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Biomedical subjects

C F Chang

Publications and source records attributed to C F Chang.

At least 181 records · Page 10Linked to original sources

Isolation of Candida albicans and their sensitivity to antifungal agents.

During 1978 and 1979 outbreaks of candidiasis were encountered in about 500,000 broiler chickens on 30 farms, 30,000 guinea fowl on 4 farms, 500 geese on 1 farm, and 10 penguins in a zoo. This represents the first report of avian candidiasis in Taiwan. Diagnoses were based on typical gross and microscopic pathology consistent isolation of Candida albicans from crop and esophageal lesions, virulence of isolates in rabbits, identification of the isolates as C. albicans serotype A by chlamydospore and germ tube formation, fermentation tests, and agglutination by specific antisera, and the lack of any sign of fowl pox or trichomoniasis. The upsurge of candidiasis is attributed to the modernization stressors which interact deleteriously with opportunistic pathogens. In vitro sensitivity testing recorded the following order of effectiveness against 20 isolates: nystatin greater than gentian violet greater than copper sulfate = propionic acid = p-hydroxy benzoic acid greater than calcium propionate = propylene glycol.

Animals↗

Pathogenesis on the experimental infections of Candida albicans in chickens.

Systemic candidiasis were induced in chickens by both intravenous and subcutaneous injections of viable Candida albicans. However, infection was not encountered by intratracheal or oral injections. Pathologically, necrotic foci were found in the brain, heart, and spleen but not in the liver, kidney and lungs of the diseased chickens. Numerous segments of the pseudomycelium were seen in the necrotic areas which were surrounded by foreign body giant cells. Pure cultures of the agent were successfully isolated from the necrotic tissues. C albicans seemed to have an affinity for the brain and heart in chickens instead of the kidney which is focus of infections in rabbits.

Animals↗

Experimental ochratoxicosis in turkey poults.

Graded concentrations of ochratoxin A (0, 1, 2, 4, and 8 micrograms/g of feed) incorporated into the diet of turkey poults from hatching until 3 weeks of age resulted in a decreased growth rate, enlarged proventriculus and gizzard, and a regressed thymus (all at 4 and 8 micrograms/g) and the sizes of liver, spleen, pancreas, kidneys, bursa of Fabricius were unaffected. Feed conversion ratio increased from 1.63 (control value) to 2.07 (8 micrograms/g). Mortality was increased significantly (P less than .05) at 8 micrograms/g. Water consumption and plasma uric acid were increased at 4 and 8 micrograms/g. Plasma glucose and the dry weight of the kidneys decreased significantly at 8 micrograms/g while total plasma proteins, prothrombin time, plasma carotenoids, and phenol red clearance rate were unaltered. A leucocytopenia, which was primarily a lymphocytopenia, was observed at 4 and 8 micrograms/g. Heterophils decreased while basophils increased at 8 micrograms/g. The oral LD50 for day-old and 3-week-old poults was 4.63 +/- .31 and 7.84 +/- .94 mg/kg, respectively. Intraperitoneally, the value for day-old birds was .16 +/- .03 +/- mg/kg and for 3-week-old birds was .34 +/- .09 mg/kg. These data suggest that ochratoxin is a potent nephrotoxin in turkeys, but that ochratoxicosis in turkeys differs markedly from the disease in other species.

Animal Feed↗

Impairment of phagocytosis by heterophils from chickens during ochratoxicosis.

The effect of graded concentrations of dietary ochratoxin A (0, O.5, 1.0, 2.0, 4.0, and 8.0 microgram/g of diet) on the in vitro phagocytic, locomotory, and bactericidal capacities of heterophils from broiler chickens was investigated. Both the percentage and the mean phagocytic activities were decreased significantly (P less than 0.05) at 4.0 and 8.0 microgram/g. Both directed and undirected locomotion of heterophila was impaired significantly at the same concentrations. A crossover experiment revealed that the reduced percentage of phagocytosis was associated with the heterophil itself and not with a serum factor such as complement. Heterophila from birds that consumed 4.0 microgram/g were not impaired in ability to kill engulfed bacteria.

Animals↗

Demonstration of an altered S-adenosylmethionine synthetase in human malignant tumors xenografted into athymic nude mice.

S-Adenosylmethionine synthetase isoenzymes (EC 2.5.1.6) were studied in human malignant tumors xenografted into athymic nude mice and were studied in normal human and rat tissues. The tumors included 7 melanomas; 4 colon carcinomas; 3 each of mammary, cervical, and ovary carcinomas; 2 each of lung carcinomas and sarcomas; and 1 each of lymphoma and stomach and nasopharyngeal carcinomas. The presence of an altered intermediate Michaelis constant (Km) isoenzyme, previously shown to be a unique characteristic of rat neoplastic tissues, in these tumors was invariably detectable, though the presence of the low-Km isoenzyme characteristic of the enzyme of normal tissues was also evident in many of these tumors. Only tumors demonstrating high rates of growth were devoid of the low-Km isoenzyme. The low-Km isoenzyme was the only enzyme detectable in many normal human and rat tissues. Thus this isoenzyme was probably the common enzyme of all tissues. Some additional organ-specific isoenzymes were found, e.g., in the liver and lactating mammary gland. The low-Km isoenzyme in malignant tumors was altered to assume a considerably higher Km value, and this alteration appeared to be a common aberration of malignant tumors.

Animals↗

Ochratoxin A-induced iron deficiency anemia.

Ochratoxin A at 8 micrograms per g of diet, but not at lower doses, fed to chickens from 1 day to 3 weeks of age resulted in significantly (P less than 0.05) decreased packed blood cell volume and hemoglobin concentration without altering the number of circulating erythrocytes. Serum iron and percentage of transferrin saturation were lowered at 4 and 8 micrograms/g. Therefore, anemia was characteristic of severe ochratoxicosis of young chickens, and the anemia was categorized as a hypochromic-microcytic anemia of the iron deficiency type. These data indicate that ochratoxin A by itself does not cause hemorrhagic anemia syndrome of chickens and that an anemia caused by a nutritional deficiency can be elicited by a mycotoxin.

Anemia, Hypochromic↗

A leucocytopenia induced in chickens by dietary ochratoxin A.

Ochratoxin A was fed (0, .5, 1.0, 2.0, 4.0, and 8.0 microgram/g) to broiler chickens from day-old to three weeks of age when the birds were bled and total leucocyte and differential counts were performed. Ochratoxin A significantly (P less than .05) reduced leucocyte counts at every dose level of ochratoxin A administered. The leucocytopenia was characterized by an increase in the relative concentration of heterophils and decrease in the relative concentration of lymphocytes. From total leucocyte and differential leucocyte counts the number of circulating cells was calculated for each type of leucocyte. The total number of circulating lymphocytes of blood decreased significantly (P less than .05) at every dose level of ochratoxin A administered, and the number of monocytes decreased at 2.0 microgram/g and above. However, the number of circulating heterophils was not altered. These data demonstrated that ochratoxin A induced a severe leucocytopenia (lympocytopenia primarily and monocytopenia to a lesser extent) and implied that the functioning of the immune system might be altered.

Animals↗

Refractory phagocytosis by chicken thrombocytes during aflatoxicosis.

The percentage phagocytosis of chicken thrombocytes was insensitive to dietary aflatoxin (10 microgram/g diet) while the mean phagocytosis was slightly but significantly (P less than .05) reduced by 5 or 10 microgram/g but not lower levels. Thrombocytic phagocytosis was dependent on a heat sensitive serum factor which is not affected during aflatoxicosis. These findings contrast with reports that other phagocytic types such as heterophils, macrophages, and monocytes are sensitive to low levels (e.g., .625 microgram/g) of dietary aflatoxin.

Animals↗

Impairment of phagocytosis in chicken monocytes during aflatoxicosis.

Graded doses of dietary aflatoxin (0, .625, 1.25, 2.5, 5.0, and 10.0 microgram/g) were tested for their effect on the phagocytic and locomotive capacities of monocytes from chicken blood. The percentage and mean phagocytic activites were decreased significantly (P less than .05) at 2.5 microgram/g and above and at 1.25 microgram/g and above, respectively. Both the directed and undirected locomotion of monocytes were impaired significantly (P less than .05) at 2.5 microgram/g and above. A serum factor with the heat sensitivity of complement and which was required for optimal phagocytosis by monocytes also was reduced in activity during aflatoxicosis. Thus, the circulating element of the mononuclear phagocyte series has reduced capacity to perform its role in host defense during aflatoxicosis.

Animals↗

Investigations on prostatic adenocarcinomas in rats.

Metastatic prostate adenocarcinomas, derived from aging germfree Wistar rats, have been propagated in rats and in tissue culture. A protocol has been developed and demonstrated for assay of treatments which retard or which accelerate the rate and extent of tumor growth and of metastasis in tumor-bearing rats. The pattern of spread has been retarded by cyclophosphamide, aspirin, indomethacin, and Corynebacterium parvum. The spread pattern has been accelerated by oral administrations of sodium barbiturate.

Adenocarcinoma↗

In vitro propagation of prostate adenocarcinoma cells from rats.

Two rat adenocarcinomas were physically dispersed and propagated in vitro. Epithelial and fibroblast cell lines were cloned from them and the monolayer cell lines derived therof were further characterized. The cells produced acid phosphatase in early in vitro cell passages, and later they turned negative. Fibroblast-like cells produced no tumors when implanted in syngeneic Lobund Wistar rats, but as few as 10 epithelial cells produced metastasizing adenocarcinomas in them. A third prostate tumor has yielded a line of epithelial cells which reproduced the original tumor type in inoculated rats, but the cells have not yet been characterized. Rat prostate adenocarcinomas provided a useful model system for in vitro and in vivo studies on prostate cancer and on metatasis.

Acid Phosphatase↗