The inhibition of MARCO by PolyG alleviates pulmonary fibrosis via regulating mitochondrial function in a silicotic rat model.

Silicon dioxide (SiO2)-induced pulmonary fibrosis is potentially associated with the impairment of mitochondrial function. Previous research found that inhibition of macrophage receptor with collagenous structure (MARCO) could alleviate particle-induced lung injury by regulating phagocytosis and mitigating mitochondrial damage. The present study aims to explore the underlying anti-fibrosis mechanism of polyguanylic acid (PolyG, MARCO inhibitor) in a silicotic rat model. Hematoxylin and eosin and Masson staining were performed to visualize lung tissue pathological changes. Confocal microscopy, transmission electron microscope, western blot analysis, quantitative real-time PCR (qPCR), and adenosine triphosphate (ATP) content assay were performed to evaluate collagen content, mitochondrial function, and morphology changes in SiO2-induced rat pulmonary fibrosis. The results suggested that SiO2 exposure contributed to reactive oxygen species aggregation and the reduction of respiratory complexes and ATP synthesis. PolyG treatment could effectively reduce MARCO expression and ameliorate lung injury and fibrosis by rectifying the imbalance of mitochondrial respiration and energy synthesis. Furthermore, PolyG could maintain mitochondrial homeostasis by promoting peroxisome proliferator-activated receptor-coactivator 1 α (PGC1α)-mediated mitochondrial biogenesis and regulating fusion and fission. Together, PolyG could ameliorate SiO2-induced pulmonary fibrosis via inhibiting MARCO to protect mitochondrial function.

XAV-939 inhibits epithelial-mesenchymal transformation in pulmonary fibrosis induced by crystalline silica via the Wnt signaling pathway.

Silicosis is an occupational lung disease that results from long-term inhalation of free silica dust, the expression is sustained inflammation response, fibroblast hyperplasia, and excessive collagen deposit, bringing about pulmonary interstitial fibrosis. Wnt signaling pathway exists in various kinds of eukaryotic cells, is a highly conservative signaling pathway in biological evolution, and participates in cell proliferation, differentiation, migration, and polarity of physiological activity, such as in embryonic development, organ morphology, and tumor. In addition, it plays an important role in the progress of fibrosis disease. At present, studies related to silicosis are increasing, but the pathogenesis of silicosis still is not clear. In recent years, more and more studies have suggested that the Wnt signaling pathway could participate in the pathogenesis of silicosis fibrosis. In the study, we explored the mechanism of the Wnt signaling pathway in the pathogenesis of silicosis fibrosis and evaluated the effect of XAV-939 treatment epithelial-mesenchymal transformation (EMT) induced by silica. In addition, the results showed that EMT and activation of the Wnt signaling pathway would occur after stimulation of silica or TGF-ß1. However, after treatment with the Wnt signaling pathway inhibitor XAV-939, EMT was reversed and the expression of the ß-catenin decreased. These results suggested that the Wnt signaling pathway is associated with EMT induced by silica and it could be a potential target for the treatment of silicosis.

Metformin alleviates crystalline silica-induced pulmonary fibrosis by remodeling endothelial cells to mesenchymal transition via autophagy signaling.

Silicosis is a severe progressive lung disease without effective treatment methods. Previous evidence has demonstrated that endothelial cell to mesenchymal transition (EndoMT) plays an essential role in pulmonary fibrosis, and pulmonary fibrosis is associated with dysregulation of autophagy, while the relationship between autophagy and EndoMT has not yet been adequately studied. Herein, we established a mouse model of silicosis, and we found that the pharmacological induction of the AMPK/mTOR-dependent pathway using 100 mg/kg Metformin (Met) enhanced autophagy in vivo, and results of the Western blot showed that autophagy-related proteins, LC3 II/I ratio, and Beclin-1 increased while p62 decreased. In addition, Met treatment attenuated silica-induced pulmonary inflammation and decreased collagen deposition by suppressing EndoMT, and the proliferation of human umbilical vein endothelial cells (HUVECs) was also inhibited. Notably, the tube forming assay showed that Met also protected the vascular endothelial cells from silica-induced morphological damage. In conclusion, Met can alleviate inflammatory response and collagen deposition in the process of pulmonary fibrosis induced by silica via suppressing EndoMT through the AMPK/mTOR signaling pathway.

Social Support, Unstable Angina, and Stroke as Predictors of Depression in Patients With Coronary Heart Disease.

BACKGROUND: Depression is known to adversely affect coronary heart disease patients in western countries; however, no study of social support and depression has been conducted in the Chinese population. OBJECTIVE: The aim of this study was to investigate the predictors of depression in patients with coronary heart disease. METHODS: Between January and December 2015, a cross-sectional sample of 105 Taiwanese patients from cardiology units completed a demographic and clinical characteristics questionnaire, Enhancing Recovery in Coronary Heart Disease Social Support Inventory, and Patient Health Questionnaire-9. RESULTS: Thirty-nine percent of the participants reported low social support, and 61.0% had depression symptoms. Eight factors predicted depression. Social support was significantly and adversely correlated with depression (r = -.481, P < .01). The other 7 factors were positively correlated with depression: age (r = .212, P < .05), reported monthly income of less than US $600 (F = 4.98, P = .001), lack of exercise (F = 3.75, P = .027), history of stroke (t = -2.45, P = .016) and kidney disease (t = -2.41, P = .018), unstable angina (F = 3.56, P = .031), and groin puncture (F = 3.27, P = .042). A hierarchical regression model explained 43.7% of the variance in depression. CONCLUSION: Social support, unstable angina, and stroke may be important predictors of depression in patients with coronary heart disease. These findings help clinical staff to understand physical and mental health problems in cardiovascular patients. Thus, we suggest that early depression prediction and sufficient social support can help patients to face their disease and thus improve depression and health care quality.

Activation of Sirtuin3 by honokiol ameliorates alveolar epithelial cell senescence in experimental silicosis via the cGAS-STING pathway.

BACKGROUND: Silicosis, characterized by interstitial lung inflammation and fibrosis, poses a significant health threat. ATII cells play a crucial role in alveolar epithelial repair and structural integrity maintenance. Inhibiting ATII cell senescence has shown promise in silicosis treatment. However, the mechanism behind silica-induced senescence remains elusive. METHODS: The study employed male C57BL/6 N mice and A549 human alveolar epithelial cells to investigate silicosis and its potential treatment. Silicosis was induced in mice via intratracheal instillation of crystalline silica particles, with honokiol administered intraperitoneally for 14 days. Silica-induced senescence in A549 cells was confirmed, and SIRT3 knockout and overexpression cell lines were generated. Various analyses were conducted, including immunoblotting, qRT-PCR, histology, and transmission electron microscopy. Statistical significance was determined using one-way ANOVA with Tukey's post-hoc test. RESULTS: This study elucidates how silica induces ATII cell senescence, emphasizing mtDNA damage. Notably, honokiol (HKL) emerges as a promising anti-senescence and anti-fibrosis agent, acting through sirt3. honokiol effectively attenuated senescence in ATII cells, dependent on sirt3 expression, while mitigating mtDNA damage. Sirt3, a class III histone deacetylase, regulates senescence and mitochondrial stress. HKL activates sirt3, protecting against pulmonary fibrosis and mitochondrial damage. Additionally, HKL downregulated cGAS expression in senescent ATII cells induced by silica, suggesting sirt3's role as an upstream regulator of the cGAS/STING signaling pathway. Moreover, honokiol treatment inhibited the activation of the NF-κB signaling pathway, associated with reduced oxidative stress and mtDNA damage. Notably, HKL enhanced the activity of SOD2, crucial for mitochondrial function, through sirt3-mediated deacetylation. Additionally, HKL promoted the deacetylation activity of sirt3, further safeguarding mtDNA integrity. CONCLUSIONS: This study uncovers a natural compound, HKL, with significant anti-fibrotic properties through activating sirt3, shedding light on silicosis pathogenesis and treatment avenues.

Nursing Staff Presenteeism Scale: Development and psychometric test.

BACKGROUND AND OBJECTIVES: Nurses tend to exhibit higher rates of presenteeism compared to other professions. Presenteeism can cause the work performance of nurses to suffer, jeopardizing their own and their patients' safety and leading to decreased quality of care and increased risks of errors. However, there is a lack of a validated assessment tool for presenteeism in Taiwan. Thus, the purpose of this study was to develop a Nursing Staff Presenteeism Scale (NSPS). METHODS: To develop questionnaire items, participants from three medical centers in Taiwan were recruited. Through convenience sampling, 500 nurses who met the selection criteria were recruited from November 1, 2022 to January 18, 2023. The scale was developed based on a systematic literature review, a previous study, and expert consultation, and 50 items were initially generated. After removing three items that lacked discriminative power, the reliability and validity of the remaining 47 items were evaluated. An exploratory factor analysis was used to establish the construct validity. A confirmatory factor analysis and structural equation modeling for cross-validation were used to assess relationships of factors with items and the overall NSPS. RESULTS: The final scale consisted of 44 items assessed on a five-point Likert scale that loaded onto three different factors of physical or mental discomfort (18 items), work performance (15 items), and predisposing factors (11 items). These three factors were found to explain 63.14% of the cumulative variance. Cronbach's alpha for the overall final scale was 0.953. The item-to-total correlation coefficients ranged 0.443 to 0.795. CONCLUSIONS: The NSPS exhibited satisfactory reliability and validity. It can be applied to assess the level of presenteeism among clinical nurses and provide medical institutions with information regarding the causes of presenteeism, predisposing factors, and the impacts of presenteeism on their work performance to enhance the safety and quality of clinical care.

Echistatin/BYL-719 impedes epithelial-mesenchymal transition in pulmonary fibrosis induced by silica through modulation of the Integrin ß1/ILK/PI3K signaling pathway.

Silicosis is a chronic fibroproliferative lung disease caused by long-term inhalation of crystalline silica dust, characterized by the proliferation of fibroblasts and pulmonary interstitial fibrosis. Currently, there are no effective treatments available. Recent research suggests that the Integrin ß1/ILK/PI3K signaling pathway may be associated with the pathogenesis of silicosis fibrosis. In this study, we investigated the effects of Echistatin (Integrin ß1 inhibitor) and BYL-719 (PI3K inhibitor) on silicosis rats at 28 and 56 days after silica exposure. Histopathological analysis of rat lung tissue was performed using H&E staining and Masson staining. Immunohistochemistry, Western blotting, and qRT-PCR were employed to assess the expression of markers associated with epithelial-mesenchymal transition (EMT), fibrosis, and the Integrin ß1/ILK/PI3K pathway in lung tissue. The results showed that Echistatin, BYL 719 or their combination up-regulated the expression of E-cadherin and down-regulated the expression of Vimentin and extracellular matrix (ECM) components, including type I and type III collagen. The increase of Snail, AKT and ß-catenin in the downstream Integrin ß1/ILK/PI3K pathway was inhibited. These results indicate that Echistatin and BYL 719 can inhibit EMT and pulmonary fibrosis by blocking different stages of Integrinß1 /ILK/PI3K signaling pathway. This indicates that the Integrin ß1/ILK/PI3K signaling pathway is associated with silica-induced EMT and may serve as a potential therapeutic target for silicosis.

Activation of AMPK signalling by Metformin: Implication an important molecular mechanism for protecting against mice silicosis via inhibited endothelial cell-to-mesenchymal transition by regulating oxidative stress and apoptosis.

Inhalation of silica particles (SiO2) causes oxidative stress-induced inflammation and cell apoptosis, ultimately resulting in irreversible pulmonary fibrosis, Unfortunately, effective treatment or preventative measures have yet to be fully established. Metformin (Met), a relatively safe and effective medication for treating diabetes, may hold promise as protective agent against early-stage pulmonary fibrosis in mice through the activation of autophagy and inhibition of endothelial cell to mesenchymal transition (EndoMT). Here, we investigated whether Met could reduce silicosis in mice by regulating inflammation, oxidative stress, and apoptosis, and to identify the underlying protective effect on endothelial cells. First, through pathological observation, we found that 21 consecutive days of Met (100 mg/kg) administration is optimal against silicosis. Next, using haematoxylin-eosin and Masson's trichrome staining and immunoblotting, we found that Met effectively blunted the inflammatory response and collagen deposition at 56 days after exposure to SiO2. We also demonstrated that Met effectively activates AMPK signalling and markedly relieves oxidative stress, the mitochondrial apoptotic pathway and EndoMT induced by SiO2 exposure both in vivo and in vitro. Overall, Met can alleviate SiO2-induced pulmonary fibrosis by regulating oxidative stress and the mitochondrial apoptotic pathway. The current study provides a rationale for the clinical treatment of SiO2-induced pulmonary fibrosis.

Pathological Comparison of Rat Pulmonary Models Induced by Silica Nanoparticles and Indium-Tin Oxide Nanoparticles.

Purpose: The objective of this study was to evaluate and compare the histopathological implications of silica nanoparticles (Nano-SiO2) and indium-tin oxide nanoparticles (Nano-ITO), in vivo. Methods: Male Sprague-Dawley rats were exposed to Nano-SiO2 (50 mg/kg) and Nano-ITO (6 mg/kg) by a single intratracheal instillation, respectively. Broncho-alveolar lavage fluid (BALF) and lung tissue were obtained at 7, 14, 28, and 56 days post exposure for analysis of BALF inflammatory factors, total protein, and for lung tissue pathology. Histopathological and ultrastructural change in lungs were investigated by hematoxylin and eosin, Masson's trichrome, sirius red staining, periodic acid Schiff stain, and transmission electron microscopy. The expression of SP-A, collagen type I and III in lung tissue was determined by immunohistochemistry and ELISA. Results: The rats in both models exhibited obvious collagen fibrosis and the severity of the lung injury increased with time after exposure to respective dosage increased. Several parameters of pulmonary inflammation and fibrosis significantly increased in both groups, which was reflected by increased LDH activity, total proteins, TNF-α, and IL-6 levels in BALF, and confirmed by histopathological examination. The results also showed that the two models exhibited different features. Exposure to Nano-ITO caused persistent chronic lung inflammation, illustrated by the infiltration of a large amount of enlarged and foamy macrophages and neutrophils into the lung parenchyma. In Nano-SiO2 exposed rat lung tissue, granulomatous inflammation was most prominent followed by progressive and massive fibrotic nodules. Compared with the Nano-SiO2 rats, Nano-ITO exposed rats exhibited significantly severe pulmonary alveolar proteinosis (PAP) pathological changes, lower fibrosis, and higher levels of inflammatory biomarkers. However, Nano-SiO2 exposed rats had greater fibrosis pathological changes and more severe granulomas than Nano-ITO exposed rats. Conclusion: This study suggests that the Nano-SiO2-induced model has greater value in research into granulomas and fibrosis, while the Nano-ITO-induced model has greater repeatability in area of PAP.

Correlational Study of Emotional Stress, Pain, and the Presence of Inpatient Companions for Cancer Inpatients during the COVID-19 Pandemic.

The outbreak of COVID-19 poses an immense global threat. Visitors to hospitalized patients during a pandemic might themselves be carriers, and so hospitals strictly control patients and inpatient companions. However, it is not easy for cancer patients to adjust the times of their medical treatment or to suspend treatment, and the impact of the pandemic on cancer inpatients and inpatient companions is relatively high. The objectives for this investigation are to study the correlations among emotional stress, pain, and the presence of inpatient companions in cancer patients during the COVID-19 pandemic. This study was a retrospective descriptive study. The participants were cancer inpatients and inpatient companions in a medical center in Taiwan. The data for this study were extracted from cross-platform structured and normalized electronic medical record databases. Microsoft Excel 2016 and SPSS version 22.0 were used for analysis of the data. In all, 75.15% of the cancer inpatients were accompanied by family, and the number of hospitalization days were 7.87 ± 10.77 days, decreasing year by year, with statistical significance of p < 0.001. The daily nursing hours were 12.94 ± 10.76, and the nursing hours decreased year by year, p < 0.001. There was no significant difference in gender among those who accompanied the patients, but there were statistical differences in the length of hospitalization, nursing hours, and pain scores between those with and without inpatient companions, with p < 0.001. The inpatient companions were mostly family members (78%). The findings of this study on cancer patient care and inpatient companions should serve as an important basis for the transformation and reform of the inpatient companion culture and for epidemic prevention care in hospitals.

Prevention of needle-stick injury among nurses in an acute ward of a hospital: a best practice implementation project.

OBJECTIVES: This evidence implementation project aimed to identify barriers leading to needle-stick injuries (NSIs) and to develop implementation strategies to prevent NSIs in the acute ward of a hospital in central Taiwan. INTRODUCTION: The incidence rate of NSIs was 5.6% in the acute ward of a hospital in Taiwan. NSIs commonly occur during the drawing of blood, intravenous insertion, needle recapping, or performing any procedure involving sharp medical devices. NSIs are critical occupational risks among healthcare workers, possibly leading to transmission of infectious diseases, especially blood-borne viruses, such as HIV, hepatitis B, and hepatitis C. METHODS: A clinical audit was undertaken using the JBI Practical Application of Clinical Evidence System (PACES) and the Getting Research into Practice (GRiP) approach. Five audit criteria that represented best practice recommendations for prevention of NSIs were used. Baseline data were collected from 177 nurses in five acute wards, followed by the implementation of multiple strategies during a 20-week period of the project. Both baseline and postimplementation audits were undertaken to determine changes in practice. RESULTS: According to the pre-audit concerning the use of safety-engineered injection devices and safe use and disposal of needles, there was 14-15% compliance, which indicated poor compliance with current best-practice criteria. Following the project implementation, the nursing staff were educated about the well tolerated use and disposal of sharps and the improved compliance rate ranged from 40 to 96.6%, with safety needle use increasing from 16 to 95.5%, safety needle operation procedure awareness increasing from 14 to 96%, needles not recapped after use increasing from 47 to 85%, and placing used needles in the sharps collection box increasing from 75 to 80%. CONCLUSION: This article suggests that standardized puncture prevention education and training enhanced nurses' awareness in the acute ward.

Chair-sitting exercise intervention does not improve respiratory muscle function in mechanically ventilated intensive care unit patients.

BACKGROUND: Chair-sitting may allow for more readily activated scalene, sternocleidomastoid, and parasternal intercostal muscles, and may raise and enlarge the upper thoracic cage, thereby allowing the thoracic cage to be more easily compressed. OBJECTIVE: To evaluate the effect of chair-sitting during exercise training on respiratory muscle function in mechanically ventilated patients. METHODS: We randomized 16 patients to a control group and 18 patients to a chair-sitting group. The patients in the chair-sitting group were transferred by 2 intensive care unit nurses from bed to armchair and rested for at least 30 min, based on the individual patient's tolerance. We measured heart rate, blood pressure, S(pO(2)), and respiratory rate. In the treatment group, before transferring the patient from bed to armchair, and 30 min after the completion of chair-sitting we measured respiratory muscle function variables, including the ratio of respiratory rate (f) to tidal volume (V(T)), S(pO(2)), maximum inspiratory pressure (P(Imax)) and maximum expiratory pressure (P(Emax)). In the control patients we took those same measurements while the patient was in semirecumbent position, before and after treatments, for at least 6 days or until the patient was discharged from the intensive care unit or died. RESULTS: The 2 groups did not significantly differ in age, sex, or clinical outcomes. Respiratory rate, V(T), f/V(T), S(pO(2)), P(Imax), and P(Emax) were not significantly better in the chair-sitting group. The study period significantly improved respiratory rate, V(T), P(Imax), and P(Emax) (all P < .001), but not f/V(T). CONCLUSIONS: Six days of chair-sitting exercise training did not significantly improve respiratory muscle function in mechanically ventilated patients.

Effectiveness of Music-Based Intervention in Improving Uncomfortable Symptoms in ICU Patients: An Umbrella Review.

BACKGROUND: Intensive care unit (ICU) patients experience multiple uncomfortable symptoms, which may be alleviated using music-based intervention, a nondrug treatment. This umbrella review aims to combine the data of systematic reviews and/or meta-analyses to evaluate the effectiveness of music-based intervention in improving uncomfortable symptoms in ICU patients. METHODS: A comprehensive literature search was performed on the PubMed, Embase, Cochrane Library, Airiti Library, CINAHL, ProQuest, and Web of Science databases, and Epistemonikos. The search had no language restrictions, and articles on the improvement of symptoms using music-based intervention in adult ICU patients were included. This review protocol was registered on PROSPERO (CRD42021240327). RESULTS: This umbrella review retrieved 5 systematic reviews and 41 original studies, including 39 randomized controlled trials, and 2 nonrandomized controlled trials. Diverse music was the most common music type used for music-based intervention, the intervention music was typically decided by the study participants (61%), and most subjects underwent one intervention session (78%). Furthermore, most music intervention sessions lasted for 30 min (44%). The positive results included decreased anxiety, decreased pain, decreased agitation, decreased anesthesia dose and sedative use, decreased chances of delirium, decreased feelings of uncomfort, and improved sleep quality. CONCLUSIONS: A systematic review on the effectiveness of music-based intervention in improving uncomfortable symptoms in ICU patients revealed that 20-30 min intervention sessions showed the best improvement in the uncomfortable symptoms in patients. This study provides a basis for using music-based intervention to relieve the uncomfortable symptoms in critically ill ICU patients, and a reference for empirical clinical practice.

Alpha-lipoic acid attenuates silica-induced pulmonary fibrosis by improving mitochondrial function via AMPK/PGC1α pathway activation in C57BL/6J mice.

Silicosis is characterized by pulmonary interstitial fibrosis that arises as a result of chronic exposure to silica. The few available treatments only delay its progression. As α-lipoic acid (ALA) has been shown to have various beneficial effects, including mitoprotective, antioxidant, and anti-inflammatory effects, we hypothesized that it may exhibit therapeutic effects in pulmonary fibrosis. Therefore, in the present study, we used a murine model of silicosis to investigate whether supplementation with exogenous ALA could attenuate silica-induced pulmonary fibrosis by improving mitochondrial function. ALA was administered to the model mice via continuous intragastric administration for 28 days, and then the antioxidant and mitoprotective effects of ALA were evaluated. The results showed that ALA decreased the production of reactive oxygen species, protected mitochondria from silica-induced dysfunction, and inhibited extracellular matrix deposition. ALA also decreased hyperglycemia and hyperlipidemia. Activation of the mitochondrial AMPK/PGC1α pathway might be responsible for these ALA-mediated anti-fibrotic effects. Exogenous ALA blocked oxidative stress by activating NRF2. Taken together, these findings demonstrate that exogenous ALA effectively prevents the progression of silicosis in a murine model, likely by stimulating mitochondrial biogenesis and endogenous antioxidant responses. Therefore, ALA can potentially delay the progression of silica-induced pulmonary fibrosis.

Overexpression of lipoic acid synthase gene alleviates diabetic nephropathy of Leprdb/db mice.

INTRODUCTION: Diabetic nephropathy (DN) develops in about 40% of patients with type 2 diabetes and remains the leading cause of end-stage renal disease. The mechanisms of DN remain to be elucidated. Oxidative stress is thought to be involved in the development of DN but antioxidant therapy has produced conflicting results. Therefore, we sought to define the role of antioxidant in retarding the development of DN in this study. RESEARCH DESIGN AND METHODS: We generated a new antioxidant/diabetes mouse model, LiasH/HLeprdb/db mice, by crossing db/db mice with LiasH/H mice, which have overexpressed Lias gene (~160%) compared with wild type, and also correspondingly increased endogenous antioxidant capacity. The new model was used to investigate whether predisposed increased endogenous antioxidant capacity was able to retard the development of DN. We systemically and dynamically examined main pathological alterations of DN and antioxidant biomarkers in blood and kidney mitochondria. RESULTS: LiasH/HLeprdb/db mice alleviated major pathological alterations in the early stage of DN, accompanied with significantly enhanced antioxidant defense. The model targets the main pathogenic factors by exerting multiple effects such as hypoglycemic, anti-inflammation, and antioxidant, especially protection of mitochondria. CONCLUSION: The antioxidant animal model is not only very useful for elucidating the underlying mechanisms of DN but also brings insight into a new therapeutic strategy for clinical applications.

Genome-wide mRNA profiling identifies the NRF2-regulated lymphocyte oxidative stress status in patients with silicosis.

BACKGROUND: The immunomodulatory abnormalities of silicosis are related to the lymphocyte oxidative stress state. The potential effect of antioxidant therapy on silicosis may depend on the variation in nuclear factor erythroid 2-related factor 2 (NRF2)-regulated antioxidant genes in peripheral blood mononuclear cells (PBMCs). As NRF2 is a redox-sensitive transcription factor, its possible roles and underlying mechanism in the treatment of silicosis need to be clarified. METHODS: Ninety-two male patients with silicosis and 87 male healthy volunteers were randomly selected. PBMCs were isolated from fresh blood from patients with silicosis and healthy controls. The lymphocyte oxidative stress state was investigated by evaluating NRF2 expression and NRF2-dependent antioxidative genes in PBMCs from patients with silicosis. Key differentially expressed genes (DEGs) and signaling pathways were identified utilizing RNA sequencing (RNA-Seq) and bioinformatics technology. Gene set enrichment analysis was used to identify the differences in NRF2 signaling networks between patients with silicosis and healthy controls. RESULTS: The number of monocytes was significantly higher in patients with silicosis than that of healthy controls. Furthermore, RNA-Seq findings were confirmed using quantitative polymerase chain reaction and revealed that NRF2-regulated DEGs were associated with glutathione metabolism, transforming growth factor-ß, and the extracellular matrix receptor interaction signaling pathway in PBMCs from patients with silicosis. The top 10 hub genes were identified by PPI analysis: SMAD2, MAPK3, THBS1, SMAD3, ITGB3, integrin alpha-V (ITGAV), von Willebrand factor (VWF), BMP4, CD44, and SMAD7. CONCLUSIONS: These findings suggest that NRF2 signaling regulates the lymphocyte oxidative stress state and may contribute to fibrogenic responses in human PBMCs. Therefore, NRF2 might serve as a novel preventive and therapeutic candidate for silicosis.

Effectiveness of Applying Evidence-based Guidelines for Nurses Training on Nasogastric Tube Care.

BACKGROUND: This study formulated clinical guidelines for assessing nasogastric tube placement and for health education guidance according to evidence-based recommendations. METHOD: This study used a single group, pre- and postintervention design. Purposive sampling was used to recruit participants from nursing institutions in Taiwan. RESULTS: Sixty-two individuals in charge of nursing institutions were recruited to participate in the in-service training program. Statistically significant differences were observed in the four major items in the self-directed learning readiness scale (t = 3.85, p < .00; t = 3.99, p < .00; t = 2.94, p < .01; t = 4.13, p < .00). With regard to program satisfaction, the mean score was 4.88 to 4.9 points. The mean score for teaching satisfaction was 4.94 to 4.9 points. Furthermore, the participants scored more than 80 points in the online course test and the nasogastric tube placement skill. CONCLUSION: The individuals in-charge are expected to be willing to apply and promote methods of literature collation and recommendation in their respective institutions. [J Contin Educ Nurs. 2021;52(7):326-334.].

Overexpression of endogenous lipoic acid synthase attenuates pulmonary fibrosis induced by crystalline silica in mice.

Oxidative stress and inflammatory processes are proposed to mediate the development of silicosis. However, antioxidant therapy has not produced consistent results during the treatment of silicosis. α-Lipoic acid synthesized by lipoic acid synthase is a powerful anti-oxidant and helps protect mitochondria. Thus far, the effect of endogenous α-Lipoic acid on silicosis has not been elucidated yet. We established an experimental model of silicosis with wildtype and LiasH/H mice, a new antioxidant mouse model which has overexpressed Lias gene (∼150 %) relative to its wild type counterpart. We systemically examined main pathological changes of pulmonary fibrosis, and explored α-lipoic acid effects on oxidative stress, inflammatory and pulmonary fibrosis biomarkers in silica-instillated mice. In LiasH/H mice over-expression of lipoic acid alleviated the severity of major pathological alterations in the early stage of pulmonary fibrosis induced by silica compared with wild type mice. Silica significantly increased oxidative stress in both wild type and LiasH/H mice. The antioxidant defense was strengthen including increased NRF2 and LIAS production in LiasH/H mice. Relieved oxidative stress resulted in decreased inflammatory response and secretion of chemokines. LiasH/H mice reduced chronic inflammatory response and inhibition of NF-κB activity after silica instillation. The LiasH/H mouse model overexpression of lipoic acid synthase gene retarded the development of silica-induced pulmonary fibrosis. Strengthen antioxidant defense by increased lipoic acid synthase is a potential strategy for protection against silica-induced pulmonary fibrosis.

Safety and efficacy of using vascular closure devices for hemostasis on sheath removal after a transfemoral artery percutaneous coronary intervention.

AIM: To determine the efficacy of vascular closure devices (VCDs) for hemostasis following transfemoral percutaneous coronary interventions (PCIs). METHODS: This two-group pre-post-test observational study with purposive sampling enrolled 73 patients between January, 2014 and February, 2015. The patients were allocated to either the intervention (vascular closure devices group, n = 34) or the control group (manual compression [MC] group, n = 39). Questionnaires were used to assess their demographic and clinical characteristics, vascular complications, visual analogue scale score for pain, and discomfort levels. Pain and discomfort were measured before and after the PCI. RESULTS: Vascular complications were observed in 15 (44.1%) VCD patients and 13 (33.3%) MC patients, with no significant between-group difference. However, the VCD patients had a higher relative risk of bruising, hematomas, and need for further treatment. After the PCI, the pain scores and discomfort levels increased significantly in both groups, but the VCD patients had more successful hemostasis, less pain, and less physical and psychological discomfort (lower-limb numbness, shoulder pain, restlessness, and worrying about walking ability, being unable to lift heavy objects in the future, and taking time off from work). CONCLUSION: The VCDs seem to be superior to the MCs, providing more successful hemostasis, less pain and discomfort, and earlier ambulation after a transfemoral PCI. These findings aid clinical nurses in understanding the risk of vascular complications, discomfort, and pain that are associated with VCD use for improving the quality of clinical care and help clinicians in determining the appropriate hemostatic method for patients undergoing a transfemoral PCI, particularly in the Chinese population.