The role of industry in improving quality of life for persons with an ostomy: a Canadian consensus

Financial and clinical resources (which include 260 enterostomal therapy nurses nationwide) to provide clinical and rehabilitative expertise to the estimated 50,000 to 60,000 Canadians living with an ostomy are limited. Hence, many persons with an ostomy fall through the cracks in the early pre- and postoperative period or are lost to follow-up afterdischarge. Problems and issues related to ostomy management continue to surface throughout their lives. As a result,the time required for rehabilitation is often lengthy, affecting the person's quality of life. The First Canadian Enterostomal Therapy Nurses' Advisory Council consisting of 10 Canadian enterostomal therapy nurses met in February 2004 to identify key issues and concerns for Canadians living the ostomy experience and to identify gaps in information and services available before surgery, during the immediate postoperative period, and as the time from surgery lengthened and patients moved through age-related life issues. The two most important gaps identified were the development of quality, pertinent resources and the dissemination of those resources. The Council also identified potential strategies to bridge these gaps, including utilizing the resources of manufacturer Customer Service departments to follow a communications protocol to provide information to patients, retailers, and providers. Finally, a process map from which individual ostomy manufacturers can build programs and processes for improving patient/provider/manufacturer communication was developed.     

Comfort Theory: a unifying framework to enhance the practice environment

The application of theory to practice is multifaceted. It requires a nursing theory that is compatible with an institution's values and mission and that is easily understood and simple enough to guide practice. Comfort Theory was chosen because of its universality. The authors describe how Kolcaba's Comfort Theory was used by a not-for-profit New England hospital to provide a coherent and consistent pattern for enhancing care and promoting professional practice, as well as to serve as a unifying framework for applying for Magnet Recognition Status.     

Serological study of an allergic agranulocytosis due to noramidopyrine

An allergic agranulocytosis induced by amidopyrine and triggered by noramidopyrine was studied. Leucoagglutinating and leucocytotoxic antibody, active only in the presence of the drug, was demonstrated. The antibody was stable, giving a titre from 1·34 to 1·62 and was present in the IgM (19S globulin) and in the IgG (7S globulin) serum fractions. The site of drug fixation was studied by use of iodoantipyrine labelled with ¹³¹I; a stable fixation was demonstrated on to the IgM and IgG globulins. Special emphasis is given to cross-reaction with compounds related to amidopyrine.     

Development of dyskinesias induced by treatment for Parkinson's disease: potential role of first exposure to L-DOPA (or phenomenon of priming)

L-DOPA-induced dyskinesias are one of the main problems encountered in treating patients with Parkinson's disease (PD). They are induced by the antiparkinsonian medications and primarily related to the degree of dopaminergic depletion, as shown by the fact that they tend to appear several years after the onset of the disease. Do the initial therapeutic decisions taken in treating a PD patient influence the point at which dyskinesias first occur? This question is raised in view of the apparent priming phenomenon that occurs in first exposure to L-DOPA. L-DOPA administrated to an MPTP intoxicated monkey rapidly corrects the animals' motor symptoms but generate dyskinesias. In contrast, the administration of dopaminergic agonists with a long half-life has a similar therapeutic effect but without inducing dyskinesias. However, a parkinsonian monkey that had received L-DOPA and developed dyskinesias, which were subsequently abolished when the treatment was withdrawn for several months, proceeded to develop dyskinesias when treatment with dopaminergic agonists with long half-life was introduced. The monkeys' previous exposure to L-DOPA (i.e. priming) thus increased its susceptibility to develop dyskinesias after exposure to drugs which would not otherwise have had this effect. Pulsatile activation of type D2 dopamine receptors is reported to be the principal factor in the triggering of dyskinesias and may well be involved in the priming phenomenon. While the pathophysiological basis of priming is not yet known, the phenomenon would not appear to be related to a hyperexpression of dopamine receptors (types D1 and D2) in the sensorimotor striatum. The results of recent experiments have given rise to several different hypothesis for the mechanisms involved in priming: the role of internalization of dopamine receptors after administration of dopaminergic drugs; change in the distribution of D3 dopamine receptor; changes in the expression of peptides (substance P, enkephalin) in efferent neurons of the striatum; and reorganization of connections at the level of the dopaminergic neurons and their target tissue. While many questions remain unanswered, it may well be that the initial therapeutic decisions taken when treating de novo patient are crucial in trying to delay the onset of dyskinesias.     

Tracer coupling of neurons in the rat retina inner nuclear layer labeled by Fluorogold

A subpopulation of neurons in the inner nuclear layer (INL) of the rat retina were labeled 9-13 weeks after application of Fluorogold (FG) to the superior colliculus. Neurobiotin injection of FG-labeled cells in the INL of flatmounted living retina revealed that these cells consisted of both displaced ganglion cells and a subset of amacrine cells. Fluorogold-labeled amacrine cells in the INL showed tracer coupling to other presumptive amacrine cells in the INL, but there was no evidence of coupling to neurons in the ganglion cell layer (GCL). As the labeling of amacrine cells by FG may be due to gap junction coupling between ganglion and amacrine cells, these data add to the evidence that tracer coupling between these cells can be unidirectional. Some of the FG-labeled displaced ganglion cells in the INL injected with Neurobiotin also showed tracer coupling to neurons in the INL or GCL.     

Brain biopsy in the diagnosis of cerebral mycosis fungoides

A case of cerebral mycosis fungoides co-existing with progressive multifocal leucoencephalopathy presented with dementia. Brain biopsy established the diagnosis of mycosis fungoides after cerebrospinal fluid examinations and computerised tomographic scanning of the brain produced non-specific abnormalities.     

Neonatal maternal separation opposes the facilitatory effect of castration on the respiratory response to hypercapnia of the adult male rat: Evidence for the involvement of the medial amygdala

Respiratory manifestations of panic disorder (PD) include a greater respiratory instability and enhanced responsiveness to CO₂ compared to normal individuals. Although the prevalence of PD is approximately three times greater in women compared to men, the origins of this sexual dimorphism remain poorly understood. Similar to PD patients, adult female rats previously subjected to neonatal maternal separation (NMS) show an increase in their ventilatory response to CO₂. Because this effect of NMS is not observed in males, we hypothesised that testosterone prevents NMS‐induced hyper‐responsiveness to CO₂. Pups subjected to NMS were placed in an incubator for 3 h d^‐1 from postnatal days 3‐12. Control pups remained undisturbed. At adulthood (8‐10 weeks of age), rats were then subjected either to sham surgery or castration. Fourteen days later, breathing was measured at rest (room air) and during acute exposure to hypercapnia (5 and 10% CO₂ for 10 minutes each) using plethysmography. To gain insight into the mechanisms involved, c‐fos expression was used as an indicator of neuronal activation. Brains were collected following air or CO₂ exposure for quantification of c‐fos positive cells by immunohistochemistry in selected regions, including the paraventricular nucleus of the hypothalamus, the dorsomedial hypothalamus and the amygdalar complex. Castration produced a 100% increase of hyperventilatory response to 10% CO₂ in control rats. Unexpectedly, castration had no effect on the hyperventilatory response of NMS rats. The intensity of the hypercapnic response was inversely correlated with c‐fos expression in the medial amygdala. We conclude that testosterone prevents the hyper‐responsiveness to CO₂, whereas NMS attenuates sensitivity to hormone withdrawal. We propose that an inhibitory influence from the medial amygdala contributes to this effect.