Prolactin and known modulators of rat splenocytes activate nuclear protein kinase C

Prolactin (PRL) and other trophic factors rapidly activate a nuclear pool(s) of protein kinase C (nPKC) in purified splenocyte nuclei. The PRL also enhanced [2-3H]glycerol incorporation into nuclear mono- and triacylglycerol. An assay was devised which not only probed the ability of the hormone to activate protein kinase C (PKC) but also demonstrated the presence of nuclear substrates. Using this methodology, a biphasic concentration-response curve to PRL was observed. Heterologous species of PRL and various growth factors also activated nPKC. The PRL-induced nPKC stimulation was antagonized by various immunomodulators, G protein-coupling inhibitors, PKC inhibitors, a calmodulin inhibitor, and a peripheral benzodiazepine agonist and antagonist. A monoclonal antibody to PKC, anti-rat PRL antiserum and a monoclonal anti-rat PRL receptor antibody antagonized PRL-induced PKC-dependent nuclear phosphorylation, further implicating nPKC and a PRL receptor-mediated activation process. Nuclear PKC may be a major target for trophic regulation in response to both positive and negative growth signals.     

Medical technology in the United States. The last decade.

This paper reviews the evolution of U.S. policy toward medical technology in areas such as cost containment, regulation of devices and drugs, and third party reimbursement. In addition the authors chronicle the diffusion of major medical technologies, procedures, and organizational innovations in the United States. Finally, the article provides tentative observations on the effect of recent policy changes and concludes with some recommendations for the future.     

Autosomal dominant neovascular inflammatory vitreoretinopathy

Twenty-eight of 61 members of a six-generation family are affected by an autosomal dominant eye disease which has not been described previously. Affected patients are asymptomatic in early adulthood, but have vitreous cells and the selective loss of the b-wave on the electroretinogram. Later, peripheral retinal scarring and pigmentation, peripheral arteriolar closure, and neovascularization of the peripheral retina at the ora serrata or occasionally neovascularization of the optic disc develop. Cystoid macular edema, vitreous hemorrhage, tractional retinal detachment, and neovascular glaucoma can cause profound visual loss. Vitrectomy reduces traction on the retina and allows for retinal reattachment. The role of argon laser photocoagulation or cryopexy in reducing the neovascular complications remains uncertain.     

Smoking--a major cause of polycythaemia.

The importance of smoking in the aetiology of polycythaemia has been assessed in a group of patients referred to a general haematology clinic. All patients with true and relative polycythaemia (excluding those with polycythaemia rubra vera) were studied. Of the 21 such patients evaluated, 14 were smokers and had raised carboxyhaemoglobin levels and had no other demonstrable cause for their polycythaemia. The commonest physiological abnormality in these patients was a raised red cell mass combined with a low plasma volume. Six of the 14 patients were able to reduce their smoking with subsequent improvement in their haematocrits. These results suggest that smoking is a major cause of polycythaemia in an unselected series of referrals to a general haematology clinic. The early identification of these patients may be useful in planning therapy.     

The stability of atracurium in clinical practice

Atracurium has an unusual intrinsic Hofmann elimination which is increased by an alkaline environment and increased temperature. Normally the relaxant is stored at pH 3.3 and kept at a temperature of 4 degrees C. However, it is convenient to have a reasonable quantity available within the operating theatre. This study examined the rate of degradation of atracurium in the operating theatre environment of 20 degrees C. Atracurium within one month of its expiry date was placed in the drawer for anaesthetic drugs in each of three operating theatres. At the end of each month, further drug was added to the stock. At the end of the study, atracurium which had been stored continuously at 4 degrees C, was at 102.9% of nominal strength, having started with 113.5% at manufacture. Atracurium which had been at room temperature for one, two and three months respectively retained 99%, 95% and 92% strength respectively. These results show that even three months' exposure to room temperature does not cause enough deterioration to be clinically significant.