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Introduction: The research on cancer patients returning to work in China is still in its infancy, and there is no research and discussion on the adaptability to returnto-work for cancer patients. It is critical to develop the Adaptability to Return-to-Work Scale (ARTWS) for cancer patients and evaluate its psychometric properties. Methods: The items of the initial scale were compiled based on the theoretical model and literature review results. Through two rounds of Delphi expert consultation (N = 15) and a pilot survey (N = 40), the initial scale was further checked and revised. Conduct a large sample survey (N = 376) and the construct validity and reliability of the ARTWS were assessed by confirmatory factor analysis (CFA) and exploratory factor analysis (EFA). Results: The final ARTWS consisted of 24 items. “Focusing on rehabilitation,” “Rebuilding Self-efficiency,” and “Adjusting plans” as common factors in determining adaptability to return to work for cancer patients, and the cumulative variance contribution rate for these three factors was 66.6%. The S-CVI of the total scale was 0.979. The Cronbach’s α coefficient was 0.937 and the 2-week test–retest reliability was 0.814. Discussion: ARTWS has good correlation validity and can be used as a tool to measure the adaptability of cancer patients’ return to work. The presentation of the manuscript in Research Square [ABSTRACT FROM AUTHOR]

Objectives: This study aimed to identify predictors of remission or low disease activity (LDA) in patients with rheumatoid arthritis (RA) and low-ultrasound inflammation. Methods: A total of 80 patients with RA who fulfilled the 1987 ACR criteria for RA with a disease activity score of 28 joints (DAS28) > 3.2 were recruited. Over 1 year of therapy, we conducted blood tests every 6 months to examine erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), monocyte chemotactic protein-1 (MCP-1), neuraminidase 3 (Neu3), and α-2,3-sialyltrasnferse I (ST3Gal-1) levels in B cells and monocytes. Additionally, we evaluated physical function by using the Health Assessment Questionnaire–Disability Index (HAQ-DI). Data on demographic and clinical parameters were collected, and musculoskeletal ultrasonography was performed twice a year on 12 specific joints to assess synovial changes. One year later, we compared all collected data and laboratory or ultrasound results between patients achieving remission or LDA and those who did not in order to determine the predictors. Results: Age, the presence or absence of rheumatoid factor, and the number of conventional disease-modifying anti-rheumatic drugs used were not correlated with remission or LDA for DAS28 or Simplified Disease Activity Index formulas. However, male sex, low CRP levels, low ESR levels, and low HAQ-DI scores were associated with a higher likelihood of achieving remission or LDA for DAS28-ESR. Negative anticyclic citrullinated peptide (CCP) and low HAQ-DI scores were predictors of remission or LDA for DAS28-MCP-1. Interestingly, having less than two comorbidities is a good predictor of a combined remission/low disease activity state for SDAI and DAS28-MCP-1. Furthermore, Neu3 and ST3Gal-1 levels and ST3Gal-1/Neu3 ratios in B cells and monocytes had no significant correlation with total ultrasound scores. Nevertheless, monocyte ST3Gal-1 and Neu3 correlated significantly with DAS28-ESR >5.1 and DAS-MCP-1 >4.8 (both categories belong to high disease activity), respectively (rho = 0.609 with p = 0.012, and rho = 0.727 with p = 0.011, respectively). Monocyte ST3Gal-1/Neu3 ratios connected with DAS28-ESR >5.1 and 3.3 < SDAI ≦ 11 (low disease activity), respectively (rho = 0.662 with p = 0.005, and rho = 0.342 with p = 0.048, respectively). Conclusions: In patients with RA in Taiwan, male sex, low CRP levels, low ESR levels, and low HAQ-DI scores are predictors of remission or LDA for DAS28-ESR, which differ from the predictors for DAS28-MCP-1. Moreover, monocyte ST3Gal-1, Neu3, and their ratios correlated with different disease activity categories of DAS28-ESR, DAS28-MCP-1, and SDAI scores. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the regulatory function of the non-coding microRNA-155 (miR-155) and suppressor of cytokine signaling 1 (SOCS1) in alcoholic hepatitis (AH) and its potential mechanism associated with the mitogen-activated protein kinase (MAPK) signaling pathway. Levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), albumin (ALB), total bilirubin (TBIL), malondialdehyde (MDA), and superoxide dismutase (SOD) were measured in a rat model of AH. The biological prediction website microRNA.org and dual-luciferase reporter gene assay were used to identify whether SOCS1 was a direct target of miR-155, and the effects of miR-155 and SOCS1 on the viability, cycle progression, and apoptosis of hepatic stellate cells were assessed using RT-qPCR, Western blot assay, MTT assay, Annexin V/PI double staining, and PI single staining. The levels of ALT, AST, MDA, and TBIL and the liver cell morphology were all prominently changed in AH model rats. miR-155 suppressed SOCS1 by specifically binding to SOCS1-3'-UTR to activate the MAPK signaling pathway. SOCS1 had low expression while miR-155 was highly expressed in AH rats. miR-155 promoted hepatic stellate cell viability and cycle progression and reduced cell apoptosis by silencing SOCS1. Together, we find that silenced miR-155 could upregulate SOCS1 and inactivate the MAPK signaling pathway, thereby inhibiting the proliferation of alcoholic hepatic stellate cells and promoting cell apoptosis. [ABSTRACT FROM AUTHOR]

Despite convincing evidence suggesting that organizations benefit from employees' flow states, when and how work flow experience generates negative effects remain largely understudied. By integrating the spillover-crossover model and perseverative cognition theory, we established a model to explain how flow experience induces employees' positive rumination after work (i.e., problem-solving pondering), which ultimately results in work-family conflict. We proposed that mindfulness acts as a buffer factor in this process but further elucidated that work-family segmentation preference serves as a boundary that may alter or even completely reverse the original effects of mindfulness. Our experience sampling method yielded 1425 data points from 186 employees and their family members across 10 workdays in China, and multilevel analyses supported our propositions. We identified the mediating role of problem-solving pondering in transmitting the effects of flow to work-family conflict. Additionally, we confirmed the three-way interaction effect among mindfulness, segmentation preference, and flow. Specifically, the harmful effect of flow is assuaged when segmentation preference and mindfulness are both high. However, flow experience causes severe work-family conflict when mindfulness is high and segmentation preference is low. Theoretical and practical implications were discussed. [ABSTRACT FROM AUTHOR]

Background: Mufangji tang (MFJT) is composed of Ramulus Cinnamomi, Radix Ginseng, Cocculus orbiculatus (Linn.) DC., and Gypsum. In clinical settings, MFJT has been effectively employed in addressing a range of respiratory disorders, notably including pulmonary arterial hypertension (PAH). However, the mechanism of action of MFJT on PAH remains unknown. Methods: In this study, a monocrotaline-induced PAH rat model was established and treated with MFJT. The therapeutic effects of MFJT on PAH rat model were evaluated. Network pharmacology was conducted to screen the possible targets for MFJT on PAH, and the molecular docking between the main active components and the core targets was carried out. The key targets identified from network pharmacology were tested. Results: Results showed significant therapeutic effects of MFJT on PAH rat model. Analysis of network pharmacology revealed several potential targets related to apoptosis, inflammation, oxidative stress, and vascular remodeling. Molecular docking showed that the key components were well docked with the core targets. Further experimental validation results that MFJT treatment induced apoptosis (downregulated Bcl-2 levels and upregulated Bax levels in lung tissue), inhibited inflammatory response and oxdative stress (decreased the levels of IL-1β, TNF-α, inducible NOS, and malondialdehyde, and increased the levels of endothelial nitric oxide synthase, nitric oxide, glutathione and superoxide dismutase), reduced the proliferation of pulmonary arterial smooth muscle cells (downregulated ET-1 and β-catenin levels and ERK1/2 phosphorylation, increased GSK3β levels). Conclusion: Our study revealed MFJT treatment could alleviate PAH in rats via induction of apoptosis, inhibition of inflammation and oxidative stress, and the prevention of vascular remodeling. [ABSTRACT FROM AUTHOR]

IMP‐3 expression is a poor prognostic factor of melanomas and it promotes melanoma cell migration and invasion by a pathway modulating HMGA2 mRNA expression. We tried to identify other putative targets of IMP‐3. We identified putative IMP‐3‐binding RNAs, including AKT1, MAPK3, RB1 and RELA, by RNA immunoprecipitation coupled with next‐generation sequencing. IMP‐3 overexpression increased AKT and RELA levels in MeWo cells. siRNAs against AKT1 and RELA inhibited MeWo/Full‐length IMP‐3 cell migration. IMP‐3 knockdown of A2058 cells decreased AKT1 and RELA expression and lowered migration ability. Co‐transfection of A2058 cells with AKT1‐ or RELA‐expressing plasmids with IMP‐3 siRNA restored the inhibitory effects of IMP‐3 knockdown on migration. HMGA2 did not influence AKT1 and RELA expression in melanoma cells. Human melanoma samples with high IMP‐3 levels also showed high HMGA2, AKT1 and RELA expression. Our results show that IMP‐3 enhances melanoma cell migration through the regulation of the AKT1 and RELA axis. [ABSTRACT FROM AUTHOR]