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Biomedical subjects

D A Rice

Publications and source records attributed to D A Rice.

At least 55 records · Page 3Linked to original sources

Promoter cassettes, antibiotic-resistance genes, and vectors for plant transformation.

We have constructed a set of plant transformation vectors, promoter cassettes, and chimeric antibiotic-resistance genes for the transformation and expression of foreign genes in plants sensitive to Agrobacterium infection. The different vectors allow for either concurrent or consecutive selection for kanamycin and hygromycin resistance and have a number of unique restriction sites for the insertion of additional DNA. The promoter cassettes utilize the CaMV 19S and CaMV 35S promoters and are constructed to allow for the easy insertion of foreign genes. The cloned gene can then easily be inserted into the transformation vectors. We have utilized the promoter cassettes to express the hygromycin-resistance gene either from the CaMV 35S or the CaMV 19S promoters, with both chimeric resistance genes allowing for the selection of hygromycin-resistant tobacco plants.

Cinnamates↗

Central to peripheral sound propagation in excised lung.

The time it takes audible sound to travel from the trachea to the pleura in five intact, excised horse lungs and one dog lung inflated with several gases was measured. Regression estimates of sound speed at total lung capacity (TLC) using straight line distance from the carina to the pleura are: helium, 775 +/- 60.5 m/s (means +/- 95% confidence limits); air, 282 +/- 23.5; carbon dioxide, 219 +/- 25.5; sulfur hexafluoride, 142 +/- 43.5. With the exception of sulfur hexafluoride, these speeds are 15%-20% less than the free-field speed of sound in each gas. Total airway length did not predict time delay any better or worse than straight line distance, but the high correlation between these two predictors (r = 0.94) prevents showing either to be the more predictive. In one lung, airway length was partitioned according to airway diameter. A regression using partitioned airway lengths significantly improved time delay prediction (p less than 0.001) over an unpartitioned model. Sound speed in the trachea equals free-field sound speed. Sound speed in air-filled airways 1 to 25 mm in diameter equals 268 +/- 44 m/s. We conclude that the first sound to reach the surface travels in the airways for at least 90% of the distance, spending at least 87% of the total travel time there.

Acoustics↗

Renal lesions in cattle fed sodium hydroxide-treated barley.

Ten 14-week-old calves were fed a diet containing 87.5% NaOH-treated barley, and killed after 29, 65, 75, 117, 140, 179, 314, 338, and 408 days. Eight control calves were fed a diet in which untreated rolled barley was substituted for alkali-treated grain. Calves receiving NaOH-treated barley became polyuric with urine pH ranging from 9.0 to 9.5, and had significantly raised plasma creatinine levels on day 29. Other clinical findings were normal, and there were no other significant alterations in blood. At necropsy, bilateral renal lesions consisted of white cortical foci, medullary stippling, and the presence of uroliths in the renal papillae and calyces. Microscopic changes included tubular dilatation, atrophy, necrosis, and mineralization, interstitial fibrosis with mononuclear cell invasion and consequent glomerular changes. It appeared that glomerular and interstitial changes were secondary to primary tubular damage. No abnormalities were detected in control calves. Feeding of NaOH-treated barley can result in nephrotoxicosis in cattle.

Animal Feed↗

Experimental myopathy in vitamin E- and selenium-depleted calves with and without added dietary polyunsaturated fatty acids as a model for nutritional degenerative myopathy in ruminant cattle.

Fourteen calves, 14 weeks old, fed a low vitamin E and selenium diet based on sodium hydroxide-treated, selenium-deficient barley showed a rapid decline in plasma alpha-tocopherol, a gradual decline in erythrocyte glutathione peroxidase (GSHPX) activity, elevated plasma creatine kinase (CK) activity, teeth grinding and (in three cases) electrocardiographic changes, but no clinical abnormalities after 127 to 137 days. Necropsy of six depleted calves at that stage revealed pale muscles in two animals and mild histopathological lesions of skeletal myopathy in all six calves. Ten control calves were fed a similar diet supplemented with alpha-tocopherol and selenium. Plasma alpha-tocopherol and erythrocyte GSHPX activity remained high in these calves and no clinical abnormalities or evidence of myodegeneration were observed. When protected linseed oil was fed as a source of polyunsaturated fatty acids to the remaining eight depleted calves, rapid elevations in plasma CK activity and linolenic acid associated with a variety of cardiopulmonary and locomotory signs, electrocardiographic changes and myoglobinuria occurred within six to 11 days. Necropsy revealed widespread severe skeletal myodegeneration (eight calves) and myocardial lesions (five calves) with preferential involvement of the left ventricular myocardium. Clinical signs and pathological changes were similar to those reported in field outbreaks of nutritional degenerative myopathy in ruminant cattle and establish the experimental regime as the first successful model for reproduction of this disease.

Animals↗

Evaluation of flow-volume curves generated by forced-expiratory spirometry in anesthetized dogs.

Positive-pressure plethysmography was used to generate partial and maximal flow-volume data in 10 anesthetized dogs. Acetylcholine (ACh) administered IV induced significant (P less than 0.05) changes in tidal breathing, as evidenced by decreased tidal volume, increased respiratory rate and dynamic resistance, and decreased dynamic compliance. Partial forced-expiratory spirometry-determined from end inspiratory capacity and functional residual capacity, revealed changes in flow and volume as a result of ACh treatment. These changes were not seen in maximal curves (determined from total lung capacity). Peak expiratory flows were limited by the presence of an endotracheal tube. Use of instantaneous time-constant variables to evaluate the concavity or convexity of the downslope of a flow-volume curve did not reveal differences after IV ACh administration. Seemingly, partial forced-expiratory spirometry was useful in detecting bronchoconstriction in anesthetized dogs. Accepted techniques of flow-volume curve analysis for the evaluation of small airway function were not sensitive enough to detect bronchoconstriction in the dog.

Animals↗

Clinical pathology of myodegeneration (pancreas disease) in Atlantic salmon (Salmo salar).

The clinical pathology and histopathology of two groups of Atlantic salmon with severe degenerative myopathy (pancreas disease) is described and compared with a third healthy group. One affected group was anorexic and had low plasma protein and albumin levels while the other was feeding and had normal levels. Both diseased groups had plasma and tissue vitamin E and selenium levels lower than the healthy group. Similarly, creatine kinase values were raised in affected groups. If representative of the syndrome as a whole, the results suggest that the myopathy of pancreas disease has a basis in a vitamin E-selenium deficiency, but whether primary or induced is not clear. The results also demonstrate that the myopathy and pancreatic atrophy do not inevitably lead to anorexia or any other clinically obvious sign of disease, despite both cardiac and oesophageal involvement.

Animals↗

Use of sodium hydroxide treated selenium deficient barley to induce vitamin E and selenium deficiency in yearling cattle.

Selenium deficient barley grown in Northern Ireland was treated with sodium hydroxide to deplete it of vitamin E. Housed cattle fed a complete diet based on this treated barley developed nutritional degenerative myopathy, showing that spontaneous myopathy in yearling cattle can be the result of vitamin E and selenium deficiency alone. The diet used is as effective and cheaper than others presently in use for inducing degenerative myopathy.

Animal Feed↗

Neuropathology of experimental 3-nitro-4-hydroxyphenylarsonic acid toxicosis in pigs.

Twenty pigs were fed a diet containing 187.5 mg kg-1 of 3-nitro-4-hydroxyphenylarsonic acid (3-nitro). Ten pigs were euthanized at intervals up to 29 days, 3-nitro was withdrawn from the diet of the remaining pigs on day 30, and these animals were subsequently euthanized at intervals up to 49 days after commencement of the experiment. A nervous syndrome characterized by clonic convulsive episodes inducible by exercise, developed at day 11. Paraparesis was apparent at day 22 progressing to paraplegia by day 33 (3 days after cessation of 3-nitro feeding). Histopathologic examination revealed myelin and axonal degeneration in the white matter of the spinal cord coincident with the onset of nervous signs. Marchi-positive degeneration was present in the dorsal funiculus at cervical level at day 22. Lesions intensified with increasing duration of toxicosis and while degenerate fibers were seen in all funiculi, there was preferential involvement of the fasciculi gracilis and cuneatus, the peripheral regions of the ventral and lateral funiculi, and a discrete area of the dorsal region of the lateral funiculus. Peripheral and optic neuropathies were evident from day 32 but were always mild and focal. The experiment establishes 3-nitro as a central-peripheral neurotoxicant of pigs.

Animals↗

Experimental 3-nitro-4-hydroxyphenylarsonic acid toxicosis in pigs.

Five times the recommended dose of 3-nitro-4-hydroxyphenylarsonic acid (187.5 mg kg-1) induces a pathognomonic clinical syndrome in pigs. The main clinical features are not continually present but are inducible only by exercise. From day 11 on the experimental diet a nervous syndrome was inducible. This manifested as muscle tremors and clonic convulsive episodes. Paraparesis developed by day 22 and paraplegia by day 33. Liver arsenic levels plateaued at 5.4 +/- 1.3 mg kg-1. The experiment confirms field observations that 3-nitro produces a characteristic toxicological syndrome, which is distinct from that of arsanilic acid. It also confirms that 3-nitro has a higher absolute toxicity than arsanilic acid in pigs as well as a lower margin of safety.

Animals↗

Automated kinetic method for D-3-hydroxybutyrate in plasma or serum.

This assay for 3-hydroxybutyrate in plasma or serum, based on kinetic initial-rate techniques, has been optimized with respect to initial rate and linearity as follows: pH 8.5, hydroxybutyrate dehydrogenase 62.5 U/L, and NAD+ concentration 20 mmol/L. We have used the assay satisfactorily with both the Gilford 103 and Hitachi 705 discrete analyzers, obtaining results that compare well with those by a segmented-flow method. Within-assay precision (CV) varied from 7.8 to 0.6%, depending on both the analyzer used and on the concentration of 3-hydroxybutyrate. Analytical recovery was also dependent on 3-hydroxybutyrate concentration, varying from 99% at 2 mmol/L to 91% at 9.5 mmol/L. Lactate dehydrogenase/lactate interference in this direct assay is eliminated by incorporating oxalate in the assay reagents. Hydrazine, commonly used in equilibrium methods of analysis for 3-hydroxybutyrate, produced no significant advantage in this assay and was omitted. The mixed reagents for the assay are stable at 4 degrees C for at least a week. The advantages of analysis for this metabolite may now be realized, so that clinical and subclinical ketosis can be identified in humans and animals.

3-Hydroxybutyric Acid↗