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With the increasing energy use and carbon emissions in the transportation industry, its impact on the greenhouse effect is gradually being recognized. Therefore, this study aims to explore the achievement of carbon emission peak and carbon neutrality in transportation through prediction. The research employs a deep learning model, the CNN-GRU-Attention model, to predict carbon emissions in the transportation industry in Jiangsu, China. We select influencing factors through an extended STIRPAT model coupled with Lasso regression, and construct the CNN-GRU-Attention traffic carbon emission prediction model according to data indicators from 1995 to 2021. The model predicts carbon emissions from the transportation industry in Jiangsu Province between 2022 and 2035 under six distinct scenarios and proposes corresponding emission reduction strategies. The results show that the model in this study has higher prediction accuracy compared with other models, with a mean absolute error (MAE) of 0.061582, root mean square error (RMSE) of 0.085025, and R2 of 0.91609 on the test set. Scenario-based predictions reveal that emission peak in the transportation industry in Jiangsu Province can be achieved under the clean development and comprehensive low-carbon scenarios, with technological innovation being the primary driver of low-carbon emission reductions. This study provides a novel approach for forecasting carbon emissions from the transportation industry and explores the implementation path of emission peak through this method. [ABSTRACT FROM AUTHOR]

Highlights from the article: Previous quantitative trait locus analysis has identified P2X7R gene as a candidate gene for hypertension ([24]). The structure of the P2X7R gene and the locations of the studied polymorphisms in the P2X7R gene. The Bonferroni correction was used to adjust for multiple testing in the analysis of individual SNP analyses and haplotype analyses.

Increasing evidence has suggested high‐fat diet (HFD) is an independent risk factor for myocardial ischemia/reperfusion (MI/R) injury. Long noncoding RNAs (lncRNAs) recently attracted much attraction in the study of MI/R injury. However, the functional questions of specific lncRNAs in HFD‐induced MI/R injury have not been well elucidated. Uc.48+ is a lncRNA from a transcribed ultraconserved region (T‐UCR) of human, mouse, and rat genomes. Here, we explored the aggravating role of uc.48+and identified purinergic P2X7 receptor (P2X7R) as a downstream regulator of uc.48+ in HFD‐induced MI/R vulnerability. We demonstrated uc.48+ expression was upregulated, accompanied by the corresponding upregulation of P2X7R in HFD I/R myocardium and HFD‐induced MI/R vulnerability. Overexpression of uc.48+enhanced, whereas silencing of uc.48 + decreased the expression of P2X7R, cardiomyocyte apoptosis, and MI/R injury. The functional relevance of uc.48+ regulated P2X7R expression and the subsequent NF‐κB signaling to promote cardiomyocyte apoptosis was supported by inhibition of P2X7R with its specific antagonist (A438079) as well as the inhibitor of NF‐κB signaling (pyrrolidine dithiocarbamate, PDTC) in H9c2 hypoxia/reoxygenation (H/R) cells transfected with pcDNA3.0‐uc.48 + plasmid, and RNA immunoprecipitation (RIP) suggested uc.48+ could interact with transcription factor Sp1. Importantly, Sp1 inhibitor (mithramycin, MIT) was found to suppress uc.48+ ‐induced P2X7R expression and the NF‐κB signaling and cardiomyocyte apoptosis. Our findings provide a potential novel mechanism through which uc.48+ boosts cardiomyocyte apoptosis and MI/R vulnerability to HFD. Thus, uc.48+ is a novel regulator of HFD‐induced MI/R injury; targeting uc.48+ may be a novel therapeutic approach of MI/R vulnerability to HFD. High‐fat diet (HFD) is an independent risk factor for myocardial ischemia/reperfusion (MI/R) injury. Uc.48+ is a long noncoding RNA (lncRNA) from a transcribed ultraconserved region (T‐UCR) of human, mouse, and rat genomes. Here, we explored the aggravating role of uc.48+ and identified purinergic P2X7 receptor (P2X7R) as a downstream regulator of uc.48+ in HFD‐induced MI/R vulnerability. Targeting uc.48+ may be a novel therapeutic approach of MI/R vulnerability to HFD. [ABSTRACT FROM AUTHOR]

Abdominal aortic aneurysm (AAA) is one of the most life-threatening cardiovascular diseases; however, effective drug treatments are still lacking. The formation of neutrophil extracellular traps (NETs) has been shown to be a crucial trigger of AAA, and identifying upstream regulatory targets is thus key to discovering therapeutic agents for AAA. We revealed that phosphoinositide-3-kinase γ (PI3Kγ) acted as an upstream regulatory molecule and that PI3Kγ inhibition reduced NET formation and aortic wall inflammation, thereby markedly ameliorating AAA. However, the mechanism of NET formation regulated by PI3Kγ remains unclear. In this study, we showed that PI3Kγ deficiency inactivated the noncanonical pyroptosis pathway, which suppressed downstream NET formation. In addition, PI3Kγ regulation of noncanonical pyroptosis was dependent on cyclic AMP/protein kinase A signaling. These results clarify the molecular mechanism and crosstalk between PI3Kγ and NETosis in the development of AAA, potentially facilitating the discovery of therapeutic options for AAA.

Background: It is well-accepted that antihypertensive therapy is the cornerstone of treatment for abdominal aortic aneurysm (AAA) patients with hypertension. Direct-acting vasodilators were used in the treatment of hypertension by directly relaxing vascular smooth muscle but may have destructive effects on the aortic wall by activating the renin-angiotensin system axis. Their roles in AAA disease remain to be elucidated. In this study, we used hydralazine and minoxidil, two classical direct-acting vasodilators, to investigate their influence and potential mechanisms on AAA disease. Methods and results: In this study, we investigated the plasma renin level and plasma renin activity in AAA patients. Simultaneously, age and gender ratio-matched patients diagnosed with peripheral artery disease and varicose veins were selected as the control group using a ratio of 1:1:1. Our regression analysis suggested both the plasma renin level and plasma renin activity are positively associated with AAA development. In view of the well-established relationship between direct-acting vasodilators and increased plasma renin concentration, we established a porcine pancreatic elastase-infused AAA mouse model, followed by oral administration of hydralazine (250 mg/L) and minoxidil (120 mg/L) to investigate effects of direct-acting vasodilators on AAA disease. Our results suggested both hydralazine and minoxidil promoted the progression of AAA with increased aortic degeneration. Mechanistically, the vasodilators aggravated aortic inflammation by increased leukocyte infiltration and inflammatory cytokine secretion. Conclusion and relevance: The plasma renin level and plasma renin activity are positively associated with AAA development. Direct vasodilators aggravated experimental AAA progression, which raised cautionary concerns about their applications in AAA disease., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Liu, Liu, Zhao, Wu, Xu and Wang.)