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Biomedical subjects

N D Costa

Publications and source records attributed to N D Costa.

At least 19 recordsLinked to original sources
PubMed2005

Clinical acidosis in a Gippsland dairy herd.

OBJECTIVE: To report on spontaneous clinical and subclinical acidosis in a large dairy herd, to evaluate the diets and feeding strategies involved, and to report on measures of rumen function in the cows affected. DESIGN: A Gippsland dairy herd was sampled as part of a wider randomised cross-sectional study that examined the prevalence, risk factors for, and effects of, acidosis on rumen function of dairy cattle. Three herds on the farm were involved in the study: the transition herd (cows 3 weeks prior to calving), the very fresh lactating herd (1 < days in milk < 10, herd 1) and the fresh lactating herd (10 < days in milk < 120, herd 2) including a small lame herd fed separately. The transition cows were fed 2 kg dry matter triticale per cow per day and hay with an estimated total dry matter intake of 4.8 kg per cow per day. The lactating cow diet included 6.75 kg dry matter triticale per cow per day with total concentrate fed being 8.1 kg dry matter per cow per day in the milking parlour. Silage, lucerne cubes, hay and pasture (herd 2 only) was also fed to the lactating cows with the estimated total dry matter intake for cows in herds 1 and 2 being 13.7 kg and 20.8 kg per cow per day respectively. Three primiparous and five multiparous cows in early lactation (< 100 days in milk) were randomly selected from each of two lactating herds: herds 1 and 2. Rumen fluid was sampled from each cow by both rumenocentesis and stomach tube. The rumenocentesis samples were tested for pH at the time of sampling. Stomach tube samples were frozen and subsequently tested for volatile fatty acid, ammonia, and D- and L-lactate concentration. RESULTS: In the very fresh herd, there was a high prevalence of severe lameness and scouring, coupled with a mean rumen pH 5.67, low mean total volatile fatty acid concentration 71.0 mM and high mean concentrations of L- and D-lactate, (7.71 mM and 7.31 mM), respectively. Cows in the fresh herd had moderate signs of scouring and lameness. A lame herd comprising approximately 50 cows separated from the fresh herd was also present on the farm. The mean rumen pH of the fresh herd was 5.74 and mean rumen concentrations of volatile fatty acids, ammonia, L- and D-lactate were within ranges considered normal. CONCLUSIONS: The transition diet failed to supply sufficient energy and protein for maintenance of cows of this live weight in late gestation. The diet fed to the very fresh herd was low in effective fibre and contained an excessive content of non-structural carbohydrate in the form of processed, rapidly fermentable grain. The sudden change from the transition diet to the diet fed to the very fresh herd probably also precipitated the outbreak of acidosis. This case report provides unique detail, including information on diets and rumen parameters, of an outbreak of acidosis in a pasture-fed herd.

Acidosis↗
PubMed2002

Effect of copper, zinc and cadmium on the promoter of selenoprotein W in glial and myoblast cells.

Rat selenoprotein W (SeW) promoter activity was investigated using different concentrations of cadmium, copper, and zinc. Two fragments (404 and 1265 bp) of the SeW promoter, containing a single metal response element (MRE), were ligated into the multiple cloning site of a pGL3-Basic reporter plasmid. The constructs were transfected into cultured C6 (rat glial) and L8 (myoblast) cells and promoter activity measured by means of luciferase reporter gene fused to the SeW promoter fragments in the reporter plasmid. With post-transfection exposure of these cell lines to these metals, copper and zinc, but not cadmium, significantly increased promoter activity of the unmutated 1265 bp (not 404 bp) construct (p<0.05) only in the C6 cells. Mutation of the MRE sequence abolished promoter response to metal exposure but did not eliminate promoter activity. The results suggest that SeW expression in glial cells can be increased on exposure to copper and zinc and that this response is dependent on the MRE sequence present in the SeW promoter.

Animals↗
PubMed2001

Bleeding reflux esophagitis: a prospective 1-year study in a university hospital.

OBJECTIVES: The prevalence of bleeding from reflux esophagitis has not been studied. The aim of the study was to evaluate the 1-yr prevalence of bleeding from reflux esophagitis, as well as the independent factors associated with bleeding. METHODS: All patients with reflux esophagitis diagnosed with upper digestive tract endoscopy in Reims Hospital in 1996 were included. Studied parameters were prospectively recorded and compared between patients with bleeding and nonbleeding reflux esophagitis. RESULTS: Endoscopy was performed in 1983 patients of whom 219 (11.0%) had overt upper digestive tract hemorrhage. Reflux esophagitis was the cause of bleeding in 32 patients (14.6%). Reflux esophagitis was diagnosed in 391 patients during the same period of time. Bleeding reflux esophagitis accounted for 8.2% of them. Independent factors associated with bleeding were grade 3 or 4 (Savary-Miller) esophagitis (odds ratio [OR]: 25.5, 95% confidence interval [CI]: 9.6-67.9), cirrhosis (OR: 5.7, 95% CI: 1.7-18.9), Eastern Cooperative Oncology Group performance status > or = 3 (OR: 4.6, 95% CI: 1.5-14.2), and anticoagulant therapy (OR: 3.9, 95% CI: 1.2-12.5). A history of reflux esophagitis or heartburn was noted in only 28.1% or 37.5% of the patients with bleeding reflux esophagitis, respectively. CONCLUSIONS: In this population of patients with reflux esophagitis, the prevalence of bleeding esophagitis was high (8.2%). Bleeding esophagitis occurred primarily in patients with severe esophagitis and was the revealing clinical form of gastroesophageal reflux disease in the majority of cases, suggesting that bleeding prevention would hardly be effective.

Adult↗
PubMed1998

Molybdenum poisoning in feedlot cattle.

OBJECTIVE: To describe a case of acute, fatal molybdenum poisoning in feedlot cattle. DESCRIPTION OF THE HERD: In total, 831 Hereford, Hereford x Angus, and Hereford x Simmental steers, aged 8 to 10 months, with an average body weight of 310 kg were fed a diet, to which sodium molybdate at a rate of 1.9% of the total ration had been accidently added. INVESTIGATION: The steers lost appetite within 3 days and deaths commenced within 6 days of the diet being first offered. The error was rectified when deaths started to occur, but steers continued to die for up to 7 months afterwards. Of the 831 steers on the feedlot, 90 died and a further 5 remained in poor condition. The cause of death was periacinar to massive hepatic necrosis and acute renal tubular necrosis. Blood and tissue samples were taken from surviving steers for 76 days, by which time plasma molybdenum concentrations had returned to normal concentrations. CONCLUSION: Sodium molybdate when fed at a rate of 1.9% of the diet results in acute renal tubular necrosis and periacinar to massive hepatic necrosis.

Animal Feed↗
PubMed1997

Chromosomal aberrations induced by defined DNA double-strand breaks: the origin of achromatic lesions.

The mechanisms of formation of chromosomal aberrations are poorly understood, despite the common use of aberrations as a measure of the genetic effects of physical and chemical agents. We have used restriction endonucleases to introduce defined DNA double-strand breaks into mammalian cells, and measured chromosomal aberration formation relative to the activity of the endonuclease. The endonucleases AluI and Sau3AI remain active for a relatively short time under simulated cellular conditions and induce achromatic lesions ('gaps') in chromatids only within the first hour or two following treatment. In contrast, the endonuclease MboI (an isoschizomer of Sau3AI) is active for an extremely long time and continues to produce chromatid gaps during the whole 12 hr sampling period. This observation strongly suggests that the aberrations classified as gaps are a manifestation of unrejoined DNA double-strand breaks. The formation of gaps may relate to the opportunities for repair of DNA breaks in relation to cell-cycle position. It is more difficult to relate the formation of structural chromatid aberrations to the endonuclease activity, although at relatively low concentrations all 3 endonucleases gave similar levels of structural aberrations.

Animals↗
PubMed1996

Mutations induced by DNA double-strand breaks: the influence of genomic site.

The transgenic CHO cell line PL61, carrying a recombinant SV40-gpt gene, was treated with restriction endonucleases to assess mutagenesis from defined DNA double-strand breaks. Mutations in gpt were measured under two conditions: a stringent condition where selection ensured that the closely-linked neo gene was retained functionally intact, or a relaxed condition without the requirement for neo gene function. Despite testing 18 different restriction endonucleases with various numbers of potential break-sites within the transgene, mutations were only found under relaxed selection conditions. These mutations commonly led to complete loss of the transgene, suggesting that large deletions predominate when selection is relaxed. It is argued, in comparison to mutation data for other genomic sites in CHO cells, that variations in the 'effective target size' for mutagenesis may explain the response of the transgene under different conditions.

Animals↗
PubMed1994

Electroporation and streptolysin O--a comparison of poration techniques.

CHO (Chinese hamster ovary), xrs5 (X-ray sensitive Chinese hamster) and HF19 (untransformed human fibroblast) cells, were exposed to a lethal dose of the restriction enzyme Pvu II during electroporation or poration with the bacterial toxin streptolysin O. The uptake of the exclusion dye trypan blue was used as a measure of poration and compared with survival as measured by subsequent colony formation. It was assumed that any surviving cells had not been permeabilized and therefore did not receive any restriction enzyme. Electroporation alone proved to be more cytotoxic to the cells, whilst streptolysin O was more efficient at permeabilizing both hamster and human cells.

Animals↗
PubMed1994

Case report: efficacy of oral carnitine therapy for dilated cardiomyopathy in boxer dogs.

This paper investigates the role of carnitine in the etiology and treatment of dilated cardiomyopathy in boxers. Two boxers were diagnosed as having dilated cardiomyopathy on the basis of clinical presentation, chest radiographs, electrocardiography and echocardiography. In one dog, carnitine was administered at 6.0 g (or approximately 250 mg/kg live weight (LW) daily per os, and this dog remained asymptomatic for 4 mo until it presented for anorexia, coughing and weakness. Necropsy and histologic findings were consistent with boxer cardiomyopathy in both dogs. Cardiac carnitine concentration was 567 nmol/g wet weight in the unsupplemented dog, which is below the normal mean +/- SD concentration of 1493 +/- 141 nmol/g wet weight. Low cardiac carnitine concentrations appear to be a consistent finding for dilated cardiomyopathy in boxers. However, in the dog that received carnitine therapy, cardiac carnitine was 2802 nmol/g wet weight, and all tissues assayed in the supplemented dog had higher carnitine concentrations than normal dogs. Elevation of tissue carnitine failed to ameliorate dilated cardiomyopathy in this dog. Oral carnitine supplementation in these therapeutic doses appears not to resolve dilated cardiomyopathy in all boxers.

Administration, Oral↗
PubMed1994

Plasma indicators of muscle damage in a model of nutritional myopathy in weaner sheep.

Subclinical nutritional myopathy was induced in 5-month-old sheep by feeding them a diet low in vitamin E and selenium. Subsequently clinical myopathy was induced by dosing with protected polyunsaturated fatty acids. Plasma activities of creatine kinase (CK), pyruvate kinase, aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase and aldolase, enzymes of muscle origin, all remained above their reference ranges in clinically affected sheep, but fluctuated widely. Similar fluctuations occurred in subclinically affected animals, resulting in some activities being within the reference ranges and some above, at different times. Plasma malondialdehyde, an indicator of lipid peroxidation, proved of no diagnostic value. Terminal plasma CK activities were significantly correlated with microscopic damage in the vastus lateralis (VL), but not the vastus intermedius (VI) or the tensor fascia lata (TFL) muscles. AST was the most highly correlated with damage in VI and VL. In two clinically affected sheep successfully treated with an oral dose of alpha-tocopherol acetate all enzymes decreased steadily to within their reference ranges, at rates probably related to their plasma half-lives. These results suggest that measurement of plasma CK activity would be useful in monitoring recovery of treated sheep.

Animals↗
PubMed1993

The effectiveness of restriction endonucleases in cell killing and mutation.

The use of restriction endonucleases (RE) to study the importance of DNA break end structures in differential cellular response has proved controversial. The number of DNA cut sites and the accessibility of RE are recognized examples of confounding factors. We have eliminated these factors by comparing the effectiveness of isoschizomers. Additionally, we considered for the first time the tolerance of the enzymes to cellular conditions. Cell killing and mutation were compared to the overall cutting ability of the enzymes in an "intracellular" buffer. We found that the activity of each RE combined with its lifetime, under simulated cellular conditions, were the overriding factors in determining effectiveness.

Animals↗
PubMed1993

Response of radiation-sensitive human cells to defined DNA breaks.

We have investigated the response of four human cell lines, representing a range of sensitivities to ionizing radiation, to enzymes which induce defined DNA double-strand breaks (dsbs). Cell lines were derived from a normal individual, from the cancer-prone disorders ataxia-telangiectasia (AT) and Bloom's syndrome (BS), and from an immunodeficient individual (46BR). The molecular defects in AT and BS are unknown, while 46BR is known to be DNA ligase I deficient. We assayed the clonogenic survival of the cell lines following in vivo scission of the DNA by the restriction endonucleases PvuII and BanI. These two enzymes differ in their action; PvuII gives rise to dsbs with blunt termini, while BanI generates staggered ends with a 4 bp overhang. We found a correlation between the sensitivity of the cell lines to X-rays and to the blunt-end cutter PvuII, but not to the cohesive-end cutter BanI.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Age-related changes in plasma biochemical values of farmed emus (Dromaius novaehollandiae).

Blood samples were collected from 40 emus (Dromaius novaehollandiae) of 4 different age groups ranging from 1 week to 14 months. Plasma values of glucose, cholesterol, uric acid, total protein, albumin, creatine kinase, aspartate amino transferase, alkaline phosphatase, calcium, phosphorus and magnesium were measured. Fourteen-month-old birds had lower plasma glucose values and enzyme activities and higher plasma protein values than younger birds. One-week-old birds had higher cholesterol and uric acid values than other age groups. Plasma calcium, phosphorus and magnesium values did not differ across the age profiles sampled.

Aging↗
PubMed1991

Elevated levels of DNA double-strand breaks (dsb) in restriction endonuclease-treated xrs5 cells correlate with the reduced capacity to repair dsb.

Recently we have reported the kinetics of DNA double-strand breaks (dsb) induced in electroporated mammalian (CHO) cells that had been treated with the restriction endonuclease PvuII, as measured by the filter elution assay at the non-denaturing pH of 9.6. A gradual accumulation of dsb was observed over a 24-h incubation period following the restriction endonuclease (RE) treatment and this was attributed to a competition between incision of the DNA by PvuII and dsb repair. In order to test this 'competition' hypothesis we have carried out similar experiments in the radiosensitive xrs5 mutant cell line, which has been shown to be deficient in dsb repair. The levels of dsb monitored by the non-denaturing filter elution assay in the xrs5 cell line treated with PvuII was found to be 3-4 times higher than that found for the wild-type CHO K1 cell line. Levels of dsb were also significantly raised in xrs5 cells treated with BamHI, as compared with the background levels observed in the CHO line. These data lend strong support to the competition hypothesis of simultaneous incision and repair of RE-induced dsb.

Animals↗
PubMed1991

Differences in accumulation of blunt- and cohesive-ended double-strand breaks generated by restriction endonucleases in electroporated CHO cells.

Restriction endonucleases (RE) have been used in cytogenetic studies to mimic the DNA double-strand break (dsb)-inducing action of radiation. In the experiments presented here, we have treated electroporated CHO cells with RE and have measured the resulting dsb using the filter elution technique under non-denaturing conditions (pH 9.6). PvuII, which generates blunt-ended dsb, gave rise to a significant number of measurable dsb. The frequency of the dsb induced by PvuII is shown to increase over a 3-12-h post-treatment incubation period, which implies that the RE is active in the cell for a considerable length of time. We postulate that the accumulation of dsb reflects a competition between enzymatic incision and repair of the DNA. The presence of araA, a known inhibitor of DNA synthesis, did not affect the frequency of PvuII-induced breaks indicating a lack of an inhibitory effect of araA on the repair of RE-induced dsb. Two RE which cause cohesive-ended dsb, namely BamHI and EcoRI, were found to be ineffective in giving rise to measurable dsb. Our interpretation of this is that for cohesive-ended dsb (caused by BamHI and EcoRI) the rate at which these breaks are rejoined matches or exceeds the rate of enzymatic incision and hence no dsb were observed. In the case of PvuII, the possibly slower rate of repair of blunt-ended termini would on this hypothesis result in the observed net accumulation of dsb.

Animals↗
PubMed1990

Neutral filter elution detects only limited inhibition of double-strand break repair by 9-beta-D-arabinofuranosyladenine.

Bradley and Kohn (1979) showed that the neutral filter elution technique detects DNA double-strand breaks (dsb), yet there is still some uncertainty regarding the interpretation of results obtained with this technique (viz. the curvilinear dose-response curve and the rapid repair kinetics). In this report we have investigated the effect of the nucleoside analogue 9-beta-D-arabinofuranosyladenine (ara A), a known inhibitor of dsb repair, on the DNA repair in X-irradiated Ehrlich ascites tumour cells as measured by this technique. We have compared the effect of ara A on repair in these cells with results previously obtained with the same cell line and using the neutral velocity sedimentation and DNA unwinding techniques (Blöcher, 1982; Bryant and Blöcher, 1982). Our results suggest that the lesions measured by the neutral elution technique are different from those measured by neutral velocity sedimentation or long-term repair measured by DNA unwinding.

Animals↗
PubMed1990

The induction of DNA double-strand breaks in CHO cells by Pvu II: kinetics using neutral filter elution (pH 9.6).

Chinese hamster CHO K1 cells were treated with the restriction endonuclease Pvu II during electroporation and assayed for DNA double-strand breaks (dsb). Dsb were measured by the non-denaturing filter elution technique (pH 9.6) at various times up to 24 h after restriction endonuclease (RE) treatment. The frequency of dsb following electroporation in the presence of 200 units/ml Pvu II increased over the post-treatment incubation period. This was found not to be due to cell or DNA degradation, indicating that Pvu II remains active for at least 24 h inside the cell. We suggest that these kinetics of dsb result from a competition between incision (by Pvu II) and dsb repair.

Animals↗