Objective:To evaluate the relationship between systemic immune-inflammatory index (SII) and prognosis of acute respiratory distress syndrome (ARDS).Methods:ARDS patients from the I Medical Information Mart for Intensive CareⅢ were selected as the study objects. Patients were followed up for one year. The primary endpoint was the 30-day mortality rate, and secondary endpoints were the 90-day and one-year mortality rates. Cox proportional hazard regression analysis was used to assess SII as an independent risk factor for ARDS patients, with propensity score matching to control for confounding factors.Results:A total of 723 ARDS patients were included in this study. Patients with SII≥ 3655 had older age, lower SpO 2 levels, and higher simplified acute physiology scoreⅡ (SAPSⅡ) and sequential organ failure assessment (SOFA) scores compared to those with SII <3655. Additionally, the 30-day, 90-day, and one-year mortality rates were higher in patients with SII ≥3655. Cox proportional hazard regression analysis showed that high SII level was an independent risk factor for the prognosis of ARDS at 30 days ( HR=1.68, 95% CI: 1.19-2.36, P=0.0028), 90 days ( HR=1.46, 95% CI: 1.07-1.99, P=0.0170), and one year ( HR=1.34, 95% CI: 1.01-1.77, P=0.0425). Propensity score matching analysis further confirmed the relationship between SII and the prognosis of ARDS patients. Conclusions:SII, as a simple and easily measurable index, is an independent risk factor for the prognosis of ARDS patients.

Objective To evaluate the effect of methylprednisolone on endoplasmic reticulum stress in rats with ventilator-induced lung injury ( VILI ) and the relationship with phosphatidylinositol 3-kinase∕serine-threonine protein kinase ( PI3K∕Akt) signaling pathway. Methods One hundred clean-grade male Sprague-Dawley rats, aged 4-5 months, weighing 270-320 g, were divided into 5 groups ( n=20 each) using a random number table method: control group ( C group) , VILI group ( V group) and different doses of methylprednisolone groups ( M1-3 groups) . Group C received no mechanical ventilation and kept spontane-ous breathing for 4 h. Rats were mechanically ventilated ( tidal volume 40 ml∕kg, respiratory rate 15-17 breaths∕min, inspiratory∕expiratory ratio 1 : 1, positive end-expiratory pressure 0, fraction of inspired oxy-gen 21％ during OLV) in group V. Methylprednisolone 2, 10 and 30 mg∕kg were intravenously injected at 20 min before mechanical ventilation in M1-3 groups, respectively, and the equal volume of normal saline was given in group V. Blood samples and lung tissues were taken at 4 h of ventilation for measurement of the lung permeability index ( LPI) and wet∕dry lung weight ratio ( W∕D ratio) , for examination of pathological changes, and for determination of apoptosis index ( AI) in lung tissues ( by TUNEL) , expression of Akt, phosphorylated Akt (p-Akt), glucose-regulated protein 78 (GRP78), CCAAT∕enhancer-binding protein homologous protein (CHOP) and caspase-12 in lung tissues (by Western blot). Injured alveoli rate (IAR) was calculated. Results Compared with group C, the W∕D ratio, LPI, IAR and AI were significantly in-creased, the expression of p-Akt was down-regulated, and the expression of GRP78, CHOP and caspase-12 was up-regulated in V and M1 groups ( P<0. 05) , and no significant change was found in the indexes mentioned above in M2 and M3 groups ( P>0. 05) . Compared with group V, the W∕D ratio, LPI, IAR and AI were significantly decreased, p-Akt expression was up-regulated, and the expression of GRP78, CHOP and caspase-12 was down-regulated in M2 and M3 groups ( P<0. 05) . Conclusion Methylprednisolone in-hibits endoplasmic reticulum stress, thus inhibiting cell apoptosis, and the mechanism is related to activa-ting PI3K∕Akt signaling pathway in rats with VILI.