When income meets faith: the development and application of the Chinese generation Z unconventional religious orientation scale.

This study seeks to analyze the psychological construction of Unconventional Religious Orientations and their association with individual income level satisfaction within Generation Z. Generation Z, individuals born between 1995 and 2010, grew up in a socio-cultural context marked by digitization and globalization. This study identifies three key dimensions of Unconventional Religious Orientations: religious spiritual dependence, religious instrumental tendencies, and religious uniqueness identity. By combining rootedness theory, semi-structured interviews, and literature review, we constructed and refined a set of relevant scales. Using exploratory and validation factor analyses (EFA and CFA), we verified the structural validity of the scale. The results of the analyses revealed significant negative correlations between satisfaction with income level and all dimensions of Unconventional Religious Orientation for Generation Z, suggesting that Unconventional Religious Orientation tends to diminish as income satisfaction increases. In addition, the significant positive correlations between these dimensions of religious inclination imply that they may share certain underlying factors in their psychological structure. This study not only successfully developed a set of psychometric instruments for Unconventional Religious Orientations, but also provided a new psychological perspective for understanding the dynamic interaction between economic satisfaction and religious psychological attitudes in Generation Z.

Effect of unfractionated heparin on high mobility group box 1-mediated expression of vascular endothelial cadherin / 中华危重病急救医学

Objective To observe the damage of high mobility group box 1 (HMGB1) on human umbilical vein endothelial cell (HUVEC) barrier permeability and the protective effect of unfractionated heparin (UFH), and to explore the down-regulated protection effect mechanism of UFH on HMGB1-mediated vascular endothelial cadherin (VE-cadherin) expression. Methods The trypsin-digested HUVEC were subcultured in culture flasks. When the cells were grown to 80%, they were randomly divided into four groups: phosphate buffer (PBS) control group (200 μL PBS), recombinant human high mobility group box 1 (rhHMGB1) treatment group (100 μg/L rhHMGB1), UFH control group (10 kU/L UFH), and UFH pretreatment group (10 kU/L UFH+100 μg/L rhHMGB1). The cells in each group were challenged with different reagent for 24 hours, and the activity of endothelial cells was determined by methyl thiazolyl tetrazolium (MTT) colorimetric assay. The permeability of endothelial cells was measured by Transwell method, and the expression and distribution of VE-cadherin was observed by immunofluorescence. The protein expressions of VE-cadherin and phosphorylated p38 mitogen-activated protein kinase (p-p38MAPK) were determined by Western Blot. Results After treatment with 100 μg/L rhHMGB1 for 24 hours, the activity of endothelial cells was not significantly different from that of the PBS control group (A value: 0.230±0.004 vs. 0.255±0.006, P > 0.05), but the permeability was significantly increased (glucan FD40 fluorescence intensity: 11.05±0.12 vs. 6.34±0.39, P < 0.05). Compared with PBS control group, the fluorescence microscopy showed that the VE-cadherin membrane localization was reduced, the distribution was loose, and there were obvious fissures between cells in rhHMGB1 treatment group, and quantitative analysis showed the protein expression of VE-cadherin was decreased significantly (VE-cadherin/β-actin: 0.16±0.04 vs. 0.31±0.03, P < 0.05), and the expression of p-p38MAPK protein was significantly increased (p-p38MAPK/β-actin: 0.79±0.03 vs. 0.26±0.05, P < 0.05). UFH pretreatment could protect HMGB1-mediated endothelial cell injury, cell permeability was significantly reduced (glucan FD40 fluorescence intensity: 9.11±0.23 vs. 11.05±0.12), fluorescence expression of VE-cadherin was enhanced, membrane localization was significantly increased, quantitative analysis showed that VE-cadherin protein expression was significantly up-regulated (VE-cadherin/β-actin: 0.24±0.02 vs. 0.16±0.04), and p38MAPK phosphorylation level was significantly decreased (p-p38MAPK/β-actin: 0.54±0.05 vs. 0.79±0.03), the difference was statistically significant as compared with rhHMGB1 treatment group (all P < 0.05). There was no significant difference in all parameters between PBS control group and UFH control group. Conclusions UFH can protect the endothelial cell barrier from the HMGB1 by regulating the expression and distribution of VE-cadherin. The mechanism may be related to the inhibition of p38MAPK phosphorylation by UFH.