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Biomedical subjects

M A Gallo

Publications and source records attributed to M A Gallo.

90 records · Page 5Linked to original sources
PubMed1983

'Tis the season.

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Animals↗
PubMed1982

Combined two-generation reproduction-teratogenesis study of zearalenone in the rat.

The toxicity of zearalenone was studied in two generations of Wistar rats over approximately 10 months. Zearalenone was administered in the diet; the dose levels used were 0, 0.1, 1.0 and 10.0 mg per kg body weight per day in all generations. Animals in the F0 generation were bred twice to produce F1A and F1B generations. The F1A generation was bred to produce the F2A generation. The only lesion found at necropsy that could be attributed to zearalenone administration was increased medullary trabeculation of the femur in animals given the high dose. A dose-related increase in absolute and relative thyroid, pituitary and adrenal gland weights occurred in male and female rats of both the F1 and F1A generation. The alteration in the weights of these endocrine organs is probably a result of the estrogenic activity of zearalenone. Feeding of zearalenone caused decreases in fertility, number of viable offspring per litter and numbers of corpora lutea, implantations and resorptions per dam. Statistically significant differences were noted in the incidences of a number of skeletal and soft tissue abnormalities in both the F1B and F2A1 fetuses, especially at doses of 1.0 and 10.0 mg kg-1. These lesions most likely indicate a delay in fetal development. Unequivocal teratogenic effects could not be defined.

Abnormalities, Drug-Induced↗
PubMed1981

Long-term carcinogenicity and toxicity studies of patulin in the rat.

Patulin is a mycotoxin produced by a variety of Penicillium and Aspergillus species which are likely natural contaminants of various foods. The present study was conducted to determine the effects of lifetime administration of patulin in FDRL Wistar rats. Animals received patulin by gastric intubation three times per week at the level of 0.0, 0.1, 0.5 and 1.5 mg per kg body weight. The animals used in this lifetime study were derived from F0 parents exposed to equivalent levels of patulin for 4 weeks before mating, and throughout mating, gestation and lactation. Patulin treatment at 0.5 and 1.5 mg kg-1 to male rats caused a significant decrease in body weight gain in comparison to controls. Body weights of treated female rats were similar to that of control rats. No consistent significant differences among groups were noted in the hematology, clinical chemistry or urine analysis parameters measured during or at the termination of the study. Patulin administered to male and female rats at 1.5 mg kg-1 caused a significantly increased mortality rate as compared to respective control animals. The cause of death appeared to be increased pulmonary and laryngotracheal inflammation. No tumorigenic effect of patulin was observed.

Animals↗
PubMed1976

Residue uptake and depletion measurements of dietary oxadiazon in mammalian and avian species.

The herbicide oxadiazon, 2-(tert-butyl)-4-(2,4-dichloro-5-isopropyloxy-phenyl)-delta 2-1,3,4-oxadiazoline 5-one, was fed in a total diet at three dosage levels to groups of dairy cows (0.5, 2.5, and 25 ppm) and to groups of male and laying female quail (20, 80, and 160 ppm) for 28 days. Control animals received basal diet rations. No residue (less than 5 ppb) was detected in milk or cream after three days withdrawal from fortified feed. The maximum plateau reached in milk was 83.8 ppb at the highest dosage fed. Tissues of cows sacrificed on the 12th day of withdrawal showed no residue (less than 20 ppb). Birds were sacrified at weekly intervals during acclimation, intake, and withdrawal periods. Eggs were collected at the same intervals. Tissues were free of oxadiazon residue (less than 40 ppb) within two to seven days of returning the quail to the basal ration, and the eggs were residue-free within seven to fourteen days. The maximum residue found in adipose tissue of quail and their fresh eggs was 3100 ppb and 5400 ppb, respectively at the greatly exaggerated dosage of 160 ppm in the diet. A comprehensive analytical methodology, including liquid-liquid partition, absorption chromatography and electron-capture gas chromatography will be discussed.

Adipose Tissue↗
PubMed1976

The dominant lethal effect of dietary triethylenemelamine.

Triethylenemelamine (TEM) was administered in the diet to adult male mice at doses of 0.1, 0.3, 1, 10 or 50 mg/kg body weight for 45 days or at doses of 0.1 or 0.3 mg/kg b.w. for 10 days. As a comparison, male mice were treated intraperitoneally with 5 daily doses of 0.25 or 0.5 mg TEM/kg b.w. At the end of the treatment period, males were mated sequentially with 2 untreated virgin females each for 2 or 3 weeks. Near mid-pregnancy the number of implantation sites and fetal deaths were determined. TEM, administered in the diet at 10 or 50 mg/kg b.w. for 45 dyas, was lethal to male mice. Surviving males from the 1 mg/kg level failed to impregnate any females during the two matings. TEM, given in the diet at 0.1 or 0.3 mg/kg for 10 or 45 dyas, decreased fertility and increased dominant lethal mutations in a dose and time dependent manner. These results were comparable to those obtained from males treated i.p. with TEM at 0.25 or 0.5 mg/kg b.w.

Animals↗
PubMedDate not supplied

Interactive effects of estradiol and 2,3,7,8-tetrachlorodibenzo-p-dioxin on hepatic cytochrome P-450 and mouse uterus.

Weanling C57B/6 female mice treated with 6 micrograms/kg 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) 3 times a week for one month (total dose 72 micrograms/kg) were observed to have greatly reduced relative uterine weights and histopathological changes in the uterus. Weanling CD-1 female mice were then treated with estradiol (E2) subcutaneously daily for 2 weeks. Half the mice also received 10 micrograms/kg TCDD in corn oil: acetone (9:1) by gavage 4 times during the second week. Control mice received either no E2 or no TCDD. Mice were killed on day 15 and autopsied. Relative uterine weights increased with increasing E2 doses; however, TCDD decreased this effect of E2 markedly. Liver microsomes from these animals showed that cytochrome P1-450 and P3-450 and, aryl hydrocarbon hydroxylase (AHH) induction by TCDD were independent of E2 dosage. Epoxide hydrolase was induced in TCDD treated animals. Gels showed an E2 dose dependent decrease in a protein migrating near epoxide hydrolase and 'P-450a' in animals receiving both E2 and TCDD. These results suggest that: E2 may act at the TCDD receptor; the TCDD receptor may be related to the estrogen receptor; the anti-estrogenic effects of TCDD are possibly independent of the Ah locus and AHH induction, and in TCDD-treated mice a protein migrating near epoxide hydrolase and 'P-450a' may be controlled by estrogen levels.

Animals↗
PubMedDate not supplied

PCR-based diagnosis of a case of herpetic whitlow in an AIDS patient.

Herpetic infections are common complications in AIDS patients. The clinical features could be uncommon and antiviral chemotherapy is imperative. A rapid diagnosis could prevent incorrect approaches and treatment. The polymerase chain reaction is a rapid, specific and sensible method for DNA amplification and diagnosis of infectious diseases, especially viral diseases. This approach has some advantages compared with conventional diagnostic procedures. Recently we have reported a new PCR protocol to rapid diagnosis of herpetic infections with suppression of the DNA extraction step. In this paper we present a case of herpetic whitlow with rapid diagnosis by HSV-1 specific polymerase chain reaction using the referred protocol.

AIDS-Related Opportunistic Infections↗
PubMedDate not supplied

Differential effects of estradiol and its analogs on cyclin D1 and CDK4 expression in estrogen receptor positive MCF-7 and estrogen receptor-transfected MCF-10AEwt5 cells.

Estradiol stimulates the growth of a majority of human breast tumors containing the estrogen receptors (ERs), proteins that mediates estrogen function. Opposing effects of estradiol have been found in cells expressing endogenous ER and those containing a transfected ER. To understand the role of estradiol structure in diverse estrogenic responses related to cell cycle regulation, we evaluated the effects of estradiol and its analogs on cell cycle progression, and the expression of cyclin D1 and the cyclin dependent kinase 4 (CDK4) in ER-positive MCF-7 and ER-transfected MCF-10AEwt5 cells. Four analogs of estradiol, with a re-positioned or a deleted hydroxyl group, were used. Our results show that estradiol and all of the analogs facilitated cell cycle progression of MCF-7 cells. In contrast, only estradiol inhibited the cell cycle progression of MCF-10AEwt5 cells significantly. Western blot analysis revealed that cyclin D1 protein increased to the maximal level by 6 h after the initiation of cell cycle from G1 phase of MCF-7 cells. The least effective analog in inducing cyclin D1 was 3-hydroxyestratriene. However, this analog was most effective at inducing CDK4, contributing to its efficacy in facilitating MCF-7 cell cycle. In contrast to MCF-7 cells, the level of cyclin D1 protein was not influenced significantly by estradiol or its analogs in MCF-10AEwt5 cells. Sucrose gradient sedimentation analysis of ER from MCF-7 cells showed that the major peak of [3H]-estradiol bound to ER could be displaced by a 10-fold excess of unlabelled estradiol or any of the analogs. In contrast, several analogs were less effective than unlabelled estradiol in competitive displacement of [3H]-estradiol bound to ER from MCF-10AEwt5 cells. These data indicate that the induction of cyclin D1 is an important part of the growth stimulatory effects of estrogens in MCF-7 cells, but it may not be involved in growth inhibition of MCF-10AEwt5 cells. Our results also show that estrogenic compounds interact with ER from MCF-10AEwt5 cells with altered ligand binding affinity, possibly due to the absence or dysfunction of certain transcription factors or ER-associated proteins that co-regulate ER function.

Breast Neoplasms↗