Understanding the distinct experience of rural interprofessional collaboration in developing palliative care programs.

INTRODUCTION: Palliative care is one component of rural generalist practice that requires interprofessional collaboration (IPC) amongst practitioners. Previous research on developing rural palliative care has created a four-phase capacity development model that included interprofessional rural palliative care teams; however, the details of rural team dynamics had not been previously explored and defined. A growing body of literature has produced models for interprofessional collaborative practice and identified core competencies required by professionals to work within these contexts. An Ontario College of Family Physicians discussion paper identifies seven essential elements for successful IPC: responsibility and accountability, coordination, communication, cooperation, assertiveness, autonomy, and mutual trust and respect. Despite the fact that IPC may be well conceptualized in the literature, evidence to support the transferability of these elements into rural health care practice or rural palliative care practice is lacking. The purpose of this research is to bridge the knowledge gap that exists with respect to rural IPC, particularly in the context of developing rural palliative care. It examines the working operations of these teams and highlights the elements that are important to rural collaborative processes. METHODS: For the purpose of this qualitative study, naturalistic and ethnographic research strategies were employed to understand the experience of rural IPC in the context of rural palliative care team development. Purposive sampling was used to recruit key informants as participants who were members of rural palliative care teams. The seven elements of interprofessional collaboration, as outline above, provided a preliminary analytic framework to begin exploring the data. Analysis progressed using a process of interpretive description to embrace new ideas and conceptualizations that emerged from the patterns and themes of the rural health providers' narratives. The questions of particular interest that guided this work were: What are the collaborative processes of a rural palliative care team? To what extent are the seven elements of IPC representative of rural teams' experiences? Are there any additional elements present when examining the experiences of rural teams? RESULTS: The analysis showed that the seven identified elements of IPC were very much integrated in rural teams' collaborative practice, and thus validated the applicability of these elements in a rural context. However, all seven elements were implemented with a rural twist: the distinctiveness of the rural environment was observed in each element. In addition, another element, specific to rural context, was observed, that being the 'automatic teams' of rural practitioners - the collaboration has been established informally and almost automatically between rural practitioners. CONCLUSIONS: This research contributes new knowledge about rural palliative care team work that can assist in implementing models for rural palliative care that apply accepted elements of collaborative practice in the rural context. Understanding the process of how rural teams form and continue to function will help further the current understanding of IPC in the context in which these professionals work.

Expression and functions of galectin-1 in sensory and motoneurons.

Galectin-1 (Gal1) was the first identified member of the galectin family of beta-galactosidase-binding proteins. Gal1 has important roles in processes fundamental to growth and survival of an organism, including cell adhesion, cell proliferation and apoptosis, and is expressed in many tissues, including the nervous system. In the 1980s, research focused on the developmental regulation of Gal1 expression during neurogenesis. Gal1 was found to be expressed mainly in peripherally-projecting neurons beginning early in neurogenesis, and its expression is maintained at high levels in subpopulations of these neurons in the adult rodent. Although the expression pattern of Gal1 implied that it may be involved in axonal guidance or targeting of subsets of sensory and motoneurons, possible roles of Gal1 in the nervous system had not been confirmed until recently. Gal1 has since been shown to be required for the proper guidance of subsets of primary olfactory axons (to targets in the olfactory bulb) and of primary somatosensory axons (to targets in the superficial dorsal horn). In addition, Gal1 has been implicated in the regenerative response of axons following peripheral nerve injury. Gal1 has been shown to promote axonal regeneration through the activation of macrophages. Also, Gal1 may act within the injured neuron to enhance regrowth: the injury-induced regulation of Gal1 in numerous types of peripherally- and centrally-projecting neurons correlates positively with the regenerative potential of their axons. In this review, we discuss the expression pattern of Gal1 in sensory and motoneurons, and the potential roles of Gal1 in development, axonal regeneration and neuropathic pain.

Regulation of neuronal and glial galectin-1 expression by peripheral and central axotomy of rat primary afferent neurons.

Galectin-1 (Gal1) is an endogenously-expressed protein important for the embryonic development of the full complement of primary sensory neurons and their synaptic connections in the spinal cord. Gal1 also promotes axonal regeneration following peripheral nerve injury, but the regulation of Gal1 by axotomy in primary afferent neurons has not yet been examined. Here, we show by immunohistochemistry and in situ hybridization that Gal1 expression is differentially regulated by peripheral nerve injury and by dorsal rhizotomy. Following peripheral nerve injury, the proportion of Gal1-positive DRG neurons was increased. An increase in the proportion of large-diameter DRG neurons immunopositive for Gal1 was paralleled by an increase in the depth of immunoreactivity in the dorsal horn, where Gal1-positive terminals are normally restricted to laminae I and II. Dorsal rhizotomy did not affect the proportions of neurons containing Gal1 mRNA or protein, but did deplete the ipsilateral dorsal horn of Gal1 immunoreactivity, indicating that it is transported centrally by dorsal root axons. Dorsal rhizotomy also resulted in an increase in Gal1 mRNA the nerve peripheral to the PNS-CNS interface (likely within Schwann cells and/or macrophages), and to a lesser extent within deafferented spinal cord regions undergoing Wallerian degeneration. This latter increase was notable in the dorsal columns and along the prior trajectories of myelinated afferents into the deeper dorsal horn. These results show that neuronal and glial expressions of Gal1 are tightly correlated with regenerative success. Thus, the differential expression pattern of Gal1 following peripheral axotomy and dorsal rhizotomy suggests that endogenous Gal1 may be a factor important to the regenerative response of injured axons.

Altered primary afferent anatomy and reduced thermal sensitivity in mice lacking galectin-1.

The transmission of nociceptive information occurs along non-myelinated, or thinly myelinated, primary afferent axons. These axons are generally classified as peptidergic (CGRP-expressing) or non-peptidergic (IB4-binding), although there is a sub-population that is both CGRP-positive and IB4-binding. During neuronal development and following injury, trophic factors and their respective receptors regulate their survival and repair. Recent reports also show that the carbohydrate-binding protein galectin-1 (Gal1), which is expressed by nociceptive primary afferent neurons during development and into adulthood, is involved in axonal pathfinding and regeneration. Here we characterize anatomical differences in dorsal root ganglia (DRG) of Gal1 homozygous null mutant mice (Gal1(-/-)), as well as behavioural differences in tests of nociception. Gal1(-/-) mice have a significantly reduced proportion of IB4-binding DRG neurons, an increased proportion of NF200-immunoreactive DRG neurons, increased depth of central terminals of IB4-binding and CGRP-immunoreactive axons in the dorsal horn, and a reduced number of Fos-positive second order neurons following thermal (cold or hot) stimulation. While there is no difference in the total number of axons in the dorsal root of Gal1(-/-) mice, there are an increased number of myelinated axons, suggesting that in the absence of Gal1, neurons that are normally destined to become IB4-binding instead become NF200-expressing. In addition, mice lacking Gal1 have a decreased sensitivity to noxious thermal stimuli. We conclude that Gal1 is involved in nociceptive neuronal development and that the lack of this protein results in anatomical and functional deficits in adulthood.

Behavioral treatment of chronic psychogenic polydipsia with hyponatremia: a unique case of polydipsia in a primary care patient with intractable hiccups.

Psychogenic polydipsia is recognized as a dangerous and potentially life threatening disorder. Few studies have focused on the treatment of polydipsia presenting in the outpatient setting. A review of the behavioral treatment literature pertaining to psychogenic polydipsia is presented. This review is followed by a case illustration of an outpatient behavioral approach to the treatment of psychogenic polydipsia in a non-psychiatric, primary car, adult, male patient suffering from intractable hiccup. An ABA single-case design was used, with sodium concentration as the dependent variable. This behavioral method appears promising in settings where restriction of fluid intake is not practical.

Mutations in CEN3 cause aberrant chromosome segregation during meiosis in Saccharomyces cerevisiae.

We investigated the structural requirements of the centromere from chromosome III (CEN3) of Saccharomyces cerevisiae by analyzing the ability of chromosomes with CEN3 mutations to segregate properly during meiosis. We analyzed diploid cells in which one or both copies of chromosome III carry a mutant centromere in place of the wild-type centromere and found that some alterations in the length, base composition and primary sequence characteristics of the central A+T-rich region (CDE II) of the centromere had a significant effect on the ability of the chromosome to segregate properly through meiosis. Chromosomes containing mutations which delete a portion of CDE II showed a high rate of premature disjunction at meiosis I. Chromosomes containing point mutations in CDE I or lacking CDE I appeared to segregate properly through meiosis; however, plasmids carrying centromeres with CDE I completely deleted showed an increased frequency of segregation to nonsister spores.

Alterations in the adenine-plus-thymine-rich region of CEN3 affect centromere function in Saccharomyces cerevisiae.

Centromere DNA from 11 of the 16 chromosomes of the yeast Saccharomyces cerevisiae have been analyzed and reveal three sequence elements common to each centromere, referred to as conserved centromere DNA elements (CDE). The adenine-plus-thymine (A + T)-rich central core element, CDE II, is flanked by two short conserved sequences, CDE I (8 base pairs [bp]) and CDE III (25 bp). Although no consensus sequence exists among the different CDE II regions, they do have three common features of sequence organization. First, the CDE II regions are similar in length, ranging from 78 to 86 bp measured from CDE I to the left boundary of CDE III. Second, the base composition is always greater than 90% A + T. Finally, the A and T residues in these segments are often arranged in runs of A and runs of T residues, sometimes with six or seven bases in a stretch. We constructed insertion, deletion, and replacement mutations in the CDE II region of the centromere from chromosome III, CEN3, designed to investigate the length and sequence requirements for function of the CDE II region of the centromere. We analyzed the effect of these altered centromeres on plasmid and chromosome segregation in S. cerevisiae. Our results show that increasing the length of CDE II from 84 to 154 bp causes a 100-fold increase in chromosome nondisjunction. Deletion mutations removing segments of the A + T-rich CDE II DNA also cause aberrant segregation. In some cases partial function could be restored by replacing the deleted DNA with fragments whose primary sequence or base composition is very different from that of the wild-type CDE II DNA. In addition, we found that identical mutations introduced into different positions in CDE II have very similar effects.