Registered nurses' experiences of communication with patients after the end-of-life breakpoint communication: A pilot interview study.

Purpose: Effective nurse-patient communication is demanding and essential when patients' treatment changes from curative to palliative approach. We aimed to illustrate nurses' experiences communicating with patients who have undergone end-of-life breakpoint communication.

Method: Six nurses from both haematology and oncology wards at a hospital in southern Sweden were interviewed.

Plasma membrane cyclic nucleotide phosphodiesterase 3B (PDE3B) is associated with caveolae in primary adipocytes.

Caveolae, plasma membrane invaginations particularly abundant in adipocytes, have been suggested to be important in organizing insulin signalling. Insulin-induced activation of the membrane bound cAMP degrading enzyme, phosphodiesterase 3B (PDE3B) is a key step in insulin-mediated inhibition of lipolysis and is also involved in the regulation of insulin-mediated glucose uptake and lipogenesis in adipocytes. The aim of this work was to evaluate whether PDE3B is associated with caveolae.

Chemical derivatization of phosphoserine and phosphothreonine containing peptides to increase sensitivity for MALDI-based analysis and for selectivity of MS/MS analysis.

Protein phosphorylation is one of the most important and common ways of regulating protein function in cells. However, phosphopeptides are difficult to analyse, ionising poorly under standard MALDI conditions. Several methods have been developed to deal with the low sensitivity and specificity of phosphopeptide analysis.

Dimethylaminopurine inhibits metabolic effects of insulin in primary adipocytes.

Dimethylaminopurine (DMAP) has previously been used as an inhibitor of phosphorylation in studies of meiotic events, and more recently to investigate TNFalpha signaling, because of its potential to inhibit activation of c-jun N-terminal kinase (JNK). Here we have addressed the effects of DMAP on metabolic insulin responses in adipocytes and on intracellular insulin signaling molecules. At 100 micromol/L, DMAP completely inhibited the ability of insulin to counteract lipolysis in isolated adipocytes.