The relationship between job satisfaction, burnout, and turnover intention among physicians from urban state-owned medical institutions in Hubei, China: a cross-sectional study

<p>Abstract</p> <p>Background</p> <p>Throughout China, a growing number of physicians are leaving or intending to depart from their organizations owing to job dissatisfaction. Little information is available about the role of occupational burnout in this association. We set out to analyze the relationship between job satisfaction, burnout, and turnover intention, and further to determine whether occupational burnout can serve as a mediator among Chinese physicians from urban state-owned medical institutions.</p> <p>Methods</p> <p>A cross-sectional survey was carried out in March 2010 in Hubei Province, central China. The questionnaires assessed sociodemographic characteristics, job satisfaction, burnout, and turnover intention. The job satisfaction and occupational burnout instruments were obtained by modifying the Chinese Physicians' Job Satisfaction Questionnaire (CPJSQ) and the Chinese Maslach Burnout Inventory (CMBI), respectively. Such statistical methods as one-way ANOVA, Pearson correlation, GLM-univariate and structural equation modeling were used.</p> <p>Results</p> <p>Of the 1600 physicians surveyed, 1451 provided valid responses. The respondents had medium scores (3.18 +/-0.73) on turnover intention, in which there was significant difference among the groups from three urban areas with different development levels. Turnover intention, which significantly and negatively related to all job-satisfaction subscales, positively related to each subscale of burnout syndrome. Work environment satisfaction (<it>b </it>= -0.074, <it>p < 0.01</it>), job rewards satisfaction (<it>b </it>= -0.073, <it>p < 0.01</it>), organizational management satisfaction (<it>b </it>= -0.146, <it>p < 0.01</it>), and emotional exhaustion (<it>b </it>= 0.135, <it>p < 0.01</it>) were identified as significant direct predictors of the turnover intention of physicians, with 41.2% of the variance explained unitedly, under the control of sociodemographic variables, among which gender, age, and years of service were always significant. However, job-itself satisfaction no longer became significant, with the estimated parameter on job rewards satisfaction smaller after burnout syndrome variables were included. As congregated latent concepts, job satisfaction had both significant direct effects (gamma₂₁= -0.32, <it>p < 0.01</it>) and indirect effects (gamma₁₁× beta₂₁= -0.13, <it>p < 0.01</it>) through occupational burnout (62% explained) as a mediator on turnover intention (47% explained).</p> <p>Conclusions</p> <p>Our study reveals that several, but not all dimensions of both job satisfaction and burnout syndrome are relevant factors affecting physicians' turnover intention, and there may be partial mediation effects of occupational burnout, mainly through emotional exhaustion, within the impact of job satisfaction on turnover intention. This suggests that enhancements in job satisfaction can be expected to reduce physicians' intentions to quit by the intermediary role of burnout as well as the direct path. It is hoped that these findings will offer some clues for health-sector managers to keep their physician resource motivated and stable.</p

A longitudinal analysis of motivation profiles at work

This paper examines the multidimensional nature of workplace motivation and the importance of a continuum structure in self-determination theory through application of complementary variable- and person-centered approaches. This approach is taken to simultaneously model the complexity of motivation and highlight interactions between motivational factors. Additionally, this study represents an initial test of the temporal stability of work motivation profiles. A sample of 510 full-time employees were recruited from a range of occupations. Results support the central importance of a general factor representing self-determination as the most influential factor in an employee’s motivation profile. However, smaller effects associated with the motivation subscales, especially identified regulation, were also noticed. Importantly, motivation profiles were found to be highly stable over the 4-month duration of this study. Results lend support to the theoretical position that while general self-determination is an essential component of motivation, it alone does not fully describe an employee’s motivation

Oral Pirfenidone in patients with chronic fibrosis resulting from radiotherapy: a pilot study

<p>Abstract</p> <p>Background</p> <p>Fibrosis is a common side effect after treatment with ionizing radiation. Several methods to ameliorate debilitating fibrosis have been employed but without consistent results. The goal of this pilot study is to determine if Pirfenidone, a novel regulator of cytokine gene expression, has the potential to ameliorate established radiation-induced fibrosis.</p> <p>Methods</p> <p>Open label, prospective pilot study of 800 mg three times/day, orally administered Pirfenidone was administered to enrolled patients who were had completed radiation therapy and who had established radiation-induced fibrosis. Range of motion (ROM) was assessed using standard measures, and subjective measures of pain, fatigue, disability and global health were measured every three months.</p> <p>Results</p> <p>Seven patients were enrolled of whom 3 had ROM assessments of 1 site and 2 had ROM assessments of 2 sites. Of these assessments, 6 revealed increased ROM during drug intervention while 1 revealed a decreased ROM. There was an overall improvement in the mental composite score of the SF36 while physical composite score was decreased and the vitality score was unchanged. Two patients were removed from the study because of syncopal episodes.</p> <p>Conclusion</p> <p>Several patients experienced improved function of at least 25% and reported subjective improvement. Pirfenidone may benefit patients with radiation-induced fibrosis and is worthy of a larger well controlled trial.</p

Ciprofloxacin, diclofenac, ibuprofen and 17α-ethinylestradiol differentially affect the activity of acetogens and methanogens in anaerobic communities

Pharmaceutical compounds end up in wastewater treatment plants but little is known on their effect towards the different microbial groups in anaerobic communities. In this work, the effect of the antibiotic Ciprooxacin (CIP), the non-steroidal anti-inammatory drugs Diclofenac (DCF) and Ibuprofen (IBP), and the hormone 17-ethinylestradiol (EE2), on the activity of acetogens and methanogens in anaerobic communities, was investigated. Microbial communities were more affected by CIP, followed by EE2, DCF and IBP, but the response of the different microbial groups was dissimilar. For concentrations of 0.01 to 0.1 mg/L, the specic methanogenic activity was not affected. Acetogenic bacteria were sensitive to CIP concentrations above 1 mg/L, while DCF and EE2 toxicity was only detected for concentrations higher than 10 mg/L, and IBP had no effect in all concentrations tested. Acetoclastic methanogens showed higher sensitivity to the presence of these micropollutants, being affect by all the tested pharmaceutical compounds although at different degrees. Hydrogenotrophic methanogens were not affected by any concentration, indicating their lower sensitivity to these compounds when compared to acetoclasts and acetogens.e Portuguese Foundation for Science and Technology (FCT) under the scope of the strategic funding of UID/BIO/04469/2019 unit and BioTecNorte operation (NORTE-01-0145-FEDER-000004) funded by the European Regional Development Fund under the scope of Norte2020 - Programa Operacional Regional do Norte. Ana Rita Silva holds a Grant from FCT, reference SFRH/BD/131905/2017info:eu-repo/semantics/publishedVersio

HEATR2 Plays a Conserved Role in Assembly of the Ciliary Motile Apparatus

Cilia are highly conserved microtubule-based structures that perform a variety of sensory and motility functions during development and adult homeostasis. In humans, defects specifically affecting motile cilia lead to chronic airway infections, infertility and laterality defects in the genetically heterogeneous disorder Primary Ciliary Dyskinesia (PCD). Using the comparatively simple Drosophila system, in which mechanosensory neurons possess modified motile cilia, we employed a recently elucidated cilia transcriptional RFX-FOX code to identify novel PCD candidate genes. Here, we report characterization of CG31320/HEATR2, which plays a conserved critical role in forming the axonemal dynein arms required for ciliary motility in both flies and humans. Inner and outer arm dyneins are absent from axonemes of CG31320 mutant flies and from PCD individuals with a novel splice-acceptor HEATR2 mutation. Functional conservation of closely arranged RFX-FOX binding sites upstream of HEATR2 orthologues may drive higher cytoplasmic expression of HEATR2 during early motile ciliogenesis. Immunoprecipitation reveals HEATR2 interacts with DNAI2, but not HSP70 or HSP90, distinguishing it from the client/chaperone functions described for other cytoplasmic proteins required for dynein arm assembly such as DNAAF1-4. These data implicate CG31320/HEATR2 in a growing intracellular pre-assembly and transport network that is necessary to deliver functional dynein machinery to the ciliary compartment for integration into the motile axoneme

The distinct role of CD4+ and CD8+ T-cells during the anti-tumour effects of targeted superantigens

To target T-cells to the tumour area we created a recombinant protein of the bacterial superantigen (SAg) Staphylococcal enterotoxin A (SEA) and the Fab-fragment of a tumour-reactive antibody. This antibody-targeted SAg immunotherapy therapy has been shown to be highly efficient, eliminating > 95% of the pulmonary metastasis in mice carrying established melanoma micrometastases. Earlier studies demonstrated that elimination of the C215-expressing B16-melanoma lung metastasis was dependent on interferon (IFN)-γ release and expression of perforin. In the present study, therapeutic effector functions were analysed both locally at the tumour site and systemically in the spleen. In order to elucidate the role of each T-cell subset during Fab–SEA therapy, CD4 knock-out (KO) and CD8 KO mice were used. Tumour size reduction was statistically significant in Fab–SEA-based tumour therapy in both types of T-cell-deficient mice compared to wild-type mice. CD4 KO mice displayed a drastic reduction in the number of tumour-infiltrating macrophages and CD8+ T-cells. Therapy-induced accumulation of perforin-containing cells at the tumour site was significantly impaired in CD8 KO mice, and marginally in CD4 KO mice. Moreover, CD4 KO mice failed to produce substantial amounts of the tumour suppressive cytokine IFN-γ. This is in sharp contrast to normal mice where a massive local release was recorded. CD8 KO mice displayed a spontaneous production of interleukin (IL)-4 and IL-10 locally in the tumour. Neither normal nor CD4 KO mice produced detectable levels of these Th-2-associated cytokines. The high level of IL-10 was demonstrated to inhibit Fab–SEA tumour therapy, since the therapeutic efficacy was significantly higher in IL-10 KO mice. These results illustrate the importance of a finely tuned cellular collaboration to regulate the various phases of an efficient anti-tumour immune response. © 1999 Cancer Research Campaig

Public Attitudes toward Consent and Data Sharing in Biobank Research: A Large Multi-site Experimental Survey in the US

Individuals participating in biobanks and other large research projects are increasingly asked to provide broad consent for open-ended research use and widespread sharing of their biosamples and data. We assessed willingness to participate in a biobank using different consent and data sharing models, hypothesizing that willingness would be higher under more restrictive scenarios. Perceived benefits, concerns, and information needs were also assessed. In this experimental survey, individuals from 11 US healthcare systems in the Electronic Medical Records and Genomics (eMERGE) Network were randomly allocated to one of three hypothetical scenarios: tiered consent and controlled data sharing; broad consent and controlled data sharing; or broad consent and open data sharing. Of 82,328 eligible individuals, exactly 13,000 (15.8%) completed the survey. Overall, 66% (95% CI: 63%–69%) of population-weighted respondents stated they would be willing to participate in a biobank; willingness and attitudes did not differ between respondents in the three scenarios. Willingness to participate was associated with self-identified white race, higher educational attainment, lower religiosity, perceiving more research benefits, fewer concerns, and fewer information needs. Most (86%, CI: 84%–87%) participants would want to know what would happen if a researcher misused their health information; fewer (51%, CI: 47%–55%) would worry about their privacy. The concern that the use of broad consent and open data sharing could adversely affect participant recruitment is not supported by these findings. Addressing potential participants’ concerns and information needs and building trust and relationships with communities may increase acceptance of broad consent and wide data sharing in biobank research

Mitochondrial Fragmentation Is Involved in Methamphetamine-Induced Cell Death in Rat Hippocampal Neural Progenitor Cells

Methamphetamine (METH) induces neurodegeneration through damage and apoptosis of dopaminergic nerve terminals and striatal cells, presumably via cross-talk between the endoplasmic reticulum and mitochondria-dependent death cascades. However, the effects of METH on neural progenitor cells (NPC), an important reservoir for replacing neurons and glia during development and injury, remain elusive. Using a rat hippocampal NPC (rhNPC) culture, we characterized the METH-induced mitochondrial fragmentation, apoptosis, and its related signaling mechanism through immunocytochemistry, flow cytometry, and Western blotting. We observed that METH induced rhNPC mitochondrial fragmentation, apoptosis, and inhibited cell proliferation. The mitochondrial fission protein dynamin-related protein 1 (Drp1) and reactive oxygen species (ROS), but not calcium (Ca2+) influx, were involved in the regulation of METH-induced mitochondrial fragmentation. Furthermore, our results indicated that dysregulation of ROS contributed to the oligomerization and translocation of Drp1, resulting in mitochondrial fragmentation in rhNPC. Taken together, our data demonstrate that METH-mediated ROS generation results in the dysregulation of Drp1, which leads to mitochondrial fragmentation and subsequent apoptosis in rhNPC. This provides a potential mechanism for METH-related neurodegenerative disorders, and also provides insight into therapeutic strategies for the neurodegenerative effects of METH