Forging green Horizons: Revealing Catalysts of pro-environmental behavior in emerging market.

In recent years, environmental pollution has started to threaten global economies. The understanding of consumer behavior within the context of sustainable development has become increasingly important to deal with this growing ecological complexity. Urbanization has accelerated in Pakistan, resulting in urban consumers raising more environmental concerns and promoting eco-friendly products. These concerns have demonstrated their commitment to sustainability and pro-environmental behaviors, such as reducing waste materials (e.g., plastics) and pollutants (i.e., smoke, dust, etc.), thus supporting eco-friendly behaviors. Today, Pakistan's urban consumers are well-aware of environmental complexities. As such, environmental knowledge is the driver of consumers' pro-environmental behavior, affective commitment and social capital also compel individuals to acquire ecological knowledge to enhance consumer behavior. This research considers customers' environmental knowledge and affective commitment, both of which actively contribute to pro-environmental activity. It explores the relationship between environmental knowledge, affection commitment, social capital, and environmental behavior in Pakistan. Data was gathered from Pakistan's urban customers and analyzed using Covariance-based Structural Equation Modeling (CB-SEM). The results indicate that affective commitment and social capital have a positive and significant effect on environmental knowledge and behavior. Notably, the relationship between social capital, affective commitment, and environmental behavior is mediated by knowledge of environmental issues. Through its findings, this study fosters an understanding of environmental behavior and explains the sense of responsibility and greater commitment in individuals, which thus leads them toward sustainability.

Effects of full-body exercise-based pulmonary rehabilitation in patients with idiopathic pulmonary fibrosis: a systematic review and meta-analysis protocol.

INTRODUCTION: Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease characterised by progressive and irreversible fibrosis of the lung parenchyma, resulting in reduced lung function. Since conventional medicines can be associated with low effective rates and adverse events, pulmonary rehabilitation may be a promising non-pharmacological therapy for IPF. Thus, we aimed to evaluate the effects of full-body exercise-based pulmonary rehabilitation on patients with IPF by conducting a systematic review and meta-analysis of randomised controlled trials (RCTs). METHODS AND ANALYSIS: This systematic review and meta-analysis has been registered in the International Prospective Register of Systematic Reviews (PROSPERO). From inception to 31 August 2022, electronic databases in English and Chinese were searched, including PubMed, Embase, Web of Science, Cochrane Central Register of Controlled Trials among the English databases. China National Knowledge Infrastructure, Chinese Biomedical Literature, VIP Chinese Science and Technology Periodical, and Wan Fang Data were among the Chinese databases. Two independent reviewers then screened the potential RCT studies, which were analysed according to the Cochrane Handbook criteria. The efficacy and safety of full-body exercise pulmonary rehabilitation for IPF were evaluated based on outcomes, including exercise capacity measured by 6 min walking distance and quality of life measured by St. George's Respiratory Questionnaire. Lung function was measured based on the forced vital capacity, total lung capacity, diffusing capacity of the lungs for carbon monoxide and dyspnoea assessed by the modified Medical Research Council scale. ETHICS AND DISSEMINATION: Ethical approval was not required for this systematic review and meta-analysis. Results will be published in a peer-reviewed journal and presented at conferences. PROSPERO REGISTRATION NUMBER: CRD42021284293.

Impact of Leading by Example on Employees' Organizational and Job Psychological Ownership: A Moderated Mediation Study.

This article studies the influence of leading by example on organizational psychological ownership and job psychological ownership. This article further introduces the mediating mechanism of organizational identification and the regulating mechanism of Leader-member Exchange (LMX). This study investigated 312 personnel from eight property management enterprises in East, Northwest, Northeast, and central China. This study adopts a quantitative research method, using survey data of project managers, team leaders, and managers of Property management projects in China. The data were collected by questionnaire survey. In terms of data analysis, AMOS 21.0 software was used to conduct structural equation modeling (SEM) using the maximum likelihood method to test direct and indirect effects. SPSS 25.0 software was used to test the moderating effect by multilevel regression analysis with the maximum variance method. Use these two methods to analyze the whole theoretical framework. The results established all assumed relationships. In this article, leading by example, one of the important dimensions of empowering leadership is studied as a new leadership style, and the predictive effect of leading by example on organizational psychological ownership and job psychological ownership is verified. This finding further verifies the influence mechanism and boundary conditions of empowering leadership in different dimensions. It is found that organizational identification has different mediating effects on leading by example and organizational psychological ownership and job psychological ownership. The moderating effect of LMX also further indicates that under the influence of Confucian pan-family culture, the leader's exemplary behavior with higher authority has a stronger influence on employees' organizational identification, organizational psychological ownership, and job psychological ownership. Their relationship is deeply influenced by the culture of China's unique organizational Circle Culture.

Evaluation of Pancreatic Fibrosis Grading by Multiparametric Quantitative Magnetic Resonance Imaging.

BACKGROUND: Early detection and grading of pancreatic fibrosis (PF) are important and challenging clinical goals. PURPOSE: To determine main pancreatic duct (MPD) diameter, pancreatic thickness, and grades of PF via magnetic resonance elastography (MRE), T1 mapping, and intravoxel incoherent motion diffusion-weighted imaging (IVIM-DWI), assessing respective diagnostic performances. STUDY TYPE: Prospective. SUBJECTS: Histopathologic and imaging records (MRE, T1 mapping, and IVIM-DWI) generated by 144 patients between December 2018 and May 2020 were collected for analysis. Grades of PF were distributed as follows: F0, 82; F1, 22; F2, 22; and F3, 18. FIELD STRENGTH/SEQUENCE: 3 T pancreatic MRI, encompassing MRE, T1 mapping, and IVIM-DWI. ASSESSMENT: In all patients, T1 relaxation times, pancreatic stiffness values, IVIM-DWI parameters, MPD diameter, and pancreatic thickness were measured. STATISTICAL TESTS: Receiver operating characteristic (ROC) analysis served to assess imaging parameters useful in diagnosing PF. To identify relations between specific parameters and grades of PF, logistic regression analysis was invoked. RESULTS: Both pancreatic stiffness (r = 0.754; P < 0.001) and T1 relaxation time (r = 0.433; P < 0.001) correlated significantly with PF (%). To determine PF grades ≥F1, a combined model (area under the curve [AUC] = 0.906) performed significantly better than pancreatic stiffness (AUC = 0.855; P < 0.001) or T1 relaxation time (AUC = 0.754; P < 0.001) alone. For PF grades ≥F2 or grade F3, both the combined model (≥F2: AUC = 0.910; F3: AUC = 0.939) and pancreatic stiffness (≥F2: AUC = 0.906; F3: AUC = 0.929) outperformed T1 relaxation time (≥F2: AUC = 0.768 [P = 0.005 and P = 0.004, respectively]; F3: AUC = 0.816 [both P < 0.005]). All IVIM-DWI parameters generated AUC values <0.700. DATA CONCLUSION: A combination of MRE and T1 mapping seems promising in diagnosing various grades of PF, particularly at an early stage. LEVEL OF EVIDENCE: 1 TECHNICAL EFFICACY: Stage 2.

Computed tomography-adjusted fistula risk score for predicting clinically relevant postoperative pancreatic fistula after pancreatoduodenectomy: Training and external validation of model upgrade.

BACKGROUND: To develop a modified Fistula Risk Score (FRS) for predicting clinically relevant postoperative pancreatic fistula (CR-POPF) after pancreatoduodenectomy (PD) based on both FRS and contrast-enhanced computed tomography (CE-CT). METHODS: In this multicenter retrospective analysis, we focused on 990 consecutive patients with pancreatoduodenectomy performed at four institutions between 2009 and 2019. The enhanced CT-FRS model initially targeted 26 pre- and intraoperative factors, including CT descriptors, FRS elements and clinical factors, using LASSO-penalized multivariable logistic regression for predicting CR-POPF events in discovery (n = 718) and externally validated (n = 272) datasets. Probabilities generated were further correlated with histologic features of pancreatic stumps in 356 patients. C-indices were analyzed to compare the predictive potential between the original FRS and the CT-FRS. FINDINGS: CR-POPF developed in 112 (15.6%) and 36 (13.2%) patients in discovery and validation datasets, respectively. The final CT-FRS construct, incorporating remnant pancreatic volume (RPV), stump area, fat and atrophy scores by CT, and main pancreatic duct size, offered significantly greater overall predictability than the original FRS in discovery (C-index: 0.825 vs 0.794; p = 0.04) and validation (0.807 vs 0.741; p = 0.05) cohorts. Importantly, it outperformed the FRS in patients at moderate risk levels (FRS: 3-6), showing remarkably improved C-indices (discovery: 0.729 vs 0.626 [p<0.001], validation: 0.722 vs 0.573 [p = 0.006]). CT-FRS probabilities increased in conjunction with less extensive pancreatic fibrosis (p<0.001), ample glandular acini (p<0.001), and advanced lipomatosis (p<0.001). INTERPRETATION: The enhanced CT-FRS performed significantly better than the original FRS in predicting CR-POPF occurrences after PD, especially at moderate FRS levels.

Pancreatic adenocarcinoma: quantitative CT features are correlated with fibrous stromal fraction and help predict outcome after resection.

OBJECTIVES: To identify quantitative imaging features of contrast-enhanced computed tomography (CE-CT) that may be prognostically favorable after resection of smaller (≤ 30 mm) pancreatic ductal adenocarcinomas (PDACs) located at head. METHODS: This retrospective study included two independent cohorts (discovery cohort, n = 212; test cohort, n = 100) of patients who underwent resection of head PDACs ≤ 30 mm and preoperative CE-CT. We examined tumor and surrounding parenchymal attenuation differences (deltas), and tumor attenuation changes across phases (ratios). Semantic features of PDACs were evaluated by two radiologists. Clinicopathologic and imaging features for predicting disease-free survival (DFS) and overall survival (OS) were analyzed via multivariate Lasso-penalized Cox proportional-hazards models. Survival rates were derived by Kaplan-Meier method. RESULTS: Imaging features achieved C-indices of 0.766 (discovery cohort) and 0.739 (test cohort) for DFS, and 0.790 (discovery cohort) and 0.772 (test cohort) for OS estimates through incorporation of clinicopathologic features. The most decisive imaging feature was delta 3, denoting attenuation differences between tumor and surrounding pancreas at pancreatic phase (DFS: HR = 2.122; OS: HR = 2.375; both p < 0.001). Compared with inconspicuous (low-delta-3, < 28 HU) tumors, conspicuous (high-delta-3) tumors correlated significantly with more aggressive histologic grades (p = 0.014) and less extensive tumor fibrous stromal fractions (p < 0.001). Patients with low-delta-3 tumors ≤ 20 mm experienced the most favorable outcomes (DFS, 36 months; OS, 42 months), whereas those with high-delta-3 tumors fared poorly, regardless of tumor size (DFS, 12 months; OS, 19 months). CONCLUSIONS: Quantifiable CT imaging features reflect heterogeneous fibrous stromal fractions and histologic grades of PDAC at head locations that help stratify patients with disparate clinical outcomes. KEY POINTS: • Quantitative and semantic imaging features achieved promising results for the prognosis of resected PDAC (≤ 30 mm) at head location, through incorporation of clinicopathologic features. • Attenuation difference at tumor-parenchyma interface (delta 3) emerged as the most decisive imaging feature, enabling further stratification of patients into distinct prognostic subtypes by tumor size. • High delta 3 signifies sharper contrast between tumor and surrounding pancreas, correlating with more aggressive histologic grades and less extensive tumor fibrous stromal fractions.

Normative Pancreatic Stiffness Levels and Related Influences Established by Magnetic Resonance Elastography in Volunteers.

BACKGROUND: Large-scale normative studies of pancreatic stiffness and potential influences have yet to be pursued via magnetic resonance elastography (MRE). PURPOSE: To determine normative MRE-based pancreatic stiffness values and to examine related influential factors. STUDY TYPE: Prospective. SUBJECTS: In all, 361 volunteers (men, 199; women, 162) with a median age of 54.0 years and a median body mass index (BMI) of 22.86 kg/m2 were prospectively recruited. Those with no histories of smoking, alcohol abuse, and diabetes mellitus (DM) were grouped as healthy volunteers, designating all others as positive controls. FIELD STRENGTH/SEQUENCE: Each volunteer underwent 3.0T pancreatic MRI at a frequency of 40 Hz. ASSESSMENT: Pancreatic stiffness values, pancreatic width and volume, waist circumference, and wave distance were measured in all subjects. STATISTICAL TESTS: Multiple linear regression analyses were performed to determine variables that influence MRE-determined stiffness. RESULTS: The mean pancreatic stiffness in all volunteers was 1.20 ± 0.16 kPa. Stiffness levels in positive control volunteers proved significantly greater than levels in healthy volunteers (1.29 ± 0.17 kPa vs. 1.14 ± 0.13 kPa; P < 0.001). In multiple linear regression analysis, sex (P = 0.004), BMI (P < 0.001), pancreatic width (P = 0.005), smoking (P < 0.001), alcohol abuse (P < 0.001), and DM (P = 0.001) emerged as significant independent factors impacting pancreatic stiffness. Smoking, alcohol abuse, DM, and wide pancreas were associated with greater pancreatic stiffness (coefficients = 0.202, 0.183, 0.149, and 0.160, respectively), while reduced pancreatic stiffness corresponded with female sex and larger BMI (coefficient = -0.155 and -0.192, respectively). DATA CONCLUSION: MRE-based pancreatic stiffness values are impacted by sex, BMI, pancreatic width, smoking, alcohol abuse, and DM. Reference values are essential for future clinical studies. LEVEL OF EVIDENCE: 1 Technical Efficacy: Stage 2 J. Magn. Reson. Imaging 2020;52:448-458.

Epigenetic differences of chronic hepatitis B in different TCM syndromes: Protocol for a case-control, non-interventional, observational clinical study.

INTRODUCTION: Chronic hepatitis B is a serious disease causing serious harm to the human health. Chinese medicine has its unique advantages in the clinical prevention and treatment, while the syndrome of Chinese medicine lacks the understanding at the micro level. There are some theoretical commonalities between the epigenetics and traditional Chinese medicine (TCM) syndromes. The biological basis of chronic hepatitis B (CHB) syndrome differentiation from the perspective of epigenetics is of great significance to diagnose and prevent the diseases. METHODS: This protocol is a case-control, noninterventional, observational clinical study. Patients with CHB for spleen-stomach damp heat and liver depression and spleen deficiency, with 12 each and 11 healthy volunteers were recruited. Peripheral venous blood was collected from the participants. DNA methylated transferase, genomic DNA methylated spectrum, methylated DNA binding protein MeCP2, chronic infection of hepatitis B virus with methylated related proteins, and miRNA target genes were analyzed. OBJECTIVES: From the perspective of DNA methylation epigenetics, "DNA methylation-miRNA-Target gene" is the main line, which further reveals the essence of TCM syndrome. To improve the level of TCM clinical syndrome differentiation and the clinical efficacy of TCM, especially in the study of TCM syndromes of CHB, discovering its underlying biological signature is necessary. TRIAL REGISTRATION: Clinical Trials Registration: ChiCTR1800017365, registered 26 July 2018.

Human Bop is a novel BH3-only member of the Bcl-2 protein family.

One group of Bcl-2 protein family, which shares only the BH3 domain (BH3-only), is critically involved in the regulation of programmed cell death. Herein we demonstrated a novel human BH3-only protein (designated as Bop) which could induce apoptosis in a BH3 domain-dependent manner. Further analysis indicated that Bop mainly localized to mitochondria and used its BH3 domain to contact the loop regions of voltage dependent anion channel 1 (VDAC1) in the outer mitochondrial membrane. In addition, purified Bop protein induced the loss of mitochondrial transmembrane potential (Δψm) and the release of cytochrome c. Furthermore, Bop used its BH3 domain to contact pro-survival Bcl-2 family members (Bcl-2, Bcl-X(L), Mcl-1, A1 and Bcl-w), which could inhibit Bop-induced apoptosis. Bop would be constrained by pro-survival Bcl-2 proteins in resting cells, because Bop became released from phosphorylated Bcl-2 induced by microtubule-interfering agent like vincristine (VCR). Indeed, knockdown experiments indicated that Bop was partially required for VCR induced cell death. Finally, Bop might need to function through Bak and Bax, likely by releasing Bak from Bcl-X(L) sequestration. In conclusion, Bop may be a novel BH3-only factor that can engage with the regulatory network of Bcl-2 family members to process intrinsic apoptotic signaling.

TANK-binding kinase 1 attenuates PTAP-dependent retroviral budding through targeting endosomal sorting complex required for transport-I.

Retroviruses need to bud from producer cells to spread infection. To facilitate its budding, some virus hijacks the multivesicular body (MVB) pathway that is normally used to cargo and degrade ubiquitylated cellular proteins, through interaction between the late domain of Gag polyproteins and the components of MVB machinery. In this study, we demonstrated that TANK-binding kinase 1 (TBK1) directly interacted with VPS37C, a subunit of endosomal sorting complex required for transport-I (ESCRT-I) in the MVB pathway, without affecting the ultrastructure or general function of MVB. Interestingly, overexpression of TBK1 attenuated, whereas short hairpin RNA interference of TBK1 enhanced HIV-1 pseudovirus release from Vero cells in type I IFN (IFN-I)-independent manner. Down-regulation of TBK1 by short hairpin RNA in TZM-bl cells also enhanced live HIV-1 NL4-3 or JR-CSF virus budding without involvement of IFN-I induction. Furthermore, infection of TBK1-deficient mouse embryonic fibroblast cells with a chimeric murine leukemia virus/p6, whose PPPY motif was replaced by PTAP motif of HIV-1, showed that lack of TBK1 significantly enhanced PTAP-dependent, but not PPPY-dependent retrovirus budding. Finally, phosphorylation of VPS37C by TBK1 might regulate the viral budding efficiency, because overexpression of the kinase-inactive mutant of TBK1 (TBK1-K38A) in Vero cells accelerated HIV-1 pseudovirus budding. Therefore, through tethering to VPS37C of the ESCRT-I complex, TBK1 controlled the speed of PTAP-dependent retroviral budding through phosphorylation of VPS37C, which would serve as a novel mechanism of host cell defense independent of IFN-I signaling.

MDA5 is SUMOylated by PIAS2ß in the upregulation of type I interferon signaling.

Retinoic acid-inducible protein I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5) are cytosolic viral RNA sensors that induce type I interferon production (IFN). In this study, we found that MDA5 undergoes inducible SUMOylation by small ubiquitin-like modifier-1 (SUMO-1) in response to polyI:C stimulation. Enhanced SUMOylation of MDA5 by exogenously expressed SUMO-conjugating enzyme Ubc9 correlated with upregulation of IFN expression and repressed virus replication. Conversely, overexpression of a SUMOylation-deficient mutant of Ubc9 or knockdown of endogenous Ubc9 reduced IFN production. Furthermore, we showed that PIAS2ß, a SUMOylation E3 ligase, could specifically interact with and enhance the SUMOylation of MDA5. Consequently, PIAS2ß knockdown reduced the SUMOylation of MDA5 and the IFN production. Collectively, these findings suggest that SUMO-1 modification of MDA5 possibly via PIAS2ß may play a role in the MDA5-mediated IFN response to viral infections.

MTMR4 attenuates transforming growth factor beta (TGFbeta) signaling by dephosphorylating R-Smads in endosomes.

Homeostasis of Smad phosphorylation at its C-terminal SXS motif is essential for transforming growth factor beta (TGFbeta) signaling. Whereas it is known that TGFbeta signaling can be terminated by phosphatases, which dephosphorylate R-Smads in the nucleus, it is unclear whether there are any cytoplasmic phosphatase(s) that can attenuate R-Smad phosphorylation and nuclear translocation. Here we demonstrate that myotubularin-related protein 4 (MTMR4), a FYVE domain-containing dual-specificity protein phosphatase (DSP), attenuates TGFbeta signaling by reducing the phosphorylation level of R-Smads in early endosomes. Co-immunoprecipitation experiments showed that endogenous MTMR4 interacts with phosphorylated R-Smads, and that this interaction is correlated with dephosphorylation of R-Smads. Further analysis showed that overexpression of MTMR4 resulted in the sequestration of activated Smad3 in the early endosomes, thus reducing its nuclear translocation. However, both point mutations at the conserved catalytic site of the phosphatase (MTMR4-C407S) and small interference RNA of endogenous Mtmr4 expression led to sustained Smad3 activation. This work therefore suggests that MTMR4 plays an important role in preventing the overactivation of TGFbeta signaling by dephosphorylating activated R-Smads that have been trafficked to early endosomes.

Troglitazone inhibits cell proliferation by attenuation of epidermal growth factor receptor signaling independent of peroxisome proliferator-activated receptor gamma.

Peroxisome proliferator-activated receptors (PPAR) belong to the nuclear hormone receptor superfamily of ligand-dependent transcription factors. Recent results have shown that agonists of PPARgamma, such as troglitazone (TGZ), can inhibit cell proliferation and promote cell differentiation independent of PPARgamma. In the present study, we provide evidence that TGZ may bind directly to EGFR and trigger its signaling and internalization independent of PPARgamma. Detailed studies revealed that prolonged incubation with TGZ effectively attenuated EGFR signaling by targeting the receptor to the endo-lysosomal degradation machinery. Although the extracellular signal-regulated kinase-signaling pathway was transiently activated by TGZ in EGFR overexpressing cancer cells, inhibition of EGF-induced Akt phosphorylation most likely accounted for the growth arrest of tumor cells caused by TGZ at pharmacologically achievable concentrations. Therefore, we have provided a new line of evidence indicating that TGZ inhibits cell proliferation by promoting EGFR degradation and attenuating Akt phosphorylation.

Internalization of CD40 regulates its signal transduction in vascular endothelial cells.

The CD40 ligand (CD40L)-CD40 dyad can ignite proinflammatory and procoagulatory activities of the vascular endothelium in the pathogenesis and progression of atherosclerosis. Besides being expressed on the activated CD4(+) T cell surface (mCD40L), the majority of circulating CD40L reservoir (sCD40L) in plasma is released from stimulated platelets. It remains debatable which form of CD40L triggers endothelial inflammation. Here, we demonstrate that the agonistic antibody of CD40 (G28.5), which mimics the action of sCD40L, induces rapid endocytosis of CD40 independent of TRAF2/3/6 binding while CD40L expressed on the surface of HEK293A cells captures CD40 at the cell conjunction. Forced internalization of CD40 by constitutively active mutant of Rab5 preemptively activates NF-kappaB pathway, suggesting that CD40 was able to form an intracellular signal complex in the early endosomes. Internalized CD40 exhibits different patterns of TRAF2/3/6 recruitment and Akt phosphorylation from the membrane anchored CD40 complex. Finally, mCD40L but not sCD40L induces the upregulation of proinflammatory cytokines and cell adhesion factors in the primary human vascular endothelial cells in vitro, although both forms of CD40L activate NF-kappaB pathway. These results therefore may help understand the molecular mechanism of CD40L signaling that contributes to the pathophysiology of atherosclerosis.