다중혈관 관상동맥 환자에서 y-문합을 이용하여 양쪽 내흉동맥만을 사용한 우회술의 조기 성적

Hydrogen sulfide: An endogenous regulator of the immune system.

Two's company.

Background Accumulation of myofibroblasts is critical to fibrogenesis in idiopathic pulmonary fibrosis (IPF). Senescence and insufficient mitophagy in fibroblasts contribute to their differentiation into myofibroblasts, thereby promoting the development of lung fibrosis. Bone morphogenetic protein 4 (BMP4), a multifunctional growth factor, is essential for the early stage of lung development; however, the role of BMP4 in modulating lung fibrosis remains unknown. Methods The aim of this study was to evaluate the role of BMP4 in lung fibrosis using BMP4-haplodeleted mice, BMP4-overexpressed mice, primary lung fibroblasts and lung samples from patients with IPF. Results BMP4 expression was downregulated in IPF lungs and fibroblasts compared to control individuals, negatively correlated with fibrotic genes, and BMP4 decreased with transforming growth factor (TGF)-β1 stimulation in lung fibroblasts in a time- and dose-dependent manner. In mice challenged with bleomycin, BMP4 haploinsufficiency perpetuated activation of lung myofibroblasts and caused accelerated lung function decline, severe fibrosis and mortality. BMP4 overexpression using adeno-associated virus 9 vectors showed preventative and therapeutic efficacy against lung fibrosis. In vitro, BMP4 attenuated TGF-β1-induced fibroblast-to-myofibroblast differentiation and extracellular matrix (ECM) production by reducing impaired mitophagy and cellular senescence in lung fibroblasts. Pink1 silencing by short-hairpin RNA transfection abolished the ability of BMP4 to reverse the TGF-β1-induced myofibroblast differentiation and ECM production, indicating dependence on Pink1-mediated mitophagy. Moreover, the inhibitory effect of BMP4 on fibroblast activation and differentiation was accompanied with an activation of Smad1/5/9 signalling and suppression of TGF-β1-mediated Smad2/3 signalling in vivo and in vitro. Conclusion Strategies for enhancing BMP4 signalling may represent an effective treatment for pulmonary fibrosis. BMP4 deficiency results in cellular senescence and defective mitophagy of fibroblasts and promotes fibrosis in the lung. This study provides a proof-of-principle that BMP4 activation may offer a promising therapeutic approach for pulmonary fibrosis. https://bit.ly/3HWIKWS

/pdf/bone-morphogenetic-protein-4-inhibits-pulmonary-fibrosis-by-1jh4rhnr.pdf

Bone morphogenetic protein 4 inhibits pulmonary fibrosis by modulating cellular senescence and mitophagy in lung fibroblasts

Epithelial-mesenchymal transition: Insights into nickel-induced lung diseases.

Airway remodeling is one of the characteristics for chronic obstructive pulmonary disease (COPD). The mechanism underlying airway remodeling is associated with epithelial-mesenchymal transition (EMT) in the small airways of smokers and patients with COPD. Sirtuin 1 (SIRT1) is able to reduce oxidative stress, and to modulate EMT. Here, we investigated the effects and mechanisms of hydrogen sulfide (H2S) on pulmonary EMT in vitro and in vivo. We found that H2S donor NaHS inhibited cigarette smoke (CS)-induced airway remodeling, EMT and collagen deposition in mouse lungs. In human bronchial epithelial 16HBE cells, NaHS treatment also reduced CS extract (CSE)-induced EMT, collagen deposition and oxidative stress. Mechanistically, NaHS upregulated SIRT1 expression, but inhibited activation of TGF-β1/Smad3 signaling in vivo and in vitro. SIRT1 inhibition by a specific inhibitor EX527 significantly attenuated or abolished the ability of NaHS to reverse the CSE-induced oxidative stress. SIRT1 inhibition also abolished the protection of NaHS against CSE-induced EMT. Moreover, SIRT1 activation attenuated CSE-induced EMT by modifying TGF-β1-mediated Smad3 transactivation. In conclusion, H2S prevented CS-induced airway remodeling in mice by reversing oxidative stress and EMT, which was partially ameliorated by SIRT1 activation. These findings suggest that H2S may have therapeutic potential for the prevention and treatment of COPD.

Hydrogen sulfide attenuates cigarette smoke-induced airway remodeling by upregulating SIRT1 signaling pathway.


 Objectives: The pandemic of the coronavirus disease 2019 (COVID-19) continuously poses a serious threat to public health, highlighting an urgent need for simple and efficient early detection and prediction. Methods: We comprehensively investigated and reanalyzed the published indexes and models for predicting severe illness among COVID‑19 patients in our dataset, and validated them on an independent dataset. Results: 696 COVID-19 cases in the discovery stage and 337 patients in the validation stage were involved. The AuROC of neutrophil to lymphocyte ratio (NLR) (0.782) was significantly higher than that of the other 11 independent risk indexes in severe outcome prediction. The combination of NLR and oxygen saturation (SaO2) (NLR+SaO2) showed the biggest AuROC calculations with a value of 0.901; with a cut-off value of 0.532, it exhibited 84.2% sensitivity, 88.4% specificity and 86.8% correct classification ratio. Moreover, we first identified that principal component analysis (PCA) is an effective tool to predict the severity of COVID-19. We obtained 86.5% prediction accuracy with 86% sensitivity when PCA was applied to predict severe illness. In addition, to evaluate the performance of NLR+SaO2 and PCA, we compared them with currently published predictive models in the same dataset. Conclusions: It showed that NLR+SaO2 is an appropriate and promising method for predicting severe illness, followed by PCA. We then validated the results on an independent dataset and revealed that they remained robust accuracy in outcome prediction. This study is significant for early treatment, intervention, triage and saving limited resources.

/pdf/nlr-combined-with-sao2-predict-severe-illness-among-covid-19-19s46gzxvd.pdf

NLR combined with SaO2 predict severe illness among COVID-19 patients: a currently updated model

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Hydrogen sulfide attenuates cigarette smoke-induced airway remodeling by upregulating SIRT1 signaling pathway.

NLR combined with SaO2 predict severe illness among COVID-19 patients: a currently updated model