Interprofessional Master of Science in Palliative Care: On Becoming a Palliative Care Community Specialist.

Background: Palliative care (PC) is a limited resource in health care systems. Many providers develop a PC interest later in their careers when it is difficult to relocate and compete for a limited number of training positions. In communities without an academic tertiary medical center, interprofessional PC community specialists are poised to deliver high-quality accessible PC to patients/families with needs beyond what can be addressed by primary care providers. Objective: An interprofessional 36-credit Master of Science in Palliative Care (MSPC) provides evidence-based education to nurses, pharmacists, physicians, physician assistants, social workers, spiritual care providers, psychologists, counselors, and other allied health professionals. Design: The predominantly online curriculum, designed and taught by an interprofessional faculty, focuses on interdisciplinary teamwork, communication skills, and practical application of biomedical and psycho-sociocultural-spiritual-ethics content. The pedagogy is narrative based, emulating in-person clinical experiences, with patient cases progressing throughout the curriculum. We have enrolled four student cohorts. Measurements: Student self-assessments pre-mid-post program. Results: Students highly rate curriculum with demonstrated application of knowledge in case integration assignments, simulations with standardized patients, and Capstone Projects. Students' self-assessed skills on a 39-item scale increased on average to the highest level of 5 (able to perform independently and teach others). Conclusions: The inaugural student cohort reports high levels of engagement and satisfaction, including mastery and synthesis of didactic and experiential content through case integration projects. Students who worked in PC/hospice settings have advanced in their professions; others have transitioned to PC work. The MSPC has capacity to meet projected PC workforce gaps.

An investigation of a possible relationship between olfactory identification deficits at first episode and four-year outcomes in patients with psychosis.

OBJECTIVE: Olfactory identification deficits are found in a significant proportion of patients with schizophrenia spectrum psychotic disorders and appear to be predictive of incomplete remission of negative and cognitive symptoms. In the current study, we examined whether patients with first episode psychosis who have olfactory identification deficits (microsmic) have poorer functional outcome than those whose olfactory status is normal (normosmic). METHOD: Sixty-six (66) first episode psychosis patients (46 M and 20 F) were assessed with the University of Pennsylvania Smell Identification Test (UPSIT) at baseline. UPSIT scores served to classify patients into subgroups. The patients' psychiatrists completed the Social and Occupational Functioning Assessment Scale (SOFAS) and the Levels of Functioning Scale (LOFS) after at least 6 months of treatment. The Premorbid Assessment Scale (PAS) was rated by a parent at baseline. RESULTS: Thirty-eight percent (38%) of the sample was identified as 'microsmic'. LOFS and SOFAS scores were significantly lower in the microsmic group than in the normosmic group. Symptoms were significantly worse in the microsmic group in comparison to the normosmic group. PAS scores did not differ between groups. CONCLUSIONS: First episode patients identified as microsmic at baseline assessment went on to demonstrate poorer functional outcome compared to normosmic patients despite no differences in premorbid adjustment. Olfactory identification deficits at first episode may provide a marker for poorer outcome. Testing olfaction is simple and inexpensive, and could provide clinically valuable information at first episode to identify those patients who might benefit from more intensive interventions promoting functional recovery.

Complete nucleotide sequence of Nootka lupine vein-clearing virus.

The complete genome sequence of Nootka lupine vein-clearing virus (NLVCV) was determined to be 4,172 nucleotides in length containing four open reading frames (ORFs) with a similar genetic organization of virus species in the genus Carmovirus, family Tombusviridae. The order and gene product size, starting from the 5'-proximal ORF consisted of: (1) polymerase/replicase gene, ORF1 (p27) and ORF1RT (readthrough) (p87), (2) movement proteins ORF2 (p7) and ORF3 (p9), and, (3) the 3'-proximal coat protein ORF4, (p37). The genomic 5'- and 3'-proximal termini contained a short (59 nt) and a relatively longer 405 nt untranslated region, respectively. The longer replicase gene product contained the GDD motif common to RNA-dependent RNA polymerases. Phylogenetically, NLVCV formed a subgroup with the following four carmoviruses when separately comparing the amino acids of the coat protein or replicase protein: Angelonia flower break virus (AnFBV), Carnation mottle virus (CarMV), Pelargonium flower break virus (PFBV), and Saguaro cactus virus (SgCV). Whole genome nucleotide analysis (percent identities) among the carmoviruses with NLVCV suggested a similar pattern. The species demarcation criteria in the genus Carmovirus for the amino acid sequence identity of the polymerase (<52%) and coat (<41%) protein genes restricted NLVCV as a distinct species, and instead, placed it as a tentative strain of CarMV, PFBV, or SgCV when both the polymerase and CP were used as the determining factors. In contrast, the species criteria that included different host ranges with no overlap and lack of serology relatedness between NLVCV and the carmoviruses, suggested that NLVCV was a distinct species. The relatively low cutoff percentages allowed for the polymerase and CP genes to dictate the inclusion/exclusion of a distinct carmovirus species should be reevaluated. Therefore, at this time we have concluded that NLVCV should be classified as a tentative new species in the genus Carmovirus, family Tombusviridae.

11beta-HSD1 inhibition ameliorates metabolic syndrome and prevents progression of atherosclerosis in mice.

The enzyme 11beta-hydroxysteroid dehydrogenase (HSD) type 1 converts inactive cortisone into active cortisol in cells, thereby raising the effective glucocorticoid (GC) tone above serum levels. We report that pharmacologic inhibition of 11beta-HSD1 has a therapeutic effect in mouse models of metabolic syndrome. Administration of a selective, potent 11beta-HSD1 inhibitor lowered body weight, insulin, fasting glucose, triglycerides, and cholesterol in diet-induced obese mice and lowered fasting glucose, insulin, glucagon, triglycerides, and free fatty acids, as well as improved glucose tolerance, in a mouse model of type 2 diabetes. Most importantly, inhibition of 11beta-HSD1 slowed plaque progression in a murine model of atherosclerosis, the key clinical sequela of metabolic syndrome. Mice with a targeted deletion of apolipoprotein E exhibited 84% less accumulation of aortic total cholesterol, as well as lower serum cholesterol and triglycerides, when treated with an 11beta-HSD1 inhibitor. These data provide the first evidence that pharmacologic inhibition of intracellular GC activation can effectively treat atherosclerosis, the key clinical consequence of metabolic syndrome, in addition to its salutary effect on multiple aspects of the metabolic syndrome itself.