Prostaglandin E2 increases the proportion of neonatal rat dorsal root ganglion neurons that respond to bradykinin

Prostaglandins sensitize some nociceptors to noxious mechanical, thermal and chemical stimuli; however, not all nociceptors are sensitized by prostaglandins. We used cultures of dorsal root ganglion neurons from neonatal rats to determine whether prostaglandins differentially alter the responsiveness of populations of neurons to the chemical stimulus bradykinin. Groups of dorsal root ganglion neurons were defined by size of the cell soma and by the presence of immunoreactivity for substance P. An increase in the concentration of free intracellular Ca2+ was used as an indicator of responsiveness to bradykinin. Pretreatment (5 min) with prostaglandin E2 (100 nM) increased the proportion of intermediate-size neurons (somal areas of 240-320 microns2) that responded to 30 nM bradykinin by two-fold but did not alter the proportion of small-size neurons (somal areas of 160-239 microns2) that responded. Pretreatment with prostaglandin E2 had no effect on the maximum increase in free intracellular Ca2+ evoked by 30 nM bradykinin in either population of neurons, defined by size. Although pretreatment with PGE2 did not increase the proportion of intermediate-size neurons that responded to a lower concentration of bradykinin (3 nM), it did increase the concentration of free intracellular Ca2+ evoked by 3 nM bradykinin. Both results were consistent with a leftward shift in the stimulus-response relationship for bradykinin following pretreatment with PGE2. Small- and intermediate-size neurons that responded to bradykinin also differed in their expression of immunoreactivity for substance P. Furthermore, intermediate-size neurons that expressed immunoreactivity for substance P were more likely to respond to bradykinin after treatment with prostaglandin E2. These results support the hypothesis that prostaglandin E2 sensitizes some normally unresponsive primary afferent neurons to chemical stimuli. One population of neurons which becomes responsive to bradykinin after treatment with prostaglandin E2 can be defined based on cell size, and furthermore, these neurons are likely to express substance P. During inflammation, recruitment of primary afferent neurons that are immunoreactive for substance P would enhance the participation of substance P in central mechanisms that contribute to hyperalgesia.     

Primary synovial chondromatosis of the ankle. A case report

A case of primary diffuse synovial chondromatosis of the ankle with long-term follow-up is reported. Trauma is implicated as a precipitating factor. This unusual, distinctive synovial neoplasm presents readily recognizable pathological features (Fig. 2). Specific diagnostic criteria are presented. The differential diagnosis of primary synovial chondromatosis includes secondary reactive synovial chondromatosis and synovial chondrosarcoma. The usual sources of osteochondritic loose bodies, on the other hand, are traumatic joint disruption, osteoarthritis, and infectious disorders. Acute primary synovial chondromatosis is adequately treated by removal of the loose bodies and synovectomy. Postoperative prognosis is dependent on the stage of the disease at the time of surgery. In this acute case, the patient had minimum impairment, and ankle roentgenograms twenty years after the arthrotomy were normal (Fig. 3).     

The Uba2 and Ufd1 proteins of Saccharomyces cerevisiae interact with poly(A) polymerase and affect the polyadenylation activity of cell extracts

We investigated calcium influx in the long lasting potentiation induced in area CA1 of rat hippocampus by brief bath application of the G-protein activator A1F4-(NaF/AlCl3). Brief (10 min) bath application of A1F4 in standard saline (with 2 mM Ca2+) consistently induced a long lasting potentiation which was not observed if A1F4 was bath-applied in nominally calcium free saline. Increasing the potential calcium influx, either by raising extracellular calcium concentration to 3.5 mM or by addition of the voltage operated calcium channel (VOCC) agonist BayK8644, failed to increase the number of slices exhibiting potentiation or the mean level of potentiation. Bath application of AlF4 in the presence of the VOCC antagonist failed to block the potentiation and A1F4- readily induced a long lasting potentiation under voltage clamp conditions, strongly suggesting that the calcium influx required for A1F4-induced potentiation is not through NMDA receptors or VOCC channels. It is suggested that the calcium required may be provided by an ongoing recharging and emptying of IP3 sensitive intracellular Ca2+ stores.     

Smooth muscle cells isolated from the neointima after vascular injury exhibit altered responses to platelet-derived growth factor and other stimuli

Health promotion is gaining widespread recognition throughout the world as the most efficacious practice in achieving health for all. In Canada, the philosophy of health promotion is driving both federal and provincial health initiatives. Such a philosophy is derived from a human science paradigm and is in direct opposition to the natural science paradigm from which the biomedical approach to health care emerged. There now exists a tension between these contrasting paradigms as health care shifts to embrace a health-promotion perspective. The nursing process is based in the natural science paradigm and on a biomedical approach to health care. In order for nurses to embrace health promotion fully, they must move away from the philosophy of the natural sciences and adopt a human science perspective. Such a shift requires a radical transformation in nursing practice as nurses move away from the 'top-down' approach of the nursing process and adopt a 'bottom-up' approach to health-promoting nursing practice. The purpose of this paper is to compare and contrast the nursing process with the principles of health promotion, and to challenge our use of the nursing process in current nursing practice. In particular, a framework for health-promoting nursing practice will be provided.