Granulocyte-macrophage colony-stimulating factor. Sensitive and receptor-mediated regulation by 1,25-dihydroxyvitamin D3 in normal human peripheral blood lymphocytes.

We show that 1,25-dihydroxyvitamin D3 (1,25[OH]2D3), the most hormonally active metabolite of vitamin D3, modulates sensitively and specifically both the protein and messenger RNA accumulation of the multilineage growth factor granulocyte-macrophage colony-stimulating factor (GM-CSF). The regulation of GM-CSF expression is seen in both normal human mitogen-activated T lymphocytes and T lymphocytes from a line (S-LB1) transformed with human T cell lymphotropic virus 1 (HTLV-1). In contrast, cells from a HTLV-1 transformed T lymphocyte line (Ab-VDR) established from a patient with vitamin D-resistant rickets type II with undetectable 1,25(OH)2D3 cellular receptors are resistant to the action of 1,25(OH)2D3. Inhibition of GM-CSF expression by 1,25(OH)2D3 can occur independently of interleukin 2 regulation and is probably mediated through cellular 1,25(OH)2D3 receptors. We conclude that 1,25(OH)2D3 may be important in the physiology of hematopoiesis.     

System for prostate brachytherapy and biopsy in a standard 1.5 T MRI scanner.

A technique for transperineal high-dose-rate (HDR) prostate brachytherapy and needle biopsy in a standard 1.5 T MRI scanner is demonstrated. In each of eight procedures (in four patients with intermediate to high risk localized prostate cancer), four MRI-guided transperineal prostate biopsies were obtained followed by placement of 14-15 hollow transperineal catheters for HDR brachytherapy. Mean needle-placement accuracy was 2.1 mm, 95% of needle-placement errors were less than 4.0 mm, and the maximum needle-placement error was 4.4 mm. In addition to guiding the placement of biopsy needles and brachytherapy catheters, MR images were also used for brachytherapy treatment planning and optimization. Because 1.5 T MR images are directly acquired during the interventional procedure, dependence on deformable registration is reduced and online image quality is maximized.     

Primary hyperaldosteronism caused by adrenocortical carcinoma

Since the syndrome of primary hyperaldosteronism was described by Jerome Conn in 1955, over 300 patients with this disorder have been identified in the medical centers of Vanderbilt University and the University of Michigan. The most frequent cause of this endocrinopathy has been a solitary adenoma of the adrenal cortex (72%); bilateral adrenocortical hyperplasia has been the cause of primary hyperaldosteronism in 27% of cases; less frequently, the cause has been multiple and/or bilateral adenomas (1%). During the last 4 years in these 2 medical centers, we have encountered 3 patients who have had biochemically proven primary hyperaldosteronism due to adrenocortical carcinoma. Each of these unusual cases is summarized with review of the recent literature.

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Resumen Desde la descripción del síndrome de hiperaldosteronismo primario por Jeremo Conn en 1955, más de 300 pacientes con esta entidad han sido identificados en nuestros 2 centros médicos, la Universidad de Vanderbilt (Nashville) y la Universidad de Michigan (Ann Arbor). La causa más frecuente de esta endocrinopatía ha sido el adenoma solitario de la corteza suprarrenal (72%); la hiperplasia adrenocortical bilateral ha sido la causa del hiperaldosteronismo primario en 27% de los casos; con menor frecuencia se han presentado los adenomas multiples y/o bilaterales (1%). En los 4 últimos años hemos encontrado 3 pacientes con hiperaldosteronismo primario comprobado bioquímicamente producido por carcinoma adrenocortical. Se presenta cada uno de estos casos poco usuales junto con una revisión de la literatura reciente.

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Résumé Depuis que le syndrome d'hyperaldostéronisme primitif a été décrit par Jerôme Conn en 1955 plus de 300 sujets qui en étaient victimes ont été identifiés à la Vanderbilt University de Nashville et à l'University of Michigan de Ann Arbor. La cause la plus fréquente de cette endocrinopathie répond à un adénome solitaire de la cortico-surrénale (72%) alors que l'hyperplasie corticale des 2 surrénales est plus rarement à son origine (27%), les adénomes multiples et/ou bilatéraux étant rarissimes (1%). Au cours des 4 dernières années 3 cas d'hyperaldosteronisme dû à un cancer de la cortico-surrénale ont été observés dans les 2 centres. Chacun de ces cas exceptionnels est exposé cependant que la littérature récente concernant l'hyperalderosteronisme est analysée.

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Presented at the International Association of Endocrine Surgeons in Paris, September 1985.     

Transluminal angioplasty of the vertebral and basilar artery

Transluminal angioplasty of brachiocephalic vessels for atherosclerotic lesions is now being performed in selected cases. We have thus far treated 17 cases of vertebral artery stenosis and one case of basilar artery stenosis by intravascular balloon dilatation techniques. Clinical presenting symptoms included vertebral basilar insufficiency, repeated transient ischemic attacks (TIAs), and multiple strokes. We performed successful transluminal angioplasty in 16 patients with marked narrowing (greater than 70%) of the dominant vertebral artery from atherosclerosis. One patient with basilar artery stenosis with tandem atherosclerotic lesions was also treated by angioplasty techniques. Repeat angiography at 3- to 12-month intervals has revealed continued patency at the angioplasty site. Complications occurred in our one patient with basilar artery angioplasty, who suffered a brainstem infarction after treatment, and in one patient who had a TIA after bilateral vertebral artery angioplasty. Two other patients had residual vertebral stenosis but remained asymptomatic after the procedure. All other patients who had successful dilatation were asymptomatic at 6 months to 2 years (mean, 15 months) of follow-up. These initial studies indicate that vertebral artery angioplasty may be effective for treating high-grade atherosclerotic lesions and for improving blood flow to the posterior circulation. Angioplasty of the basilar artery is technically more difficult and has a higher degree of risk because of the many perforating branches supplying the brainstem.     

Anaesthetic potency of inhalation agents is independent of membrane microviscosity

The decrease in membrane microviscosity of erythrocyte ghosts in the presence of clinically relevant concentrations of seven inhalation anaesthetic agents was studied using fluorescence polarization anisotropy of the membrane incorporated fluorescent probes 1,6-diphenyl- 1,3,5-hexatriene and 1-[4-trimethylammoniumphenyl]-6-phenyl-1,3,5- hexatriene. All anaesthetic agents produced a dose-dependent decrease in anisotropy of both probes, indicating decreased membrane microviscosity. The reduction in anisotropy measured at the minimum alveolar concentration (ED50) for anaesthesia was related inversely to the anaesthetic potency of the agent and was directly proportional to the hypothetical concentration of agent in the membrane calculated from lipid-water partition coefficients. These findings do not support the hypothesis that volatile anaesthetic agents act by increasing membrane microviscosity of the bulk lipid bilayer to produce anaesthesia.