Endoplasmic reticulum stress is involved in ventilator-induced lung injury in mice via the IRE1α-TRAF2-NF-κB pathway

Inflammation plays a critical role in the development of ventilator-induced lung injury (VILI). Endoplasmic reticulum (ER) stress is associated with a variety of diseases through the modulation of inflammatory responses. However, little is known about how ER stress is implicated in VILI. In this study, murine mechanical ventilation models were constructed. Total protein and inflammatory cytokines were measured in bronchoalveolar lavage fluid (BALF), and lung tissue injury was assessed by histology. Our data revealed that mice subjected to high tidal ventilation (TV) for 4 h showed more severe pulmonary edema and inflammation than those of mice with spontaneous breathing and low TV-treatment. In addition, the high TV-treated animals upregulated the ER stress markers GRP78, CHOP, p-IRE1α, TRAF2, and p-NF-κB expression at both the mRNA and protein levels in lung tissue. Administration of thapsigargin exacerbated the histological changes, inflammation and expression of GRP78 and CHOP after high TV, but treatment with ER stress and IRE1α kinase inhibitors attenuated the pathological damage and downregulated the high expression of GRP78, CHOP, p-IRE1α, TRAF2, and p-NF-κB, suggesting that ER stress is involved in VILI though the IRE1α/TRAF2/NF-κB signaling pathway in mice.     

Skin temperature and vascular attributes as early warning signs of pressure injury

ObjectivesThis study aimed to validate the skin temperature on sacral region and vascular attributes as early warning signs of pressure injury.MethodsTotally 415 patients admitted to the adult intensive care unit from August 2018 to April 2019 were prospectively screened. Daily blood pressure and blood glucose affecting vascular attributes and the relative skin temperature of sacral region were measured for 10 consecutive days. Collect the changes of these indicators during the occurrence of pressure injury. The optimal cut-off values of indicators were determined by X-tile analysis. The risk ratios of indicators associated with pressure injury were compared using the Cox proportional hazards regression model.ResultsThere were no obvious interactions among blood pressure, blood glucose and relative skin temperature (P > 0.05). The optimal cutoff value for above indicators was 63.5 mmHg, 9.9 mmol/L and −0.1 °C, respectively. The incidence of pressure injury peaked on the 4th and 5th day after hospitalization when categorizing the patients into low- and high-risk groups according to the cutoff values (P < 0.05). Based on relative skin temperature, patients in the high-risk group were more likely to develop pressure injury (hazard ratio = 6.36, 95% confidence interval = 3.91, 10.36), when compared to the other two indicators of blood pressure and blood glucose.ConclusionStringent skin temperature and vascular attributes measurements were necessary for preventing pressure injury. Nursing measures should be taken according to warning sings to reduce the incidence of pressure injury.     

腮腺切除术中沿面神经总干顺行解剖面神经的效果及安全性

目的探讨腮腺切除术中应用沿面神经总干顺行解剖面神经的治疗效果及安全性。方法选取我院2016年2月至2019年3月收治的60例择期行腮腺切除术的患者,随机分为观察组与对照组各30例。对照组沿面神经总干逆行解剖面神经,观察组沿面神经总干顺行解剖面神经,观察两组患者术后1个月面神经功能及术后并发症发生情况。结果术后1个月,两组患者的面神经功能分级比较无统计学差异(P>0.05);观察组的术后并发症发生率为10.00%,明显低于对照组的33.33%(P <0.05)。结论临床行腮腺切除术中,沿面神经总干顺行解剖面神经可降低术后并发症发生率,值得推广。     

Emodin attenuates acute lung injury in Cecal-ligation and puncture rats

Acute lung injury (ALI) is a major cause of sepsis-induced acute respiratory failure. Emodin has been considered to play a protective role for acute lung edema in cecal ligation and puncture (CLP)-induced sepsis model. In this study we aimed to investigate whether emodin could improve CLP-induced lung sepsis via regulating aquaporin (AQP) and tight junction (TJ), inflammatory factors, and pulmonary apoptosis. The results showed that sepsis-induced pulmonary pathological changes were significantly improved after emodin treatment. Emodin was found to upregulate AQP and TJ expression in the CLP model. Meanwhile, inflammatory cytokine release and pulmonary apoptosis was remarkably reduced after emodin treatment in lung sepsis. Our data demonstrated that emodin could suppresse inflammation, restore pulmonary epithelial barrier and reduce mortality in CLP-induced ALI, suggesting the potential therapeutic application of emodin in sepsis.