Development and psychometric evaluation of the hidden curriculum assessment scale in nursing education: A validity and reliability study.

AIMS: The study aimed to develop and psychometrically evaluate a measurement scale for identifying and assessing the hidden curriculum in undergraduate nursing education. BACKGROUND: The hidden curriculum is a general term for educational information that exists outside of the teaching program and mainly affects students' knowledge, emotions, behaviors, beliefs, values and professional ethics. However, a specific instrument to comprehensively define and assess the hidden curriculum in nursing education has not yet been developed in China. DESIGN: A descriptive and explorative study design was used. METHODS: We developed the initial scale through a literature review, focus group discussion, Delphi expert consultation and pre-survey. From February to April 2023, the data were collected from a convenient sample of 512 nursing students enrolled in five medical universities in China to conduct exploratory factor analysis and confirmatory factor analysis for validity testing. In addition, reliability analysis was conducted by calculating Cronbach's alpha coefficients, split-half reliability and test-retest reliability. The nursing students' responses were evaluated using a five-point Likert scale. RESULTS: The Hidden Curriculum Assessment Scale in Nursing Education (HCAS-NE) was formulated, consisting of 4 dimensions and 35 items. Exploratory factor analysis extracted four factors, with a cumulative variance contribution rate of 66.863 % and confirmatory factor analysis indicated that the fit indices values of the scale structure model met the criteria for an ideal level. the Cronbach's α coefficient of the scale was 0.965, the Guttman split-half was 0.853 and the test-retest reliability was 0.967. CONCLUSION: This study demonstrated that the Hidden Curriculum Assessment Scale in Nursing Education (HCAS-NE) has ideal reliability and validity, which provides a valid and reliable tool for identifying and assessing the hidden curriculum in nursing education.

Advances in amelioration of plasma electrolytic oxidation coatings on biodegradable magnesium and alloys.

Magnesium and its alloys are considered excellent materials for biodegradable implants because of their good biocompatibility and biodegradability as well as their mechanical properties. However, the rapid degradation rate severely limits their clinical applications. Plasma electrolytic oxidation (PEO), also known as micro-arc oxidation (MAO), is an effective surface modification technique. However, there are many pores and cracks on the coating surface under conventional PEO process. The corrosive products tend to penetrate deeply into the substrate, reducing its corrosion resistance and the biocompatibility, which makes PEO-coated Mg difficult to meet the long-term needs of in vivo implants. Hence, it is necessary to modify the PEO coating. This review discusses the formation mechanism and the influential parameters of PEO coatings on Mg. This is followed by a review of the latest research of the pretreatment and typical amelioration of PEO coating on biodegradable Mg alloys in the past 5 years, including calcium phosphate (Ca-P) coating, layered double hydroxide (LDH)-PEO coating, ZrO2 incorporated-PEO coating, antibacterial ingredients-PEO coating, drug-PEO coating, polymer-PEO composite coating, Plasma electrolytic fluorination (PEF) coating and self-healing coating. Meanwhile, the improvements of morphology, corrosion resistance, wear resistance, biocompatibility, antibacterial abilities, and drug loading abilities and the preparation methods of the modified PEO coatings are deeply discussed as well. Finally, the challenges and prospects of PEO coatings are discussed in detail for the purpose of promoting the clinical application of biodegradable Mg alloys.

Phosphorylation-dependent deubiquitinase OTUD3 regulates YY1 stability and promotes colorectal cancer progression.

Yin Yang 1 (YY1) is a key transcription factor that has been implicated in the development of several malignancies. The stability of YY1 is regulated by the ubiquitin-proteasome system. The role of deubiquitinases (DUBs) and their impact on YY1 remain to be fully elucidated. In this study, we screened for ubiquitin-specific proteases that interact with YY1, and identified OTUD3 as a DUB for YY1. Over-expressed OTUD3 inhibited YY1 degradation, thereby increasing YY1 protein levels, whereas OTUD3 knockdown or knockout promoted YY1 degradation, thereby decreasing the proliferation of colorectal cancer (CRC). Furthermore, PLK1 mediates OTUD3 S326 phosphorylation, which further enhances OTUD3 binding and deubiquitination of YY1. In CRC tissues, elevated the expression level of OTUD3 and YY1 were significantly associated with poor prognostic outcomes. These findings suggest that the OTUD3-YY1 pathway has therapeutic potential in CRC, and OTUD3 plays a critical role in regulating YY1.

Nicotinamide mononucleotide attenuates airway epithelial barrier dysfunction via inhibiting SIRT3 SUMOylation in asthma.

Nicotinamide adenine dinucleotide (NAD+) is an essential element in cellular metabolism that regulates fundamental biological processes. Growing evidence suggests that a decline in NAD+ is a common pathological factor in various diseases and aging. However, its role in airway epithelial barrier function in response to asthma remains underexplored. The current study aims to explore the efficacy of restoring cellular NAD+ concentration through supplementation with the NAD+ precursor, nicotinamide mononucleotide (NMN), in the treatment of allergic asthma and to investigate the role of SIRT3 in mediating the effects of NAD+ precursors. In this research, NMN alleviated airway inflammation and reduced mucus secretion in house dust mite (HDM)-induced asthmatic mice. It also mitigated airway epithelial barrier disruption in HDM-induced asthma in vitro and in vivo. But inhibition of SIRT3 expression abolished the effects of NMN. Mechanistically, HDM induced SIRT3 SUMOylation and proteasomal degradation. Mutation of these two SIRT3 SUMO modification sites enhanced the stability of SIRT3. Additionally, SIRT3 was targeted by SENP1 which acted to de-conjugate SUMO. And down-regulation of SENP1 expression in HDM-induced models was reversed by NMN. Collectively, these findings suggest that NMN attenuates airway epithelial barrier dysfunction via inhibiting SIRT3 SUMOylation in asthma. Blockage of SIRT3 SUMOylation emerges as for the treatment of allergic asthma.

Inhibition of Pard3 promotes breast cancer metastasis via the USP28 mediated deubiquitination of Snail1.

Pard3 is a core component of the Par complex and is a critical regulator of cell polarity. However, the biological role of Pard3 in breast cancer (BC) remains unclear. In this study we found that Pard3 levels were down-regulated in BC cells and tissues. Pard3 down-regulation was associated with the TNM stage of BC. Further, Pard3 knockdown enhanced colony formation and metastasis in vitro and in vivo. Interestingly, Pard3 knockdown also enhanced Snail1 deubiquitination and promoted BC invasion and migration via Snail1. Moreover, Pard3 silencing led to activation of the NFκB pathway, promoting the expression of USP28. Subsequently, USP28 interacted with and deubiquitinated Snail1; these effects were dependent on GSK-3ß-mediated phosphorylation. Together, the findings indicated that Pard3 knockdown facilitated the migration and invasion of BC cells by enhancing USP28-mediated Snail1 deubiquitination. Collectively, targeting the Pard3/NFκB/USP28/Snail1 signaling pathway might be a promising treatment option for breast cancer.

SEMA4D/VEGF surface enhances endothelialization by diminished-glycolysis-mediated M2-like macrophage polarization.

Cardiovascular disease remains the leading cause of death and morbidity worldwide. Inflammatory responses after percutaneous coronary intervention led to neoathrosclerosis and in-stent restenosis and thus increase the risk of adverse clinical outcomes. In this work, a metabolism reshaped surface is engineered, which combines the decreased glycolysis promoting, M2-like macrophage polarization, and rapid endothelialization property. Anionic heparin plays as a linker and mediates cationic SEMA4D and VEGF to graft electronically onto PLL surfaces. The system composed by anticoagulant heparin, immunoregulatory SEMA4D and angiogenic VEGF endows the scaffold with significant inhibition of platelets, fibrinogen and anti-thrombogenic properties, also noteworthy immunometabolism reprogram, anti-inflammation M2-like polarization and finally leading to rapid endothelializaiton performances. Our research indicates that the immunometabolism method can accurately reflect the immune state of modified surfaces. It is envisioned immunometabolism study will open an avenue to the surface engineering of vascular implants for better clinical outcomes.

Fruits are vehicles of drug-resistant pathogenic Candida tropicalis.

IMPORTANCE: Of 123 identified isolates from the fruit surface, C. tropicalis was the most frequently found species, followed by Meyerozyma caribbica and Candida krusei. All three fluconazole-resistant C. tropicalis were non-susceptible to voriconazole and belonged to the same predominant genotype of azole-resistant C. tropicalis causing candidemia in patients in Taiwan. Our findings provide evidence that fruit should be washed before eaten not only to remove chemicals but also potential drug-resistant pathogenic microbes, especially for immunocompromised individuals. To keep precious treatment options in patients, we not only continuously implement antimicrobial stewardship in hospitals but also reducing/stopping the use of agricultural fungicide classes used in human medicine.

Effects of the mini-clinical evaluation exercise teaching mode based on nurse-faculty cooperation in Fundamentals of Nursing course: A quasi-experimental study.

Objectives: This study aimed to explore the effects of the mini-clinical evaluation exercise (mini-CEX) teaching model based on nurse-faculty collaboration in Fundamentals of Nursing course. Methods: A quasi-experimental design was conducted. A total of 111 nursing students of two parallel classes were recruited from a nursing college in Guilin, China from February to December 2022, and allocated to the intervention group (n = 56) and control group (n = 55). The intervention group received a mini-CEX teaching model based on nurse-faculty collaboration, the teaching-learning process included scenario creation (10 min), inquiry-based learning (30 min), case report (30 min), scenario simulation exercise (40 min), and effectiveness evaluation (10 min). While the control group received conventional teaching method. All students were invited to complete the College Classroom Climate Assessment Scale (CCCA) and the Chinese version of the Competency Inventory for Nursing Students (CINS-CV) before and after the intervention. Course achievement of students was evaluated. After the intervention, the intervention group was asked an open-ended question to explore the difficulties or challenges they had encountered. Results: After intervention, the CCCA score (208.36 ± 23.25 vs. 190.60 ± 28.83), CINS-CV score(106.95 ± 14.48 vs. 99.55 ± 14.60), the oretical exam score (83.01 ± 4.27 vs. 79.75 ± 5.45), and scenario simulation exam score (89.23 ± 3.17 vs. 81.42 ± 7.19) of intervention group were higher than those of the control group (P＜0.01). The open-ended questionnaire survey revealed that the difficulties or challenges faced by the intervention group were mainly related to case analysis, group cooperation, learning material acquisition, and teacher guidance. Conclusion: Applying the mini-CEX teaching model based on nurse-faculty collaboration could cultivate nursing students' competency, build a positive classroom climate, and improve the course achievement of students.

Cbx4 governs HIF-1α to involve in Th9 cell differentiation promoting asthma by its SUMO E3 ligase activity.

The potential role of polycomb chromobox 4 (Cbx4), as a small ubiquitin-like ligase (SUMO) E3 ligase, in the development and exacerbation of asthma remains unclear. Hypoxia inducible factor-1 (HIF-1) is a key transcription factor in the cellular response to hypoxia and contributes to the pathogenesis and progression of a range of diseases, including asthma. Here, we aimed to investigate the interaction of Cbx4 with Hypoxia inducible factor-1α (HIF-1α) and the potent mechanism of action in asthma progression. In present study, in vitro and ex vivo results demonstrated that Cbx4 interacts with HIF-1α protein through its SUMO E3 ligase activity and enhances the sumoylation, which increases HIF-1 transactivation through Cbx4 and promotes the differentiation of Th9 cells, then in turn promotes the process of asthma. Treatment of inhibitors targeting SUMO E3 ligase activity of Cbx4 or HIF-1α can effectively reduce HIF-1α activation and differentiation of Th9 cells, which further attenuates the asthma in mouse model. Current results collectively demonstrated Cbx4 can govern HIF-1α to involve in Th9 cell differentiation promoting asthma by its SUMO E3 ligase activity, providing a new direction for clinical treatment of asthma.

Real-time semi-quantitative assessment of anastomotic blood perfusion in mini­invasive rectal resections by Sidestream Dark Field (SDF) imaging technology: a prospective in vivo pilot study.

PURPOSE: Anastomotic leakage (AL) is one of the severe complications after rectal surgery, and anastomotic ischemia is one of the main factors. This prospective in vivo pilot study aimed to evaluate the effectiveness of Sidestream Dark Field (SDF) imaging in quantitative assessment of anastomotic microcirculation and to analyze its correlation with AL. METHODS: Thirty-three patients with rectal cancer who underwent laparoscopic low anterior resection from 2019 to 2020 were enrolled. Microcirculation was measured by SDF imaging at the descending colon, the mesocolon transection line (MTL), and 1 cm and 2 cm distal to the MTL. Anastomotic microcirculation was measured at the stapler anvil edge before anastomosis. Quantitative perfusion-related parameters were as follows: microcirculation flow index (MFI), perfused vessel density (PVD), proportion of perfused vessels (PPV), and total vessel density (TVD). RESULTS: All patients obtained stable microcirculation images. Functional microcirculation parameters (MFI, PPV, PVD) decreased successively from the descending colon, the colon at MTL, and 1 cm and 2 cm distal to the MTL (all P < 0.01). Extremely poor microcirculation was found at the intestinal segment 2 cm distal to the MTL. Micro-perfusion was significantly lower at the colonic limb of the anastomosis compared with the descending colon (all P < 0.001). Anastomotic leakage occurred in 3 patients (9.1%) whose anastomotic microcirculation was significantly lower than those without AL (all P < 0.01). Blood perfusion at the colonic limb of the anastomosis was significantly higher in patients with left colic artery preservation than in controls. CONCLUSION: SDF imaging is a promising technique for evaluating anastomotic microcirculation and has potential clinical significance for risk stratification of AL.

Homeostatic control of an iron repressor in a GI tract resident.

The transition metal iron plays a crucial role in living cells. However, high levels of iron are potentially toxic through the production of reactive oxygen species (ROS), serving as a deterrent to the commensal fungus Candida albicans for colonization in the iron-rich gastrointestinal tract. We observe that the mutant lacking an iron-responsive transcription factor Hap43 is hyper-fit for colonization in murine gut. We demonstrate that high iron specifically triggers multiple post-translational modifications and proteasomal degradation of Hap43, a vital process guaranteeing the precision of intestinal ROS detoxification. Reduced levels of Hap43 de-repress the expression of antioxidant genes and therefore alleviate the deleterious ROS derived from iron metabolism. Our data reveal that Hap43 functions as a negative regulator for oxidative stress adaptation of C. albicans to gut colonization and thereby provide a new insight into understanding the interplay between iron homeostasis and fungal commensalism.

Mettl14 sustains FOXP3 expression to promote the differentiation and functions of induced-regulatory T cells via the mTOR signaling pathway.

Induced regulatory T cell (iTregs) can be generated in vitro. Thus, iTregs-based therapeutics are receiving increased attention for their potential to treat autoimmune diseases and prevent transplant rejection. However, iTregs fail to maintain FoxP3 expression and suppressive activity, which limits their clinical application. Increasing lines of evidence suggest that methyltransferase-like 14 (METTL14), a critical component of the m6A writer complex, regulates the stability and function of the Treg cells. However, beyond meeting the epigenetic modification of Treg cells, whether Mettl14 plays a role in the fate determination of iTregs is unclear. Here, we systemically investigated the potential function of METTL14 in iTregs differentiation and regulatory activity. In our study, iTregs were generated from CD4+ naïve T cells under iTreg-polarizing conditions, we found that the expression of METTL14 was increased in iTregs compared with CD4+naïve T cells. Subsequently, the expression of METTL14 was knocked down by siRNA-METTL14 interference in CD4+ naïve T cells and cultured under iTreg-polarizing conditions. According to the results, Mettl14 deficiency resulted in the disruption of iTregs differentiation evidenced by the limited FoxP3 expression. Meanwhile, inflammatory cytokines such as IFN-γ and IL-17a were upregulated in cultured iTregs. We next determined the functional change in METTL14-deficient iTregs. The results of the colitis development in Rag1-/- mice and CFSE assays revealed that loss of METTL14 significantly compromised the suppressive function of iTregs in vivo and in vitro. We further checked the altered signaling pathway in METTL14-deficient iTregs. We found that reduced METTL14 leads to activation of the mTOR pathway with increased p-mTOR and p-p70S6K, which are known to modulate the suppressive function of iTregs. In conclusion, our study revealed that Mettl14 plays a critical role in the development and suppressive function of iTregs in vitro and could thus serve as a regulatory element for stabilizing iTregs in cell-based therapy.

Dietary interventions for pediatric patients with functional abdominal pain disorders: a systematic review and network meta-analysis.

Dietary therapies are recommended for the treatment of pediatrics with functional abdominal pain disorders (FAPDs), but the comparative effectiveness among them is unclear. Therefore, the main aim of this systematic review and meta-analysis was to compare the effectiveness of differential dietary therapies in pediatrics with functional abdominal pain disorders. We searched PubMed, Embase, and the Cochrane Central Register of Controlled Trials databases from inception to February 28, 2023. Randomized clinical trials of dietary treatments for pediatric patients with functional abdominal pain disorders were included. The primary outcome was the improvement in abdominal pain. The secondary outcomes were changes in pain intensity and pain frequency. Thirty-one studies after screening 8695 retrieved articles were included, and 29 studies were available for network meta-analysis. Compared with placebo, fiber (RR, 4.86; 95%CI, 1.77 to 13.32; P-score = 0.84), synbiotics (RR, 3.92; 95%CI, 1.65 to 9.28; P-score = 0.75), and probiotics (RR, 2.18; 95%CI, 1.46 to 3.26; P-score = 0.46) had significantly larger effect on the improvement in abdominal pain, the three treatments had larger effect than placebo but statistically insignificant in difference in improving pain frequency and intensity. Similarly, there were no significant differences between the dietary treatments after indirect comparisons of the three outcomes.  Conclusion: Fiber supplements, synbiotics, and probiotics were efficacious in improving abdominal pain of FAPDs in children, suggested by very low or low evidence. The evidence of the efficacy of probiotics is more convincing than fiber and synbiotics when sample size and statistical power were considered. No difference in the efficacy of the three treatments. High-quality trials are needed to further investigate the efficacy of dietary interventions. What is Known: • Multiple dietary treatment options are available for functional abdominal pain disorders in the pediatric population, of which the most beneficial one is currently unknown. What is New: • This NMA found very low to low certainty of the evidence suggesting that fiber, synbiotics, and probiotics might be more efficacious in improving abdominal pain of FAPDs in children than the other dietary treatments. • There were no significant differences between active dietary treatments for changes in abdominal pain intensity.

Comparison of the efficacy of different biodegradable membranes in guided bone/tissue regeneration: a systematic review and network meta-analysis.

Guided bone/tissue regeneration (GBR/GTR) is commonly used in dental treatment. The desired bone/tissue regeneration is achieved by placing a barrier membrane over the defect to avoid the downward growth of faster-growing connective and epithelial tissue into the defect. This review aimed to evaluate osteogenic properties, degradation characteristics, and postoperative complications of eight biodegradable membranes in animal experiments, including non-crosslinked collagen membrane (NCCM), crosslinked collagen membrane (CCM), silk membrane (SM), polylactic-co-glycolic acid, polylactic acid, polyethylene glycol hydrogel, polycaprolactone (PCL), and magnesium alloys. Seven electronic databases (PubMed, Embase, Web of Science, Cochrane Library, Science Direct, Wiley, Scopus and Google Scholar) were screened. Study selection, data extraction and quality assessment were made in duplicate. The SYRCLE assessment tool, CERQual (Confidence in the Evidence from Reviews of Qualitative Research) tool and GRADE tool were used to grade the risk of bias and level of evidence. A total of 2512 articles were found in the electronic database. Finally, 94 articles were selected, of which 53 were meta-analyzed. Surface under the cumulative ranking curve showed the best results for new bone formation in the magnesium barrier membrane group, followed by SM, PCL, NCCM, and CCM. Qualitative analysis showed good biocompatibility for natural polymer membranes and a longer degradation time for synthetic polymer membranes. In addition, 34 studies all showed high bias risks, while other studies had unclear bias risks. Natural polymer membranes were more effective for bone regeneration and magnesium alloys were proved to be promising barrier materials that warrant future research.

RNF130 protects against pulmonary fibrosis through suppressing aerobic glycolysis by mediating c-myc ubiquitination.

BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a chronic and fatal disease,characterized by an excessive accumulation of extracellular matrix (ECM) proteins in response to chronic lung injury. Current evidence suggests that metabolic reprogramming is always accompanied by myofibroblast activation in IPFof whichthe underlying mechanisms remain unclear. Ring finger protein 130 (RNF130), was demonstrated involved in multiple diseases. However, whether RNF130 plays a critical role in the pathogenesis of IPF needs to be clarified. METHODS: We first investigated the expression of RNF130 in pulmonary fibrosis in vivo and in vitro. We then observed the effect and explored the molecular mechanism of RNF130 on the transition of fibroblast to myofibroblast and aerobic glycolysis. Further, we assessed the effects of adeno-associated virus (AAV)-induced RNF130 overexpression in the pulmonary fibrosis model, conducting pulmonary function, assessment of collagen depositionusing the hydroxyproline assay, and biochemical and histopathological analyses. RESULTS: We found that RNF130 was down-regulated in lung tissues of mice with bleomycin-induced pulmonary fibrosis and lung fibroblasts treated with transforming growth factor-ß1 (TGF-ß1). Then we demonstrated that RNF130 inhibitedthe transition of fibroblast to myofibroblast by suppressing aerobic glycolysis. Mechanistically, we revealed that RNF130 promotedc-myc ubiquitination and degradation, while c-myc overexpression reverses the inhibitory effects of RNF130. Importantly, pulmonary function, collagen deposition and fibroblast differentiation were significantly alleviated in adeno-associated virus serotype (AAV)6-RNF130 treated mice, which further validated the contribution of RNF130/c-myc signaling axis in pulmonary fibrosis pathological process. CONCLUSIONS: In summary, RNF130 participates in the pathogenesis of pulmonary fibrosis by inhibiting the transition of fibroblast to myofibroblast and aerobic glycolysis through promoting c-myc ubiquitination and degradation. Targeting RNF130-c-myc axismightrepresent a promising strategy to alleviate the progression of IPF.

Experimental and numerical study of Conoscopic Interferometry sensitivity for optimal acoustic pulse detection in ultrafast acoustics.

Conoscopic interferometry is a promising detection technique for ultrafast acoustics. By focusing a probe beam through a birefringent crystal before passing it through a polarizer, conoscopic interferences sculpt the spatial profile of the beam. The use of these patterns for acoustic wave detection revealed a higher detection sensitivity over existing techniques, such as reflectometry and beam distortion detection. However, the physical origin of the increased sensitivity is unknown. In this work, we present a model, describing the sensitivity behavior of conoscopic interferometry with respect to the quarter-wave plate orientation and the diaphragm aperture, which is validated experimentally. Using the model, we optimize the detection sensitivity of conoscopic interferometry. We obtain a maximal sensitivity of detection when placing the diaphragm edge on the dark fringes of the conoscopic interference patterns. In the configurations studied in this work, conoscopic interferometry can be 18 dB more sensitive to acoustic waves than beam distortion detection.

TGF-ß1 promotes SCD1 expression via the PI3K-Akt-mTOR-SREBP1 signaling pathway in lung fibroblasts.

BACKGROUND: Lung fibroblast activation is associated with airway remodeling during asthma progression. Stearoyl-CoA desaturase 1 (SCD1) plays an important role in the response of fibroblasts to growth factors. This study aimed to explore the effects of SCD1 on fibroblast activation induced by transforming growth factor-ß1 (TGF-ß1) and the role of the phosphatidylinositol-3-kinase-AKT serine-threonine protein kinase-mechanistic target of rapamycin (PI3K-Akt-mTOR) pathway on the regulation of SCD1 expression in airway remodeling. METHODS: Female C57BL/6 mice were sensitized and challenged with house dust mites to generate a chronic asthma model. The inhibitor of SCD1 was injected i.g. before each challenge. The airway hyper-responsiveness to methacholine was evaluated, and airway remodeling and airway inflammation were assessed by histology. The effects of SCD1 on fibroblast activation were evaluated in vitro using an SCD1 inhibitor and oleic acid and via the knockdown of SCD1. The involvement of the PI3K-Akt-mTOR-sterol regulatory element-binding protein 1 (SREBP1) pathway in lung fibroblasts was investigated using relevant inhibitors. RESULTS: The expression of SCD1 was increased in fibroblasts exposed to TGF-ß1. The inhibition of SCD1 markedly ameliorated airway remodeling and lung fibroblast activation in peripheral airways. The knockdown or inhibition of SCD1 resulted in significantly reduced extracellular matrix production in TGF-ß1-treated fibroblasts, but this effect was reversed by the addition of exogenous oleic acid. The PI3K-Akt-mTOR-SREBP1 pathway was found to be involved in the regulation of SCD1 expression and lung fibroblast activation. CONCLUSIONS: The data obtained in this study indicate that SCD1 expression contributes to fibroblast activation and airway remodeling and that the inhibition of SCD1 may be a therapeutic strategy for airway remodeling in asthma.

Modelling of pH changes in alkaline lakes with water transfer from a neutral river.

While water transfer from rivers to alkaline lakes has been proposed to solve lake water level drawdown and ecological degradation problems, its effectiveness for achieving ecological goals is often questionable. A sudden pH decline in alkaline lakes due to water transfer is considered likely to harm the lake ecology. However, it remains unclear to what extent water transfer affects alkaline lake pH. Thus, a three-dimensional numerical model coupling a pH calculation method considering the carbonate balance with the MIKE3 hydrodynamic model was developed to predict pH changes in an alkaline lake. Laboratory and field measurements verified the model reliability. The model accurately simulated the mixed-water pH during water transfer, with a root mean square error of 0.03-0.07 and a coefficient of determination of 0.894-0.998. The model was then applied to predict the pH response to water transfer in Lake Chenghai. The results showed that the pH response to water transfer demonstrated spatial and temporal variability, and a low-pH diffusion zone (pH ≤ 9) formed in the northern parts of the lake during annual water transfer; the effects of water transfer on the pH in the lake were cumulative over time, and the average pH in Lake Chenghai after five years decreased by 0.2 units; strong wind and low inflow could effectively reduce the low-pH diffusion area; and daily thermal stratification of the plateau region threatened the low-pH diffusion area control in Lake Chenghai. Our results provide a new reference for formulating ecological water transfer strategies for alkaline lakes and similar water bodies.