Thriving at work as a mediator of the relationship between psychological resilience and the work performance of clinical nurses.

OBJECTIVE: This study aims to investigate the relationship between psychological resilience, thriving at work, and work performance among nurses, as well as analyse the mediating role of thriving at work in the relationship between psychological resilience and the work performance of nurses. The findings are intended to serve as a reference for nursing managers to design tailored work performance intervention programs. METHOD: Using convenience sampling, 308 clinical nurses were selected from a tertiary hospital in Changsha City, Hunan Province, China, from February to April 2023. The Connor-Davidson Resilience Scale (CD-RISC), the Thriving at Work Scale, and the Work Performance Scale were employed for the questionnaire survey. Pearson correlation analysis was used to explore the relationship between psychological resilience, thriving at work and work performance. The SPSS 26.0 software's 'Process' plugin was utilised for mediation effect analysis. RESULTS: Significantly positive correlations were found between psychological resilience and thriving at work (r = 0.806, P < 0.01), thriving at work and work performance (r = 0.571, P < 0.01) as well as psychological resilience and work performance (r = 0.572, P < 0.01). Psychological resilience significantly predicted work performance positively (ß = 0.558, t = 11.165, P < 0.01), and this prediction remained significant when thriving at work (the mediating variable), was introduced (ß = 0.371, t = 4.772, P < 0.01). Psychological resilience significantly predicted thriving at work positively (ß = 0.731, t = 20.779, P < 0.01), and thriving at work significantly predicted work performance positively (ß = 0.256, t = 3.105, P < 0.05). The mediating effect size of thriving at work between psychological resilience and work performance was 33.49% (P < 0.05). CONCLUSION: Thriving at work plays a partial mediating role between psychological resilience and work performance. The level of work performance among clinical nurses was relatively high. Nursing managers can enhance thriving at work by fostering psychological resilience among clinical nurses, thereby further improving their work performance to ensure high-quality and efficient nursing care.

[Expression level and clinical significance of CD44 and CD33 in 77 patients with benign lymphoadenosis of oral mucosa].

PURPOSE: To investigate the expression and clinical significance of CD44 and CD33 in benign lymphoadenosis of oral mucosa(BLOM). METHODS: From January 2017 to March 2020, seventy-seven BLOM wax blocks from the Department of Pathology of Qingdao Traditional Chinese Medicine Hospital were selected as the experimental group, and 63 cases of normal oral mucosal tissue wax blocks during the same period were selected as the control group. Immunohistochemical method was used to detect the positive expression of CD44 and CD33 in the two groups.Spearman correlation analysis was used to analyze the correlation between the positive expression of CD33 and the positive expression of CD44 in the diseased tissues of BLOM patients.The general information about patients were collected.The relationship between the expression of CD33 and CD44 in the diseased tissues of BLOM patients and the clinicopathological characteristics of BLOM patients were analyzed. SPSS 21.0 software package was used for statistical analysis of the data. RESULTS: The positive expression rates of CD33 in the control group and the experimental group were 95.24% and 63.64%, respectively, and the difference was statistically significant(P＜0.05). The positive expression rates of CD44 in the control group and the experimental group were 93.65% and 67.53%, respectively, and the difference was statistically significant(P＜0.05). The results of Spearman correlation analysis showed that the positive expression of CD33 in the diseased tissues of BLOM patients was positively correlated with the positive expression of CD44 (r=0.834, P=0.002). The expression of CD33 and CD44 in the diseased tissues of patients with BLOM were related to clinical type, degree of inflammation, presence or absence of lymphoid follicles, and lymphocyte infiltration(P＜0.05), but not related to age, gender, course of disease, location, and epithelial surface keratinization(P＞0.05). CONCLUSIONS: The positive expression rate of CD33 and CD44 in the BLOM tissues decreased, which was closely related to the clinical type, degree of inflammation, presence or absence of lymphoid follicles, and lymphocyte infiltration.

Representation of In-Service Performance for Cable-Stayed Railway-Highway Combined Bridges Based on Train-Induced Response's Sensing Data and Knowledge.

Real-time representation of the current performance of structures is an important task for perceiving potential danger in in-service bridges. Methods driven by the multisource sensing data of structural health monitoring systems are an effective way to achieve this goal. Due to the explicit zero-point of signals, the live load-induced response has an inherent advantage for quantitatively representing the performance of bridges. Taking a long-span cable-stayed railway-highway combined bridge as the case study, this paper presents a representation method of in-service performance. First, the non-stationary sections of train-induced response are automatically extracted by wavelet transform and window with threshold. Then, the data of the feature parameter of each non-stationary section are automatically divided into four cases of train load according to the calculational theory of bridge vibration under train effect and clustering analysis. Finally, the performance indexes for structural deformation and dynamics are determined separately, based on hierarchical clustering and statistical modeling. Fusing the real variability of massive data from monitoring and the knowledge of mechanics of theoretical calculations, accurate and robust indexes of bridge deflection distribution and forced vibration frequency are obtained in real time. The whole process verifies the feasibility of the representation of bridge in-service performance from massive multisource sensing data. The presented method, framework, and analysis results can be used as a reference for the design, operation, and maintenance works of long-span railway bridges.

Puerarin ameliorated pressure overload-induced cardiac hypertrophy in ovariectomized rats through activation of the PPARα/PGC-1 pathway.

Estrogen deficiency induces cardiac dysfunction and increases the risk of cardiovascular disease in postmenopausal women and in those who underwent bilateral oophorectomy. Previous evidence suggests that puerarin, a phytoestrogen, exerts beneficial effects on cardiac function in patients with cardiac hypertrophy. In this study, we investigated whether puerarin could prevent cardiac hypertrophy and remodeling in ovariectomized, aortic-banded rats. Female SD rats subjected to bilateral ovariectomy (OVX) plus abdominal aortic constriction (AAC). The rats were treated with puerarin (50 mg·kg-1 ·d-1, ip) for 8 weeks. Then echocardiography was assessed, and the rats were sacrificed, their heart tissues were extracted and allocated for further experiments. We showed that puerarin administration significantly attenuated cardiac hypertrophy and remodeling in AAC-treated OVX rats, which could be attributed to activation of PPARα/PPARγ coactivator-1 (PGC-1) pathway. Puerarin administration significantly increased the expression of estrogen-related receptor α, nuclear respiratory factor 1, and mitochondrial transcription factor A in hearts. Moreover, puerarin administration regulated the expression of metabolic genes in AAC-treated OVX rats. Hypertrophic changes could be induced in neonatal rat cardiomyocytes (NRCM) in vitro by treatment with angiotensin II (Ang II, 1 µM), which was attenuated by co-treatemnt with puerarin (100 µM). We further showed that puerarin decreased Ang II-induced accumulation of non-esterified fatty acids (NEFAs) and deletion of ATP, attenuated the Ang II-induced dissipation of the mitochondrial membrane potential, and improved the mitochondrial dysfunction in NRCM. Furthermore, addition of PPARα antagonist GW6471 (10 µM) partially abolished the anti-hypertrophic effects and metabolic effects of puerarin in NRCM. In conclusion, puerarin prevents cardiac hypertrophy in AAC-treated OVX rats through activation of PPARα/PGC-1 pathway and regulation of energy metabolism remodeling. This may provide a new approach to prevent the development of heart failure in postmenopausal women.

Contributions of Nrf2 to Puerarin Prevention of Cardiac Hypertrophy and its Metabolic Enzymes Expression in Rats.

Previous evidence has suggested that puerarin may attenuate cardiac hypertrophy; however, the potential mechanisms have not been determined. Moreover, the use of puerarin is limited by severe adverse events, including intravascular hemolysis. This study used a rat model of abdominal aortic constriction (AAC)-induced cardiac hypertrophy to evaluate the potential mechanisms underlying the attenuating efficacy of puerarin on cardiac hypertrophy, as well as the metabolic mechanisms of puerarin involved. We confirmed that puerarin (50 mg/kg per day) significantly attenuated cardiac hypertrophy, upregulated Nrf2, and decreased Keap1 in the myocardium. Moreover, puerarin significantly promoted Nrf2 nuclear accumulation in parallel with the upregulated downstream proteins, including heme oxygenase 1, glutathione transferase P1, and NAD(P)H:quinone oxidoreductase 1. Similar results were obtained in neonatal rat cardiomyocytes (NRCMs) treated with angiotensin II (Ang II; 1 µM) and puerarin (100 µM), whereas the silencing of Nrf2 abolished the antihypertrophic effects of puerarin. The mRNA and protein levels of UGT1A1 and UGT1A9, enzymes for puerarin metabolism, were significantly increased in the liver and heart tissues of AAC rats and Ang II-treated NRCMs. Interestingly, the silencing of Nrf2 attenuated the puerarin-induced upregulation of UGT1A1 and UGT1A9. The results of chromatin immunoprecipitation-quantitative polymerase chain reaction indicated that the binding of Nrf2 to the promoter region of Ugt1a1 or Ugt1a9 was significantly enhanced in puerarin-treated cardiomyocytes. These results suggest that Nrf2 is the key regulator of antihypertrophic effects and upregulation of the metabolic enzymes UGT1A1 and UGT1A9 of puerarin. The autoregulatory circuits between puerarin and Nrf2-induced UGT1A1/1A9 are beneficial to attenuate adverse effects and maintain the pharmacologic effects of puerarin.

microRNA-802/Rnd3 pathway imposes on carcinogenesis and metastasis of fine particulate matter exposure.

Recent studies have linked ambient fine particulate matter (PM2.5) to increased lung cancer mortality and morbidity. However, the underlying mechanism causing the adverse effects of PM2.5 is less clear. In the present study, post-transcriptional profiling was used to explore biological pathways involved in PM2.5-induced pulmonary disorders. The carcinogenesis and metastasis of PM2.5 exposure were evaluated by long-term PM2.5 exposure tests. We observed dysregulation of actin in A549 cells line and dysplasia in the lungs of mice exposed to PM2.5. Both PM2.5-exposed cells and animals showed increased Rnd3 expression levels. Moreover, miR-802 mimics rescued actin disorganization in vitro and alveolitis in vivo. Long-term exposure to PM2.5 promoted carcinogenesis and metastasis of pulmonary cells. Decreased miR-802 expression levels in the serum samples of PM2.5-treated mice and individuals from moderately polluted cities were observed. Increased Rnd3 expression levels in lung cancers tissues have been identified by a genome database TCGA, and have been linked to less overall survival probabilities of lung cancer patients. Our findings suggest that dysregulation of actin cytoskeleton and down-regulation of miR-802 expression might be the underlying mechanism involved in the adverse effects of PM2.5 exposure. In addition, long-term exposure to PM2.5 demonstrated strong associations with malignant pulmonary disorders.

Inhibition of lectin-like oxidized low-density lipoprotein receptor-1 reduces cardiac fibroblast proliferation by suppressing GATA Binding Protein 4.

Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) and GATA Binding Protein 4 (GATA4) are important for the growth of cardiac fibroblasts (CFs). When deregulated, LOX-1 and GATA4 can cause cardiac remodeling. In the present study, we found novel evidence that GATA4 was required for the LOX-1 regulation of CF proliferation. The inhibition of LOX-1 by RNA interference LOX-1 lentivirus resulted in the loss of PI3K/Akt activation and GATA4 protein expression. The overexpression of LOX-1 by lentivirus rescued CF proliferation, PI3K/Akt activation, and GATA4 protein expression. Moreover, GATA4 overexpression enhanced CF proliferation with LOX-1 inhibition. We also found that the inhibition of PI3K/Akt activation by LY294002, a PI3K inhibitor, reduced cell proliferation and protein level of GATA4. In summary, GATA4 may play an important role in the LOX-1 and PI3K/Akt regulation of CF proliferation.

Insulin-like growth factor 1 opposes the effects of C-reactive protein on endothelial cell activation.

Emerging evidence demonstrates that high plasma C-reactive protein (CRP) levels or low plasma insulin-like growth factor 1 (IGF-1) concentrations may be separately associated with the increased risk of coronary artery disease or myocardial infarction. Interestingly, animal model studies and epidemiological investigations indicate that circulating IGF-1 and CRP levels have an inverse correlation. The present study aims to evaluate if IGF-1 can directly oppose the effects of CRP on endothelial cell (EC) activation. We found that IGF-1 rescues endothelial nitric oxide synthase activity and decreases the release of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 from ECs. We also showed that IGF-1 antagonizes the effects of CRP by activating the PI3K/Akt pathway and suppressing the JNK/c-Jun and MAPK p38/ATF2 signaling pathways, rather than inhibiting ERK1/2 activity. These findings provide evidence of the physiopathological mechanisms of endothelial activation and novel insights into the protective properties of IGF-1.

[Expressions of JWA protein and heat stress protein 70 induced by cell differentiation inducers combined with heat stress in K562 cells].

OBJECTIVE: To study how the combined effects of various differentiation inducers and heat stress on the expression of JWA protein in K562 cell, the relationship between JWA and Hsp70 expression, and the signal regulation mechanism possibly involved. METHODS: The experimental model was established in K562 cells. Various directional differentiation inducers (TPA, Ara-C, hemin, adriamycin, ATRA and As(2)O(3)) were used alone or combined with heat shock treatment (42 degrees C, 2 h). Western blot was used for detecting expressions of JWA, Hsp70, heat stress factor 1 (HSF1) and HSF2. RESULTS: (1) The expressions of both JWA protein and Hsp70 were significantly up-regulated after K562 cells treated by TPA (100, 200 ng/ml) or adriamycin (4 x 10(-8) mol/L) 48 h, and followed by heat shock (42 degrees C, 2 h). However, the opposite effects were observed when the cells treated by hemin (3 x 10(-5) mol/L, 48 h), Ara-C (80 ng/ml, 48 h) and As(2)O(3) (1 x 10(-6) mol/L, 48 h) followed by 2 h heat shock. No obvious changes were found when the cells treated by ATRA (1 x 10(-6) mol/L, 48 h) alone or followed by heat shock. (2) Both the heat shock transcriptional factors HSF1 and HSF2 did not show any significant changes when K562 cells were treated with various differentiation inducers and followed by heat stress. CONCLUSION: JWA not only takes part in the regulation of K562 cellular differentiation, but also of heat stress, it might be the co-target gene of several differentiation inducers and heat stress. The expression of Hsp70 seems not mediated by both HSF1 and HSF2 in K562 cells undergoing directional differentiation or heat stress treatment. JWA is likely to be a new signal molecule similar to Hsp70 signal pathways. The results show that JWA takes part in the mechanism of K562 cell response to heat stress.

[Application of the nasal lining flap to correct the wide unilateral complete cleft lip].

OBJECTIVE: To study use of nasal lining flap in correction of the wide complete unilateral cleft lip. METHODS: 78 patients with wide complete cleft lip were. operated, firstly to be sure. That the lip length on both sides was equal. Then the nasal lining flap was used to enhance the height of the lip on cleft side for keeping symmetry with the non-cleft side. The rest of procedures was the same as "Millard" method. RESULTS: 84.6 percent of patients had good appearance at one and half years after surgery. CONCLUSIONS: It is an effective way to take advantage of the nasal lining flap to correct the wide complete unilateral cleft lip.

[Effect of differentiation inducer and heat stress on the expression of JWA protein and Hsp70 of K562 cells].

OBJECTIVE: To study the expression of JWA protein and heat shock protein (Hsp70), and to explore these relationship and the possible mechanism of JWA gene involved in induced differentiation and heat stress (42 degrees C) of K562 cells. METHODS: The models of differentiation and heat stress of K562 cells were established. Western blot was used for detecting expressed proteins of JWA gene, Hsp70, heat shock factor (HSF1 and HSF2). RESULTS: (1) Under the condition of differentiations induced by TPA (100 ng/ml), hemin (3 x 10(-5) mol/L), Ara-C (80 ng/ml), adriamycin (4 x 10(-8) mol/L), ATRA (1 x 10(-6) mol/L) and As(2)O(3) (1 x 10(-6) mol/L) for 48 h respectively, the expression of JWA protein and Hsp70 were more significantly increased than control; the level of HSF2 protein was increased by inductions of hemin, Ara-C and adriamycin, respectively. (2) After heat exposure to 42 degrees C for 10, 20, 30, 45, 60, 90 min, and heat exposure to 39 degrees C, 42 degrees C, 45 degrees C, the trend of changing in expression of Hsp70 was similar to that of JWA protein, and HSF1 was expressed in earlier stage. CONCLUSION: The expression of JWA protein and Hsp70 were upregulated in induced differentiation and in heat stress, and the change of expression of JWA protein were similar to that of Hsp70, but the intracellular transduction signal pathways involved may be various. JWA might not be specifically related with both HSF1 and HSF2.

Anatomy of the nasal cartilages of the unilateral complete cleft lip nose.

The purpose of this study was to disclose the relationship between the anomaly of the cartilaginous framework and the nasal deformity of cleft lip. The noses of six stillborn infants with unilateral complete cleft lip were carefully dissected. The size and weight of the lower lateral cartilages were measured to determine whether there was a significant difference between the normal and involved sides. The position of the nasal cartilages was observed, and the distance between them was measured to determine whether they were normal. The surgical dissection revealed that the lower lateral cartilages from both sides were asymmetrical in three dimensions, indicating the displacement of the lower lateral cartilage on the involved side. There was displacement of the cartilaginous septum and the upper lateral cartilage. The statistical evaluation did not demonstrate a significant difference between weight and size of the two sides. One of the major causative factors of nasal deformity is displacement of the nasal cartilages. There is no hypoplasia of nasal cartilage in newborn infants with cleft lip.