A novel coronavirus disease 2019 (COVID‐19) broke out at 2019 and had caused a pandemic around the world. This disease was found resulting from the infection of 2019 novel coronavirus (2019‐nCoV) (Zhu, et al 2020). The severity of COVID‐19 disease has a wide range and varies from asymptomatic to critical severe, clinical researches reported that 10‐15% of the patients were in the severe situation and required a great deal of attention of treatment and nursing (WHO‐China‐Joint‐Mission 2020).

Background and Purpose: Endothelium‐derived hyperpolarizing factor (EDHF) has been suggested as a therapeutic target for vascular protection against ischaemic brain injury. However, the molecular entity of EDHF and its action on neurons remains unclear. This study was undertaken to demonstrate whether the hydrogen sulfide (H₂S) acts as EDHF and exerts neuroprotective effect via large‐conductance Ca²⁺‐activated K⁺ (BK_Ca/K_Ca1.1) channels.Experimental Approach: The whole‐cell patch‐clamp technology was used to record the changes of BK_Ca currents in rat neurons induced by EDHF. The cerebral ischaemia/reperfusion model of mice and oxygen–glucose deprivation/reoxygenation (OGD/R) model of neurons were used to explore the neuroprotection of EDHF by activating BK_Ca channels in these neurons.Key Results: Increases of BK_Ca currents and membrane hyperpolarization in hippocampal neurons induced by EDHF could be markedly inhibited by BK_Ca channel inhibitor iberiotoxin or endothelial H₂S synthase inhibitor propargylglycine. The H₂S donor, NaHS‐induced BK_Ca current and membrane hyperpolarization in neurons were also inhibited by iberiotoxin, suggesting that H₂S acts as EDHF and activates the neuronal BK_Ca channels. Besides, we found that the protective effect of endothelium‐derived H₂S against mice cerebral ischaemia/reperfusion injury was disrupted by iberiotoxin. Importantly, the inhibitory effect of NaHS or BK_Ca channel opener on OGD/R‐induced neuron injury and the increment of intracellular Ca²⁺ level could be inhibited by iberiotoxin but enhanced by co‐application with L‐type but not T‐type calcium channel inhibitor.Conclusion and Implications: Endothelium‐derived H₂S acts as EDHF and exerts neuroprotective effects via activating the BK_Ca channels and then inhibiting the T‐type calcium channels in hippocampal neurons.

Currently, the treatment of septic myopathy presents significant challenges with implications for increased mortality rates and prolonged hospitalizations. Effective therapeutic strategies for septic myopathy remain elusive, highlighting an urgent need for novel therapeutic approaches. High‐mobility group box 1 (HMGB1) is a conserved nonhistone nuclear protein that is released passively from deceased cells or actively secreted by activated immune cells, influencing both infectious and noninfectious inflammatory responses. Studies have indicated that HMGB1 likely plays a pivotal role in the pathogenesis of septic myopathy by crucial pathways associated with muscle atrophy and contributing to muscle regeneration under certain conditions. This review aims to summarize the possible mechanisms of HMGB1 in muscle atrophy and its potential in muscle regeneration, providing a theoretical basis for HMGB1 treatment of septic myopathy. Research shows that the dual role of HMGB1 is related to its specific forms, which are influenced to varying degrees by environmental factors. HMGB1 is a key participant in septic muscle atrophy, whereas HMGB1 shows therapeutic potential in muscle regeneration. One key mechanism by which HMGB1 contributes to septic muscle atrophy is through the exacerbation of inflammation. HMGB1 can amplify the inflammatory response by promoting the release of pro‐inflammatory cytokines, which further damages muscle tissue. HMGB1 is also involved in promoting cell death in sepsis, which contributes to muscle degradation. Another important mechanism is the regulation of protein degradation systems. HMGB1 can activate the ubiquitin–proteasome system and autophagy–lysosome pathway, both of which are crucial for the breakdown of muscle proteins during atrophy. Conversely, targeting HMGB1 has shown the potential to ameliorate muscle atrophy in various diseases. For instance, HMGB1 has been shown to promote muscle vascular regeneration, modify stem cell status and enhance stem cell migration and differentiation, all of which are beneficial for muscle repair and recovery. Pharmacological inhibition of HMGB1 has been explored, with several drugs demonstrating efficacy in reducing inflammation and muscle degradation in sepsis models. These findings suggest that HMGB1 inhibition could be a viable therapeutic approach for septic myopathy. However, the function of promoting muscle regeneration in septic myopathy needs further research. HMGB1 emerges as a promising therapeutic target for the treatment of muscle atrophy in sepsis. This review focuses on identifying the correlation between HMGB1 and septic myopathy, analysing the possible role of HMGB1 in disease development and examining the feasibility of HMGB1 as a therapeutic target.

Review question / Objective: We aimed to compare the death risk of operating room thoracotomy and emergency department thoracotomy for patients with severe thoracic injuries by conducting systematic review and meta-analysis. Condition being studied: Duo to the high mortality of severe thoracic and cardiac trauma, treatment for severe thoracic trauma patients has become a great challenge. Resuscitative thoracotomy, which included emergency department thoracotomy (EDT) and operating room thoracotomy (ORT), is a surgical procedure to rescue severe thoracic patients, especially for patients with traumatic cardiac arrest and tamponade. However, it was still controversial that whether EDT or ORT was superior to the patients suffered from severe thoracic injuries.