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Biomedical subjects

M M Walser

Publications and source records attributed to M M Walser.

At least 19 recordsLinked to original sources

Hepatoblastoma with erythrocytosis in a young female horse.

A 2.5-year-old female Thoroughbred was examined because of lethargy, anorexia, and weight loss. Analysis of a CBC revealed erythrocytosis and an increase in PCV. Serum biochemical analysis revealed increases in activities of several hepatic enzymes. Ultrasonography revealed hepatomegaly and a heterogeneous appearance of the hepatic parenchyma. The horse did not improve despite supportive care, and it was euthanatized. Necropsy revealed numerous raised white to gray foci in the liver. Histologically, these foci consisted of neoplastic cells that resembled fetal hepatocytes, embryonal-type cells, and cells with features intermediate between those 2 cell types. Immunohistochemical staining revealed that hepatocytes stained strongly with anti-alpha-fetoprotein. On the basis of these results, hepatoblastoma was diagnosed. Diagnosis of hepatoblastoma is difficult, because it can appear histologically similar to other hepatic tumors, such as hepatocellular carcinomas. Definitive diagnosis requires histologic evaluation of tumor architecture and cell morphology. Immunohistochemical staining for alpha-fetoprotein in tumor cells may serve as a tumor marker but is not pathognomonic of hepatoblastoma. Paraneoplastic syndromes, such as erythrocytosis, can accompany hepatoblastoma. The prognosis for horses with hepatoblastoma is grave.

Animals↗

Effect of dietary phosphorus, calcium, and phytase on performance of growing turkeys.

Female and male turkeys were fed 110, 73, 52, and 30% of the NRC (1994) nonphytate P (NPP) requirement without and with 500 phytase units (FTU)/kg during 4 to 14 or 16 wk of age, respectively. At 110% P (control; also 110% of NRC Ca), phytase was without effect. At 73% of NPP (100% Ca), without phytase, performance was similar to the control; with phytase, performance was equivalent, and in some stages, superior to the control. At 52% of NPP (90% Ca), performance was inferior without phytase and was variably similar or poorer than the control with phytase. At 30% NPP without phytase, poults gained poorly and showed a high incidence of leg disorder at 8 wk when they were removed from experiment; poults gained better with 80% NRC Ca compared with 110%. At 30% NPP with phytase, turkeys performed remarkably well, although suboptimally, at 80 or 110% NRC Ca. Phytase at 400, 300, and 200 FTU/kg with increasing age periods performed as well as 500 FTU/kg with 73% of NRC NPP (100% Ca) and 52% NRC NPP (90% Ca). These lower phytase levels were not as sufficient as 500 FTU/kg with 30% of NRC NPP; this inadequacy was more severe with higher dietary calcium. Phytase was effective in reducing dietary P requirements of growing turkeys when the NPP levels were below NRC (1994) requirements.

6-Phytase↗

Synovial chondromatosis in raptors.

Fourteen raptors, consisting of 13 great horned owls (Bubo virginianus) and one red-tailed hawk (Buteo jamaicensis), from central and north central Minnesota, western Wisconsin, and eastern South Dakota (USA) were admitted to a raptor rehabilitation center between June 1992 and June 1995, with perisynovial and synovial chondromatosis affecting multiple joints. Birds were severely debilitated primarily due to loss of shoulder motion. The etiology of these lesions in raptors is unknown.

Animals↗

Suppressor macrophages mediate depressed lymphoproliferation in chickens infected with avian reovirus.

A previous study indicated that spleens from reovirus-infected chickens contained macrophages that were primed to produce nitric oxide (NO). The presence of these primed macrophages correlated with depressed in vitro T cell mitogenesis. The current studies indicated that splenic adherent macrophages from virus-exposed chickens inhibited concanavalin A (ConA) induced proliferation of normal spleen cells. ConA-stimulated spleen cells from uninfected chickens, but not virus-exposed chickens, produced large quantities of interleukin-2 (IL-2) and a factor that induced NO production. This factor was tentatively named NO inducing factor (NOIF). The removal of macrophages from the spleens of virus-exposed chickens by plastic adherence resulted in partial recovery of ConA-induced proliferation and the production of normal levels of IL-2 and increased levels of NOIF, although these remained below normal. However, nonadherent spleen cells produced substantial quantities of NO, which indicated an incomplete removal of macrophages. Because removal by plastic adherence did not result in the depletion of all macrophages, spleen cells were panned with anti-CD3 antibody to obtain an almost pure population of T cells. Fractionated T cells from virus-exposed chickens proliferated vigorously to ConA and produced normal levels of IL-2 and NOIF. When splenic adherent cells from virus-exposed chickens were added to purified T cells, the T cells failed to respond to ConA. Addition of splenic adherent cells from virus-free chickens did not induce mitogenic inhibition. Further, the addition of purified T cells from the spleens of reovirus-infected chickens to T cells from virus-free birds did not adversely affect T cell mitogenesis. These data indicated that reovirus infection in chickens does not compromise the functional capabilities of T cells but induces suppressor macrophages that inhibit T cell functions.

Animals↗

Immunohistochemical detection of lymphocyte subpopulations in the tarsal joints of chickens with experimental viral arthritis.

We characterized the lymphocytes in the tarsal joint synovium of chickens inoculated with an arthrotropic strain of avian reovirus. Cryostat sections of whole joints taken from 2 days to 35 days postinoculation were analyzed using monoclonal antibodies directed against B lymphocytes, T lymphocytes, and chicken Ia antigen. Plasma cells were morphologically identified using stained sections of whole joints. Time-dependent changes were found in the type and number of positively staining cells. Synoviocytes and cells with a dendritic morphology stained positive for Ia in normal joint sections. T cells, mostly CD8 positive, were present in low numbers in acute phase arthritis (2-6 days postinfection) in the perivascular and superficial regions of the synovium. Subacute arthritis (8-14 days postinfection) was characterized by increased numbers of CD4 and Cd8 T cells in the perivascular and superficial regions. The perivascular T cells began to organize into aggregates, with IgM-positive B cells and plasma cells on the periphery of these aggregates. Some CD8-positive cells were detected on the surface of the articular cartilage. Cells staining positively for Ia were not lymphocytes. Chronic arthritis ( > 14 days postinfection) was characterized by large numbers of T cells in the perivascular and superficial regions, with the CD4-positive T cells found primarily in the lymphoid aggregates of the perivascular regions. IgM-positive B cells were fewer, but more plasma cells, few of which stained positive for IgM, were present. Lymphocytes in chronic arthritis stained positively for Ia. These data suggest that the types, numbers, and activation level of lymphocytes present in the tarsal joints are similar but not identical to those seen in rheumatoid arthritis.

Animals↗

Reovirus infection in chickens primes splenic adherent macrophages to produce nitric oxide in response to T cell-produced factors.

In this study, we examined the mechanisms by which avian reovirus infection of chickens depresses in vitro proliferative responses of spleen cells to T cell mitogens. We showed an enhanced production of nitric oxide (NO) by phytohemagglutinin (PHA)-stimulated spleen cells from reovirus-infected birds but not from virus-free birds. Since macrophages are a primary source of NO, we compared splenic adherent macrophages from virus-free and virus-exposed chickens. There was a fourfold increase in the number of adherent macrophages from the spleens of virus-exposed chickens. Production of NO by macrophages from virus-exposed chickens required T-cell-produced factors and was not due to direct stimulation of macrophages by PHA. Although T cell products were needed for NO production by macrophages, in an apparent paradox, we found significantly reduced levels of NO-inducing activity in the supernatants of PHA-stimulated spleen cells from virus-exposed chickens than in supernatants from PHA-stimulated normal spleen cells. Cocultures of adherent cells from infected chickens with normal spleen cells indicated that although macrophages secreted NO following PHA stimulation, macrophages ultimately suppressed the continued production of NO-inducing factors by normal spleen cells. We further showed in experiments utilizing NG-monomethyl-L-arginine, an NO synthesis inhibitor, that NO was not responsible for the mitogenic inhibition of spleen cells from virus-exposed chickens. In summary, our results indicated that following reovirus infection, macrophages are primed in vivo and activated in vitro by T-cell-produced factors. Despite the requirement of T cell cytokines for NO production, T cells did not proliferate to mitogenic stimuli, which indicated that the early events (i.e., cytokine secretion) but not the late events (i.e., proliferation) of the T cell activation cascade were functional. Macrophage priming following reovirus infection may have important implications for impaired T cell responsiveness.

Animals↗

The natural occurrence of aflatoxin B1 in Moroccan poultry feeds.

The occurrence of AFB1 in Moroccan poultry feeds and their ingredients was evaluated. Thirty poultry farms and 4 feedmills were surveyed from September 1989 to June 1991, and 300-500 g each of feeds (corn, sorghum, wheat bran, soybean meal, cottonseed meal, sunflower meal, finished feeds) were sampled. Additionally, on farms with suspected mycotoxin problems, necropsies of affected chickens were performed for gross and microscopic examinations. A total of 315 samples were analysed for AFB1 using a semi-quantitative enzyme linked immuno-sorbent assay (ELISA kits) and thin-layer chromatography. In feedmills, 4% of samples contained AFB1; 17% among sunflower meal samples (20-80 ppb) and 4% among corn (110 ppb) and mixed feed samples (20-110 ppb). On poultry farms, 17% of samples were found contaminated with AFB1; 20% were positive among pellets and 16% among crumbles and 15% mash feeds. The level of contamination ranged from 20 ppb to 200 ppb, except for 4 samples that contained high levels of AFB1 (2000-5625 ppb). These highly-contaminated samples were associated with clinical aflatoxicosis in broiler chickens. The most frequent incidence of AFB1 contamination and the highest AFB1 contamination occurred in feeding troughs (23%). Aflatoxins should be considered potential contaminants of poultry feeds under Moroccan conditions.

Aflatoxin B1↗

Phosphorus availability bioassay using bone ash and bone densitometry as response criteria.

Two experiments were conducted to examine the relative precision of bone densitometry and bone ash methodologies as response criteria in measurement of bioavailability of phosphorus from various supplements for turkeys. Multivariate analyses of variance were used to analyze data collected. Coefficients of correlation and variation and F ratios were used for evaluation. Bone densitometry with one scan at each of 3 points on the bone was faster than bone ash and as precise as bone ash analysis in measuring phosphorus availability in turkeys. The coefficient of correlation between percentage ash (of dry bone) and scan density (milligrams per centimeter length of bone) measurements for treatment effects was .986. The coefficient of variation was about the same for the bone ash (5.8) and the three-point bone scan (6.9) methods. As indicated by the F ratio for testing treatment effects, bone densitometry was better able to detect differences among phosphorus sources. A technician may scan 50 cleaned bones in 3 hr, but with the bone ash method, drying, ashing, and weighing may require 3 working days. Bone sampling technique, multiple operators, different bone sizes, and decay of iodine source were the major factors affecting precision of the bone densitometry technique. Relative biological availabilities of phosphorus from various supplements were about the same by the two methods.

Animals↗

Pain threshold changes in adjuvant-induced inflammation: a possible model of chronic pain in the mouse.

A chronic hyperalgesic condition was induced in mice by the injection of Freund's complete adjuvant (FCA) into the lower lumbar region or directly into the hind footpads. Although little or no visible inflammation was observed after a single intradermal injection of FCA into the lower lumbar area of rats or mice, significant alterations in nociceptive thresholds occurred in each species as determined by decreases in response latency in tail-flick and hot-plate assays. Unilateral intraplantar administration of FCA in mice resulted in visible inflammation in the area of the tibiotarsal (ankle) joint. Changes in the response latency to a noxious stimulus in the areas surrounding the inflamed joint were similar to those observed in non-inflamed limbs, suggesting that changes in sensitivity to noxious stimuli were not merely the result of local hypersensitivity of the inflamed tissue, but may also be due to alterations in nociception at the level of the central nervous system (CNS). When the chronic inflammatory condition induced in the mouse tibiotarsal joint was evaluated by histological and morphological techniques, it was found to have the same characteristics as described in the early stages of FCA-induced arthritis in rats. The similarities between the response to FCA in rat and mouse suggest that injection of FCA in mice may prove to be a useful model for the study of chronic pain in mice as well as in rats.

Adjuvants, Immunologic↗

Ultrastructure of Fusarium-induced tibial dyschondroplasia in chickens: a sequential study.

Female broiler chicks were randomly placed into two groups; one was treated twice daily with TDP-1 (a mycotoxin produced by Fusarium roseum), the other was controls. Chicks were sacrificed after 2, 4, 6, 8, 10, and 14 days of treatment and were evaluated for tibial dyschondroplasia. TDP-1-treated chicks examined after 2, 4, or 6 days of treatment had either no gross lesions (2 days) or mild gross lesions (4 and 6 days); growth plates from these groups did not have ultrastructural changes. TDP-1-treated chicks examined after 8, 10, or 12 days of treatment had moderate to severe gross lesions of tibial dyschondroplasia. These groups also had intracellular lipid accumulation and necrosis of chondrocytes within the retained cartilage. It was concluded that the cellular changes in tibial dyschondroplasia develop only after the cartilage accumulates; the changes are sequelae, possibly due to nutrient depletion from an increased distance between chondrocytes and perforating epiphyseal vessels, their nutrient source.

Amino Acids↗

The interaction of dietary vitamin A and vitamin D related to skeletal development in the turkey poult.

Large white male turkey poults were fed diets with different levels of vitamins A and D to study the interaction of these vitamins with regard to skeletal development. Poults fed a basal diet deficient in both vitamins A and D developed severe lameness, growth depression, mortality and lesions consistent with rickets. Birds fed a diet containing the required level of vitamin D (900 ICU/kg, NRC estimated requirement) and a high level of vitamin A (400,000 IU/kg) also developed severe lameness, growth depression and a rachiticlike condition, characterized by thicker than normal proximal tibial epiphyseal plates and lower than normal bone mineral content. When fed a diet containing the required level of vitamin A (4,000 IU/kg, NRC estimated requirement) and a high level of vitamin D (900,000 ICU/kg), poults developed hypervitaminosis D as evidenced by mild growth depression and renal tubular mineralization. When poults were fed a diet containing high levels of both vitamins A and D growth rate and bone mineral content were similar to control poults fed a diet containing the required levels of vitamins A and D. In addition, lameness and renal tubular mineralization were not apparent in the poults fed a diet containing high levels of both vitamins A and D. It was concluded that there is an antagonistic interaction between vitamins A and D.

Animals↗

TDP-1, a toxic component causing tibial dyschondroplasia in broiler chickens, and trichothecenes from Fusarium roseum 'Graminearum'.

Fusarium roseum 'Graminearum' was isolated from overwintered oats in Alaska and was tested for its ability to cause tibial dyschondroplasia (TDP) in broiler chickens. The water-soluble fraction was tested and found to cause TDP. In addition, diacetoxyscirpenol and 7-hydroxydiacetoxyscirpenol were identified in the acetonitrile fraction of the extracts and caused mild mouth lesions in chickens. Six major water-soluble components were purified by thin-layer chromatography and tested for toxicity to chick embryos. One of the six components, called TDP-1, was found to be lethal to chick embryos. There was a 100% incidence of TDP in chickens fed a diet containing 75 ppm (wt/wt) of pure TDP-1, thus establishing the cause and effect relationship between TDP and TDP-1. Analyses by thin-layer chromatography and mass spectrometry revealed that TDP-1 is polar and ninhydrin positive, exhibits fluorescence with UV irradiation, and is a nitrogen-containing component with an empirical formula of C15H20N2O4.

Alaska↗

Morphogenesis of Fusarium sp-induced tibial dyschondroplasia in chickens.

Tibial dyschondroplasia was induced in female broiler chicks by the incorporation of 2% Fusarium roseum "Alaska" culture into their starter ration. Chicks were placed on this diet at one day of age and maintained until they were killed at four days or one week. Proximal tibial physes were grossly thickened into cone-shaped masses of cartilage by one week of age. Microscopically, lesions were in both ages of treated chickens and were characterized by thickening of the transitional zone which was especially prominent in the center of the growth plate. This zone was unmineralized, avascular, and contained chondrocytes which were crenated and densely eosinophilic. The cartilage matrix was pale and contained some patchy eosinophilic foci. Four growth plates with tibial dyschondroplasia and four normal growth plates from each of the four-day and one-week-old age groups were evaluated based on the following parameters: number of metaphyseal vascular sprouts, distance between the proliferative/transitional junction and the tip of the metaphyseal vascular sprouts, width of the tips of the metaphyseal sprouts, distance between tips of adjacent metaphyseal vascular sprouts, and number of perforating vessels in the proliferative zone. The distance between the proliferative/transitional junction and the metaphyseal sprout tips was greatly increased (p less than 0.01) in the affected four-day and one-week-old chickens compared to age-matched controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Chondroclasts in fusarium-induced tibial dyschondroplasia. A histomorphometric study.

The role of chondroclasts in the pathogenesis of Fusarium roseum-induced tibial dyschondroplasia (TD) was examined in a histomorphometric study. TD developed rapidly in broiler chickens placed at 1 day of age on rations containing either 3% (Experiment 1) or 2% (Experiment 2) F roseum cultures. In Experiment 1 the frequency of TD in birds killed at 4 weeks of age was 90%. In Experiment 2, birds were killed at intervals from 4 days until 4 weeks of age. By 1 week of age, 70% of birds examined had characteristic accumulations of prehypertrophic cartilage at the proximal tibial physis, and the frequency of TD in 4-week-old birds was 80%. Sections of hypertrophic cartilage from F roseum-fed and control birds from both experiments were examined for determination of the volume density of chondroclasts along the vascular channel boundary. Chondroclast density was consistently lower in F roseum-fed than in control birds, but the difference was significant only at 4 weeks of age. The fact that gross lesions were evident before a significant decrease in chondroclast density occurred indicates that a decrease in the density of chondroclasts was not an essential factor in the accumulation of cartilage characteristic of TD.

Age Factors↗

Bioavailability of phosphorus in commercial phosphate supplements for turkeys.

Forty-seven commercial phosphorus supplements were obtained from feed manufacturers and subjected to biological phosphorus availability assay using the turkey poult. Bone ash was the response criterion. Compared to a reference source of commercial mono/ dicalcium phosphate (assigned 100), 7 other mono/ dicalcium phosphates averaged 97.1 (range 88.6 to 110.0), 20 dicalcium phosphate sources averaged 90.6 (76.3 to 104.8), and 20 defluorinated phosphate sources averaged 78.4% (68.6 to 89.6) availabilities. Combining equal parts of all sources of each type of phosphorus supplement and using purified grade calcium phosphate monobasic monohydrate as a defined standard, the commercial mono/ dicalcium phosphates, dicalcium phosphates, and defluorinated phosphates averaged (with 95% confidence limits) 93.6 +/- 7.6, 88.3 +/- 8.2, and 70.2 +/- 7.2% phosphorus availability in a slope ratio bioassay. Calculating the requirement intercepts utilizing the blended phosphorus supplements indicated apparent requirements using mono/ dicalcium phosphate, dicalcium phosphate, and defluorinated phosphate of .74, .76, and .83% total phosphorus in the diet, respectively. Considering 1) the variability in availability of the sources, 2) variation in feed mixing, 3) the National Research Council requirement of .80%, and 4) that newly hatched poults are completely dependent on one batch of prestarter feed during 0 to 10 days of life, it is suggested that in certain instances field rickets could result from deficiency of dietary phosphorus.

Animal Feed↗

Protective effect of organic cation transport inhibitors on cis-diamminedichloroplatinum-induced nephrotoxicity.

Cis-diamminedichloroplatinum (II) (cisplatin) is a frequently used cancer chemotherapeutic agent. Nephrotoxicity is a serious dose-limiting side effect. Many approaches have been studied for protective action against cisplatin-induced nephrotoxicity, but with the exception of diuretics and hydration none are in widespread use. We have used a modified Sperber technique in unanesthetized hens to examine the effect of cisplatin on renal organic cation and anion transport and on renal morphology. The effects of the organic cation transport inhibitors quinine and cyanine on cisplatin-induced toxicity also were evaluated. Administration of cisplatin (3.0 mg/kg i.v.) produced nephrotoxic and lethal effects. Four days after cisplatin administration there was a significant inhibition of renal tubular excretory transport of the organic cation tetraethylammonium and the organic anion p-aminohippuric acid. Acute multifocal tubular necrosis of the proximal tubules was present. Administration of quinine (1.5 mumol/min) and cyanine (0.122 mumol/min) protected against the lethal effects, the inhibition of renal organic cation and anion transport and the renal lesions induced by cisplatin.

Animals↗

Effect of dietary sodium fluoride on growth and bone development in growing turkeys.

Large White male turkeys were fed rations containing 0, 12.5, 25, 50, 100, 200, 400, and 800 ppm added fluoride (F) from sodium fluoride in a corn-soybean assay diet containing tricalcium phosphate and 3 to 5 ppm F. The 800 ppm treatment was discontinued at 8 weeks because of low weight gains and a high incidence of leg disorders. Turkeys receiving defluorinated phosphate (32% calcium, 18% phosphorus) had significantly higher 4-week body weights than turkeys receiving tricalcium phosphate. Turkeys fed 0, 400, and 800 ppm F had significantly lower body weights at 8 weeks than turkeys fed 50 ppm F. A similar weight pattern was seen at 18 weeks, although the differences were not statistically significant. Based on growth response in this study, a requirement of 20 ppm F is proposed. Increasing levels of dietary F resulted in large increases in tibia F. Removal of high dietary F in certain groups at 8 weeks resulted in growth recovery and reduction in tibia F by 18 weeks. Elevated plasma alkaline phosphatase activity was observed with added dietary F of 400 and 800 ppm. At 4 weeks, tibiae from turkeys receiving high F had a trend (not statistically significant) toward lower percentage ash and a significantly lower breaking strength than controls. Compared to controls, tibiotarsi from turkeys on high F rations were significantly shorter, had thinner cortices, and had a narrower proliferative zone of proximal growth plates. A high incidence of tibial dyschondroplasia was observed, but it was not correlated with dietary treatment.

Alkaline Phosphatase↗