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IntroductionAs China advances its dual carbon targets, the carbon market has become a key policy instrument. However, climate policy uncertainty (CPU) can disrupt expectations and amplify risks in carbon trading prices (CTP), creating challenges for market stability and policy effectiveness.MethodsTo address this issue, this study constructs a weekly China-specific CPU (CCPU) index using text analysis of domestic newspapers and employs the Quantile Vector Autoregression–Diebold-Yilmaz (QVAR-DY) framework to assess its spillover effects on returns and volatility across six regional carbon markets. The quantile Granger-causality test is also applied to further validate the direction and significance of spillovers under different market conditions.ResultsThe analysis shows that spillovers remain moderate under normal conditions but intensify considerably under extreme states, particularly at higher quantiles, as confirmed by the quantile Granger-causality tests. The most striking finding is that spillovers from CCPU to volatility are consistently stronger than to returns, indicating that systemic risk contagion is more pronounced through volatility channels.DiscussionBy integrating a quantile perspective with dynamic spillover analysis, this study reveals the asymmetric transmission of policy uncertainty in China’s carbon markets and provides new insights for risk monitoring and policy design in the low-carbon transition.

Background Pleckstrin homology (PH) domain leucine-rich repeat protein phosphatases (PHLPP) has been associated with several neurodegenerative diseases, however, few studies have investigated the role of PHLPP in Parkinson’s disease (PD). The present study aimed to answer this question through establishing a Parkinson’s disease (PD) model using the Phlpp1-/- and wild-type (WT) mice and testing their behavioral as well as molecular changes. Methods: MPTP was intraperitoneal injected into mice to generate a PD model. Neurobehavioral parameters, protein expression and inflammatory cytokines release were measured by the open filed test, the pole test, immunohistochemistry, immunoblotting, immunoprecipitation, and quantitative reverse transcription PCR. Results MPTP-induced neurobehavioral deficits were more significantly ameliorated in PHLPP-KO-MPTP mice compared to WT-MPTP mice. The survival rate of TH + neurons in the PHLPP-KO-MPTP group was higher than that in the WT-MPTP group (66% vs. 38%). Additionally, PHLPP1 knockout in KO-MPTP mice markedly reduced levels of IL-1β, IL-6, TNF-α, and iNOS, and increased levels of TGF-β compared to those of WT-MPTP mice. Furthermore, PHLPP1 was found to bind to NLRP3 and that PHLPP1 knockout inhibited MPTP-induced expression of IL-1β and caspase-1 in substantia nigra of PD model mice. Conclusion Our results demonstrates that PHLPP1 knockout in PD model is positively associated with the survival of TH + neurons by suppressing inflammatory response in substantia nigra, suggesting that PHLPP1 plays a critical role in the development of PD.

Although the impact of the variants of COVID-19 on the general population is diminishing, there is still a certain mortality rate for severe and critically ill patients, especially for the elderly with comorbidities. The present study investigated whether the D-dimer to albumin ratio (DAR) can predict the severity of illness and mortality in COVID-19 patients. A total of 1,993 patients with COVID-19 were retrospectively reviewed and the association of DAR with severe or critical illness or death during hospitalization was analyzed. The area under the ROC curve was used to screen the best indicators, Chi-square test, rank sum test, and univariate and multivariate binary logistic regression analysis were used to calculate the mean value of difference and adjusted odds ratio (aORs) with their 95% CI, and finally, survival was analyzed using Kaplan-Meier (KM) curves. Among 1,993 patients with COVID-19, 13.4% were severely ill, and the mortality rate was 2.3%. The area under the curve (AUC) using DAR to predict severe and critically ill patients was higher than that using other parameters. The best cut-off value of DAR was 21 in the ROC with a sensitivity of 83.1% and a specificity of 68.7%. After adjusting age, gender, comorbidities, and treatment, the binary logistic regression analysis showed that elevated DAR was an independent risk factor for severely ill and mortality of COVID-19 patients. The KM curve suggested that patients with a higher DAR was associated with worse survival. The negative predictive value of DAR (21) for adverse prognosis and death was 95.98 and 99.84%, respectively, with a sensitivity of 80.9 and 95.65%, respectively. The DAR may be an important predictor for severe illness and mortality in COVID-19 patients.

COVID-19 pandemic has imposed tremendous stress and burden on the economy and society worldwide. There is an urgent demand to find a new model to estimate the deterioration of patients inflicted by Omicron variants. This study aims to develop a model to predict the deterioration of elderly patients inflicted by Omicron Sub-variant BA.2. COVID-19 patients were randomly divided into the training and the validation cohorts. Both Lasso and Logistic regression analyses were performed to identify prediction factors, which were then selected to build a deterioration model in the training cohort. This model was validated in the validation cohort. The deterioration model of COVID-19 was constructed with five indices, including C-reactive protein, neutrophil count/lymphocyte count (NLR), albumin/globulin ratio (A/G), international normalized ratio (INR), and blood urea nitrogen (BUN). The area under the ROC curve (AUC) showed that this model displayed a high accuracy in predicting deterioration, which was 0.85 in the training cohort and 0.85 in the validation cohort. The nomogram provided an easy way to calculate the possibility of deterioration, and the decision curve analysis (DCA) and clinical impact curve analysis (CICA)showed good clinical net profit using this model. The model we constructed can identify and predict the risk of deterioration (requirement for ventilatory support or death) in elderly patients and it is clinically practical, which will facilitate medical decision making and allocating medical resources to those with critical conditions.

Background Blepharoplasty is a common surgical technique performed in individuals seeking aesthetic enhancement. Thus, it is essential to investigate the factors influencing postoperative satisfaction from the patient’s perspective. In this study, patient-rated outcome measure questionnaires were used to identify the factors affecting patient satisfaction after full-incision upper blepharoplasty. Methods This retrospective study analyzed patients who underwent full-incision upper blepharoplasty at an outpatient clinic in China. The questionnaire responses were collected by telephone, text messaging, or email at 6 and 12 months postoperatively. Results In total, 149 questionnaires were collected. After a mean follow-up of 23.23 months, the patients’ overall satisfaction rate was 89.43%. The factors that significantly affected postoperative satisfaction were the patient’s education level, the source of referral to the surgeon, the patient’s understanding of the surgical risks, application of a cold compress after surgery as recommended, unsatisfactory postoperative double-eyelid width, postoperative bilateral asymmetry, apparent postoperative cicatrices, and postoperative caterpillar-like appearance of the double eyelids. Education level, apparent postoperative cicatrices, and postoperative bilateral asymmetry influenced the patient’s satisfaction with the surgical outcome. The patient’s understanding of the surgical risks, unsatisfactory postoperative double-eyelid width, postoperative bilateral asymmetry, apparent postoperative cicatrices, and postoperative caterpillar-like appearance influenced the satisfaction of the patient’s family and friends. Conclusions Postoperative bilateral asymmetry, apparent postoperative cicatrices, and a low education level of the patient are independent factors that negatively affect patient satisfaction with the outcome of double-eyelid blepharoplasty. Level of Evidence IV This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .

Autophagy may be a major mechanism by which osteoblasts (OBs) protect against the negative effects of chronic glucocorticoid (GC) usage. OBs are closely associated with the remodeling that occurs in GC-induced osteoporosis (GIO). In osteocytes, in response to stress induced by GCs, several pathways are activated, including cell necrosis, apoptosis and autophagy. However, the role of autophagy in OBs following treatment with excess GCs has not been addressed. In the current study, confocal microscopy observation of green fluorescent protein-microtubule-associated protein 1 light chain 3β (LC3) punctuate, and western blotting for LC3II and Beclin 1 were performed for detection of autophagy in the MC3T3-E1 osteoblastic cell line. Flow cytometry and western blotting were used for the examination of apoptosis and expression of BAX apoptosis regulator (Bax)/apoptosis regulator Bcl-2 (Bcl-2). The expression of genes associated with osteoblastic function, runt-related transcription factor 2, α-1 type 1 collagen and osteocalcin, were measured by reverse transcription-quantitative polymerase chain reaction. The results indicated that autophagy was induced in OBs during dexamethasone (Dex) treatment in a dose-dependent manner. The level of autophagy did not continue to increase over time, but peaked at 48 h and then decreased gradually. Subsequently, flow cytometry was used to demonstrate that inhibition of autophagy induced apoptosis in OBs under Dex treatment, and was associated with the upregulation of Bax and the downregulation of Bcl-2 protein expression. Furthermore, the data suggested that the inhibition of autophagy also suppressed the expression of osteoblastic genes. By contrast, the stimulation of autophagy maintained the gene expression level under Dex treatment. The data revealed that autophagy is an important regulator of osteoblastic apoptosis through its interaction with Bax/Bcl-2, and maintains the osteoblastic function of MC3T3-E1 cells following GC exposure. In addition, these results indicated that the suppression of autophagy in OBs under chronic GC therapy may increase the prevalence of GIO and fragility fractures.

Abstract Background Infected wounds caused by bacteria such as Escherichia coli and Staphylococcus aureus pose significant challenges during the healing process. Hydrogels have emerged as promising materials for the treatment of such infections, as they have the potential to deliver therapeutic agents while supporting tissue repair. This study aimed to develop ε-PLL@SA/Gel (PSG) hydrogels by incorporating varying concentrations of ε-poly-L-lysine (ε-PLL) into sodium alginate/gelatin (SA/Gel) using calcium chloride as a crosslinking agent, and to evaluate their antibacterial efficacy. Methods The mechanical properties, biocompatibility, antibacterial activity of hydrogels were evaluated. Biocompatibility was examined by measuring cell viability and proliferation of human skin fibroblasts in vitro. Antibacterial efficacy against Escherichia coli and Staphylococcus aureus was quantified using bacterial inhibition assays. The wound healing efficacy of the hydrogels were evaluated in mouse models of infected wounds. Results PSG hydrogels exhibited excellent mechanical strength, injectability, and self-adhesive properties. In vitro, hydrogel treatment resulted in high cell viability and promoted human skin fibroblast proliferation. PSG15 exhibited the highest antibacterial activity and inhibited E. coli and S. aureus by 89.53% and 92.21%, respectively. In vivo, PSG15 significantly accelerated wound healing, enhanced angiogenesis, and regulated macrophage polarization by increasing CD206 expression and decreasing CD80 expression. Additionally, PSG15 modulated the skin microbiota, reduced pathogenic bacterial abundance and maintained microbiota diversity. Conclusions The PSG15 hydrogel is a promising candidate for the treatment of infected wounds because it inhibits bacterial growth, promotes tissue repair, and modulates the wound microbiota. Graphical Abstract Graphical Abstract

The aim of the present study was to identify key genes and signaling pathways associated with the pathogenesis of juvenile spondyloarthritis (JSA). The gene expression profile dataset GSE58667, including data from 15 human whole blood samples collected from 11 patients with JSA and four healthy controls, was analyzed to identify differentially expressed genes (DEGs) associated with disease characteristics. Additionally, Gene Ontology term and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses of the DEGs were performed. Protein-protein, microRNA-transcription factor and chemical-gene interaction networks were constructed. A total of 326 DEGs, 196 upregulated and 130 downregulated, were identified. DEGs, including C-X-C motif chemokine ligand 5 (CXCL5), BCL2 interacting protein 3 like (BNIP3L), dual specificity phosphatase 5 (DUSP5) and tumor protein p53 (TP53) were enriched in functions associated with apoptosis, the cell cycle and immune responses. KEGG pathway enrichment analysis revealed that pathways associated with inflammation and the mitogen-activated protein kinase 1 (MAPK) signaling pathway were the most enriched by DEGs. The results of the present study indicated that the MAPK signaling pathway and four genes, including CXCL5, BNIP3L, DUSP5 and TP53, may be implicated in the pathogenesis of JSA.

The aim of the present study was to explore the effects of pannexin1 (Px1) protein channels on osteogenic differentiation of mesenchymal stem cells (MSCs) under mechanical stress stimulation. MSCs were isolated from Sprague Dawley rats (3 weeks old, weighing 100-120 g) and cultured in vitro. A safe concentration of carbenoxolone was determined (CBX, an inhibitor of Px1 channels; 100 µM) on MSCs using the Cell Counting Kit-8 (CCK8) method. MSCs were divided into 6 groups: Control, stress (4,000 µ strain), and stress following 3, 6, 12, and 24 h pretreatment with CBX. Stress groups were stimulated with mechanical stress for 15 min. Alkaline phosphatase (ALP) activity, type I collagen expression, intracellular calcium ion (Ca2+) concentration, Px1 expression, p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated phosphorylation were determined. ALP activity was increased in the stress group, and this was prevented by pretreatment with CBX. Similarly, stress-induced increases in type I collagen expression, Ca2+ concentration, Px1 expression, and p38 MAPK phosphorylation decreased in the presence of CBX. ERK phosphorylation was decreased by stress, however was not affected by CBX treatment. Altogether, the results suggest that mechanical stress promoted the osteogenic differentiation of MSCs, and this promotion was inhibited by pretreatment with CBX, possibly through regulating the phosphorylation of p38 MAPK.

The aim of the present study was to identify key genes and signaling pathways associated with the pathogenesis of juvenile spondylarthritis (JSA). The gene expression profile dataset GSE58667, including data from 15 human whole blood samples collected from 11 patients with JSA and four healthy controls, was analyzed to identify differentially expressed genes (DEGs) associated with disease characteristics. Additionally, Gene Ontology term and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses of the DEGs were performed. Protein-protein, microRNA-transcription factor and chemical-gene interaction networks were constructed. A total of 326 DEGs, 196 upregulated and 130 downregulated, were identified. DEGs, including C-X-C motif chemokine ligand 5 (CXCL5), BCL2 interacting protein 3 like (BNIP3L), dual specificity phosphatase 5 (DUSP5) and tumor protein p53 (TP53) were enriched in functions associated with apoptosis, the cell cycle and immune responses. KEGG pathway enrichment analysis revealed that pathways associated with inflammation and the mitogen-activated protein kinase 1 (MAPK) signaling pathway were the most enriched by DEGs. The results of the present study indicated that the MAPK signaling pathway and four genes, including CXCL5, BNIP3L, DUSP5 and TP53, may be implicated in the pathogenesis of JSA.