J. McK. Watts
Flinders Medical Centre
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Featured researches published by J. McK. Watts.
BMJ | 1966
F. T. de Dombal; J. McK. Watts; G. Watkinson; J. C. Goligher
because of disordered function of the temporal lobe, which may be related to disorder of structure when morphological study is available. It follows that even though the lesion may be a small one the patient is brain-damaged, to use a topical phrase. As the part of the brain damaged is responsible for the integration of all sensation into total experience, and as that experience is primarily responsible for behaviour, it would not be surprising if the epilepsy was associated with psychological disorders reflected in disturbance of mood or attitude, or evidenL in disturbed social behaviour. That of course is the case, tor so many people with aggressive psychopathic behaviour also have disturbance of this part of the brain either reflected in the electroencephalogram or in morbid anatomical studies. If the clinician will keep clearly before him the distinction between what happens in the attack itself (the ictus) and what results from the post-ictal confusional state, and will then divorce these events from the total behaviour of the patient, he will be doing just what the neurologist does when he is faced with the much simpler situation in a patient who has a parietal lobe lesion. In this case there may be a hemiplegia with disturbance of feeling which will affect the patients behaviour at a lower level of functional integration, and this disturbance of movement or behaviour may well be associated with attacks of a parietal lobe kind-that is to say, a focal fit affecting arm or leg,. In this simple situation there is no difficulty in distinguishing between the intermittent epileptic event and the continued life handicap. Although the distinction is much less obvious with temporal lobe lesions, it exists, and in practice it can in most cases be made. To know that it exists will prevent serious mistakes. Lastly, a point which has been made before must be re-emphasized-that in any epileptic patient the impact of the attacks upon the subjects life is apt to lead to psychological difficulties the effects of which are to increase the frequency of attacks and severity of epilepsy ; when the epilepsy includes in its experiences psychic disturbances it is particularly prone to be aggravated by psychological distress.
BMJ | 1966
J. McK. Watts; F. T. de Dombal; G. Watkinson; J. C. Goligher
Brooke, B. N. (1961). Dis. Colon Rect., 4, 393. Brown, M. L., Kasich, A. M., and Weingarten, B. (1951). Amer. 7. dig. Dis., 18, 52. Carleson, R., Fristedt, B., and Philipson, J. (1963). Acta chir. scand., 125, 486. Castleman, B., and Krickstein, H. I. (1962). New Engl. 7. Med., 267, 469. Counsell, P. B., and Dukes, C. E. (1952). Brit. 7. Surg., 39, 485. Crohn, B. B., and Rosenberg, H. (1925). Amer. 7. med. Sci., 170, 220. Dawson, I. M. P., and Pryse-Davies, J. (1959). Brit. 7. Surg., 47, 113. de Dombal, F. T., Watts, J. M., Watkinson, G., and Goligher, J. C. (1966). Awaiting publication. --(1965). Proc. roy. Soc. Med., 58, 713. Dennis, C., and Karlson, K. E. (1961). Surgery, 50, 568. Dukes, C. E. (1954). Ann. roy. Coll. Surg. Engl., 14, 389. Edwards, F. C., and Truelove, S. C. (1964). Gut, 5, 1. Goldgraber, M. B., Humphreys, E. M., Kirsner, J. B., and Palmer, W. L. (1958). Gastroenterology, 34, 809. Jackman, R. J. (1954). Arch. intern. Med., 94, 420. MacDougall, I. P. M. (1954). Brit. med. 7., 1, 852. (1964). Lancet, 2, 655. Michener, W. M., Gage, R. P., Sauer, W. G., and Stickler, G. B. (1961). New Engl. 7. Med., 265, 1075. Nefzger, M. D., and Acheson, E. D. (1963). Gut, 4, 183. Registrar-General (1962). Statistical Review of England and Wales, 1962. Part 1, Tables, Medical. H.M.S.O., London. Rosenqvist, H., Ohrling, H., Lagercrantz, R., and Edling, N. (1959). Lancet, 1, 906. Russell, I. S., and Hughes, E. S. R. (1961). Aust. N.Z. 7. Surg., 30, 306. Slaney, Q., and Brooke, B. N. (1959). Lancet, 2, 694. Sloan, W. P., Bargen, J. A., and Baggenstoss, A. H. (1950). Proc. Mayo Clin., 25, 240, Svartz, N., and Ernberg, T. (1949). Acta med. scand., 135, 444. Texter, E. C. (1957) 7. chron. Dis., 5, 347 Truelove, S. C., and Witts, L. J. (1955). Brit. med. 7., 2, 1041. Van Prohaska, J., and Siderius, N. J. (1962). Surg. Clin. N. Amer., 42, 1245. Watts, J. McK., de Dombal, F. T., Watkinson, G., and Goligher, J. C. (1966). Brit. med. 7., 1, 1447.
BMJ | 1972
R. A. Smallwood; Paula Jablonski; J. McK. Watts
Gall bladder and hepatic bile was sampled from 66 patients undergoing elective operations on the biliary tract. Fifty-one patients had cholesterol gall stones but only 59% of these were found to have bile which was supersaturated with cholesterol. Repeated sampling of hepatic bile from patients with T-tubes showed that the secretion of supersaturated bile was intermittent. These results indicate that it is impossible to separate patients with cholesterol stones from controls simply by examination of the lipid composition of their bile, since an appreciable number of bile samples from patients with cholesterol stones were unsaturated. The fact that cholesterol gall stones form when the bile is supersaturated with cholesterol only intermittently suggests that the gall bladder may also have a part in their formation.
Journal of Gastroenterology and Hepatology | 1986
M. J. Whiting; J. McK. Watts
Abstract Glycoprotein synthesis by the gall‐bladder was studied during cholesterol gallstone formation in mice fed a diet supplemented with 1% cholesterol and 0.5% cholic acid for up to 6 weeks. Within 1 week, this lithogenic diet induced a 5 fold increase in the cholesterol saturation of gall‐bladder bile, which remained near‐saturated for the next 5 weeks. Cholesterol gallstones were infrequent until the fourth week of the diet. Glycoprotein synthesis was measured as the incorporation of 3H‐glucosamine by mouse gall‐bladder explants in organ culture and was found to double after 4 weeks of the diet when expressed per gall‐bladder. This increase could be explained by a marked enlargement of the gall‐bladder with a greater number of mucus‐secreting cells. Gall‐bladder glycoprotein synthesis and secretion did not appear to be regulated by prostaglandins, since indomethacin blocked prostaglandin synthesis but did not inhibit glycoprotein synthesis. High molecular weight mucin glycoprotein accounted for around one‐third of gall‐bladder glycoprotein secretion.
Digestion | 1984
M. J. Whiting; B.M. Bradley; John C. Hall; J. McK. Watts
The ability of chenodeoxycholic acid to dissolve gallstones was compared using different dosage regimens in two groups of 21 patients. The groups were closely matched for patient factors and stone characteristics known to influence the outcome of dissolution treatment. The patients in one group received a standard dose of chenodeoxycholic acid (15 mg/kg/day) taken at mealtimes. The patients in the second group received a bedtime dose of chenodeoxycholic acid which was sufficient to result in a proportion of this bile acid of 70% in the bile acid pool. This dose was monitored using serum bile acid profiles and varied within this test group (range 5.1-13.9 mg/kg/day). The number of patients whose stones completely dissolved in 12 months was similar in the standard-dose (7 of 21) and monitored-dose (8 of 21) groups. These results suggest that a bedtime dose of chenodeoxycholic acid, which is monitored to produce a level of 70% chenodeoxycholic acid in the biliary bile acid pool, is lower than the standard dose taken after meals but is of comparable efficacy. Lower dosage has the advantage of reducing costs and side effects from the drug, although serum bile acid profiling increases the cost of treatment.
British Journal of Surgery | 1966
J. McK. Watts; F. T. de Dombal; J. C. Goligher
British Journal of Surgery | 1965
J. C. Goligher; H. L. Duthie; F. T. deDOMBAL; J. McK. Watts
British Journal of Surgery | 1986
T. G. Wilson; John C. Hall; J. McK. Watts
British Journal of Surgery | 1977
J. McK. Watts; E. S. R. Hughes
British Journal of Surgery | 1966
J. McK. Watts; F. T. de Dombal; J. C. Goligher