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This study aimed to assess healthcare professionals’ knowledge, attitudes, and practices (KAP) regarding perioperative enhanced recovery after surgery (ERAS) in video-assisted thoracoscopic lobectomy. A cross-sectional study was conducted from April to July 2024 across 10 tertiary hospitals in Shanxi Province. Healthcare professionals from the Departments of Anesthesiology and Thoracic Surgery were surveyed using a self-administered questionnaire. A total of 289 valid responses were included. The mean scores for knowledge, attitude, and practice were 19.99 ± 5.89 (range: 0–28), 36.71 ± 4.09 (range: 8–40), and 49.84 ± 5.40 (range: 11–55), respectively. Correlation analysis revealed significant positive relationships: knowledge correlated with attitude ( r  = 0.423, P  < 0.001) and practice ( r  = 0.475, P  < 0.001); attitude also correlated strongly with practice ( r  = 0.731, P  < 0.001). The structural equation model revealed that knowledge directly influenced attitude (β = 0.450) and practice (β = 0.162) and indirectly affected practice via attitude (β = 0.339) (all P  < 0.001). Healthcare professionals in Shanxi Province demonstrated generally adequate knowledge, positive attitudes, and proactive practices concerning perioperative ERAS protocols in video-assisted thoracoscopic lobectomy. Targeted training and education for healthcare professionals are recommended to enhance ERAS protocol implementation.

Background Nanoplastics (NPs) are now a new class of pollutants widely present in the soil, atmosphere, freshwater and marine environments. Nanoplastics can rapidly penetrate cell membranes and accumulate in human tissues and organs, thus posing a potential threat to human health. The heart is the main power source of the body. But up to now, the toxicological effects of long-term exposure to nanoplastics on the heart has not been revealed yet. Results We evaluated the effects of long term exposure of nanoplastics on cardiac cell/tissue in vitro and in vivo model. Furthermore, we explored the molecular mechanism by which nanoplastics exposure causes myocardial cell senescence. Immunohistochemistry, indirect immunofluorescence and ELISA were performed to detect the effects of nanoplastics on heart aging. We found that nanoplastics were able to induce significant cardiac aging through a series of biochemical assays in vivo. In vitro, the effects of nanoplastics on cardiac cell were investigated, and found that nanoplastics were able to internalize into cardiomyocytes in time and dose-dependant manner. Further biochemical analysis showed that nanoplastics induces cardiomyocytes senescence by detecting a series of senescence marker molecules. Molecular mechanism research shows that nanoplastics may cause mitochondrial destabilization by inducing oxidative stress, which leads to the leakage of mtDNA from mitochondria into the cytoplasm, and then cytoplasm-localized mt-DNA activates the cGAS-STING signaling pathway and promotes inflammation response, ultimately inducing cardiomyocytes senescence. Conclusions In this work, we found that nanoplastics exposure induces premature aging of heart. Current research also reveals the molecular mechanism by which nanoplastics induces cardiomyocyte senescence. This study laid the foundation for further studying the potential harm of nanoplastics exposure on heart. Graphical abstract

Steel plate shear walls (SPSWs) are widely used in earthquake-prone areas, and they usually undergo multiple earthquakes throughout their service lives. The performances of SPSWs under a single shot of an earthquake have been widely studied, although the secondary seismic performance of earthquake-damaged structures remains unclear. Damage to an SPSW structure during an earthquake is difficult to evaluate. In this study, the degradation of the seismic performance of SPSWs during earthquakes was investigated. A test specimen was subjected to a two-stage quasistatic load. The plastic development and failure modes of SPSW specimens were investigated. The degradation of bearing capacity, stiffness, and energy dissipation performance was analyzed. On the basis of the experimental investigation, finite-element models introducing the ductile damage criterion and the cyclic constitutive model of steel were established. The degradation of the seismic performance of SPSWs under secondary earthquakes was studied. The results indicate that the stiffness of the SPSWs degrades more significantly than the bearing capacity. The larger the height-to-thickness ratio of the embedded plate, the more obvious the decrease in the bearing capacity, and the smaller the decrease in stiffness. With the increase in the maximum lateral displacement reached by the structure in an earthquake, and as the pinch phenomenon of the hysteresis curve of the SPSW becomes more serious, the energy dissipation capacity shows a uniform downward trend.

Background: Myocarditis, an autoimmune disease characterized by inflammation of the heart muscle, can lead to impaired cardiac function. Understanding the cellular subpopulations within the myocarditis microenvironment is crucial for improving diagnosis and treatment strategies. Methods: We first performed differential expression analysis using bulk RNA sequencing data from myocarditis mouse models, to identify key genes and pathways. Subsequently, we integrated single-cell RNA sequencing data to explore different cell subpopulations through clustering analysis, utilizing GSEA, GSVA, and CellChat to examine their functions and interactions. Results: Differential expression analysis revealed 690 upregulated genes associated with immune regulation and inflammation, as well as pathways related to cardiovascular diseases, such as viral myocarditis and lipid metabolism. Analysis of fibroblasts indicated significant heterogeneity, including normal fibroblasts, inflammatory fibroblasts, myofibroblasts, and antigen-presenting fibroblasts. We observed a marked increase in Nfkbia + M1 macrophages during myocarditis, along with pre-exhausted Ccl5+ CD8+ cytotoxic T cells within T/NK cell subgroups, which receive antigen presentation signals from fibroblasts and macrophages. Conclusion: Our study reveals novel insights into the cellular complexity of the myocarditis microenvironment, particularly the identification of distinct fibroblast subpopulations, the role of Nfkbia + M1 macrophages in inflammation, and the pre-exhausted state of Ccl5+ CD8+ T cells. These findings not only provide a deeper understanding of the immune mechanisms underlying myocarditis but also highlight potential therapeutic targets and avenues for future research aimed at improving the diagnosis and treatment of myocarditis.

Racemic new cyclohexenone and cyclopentenone derivatives, (±)-(4R*,5S*,6S*)-3-amino-4,5,6-trihydroxy-2-methoxy-5-methyl-2-cyclohexen-1-one (1) and (±)-(4S*,5S*)-2,4,5-trihydroxy-3-methoxy-4-methoxycarbonyl-5-methyl-2-cyclopenten-1-one (2), and two new xanthone derivatives 4-chloro-1,5-dihydroxy-3-hydroxymethyl-6-methoxycarbonyl-xanthen-9-one (3) and 2,8-dimethoxy-1,6-dimethoxycarbonyl-xanthen-9-one (4), along with one known compound, fischexanthone (5), were isolated from the culture of the mangrove endophytic fungus Alternaria sp. R6. The structures of these compounds were elucidated by analysis of their MS (Mass), one and two dimensional NMR (nuclear magnetic resonance) spectroscopic data. Compounds 1 and 2 exhibited potent ABTS [2,2′-azino-bis(3-ethylbenzthiazoline-6-sulphonic acid)] scavenging activities with EC50 values of 8.19 ± 0.15 and 16.09 ± 0.01 μM, respectively. In comparison to Triadimefon, compounds 2 and 3 exhibited inhibitory activities against Fusarium graminearum with minimal inhibitory concentration (MIC) values of 215.52 and 107.14 μM, respectively, and compound 3 exhibited antifungal activity against Calletotrichum musae with MIC value of 214.29 μM.

The role of airway microbiota in COPD is highly debated. Symptomology assessment is vital for the management of clinically stable COPD patients; however, the link between symp toms and the airway microbiome is currently unknown. The present study aimed to evaluate the relationship among stable COPD patients. We conducted pyrosequencing of bacterial 16S rRNA using induced sputum samples in a Han Chinese cohort that included 40 clinically stable COPD patients and 19 healthy controls. Alterations in community composition and core bacte rial taxa (Neisseria subflava, etc.) were observed in patients with severe symptoms compared with controls. The co-occurrence network indicated that the key microbiota enriched in COPD patients showed higher expression in patients with severe symptoms. The association pattern of symptoms with the sputum microbiome was obviously different from that of lung function in COPD patients. These findings broaden our insights into the relationship between the sputum microbiota and the symptom severity in COPD patients, emphasizing the role of symptoms in the airway microbiome, independent of lung function.

Suppressor of variegation 3-9 homolog 1 (SUV39H1), a histone methyltransferase, catalyzes historie 3 lysine 9 trimethylation and is involved in heterochromatin organization and genome stability. However, the mechanism for regulation of the enzymatic activity of SUV39H1 in cancer cells is not yet well known. In this study, we identified SET domain-containing protein 7 (SET7/9), a protein methyltransferase, as a unique regulator of SUV39H1 activity. In response to treatment with adriamycin, a DNA damage inducer, SET7/9 interacted with SUV39H1 in vivo, and a GST pull-down assay confirmed that the chromodomain-containing region of SUV39H1 bound to SET7/9. Western blot using antibodies specific for antimethylated SUV39H1 and mass spectrometry demonstrated that SUV39H1 was specifically methylated at lysines 105 and 123 by SET7/9. Although the half-life and localization of methylated SUV39H1 were not noticeably changed, the methyltransferase activity of SUV39H1 was dramatically down-regulated when SUV39H1 was methylated by SET7/9. Consequently, H3K9 trimethylation in the heterochromatin decreased significantly, which, in turn, led to a significant increase in the expression of satellite 2 (Sat2) and α-satellite (α-Sat), indicators of heterochromatin relaxation. Furthermore, a micrococcal nuclease sensitivity assay and an immunofluorescence assay demonstrated that methylation of SUV39H1 facilitated genome instability and ultimately inhibited cell proliferation. Together, our data reveal a unique interplay between SET7/9 and SUV39H1—two histone methyltransf erases—that results in heterochromatin relaxation and genome instability in response to DNA damage in cancer cells.

Long non-coding RNA (lncRNA) is widely reported to be involved in cardiac (patho)physiology. Acute myocardial infarction, in which cardiomyocyte apoptosis plays an important role, is a life-threatening disease. Here, we report the lncRNA Chaer that is anti-apoptotic in cardiomyocytes during Acute myocardial infarction. Importantly, lncRNA Chaer is significantly downregulated in both oxygen-glucose deprivation (oxygen-glucose deprivation)-treated cardiomyocytes in vitro and AMI heart. In vitro , overexpression of lncRNA Chaer with adeno virus reduces cardiomyocyte apoptosis induced by OGD-treated while silencing of lncRNA Chaer increases cardiomyocyte apoptosis instead. In vivo , forced expression of lncRNA Chaer with AAV9 attenuates cardiac apoptosis, reduces infarction area and improves mice heart function in AMI. Interestingly, overexpression of lncRNA Chaer promotes the phosphorylation of AMPK, and AMPK inhibitor Compound C reverses the overexpression of lncRNA Chaer effect of reducing cardiomyocyte apoptosis under OGD-treatment. In summary, we identify the novel ability of lncRNA Chaer in regulating cardiomyocyte apoptosis by promoting phosphorylation of AMPK in AMI.

Protein posttranslational modifications play important roles in cardiovascular diseases. The authors’ previous report showed that the abundance of succinylated and glutarylated proteins was significantly lower in the serum of patients with acute myocardial infarction (AMI) than in that of healthy volunteers, suggesting a potential relationship between protein acylation and AMI. Sirtuin 5 (SIRT5) facilitates the removal of malonyl, succinyl, and glutaryl modification; however, its effects on AMI remain unknown. In this study, the levels of SIRT5 in AMI mouse model was compared. Results showed elevated hepatic SIRT5 after myocardial infarction. Hepatocyte-specific SIRT5 overexpressing mice (liver SIRT5 OE) were generated to address the possible involvement of hepatic SIRT5 in AMI. The areas of myocardial infarction, myocardial fibrosis, and cardiac function in a model of experimental myocardial infarction were compared between liver SIRT5 OE mice and wild-type (WT) mice. The liver SIRT5 OE mice showed a significantly smaller area of myocardial infarction and myocardial fibrosis than the WT mice. The fibroblast growth factor 21 (FGF21) in the blood and myocardium of liver SIRT5 OE mice after AMI was markedly elevated compared with that in WT mice. The results of mass spectrometry showed increased levels of proteins regulating tricarboxylic acid cycle, oxidative phosphorylation, and fatty acid β-oxidation pathways in the liver mitochondria of liver SIRT5 OE mice. These findings showed that SIRT5 may exhibit a cardioprotective effect in response to acute ischemia through a liver-cardiac crosstalk mechanism, probably by increasing the secretion of FGF21 and the improvement of energy metabolism.

Toxoplasma gondii uracil phosphoribosyltransferase (UPRT) converts 4‐thiouracil (4TUc) into 4‐thiouridine (4TUd), which is incorporated into nascent RNAs and can be biotinylated, then labelled with streptavidin conjugates or isolated via streptavidin‐affinity methods. Here, we generated mice that expressed T. gondii UPRT only in cardiomyocytes (CMUPRT mice) and tested our hypothesis that CM‐derived miRNAs (CMmiRs) are transferred into remote organs after myocardial infarction (MI) by small extracellular vesicles (sEV) that are released from the heart into the peripheral blood (PBsEV). We found that 4TUd was incorporated with high specificity and sensitivity into RNAs isolated from the hearts and PBsEV of CMUPRT mice 6 h after 4TUc injection. In PBsEV, 4TUd was incorporated into CM‐specific/enriched miRs including miR‐208a, but not into miRs with other organ or tissue‐type specificities. 4TUd‐labelled miR208a was also present in lung tissues, especially lung endothelial cells (ECs), and CM‐derived miR‐208a (CMmiR‐208a) levels peaked 12 h after experimentally induced MI in PBsEV and 24 h after MI in the lung. Notably, miR‐208a is expressed from intron 29 of α myosin heavy chain (αMHC), but αMHC transcripts were nearly undetectable in the lung. When PBsEV from mice that underwent MI (MI‐PBsEV) or sham surgery (Sham‐PBsEV) were injected into intact mice, the expression of Tmbim6 and NLK, which are suppressed by miR‐208a and cooperatively regulate inflammation via the NF‐κB pathway, was lower in the lungs of MI‐PBsEV–treated animals than the lungs of animals treated with Sham‐PBsEV or saline. In MI mice, Tmbim6 and NLK were downregulated, whereas endothelial adhesion molecules and pro‐inflammatory cells were upregulated in the lung; these changes were significantly attenuated when the mice were treated with miR‐208a antagomirs prior to MI surgery. Thus, CMUPRT mice enables us to track PBsEV‐mediated transport of CMmiRs and identify an miR‐208a‐mediated mechanism by which myocardial injury alters the expression of genes and inflammatory response in the lung.