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Biomedical subjects

B C Yang

Publications and source records attributed to B C Yang.

At least 19 recordsLinked to original sources
PubMed2003

Characterization of surface oxide films on titanium and adhesion of osteoblast.

The relationship between surface characteristics of titanium and initial interactions of titanium-osteoblasts was investigated. Titanium plates were heat-treated in different oxidation atmospheres. The third passage rabbit osteoblasts were cultured on the titanium plates for 24h. After the heat-treatment, the crystal structure of the surface oxide films on titanium was identified using X-ray diffractometer and X-ray photoelectron spectroscopy (XPS). The surface roughness of titanium was measured with a profilometer. The surface energy was obtained by measurement of contact angles and calculation with Owens-Wendt-Kaeble's equation. The amount of surface hydroxyl (OH)(s) groups was examined using XPS. The change of binding energy of the some elements on the substrate surface suggested that the interactions between the cells and the titanium involved chemical reactions. The greater surface roughness, higher surface energy and more surface hydroxyl groups resulted in greater numbers of adhered osteoblasts and higher cell activity. Compared to the acidic hydroxyl (OH)(a) groups in (OH)(s) groups and the dispersion component of the total surface energy, the basic hydroxyl (OH)(b) groups and the polar component play more important roles in the osteoblast-titanium interaction.

Alkaline Phosphatase↗
PubMed2001

Down-regulation of Fas-L in glioma cells by ribozyme reduces cell apoptosis, tumour-infiltrating cells, and liver damage but accelerates tumour formation in nude mice.

Fas-L (CD95L, APO-1L) expresses in a variety of tumours and has been proposed to play a role in tumour formation and metastasis. The contribution of Fas-L to tumour growth, however, is not conclusive especially in systems using cells with over-expressed Fas-L. In this study we down-regulated the expression o Fas-L in human glioma cells by a hammerhead ribozyme (Fas-L(ribozyme)) targeting against Fas-L mRNA. Fas-L(ribozyme)-carrying cells exhibited slightly enhanced growth rate and less degree of spontaneous apoptosis in vitro as compared with vector controls. In nude mice, Fas-L(ribozyme)-carrying cells grew faster with lesser apoptosis, formed bigger tumour with significantly fewer infiltrating cells in the tumour area, and triggered relatively milder tumour-associated liver damage than vector controls did. Thus, down-regulation of Fas-L not only improved viability of glioma cells but also reduces local immune responses that may consequently affect tumour formation. Taken together, our findings imply that endogenous expression of Fas-L in malignant cells is not always growth promoting.

Animals↗
PubMed2001

The inhibitory effects of lead on steroidogenesis in MA-10 mouse Leydig tumor cells.

Lead is an environmental and occupational pollutant. It has been reported that lead affects the male reproductive system in humans and animals. However, the cellular mechanism of the adverse effect of lead on Leydig cell steroidogenesis remains unknown. To clarify whether lead has a direct effect on Leydig cells and how lead affects Leydig cells, MA-10 cells, a mouse Leydig tumor cell line, were exploited in this study. Lead acetate significantly inhibited hCG- and dbcAMP-stimulated progesterone production in MA-10 cells at 2 h. Steroid production stimulated by hCG or dbcAMP were reduced by lead. The mechanism of lead in reducing MA-10 cell steroidogenesis was further investigated. The expression of Steroidogenic Acute Regulatory (StAR) protein and the activities of P450 side-chain cleavage (P450scc) and 3beta-hydroxysteroid dehydrogenase (3beta-HSD) enzymes were detected. Cells were treated with dbcAMP, 22R-hydroxycholesterol or pregnenolone alone or in combination with lead acetate ranging from 10(-8) to 10(-5) M for 2 h. The expression of StAR protein stimulated by dbcAMP was suppressed by lead at about 50%. Progesterone productions treated with 22R-hydroxycholesterol or pregnenolone were reduced 30-40% in lead-treated MA-10 cells. These data suggest that lead directly inhibited steroidogenesis by decreasing StAR protein expression and the activities of P450scc and 3beta-HSD enzymes with a dose-response trend in MA-10 cells. Moreover, cadmium, a calcium channel blocker, abolished inhibitory effect of lead on MA-10 cell steroid production. This indicates that lead might act on calcium channel to regulate MA-10 cell steroidogenesis.

3-Hydroxysteroid Dehydrogenases↗
PubMed2001

UV-induced increase in RNA polymerase activity in Xanthomonas oryzae pathovar oryzae.

UV radiation is thought to inhibit transcriptional elongation, as a result of the formation of pyrimidine dimers in the DNA template, as well as to activate specific transcription factors. However, the effect of UV radiation on the enzymatic activity of RNA polymerase has remained unknown. With the use of an in vitro assay, UV irradiation of Xanthomonas oryzae pathovar oryzae has now been shown to increase RNA polymerase activity. This effect was maximal at a UV dose of approximately 12 J m(-2) and at approximately 60 min after irradiation. It was also not inhibited by pretreatment of cells with chloramphenicol, an inhibitor of protein synthesis. Immunoprecipitation with antibodies to the RNA polymerase core enzyme revealed that exposure of the bacterial cells to UV radiation induced the association of the core enzyme with a protein of approximately 29 kDa. These results demonstrate that UV radiation increases the activity of RNA polymerase, and they suggest that this effect may be related to the repair of DNA damage.

Bacterial Proteins↗
PubMed2001

[Laser-induced fluorescence detection in micro-column separation].

Laser-induced fluorescence detection (LIFD) has been used extensively in micro-column separation due to its high sensitivity and selectivity. A review is presented on the present status and the trends of development of LIF detector with 52 references cited. The detection cells of the LIFD are mainly discussed.

Amino Acids↗
PubMed2000

In vitro aberrant gene expression as the indicator of lead-induced neurotoxicity in U-373MG cells.

Lead is an important neurobehavioral toxicant and may interfere with developmental processes in the brain resulting in impairment of its functions. U-373MG, a human glioma cell line, was cultured in Dulbecco's modified Eagles' medium supplemented with either 20 or 10% FBS (fetal bovine serum) to explore the possible indications for lead-induced toxicity. Although lead did not affect cell growth rate in concentrations ranging from 0.01 to 10 microM, it substantially altered gene expression analyzed by reverse-transcription polymerase chain reaction. With 10% FBS culture, lead affected the gene expression in a dose-dependent relationship. It enhanced the expression of tumor necrosis factor-alpha (TNF-alpha), but decreased those of interleukin-1beta (IL-1beta), interleukin-6 (IL-6), gamma-aminobutyric acid (GABA) transaminase, and glutamine synthetase. With 20% FBS culture, lead also profoundly increased TNF-alpha and IL-1beta; however, it did not extensively affect the other genes examined above. Thus, the highly sensitive changes of gene expression of these cytokines or metabolic enzymes after treatments with lead acetate evidenced their usefulness as indicators for in vitro measurement of lead-induced neurotoxicity.

Brain Neoplasms↗
PubMed2000

Ras signaling is involved in the expression of Fas-L in glioma.

Fas-L expresses on a variety of tumors and is suspected to modify the dialog between tumor and the immune system. However, the cellular abnormality in tumor cells leading to an aberrant expression of Fas-L is unclear. In this study, we demonstrate the involvement of Ras signaling in the Fas-L expression in several ways. First, the activated Ha-rasval12 gene enhanced the Fas-L expression of primary human glial cells. Second, blocking the Ras signal pathway in glioma cells by lovastatin or the Ha-rasAsn17 dominant-negative mutant gene resulted in reduced Fas-L expression. Transfection of the Ha-rasAsn17 into glioma cells also inhibited the activation of NFKB, which is a downstream component of Ras signaling. Accordingly, the membrane-permeable NFKB competitor suppressed the Fas-L expression. Furthermore, the Fas-L expression coincided with the Ras activity in the murine 212 cells, in which the Ras activity could be induced by isopropyl 3-D-thiogalactoside. In summary, these results suggest that the enhanced Ras signaling with consequential NFKB activation, which is a frequent defect found in tumors, could mediate the Fas-L expression of tumors.

Antineoplastic Agents↗
PubMed2000

Overexpression of Fas-ligand in human nasal polyps.

Apoptosis mediated through the Fas/Fas-L system is essential in regulating immune function, developing organs, and conferring immune privilege. To illustrate the role of the Fas/Fas-L system in the pathogenesis of human nasal polyps, we investigated the transcripts and protein level of the Fas-L gene in 8 human nasal polyp tissues and 7 nasal turbinate mucosa specimens using reverse transcription-polymerase chain reaction and Western blotting. Localization of Fas-L was performed with immunohistochemistry. The transcripts of the Fas-L gene were detected at similar levels in both polyps and nasal mucosa. There was a significant overexpression of Fas-L protein on nasal polyps compared to nasal mucosa. Fas-L-positive cells were localized on the epithelial layers of cystically dilated glands and the down-growing epithelium of nasal polyps. Fas-L may play an important role in the pathogenesis of human nasal polyps, including cystic degeneration of submucosal glands and conferring of immune privilege to nasal polyp formation.

Blotting, Western↗
PubMed1999

Selective activation of Ha-ras(val12) oncogene increases susceptibilityof NIH/3T3 cells to TNF-alpha.

This is the first report demonstrating that NIH/3T3 fibroblasts utilize the Raf-1/MAPK pathway to sensitize themselves to tumor necrosis factor-alpha (TNF-alpha) cytotoxicity under Ha-rasVal12 oncogene-overexpressed conditions. This paper clearly shows that the sensitivity of NIH/3T3 cells to TNF-alpha cytotoxicity positively correlated with the expression level of activated Ha-ras transgene, which was manipulated either positively by isopropyl-beta-d-thiogalactoside (IPTG) induction or negatively by a ribozyme or a dominant negative Ras suppression. Further analysis revealed that after TNF-alpha treatment, Ha-ras-overexpressed transformants underwent apoptosis. Overexpression of dominant negative Raf-1, Rac1, or RhoA in the Ha-ras transformants clarified that among these factors, only dominant negative Raf-1 could reverse the cell sensitivity to TNF-alpha, indicating that Raf-1, as a proapoptotic factor, indeed participates in TNF-alpha cytotoxicity. The anti-apoptotic roles of Bcl-2 and PI(3) kinase are also demonstrated by the Ha-ras transformants which became more resistant to TNF-alpha while overexpressing Bcl-2 or the activated p110 catalytic subunit. The analyses of the cell cycle and nuclear transcription factor activities revealed that TNF-alpha treatment caused the Ha-ras overexpressed transformants to shift from S to G0/G1 phase and increased the responses of AP-1, c-fos, and c-myc. Taken together, we suggest that the possible action of Ha-ras overexpression to sensitize TNF-alpha-treated fibroblasts is predominantly through the Ras/Raf-1/MAPK pathway to increase the responses of AP-1, c-fos, and c-myc, which are possibly involved in the aberration of cell cycle machinery, and subsequently to turn on the death program.

Apoptosis↗
PubMed1999

The order of calcium and phosphate ion deposition on chemically treated titanium surfaces soaked in aqueous solution.

The mechanism of apatite deposition on chemically treated Ti surfaces still is being studied. In this study, simulated body fluid, calcium aqueous solution, phosphate aqueous solution, and accelerated calcification solution are used as media to investigate the order of calcium and phosphate ion deposition on chemically treated Ti surfaces. The results of inductively coupled plasma spectra, scanning electron microscopy, and energy dispersive X-ray analysis show that calcium deposition is the prerequisite for phosphate ion deposition.

Biocompatible Materials↗
PubMed1999

Transient apoptosis elicited by insulin in serum-starved glioma cells involves Fas/Fas-L and Bcl-2.

The expression of fas gene in glioma cells varies with growth stage. When insulin-elicited transient apoptosis of glioma cells was in progress, the expression of fas gene increased at both transcriptional and translational levels. In contrast, the expression of fas-L gene in glioma cells remained constant. Apoptosis occurred in the cells having high level of surface Fas protein. When the expression of Fas-L in U-373MG cells was suppressed by ribozyme, the insulin-elicited transient apoptosis vanished. Overexpression of Bcl-2 in U-373MG cells did not alter significantly the cell cycle progression and the expression of fas gene. However, these cells were resistant to insulin-trigged death. Therefore, insulin-elicited apoptosis involved Fas-related death signal, and which could be prevented by the protective effect of Bcl-2.

Antigens, Surface↗
PubMed1999

Alpha 1-acid glycoprotein-induced tumor necrosis factor-alpha secretion of human monocytes is enhanced by serum binding proteins and depends on protein tyrosine kinase activation.

The acute phase protein, alpha1 acid glycoprotein (AGP), stimulated human mononuclear cells as well as monocytes to secrete tumor necrosis factor-alpha (TNFalpha) which was demonstrated by ELISA, RT-PCR and functional assays. AGP-induced TNFalpha secretion of monocytes was enhanced in the presence of human plasma and inhibited by protein kinase inhibitors, indicating it is serum and tyrosine kinase dependent. The activation of tyrosine kinase in AGP-stimulated monocytes was further confirmed by immunoblotting of tyrosine phosphorylated proteins of monocytes at different time after AGP stimulation. Furthermore, several serum proteins such as C3, sCD14 and IgG were able to bind to AGP and enhanced TNFalpha secretion of human monocytes induced by AGP. Taken together, these results suggest serum proteins binding to AGP enhance its ability to stimulate human monocytes to secrete pro-inflammatory cytokines through a tyrosine kinase dependent pathway.

Blood Proteins↗
PubMed1999

Analysis of the expression of Fas-L in nasopharyngeal carcinoma tissues.

Nasopharyngeal carcinoma (NPC) is an epithelial cancer with a high incidence in Southeast Asia. How it escapes attack from the host immune system is not fully understood. Recently, pieces of evidence show that Fas-ligand (Fas-L)-mediated apoptosis may be involved in immune privilege of tumours. To determine whether a similar mechanism may exist in NPC, the expression of Fas-L was analysed. Biopsy specimens of the nasopharynx were taken from 27 NPC patients. Histologically, they were either non-keratinizing or undifferentiated carcinomas. Nasopharyngeal biopsies of 11 other patients that proved to have no tumour served as control. The transcripts of Fas-L were detected by reverse transcription-polymerase chain reaction. Localization of Fas-L protein was performed with immunohistostaining using an antibody recognizing human Fas-L. All nasopharyngeal tissues have a similar amount of transcripts of Fas-L. However, the Fas-L protein was detected exclusively on the cell surface of malignant epithelial cells of NPC. The present findings suggest that Fas-L protein may be involved in evading immune attack of NPC.

Fas Ligand Protein↗
PubMed1999

Attenuation of house dust mite Dermatophagoides farinae-induced airway allergic responses in mice by dehydroepiandrosterone is correlated with down-regulation of TH2 response.

BACKGROUND: Dehydroepiandrosterone (DHEA), an abundant androgen in circulation, has important immunomodulating effects on T-cell differentiation; however, it is not known whether this hormone influences allergic responses. OBJECTIVE: We have established a murine model of airway inflammation induced by house dust mite Dermatophagoides farinae (Der f). Der f challenge of sensitized mice would elicit a pulmonary eosinophilic inflammation. In the present study, we employed this model system to explore the effect of DHEA on allergic responses. METHODS: Female BALB/c mice were fed with a standard diet incorporated with 1.5% (w/w) of DHEA for 1 week before sensitization and every other day for an additional 2 weeks after sensitization. After intratracheal inoculation of allergen, the Der f-induced airway inflammation, immunoglobulin (Ig)E antibody production, and cytokine expression were compared between control and DHEA-fed mice. RESULTS: In control mice the Der f-induced eosinophilia in bronchoalveolar lavage (BAL) fluids was accompanied by an increase in production of interleukin (IL)-4, IL-5, and interferon IFN-gamma systemically and locally. DHEA supplementation did not affect the body weight of mice. However, in mice that were receiving DHEA, the numbers of eosinophils and lymphocytes in BAL fluids significantly decreased at days 2 and 6 after challenge as compared with control mice. Concomitantly, total IgE antibody concentrations as well as IL-4, IL-5, and IFN-gamma levels in BAL fluids or serum also significantly reduced. Immunocytochemical staining of BAL cells revealed that there were fewer IL-4-, IL-5-, IL-10-, but not IFN-gamma-positive stained cells in DHEA-fed mice than in mice who consumed unsupplemented diet. Reverse transcription-polymerase chain reaction analysis demonstrated DHEA decreased the expression of IL-5 and IL-10 transcripts in BAL cells. CONCLUSIONS: Our results showed that administration of DHEA during allergic sensitization could attenuate the subsequent allergic responses elicited by challenge, and that the suppressive effect of DHEA was associated with a down-regulation of TH2 response.

Animals↗
PubMed1999

Antioxidant administration inhibits exercise-induced thymocyte apoptosis in rats.

PURPOSE: The purpose of this study was to investigate the effect of antioxidant on exercise-induced apoptosis in rat thymocytes. METHODS: After exercise at 13.8 m x min(-1) for 60-90 min x d(-1) on a motor-driven drum exerciser for 2 consecutive days, rat thymocyte apoptosis was monitored by the feature of DNA fragmentation. To study the effect of antioxidant, rats were administered with butylated hydroxyanisole (BHA) for 7 d before exercise. RESULTS: Exercise could induce thymocyte DNA fragmentation as detected on electrophoretic gel and by cell death detection ELISA kit. Further studies indicated that pretreatment with antioxidant BHA to rats resulted in a blockage of exercise-induced DNA fragmentation. The concentrations of glutathione (GSH) were not significantly changed in rat thymocytes after exercise with or without BHA treatment. CONCLUSION: These results suggest that reactive oxygen species may play a role in thymocyte apoptosis induced by exercise. However, changes in GSH levels were not observed in this exercise model.

Analysis of Variance↗
PubMed1999

Fosinopril: pharmacokinetics and pharmacodynamics in Chinese subjects.

This study examined thepharmacokinetics and pharmacodynamics of fosinopril (IVand oral) in Chinese subjects to determine whether they were different from a group of somewhat heavier and older Western control subjects previously published using the same methods. It was an open-label, randomized, balanced, two-way crossover study comparing oral and IV pharmacokinetics in 12 healthy Chinese subjects in a clinic in Taiwan. Each subject received 10 mg of oral fosinopril or 7.5 mg of IV fosinoprilatin a randomized sequence with sampling for fosinoprilat concentrations over 48 hours. Standard pharmacokinetics, including AUC, Cmax Tmax, T 1/2, Vss, bioavailability, total clearance, and renal and nonrenal clearance, were determined as well as pharmacodynamic effects on angiotensin-converting enzyme (ACE) activity. Following oral administration of 10 mg fosinopril, AUC0-T and AUCinf were 1,556 +/- 586 ng x hr/mL and 1,636 +/- 620 ng x hr/mL, respectively; T 1/2 was 17.4 +/- 11.4 hr; Cmax was 183.4 +/- 59.4 ng/mL; and median Tmax was 4.0 hr, with > 99% protein binding. Following IV administration of 7.5 mg fosinoprilat, AUC0-T and AUCinf were 7,727 +/- 2,638 ng x hr/mL and 7,816 +/- 2,693 ng x hr/mL, respectively; T 1/2 was 13.0 +/- 5.2 hr; and median Tmax was 4.0 hr, with 99.5% +/- 0.22% protein binding and a Vss of 5,850 +/- 2,780 mL. Bioavailability was 22.3% +/- 7.9%. Percent urinary excretion was 7.6% +/- 2.6% after oral dosing and 42.6% +/- 6.1% after IV dosing. After IV, dosing total clearance was 1,088 +/- 439 mL/hr, renal clearance was 472 +/- 213 mL/hr, and nonrenal clearance was 617 +/- 246 mL/hr. ACE inhibition was essentially complete through 12 hours and markedly reduced through 24 hours. Compared to a somewhat heavier and older previously reported control group, pharmacokinetic values were similar except for a slightly lower AUC and total clearance in Chinese and a statistically significantly lower nonrenal clearance. Pharmacodynamic effects on ACE activity were essentially identical. There is no reason to expect significant differences in fosinopril dosing or effect in a Chinese population compared to a Western population.

Administration, Oral↗
PubMed1999

Role of TGF-beta1 in platelet-mediated cardioprotection during ischemia-reperfusion in isolated rat hearts.

Platelets protect myocardium against ischemia-reperfusion injury. This study examined the role of platelet-derived TGF-beta1 in cardioprotection during ischemia-reperfusion. Isolated Sprague Dawley rat hearts were perfused with K-H buffer and subjected to 25 min of global ischemia followed by 30 min of reperfusion. Ischemia-reperfusion resulted in myocardial dysfunction indicated by increase in CPP and LVEDP, and decrease in dLVP. Perfusion of hearts with washed platelets or supernatant of aggregated platelets attenuated (P < 0.01) of myocardial dysfunction following ischemia-reperfusion. Ischemia-reperfusion resulted in a decrease in myocardial TGF-beta1 determined by immunohistochemistry. ELISA showed an increase in latent TGF-beta1, but a decrease in active TGF-beta1. Perfusion of hearts with platelets or aggregated platelet supernatant preserved myocardial TGF-beta1 content upon ischemia-reperfusion. Perfusion of hearts with recombinant TGF-beta1 also resulted in cardioprotection following ischemia-reperfusion qualitatively similar to that observed with platelets or aggregated platelet supernatants. RT-PCR analysis showed an increase in myocardial TGF-beta1 mRNA following ischemia-reperfusion. These observations indicate that platelets protect the myocardium against ischemia-reperfusion-mediated dysfunction at least in part by releasing TGF-beta1. Increase in both TGF-beta1 mRNA and latent TGF-beta1 does not indicate a defect in the translation of mRNA. Reduction in myocardial TGF-beta1 following ischemia-reperfusion suggests a defect in the conversion of latent TGF-beta1 to active TGF-beta1.

Animals↗