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Dive into the research topics where J. S. Robson is active.

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Featured researches published by J. S. Robson.


BMJ | 1971

Serum and urinary fibrin-fibrinogen degradation products in glomerulonephritis.

A. R. Clarkson; Mary K. MacDonald; J. J. B. Petrie; John D. Cash; J. S. Robson

The serum and urine concentrations of fibrin/fibrinogen degradation products (F.D.P.) were estimated in 172 patients with glomerulonephritis. In each case the diagnosis was established on the basis of clinical, renal histological, and ultrastructural findings. Serum F.D.P. concentrations were often raised in all types of glomerulonephritis, though more consistently in active proliferative forms. The urinary concentration provided a reliable and sensitive index of activity, progression, and natural history in proliferative glomerulonephritis. In these forms the urinary F.D.P. content was thought to reflect predominantly lysis of intraglomerular fibrin deposits. In minimal lesion and membranous glomerulonephritis low but abnormal concentrations of urinary F.D.P. were consistently found. It is suggested that in these cases the products are derived from limited proteolysis of fibrinogen filtered through an abnormally permeable basement membrane. Daily measurement of urinary F.D.P. concentration is of potential value in the differential diagnosis of patients with glomerulonephritis and at the same time provides a sensitive assessment of the activity and natural history of proliferative disease.


BMJ | 1973

Intravascular coagulation complicating influenza A virus infection.

A M Davison; D Thomson; J. S. Robson

Kuchel, O., Horky, K., Gregorova, I., and Petrasek, J. (1965). Klinische Wochenschrift, 43, 1318. Lambrew, C. T., Carver, S. T., Peterson, R. E., and Horwith, M. (1961). American Journal of Medicine, 31, 81. McGiff, J. C., et al. (1970). American Journal of Medicine. 48, 247. Mellinger, R. C., Petermann, F. L., and Jurgenson, J. C. (1972). Journal of Clinical Endocrinology, 34, 85. Morse, W. J., et al. (1959). American Journal of Medicine, 26, 315. Murphy, B. E. P. (1967). Journal of Clinical Endocrinology and Metabolism, 27, 973. Perez, G., Siegel, L., and Schreiner, G. E. (1971). Clinical Research, 19, 543. Perez, G., Siegel, L., and Schreiner, G. E. (1972). Annals of Internal Medicine, 76, 757. Posner, J. B., and Jacobs, D. R. (1964). Metabolism, 13, 513. Rick, W., Winkler, G., Koch, E., and Bohn, H. (1962). Acta Endocrinologica (K,6benhavn), Suppl. No. 67, p. 103. Schambelan, M., Stockigt, J. R., Collins, R. D., and Biglieri, E. G. (1972). Clinical Research, 20, 220. Sharma, D. C., Nerenberg, C. A., and Dorfman, R. I. (1967). Biochemistry, 6, 3472. Skanse, B., and Hokfelt, B. (1958). Acta Endocrinologica (K#benhavn), 28, 29. Stockigt, R. D., Collins, R. D., Schambelan, M., Brust, N., and Biglieri, E. G. (1971). Clinical Research, 19, 382. Tree, M. (1973).3Journal of Endocrinology, 56, 159. Tree, M. (1972). Ph.D. Thesis. University of Glasgow. Ulick, S., et al. (1964). Journal of Clinical Endocrinology and Metabolism, 24, 669. Vagnucci, A. H. (1969). Jrournal of Clinical Endocrinology and Metabolism, 29, 279. Vagnucci, A. H. (1970). Nephron, 7, 524. Visser, H. K. A., and Cost, W. S. (1964). Acta Endocrinologica (Klbenhavn), 47, 589. Waite, M. A. (1972a). Journal of Physiology, 222, 88P. Waite, M. A. (1973b). Clinical Science. In press. Weidman, P., et al. (1972). Clinical Research, 20, 249. Wilson, I. D., and Goetz, F. C. (1964). American3Journal of Medicine, 36, 635. Wrong, O., and Davies, H. E. F. (1959). Quarterly Journal of Medicine, 28, 259.


Journal of Clinical Pathology | 1973

The role of the mesangial cell in proliferative glomerulonephritis

A. M. Davison; David Thomson; Mary K. Macdonald; W. S. Uttley; J. S. Robson

In 40 patients with a histological diagnosis of proliferative glomerulonephritis the deposition of immunoglobulins, complement (C3), and fibrin/fibrinogen has been assessed by immunofluorescence and electron microscopy. The results of such examinations have been correlated with the outcome of the illness. In minor or resolving disease there is usually minor functional impairment, a good response to therapy or spontaneous resolution, the deposition of small amounts of material in glomerular capillary walls, and active mesangial removal. In moderate to marked disease there is initially a moderately severe functional disorder, a good response to therapy, considerable deposition of material in glomerular capillary walls but with less active mesangial regions than in the previous group. In progressive glomerulonephritis there was initial severe functional disorder, poor response to therapy, large amounts of material deposited within capillary walls, and active mesangial regions which were greatly enlarged, containing numerous deposits. In the rapidly progressive group there was severe functional disorder with poor response to therapy, the deposition of only small amounts of material within capillary walls, the lack of any significant mesangial cell reaction, and the formation of epithelial crescents. The results of the study indicate that in proliferative glomerulonephritis following the deposition of material in glomerular capillary loops, the progression of the disease is, to some extent at least, dependent upon the ability of the mesangial cell to remove such material.


BMJ | 1972

Modification by drugs of urinary fibrin/fibrinogen degradation products in glomerulonephritis.

A.R. Clarkson; Mary K. MacDonald; John D. Cash; J. S. Robson

Treatment with indomethacin, aspirin, or prednisone has been shown to reduce urinary fibrin/fibrinogen degradation products (F.D.P.) in approximately two-thirds of patients with proliferative glomerulonephritis. This reduction which is dose-dependent for prednisone but not for indomethacin or aspirin in the range of doses used occurs within two to three days of beginning treatment and is thought to result from decreased intraglomerular fibrin deposition rather than alteration of glomerular permeability to F.D.P. In patients who responded in this manner treatment was associated with reductions in the degree of proteinuria and maintenance or improvement in renal function.


The American Journal of Medicine | 1959

Cortisone-induced polyuria following hypophysectomy

J. S. Robson; Anne T. Lambie

Abstract 1. 1. A study has been made of the nature of the polyuria induced by cortisone occurring in two patients who had undergone hypophysectomy. 2. 2. In these two patients the polyuria has been shown not to be due to an increase in the load of urinary solute nor to deterioration in those renal functions concerned with water conservation. 3. 3. The view that the phenomenon is due to primary polydipsia seems inescapable. A review of the literature suggests that this mechanism is probably responsible for the syndrome in similar patients described by other workers, with the exception of the patient reported by Leaf et al. [2] in whom alteration in solute load determined the increase in urinary volume. In these circumstances it is inappropriate to refer to the syndrome as diabetes insipidus. 4. 4. In our patients the administration of cortisone has been shown to improve the renal capacity to absorb solute-free water during osmotic diuresis under conditions of hydropenia. 5. 5. This effect is discussed in the light of the Wirz countercurrent hypothesis and in relation to the view that the action of ADH is one of increasing the permeability of the renal tubules to the movement of water along osmotic gradients. The increase in solute-free water reabsorption brought about by cortisone might then be explained by the effect of the steroid in augmenting reabsorption of sodium.


Proceedings of the Association of Clinical Biochemists | 1964

Influence of Extracorporeal Haemodialysis on the Mean Whole-Body Intracellular pH

J. F. Cowie; Anne Lambie; J. S. Robson

Cortisol production rate estimated by the urine method, was applied to the follow-up of three cases of Cushings syndrome treated by the operation of bilateral adrenalectomy with transplantation of one sixth of the total adrenal tissue into the rectal sheath of the anterior abdominal wall. In two patients, lower than normal cortisol production rates associated with hypoadrenocorticism were detected several months after the operation and steroid therapy had to be started. It is believed that control cortisol production rate estimation should be taken as the basis in considering the amount of adrenocortical tissue to be transplanted before deciding whether, this factor or some other factors related to this surgical technique itself, is responsible for the failure of some of this type of operation.


QJM: An International Journal of Medicine | 1968

IRREVERSIBLE POST-PARTUM RENAL FAILURE

J. S. Robson; A. M. Martin; V. Anne Ruckley; Mary K. Macdonald


QJM: An International Journal of Medicine | 1970

GLOMERULAR COAGULATION IN ACUTE ISCHAEMIC RENAL FAILURE1

A. R. Clarkson; Mary K. Macdonald; Valentin Fuster; John D. Cash; J. S. Robson


The Journal of Pathology | 1983

Mesangiocapillary glomerulonephritis: A long-term study of 40 cases

Charles Swainson; J. S. Robson; David Thomson; Mary K. MacDonald


The Lancet | 1961

TRANSPLANTATION OF A KIDNEY FROM AN IDENTICAL TWIN

M.F.A. Woodruff; J. S. Robson; J.A. Ross; B. Nolan; AnneT. Lambie

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John D. Cash

Scottish National Blood Transfusion Service

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AnneT. Lambie

Edinburgh Royal Infirmary

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J. F. Cowie

University of Edinburgh

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Valentin Fuster

Icahn School of Medicine at Mount Sinai

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A.R. Clarkson

Western General Hospital

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B. Nolan

Edinburgh Royal Infirmary

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