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Biomedical subjects

C F Yang

Publications and source records attributed to C F Yang.

At least 19 recordsLinked to original sources
PubMed2001

Protection of salvia miltiorrhiza against aflatoxin-B1-induced hepatocarcinogenesis in Fischer 344 rats dual mechanisms involved.

Extract of Salvia Miltiorrhiza (SM) has been widely used in traditional Chinese medicine for treating liver diseases. Recent experimental evidence indicates that it has anti-tumor potential. In this study, the effect of SM on alfatoxin B1 (AFB1)-induced hepatocarcinogenesis was investigated in male Fischer 344 rats. AFB1 (40 microg/100 g body wt, by gavage) was administered once a week for 24 weeks. In SM treatment group, rats were given SM (0.25g/100g body wt, 5 days/week by gavage) for a total of 28 weeks, including 4 weeks before and 24 weeks during AFB1 exposure. Results showed that the elevation of serum alanine aminotransferase and aspartate aminotransferase activities due to AFB1 dosing was almost completely abolished by the treatment of SM, indicating that SM could prevent AFB1-induced liver cell injury. It was further observed that SM substantially reduced glutathione S-transferase placenta form (GST-P) positive foci formation and GST-P mRNA expression caused by AFB1, which clearly suggests that SM is effective in preventing AFB1-induced hepatocarcinogenesis. Furthermore, the inhibition on AFB1 hepatocarcinigenesis was associated with a corresponding decrease in AFB1-DNA adducts formation as well as AFB1-induced oxidative DNA damage (8-hydroxydeoxyguanosine) in rat liver. Our results also indicate that the protective effect of SM might be mediated through dual mechanisms: (i) the enhancement of AFB1 detoxification pathway, especially the induction of GST-Yc2 mRNA expression, and (ii) the antioxidant property of SM.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2001

Detection of Kaposi sarcoma-associated herpesvirus in bone marrow biopsy samples from patients with multiple myeloma.

BACKGROUND: Kaposi sarcoma-associated herpesvirus (KSHV) recently has been identified in the bone marrow (BM) dendritic cell of multiple myeloma (MM) patients. However, whether or not KSHV is associated with MM remains controversial because many studies have failed to detect the presence of KSHV DNA sequences in the BM of their MM patients. METHODS: We have assayed for KSHV DNA sequences in the BM biopsy samples from 49 patients with MM and from 8 patients with normal BM, using nested polymerase chain reaction and dot blot analysis. The polymerase chain reaction product of KSHV was further determined by single-strand conformation polymorphism and sequence analyses. RESULTS: KSHV DNA was detectable in 22 of 49 patients (44.9%) with MM but was not detectable in normal BM cells. Single-strand conformation polymorphism and sequence analyses showed that there were interpatient specific mutations. Sixteen out of 22 KSHV DNA sequences belonged to a previously defined subgroup, and the other 6 remain unclassified and may represent distinct strains of KSHV in Taiwan. CONCLUSIONS: Data strongly supported that KSHV infection did exist in the BM of the current study patients with MM. However, the role of KSHV in the pathogenesis of multiple myeloma remains to be determined.

Adult↗
PubMed2001

Superoxide radical-initiated apoptotic signalling pathway in selenite-treated HepG(2) cells: mitochondria serve as the main target.

The exact role of superoxide radicals (O(2)(*)(-)) in apoptosis is still a matter of debate. The main objective of the present study is to evaluate the apoptotic signalling pathway initiated by O(2)(*)(-). The reductive reaction of sodium selenite with glutathione was used as the intracellular O(2)(*)(-)-generating system. When cells were exposed to 5 to 25 microM selenite, a temporal pattern of apoptotic events was observed following the elevation of O(2)(*)(-), in which cytochrome c release and mitochondrial depolarization preceded caspase-3 activation and DNA fragmentation. The simultaneous treatment with N-acetylcysteine and 4-hydroxy-2,2,6, 6-tetramethylpiperidine-N-oxyl markedly reduced O(2)(*)(-) level and suppressed the mitochondrial changes and the downstream apoptotic events. Moreover, pretreatment with cyclosporin A plus trifluoperazine, two mitochondrial permeability transition (MPT) inhibitors, was capable of attenuating O(2)(*)(-)-mediated cytochrome c release and mitochondrial depolarization, and subsequently inhibiting apoptosis. Thus, the present results provide convincing evidence that O(2)(*)(-) generated from the reductive reaction of selenite with GSH is capable of triggering a mitochondria-dependent apoptotic pathway. Such knowledge may not only help to obtain a better understanding of the apoptotic effect of selenite per se, but of the role of O(2)(*)(-) in initiation and execution of apoptosis.

Acetylcysteine↗
PubMed2001

Adsorptive behavior and electrochemical determination of the anti-fungal agent ketoconazole.

The adsorptive properties and electrochemical behavior of ketoconazole, an oral anti-fungal agent, are demonstrated at a glassy carbon electrode. The adsorption of the compound obeys the Frumkin isotherm with an interaction factor (alpha) of 0.985 and adsorptive coefficient (beta) of 1.98 x 10(6) L mol(-1). The Gibbs energy of adsorption (deltaG) is -3.59 x 10(4) J mol(-1) at 25 degrees C. A very sensitive electroanalytical method has been developed for determination of the drug with a detection limit of 4.0 x 10(-11) mol L(-1). Relationships between stripping current and concentration of ketoconazole were linear in the range 10(-6)-10(-10) mol L(-1) with different preconcentration periods. The method has been used to measure the ketoconazole content of tablets.

Adsorption↗
PubMed2001

In vivo proton MR spectroscopy of chorea-ballismus in diabetes mellitus.

The most common cause of chorea-ballismus (CB) is a vascular lesion; it is also associated with nonketotic hyperglycaemia in diabetes mellitus (DM) and may be the first manifestation of this disorder. We describe the CT, MRI and proton MR spectroscopy (1H-MRS) of CB in eight patients. Six had hemichorea-hemiballismus (HC-HB) and two bilateral CB. Single-voxel (SV) 1H-MRS was performed using point-resolved spectroscopy (PRESS). Voxels were positioned in the basal ganglia of the patients and control subjects. PRESS was also used to obtain spectroscopic imaging (1H-MRSI) of the slice of interest in two patients. CT showed a slightly dense striatum in all the patients with CB, and T1-weighted images revealed high signal. The CB correlated well with the neuroimaging findings. SV 1H-MRS showed the mean (+/- SD) N-acetylaspartate (NAA)/ creatine (Cr) ratio to be 1.45 +/- 0.19 in HC-HB and 1.82 +/- 0.06 on the opposite normal side (P = 0.01). The choline (Cho)/ Cr ratio was 1.3 +/- 0.12 in HC-HB and 1.11 +/- 0.13 on the opposite normal side (P = 0.005). A lactate peak was seen in seven patients. The NAA/Cr ratio was 1.44 +/- 0.15 in bilateral CB and 1.74 +/- 0.16 in the controls (P = 0.017); the Cho/Cr ratios were 1.36 +/- 0.1 and 1.19 +/- 0.07 (P = 0.015). The low NAA/Cr suggests neuronal loss or damage and the high Cho/Cr probably indicates gliosis. The presence of lactate may suggest mild ischaemia due to acute vascular events during hyperglycaemia and underlying chronic focal cerebrovascular diseases in DM.

Aged↗
PubMed2001

Mutation analysis of Crouzon syndrome and identification of one novel mutation in Taiwanese patients.

BACKGROUND: Crouzon syndrome is an autosomal dominant disorder causing premature fusion of the cranial suture. Mutations have been reported in exon IIIa or IIIc of the fibroblast growth factor receptor 2 (FGFR2) gene. METHODS: In the present study, nine unrelated Crouzon syndrome patients were screened for mutations in the two exons of FGFR2 by polymerase chain reaction and direct sequencing. RESULTS: Mutations were detected in 67% (6/9) of all cases. More than half the studied Crouzon patients carried a mutation resulting in either the loss or gain of a cysteine residue. A novel mutation, Tyr281Cys substitution, was discovered at exon IIIa. CONCLUSIONS: The mechanisms by which the same genotypes cause different phenotypes for each type of craniosynostosis syndrome in still uncertain. However, the molecular identification of the FGFR gene has made a great impact on the clinical classification of craniosynostosis syndromes; a new classification based on genotypes seems to be unavoidable.

Asian People↗
PubMed2001

Non-point pollution from China's rural areas and its countermeasures.

Most lakes in the eastern part of China are eutrophic and non-point pollution accounts for more than half of the nutrient load to the lakes and reservoirs. Some efforts have been made to reduce the non-point source pollution in the catchments of sensitive water bodies. Technologies for the control of non-point pollution in Chinese rural areas are multipond systems, biogas fermentation, hilly area ecological agriculture, constructed wetlands, ecotone engineering and others. They are effective in the removal of nutrients from the runoff water or reduction of waste, and they are used with multi-purposes. To control non-point pollution, the cooperation with farmers and other residents in the countryside is the key to success, and the program has to consider their benefits. There are still many difficulties with its control, and more efforts are needed to develop suitable technologies and environmental education.

Agriculture↗
PubMed2001

Mucopolysaccharidosis type VI: Report of two Taiwanese patients and identification of one novel mutation.

Mucopolysaccharidosis type VI (MPS VI) is an autosomal recessive lysosomal storage disease caused by a deficiency of N-acetylgalactosamine-4-sulphatase (arylsulfatase B, ASB). We report the clinical investigation and mutation analysis of two Taiwanese patients with severe (Case 1) and intermediate (Case 2) phenotypes of MPS VI. Three missense mutations and one polymorphism were identified. Case 1 was found to have a novel heteroallelic C-to-G transversion at nucleotide 1197 causing a phenylalanine to leucine substitution at residue 399 (Phe399Leu), and a heteroallelic Gln239Arg mutation. In Case 2, a heterozygous Cys192Arg mutation and a Val358Met polymorphism were identified. Among these three mutations, the Gln239Arg and Phe399Leu substitutions have so far been observed only in the Taiwanese population. The correlation between genotype and phenotype contributes to molecular pre- and post-natal diagnosis for MPS VI patients.

Adolescent↗
PubMed2001

Intramedullary spinal cryptococcoma: a case report.

Intramedullary spinal cryptococcosis is very rare. We describe a case of intramedullary spinal cryptococcoma at the T12 level in a 60-year-old man who presented with a 3-month history of progressive bilateral lower limb weakness and no obvious immunocompromise. Magnetic resonance (MR) imaging revealed a 1.2 cm diameter mass within the spinal cord at T12 with intermediate signal intensity on T1-weighted images, a slight degree of homogeneous low signal intensity on T2-weighted images, and intense enhancement after infusion of gadopentetate dimeglumine. These findings led to a preoperative diagnosis of intramedullary tumor. After 2 months of postoperative antifungal treatment, the patient's clinical condition had markedly improved. Cryptococcoma should be considered when an enhancing lesion of the spinal cord is found on MR imaging, even in apparently immunocompetent patients. A careful lumbar puncture for cerebrospinal fluid analysis to diagnose cryptococcosis of the central nervous system should be made promptly, as early treatment is associated with a good prognosis.

Cryptococcosis↗
PubMed2000

Intracellular thiol depletion causes mitochondrial permeability transition in ebselen-induced apoptosis.

Ebselen, a selenoorganic compound, has recently been shown to display a novel property of inducing apoptosis through rapid depletion of intracellular thiols in human hepatoma cells, HepG(2). The present study was thus designed to explore the mechanism of how ebselen triggers apoptosis upon depletion of intracellular thiols. The results demonstrated that ebselen treatment triggered mitochondrial permeability transition rather rapidly as revealed by redistribution of calcein green fluorescence from cytosol into mitochondria. Ebselen treatment also caused a dose- and time-dependent loss of mitochondrial membrane potential (MMP) and release of cytochrome c. Pretreatment with N-acetylcysteine, a precursor of intracellular reduced glutathione (GSH) synthesis, significantly attenuated the ebselen-induced MMP disruption and subsequently inhibited the apoptosis. In contrast, pretreatment with buthionine sulfoximine, a specific inhibitor of intracellular GSH synthesis, significantly augmented the ebselen-induced MMP alteration, and enhanced the apoptosis. Although ebselen treatment significantly increased the intracellular superoxide radical and calcium concentrations, superoxide dismutase, and BAPTA (a calcium chelator), however, failed to prevent ebselen-induced MMP loss and apoptosis. Neither caspase-9 nor caspase-3 activation was detected in ebselen-treated cells. Z-VAD-FMK, a general caspase inhibitor, also had no effect on ebselen-induced MMP decrease and apoptosis. The overall findings thus suggest that mitochondrial permeability transition resulted from intracellular thiol depletion is a critical event in ebselen-induced apoptosis.

Acetylcysteine↗
PubMed2000

Ebselen induces apoptosis in HepG(2) cells through rapid depletion of intracellular thiols.

Ebselen, 2-phenyl-1,2-benzisoselenazol-3(2H)-one, is a synthetic seleno-organic compound with antioxidant capability. In the present study, we systematically examined the ability of ebselen to induce apoptosis in a human hepatoma cell line, HepG(2). Ebselen-induced apoptosis was evaluated by (i) TdT-mediated dUTP nick end labeling assay; (ii) analysis of sub-G1 cells; (iii) cell morphology, including cell size and granularity examination; and (iv) DNA gel electrophoresis. The results showed that ebselen was able to induce typical apoptosis in HepG(2) cells in a dose- and time-dependent manner. In order to explore the possible mechanisms involved in ebselen-induced apoptosis, the effect of ebselen on intracellular thiol concentrations including reduced glutathione (GSH) and protein thiols and the effect of N-acetylcysteine (NAC) and buthionine sulfoximine (BSO) pretreatment on ebselen-induced apoptosis were investigated. It was found that (i) ebselen rapidly depleted intracellular GSH and protein thiols, moreover, the depletion preceded the occurrence of apoptosis; (ii) NAC, a precursor of intracellular GSH synthesis, significantly alleviated ebselen-induced apoptosis; and (iii) BSO, a specific inhibitor of intracellular GSH synthesis, augmented ebselen-induced apoptosis significantly. Taken together, the present study demonstrates that ebselen is able to induce apoptosis in HepG(2) cells, most probably through rapid depletion of intracellular thiols.

Antioxidants↗
PubMed2000

Molecular analysis of Wilson disease in Taiwan: identification of one novel mutation and evidence of haplotype-mutation association.

Wilson disease (WND) is caused by a deficiency of the copper-transporting enzyme, P-type ATPase (ATP7B). Twelve different mutations have previously been identified in Taiwan Chinese with Wilson disease. We, herein, report another 4 missense mutations, 1 of which is novel. We did haplotype analysis of Taiwanese WND chromosomes, using three well characterized short tandem repeat markers (haplotype was assigned in the order of D13S314-D13S301-D13S316). Association correlation was found between the mutations and their respective haplotypes. Haplotype-deduced pedigree analysis was shown to be helpful in the mutation analysis of WND chromosomes and in the molecular assessment of both pre-symptomatic WND patients and carriers. Given the complexity and heterogeneity of the mutation spectrum of ATP7B, we suggest that haplotype analysis should be performed before full-scale mutation analysis.

Adenosine Triphosphatases↗
PubMed2000

Protective effect of ebselen on aflatoxin B1-induced cytotoxicity in primary rat hepatocytes.

Recent studies have shown that aflatoxin B1 enhances reactive oxygen species formation and causes oxidative damage, which may ultimately contribute to the cytotoxicity and carcinogenic effect of aflatoxin B1. Ebselen, 2-phenyl-1,2-benzoisoseleazol-3(H)-one, a synthetic seleno-organic compound has been shown to possess glutathione peroxidase-like activity and free radical scavenging ability. Thus present study was designed to investigate the protective effect of ebselen on aflatoxin B1-induced cytotoxicity in primary rat hepatocytes. Aflatoxin B1-induced cytotoxicity and lipid peroxidation were determined by lactate dehydrogenase leakage and malondialdehyde generation, respectively. Intracellular reactive oxygen species level was measured using the fluorescent probe 2',7'-dichlorofluorescin diacetate, and the intracellular reduced glutathione concentration was determined with a fluorometric method. Ebselen was found to display a dose-dependent protective effect on lactate dehydrogenase leakage and malondialdehyde generation caused by aflatoxin B1 exposure. The results also demonstrate that ebselen efficiently inhibits the intracellular reactive oxygen species formation in aflatoxin B1-treated hepatocytes in a dose and time-dependent manner. It was also noted that ebselen was able to increase the intracellular reduced glutathione concentration, both in the control and in aflatoxin B1-treated hepatocytes. The protection of ebselen against aflatoxin B1 cytotoxicity, however, was not affected by lowering the concentration of intracellular reduced glutathione. The overall data indicate that ebselen possesses a potent protective effect against aflatoxin B1-induced cytotoxicity, and the main mechanism involved in the protection may be its strong capability in inhibiting intracellular reactive oxygen species formation and preventing oxidative damage.

Aflatoxin B1↗
PubMed2000

Inhibition of ebselen on aflatoxin B(1)-induced hepatocarcinogenesis in Fischer 344 rats.

Aflatoxin B(1) (AFB(1)), a potent hepatocarcinogen, enhances ROS formation and causes oxidative DNA damage, which may play a role in its carcinogenicity. We have demonstrated recently that ebselen, an organic selenium compound, protects against the cytotoxicity of AFB(1) through its antioxidant capability. The present study was designed to investigate the effect of ebselen on AFB(1)-induced hepatocarcinogenesis in an animal model. Fischer 344 rats were first treated with either deionized water or ebselen (5 mg/kg, 5 days/week) via gavage for 4 weeks, then given AFB(1) (0.4 mg/kg, gavage, once a week) or AFB(1) plus ebselen (5 mg/kg, 5 days/week) for another 24 weeks. The results showed that the hepatocarcinogenicity of AFB(1) in rats was significantly reduced by ebselen treatment as indicated by a decrease in: (i) serum gamma-glutamyl transpeptidase activity; (ii) expression of mRNAs of liver alpha-fetoprotein and the placental form of glutathione S-transferase (GST-P); and (iii) the area and mean density of staining of liver GST-P foci. Ebselen treatment significantly reduced the formation of hepatic AFB(1)-DNA adducts and 8-hydroxydeoxyguanosine caused by AFB(1) exposure. These findings suggest that ebselen can inhibit the carcinogenicity of AFB(1). In addition to the reduction of AFB(1)-DNA adduct formation, the protective effect of ebselen against AFB(1)-induced oxidative DNA damage may also, at least in part, contribute to its anticarcinogenic property.

8-Hydroxy-2'-Deoxyguanosine↗