at an apparent relative molecular weight of approximately 2.0 x 10(6). Anti-PS1 antibody immunoprecipitates gamma-secretase activity from the solubilized gamma-secretase preparation. These data suggest that gamma-secretase activity is catalyzed by a PS1-containing macromolecular complex.

Alzheimer Disease↗
PubMed2000

Src and Cas mediate JNK activation but not ERK1/2 and p38 kinases by reactive oxygen species.

c-Jun NH(2)-terminal kinase (JNK) is activated by a number of cellular stimuli such as inflammatory cytokines and environmental stresses. Reactive oxygen species also cause activation of JNK; however, the signaling cascade that leads to JNK activation remains to be elucidated. Because recent reports showed that expression of Cas, a putative Src substrate, stimulates JNK activation, we hypothesized that the Src kinase family and Cas would be involved in JNK activation by reactive oxygen species. An essential role for both Src and Cas was demonstrated. First, the specific Src family tyrosine kinase inhibitor, PP2, inhibited JNK activation by H(2)O(2) in a concentration-dependent manner but had no effect on extracellular signal-regulated kinases 1 and 2 and p38 activation. Second, JNK activation in response to H(2)O(2) was completely inhibited in cells derived from transgenic mice deficient in Src but not Fyn. Third, expression of a dominant negative mutant of Cas prevented H(2)O(2)-mediated JNK activation but had no effect on extracellular signal-regulated kinases 1 and 2 and p38 activation. Finally, the importance of Src was further supported by the inhibition of both H(2)O(2)-mediated Cas tyrosine phosphorylation and Cas.Crk complex formation in Src-/- but not Fyn-/- cells. These results demonstrate an essential role for Src and Cas in H(2)O(2)-mediated activation of JNK and suggest a new redox-sensitive pathway for JNK activation mediated by Src.

Animals↗