Evidence for coexistence of dopamine and CCK in meso-limbic neurones.

Vanderhaeghen et al. reported the occurrence of gastrin-like immunoreactivity in the mammalian brain. Subsequent studies have revealed that this immunoreactivity corresponded mainly to the COOH-terminal octapeptide of cholecystokinin (CCK-8), which has a COOH-terminal pentapeptide identical to gastrin. Also, two peptides resembling the NH- and the COOH-terminal tetrapeptide fragments of CCK-8 are present in the central nervous system (CNS). Using COOH-terminal-specific antisera raised to gastrin and/or CCK, the distribution of CCK neurones has been described with immunohistochemical techniques. Although high numbers of cells and nerve terminals are found in cortical areas, the CCK systems are also present in most other parts of the brain and spinal cord. In the CNS, true gastrin molecules, gastrin-17 and gastrin-34 have been located only in the neurohypophysis, hypothalamus and occasionally in the medulla oblongata (unpublished results). We describe here the occurrence of peptides in meso-limbic dopamine neurones in the rat brain. Evidence has also been obtained that mesencephalic dopamine neurones in the human brain contain similar peptides.

Acute phase of sarcoidosis with splenomegaly and hypercalcemia. Description of a case, including a report about splenectomy and the preparation and testing of a Kveim antigen from the spleen.

A young man had a mild, slightly progressive pulmonary sarcoidosis. After 4 years he developed an acute disease with splenomegaly, anemia, marked elevation of ESR, hypercalcemia and mild renal insufficiency. The anemia and ESR elevation disappeared after splenectomy, whereas the hypercalcemia still needs corticosteroid treatment. Attempts to withdraw this treatment resulted in recurrence of the hypercalcemia, but no other abnormalities. In contrast to other organs examined, the sarcoid tissue in the spleen revealed necrosis formation, consistent with a recent process. A Kveim antigen preparation from the spleen was less potent than antigen from mediastinal lymph nodes. It is suggested that the acute phase of the disease involved mainly the spleen. Speculations about the possible role of infectious agent(s) are put forward.

Effect of somatostatin on basal and glucose induced insulin release in five patients with hyperinsulinaemia.

Somatostatin in a dose of 490 mug over 90 min inhibited basal insulin release in one subject with hyperplasia of the pancreatic islets and in two with benign insulin secreting adenomas. These three subjects also showed a marked insulin response to glucose infusion. No inhibitory effect of somatostatin was observed in two patients with benign insulinomas who demonstrated only a minor response to glucose. In the patient with islet hyperplasia and in one of the adenoma patients, who had an exaggerated insulin response to glucose (maximal response 10-30 times the basal insulin value), somatostatin also suppressed glucose induced insulin release. Our data suggest a beneficial therapeutic effect of somatostatin in patients with spontaneous hyperinsulinism with a pronounced insulin response to glucose.

The alveolar lining layer in experimental paraquat poisoning.

Rats were injected with paraquat, 35 mg/kg, and killed 8 or 12 hours later. Electron microscopic studies of the lungs revealed degenerative changes in alveolar epithelium and alveolar capillary endothelium after 8 hours. After 12 hours, the alveolar lining layer was contaminated with cellular debris from disintegrating alveolar epithelium. This contamination is probably responsible for the inactivation of lung surfactant that can be demonstrated in early stages of experimental paraquat poisoning.