Xiamen Municipal Bureau of Science and Technology

IntroductionWith the proposal of China’s “Dual Carbon” targets, how to measure carbon footprint in detail is particularly important. However, the current carbon footprint measurement mainly focuses on the production process, ignoring the high carbon emission caused by the transport phase. In this paper, we take the tobacco industry as the research object, and include the transport phase in the carbon footprint measurement.MethodsBased on the existing statistical data, this paper adopts the Life Cycle Assessment (LCA) to comprehensively measure and analyze the carbon footprint of China’s tobacco industry from 2011 to 2020.ResultsThe results show that the average carbon footprint per hectare of the tobacco industry is about 21.57 tons of carbon dioxide equivalent, while showing a slowly increasing trend in recent years. In terms of linkage and raw material composition, the carbon footprints of fertilizer application, agricultural film input, initial curing and air transportation is relatively high, accounting for 8.2%, 66% and 4.7% of the total emissions respectively. Combined with the cost of tobacco planting, it can be found that Yunnan, Guizhou and Jiangxi are facing the problems of high input, low output and high emission.DiscussionThe results are of great significance in promoting low-carbon tobacco growing and green transport.

BackgroundThe smartphone use profoundly affects human health. At present, the effect of smartphone use on the risk of hypertension in adults aged 50 years and older remains unknown. This study aimed to explore the association between smartphone use and hypertension in this population.MethodsFrom 2018 to 2019, people aged 50 years and older were enrolled in the Fujian Provincial Eye Study (FJES), a population-based cross-sectional survey of the public’s general and ocular health in Fujian Province, China. Information on smartphone use was obtained from the baseline survey, and blood pressure measurements were obtained via standardized on-site examination. Univariate and multivariable logistic regression analyses were performed on the study variables. P<0.05 were considered statistically significant.ResultsThis study ultimately enrolled 8,211 eligible participants aged ≥50 years, and the mean age was 64.39±8.87 years. The risk of hypertension decreased significantly with increasing smartphone use time, although people who spent more time on smartphones had higher systolic blood pressure (SBP). There was no significant association between smartphone use time and diastolic blood pressure (DBP). Multivariate logistic regression analysis showed that smartphone use time, along with age, BMI, diabetes and education level, was an independent predictor of hypertension risk.ConclusionThe duration of smartphone use demonstrated a significant inverse association with hypertension risk and was identified an independent predictor of hypertension risk in adults aged 50 years and older. Thus, smartphone use duration is a potentially useful indicator for assessing the risk of hypertension in this population.

ObjectiveThis study aims to investigate pulmonary protective and antiinflammatory effects of dexmedetomidine (DEX) in patients undergoing cardiac surgery with cardiopulmonary bypass (CPB) by meta-analysis.MethodsSix databases were searched to collect trials on the pulmonary protective and anti-inflammatory effects of DEX in cardiac surgery with CPB. The search period was from the establishment of each database to August 1, 2024. Alveolar arterial oxygen partial pressure difference (AaDO2), Oxygenation index (OI), respiratory index (RI), IL-6, TNF-α, and CRP values were collected in CPB progress, end of operation, postoperative 6 h(POH6), and postoperative 24 h(POH24). The control group was treated with normal saline after anesthesia induction, while the experimental group with DEX.ResultsA total of 9 articles were included. In the overall analysis, AaDO2 (SMD=-1.03, 95%CI:-1.62 to -0.44) and RI (SMD=-1.03, 95%CI:-1.90 to -0.16) in the DEX group were significantly lower than those in the control group, whereas OI was significantly increased (SMD = 0.44, 95%CI: 0.29–0.60). For inflammatory markers, levels of IL-6 (SMD= -1.96, 95%CI: -2.31-1.62) and TNF-α (SMD= -1.81, 95%CI: -2.36-1.26) were significantly decreased in the DEX group. Subgroup analyses based on the course of surgery presented a significant reduction in AaDO2 at the end of operation. At the end of operation, OI was significantly increased, while IL-6 and TNF-α were significantly decreased at POH6 and POH12. At POH24, no significant difference was found in CRP between the two groups (P > 0.05).ConclusionDEX has pulmonary protective and anti-inflammatory effects in patients undergoing cardiac surgery with CPB.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12871-025-03286-6.

Acute kidney injury (AKI) is a frequent complication in acute heart failure (AHF) patients, yet few studies have examined the prognostic implications of different dynamic KDIGO AKI stages in this population. This retrospective cohort study aimed to rigorously investigate the impact of dynamic KDIGO AKI staging on outcomes in ICU patients with AHF using robust statistical methods like propensity score matching and doubly robust analysis. Utilizing the MIMIC-IV database of 5136 adult AHF patients from 2008 to 2022, doubly robust analysis revealed no significant differences in 28-day, 180-day, and 1-year mortality between non-AKI and mild AKI groups. However, moderate-to-severe AKI had significantly higher mortality at all timepoints compared to normal or mild AKI. Patients exhibiting mild AKI, termed “subclinical AKI” as their prognosis often parallels non-AKI, face a markedly worsened outlook if their condition progresses to moderate-to-severe AKI during hospitalization. However, it is worth noting that further sensitivity analysis showed that in patients with AHF as the first diagnosis, transient AKI caused by intensive decongestion therapy and other interventions did not have a significant impact on long-term outcomes.

Adverse aortic remodeling increases the risk of aorta-related adverse events (AAEs) after thoracic endovascular aortic repair (TEVAR) and affects the overall prognosis of aortic dissection (AD). It is imperative to delve into the exploration of prognostic indicators to streamline the identification of individuals at elevated risk for postoperative AAEs, and therapeutic targets to optimize the efficacy of TEVAR for patients with AD. Here, we perform proteomic and single-cell transcriptomic analyses of peripheral blood and aortic lesions, respectively, from patients with AD and healthy subjects. The integrated multi-omics profiling identifies that highly phenotype-associated macrophages orchestrate neutrophil extracellular traps (NETs) through CXCL3/CXCR2 axis, thereby promoting the development of AD. Increased NETs formation is a defining feature of systemic immunity and aortic microenvironment of AD. Inhibiting NETs formation through the blockade of citrullinated histone H3 or CXCL3/CXCR2 axis ameliorates the progression and rupture of aortic dissection in male mice. The plasma level of citrullinated histone H3 predicts AAEs following endovascular therapy, facilitating the risk stratification and prognostic evaluation for patients with AD.

Recent studies have suggested that ferroptosis participates in various renal diseases. However, its effect on focal segmental glomerulosclerosis remains unclear. This study analyzed the GSE125779 and GSE121211 datasets to identify the differentially expressed genes (DEGs) in renal tubular samples with and without FSGS. The Cytoscape was used to construct the protein–protein interaction network. Moreover, the ferroptosis-related genes (FRGs) were obtained from the ferroptosis database, while ferroptosis-related DEGs were obtained by intersection with DEGs. The target genes were analyzed using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. The GSE108112 dataset was used to verify the expression of target FRGs. Besides, we built the mRNA-miRNA network regarding FRGs using the NetworkAnalyst database, and circRNAs corresponding to key miRNAs were predicted in the ENCORI database. In this study, 16 ferroptosis-related DEGs were identified between FSGS and healthy subjects, while five co-expressed genes were obtained by three topological algorithms in Cytoscape. These included the most concerned Hub genes JUN, HIF1A, ALB, DUSP1 and ATF3. The KEGG enrichment analysis indicated that FRGs were associated with mitophagy, renal cell carcinoma, and metabolic pathways. Simultaneously, the co-expressed hub genes were analyzed to construct the mRNA-miRNA interaction network and important miRNAs such as hsa-mir-155-5p, hsa-mir-1-3p, and hsa-mir-124-3p were obtained. Finally, 75 drugs targeting 54 important circRNAs and FRGs were predicted. This study identified the Hub FRGs and transcriptomic molecules from FSGS in renal tubules, thus providing novel diagnostic and therapeutic targets for FSGS.

Proprotein convertase subtilisin/kexin 9 (PCSK9) inhibitors have been shown to regulate lipid metabolism and reduce the risk of cardiovascular events. This study explores the effect and potential mechanism of PCSK9 inhibitors on lipid metabolism and coronary atherosclerosis. HepG2 cells were incubated with PCSK9 inhibitor. ApoE-/- mice were fed with a high fat to construct an atherosclerosis model, and then treated with PCSK9 inhibitor (8mg/kg for 8 w). PCSK9 inhibitor downregulated microRNA (miRNA)-130a-3p expression in a dose-dependent manner. And, miR-130a-3p could bind directly to the 3' untranslated region (3'-UTR) region of LDLR to down-regulate LDLR expression in HepG2 cells, as confirmed by the luciferase reporter gene assay. In addition, miR-130a-3p overexpression significantly attenuated the promoting effect of PCSK9 inhibitor on LDLR and DiI-LDL uptake in HepG2 cells. More importantly, in vivo experiments confirmed that PCSK9 inhibitor could significantly inhibit miR-130a-3p levels and promote LDLR expression in liver tissues, thus regulating serum lipid profile and alleviating the progression of coronary atherosclerosis. PCSK9 inhibitor could moderately improve coronary atherosclerosis by regulating miR-130a-3p/LDLR axis, providing an exploitable strategy for the treatment of coronary atherosclerosis.