Linking undergraduates' future work self and employability: a moderated mediation model.

BACKGROUND: The career intentions of students play a crucial role in shaping the growth of the hospitality and tourism industry. Previous research underlines the significance of future work self in predicting outcomes related to one's career. However, there is limited knowledge regarding the precise ways, timing, and conditions under which the future work self of undergraduate students can enhance their employability. METHODS: This paper aims to address the existing research gap by employing career construction theory and self-determination theory to propose a moderated mediation model-i.e., career exploration serves as a mediator and job market knowledge functions as a moderator in the relationship between future work self and employability. We conducted two independent studies (i.e., an experimental study and a time-lagged field study) to test the proposed model. Specifically, in Study 1 we employed an experimental research design to recruit 61 students majoring in tourism management to participate. They were randomly assigned to two scenarios (future work self: high vs. low), and we manipulated different levels of future work self by means of scenario descriptions. In Study 2, we used the time-lagged research design to collect data via submitting questionnaires among 253 Chinese undergraduates who majored in hospitality and tourism at a university in the middle area of China. RESULTS: The results indicate a positive correlation between undergraduates' future work self and their employability. Furthermore, this relationship is mediated by a mediator of career exploration. It is important to note that this mediating relationship is also contingent upon the moderator variable of undergraduates' job market knowledge when considering the impact of career exploration on employability. CONCLUSION: The findings contribute to enriching the current understanding of the positive effects of future work self on undergraduates' desirable outcomes in employability.

Network analysis of perception of exercise benefits/barriers and kinesiophobia among patients with cardiovascular diseases.

BACKGROUND: Perception of exercise benefits/barriers and kinesiophobia are important predictors of low exercise behaviors in patients with cardiovascular diseases (CVDs). Little is known about the complex intercorrelations between different components of perception of exercise benefits/barriers and kinesiophobia. OBJECTIVES: To identify the central components of kinesiophobia and to explore the interconnectedness between perception of exercise benefits/barriers and kinesiophobia. METHODS: A total of 258 patients with CVDs were recruited in this study. The Tampa Scale for Kinesiophobia Heart and the Exercise Benefits/Barriers Scale were used to assess kinesiophobia and perception of exercise benefits/barriers. R software was used to visualize the networks and analyze the centrality of the networks. The index "expected influence" and "bridge expected influence" were employed to identify the central components and the bridge components of the networks. RESULTS: In the item network of kinesiophobia, three items ("It is really not safe for a person in my condition to be physically active/exercise", "I cannot do the same things as others because there is a too big risk that I will get heart problems", and "If I tried to be physically active/exercise my heart problem would increase") had the highest expected influence. In the exercise benefits/barriers-kinesiophobia network, the dimension of physical exertion had the highest positive bridge expected influence, while psychological outlook had highest negative value. CONCLUSIONS: The three central components of kinesiophobia and the two bridge components (perception exercise barriers of physical exertion and perception exercise benefits of psychological outlook) should be targeted in specific intervention for relieving kinesiophobia and further promoting exercise behaviors.

Future orientation and perceived employability of chinese undergraduates: a moderated mediation model.

Although scholars and practitioners have highlighted the significance of students' attitudes for their future employment, few empirical examinations have attempted to determine the potential association between students' future orientation and their perceived employability. Thus, drawing on career construction theory, we test the positive effect of students' future orientation on their perceived employability by exploring the mediator of problem-based learning and the moderators of job market knowledge and proactive personality. Collecting our data via a time-lagged design (N = 368), we have found that the positive association between future orientation and employability is mediated by problem-based learning. Our moderation analyses further revealed that job market knowledge positively moderates the relationship between future orientation and problem-based learning and that students' proactive personality positively moderates the relationship between problem-based learning and perceived employability.

Clinical efficacy of endoscopic antireflux mucosectomy vs. Stretta radiofrequency in the treatment of gastroesophageal reflux disease: a retrospective, single-center cohort study.

Background: Currently, antireflux mucosectomy (ARMS) and Stretta radiofrequency (SRF) are the most commonly used minimally invasive antireflux therapies. To date, there have not been any reports comparing ARMS and SRF. Our aim was to compare the clinical efficacies of these two therapeutic methods. Methods: We analyzed data from gastroesophageal reflux disease (GERD) patients, including 39 who received ARMS treatment and 30 who received SRF treatment between January 2020 and May 2021. Symptom control, gastroesophageal reflux disease questionnaire (GERDQ) score, gastroesophageal reflux disease health-related quality of life (GERD-HRQL) score, proton pump inhibitor (PPI) withdrawal, and PPI reduction were analyzed and compared. Results: After 6 months of follow-up, the results showed that both therapies were effective in improving symptoms and quality of life. No difference was found between the ARMS group and SRF group in GERDQ score, GERD-HRQL score, PPI withdrawal rate, or PPI reduction rate (P>0.05). There was no significant difference in the PPI withdrawal rate between the two therapies among patients with gastroesophageal flap valve (GEFV) grade II and grade III (P>0.05), but the PPI withdrawal rate in the ARMS group was significantly higher than that in the SRF group among patients with GEFV grade IV (P<0.05). Conclusions: The clinical efficacies of ARMS and SRF 6 months postoperation were equivalent. The results showed that both ARMS and SRF treatment were acceptable for patients with GEFV grades II and III, while ARMS should be selected for patients with GEFV grade IV.

Gastroesophageal reflux disease: recent innovations in endoscopic assessment and treatment.

Innovations in endoscopy have brought about some impressive improvements in diagnosing and treating gastroesophageal reflux disease (GERD). GERD, as one of the most prevalent gastrointestinal disorders in the world, has always been on the cutting edge of endoscopic interventions. A primary diagnosis of GERD is based on symptoms and an initial trial of proton-pump inhibitor (PPI) therapy, which is devoid of adequately instructive value for therapeutic strategies. Endoscopy and optional biopsies can be used to directly observe and determine the abnormal structural and pathophysiological damage in the esophagus. The emergence of minimally invasive endoscopic therapy fills the gap between patients who are reluctant or insensitive to PPIs and candidates who are not indicated for surgical anti-reflux fundoplication. In this review, we discuss the utility of endoscopy and biopsy in patients with persistent GERD-related manifestations after proper medical anti-reflux treatment. Moreover, we portray a landscape of four current endoscopic GERD therapies and clarify the merits and disadvantages of each technique. Future research needs to concentrate on stratifying GERD patients based on personal conditions and elucidating the primary pathophysiology of GERD.

How Can Hotel Employees Produce Workplace Environmentally Friendly Behavior? The Role of Leader, Corporate and Coworkers.

Although previous studies have acknowledged that leaders' such environmental behaviors and environmental issues are becoming critical for long-term development, little research has focused on why, how and when perceived environmentally specific servant leadership contributes to employees' workplace environmentally friendly behavior in the hotel industry. This paper aims to fill this research gap by using social identity theory to test employees' green role identity as a mediator and their perceived corporate environmental responsibility and perceived coworkers' work group green advocacy as moderators in the relationship between perceived environmentally-specific servant leadership and workplace environmentally friendly behavior. Using a sample of 527 leader-follower dyads from six hotels in mainland China at two points in time, we found that employees' green role identity mediates the positive relationship between perceived environmentally specific servant leadership and employees' workplace environmentally friendly behavior. Moreover, employees' perceived corporate environmental responsibility and perceived coworkers' work group green advocacy were found to positively moderate the relationship between perceived environmentally-specific servant leadership and green role identity and between green role identity and workplace environmentally friendly behavior, respectively. Theoretical and practical implications are discussed.

Effects of dexmedetomidine on intraoperative hemodynamics, recovery profile and postoperative pain in patients undergoing laparoscopic cholecystectomy: a randomized controlled trial.

BACKGROUND: To investigate the optimal dose of dexmedetomidine to maintain hemodynamic stability, prevent of cough and minimize postoperative pain for patients undergoing laparoscopic cholecystectomy. METHODS: One hundred twenty patients were randomly divided into D1, D2, D3 and NS groups, and dexmedetomidine 0.4, 0.6, 0.8µg/kg and normal saline were administrated respectively. Patients' heart rate, systolic blood pressure and diastolic blood pressure were measured at T1-T7. The incidence of cough was recorded. Other parameters were noted, the time of spontaneous respiratory recovery and extubation, visual analogue scale scores and dosage of tramadol. RESULTS: The heart rate, systolic blood pressure and diastolic blood pressure of D2 and D3 groups has smaller fluctuations at T2-3 and T7 compared with NS and D1 groups (P < 0.05). The incidence of cough was lower in D2 and D3 groups than NS group (P < 0.05). The visual analogue scale scores and tramadol dosage of D2 and D3 groups were lower than NS group (P < 0.05). The time of spontaneous respiratory recovery and extubation in D3 group was longer than that in D1 and D2 groups (P < 0.05). CONCLUSIONS: Intravenous infusion of 0.6µg/kg dexmedetomidine before induction can maintain hemodynamic stability, decrease cough during emergence, relieve postoperative pain of patients undergoing laparoscopic cholecystectomy. TRIAL REGISTRATION: ChiCTR1900024801 , registered at the Chinese Clinical Trial Registry, principal investigator: Qin Ye, date of registration: July 28, 2019.

How Environmental Leadership Boosts Employees' Green Innovation Behavior? A Moderated Mediation Model.

We examined employees' green organizational identity as a mediator and green organizational climate as a moderator in the relationship between environmental leadership and follower green innovation behavior. Through collecting data (N = 313) from public organizations in China at different times, we found that environmental leadership is positively related to employees' green innovation behavior through increasing their green organizational identity. Meanwhile, the mediating relationship is conditional on the moderator of green organizational climate. The current study aims to clarify the mechanism and boundary condition in the relationship between environmental leadership and employees' green innovation behaviors.

The relationship between KRAS gene mutation and intestinal flora in tumor tissues of colorectal cancer patients.

BACKGROUND: Colorectal cancer is among the most prominent malignant tumors endangering human health, with affected populations exhibiting an increasingly younger trend. The Kirsten ras (KRAS) gene acts as a crucial regulator in this disease and influences multiple signaling pathways. In the present study, the KRAS gene mutation-induced alteration of intestinal flora in colorectal cancer patients was explored, and the intestinal microbes that may be affected by the KRAS gene were examined to provide new insights into the diagnosis and treatment of colorectal cancer. METHODS: Deoxyribonucleic acid (DNA) was extracted from 177 colorectal cancer patients in our hospital. The mutation of the KRAS gene was subsequently detected using real-time fluorescence quantitative polymerase chain reaction (qPCR), and survival analysis was performed. Moreover, genomic DNA was extracted from the fecal microbes in 30 of these patients, and the differences in the intestinal flora between mutation and non-mutation groups were evaluated using linear discriminant analysis (LDA) Effect size (LEfSe) analysis. RESULTS: KRAS gene mutation substantially affected the distant metastasis of colorectal cancer, and the survival prognosis in the non-mutation group was significantly superior compared to the mutation group. The mutation group had a notably higher prevalence of microbes including Roseburia, Parabacteroides, Metascardovia, Staphylococcus, Staphylococcaceae, and Bacillales than the non-mutation group. The presence of microbes in the non-mutation group, such as Clostridiales, Bacteroidetes, Lachnospiraceae, Coprococcus, and Ruminococcaceae was markedly higher than in the mutation group. Firmicutes were negatively correlated with the presence of Actinomyces and Bacteroidetes, while Bacteroidetes were positively associated with the level of Actinomyces. CONCLUSIONS: In colorectal cancer, KRAS gene mutation can remarkably affect the survival prognosis and change the composition and abundance of intestinal flora, such as Roseburia, Parabacteroides, Metascardovia, Staphylococcus, and Bacillales, thereby influencing tumor development.

The angiocrine Rspondin3 instructs interstitial macrophage transition via metabolic-epigenetic reprogramming and resolves inflammatory injury.

Macrophages demonstrate remarkable plasticity that is essential for host defense and tissue repair. The tissue niche imprints macrophage identity, phenotype and function. The role of vascular endothelial signals in tailoring the phenotype and function of tissue macrophages remains unknown. The lung is a highly vascularized organ and replete with a large population of resident macrophages. We found that, in response to inflammatory injury, lung endothelial cells release the Wnt signaling modulator Rspondin3, which activates ß-catenin signaling in lung interstitial macrophages and increases mitochondrial respiration by glutaminolysis. The generated tricarboxylic acid cycle intermediate α-ketoglutarate, in turn, serves as the cofactor for the epigenetic regulator TET2 to catalyze DNA hydroxymethylation. Notably, endothelial-specific deletion of Rspondin3 prevented the formation of anti-inflammatory interstitial macrophages in endotoxemic mice and induced unchecked severe inflammatory injury. Thus, the angiocrine-metabolic-epigenetic signaling axis specified by the endothelium is essential for reprogramming interstitial macrophages and dampening inflammatory injury.

IL-1ß suppression of VE-cadherin transcription underlies sepsis-induced inflammatory lung injury.

Unchecked inflammation is a hallmark of inflammatory tissue injury in diseases such as acute respiratory distress syndrome (ARDS). Yet the mechanisms of inflammatory lung injury remain largely unknown. Here we showed that bacterial endotoxin lipopolysaccharide (LPS) and cecal ligation and puncture-induced (CLP-induced) polymicrobial sepsis decreased the expression of transcription factor cAMP response element binding (CREB) in lung endothelial cells. We demonstrated that endothelial CREB was crucial for VE-cadherin transcription and the formation of the normal restrictive endothelial adherens junctions. The inflammatory cytokine IL-1ß reduced cAMP generation and CREB-mediated transcription of VE-cadherin. Furthermore, endothelial cell-specific deletion of CREB induced lung vascular injury whereas ectopic expression of CREB in the endothelium prevented the injury. We also observed that rolipram, which inhibits type 4 cyclic nucleotide phosphodiesterase-mediated (PDE4-mediated) hydrolysis of cAMP, prevented endotoxemia-induced lung vascular injury since it preserved CREB-mediated VE-cadherin expression. These data demonstrate the fundamental role of the endothelial cAMP-CREB axis in promoting lung vascular integrity and suppressing inflammatory injury. Therefore, strategies aimed at enhancing endothelial CREB-mediated VE-cadherin transcription are potentially useful in preventing sepsis-induced lung vascular injury in ARDS.

How Servant Leadership Leads to Employees' Customer-Oriented Behavior in the Service Industry? A Dual-Mechanism Model.

Although servant leadership has been acknowledged as an important predictor of employees' behavioral outcomes in the service industry, there is still no cohesive understanding of the positive association between servant leadership and employees' customer-oriented behavior (COB). This research, drawing on cognitive affective processing system theory (CAPS), empirically investigates the influence of servant leadership on employees' COB by exploring two mediators (i.e., organizational identification and vitality). We conducted two studies in China, using a cross-sectional design to survey employees in service-oriented technical organizations (Study 1) and a time-lagged design to survey hospitality employees with frontline service jobs in star-level hotels (Study 2). Across both samples, we found that servant leadership enhanced employees' COB by simultaneously increasing their organizational identification and vitality. We discuss the implications of these results for future research and practice.

mtDNA Activates cGAS Signaling and Suppresses the YAP-Mediated Endothelial Cell Proliferation Program to Promote Inflammatory Injury.

Cytosolic DNA acts as a universal danger-associated molecular pattern (DAMP) signal; however, the mechanisms of self-DNA release into the cytosol and its role in inflammatory tissue injury are not well understood. We found that the internalized bacterial endotoxin lipopolysaccharide (LPS) activated the pore-forming protein Gasdermin D, which formed mitochondrial pores and induced mitochondrial DNA (mtDNA) release into the cytosol of endothelial cells. mtDNA was recognized by the DNA sensor cGAS and generated the second messenger cGAMP, which suppressed endothelial cell proliferation by downregulating YAP1 signaling. This indicated that the surviving endothelial cells in the penumbrium of the inflammatory injury were compromised in their regenerative capacity. In an experimental model of inflammatory lung injury, deletion of cGas in mice restored endothelial regeneration. The results suggest that targeting the endothelial Gasdermin D activated cGAS-YAP signaling pathway could serve as a potential strategy for restoring endothelial function after inflammatory injury.

Alveolar Stretch Activation of Endothelial Piezo1 Protects Adherens Junctions and Lung Vascular Barrier.

Disruption of alveolar-capillary barriers is a major complication of high-volume mechanical ventilation referred to as "ventilator-induced lung injury." The stretching force in alveoli is transmitted to endothelial cells, increasing the tension on underlying endothelial plasma membrane. The mechanosensor Piezo1, a plasma membrane cation channel, was inducibly deleted in endothelial cells of mice (Piezo1iEC-/-), which allowed us to study its role in regulating the endothelial barrier response to alveolar stretch. We observed significant increase in lung vascular permeability in Piezo1iEC-/- mice as compared with control Piezo1fl/fl mice in response to high-volume mechanical ventilation. We also observed that human lung endothelial monolayers depleted of Piezo1 and exposed to cyclic stretch had increased permeability. We identified the calcium-dependent cysteine protease calpain as a downstream target of Piezo1. Furthermore, we showed that calpain maintained stability of the endothelial barrier in response to mechanical stretch by cleaving Src kinase, which was responsible for disassembling endothelial adherens junctions. Pharmacological activation of calpain caused Src cleavage and thereby its inactivation, and it restored the disrupted lung endothelial barrier seen in Piezo1iEC-/- mice undergoing high-volume mechanical ventilation. Our data demonstrate that downregulation of Piezo1 signaling in endothelium is a critical factor in the pathogenesis of ventilator-induced lung injury, and thus augmenting Piezo1 expression or pharmacologically activating Piezo1 signaling may be an effective therapeutic strategy.

Reflux finding score is associated with gastroesophageal flap valve status in patients with laryngopharyngeal reflux disease: a retrospective study.

Endoscopic grading of gastroesophageal flap valve (GEFV) is simple and reproducible and offers useful information for reflux activity. To investigate the potential correlation between GEFV grading and reflux finding score (RFS) in patients with laryngopharyngeal reflux disease (LPRD), 225 consecutive Patients with suspected LPRD who underwent both routine upper gastrointestinal endoscopy and laryngoscope were enrolled in our study. Patients with a RFS of more than 7 were diagnosed with LPRD. The GEFV was graded as I through IV according to Hill's classification and was classified into two groups: normal GEFV group (grades I and II) and the abnormal GEFV group (grades III and IV). The percent of GEFV grades I to IV was 39.1%, 39.1%, 12.4%, and 9.3%, respectively. Age was significantly related to an abnormal GEFV (p = 0.002). Gender, BMI, smoke and alcohol were not related to GEFV grade. Fifty-one patients (22.67%) had positive RFS. Reflux finding scores were higher in GEFV grades III and IV than I and II (p < 0.05). Endoscopic grading of GEFV is well correlated with reflux finding score in patients with LPRD. This is a simple and useful technique that provides valuable diagnostic information of LPRD.

A Tie2-Notch1 signaling axis regulates regeneration of the endothelial bone marrow niche.

Loss-of-function studies have determined that Notch signaling is essential for hematopoietic and endothelial development. By deleting a single allele of the Notch1 transcriptional activation domain we generated viable, post-natal mice exhibiting hypomorphic Notch signaling. These heterozygous mice, which lack only one copy of the transcriptional activation domain, appear normal and have no endothelial or hematopoietic phenotype, apart from an inherent, cell-autonomous defect in T-cell lineage development. Following chemotherapy, these hypomorphs exhibited severe pancytopenia, weight loss and morbidity. This phenotype was confirmed in an endothelial-specific, loss-of-function Notch1 model system. Ang1, secreted by hematopoietic progenitors after damage, activated endothelial Tie2 signaling, which in turn enhanced expression of Notch ligands and potentiated Notch1 receptor activation. In our heterozygous, hypomorphic model system, the mutant protein that lacks the Notch1 transcriptional activation domain accumulated in endothelial cells and interfered with optimal activity of the wildtype Notch1 transcriptional complex. Failure of the hypomorphic mutant to efficiently drive transcription of key gene targets such as Hes1 and Myc prolonged apoptosis and limited regeneration of the bone marrow niche. Thus, basal Notch1 signaling is sufficient for niche development, but robust Notch activity is required for regeneration of the bone marrow endothelial niche and hematopoietic recovery.

Caspase-11-mediated endothelial pyroptosis underlies endotoxemia-induced lung injury.

Acute lung injury is a leading cause of death in bacterial sepsis due to the wholesale destruction of the lung endothelial barrier, which results in protein-rich lung edema, influx of proinflammatory leukocytes, and intractable hypoxemia. Pyroptosis is a form of programmed lytic cell death that is triggered by inflammatory caspases, but little is known about its role in EC death and acute lung injury. Here, we show that systemic exposure to the bacterial endotoxin lipopolysaccharide (LPS) causes severe endothelial pyroptosis that is mediated by the inflammatory caspases, human caspases 4/5 in human ECs, or the murine homolog caspase-11 in mice in vivo. In caspase-11-deficient mice, BM transplantation with WT hematopoietic cells did not abrogate endotoxemia-induced acute lung injury, indicating a central role for nonhematopoietic caspase-11 in endotoxemia. Additionally, conditional deletion of caspase-11 in ECs reduced endotoxemia-induced lung edema, neutrophil accumulation, and death. These results establish the requisite role of endothelial pyroptosis in endotoxemic tissue injury and suggest that endothelial inflammatory caspases are an important therapeutic target for acute lung injury.

Role of the phagosomal redox-sensitive TRP channel TRPM2 in regulating bactericidal activity of macrophages.

Acidification of macrophage phagosomes serves an important bactericidal function. We show here that the redox-sensitive transient receptor potential (TRP) cation channel TRPM2 is expressed in the phagosomal membrane and regulates macrophage bactericidal activity through the activation of phagosomal acidification. Measurement of the TRPM2 current in phagosomes identified TRPM2 as a functional redox-sensitive cation channel localized in the phagosomal membrane. Simultaneous measurements of phagosomal Ca2+ changes and phagosome acidification in macrophages undergoing phagocytosis demonstrated that TRPM2 was required to mediate the efflux of cations and for phagosomal acidification during the process of phagosome maturation. Acidification in phagosomes was significantly reduced in macrophages isolated from Trpm2-/- mice as compared to wild type, and acidification was coupled to reduced bacterial clearance in Trpm2-/- mice. Trpm2+/+ macrophages treated with the vacuolar H+-ATPase inhibitor bafilomycin showed reduced bacterial clearance, similar to that in Trpm2-/- macrophages. Direct activation of TRPM2 using adenosine diphosphate ribose (ADPR) induced both phagosomal acidification and bacterial killing. These data collectively demonstrate that TRPM2 regulates phagosomal acidification, and is essential for the bacterial killing function of macrophages.

Oxidant Sensing by TRPM2 Inhibits Neutrophil Migration and Mitigates Inflammation.

Blood neutrophils perform an essential host-defense function by directly migrating to bacterial invasion sites to kill bacteria. The mechanisms mediating the transition from the migratory to bactericidal phenotype remain elusive. Here, we demonstrate that TRPM2, a trp superfamily member, senses neutrophil-generated reactive oxygen species and restrains neutrophil migration. The inhibitory function of oxidant sensing by TRPM2 requires the oxidation of Cys549, which then induces TRMP2 binding to formyl peptide receptor 1 (FPR1) and subsequent FPR1 internalization and signaling inhibition. The oxidant sensing-induced termination of neutrophil migration at the site of infection permits a smooth transition to the subsequent microbial killing phase.