Psychological stress and associated factors in caring for patients with delirium among intensive care unit nurses: A cross-sectional study.

BACKGROUND: Caring for patients with delirium is challenging and overwhelming for intensive care unit (ICU) nurses. Investigating the psychological impact of delirium care on ICU nurses is crucial to maintaining their psychological health and improving the quality of care. OBJECTIVE: The objective of this study was to investigate the psychological stress of ICU nurses in caring for patients with delirium and potential factors. METHODS: A total of 355 nurses from three tertiary care hospitals in Hunan Province, China, participated in this cross-sectional survey. Data were collected using the demographic sheet, Impact of Event Scale-Revised, Connor-Davidson Resilience Scale, and Occupational Coping Self-Efficacy Scale for Nurses. Descriptive and multiple linear regression analyses were used to examine the factors associated with psychological stress. RESULTS: ICU nurses suffered moderate psychological stress related to delirium care. The recent time to care for patients with delirium (P < 0.001), familiarity with delirium-related knowledge (P = 0.002), satisfaction with delirium-related support (P = 0.046), psychological resilience (P < 0.001), and occupational coping self-efficacy (P < 0.001) were significant contributors to psychological stress. CONCLUSION: Nurse managers and researchers need to focus on the psychological well-being of ICU nurses in caring for patients with delirium, especially those who are currently caring for patients with delirium, and provide tailored support, increase their knowledge of delirium, and also boost psychological resilience and coping skills.

The bZIP Transcription Factors in Current Jasmine Genomes: Identification, Characterization, Evolution and Expressions.

Jasmine, a recently domesticated shrub, is renowned for its use as a key ingredient in floral tea and its captivating fragrance, showcasing significant ornamental and economic value. When cultivated to subtropical zone, a significant abiotic stress adaptability occurs among different jasmine varieties, leading to huge flower production changes and plantlet survival. The bZIP transcription factors (TFs) are reported to play indispensable roles in abiotic stress tolerance. Here, we performed a genome-level comparison of bZIPs using three-type jasmine genomes. Based on their physicochemical properties, conserved motif analysis and phylogenetic analysis, about 63 bZIP genes were identified and clustered in jasmine genomes, noting a difference of one member compared to the other two types of jasmines. The HTbZIP genes were categorized into 12 subfamilies compared with A. thaliana. In cis-acting element analysis, all genes contained light-responsive elements. The abscisic acid response element (ABRE) was the most abundant in HTbZIP62 promoter, followed by HTbZIP33. Tissue-specific genes of the bZIPs may play a crucial role in regulating the development of jasmine organs and tissues, with HTbZIP36 showing the most significant expressions in roots. Combined with complicated protein interactions, HTbZIP62 and HTbZIP33 might play a crucial role in the ABA signaling pathway and stress tolerance. Combined with RT-qPCR analysis, SJbZIP37/57/62 were more sensitive to ABA response genes compared with other bZIPs in DJ amd HT genomes. Our findings provide a useful resource for further research on the regulation of key genes to improve abiotic stress tolerance in jasmine.

The collaborative mode by PmSVPs and PmDAMs reveals neofunctionalization in the switch of the flower bud development and dormancy for Prunus mume.

Prunus mume (Rosaceae, Prunoideae) serves as an excellent ornamental woody plant with a large-temperature-range cultivation scope. Its flower buds require a certain low temperature to achieve flowering circulation. Thus, it is important to delve into the processes of flower bud differentiation and dormancy, which affected its continuous flowering. These processes are generally considered as regulation by the MADS-box homologs, SHORT VEGETATIVE PHASE (SVP), and DORMANCY-ASSOCIATED MADS-BOX (DAM). However, a precise model on their interdependence and specific function, when acting as a complex in the flower development of P. mume, is needed. Therefore, this study highlighted the integral roles of PmDAMs and PmSVPs in flower organ development and dormancy cycle. The segregation of PmDAMs and PmSVPs in a different cluster suggested distinct functions and neofunctionalization. The expression pattern and yeast two-hybrid assays jointly revealed that eight genes were involved in the floral organ development stages, with PmDAM1 and PmDAM5 specifically related to prolificated flower formation. PmSVP1-2 mingled in the protein complex in bud dormancy stages with PmDAMs. Finally, we proposed the hypothesis that PmSVP1 and PmSVP2 could combine with PmDAM1 to have an effect on flower organogenesis and interact with PmDAM5 and PmDAM6 to regulate flower bud dormancy. These findings could help expand the current molecular mechanism based on MADS-box genes during flower bud development and dormancy.

Plasma complement C3 and C3a are increased in major depressive disorder independent of childhood trauma.

BACKGROUND: Dysregulated complement system is linked to pathophysiology of major depressive disorder (MDD). Childhood trauma has been associated with an increased incidence of adult depression via a putative mechanism of immune activation. This study aimed to measure and compare peripheral levels of complement C3, C3a, C1q and C-reactive protein (CRP) in MDD patients and healthy controls and explore the relationship between these molecule levels and childhood trauma history in the participants. METHODS: The participants were 49 medication-free MDD patients and 45 healthy controls. All participants were asked to finish the Childhood Trauma Questionnaire, followed by blood sampling for measurement of plasma complement C3, C3a, C1q and CRP by means of enzyme-linked immunosorbent assay. RESULTS: Peripheral plasma concentration of C3 and C3a in medication-free MDD group was significantly higher than that in the healthy controls; whereas the concentration of plasma C1q and CRP in depressed patients was comparable to that in healthy controls. All these inflammatory factors were not associated to childhood trauma experience in patients with MDD. CONCLUSION: Our data suggest that complement C3 and C3a may be implicated in the pathophysiology of MDD, although traumatic childhood experiences were not associated with the circulating levels of complement C3, C3a, C1q and CRP.

Downregulation of miR-223 promotes HMGB2 expression and induces oxidative stress to activate JNK and promote autophagy in an in vitro model of acute lung injury.

BACKGROUND: Excessive autophagic activity in alveolar epithelial cells is one of the main causes of acute lung injury (ALI), but the underlying molecular mechanism has not been fully elucidated. Previous studies have shown that microRNAs (miRs) are involved in regulating autophagy in several diseases. This study aimed to determine the role of miR-223 in excessive autophagic activity in alveolar epithelial cells and the underlying mechanism to identify a novel therapeutic targets for the development of new drugs to treat acute respiratory distress syndrome (ARDS). METHODS: A549 cells were treated with lipopolysaccharide (LPS) to establish an ALI in vitro model. The expression of miR-223 and its role of miR-223 in regulating oxidative stress and autophagy in the LPS-treated A549 cells, were examined using RT-PCR, flow cytometry and ELISA. A luciferase reporter assay was performed to verify the interaction between miR-223 and the high-mobility group box 2 (HMGB2) protein. RESULTS: The results showed that the LPS treatment downregulated miR-223 expression in alveolar epithelial cells. We further proved that miR-223 directly targeted the 3-untranslated region of the HMGB2 gene and the downregulation of miR-223 increased HMGB2 protein level, which activated the JNK signalling pathway and thus induced oxidative stress and autophagy in LPS-treated alveolar epithelial cells. Knockdown of HMGB2 protein deactivated the JNK signalling pathway and inhibited autophagy and oxidative stress in alveolar epithelial cells. CONCLUSIONS: The results of this study suggest that miR-223 regulates oxidative stress and autophagy in alveolar epithelial cells by targeting HMGB2 via the JNK signalling pathway.

Curcumin protects rat hippocampal neurons against pseudorabies virus by regulating the BDNF/TrkB pathway.

Pseudorabies virus (PRV) infection can elicit nervous system disorders. Curcumin has been reported to have neuroprotective effects. However, whether curcumin can protect neurons against PRV infection and the underlying mechanisms remain unclear. In the present study, for the first time, the protective effects of curcumin against PRV-induced oxidative stress, apoptosis, and mitochondrial dysfunction in rat hippocampal neurons and the brain-derived neurotrophic factor (BDNF)/tropomyosin-related kinase B (TrkB) pathway were investigated. Results indicated that PRV with a titer of 3.06 × 106 TCID50 (50% tissue culture infective dose) induced oxidative damage of hippocampal neurons 2 h post-infection and that 10 µM curcumin improved the viability of PRV-infected hippocampal neurons. Blocking the BDNF/TrkB pathway reversed the neuroprotective effects of curcumin, which were imparted by decreasing the PRV-induced upregulation of nitric oxide synthase expression, repressing the PRV-activated mitochondrial apoptotic pathway, and mitochondrial dysfunction. To conclude, curcumin exhibited a neuroprotective role against PRV infection by upregulating the BDNF/TrkB pathway. This study provides insight into the anti-PRV neuroprotective application of curcumin and the underlying mechanism in the prophylaxis and treatment of neurological disorders caused by PRV infection.

Virulence gene profiles and molecular genetic characteristics of diarrheagenic Escherichia coli from a hospital in western China.

BACKGROUND: Diarrheagenic Escherichia coli (DEC) is one of the most important etiological agents of diarrheal diseases. In this study we investigated the prevalence, virulence gene profiles, antimicrobial resistance, and molecular genetic characteristics of DEC at a hospital in western China. METHODS: A total of 110 Escherichia coli clinical isolates were collected from the First Affiliated Hospital of Chengdu Medical College from 2015 to 2016. Microbiological methods, PCR, antimicrobial susceptibility test, pulsed-field gel electrophoresis and multilocus sequence typing were used in this study. RESULTS: Molecular analysis of six DEC pathotype marker genes showed that 13 of the 110 E. coli isolates (11.82%) were DEC including nine (8.18%) diffusely adherent Escherichia coli (DAEC) and four (3.64%) enteroaggregative Escherichia coli (EAEC). The adherence genes fimC and fimH were present in all DAEC and EAEC isolates. All nine DAEC isolates harbored the virulence genes fyuA and irp2 and four (44.44%) also carried the hlyA and sat genes. The virulence genes fyuA, irp2, cnf1, hlyA, and sat were found in 100%, 100%, 75%, 50%, and 50% of EAEC isolates, respectively. In addition, all DEC isolates were multidrug resistant and had high frequencies of antimicrobial resistance. Molecular genetic characterization showed that the 13 DEC isolates were divided into 11 pulsed-field gel electrophoresis patterns and 10 sequence types. CONCLUSIONS: To the best of our knowledge, this study provides the first report of DEC, including DAEC and EAEC, in western China. Our analyses identified the virulence genes present in E. coli from a hospital indicating their role in the isolated DEC strains' pathogenesis. At the same time, the analyses revealed, the antimicrobial resistance pattern of the DEC isolates. Thus, DAEC and EAEC among the DEC strains should be considered a significant risk to humans in western China due to their evolved pathogenicity and antimicrobial resistance pattern.