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The 20 patients described could be included in the group of patients diagnosed as ;idiopathic steatorrhoea'. However, their histories were short and diarrhoea was not a major feature. Since megaloblastic anaemia due to folic acid deficiency was a common feature it is suggested that these patients may form a homogeneous group and the diagnostic label of temperate sprue is suggested.

Theories regarding the chemistry of the contraction process in striped muscle have been revolutionised during the last year. The Hill-Meyerhof theory was based on the assumption that the contraction process was due to the liberation of lactic acid by the break-down of glycogen, a non-oxidative reaction, and that the recovery process consisted in the oxidation of part of the lactic acid and the resynthesis of glycogen from the remainder. Meyerhof now believes (1, p. 305) that contraction is produced by the break-down of creatin-phosphoric acid (phosphagen), and that the energy produced by carbohydrate break-down is utilised to resynthesise phosphagen.

Summary The effect of a low animal fat diet and of Triparanol (MER 29) was studied in ten cases of cardiovascular disease and in four cases of xanthomatosis with hypercholesterolaemia who had no known vascular involvement. With this treatment, cholesterol levels were effectively reduced in 57 % of cases. Triparanol given alone was effective in 36 %, and dietary control alone in 38 %. Serum phospholipids were apparently not affected by Triparanol, but in 33 % of cases they were reduced by dietary control alone. The response of serum total fatty acids was inconclusive. Attention is drawn to the difficulties in interpreting these results, and particularly to the tendency in a significantly high proportion of cases for the base-line levels of serum cholesterol to fluctuate widely. This method of control of serum lipids is apparently not effective unless the serum cholesterol is greater than 300 mg/100 ml, in which case dietary control should be applied first, supplemented later by Triparanol if necessary, and if effective.

The case history of a 40-year-old woman with a fatal haemorrhage from a duodenal ulcer, jejunitis, renal lithiasis, hypertrophy of the adrenal glands, multiple adenomas of the pancreas, and three adenomas of both the parathyroid and pituitary glands is reported. Though there was histological evidence, in the bones, of hyperparathyroidism, the serum levels of calcium, phosphorus, and phosphatase and the urinary excretion of calcium were normal. The significance of low calcium and high phosphorus excretion in the urine as an indication of parathyroid disorder is discussed."Multiple endocrine adenoma syndrome" is suggested as the appropriate designation for the clinical disorders in which adenomas of one or more endocrine glands are associated with disorders of the alimentary tract when patients present with recurrent peptic ulceration, pancreatic dysfunction, or watery diarrhoea.

Summary Comparative survey of a limited number of cases has shown a tendency for the effects of Atromid and phenindione to be modified when both are given simultaneously. Phenindione may have some inhibiting influence upon the action of Atromid in lowering serum cholesterol, and Atromid increased the responsiveness of patients to phenindione. But it does not follow that other anticoagulants will behave in the same way, and these effects might be independent of the anticoagulant action of phenindione. Phenindione increased the whole blood clotting time, sometimes by a considerable amount, but this tendency was not greater in cases also having Atromid. An unexpected and so far unexplained finding was the apparently consistent fluctuation in the haemoglobin. Both these last two aspects merit further investigation.

The B12 activity as estimated by Lactobacillus leichmannii, the folic-acid-like activity by Streptococcus faecalis (F.A.A.) and the ascorbic acid concentration have been determined in the blood and buffy coat of bone marrow of normal subjects, 10 patients with pernicious anemia in relapse, a group of patients with non-Addisonian megaloblastic anemia and some patients with iron deficiency. A correlation between the serum B12 and the plasma ascorbic acid and their respective levels in bone marrow was observed. The marrow and serum B12 levels in prenicious anemia were abnormally low, but they did not differ from a group of 5 patients with hypochromic normoblastic anemia who had both low serum and marrow levels. The concentration of F.A.A. in the marrow of patients with pernicious anemia was reduced, but it was felt that this was more likely a manifestation of the megaloblastic anemia rather than a causative factor. One of six patients with megaloblastic anemia of pregnancy had no detectable deficiency, while the other five had reduced B12, folic acid and ascorbic acid concentrations. The possible therapeutic implications are discussed. There was a significant reduction in the bone marrow concentration of ascorbic acid in all patients with megaloblastic anemia.

A study of 33 patients with jejunal diverticula showed that all except four had symptoms or metabolic upsets attributable to the presence of the diverticula. A disturbance of vitamin B12 metabolism or absorption was found in 16 patients and neuropathy was found in 12 patients. It is considered that abnormal bacterial activity in the small intestine is an important factor in these patients.

A clinical, biochemical, and pathological study is recorded of 50 patients in whom a diagnosis of idiopathic steatorrhea had been made and who had `flat' jejunal biopsies. It is suggested that there is an underlying constitutional defect, not yet clearly defined, and that possibly secondary intestinal infection allows the intestinal mucosa to become sensitized to substances in the diet. Of these gluten is the commonest; milk adversely affects others; and there may be other factors.

The clinical and haematologic findings in seven patients with scurvy are presented. Although all had overt scurvy, two were not anaemic. Four had hypochromic normoblastic erythropoiesis and one had a megaloblastic anaemia subsequently shown to be Addisonian, Complete haematologic remission was obtained with ascorbic acid in two patients. In two, the response to folic acid appeared to be insignificant and the complete response was attributable to ascorbic acid only. No haematologic change was produced in the patient with megaloblastic anaemia. In two patients the simultaneous occurrence of both scurvy and deficiency of vitamin B 12 did not result in a megaloblastic anaemia. Therapy with ascorbic acid resulted in reduction of the urinary excretion of folic acid-like activity, with no significant changes in the excretion of citrovorum factor. The role of ascorbic acid in erythropoiesis is discussed and a hypothesis presented to explain the therapeutic responses to this vitamin of megaloblastic anaemias in scurvy reported by others.