Biomedical subjects

Y F Chang

Publications and source records attributed to Y F Chang.

131 records · Page 8Linked to original sources

PubMed1969

Hexuronic acid dehydrogenase of Agrobacterium tumefaciens.

Growth of Agrobacterium tumefaciens on d-glucuronic acid (GlcUA) or d-galacturonic acid (GalUA) induces formation of hexuronic acid dehydrogenase [d-aldohexuronic acid: nicotinamide adenine dinucleotide (NAD) oxidoreductase]. The dehydrogenase, which irreversibly converts GlcUA or GalUA to the corresponding hexaric acid with the concomitant reduction of NAD, but not of nicotinamide adenine dinucleotide phosphate was purified 60-fold by MnCl(2) treatment, (NH(4))(2)SO(4) fractionation, chromatography on diethylaminoethyl Sephadex and negative adsorption with Ca(3)(PO(4))(2) gel. The pH optimum is 8.0. Other uronic acids, aldohexoses, aldopentoses, and polyols, are not substrates. Reduced nicotinamide adenine dinucleotide is an inhibitor strictly competitive with NAD. Kinetic data indicate that the dehydrogenase induced by growth on GlcUA may not be identical with that induced by growth on GalUA.

Glucuronates↗

PubMedDate not supplied

An evaluation of the incidence of work-related asthma in the United States.

The objective of the study was to estimate the incidences of physician-diagnosed cases of work-related asthma (WRA) in Michigan and the entire United States. The statewide surveillance system for WRA in Michigan receives reports primarily from three sources: physicians, hospital discharge data, and worker's compensation claims. Knowledge of the overlap in reports from these sources was used in conjunction with capture-recapture methods to estimate the total number of diagnosed cases of WRA, and incidence rates were calculated using the estimated number of civilian employees in Michigan as the population at risk. For the entire United States, the product of a national incidence rate for asthma among adults and estimates of the proportion that is work-related was used. A total of 933 cases of WRA were reported to the Michigan surveillance program during 1988-1995, of which 904 were reported by at least one of the three main sources and equaled an average incidence of 27 cases/10(6)/year. This estimate was less than the range of estimates 58 to 204 cases/10(6)/year in Michigan arrived at using the capture-recapture methods. The national estimates of WRA ranged from 63 to 441 cases/10(6)/year. The authors' indirect estimates are closer to estimates from Canada, Sweden, and Finland than most existing direct estimates in the United States, but probably still underestimates the magnitude of WRA incidence because of the limitations of physician recognition of the work-relatedness of asthma among adults.

Adult↗

PubMedDate not supplied

Gastric function in dogs with naturally acquired gastric Helicobacter spp. infection.

The association of Helicobacter pylori with gastritis, peptic ulcers, and gastric neoplasia has led to fundamental changes in the understanding of gastric disease in humans. The relationship of Helicobacter spp. infection to gastric disease in dogs is unclear. The objective of this study was to determine if Helicobacter infection affects the gastric secretory axis of dogs. Eight Beagle dogs with naturally acquired Helicobacter spp. infection were studied before and after (4 and 29 days) the attempted eradication of Helicobacter spp. with a combination of amoxicillin, metronidazole, and famotidine (AMF). Six specific-pathogen-free, Helicobacter-free Beagle dogs served as controls. The electron microscopic appearance of spiral organisms in infected dogs indicated coinfection with Helicobacter felis- and H bizzozeronii-like organisms. Unstimulated gastric pH and fasting, postprandial, and bombesin-stimulated plasma gastrin were similar in both infected and uninfected dogs, although a trend (P = .09) toward higher meal-stimulated gastrin was observed in infected dogs at 60 minutes. Pentagastrin-stimulated maximal acid output (mmol HCI/kg0.75/hour) and titratable acidity (mmol HCl/mL) were similar in both infected and uninfected dogs, but gastric pH during maximal acid output was lower (P < .01) in uninfected dogs. Mild gastric inflammation was present in both infected and uninfected dogs. Gastric spiral organisms were undetectable in 6/8 infected dogs 4 days after AMF but had recurred in 8/8 dogs 29 days after AMF. Analysis of gastric DNA with Helicobacter-specific primers indicated persistence of Helicobacter DNA at 4 and 29 days after antibiotic therapy. Acid secretion, plasma gastrin, and mucosal inflammation were not affected by the transient suppression of Helicobacter spp. by AMF. These findings suggest that gastric secretory function in dogs is not markedly perturbed by naturally acquired Helicobacter spp. infection and that treatment with amoxicillin, metronidazole, and famotidine causes suppression rather than eradication of gastric Helicobacter spp. in dogs.

Animals↗

PubMedDate not supplied

Differential paclitaxel-induced cytotoxicity in rodent and human hepatoma cell lines.

Hepatoma is the leading cause of death in male cancer patients in Taiwan. In this study, we examined the effect of Paclitaxel on the in vitro growth of 2 rodent and 4 human hepatoma cell lines. Differential Paclitaxel-induced cytotoxicity was observed among hepatoma cell lines. In Paclitaxel-sensitive Hep3B and N1S1 cells, Paclitaxel-induced cytotoxicity was dose- and time-dependent. The effective doses of Paclitaxel were in the range 0.1-1.0 microM. Flow cytometric analysis showed that Paclitaxel-treated hepatoma cells were arrested in G2-M phases prior to apoptosis. In addition, growth inhibition by Paclitaxel was accompanied by an increase in the expression of proliferating cell nuclear antigen (PCNA) in hepatoma cells. For Paclitaxel-resistant hepatoma cells, cytostatic response and/or polyploidization was observed. Our results indicated that two thirds of the hepatoma cell lines examined showed some degree of resistance to Paclitaxel treatment in vitro. The expression of p53 gene had no direct effect on Paclitaxel-induced cytotoxicity. The expression of PCNA and the development of polyploidization appear to be good markers for measuring Paclitaxel response. These findings suggest that Paclitaxel alone appears to by cytostatic to hepatoma cells, combination of Paclitaxel with other chemotherapeutic agents may show better cytotoxic effects.

Animals↗

PubMedDate not supplied

Submicromolar paclitaxel induces apoptosis in human gastric cancer cells at early G1 phase.

Paclitaxel induced apoptosis has been reported in many cancer cell lines, but the relationship between G2/M phase arrest and apoptosis is not clear. We have reported that low dose (10 nM) paclitaxel induced apoptosis in gastric cancer cells without G2/M phase arrest. In this study, SC-M1 gastric cancer cells were synchronized at early G1, late G1, S and G2/M phases by staurosporine, mimosine, hydroxyurea and berberine, respectively. We have found that paclitaxel could not induce apoptosis of gastric cancer cells in late G1, S and G2/M phases; however, paclitaxel induced apoptosis in the early G1 phase. Our results suggest that cells arrested at G2/M phase by paclitaxel eventually entered the early G1 phase then proceeded to apoptosis.

Antineoplastic Agents, Phytogenic↗