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Abstract Aim To examine the status quo and influencing factors of sleep quality and work engagement of nurses participating in COVID‐19 during the post‐epidemic era and to study the relationship between them. Design We conducted a cross‐sectional survey and correlational and predictive logic to determine the association between sleep quality and work engagement among nurses in Shanghai during the post‐epidemic era. Methods This design involved 1060 frontline nurses in Shanghai. The Pittsburgh Sleep Quality Index questionnaire and the Utrecht Work Engagement Scale‐9 scales were used for data collection. Results This study found that the sleep quality of frontline nurses was impaired and the nurses with poor sleep accounted for 48.20% during the post‐epidemic era. The work engagement of frontline nurses was at the medium level. Factors affecting nurses' sleep quality were the number of nurse night shifts, family support and nurse health. The factors affecting the nurse work engagement were monthly income, profession title, family support and self‐health status. There was a positive correlation between nurses' sleep quality and work engagement.

In this paper, the factors causing the change in carbon emissions from direct energy consumption in the construction industry in Beijing–Tianjin–Hebei are decomposed using the logarithmic mean divisia index (LMDI) method to analyze the effect values and contribution rates of each macrofactor. Based on the decomposition results and given relevant national policies, five scenarios are set up for each influencing factor, and a regression stochastic impact on population, affluence, and technology (STIRPAT) with ridge regression analysis is applied to each scenario combination for scenario prediction, forming a scientific and reasonable theoretical system to predict the future time of carbon peaking and carbon neutrality in the construction industry of Beijing–Tianjin–Hebei. The results show that (1) energy intensity and energy structure have a suppressive effect on direct energy consumption carbon emissions in the construction industry in Beijing–Tianjin–Hebei, and the industrial structure, economy, and population will promote an increase in carbon emissions. Energy intensity and the economy have a more significant effect on carbon emissions in the construction industry. (2) The peak year of carbon emissions varies with different scenarios, and the energy efficiency scenario achieves peak carbon in 2028, the earliest peak time, and the lowest peak, as it is the optimal emission reduction projection scenario.

Background Obesity is an established risk factor for hypertension. Although obesity‐induced gut barrier breach leads to the leakage of various microbiota‐derived products into host circulation and distal organs, the roles of microbiota in mediating the development of obesity‐associated adrenomedullary disorders and hypertension have not been elucidated. We seek to explore the impacts of microbial DNA enrichment on inducing obesity‐related adrenomedullary abnormalities and hypertension. Methods and Results Obesity was accompanied by remarkable bacterial DNA accumulation and elevated inflammation in the adrenal glands. Gut microbial DNA containing extracellular vesicles (mEVs) were readily leaked into the bloodstream and infiltrated into the adrenal glands in obese mice, causing microbial DNA enrichment. In lean wild‐type mice, adrenal macrophages expressed CRIg (complement receptor of the immunoglobulin superfamily) that efficiently blocks the infiltration of gut mEVs. In contrast, the adrenal CRIg+ cell population was greatly decreased in obese mice. In lean CRIg−/− or C3−/− (complement component 3) mice intravenously injected with gut mEVs, adrenal microbial DNA accumulation elevated adrenal inflammation and norepinephrine secretion, concomitant with hypertension. In addition, microbial DNA promoted inflammatory responses and norepinephrine production in rat pheochromocytoma PC12 cells treated with gut mEVs. Depletion of microbial DNA cargo markedly blunted the effects of gut mEVs. We also validated that activation of cGAS (cyclic GMP‐AMP synthase)/STING (cyclic GMP–AMP receptor stimulator of interferon genes) signaling is required for the ability of microbial DNA to trigger adrenomedullary dysfunctions in both in vivo and in vitro experiments. Restoring CRIg+ cells in obese mice decreased microbial DNA abundance, inflammation, and hypertension. Conclusions The leakage of gut mEVs leads to adrenal enrichment of microbial DNA that are pathogenic to induce obesity‐associated adrenomedullary abnormalities and hypertension. Recovering the CRIg+ macrophage population attenuates obesity‐induced adrenomedullary disorders.

With the accelerated urbanization and the need for sustainable development in China, the construction projects’ social responsibility (CPSR) has received increasing attention from scholars, but reliable empirical evidence on whether the project executive’s (PE’s) ethical leadership can promote the implementation of the CPSR is insufficient. This study constructs a moderated mediation model in which we examine the role of employees’ organizational identification and organizational justice in the relationship between the PE’s ethical leadership and the organizational CPSR through data of 367 samples collected validly. Through the research, we found that the PE’s ethical leadership has a positive impact on the CPSR, the employee’s organizational identification mediates the relationship between the PE’s ethical leadership and the organizational CPSR, and organizational justice moderates between the PE’s ethical leadership and employee’s organizational identification. The outcomes indicate that the PE’s ethical leadership can promote the implementation of the organizational CPSR. This study reveals the intrinsic action mechanism of the PE’s ethical leadership and the implementation of the organizational CPSR, which has certain implications for improving the performance of CPSR and achieving the sustainable development of the projects.

Abstract Rationale Neutrophils constitute massive cellular constituents in inflammatory human gastric cancer (GC) tissues, but their roles in pathogenesis of inflammatory T helper (Th) subsets are still unknown. Methods Flow cytometry analysis and immunohistochemistry were used to analyze the responses and phenotypes of neutrophils in different samples from 51 patients with GC. Kaplan‐Meier plots and Multivariate analysis for the survival of patients were used by log‐rank tests and Cox proportional hazards models. Neutrophils and CD4+ T cells were purified and cultured for ex vivo, in vitro and in vivo regulation and function assays. Results GC patients exhibited increased tumoral neutrophil infiltration with GC progression and poor patient prognosis. Intratumoral neutrophils accumulated in GC tumors via CXCL6/CXCL8‐CXCR1‐mediated chemotaxis, and expressed activated molecule CD54 and co‐signaling molecule B7‐H2. Neutrophils induced by tumors strongly expressed CD54 and B7‐H2 in both dose‐ and time‐dependent manners, and a close correlation was obtained between the expressions of CD54 and B7‐H2 on intratumoral neutrophils. Tumor‐derived tumor necrosis factor‐α (TNF‐α) promoted neutrophil activation and neutrophil B7‐H2 expression through ERK‐NF‐κB pathway, and a significant correlation was found between the levels of TNF‐α and CD54+ or B7‐H2+ neutrophils in tumor tissues. Tumor‐infiltrating and tumor‐conditioned neutrophils effectively induced IL‐17A‐producing Th subset polarization through a B7‐H2‐dependent manner ex vivo and these polarized IL‐17A‐producing Th cells exerted protumorigenic roles by promoting GC tumor cell proliferation via inflammatory molecule IL‐17A in vitro, which promoted the progression of human GC in vivo; these effects could be reversed when IL‐17A is blocked. Moreover, increased B7‐H2+ neutrophils and IL‐17A in tumors were closely related to advanced GC progression and predicted poor patient survival. Conclusion We illuminate novel underlying mechanisms that TNF‐α‐activated neutrophils link B7‐H2 to protumorigenic IL‐17A‐producing Th subset polarization in human GC. Blocking this pathological TNF‐α‐B7‐H2‐IL‐17A pathway may be useful therapeutic strategies for treating GC.

Abstract Objectives Host immune responses are indispensable to combat the disease. We report the dynamics of peripheral immune cells, cytokines, and human leucocyte antigen‐G (HLA‐G) and its receptor expressions in a patient suffering from critical COVID‐19 pneumonia to convalescence. Methods Clinical data of the patient were collected from medical records. The expressions of HLA‐G and receptors ILT2, ILT4 and KIR2DL4 in peripheral immune cells were measured with flow cytometry. Results From critical COVID‐19 to the convalescent stage, early lymphopenia was improved (median: 0.6 × 109 L−1 vs. 0.9 × 109 L−1, P = 0.009), and an obvious fluctuation in WBC and neutrophil counts was observed. Initially, low levels of CD4+ T cells (from 120 to 528 μL−1) and CD8+ T cells (from 68 to 362 μL−1) gradually increased to normal levels. Meanwhile, high IL‐6 (from 251.8 to 6.32 pg mL−1), IL‐10 (from 39.53 to 5.21 pg mL−1) and IFN‐γ (from 13.55 to 3.16 pg mL−1) levels decreased, and IL‐4 (from 2.36 to 3.19 pg mL−1) and TNF‐α (from 2.27 to 20.2 pg mL−1) levels increased quickly when the viral RNA returned negative. Moreover, the percentage of HLA‐G+ T cells, B cells and monocytes follows high–low–high pattern, while the percentage of receptors ILT2‐, ILT4‐ and KIR2DL4‐expressing cells remained relatively stable. Conclusion Our findings provide valuable information on the dynamics of early peripheral immunological responses in SARS‐CoV‐2 infection. CD4+ and CD8+ T cells, cytokines and HLA‐G+ immune cells are associated with the natural history of the critical COVID‐19 patient; however, future studies are necessary.

Abstract Background Asians are diagnosed with breast cancer at a younger age than Caucasians are. We studied the effect of age on locoregional recurrence and the survival of Asian breast cancer patients treated with breast-conserving therapy. Methods Medical records of 2492 patients treated with breast-conserving therapy between 1989 and 2012 were reviewed. The Kaplan–Meier method was used to estimate locoregional recurrence, breast cancer-free survival, and breast cancer-specific survival rates. These rates were then compared using log-rank tests. Outcomes and age were modeled by Cox proportional hazards. Fractional polynomials were then used to test for non-linear relationships between age and outcomes. Results Patients ≤ 40 years old were more likely to have locoregional recurrence than were older patients (Hazard ratio [HR] = 2.32, P