Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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Background: Both sepsis-induced cardiomyopathy and worsening of preexisting cardiac disease can contribute to circulatory shock in septic patients. The early use of pulmonary artery catheter (PAC) could play a pivotal role in the management of sepsis-associated cardiogenic shock. In this study, we aimed to evaluate the impact of early invasive hemodynamic monitoring with PAC in patients with sepsis-associated cardiogenic shock. ⋯ The use of PAC was also associated with increased use of mechanical circulatory support in those with sepsis-associated cardiogenic shock (aOR = 12.26, 95% CI = 9.37-16.03, P < 0.001). For patients with sepsis-associated cardiogenic shock, the use of PAC after 2 days of admission was associated with significantly higher in-hospital mortality and decreased use of mechanical circulatory support. Conclusion: The use of pulmonary artery catheters in sepsis-associated cardiogenic shock was associated with significantly lower in-hospital mortality and increased use of mechanical circulatory supports in patients with sepsis-associated cardiogenic shock.
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Myocardial ischemia-reperfusion injury (MIRI) is a vital risk factor for cardiovascular diseases. Some circular RNAs have been identified as modulators of MIRI. However, the effects of circ-mitochondrial amidoxime reducing component 2 (circ-MARC2) in MIRI are unclear. ⋯ In addition, transient receptor potential cation channel subfamily M member 7 (TRPM7) was identified as the target gene of miR-335-5p. Overexpression of miR-335-5p relieved H/R-induced AC16 cell damage, whereas TRPM7 elevation abolished the effect. Circ-MARC2 knockdown was able to relieve H/R-induced AC16 cell injury through miR-335-5p/TRPM7 axis.
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Purpose : The objective of this study is to establish a nomogram that correlates optimized Acute Physiology and Chronic Health Evaluation II (APACHE II) score with sepsis-related indicators, aiming to provide a robust model for early prediction of sepsis prognosis in clinical practice and serve as a valuable reference for improved diagnosis and treatment strategies. Methods : This retrospective study extracted sepsis patients meeting the inclusion criteria from the MIMIC-IV database to form the training group. An optimized APACHE II score integrated with relevant indicators was developed using a nomogram for predicting the prognosis of sepsis patients. ⋯ Calibration curves and decision curve analyses also confirmed its good predictive ability, surpassing the APACHE II score and Sequential Organ Failure Assessment score in identifying high-risk patients. Conclusions : The nomogram was established in this study using the MIMIC-IV database and validated with external data, demonstrating its robust discriminability, calibration, and clinical practicability for predicting 28-day mortality in sepsis patients. These findings aim to provide substantial support for clinicians' decision making.
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Background : Sepsis-induced cardiomyopathy ( SIC ) is a common complication of sepsis with high morbidity and mortality but lacks specific therapy. The purpose of this study was to investigate the role of circularRNA_0003907 (circ_0003907) in myocardium injury induced by sepsis. Methods: In this experiment, human AC16 cells were treated with lipopolysaccharide (LPS) to induce an in vitro cardiomyocyte injury model. ⋯ In mechanism, circ_0003907 acted as a sponge for miR-944 to increase MYD88 expression. Meanwhile, the absence of circ_0003907 induced miR-944 expression and suppressed MYD88/NLRP3/NF-κB levels. Conclusion: Circ_0003907 sponged miR-944 to aggravate LPS-induced AC16 cell dysfunction via activating the MYD88/NLRP3/NF-κB axis during sepsis, which might provide a new direction for the treatment of SIC .
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Background: Recent studies have shown that ferroptosis is involved in the evolution of acute lung injury (ALI), a serious respiratory pathological process leading to death. However, the regulatory mechanisms underlying ferroptosis in ALI remain largely unknown. The current study analyzed and identified a ferroptosis-related gene signature for ALI. ⋯ Besides, the ferroptosis-related molecules GPX4 and ACSL4 showed remarkable difference in these models. Conclusion: These results indicate that PROK2 , IL6 , TNF , and SLC7A11 may be key regulatory targets of ferroptosis during ALI. This study proved that ferroptosis is a common pathophysiological process in three ALI models.