Serum angiotensin I converting enzyme (ACE) and lysozyme have been measured in 23 controls, 115 patients with sarcoidosis, and 64 with other chest diseases. Both enzymes were significantly raised in sarcoidosis. ACE was raised above the normal range in 21 of 72 (29%) patients with definite sarcoidosis and in 17 of 38 (45%) of those who were untreated and seen within one year of presentation. The rise discriminated usefully between those with stable and progressive disease (5% and 62% respectively). Lysozyme was raised in 50 of 72 (69%) patients with sarcoidosis but also in 11 of 54 (20%) patients with other chest diseases. Discrimination between stable and progressive disease was useful only if very high levels were considered. Five patients had serial measurements after treatment with oral steroids and showed a progressive fall in levels of both enzymes, but patients with other diseases also showed a significant fall within the normal range when so treated. Measurement of these enzymes may help in the management of some cases of sarcoidosis, but results require critical interpretation.

Background: The natural history of untreated aneurysmal subarachnoid haemorrhage carries a dismal prognosis. Case fatalities range between 32% and 67%. Treatment with either surgical clipping or endovascular coiling is highly successful at preventing re-bleeding and yet the diagnosis is still missed. Methods: Based on the national guidelines for analysis of cerebrospinal fluid for bilirubin in suspected subarachnoid haemorrhage and a review of other available literature this study has compiled guidance in making the diagnosis. Conclusion: In patients presenting with a suspected non-traumatic subarachnoid haemorrhage, computed tomography within 12 hours will reliably show 98% of subarachnoid haemorrhage. In patients who present after 12 hours with a negative computed tomogram, formal cerebrospinal fluid spectophotometry will detect subarachnoid haemorrhage for the next two weeks with a reliability of 96%. Between the early diagnosis with the aid of computed tomography and the later diagnosis with the added benefit of spectophotometry in the period where computed tomograms become less reliable, it should be possible to diagnose most cases of subarachnoid haemorrhage correctly.

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A method for the analysis of proteins in cerebrospinal fluid (CSF) using free solution capillary electrophoresis (FSCE) was developed, in which the adsorption of proteins to the fused silica capillary wall was virtually eliminated. FSCE was carried out on 30 randomly selected CSF samples. Good sensitivity and resolution was obtained with minimal baseline noise. These preliminary results clearly demonstrated the potential of FSCE to analyse proteins in CSF, both qualitatively and quantitatively more rapidly than has been possible hitherto. A total run time of approximately 30 min allowed between 20 to 25 peaks to be separated. Many peaks with long migration times were detected in CSF that appeared to be specific since they were not detectable in corresponding serum samples. The separation patterns for most of the CSF samples selected showed relatively similar patterns but there were often minor qualitative and quantitative differences. Four CSF samples showed patterns that were significantly different from the others, primarily in the peaks with long migration times. A larger clinical study is now being undertaken.

It has been calculated that to achieve an adequate concentration of a drug for a therapeutically significant period of time in the central core of a 6 cm diameter glioblastoma multiforme at a depth of 1-3 cm from the perfused rim, a plasma level would have to be maintained at therapeutic concentrations for 10-24 hours.' This is difficult to achieve clinically which perhaps goes some way to explaining the disappointing results of chemotherapy in the treatment of human cerebral gliomas. Cerebral gliomas are unique in one particular respect in that in no other tumour is there such a clear kinetic difference between the neoplastic and the normal tissue. The limited effectiveness of certain cell cycle specific drugs such as bleomycin in the treatment of human cerebral gliomas might be due therefore in part to the difficulty in maintaining adequate therapeutic concentrations of drug at the tumour site, rather than an inate ineffectiveness of the drug. Bleomycin has been found to be very effective in the treatment of human ectodermally derived tumours2 and animal