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A method for producing carrier free 66Ga (T1/2:9.4 h; beta +) by 4He bombardment of natural copper targets is presented. 66Ga is formed by means of the 63Cu (4He, n) 66Ga reaction. Production yields are given in the 17.5 to 8 MeV 4He energy range. Chemical purification of 66Ga from the copper target is described. The only radionuclidic impurity found in the final product was 67Ga. Albumin colloids from commercially available kits designed for use with 99mTc could easily be labeled with 66Ga and employed for studies of the lymphatic system by positron emission tomography.

that enhancement of the signal-to-noise ratio could be obtained by ensemble averaging the data for a dilute solution rather than making single determination of a larger sample which gave approximately the same overall signal. Therefore, the application of ensemble averaging techniques to trace analysis should often be more desirable than precon-

Aggregation of suspended HeLa cells is increased on removal of cell surface sialic acid. Calcium ions promote aggregation whereas magnesium ions have no effect. The calcium effect is abolished by previous treatment of the cells with neuraminidase. Trypsinization of the HeLa cells followed by thorough washing diminishes the rate of mutual cell aggregation. Subsequent incubation with neuraminidase restores the aggregation rate to the original value before trypsin treatment. Cells which had acquired a greater tendency for aggregation after removal of peripheral sialic acid lose this property when subsequently treated with trypsin. Calcium ions have no aggregative effect on trypsinized cells. In contrast to HeLa cells, aggregation of human erythrocytes was not increased after treatment with neuraminidase or on addition of calcium. The results with HeLa cells are interpreted as follows: (a) Trypsin-releasable material confers adhesiveness upon the cells. (b) The adhesive property of this material is counteracted by the presence of cell surface sialic acids. (c) Calcium ions exert their effect by attenuating the adverse effect of sialic acid.

Tumour uptake of 13N-labelled ammonia was studied by means of positron emission computerised axial tomography in 46 patients with various extensive neoplastic conditions. Eleven of the patients have been followed sequentially before, during and after radio- and/or chemotherapeutic treatment. Substantial accumulation of 13NH3 (up to five times the amount found in comparable normal tissues) was noted in some cases of breast cancer and their metastases, as well as in soft tissue sarcomas, in malignant neck nodes secondary to head and neck tumours, in lung tumours and their metastases, in melanomas, in malignant lymphomas, in metastasis prostatic carcinoma and in the case of ovarian carcinoma examined. Little or no extra uptake of 13NH3 was found ion necrotic or non-malignant tumours or in primary brain tumours, or in some primary breast cancer which otherwise appeared well vascularized and actively growing. In those patients who were followed sequentially, 13NH3 uptake could be seen to decrease with tumour regression. However, during the course of a radiotherapeutic treatment a transitory increase of 13NH3 uptake could be observed. If the therapy had not been successful, 13NH3 uptake was found to persist after treatment. Uptake of 13NH3 in tumours is to be regarded as the result of a complex interaction of both circulatory and metabolic influences. Studies using more specific tracers of flow and tissue metabolism will probably help to unravel the contributory physiological components.

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Cerebral blood flow and oxygen metabolism have been measured with the steady-state oxygen-15 technique and positron emission tomography in anesthetized dogs. Regional microembolization was induced by infusing Sephadex particles (diameter, 40 /am) into one of the common carotid arteries. In the first series of experiments, 2.5 mg Sephadex was infused, and the dogs were examined within 3-4 hours after embolization. In a second series 0.55 mg Sephadex was infused, and the dogs were examined either in the first 3-4 hours or 24-48 hours after embolization. Cerebral blood flow, oxygen extraction ratio, and cerebral oxygen utilization were measured at 3 Pco 2 levels. In the acute experiments, cerebral oxygen utilization in the embolized hemisphere was 6 (0.55 mg Sephadex) and 25% (2.5 mg Sephadex) lower than on the contralateral side. While cerebral blood flow was symmetrically distributed in normocapnia and hypocapnia, it was 9 (0.55 mg Sephadex) and 35% (2.5 mg Sephadex) lower in the embolized hemisphere during hypercapnia. In normocapnia and hypocapnia the lower oxygen utilization in the embolized hemisphere was characterized by a lower oxygen extraction ratio, and in hypercapnia by an unchanged (0.55 mg Sephadex) or by a higher (2.5 mg Sephadex) extraction ratio. The different effect on oxygen extraction ratio in the control and embolized hemispheres resulted in images of uncoupling between perfusion and oxygen demand that varied according to the Pco 2 . The experiments also showed a fall in cerebral blood flow in the embolized hemisphere after 3-4 hours, indicating delayed hypoperfusion. After 24-48 hours, blood flow was about 10% higher in the embolized hemisphere, and this was observed at the 3 Pco 2 levels, while the oxygen extraction ratio was systematically lower. Oxygen utilization in the embolized hemisphere was depressed to practically the same extent as in acute experiments. It can be concluded that between 4 and 24 hours after microembolization the cerebral microcirculation shows important changes, with installation of luxury perfusion in the face of an unchanging decreased oxygen metabolism. (Stroke 1987;18:128-137)