The Impact of Mentorship on Nurses’ Level of Self-Efficacy and Motivation to Pursue Board Leadership Positions

Background: Nurses comprise the largest component of the healthcare workforce and possess a unique understanding of healthcare operations and patient care. On average, the proportion of nurses serving on hospital boards range from 2 to 6%, with the proportion of physicians averaging 20%. Over the last decade, much attention has been placed on emphasizing the importance of a nurse’s presence on boards. Despite these initiatives, nurses continue to display an overall hesitancy towards board service. Objectives: The aim of this project was to implement an evidence-based mentorship program to address barriers to board leadership and increase overall self-efficacy and motivation to pursue these positions. Methods: Eleven nurse leader mentees and eleven mentors participated in a voluntary mentorship program that addressed barriers to board leadership and gave guidance to seeking out board positions. Mentees completed the Sundean Healthcare Index for Preparedness in Board Competency (SHIP-BC) survey pre and post participation to measure changes in self-efficacy. Mentors and mentees also completed additional surveys to measure overall satisfaction with the program. Results: There were increases in the mentees average score on the SHIP-BC survey after program completion with a statistically significant difference in personal – interpersonal skills, as exhibited by a two-sided exact p-value of 0.027. Both groups expressed satisfaction in the program, expressing the value of formal mentorship and increased comfort level surrounding pursuing board leadership positions. Conclusions: Nurses possess a unique understanding of the healthcare sphere that make them valuable resources for board positions. Through these roles, nurses would have increased opportunities to advocate for patients and influence healthcare transformation. Utilization of an evidence-based mentorship model can assist in increasing nurses’ understanding of the importance of board leadership and overall feelings of self-efficacy

Oestradiol and prostaglandin F2 alpha regulate sexual displays in females of a sex-role reversed fish

The mechanisms regulating sexual behaviours in female vertebrates are still poorly understood, mainly because in most species sexual displays in females are more subtle and less frequent than displays in males. In a sex-role reversed population of a teleost fish, the peacock blenny Salaria pavo, an external fertilizer, females are the courting sex and their sexual displays are conspicuous and unambiguous. We took advantage of this to investigate the role of ovarian-synthesized hormones in the induction of sexual displays in females. In particular, the effects of the sex steroids oestradiol (E2) and testosterone (T) and of the prostaglandin F2 alpha (PGF2 alpha) were tested. Females were ovariectomized and their sexual behaviour tested 7 days (sex steroids and PGF2 alpha) and 14 days (sex steroids) after ovariectomy by presenting females to an established nesting male. Ovariectomy reduced the expression of sexual behaviours, although a significant proportion of females still courted the male 14 days after the ovary removal. Administration of PGF2 alpha to ovariectomized females recovered the frequency of approaches to the male's nest and of courtship displays towards the nesting male. However, E2 also had a positive effect on sexual behaviour, particularly on the frequency of approaches to the male's nest. T administration failed to recover sexual behaviours in ovariectomized females. These results suggest that the increase in E2 levels postulated to occur during the breeding season facilitates female mate-searching and assessment behaviours, whereas PGF2 alpha acts as a short-latency endogenous signal informing the brain that oocytes are mature and ready to be spawned. In the light of these results, the classical view for female fishes, that sex steroids maintain sexual behaviour in internal fertilizers and that prostaglandins activate spawning behaviours in external fertilizers, needs to be reviewed.Portuguese Foundation for Science and Technology (FCT) [POCTI/BSE/38395/2001, PTDC/MAR/69749/2006, 331/2001]; Macao Science and Technology Development Fund (FDCT) [012/2012/A1]; FCT [SFRH/BPD/30367/2006

Immune reconstitution and clinical recovery following anti-CD28 antibody (TGN1412)-induced cytokine storm

Cytokine storm can result from cancer immunotherapy or certain infections, including COVID-19. Though short-term immune-related adverse events are routinely described, longer-term immune consequences and sequential immune monitoring are not as well defined. In 2006, six healthy volunteers received TGN1412, a CD28 superagonist antibody, in a first-in-man clinical trial and suffered from cytokine storm. After the initial cytokine release, antibody effect-specific immune monitoring started on Day + 10 and consisted mainly of evaluation of dendritic cell and T-cell subsets and 15 serum cytokines at 21 time-points over 2 years. All patients developed problems with concentration and memory; three patients were diagnosed with mild-to-moderate depression. Mild neutropenia and autoantibody production was observed intermittently. One patient suffered from peripheral dry gangrene, required amputations, and had persistent Raynaud's phenomenon. Gastrointestinal irritability was noted in three patients and coincided with elevated γδT-cells. One had pruritus associated with elevated IgE levels, also found in three other asymptomatic patients. Dendritic cells, initially undetectable, rose to normal within a month. Naïve CD8+ T-cells were maintained at high levels, whereas naïve CD4+ and memory CD4+ and CD8+ T-cells started high but declined over 2 years. T-regulatory cells cycled circannually and were normal in number. Cytokine dysregulation was especially noted in one patient with systemic symptoms. Over a 2-year follow-up, cognitive deficits were observed in all patients following TGN1412 infusion. Some also had signs or symptoms of psychological, mucosal or immune dysregulation. These observations may discern immunopathology, treatment targets, and long-term monitoring strategies for other patients undergoing immunotherapy or with cytokine storm

Skin- and gut-homing molecules on human circulating gamma delta T cells and their dysregulation in inflammatory bowel disease

Changes in phenotype and function of γδ T cells have been reported in inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC). Dysregulation of lymphocyte migration plays a key role in IBD pathogenesis; however, data on migratory properties of γδ T cells are scarce. Human circulating γδ T cells from healthy controls (n = 27), patients with active CD (n = 15), active UC (n = 14) or cutaneous manifestations of IBD (n = 2) were characterized by flow cytometry. Circulating γδ T cells in healthy controls were CD3(hi) and expressed CD45RO. They expressed gut-homing molecule β7 but not gut-homing molecule corresponding chemokine receptors (CCR)9, or skin-homing molecules cutaneous lymphocyte-associated antigen (CLA) and CCR4, despite conventional T cells containing populations expressing these molecules. CCR9 expression was increased on γδ T cells in CD and UC, while skin-homing CLA was expressed aberrantly on γδ T cells in patients with cutaneous manifestations of IBD. Lower levels of CD3 expression were found on γδ T cells in CD but not in UC, and a lower proportion of γδ T cells expressed CD45RO in CD and UC. Enhanced expression of gut-homing molecules on circulating γδ T cells in IBD and skin-homing molecules in cutaneous manifestations of IBD may be of clinical relevance

Immunotherapy targeting isoDGR-protein damage extends lifespan in a mouse model of protein deamidation

\ua9 2023 The Authors. Published under the terms of the CC BY 4.0 license. Aging results from the accumulation of molecular damage that impairs normal biochemical processes. We previously reported that age-linked damage to amino acid sequence NGR (Asn-Gly-Arg) results in “gain-of-function” conformational switching to isoDGR (isoAsp-Gly-Arg). This integrin-binding motif activates leukocytes and promotes chronic inflammation, which are characteristic features of age-linked cardiovascular disorders. We now report that anti-isoDGR immunotherapy mitigates lifespan reduction of Pcmt1−/− mouse. We observed extensive accumulation of isoDGR and inflammatory cytokine expression in multiple tissues from Pcmt1−/− and naturally aged WT animals, which could also be induced via injection of isoDGR-modified plasma proteins or synthetic peptides into young WT animals. However, weekly injection of anti-isoDGR mAb (1 mg/kg) was sufficient to significantly reduce isoDGR-protein levels in body tissues, decreased pro-inflammatory cytokine concentrations in blood plasma, improved cognition/coordination metrics, and extended the average lifespan of Pcmt1−/− mice. Mechanistically, isoDGR-mAb mediated immune clearance of damaged isoDGR-proteins via antibody-dependent cellular phagocytosis (ADCP). These results indicate that immunotherapy targeting age-linked protein damage may represent an effective intervention strategy in a range of human degenerative disorders

Multi-wavelength observations of the energetic GRB 080810: detailed mapping of the broadband spectral evolution

GRB 080810 was one of the first bursts to trigger both Swift and the Fermi Gamma-ray Space Telescope. It was subsequently monitored over the X-ray and UV/optical bands by Swift, in the optical by ROTSE and a host of other telescopes and was detected in the radio by the VLA. The redshift of z= 3.355 +/- 0.005 was determined by Keck/HIRES and confirmed by RTT150 and NOT. The prompt gamma/X-ray emission, detected over 0.3-10^3 keV, systematically softens over time, with E_peak moving from ~600 keV at the start to ~40 keV around 100 s after the trigger; alternatively, this spectral evolution could be identified with the blackbody temperature of a quasithermal model shifting from ~60 keV to ~3 keV over the same time interval. The first optical detection was made at 38 s, but the smooth, featureless profile of the full optical coverage implies that this originated from the afterglow component, not the pulsed/flaring prompt emission. Broadband optical and X-ray coverage of the afterglow at the start of the final X-ray decay (~8 ks) reveals a spectral break between the optical and X-ray bands in the range 10^15 - 2x10^16 Hz. The decay profiles of the X-ray and optical bands show that this break initially migrates blueward to this frequency and then subsequently drifts redward to below the optical band by ~3x10^5 s. GRB 080810 was very energetic, with an isotropic energy output for the prompt component of 3x10^53 erg and 1.6x10^52 erg for the afterglow; there is no evidence for a jet break in the afterglow up to six days following the burst.Comment: 15 pages, 9 figures, 4 in colour. Accepted for publication in MNRA

Exploring the uncertainties of early detection results: model-based interpretation of mayo lung project

Background: The Mayo Lung Project (MLP), a randomized controlled clinical trial of lung cancer screening conducted between 1971 and 1986 among male smokers aged 45 or above, demonstrated an increase in lung cancer survival since the time of diagnosis, but no reduction in lung cancer mortality. Whether this result necessarily indicates a lack of mortality benefit for screening remains controversial. A number of hypotheses have been proposed to explain the observed outcome, including over-diagnosis, screening sensitivity, and population heterogeneity (initial difference in lung cancer risks between the two trial arms). This study is intended to provide model-based testing for some of these important arguments.Method: Using a micro-simulation model, the MISCAN-lung model, we explore the possible influence of screening sensitivity, systematic error, over-diagnosis and population heterogeneity.Results: Calibrating screening sensitivity, systematic error, or over-diagnosis does not noticeably improve the fit of the model, whereas calibrating population heterogeneity helps the model predict lung cancer incidence better.Conclusions: Our conclusion is that the hypothesized imperfection in screening sensitivity, systematic error, and over-diagnosis do not in themselves explain the observed trial results. Model fit improvement achieved by accounting for population heterogeneity suggests a higher risk of cancer incidence in the intervention group as compared with the control group