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Biomedical subjects

J A Render

Publications and source records attributed to J A Render.

At least 19 recordsLinked to original sources

Reproductive toxicity of ergot alkaloids in mink.

Ergot alkaloids are-synthesized by fungi of the Claviceps family that infect rye as well as other cereals and grains. Since a portion of the ranch mink diet is cereal, mink are at a risk of being exposed to ergot alkaloids. This study was performed to determine the reproductive toxicity of ergot alkaloids derived from ergot-contaminated oats in mink. Four groups of 12 female mink each were fed diets containing 0, 3, 6 or 12 ppm ergot alkaloids from 2w prior to the breeding season until the kits were approximately 33-d old (133 d). Females were mated with untreated males. Ergo talkaloids caused a transient decrease in feed consumption, but body weights were unaffected. The gestation period of the mink in the 6 ppm group was longer compared to controls. The number of mink whelping varied significantly with 9 mink whelping each in the control and 3 ppm groups compared to 4 mink in the 6 ppm group and 1 in the 12 ppm group. Ergot alkaloids had a significant effect on kit survivabilitywith no kits surviving in the 12 ppm group. Serum prolactin was significantly depressed in the 3 ergot alkaloid groups compared to the control group. This study indicated that ingestion of ergot alkaloids at 3 ppm or higher resulted in reproductive toxicity in mink.

Animals↗

Persistent fetal intraocular vasculature in the European ferret (Mustela putorius): clinical and histological aspects.

OBJECTIVE: To describe the clinical and histological appearance of persistent fetal intraocular vasculature in a colony of ferrets. Design Prospective study. ANIMALS STUDIED: Eighty-six European ferrets (Mustela putorius). Procedure Both eyes of 76 genetically related progeny and 10 breeding, adult, colony-raised ferrets were studied using a slit lamp biomicroscope and an indirect ophthalmoscope. Ferret progeny were examined after eyelid opening at 5-6 weeks of age, and at 12 months of age. After euthanasia, globes were enucleated and examined histologically. RESULTS: Persistent fetal intraocular vasculature was evident in 21 progeny ferrets at 5-6 weeks of age and in three mature progenitor ferrets. Clinical appearance of diminutive vasculature was characterized by focal remnants of the posterior tunica vasculosa lentis, muscae volitantes, and an occluded hyaloid artery extending from the optic papilla and terminating in the anterior vitreous body. Extensive persistent vasculature was characterized by a perfused hyaloid artery, vasa hyaloidea propria and posterior tunica vasculosa lentis, posterior cortical and capsular cataract, and proliferation of fibrovascular tissue along the posterior lens capsule. Fetal vasculature persisted in 7 of 21 progeny ferrets at one year of age and in three progenitor ferrets. Results of histologic examination showed persistence of the hyaloid vasculature, proliferation of retrolental fibrovascular tissue with osseous metaplasia, posterior capsular and cortical cataract, and occasional retinal detachment. CONCLUSIONS: Persistent fetal intraocular vasculature in ferrets appears similar clinically and histologically to persistent fetal intraocular vasculature reported in humans and dogs. The ferret may be a suitable animal model for vasculogenic mechanisms of persistent fetal intraocular vasculature and for evaluating vasoinhibitory growth factors and angiostatic test compounds.

Animals↗

Squamous epithelial proliferation in the jaws of mink fed diets containing 3,3',4,4',5-pentachlorobiphenyl (PCB 126) or 2,3,7,8-tetrachlorodibenzo-P-dioxin (TCDD).

Previous research has shown that ingestion of 3,3',4,4',5-pentachlorobiphenyl (PCB 126) by juvenile mink (kits) caused a lesion in the mandible and maxilla that consisted of proliferation of sQuamous epithelium in the periodontal ligament, osteolysis of adjacent alveolar bone, and loose and displaced teeth. Similar, but less severe changes, developed in adult mink fed 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). The present study was conducted to compare similarities and differences of the lesion within the jaws of mink fed these 2 polyhalogenated hydrocarbons. Diets containing 24 ppb PCB 126 or 2.4 ppb TCDD were fed to 6-w-old kits for 36 d. Similar diets were fed to 12-w-old kits for 35 d. Some of these mink were then fed untreated feed for an additional 50 d. All mink treated with PCB 126 or TCDD had reductions in body weight gains which were more severe in the 6-w-old kits than the 12-week-old kits. By 28 days of exposure, many of the 6- and 12-week-old mink treated with PCB 126 or TCDD had loose and displaced incisor teeth. Canine teeth were grossly more prominant. Radiographs showed maxillary and mandibular osteolysis with lysis of the lamina dura in treated mink. Withdrawal of the toxicants from the diets of the 12-w-old mink failed to alleviate the lesions, which continued to be progressively more severe.

Administration, Oral↗

Chronic toxicity of dietary 2,3,7,8-tetrachlorodibenzo-p-dioxin to mink.

Mature female natural dark mink (Mustela vison) were fed 0.0006 (control), 0.016, 0.053, 0.180, or 1.40 ppb 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) for 131-132 d to ascertain the chronic toxic effects of TCDD in mink, including reproduction. Consumption of the 1.4 ppb TCDD diet resulted in lethargy, bloody stools, and 16.7% mortality. Final mink body weights were inversely proportional to the dietary TCDD concentrations. Due to subnormal mink breeding, definitive effects of TCDD on mink reproductive performance were not ascertained; however, there were significant dose-dependent decreases in kit (young mink) birth weight and survival from birth to 3 w of age in the groups that had reproduction. There were also significant differences in adult minkwhite blood cell counts, plasma total solids, serum iron, phosphorus, albumin, total protein, total CO2, cholesterol, osmolality, and anion gap concentrations, and alanine aminotransaminase activity between the various dietary groups. During the latter stages alopecia and thickened, deformed, and elongated toenails were observed in the adult mink fed 1.4 ppb TCDD. At termination the mink fed 1.4 ppb TCDD had ascites, gastric ulcers, intestinal hemorrhages, depletion of adipose tissue, and mottled and/or discolored livers, spleens, and kidneys. Focal lymphocytic meningitis in region of the olfactory bulb was present in 42% of the mink fed 1.4 ppb TCDD. These results confirmed the high sensitivity of mink to TCDD and revealed a toenail abnormality not previously reported for mink fed TCDD.

Animals↗

Clinical and pathologic aspects of spontaneous canine prostate carcinoma: a retrospective analysis of 76 cases.

BACKGROUND: Pet dogs and men share a vulnerability for the development of prostate carcinoma. The purpose of this study was to further characterize the clinical and pathologic features of spontaneous canine prostate carcinoma. METHODS: A multiinstitutional, retrospective study was conducted using 76 dogs with prostate carcinoma that underwent postmortem evaluation. For each case, clinical and pathologic data were tabulated and hematoxylin/eosin-stained tissue sections from the primary tumor and metastatic lesions were evaluated. Prostatic carcinomas were subclassified based upon the presence of glandular, urothelial, squamoid, or sarcomatoid differentiation. We focused our analysis on dogs that differed with respect to morphologic features of the primary tumor, lifetime duration of testicular hormone exposure, and presence of skeletal metastases. RESULTS: The vast majority of canine prostate carcinomas affected elderly sexually intact dogs or dogs that underwent surgical castration after sexual maturity. Adenocarcinoma was the most frequent histologic type, although more than half of canine prostate carcinomas exhibited intratumoral heterogeneity. In many cases, primary tumors showed mixed morphology, characterized by two or more types of differentiation. Duration of testicular hormone exposure was significantly different between dogs with adenocarcinoma and dogs with mixed morphology tumor, but did not appear to influence the frequency or pattern of metastases. Overall, gross metastases were present in 80% of dogs with prostate carcinoma. Skeletal metastases were present in 22% of cases, and the predominantly axial skeletal distribution of these lesions was similar to that reported in men with prostate carcinoma. Young dogs were at highest risk for development of skeletal metastases. CONCLUSIONS: This study provides a more complete characterization of spontaneous prostate carcinoma of dogs in terms of morphologic heterogeneity, skeletal metastases, and the influence of testicular hormones. Prostate carcinoma in pet dogs provides an immunocompetent, autochthonous tumor system that mimics certain aspects of human prostate cancer. This spontaneous model may contribute to our understanding of the factors that regulate carcinogenesis within the aged prostate, and to the development of chemoprevention strategies or bone-targeted therapies.

Adenocarcinoma↗

Proliferation of maxillary and mandibular periodontal squamous cells in mink fed 3,3',4,4',5-pentachlorobiphenyl (PCB 126).

This report characterizes squamous cell proliferation in young farm mink (Mustela vison) fed a diet supplemented with 0.024 ppm 3,3',4,4',5-pentachlorobiphenyl (polychlorinated biphenyl [PCB] congener 126). One to 2 months of dietary exposure to PCB 126 resulted in gross lesions of the upper and lower jaws consisting of mandibular and maxillary nodular proliferation of the gingiva and loose teeth. The maxilla and mandible of the PCB-treated mink were markedly porous because of loss of alveolar bone. Histologically, this osteoporosis was caused by proliferation of squamous cells that formed infiltrating cords. This report clearly documents the fact that the environmental contaminant PCB 126 can cause osteoinvasive squamous proliferation in young mink, although the dose used in the present study was 7 and 36 times higher than what is typically encountered in contaminated bird eggs and fish, respectively.

Administration, Oral↗

Effects of waterborne exposure to 4-nonylphenol and nonylphenol ethoxylate on secondary sex characteristics and gonads of fathead minnows (Pimephales promelas).

Fathead minnows were exposed to 4-nonylphenol (NP) or nonylphenol ethoxylate (NPEO) to determine the effects of these weak estrogen agonists on secondary sex characteristics and gonads of sexually mature males and females during 42-day continuous-flow exposures. Neither NP nor NPEO caused statistically significant effects on tubercles or fatpad size at the concentrations tested. Exposure to 1. 1 or 3.4 micrograms NP/L caused changes in the number and size of Sertoli cells and germ cell syncytia. Necrotic aggregates of various stages of germ cells in the spermatogenic sequence were observed in the testes of males exposed to NP. Electron microscopy of the testes of NP-exposed males revealed the presence of phagocytic cells in the lumina of seminiferous tubules. The cytoplasm of some Sertoli cells was distended with myelin figures and necrotic spermatozoa. No significant effects on the stages of follicular development were observed in females exposed to NP. There were no differences in the gonads or secondary sex characteristics of males or females exposed to 5.5 micrograms NPEO/L, the greatest concentration studied. The histologic responses observed are sensitive indicators of waterborne exposure to NP at environmentally relevant concentrations, but not as sensitive as induction of plasma vitellogenin. The secondary sex characteristics were not affected by concentrations of NP or NPEO as great as 3.4 or 5.5 micrograms/L, respectively. Histologic responses occurred at concentrations that were less than the final chronic value based on survival and approximately the same as those required to cause effects on egg production. The histologic effects caused by NP were similar to, but not exactly the same as those caused by exposure of fathead minnows to 17 beta-estradiol.

Animals↗

Amylopectinosis in fetal and neonatal Quarter Horses.

Three Quarter Horses, a stillborn filly (horse No. 1), a female fetus aborted at approximately 6 months of gestation (horse No. 2), and a 1-month-old colt that had been weak at birth (horse No. 3), had myopathy characterized histologically by large spherical or ovoid inclusions in skeletal and cardiac myofibers. Smaller inclusions were also found in brain and spinal cord and in some cells of all other tissues examined. These inclusions were basophilic, red-purple after staining with periodic acid-Schiff (both before and after digestion with diastase), and moderately dark blue after staining with toluidine blue. The inclusions did not react when stained with Congo red. Staining with iodine ranged from pale blue to black. Their ultrastructural appearance varied from amorphous to somewhat filamentous. On the basis of staining characteristics and diastase resistance, we concluded that these inclusions contained amylopectin. A distinctly different kind of inclusion material was also present in skeletal muscle and tongue of horse Nos. 1 and 3. These inclusions were crystalline with a sharply defined ultrastructural periodicity. The crystals were eosinophilic and very dark blue when stained with toluidine blue but did not stain with iodine. Crystals sometimes occurred freely within the myofibers but more often were encased by deposits of amylopectin. This combination of histologic and ultrastructural features characterizes a previously unreported storage disease in fetal and neonatal Quarter Horses, with findings similar to those of glycogen storage disease type IV. We speculate that a severe inherited loss of glycogen brancher enzyme activity may be responsible for these findings. The relation of amylopectinosis to the death of the foals is unknown.

Amylopectin↗

Disseminated Rhodococcus equi infection in two goats.

Rhodococcus equi infection was diagnosed in two goats from the same herd. At necropsy, numerous caseating granulomas were disseminated throughout the liver, lungs, abdominal lymph nodes, medulla of right humerus, and the right fifth rib of goat No. 1, and the liver of goat No. 2. Histopathologic examination confirmed the presence of multiple caseating granulomas in these organs. Numerous gram-positive and Giemsa-positive coccobacilli were identified within the cytoplasm of macrophages. Aerobic bacterial cultures of the liver and lung from both goats yielded a pure growth of R. equi. R. equi antigens were immunohistochemically identified in caseating granulomas from both goats. However, the 15- to 17-kd virulence antigens of R. equi were not detected, suggesting possible infection by an avirulent strain of this organism.

Actinomycetales Infections↗

Effects of formalin on bacterial growth in mink feed, feed consumption and reproductive performance of adult mink, and growth of mink kits.

Feed that is typically used on commercial mink ranches is an ideal environment for bacterial growth because of the raw animal by-products used as ingredients. Recently, formaldehyde was approved for use as an antimicrobial agent in poultry feed. Experiments in our laboratory were carried out to investigate the effects of incorporating different concentrations of formalin into the feed of mink on the growth of gram-negative and gram-positive bacteria. Feed containing 0, 550 or 1100 ppm formalin was kept refrigerated for up to 7 d and the number of colony forming units of gram-negative and gram-positive bacteria derived from the feed was determined each day. Colony forming units in the formalin-treated feed were significantly fewer than colony forming units in untreated feed. In the second trial, feed containing the same concentrations of formalin was maintained at 30 C for 24 h and cultured bacterial colonies were counted at 0, 12 or 24 h of feed incubation. Both concentrations of formalin were effective in significantly reducing the number of colony forming units. A feed consumption trial determined if mink (Mustela vison) preferred formalin-treated feed to non-treated feed kept refrigerated for up to 7 d. Consumption of feed treated with 1100 ppm formalin was significantly lower than consumption of the non-treated feed on d 1, 2, 4 and 5, but body weight was not affected. A long-term feeding trial determined the effects of formalin on mink reproduction, early growth of offspring and quality of fur. Mink were fed formalin at concentrations of 0, 550 or 1100 ppm for approximately 140 d beginning 1 mo prior to mating until kits were weaned at 6 w of age. Mating success was not affected by consumption of formalin-treated diets, but kit survival at birth was adversely affected in mink consuming 1100 ppm formalin. Hemoglobin concentration, hematocrit, mean corpuscular volume, and mean corpuscular hemoglobin were significantly decreased in 6-w-old kits, but there were no significant differences in any of these parameters between the kits exposed to 0 and 550 ppm formalin. In a second phase, some kits and their dams were continued on their respective dietary treatments from weaning through pelting (approximately 220 and 320 d, respectively). At pelting, hematocrits and hemoglobin concentrations for the kits fed 1100 ppm formalin were significantly less compared to the control and 550 ppm formalin groups. There were no significant differences in body weights among female kits or adult female mink. The body weights of male kits in the 1100 ppm formalin group became significantly less than the body weights of male kits in the control and 550 ppm formalin groups as the trial progressed. The quality of fur was highest for mink in the control group and lowest for mink in the 1100 ppm formalin group. While dietary 1100 and 550 ppm formalin were effective in suppressing bacterial growth in the feed of mink, the deleterious effects of 1100 ppm formalin on kit survival, hematologic parameters, body weight, and quality of fur preclude formalin use at this concentration.

Animal Feed↗

Fatal cysticercosis by Taenia crassiceps (Cyclophyllidea: Taeniidae) in a presumed immunocompromised canine host.

Cysticercosis in a canine host (Canis familiaris) attributable to the taeniid cestode Taenia crassiceps is reported for the first time in North America. Numerous parent and daughter cysticerci occurred in a massive intrapleural and intraperitoneal infection in an apparently immunocompromised host. The largest cysticerci were ovoid to elongate, 5-9 mm in maximum length, and armed with 32-34 rostellar hooks in 2 rows; small hooks measured 114-143 microm long (x = 124+/-8.2 microm), and large hooks were 156-180 microm (x = 163+/-7.4 microm). Taenia crassiceps is widespread in boreal North America and, like a number of other taeniids, constitutes a potential risk as a zoonotic parasite. The immunological status of the host may be important in determining the outcome of infections for this and other taeniids in atypical hosts.

Animals↗

Multigenerational study of the effects of consumption of PCB-contaminated carp from Saginaw Bay, Lake Huron, on mink. 1. Effects on mink reproduction, kit growth and survival, and selected biological parameters.

This study was conducted to determine the multigenerational effects of consumption of PCB-contaminated carp (Cyprinus carpio) from Saginaw Bay (Lake Huron) on mink (Mustela vison) reproduction and health and to examine selected biomarkers as potential indicators of polyhalogenated hydrocarbon toxicity in mink. The mink were fed diets formulated to provide 0 (control), 0.25, 0.5, or 1.0 ppm polychlorinated biphenyls (PCBs) through substitution of Saginaw Bay carp for ocean fish in the diets. To determine whether the effects of PCB exposure were permanent, half of the parental (P1) animals were switched from their respective treatment diets to the control diet after whelping the first of two F1 generations. Effects of in utero and lactational exposure to PCBs on subsequent reproductive performance of the F1 animals were examined by switching half of the first-year F1 offspring (kits) to the control diet at weaning, while the other half was continued on their parental diet (continuous exposure). Continuous exposure to 0.25 ppm, or more, of PCBs delayed the onset of estrus (as determined by vulvar swelling and time of mating) and lessened the whelping rate. Litters whelped by females continually exposed to 0.5 ppm, or more, of PCBs had greater mortality and lesser body weights than controls. Continuous exposure to 1.0 ppm PCBs had a variable effect on serum T4 and T3 concentrations. Compared to the controls, there were significant differences in kidney, liver, brain, spleen, heart, and thyroid gland weights of the mink continually exposed to 1.0 ppm PCBs. There was an increase in the incidence of periportal and diffuse vacuolar hepatocellular lipidosis in the P1 mink with continuous exposure to increasing concentrations of PCBs. Plasma and liver PCB concentrations of the adult and kit mink were, in general, directly related to the dietary concentration of PCBs and the duration and time of exposure. Short-term parental exposure to PCBs had detrimental effects on survival of subsequent generations of mink conceived months after the parents were placed on "clean" feed. The lowest observed adverse effect level (LOAEL) for dietary PCBs in this study was 0.25 ppm.

Animals↗

Subacute and reproductive effects in mink from exposure to Fusarium fujikuroi culture material (M-1214) containing known concentrations of moniliformin.

This study was conducted to ascertain the subacute and reproductive effects in mink (Mustela vison) resulting from exposure to moniliformin, a toxic mycotoxin produced by Fusarium fungi. In a preliminary trial, adult mink were presented diets that contained targeted concentrations of 10, 20, 40, 80, 160, or 240 ppm moniliformin provided by F. fujikuroi culture material (M-1214). The mink fed diets that contained more than 40 ppm moniliformin refused to eat significant quantities of feed. Feeding adult mink diets that contained 8.1 or 17.0 ppm (wet weight) moniliformin, provided by F. fujikuroi culture material, in a 30-day subacute trial produced no significant adverse effects on feed consumption, body weights, hematologic parameters, or serum chemical values, and notable histologic changes in tissues that were examined. In the reproduction trial, female mink were exposed to the same dietary concentrations of moniliformin provided by F. fujikuroi culture material as in the subacute test from 2 weeks prior to the breeding season until their offspring (kits) were 8 weeks old. Consumption of the high-dose (17 ppm) diet resulted in significant neonatal mortality and reduced kit body weights at birth and at 8 weeks of age. Necropsy of 8-week-old kits from the control and high-dose groups revealed no gross or histologic lesions or alterations in liver, lung, or heart tissues that could account for the mortality observed in the kits exposed to the culture material. These results indicate that long-term (105-135 days) dietary exposure to F. fujikuroi culture material containing 17 ppm moniliformin is not lethal to adult female mink, but can have adverse effects on neonatal mink.

Animals↗

Caprine mucopolysaccharidosis-IIID: clinical, biochemical, morphological and immunohistochemical characteristics.

Several animal models have been developed for the mucopolysaccharidoses (MPSs), a group of lysosomal storage disorders caused by lysosomal hydrolase deficiencies that disrupt the catabolism of glycosaminoglycans (GAG). Among the MPS, the MPS-III (Sanfilippo) syndromes lacked an animal counterpart until recently. In this investigation of caprine MPS-IIID, the clinical, biochemical, morphological, and immunohistochemical studies revealed severe and mild phenotypes like those observed in human MPS III syndromes. Both forms of caprine MPS IIID result from a nonsense mutation and consequent deficiency of lysosomal N-acetylglucosamine 6-sulfatase (G6S) activity and are associated with tissue storage and urinary excretion of heparan sulfate (HS). Using special stains, immunohistochemistry, and electron microscopy, secondary lysosomes filled with GAG were identified in most tissues from affected goats. Primary neuronal accumulation of HS and the secondary storage of gangliosides were observed in the central nervous system (CNS) of these animals. In addition, morphological changes in the CNS such as neuritic expansions and other neuronal alterations that may have functional significance were also seen. The spectrum of lesions was greater in the severe form of caprine MPS IIID and included mild cartilaginous, bony, and corneal lesions. The more pronounced neurological deficits in the severe form were partly related to a greater extent of CNS dysmyelination. These findings demonstrate that caprine MPS IIID is a suitable animal model for the investigation of therapeutic strategies for MPS III syndromes.

Animals↗

Influence of exogenous hyaluronan on synthesis of hyaluronan and collagenase by equine synoviocytes.

OBJECTIVE: To evaluate the influence of exogenous hyaluronan (HA) on in vitro synthesis of HA and collagenase by equine synoviocytes from normal and inflamed joints. ANIMALS: 9 adult horses. PROCEDURE: Synoviocytes for culture were taken from the middle carpal joint of 3 horses with normal joints (control) and 6 horses with osteochondral fractures (principal). Synoviocytes were propagated in monolayer cultures and were incubated with 3 commercial HA products at concentrations of 0, 200, 400, and 1,500 micrograms/ml. Newly synthesized HA was radiolabeled with [3H]glucosamine and quantified by cetylpyridinium chloride precipitation and liquid scintillation counting. The hydrodynamic size of radioactive HA was determined by high-performance liquid chromatography, and collagenase activity was evaluated by use of a quantitative radioactive collagen film assay. RESULTS: Exogenous HA influenced neither the rate of synthesis nor the hydrodynamic size of the newly produced HA by control or principal cell cultures. Culture supernatants from abnormal synovium, exposed to 400 and 1,500 micrograms of exogenous HA/ml, contained significantly more collagenase activity than did those exposed to lower concentrations. CONCLUSION: Although HA is thought to have beneficial effects in equine arthropathies, the principal mechanisms of action of HA do not appear to be stimulation of synthesis of HA of augmented molecular weight or marked inhibition of collagenase synthesis.

Animals↗