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Birch, H. L., Bailey, A. J., & Goodship, A. E. (1998). Macroscopic 'degeneration' of equine superficial digital flexor tendon is accompanied by a change in extracellular matrix composition. Equine Vet J, 30(6), 534–539.
Abstract: Injuries to the superficial digital flexor tendon are common in horses required to gallop and jump at speed. Partial rupture of this tendon usually occurs in the central core of the midmetacarpal region and may be preceded by localised degenerative changes. Post mortem examination of apparently normal equine flexor tendons has revealed an abnormal macroscopic appearance in the central core, characterised by a reddish discolouration. We have previously shown that there is also physical damage to the collagen fibres. In the present study we tested the hypothesis that the abnormal appearance is accompanied by changes in the composition of the extracellular matrix of the tendon. Biochemical analysis of the extracellular matrix demonstrated an increase in total sulphated glycosaminoglycan content, increase in the proportion of type III collagen and decrease in collagen linked fluorescence in the central core of 'degenerated' tendons relative to tissue from the peripheral region of the same tendon. Dry matter content and total collagen content were not significantly different between tendon zones or normal and 'degenerated' tendons. These changes suggest a change in cell metabolism and matrix turnover in the central core of the tendon and are likely to contribute to a decrease in mechanical properties in this part of the tendon, predisposing to the characteristic partial rupture of the tendon.
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Beerwerth, W., & Schurmann, J. (1969). [Contribution to the ecology of mycobacteria]. Zentralbl Bakteriol [Orig], 211(1), 58–69.
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Andrews, F. M., Ralston, S. L., Sommardahl, C. S., Maykuth, P. L., Green, E. M., White, S. L., et al. (1994). Weight, water, and cation losses in horses competing in a three-day event. J Am Vet Med Assoc, 205(5), 721–724.
Abstract: Body weight of 48 horses competing in a 3-day event was measured the day before the event (baseline), following the dressage phase of the event (day 1), after the endurance phases of the event (day 2), and 18 to 24 hours after the endurance phases (day 3). Plasma sodium and potassium concentrations were measured the evening before, immediately after, and 10 minutes after the endurance phases. Total body water, water loss, and net exchangeable cation loss were then calculated. Body weight and total body water were significantly decreased, compared with baseline values, at all times during the event, and significant water loss was detected. The largest changes were recorded after the endurance phases of the event. Water deficits were still detected 18 to 24 hours after the endurance phases of the event. Mean plasma sodium concentration was significantly increased immediately after the endurance phases of the event, compared with concentration measured the evening before, and remained increased after the 10-minute recovery period, presumably because of dehydration. Mean plasma potassium concentration was significantly increased immediately after the endurance phases of the event, compared with concentration measured the evening before, but was not increased after the 10-minute recovery period.
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Andersson, P., Kvassman, J., Lindstrom, A., Olden, B., & Pettersson, G. (1981). Effect of NADH on the pKa of zinc-bound water in liver alcohol dehydrogenase. Eur J Biochem, 113(3), 425–433.
Abstract: Equilibrium constants for coenzyme binding to liver alcohol dehydrogenase have been determined over the pH range 10--12 by pH-jump stop-flow techniques. The binding of NADH or NAD+ requires the protonated form of an ionizing group (distinct from zinc-bound water) with a pKa of 10.4. Complex formation with NADH exhibits an additional dependence on the protonation state of an ionizing group with a pKa of 11.2. The binding of trans-N,N-dimethylaminocinnamaldehyde to the enzyme . NADH complex is prevented by ionization of the latter group. It is concluded from these results that the pKa-11.2-dependence of NADH binding most likely derives from ionization of the water molecule bound at the catalytic zinc ion of the enzyme subunit. The pKa value of 11.2 thus assigned to zinc-bound water in the enzyme . NADH complex appears to be typical for an aquo ligand in the inner-sphere ligand field provided by the zinc-binding amino acid residues in liver alcohol dehydrogenase. This means that the pKa of metal-bound water in zinc-containing enzymes can be assumed to correlate primarily with the number of negatively charged protein ligands coordinated by the active-site zinc ion.
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Alexander, F. (1978). The effect of some anti-diarrhoeal drugs on intestinal transit and faecal excretion of water and electrolytes in the horse. Equine Vet J, 10(4), 229–234.
Abstract: The effect of morphine, Tinct. opii, loperamide, pethidine and atropine on intestinal transit and the faecal and urinary excretion of water and electrolytes was studied in ponies. The rate of passage of a particulate marker was slowed by morphine, hastened then slowed by loperamide and Tinct. opii, and hastened by atropine. The liquid marker was slowed by Tinct. opii and hastened then slowed by the other drugs. Only loperamide decreased the faecal sodium excretion. This drug also decreased faecal water and weight; it appeared worthy of clinical trial in diarrhoea. Tinct. opii decreased by morphine, pethidine and atropine increased faecal water.
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Alexander, F. (1977). The effect of diuretics on the faecal excretion of water and electrolytes in horses. Br J Pharmacol, 60(4), 589–593.
Abstract: 1. The effect on plasma, urinary and faecal electrolytes of frusemide and hydrochlorthiazide was measured in ponies, mean weight 180 kg. 2. The rapid loss in urine of large quantities of sodium had only a small effect on plasma sodium concentration. 3. Faecal sodium excretion was increased substantially after the administration of frusemide. 4. Frusemide increased faecal potassium during the 48 h following administration and faecal water in the 24/48 h period. It also produced a hypopotassaemia. 5. Hydrochlorthiazide increased faecal chloride during the 24 h after administration. 6. Frusemide increased the intestinal transit time of both liquid (polyethylene glycol) and particulate (Cr2O3) markers.
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