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The fundamental pathological processes of diseases involving generalized disturbance of skeletal mineralization are ill understood, and treatment is often unsatisfactory. Radiographic techniques are widely used in the diagnosis and management of bone disease. Such techniques are fundamentally dependent on the radio-opacity of skeletal calcium. The most careful radiological assessments may not detect skeletal demineralization until as much as 40% of skeletal calcium is lost (Simon, 1965 possible to achieve uniformity of neutron flux over a field large enough to accommodate a human subject at 2 m. from the source. Details of the experiments and the reason for using neutrons.of this energy are given by Chamberlain et al. (1968aChamberlain et al. ( , 1968b.On the basis of these preliminary experiments neutron activation was carried out on cadavers. A total of seven activations were performed on three cadavers. A wooden coffin (1.5 cm. thick) conveniently provided the necessary moderation of fast neutrons. Uniformity of activation was achieved by irradiating first posteroanteriorly and then from the opposite direction. The irradiation times were arranged to compensate for the decay of 4'Ca during the first half of activation; the total irradiation time was 5 minutes 16 seconds.The slow neutron flux was measured by the activity produced in indium foils, suitably placed in the neutron field. After activation the cadaver was quickly transferred to the whole body counter. The whole body counter is based on four 12.1 by 10.5 cm. sodium iodide crystals, completely shielded by 15 cm. of armour-plate steel lined by 3 mm. of lead. The spectrum is analysed by a 512-channel pulse-height analyser, and processed by a programme using the KDF9 computer of the University of Birmingham. The 49Ca activity (3.05 MeV) is based on the 2.92-3.30 MeV range. Repeated counting showed that the activity in this range had a half-life closely corresponding with 49Ca (8.9 minutes). The results of seven activations in three cadavers are shown in Table I. Included

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Summary. Twenty‐two patients with accelerated hypertension and varying degrees of renal involvement have been studied in order to assess the significance of microangiopathic haemolytic anaemia (MAHA) and the possible pathogenic role of intravascular fibrin deposition in this condition. Vascular damage was assessed by retinal photography including fluorescein angiography. Haematological investigations including examination of peripheral films and assessment of red cell fragmentation were carried out. Fibrinogen catabolism was measured using radio‐iodine labelled fibrinogen. No correlation between the degree of vascular damage in the retinal vessels and the blood pressure, degree of red cell fragmentation or evidence of renal damage was found. There was a significant increase in red cell fragmentation when the creatinine clearance was 20 ml/min or less. Fibrinogen derivatives were demonstrated in the serum in the minority and in the urine of the majority of those patients with MAHA. Fibrinogen catabolism was normal in all cases. The significance of microangiopathic haemolytic anaemia in accelerated hypertension is discussed. It is suggested from these data that the red cell fragmentation occurs predominantly within the kidney and that there is no evidence that fibrinogen deposition plays an important role in red cell damage, or that it is an important pathogenic factor in producing accelerated hypertension.

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