Background Myocardium irreversibly injured by ischemic stress must be efficiently repaired to maintain tissue integrity and contractile performance. Macrophages play critical roles in this process. These cells transform across a spectrum of phenotypes to accomplish diverse functions ranging from mediating the initial inflammatory responses that clear damaged tissue to subsequent reparative functions that help rebuild replacement tissue. Although macrophage transformation is crucial to myocardial repair, events governing this transformation are poorly understood. Methods Here, we set out to determine whether innate immune responses triggered by cytoplasmic DNA play a role. Results We report that ischemic myocardial injury, and the resulting release of nucleic acids, activates the recently described cGAS (GMP-AMP synthase)-STING (stimulator of interferon genes) pathway. Animals lacking cGAS display significantly improved early survival post-MI, diminished pathological remodeling including ventricular rupture, enhanced angiogenesis, and preserved ventricular contractile function. Furthermore, cGAS loss-of-function abolishes the induction of key inflammatory programs such as iNOS and promotes the transformation of macrophages to a reparative phenotype, which results in enhanced repair and improved hemodynamic performance. Conclusions These results reveal, for the first time, that the cytosolic DNA receptor cGAS functions during cardiac ischemia as a pattern recognition receptor in the sterile immune response. Further, we report that this pathway governs macrophage transformation, thereby regulating post-injury cardiac repair. As modulators of this pathway are currently in clinical use, our findings raise the prospect of new treatment options to combat ischemic heart disease and its progression to heart failure.

SOC is the main channel for the influx of Ca(2+) during hepatic I/R injuries. Calcium channel blockers, 2-APB, SK and F96365, econazole and miconazole, have obviously protective effects on I/R injury, probably by inhibiting I(SOC) in Kupffer cells and preventing the activation of Kupffer cells.

Carina resection and reconstruction is required when a tracheal tumor invades the tracheal carina. It is a relatively complicated surgical procedure that requires complex reconstruction to maintain airway continuity. The technical difficulty lies in minimizing the influence of anesthetic endotracheal intubation and maintaining good ventilation function during surgery by establishing appropriate ventilation channels, which are contradictory in many cases. Therefore, in order to achieve the optimal surgical outcome, we performed intratracheal tumor resection and carina reconstruction with the help of extracorporeal membrane oxygenation.

Introduction: Propofol is a general anesthetic option for deep brain stimulation (DBS) of the subthalamic nucleus (STN) of patients with Parkinson's disease (PD). However, its effects on STN activity and neuropsychological outcomes are controversial. The optimal propofol anesthesia for asleep DBS is unknown. This study investigated the safety and effectiveness of an optimized propofol anesthesia regimen in asleep DBS. Methods: This retrospective study enrolled 68 PD patients undergoing bilateral STN-DBS surgery. All patients received local scalp anesthesia, with (asleep group, n = 35) or without (awake group, n = 33) propofol-remifentanil general anesthesia by target-controlled infusion under electroencephalogram monitoring. The primary outcome was subthalamic neuronal spiking characterization during microelectrode recording. The secondary outcomes were clinical outcomes including motor, cognition, mind, sleep, and quality of life at 6 months. Results: Significantly increased delta and theta power were obtained under propofol anesthesia (awake vs. asleep group, mean ± standard deviation; delta: 31.97 ± 9.87 vs. 39.77 ± 10.56, p \ 0.01; theta: 21.09 ± 5.55 vs. 24.82 ± 6.63, p = 0.01). After excluding the influence of confounding factors of age and preoperative motor scores, there was a statistically significant influence on the delta, theta, and alpha power of STN neuronal activity under different anesthesia regimens (delta: b = 2.64, p \ 0.01; theta: b = 2.11, p \ 0.01; alpha: b = 1.42, p = 0.01). There were no differences in modified burst index, firing rate, tract numbers of microelectrode recording, and other clinical outcomes between the two groups.Nan Jiang and Yu-Ting Ling contributed equally to this work.

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