In aortic dissection (AD), long-term medical therapy is usually prescribed to decrease the stress on the aortic wall and prevent aortic expansion or rupture.¹ Medication therapy for AD is still based on historical observational studies and expert opinion. Guidelines from the European Society of Cardiology,² American College of Cardiology/American Heart Association,³ and Japanese Circulation Society⁴ recommend β-blockers for the initial management of acute AD. Observational studies show that the use of β-blockers may decrease the aortic dilatation rate in aortic disease.^5,6

To investigate the incidence, outcomes, and risk factors of postoperative acute respiratory distress syndrome (ARDS) in patients undergoing surgical repair for acute type A aortic dissection. This retrospective study involved 270 patients who underwent surgical repair for acute type A aortic dissection between January 2009 and December 2015. Data on clinical characteristics and outcomes were collected. Patients who immediately died after surgery and with preoperative myocardial dysfunction were excluded. The included patients were divided into the ARDS (ARDS patients who met the Berlin definition) and non-ARDS groups. Primary outcome was postoperative ARDS, according to the 2012 Berlin definition for ARDS and was reviewed by 2 qualified physicians with expertise in critical care and cardiac surgery. Outcomes of interest were the incidence and severity of risk factors for ARDS in this population, and perioperative outcomes and survival rates were compared with patients with or without ARDS. A total of 233 adult patients were enrolled into this study; of these, 37 patients (15.9%) had ARDS. Three, 20, and 14 patients had mild, moderate, and severe ARDS, respectively, according to the Berlin definition, with no significant difference in age, sex, and underlying disease. The ARDS group had lower mean oxygenation index (OI) than the non-ARDS group in the first 3 days post-surgery and demonstrated an improvement in lung function after the fourth day. Postoperative complication risks were higher in the ARDS group than in the non-ARDS group. However, no significant difference was observed in in-hospital mortality between the 2 groups (10.8% vs 5.6%, P = .268). Additionally, there was also no significant difference in the 3-year mortality rate between the 2 groups (P of log-rank test = .274). Postoperative hemoglobin level (odds ratio [OR]: 0.78; 95% confidence interval [CI]: 0.62–0.99) and perioperative blood transfusion volume (OR: 1.07; 95% CI: 1.03–1.12) were associated with ARDS risk. Postoperative ARDS after type A aortic dissection repair surgery was associated with risks of postoperative complications but not with risk of in-hospital mortality or 3-year mortality. A higher perioperative blood transfusion volume and a lower postoperative hemoglobin level may be risk factors for ARDS.

Recent experimental studies have highlighted the beneficial effects of curcumin on liver injury induced by acetaminophen (APAP). However, the specific molecular mechanisms underlying curcumin’s hepatoprotective effects against APAP-induced liver injury remain to be fully elucidated. This study aimed to investigate the therapeutic effect of curcumin on APAP-induced liver injury using a mouse model. In the experiment, mice were subjected to an intraperitoneal hepatotoxic dose of APAP (300 mg/kg) to induce hepatotoxicity. After 30 min of APAP administration, the mice were treated with different concentrations of curcumin (0, 10, 25, or 50 mg/kg). After 16 h, mice with hepatotoxicity showed elevated levels of serum alanine transaminase (ALT), aspartate transaminase (AST), hepatic myeloperoxidase (MPO), TNF-α, and IL-6, and decreased levels of glutathione (GSH). Moreover, there was an increased infiltration of neutrophils and macrophages following intraperitoneal injection of APAP. However, curcumin-treated mice displayed a pronounced reduction in serum ALT, AST, hepatic MPO, TNF-α, and IL-6 levels, coupled with a notable elevation in GSH levels compared to the APAP-treated hepatotoxic mice. Moreover, curcumin treatment led to reduced infiltration of neutrophils and macrophages. Additionally, curcumin inhibited the phosphorylation of ERK and NF-kB proteins while reducing the expression of cyclooxygenase-2 (COX-2). These findings highlight the hepatoprotective potential of curcumin against APAP-induced liver injury through the suppression of the ERK, NF-kB, and COX-2 signaling pathways.

Objectives Outcomes of sex differences in major cardiac surgery remain controversial. A comprehensive understanding of sex differences in major adult cardiac surgery could provide better knowledge of risk factors, management strategy and short-term or long-term outcomes. The present study aimed to investigate sex differences in the risks of outcomes of major cardiac surgeries and subgroup analyses of different valve types. Design Population-based nationwide cohort study. Setting Data were obtained from National Health Insurance Research Database (NHIRD) in Taiwan. Participants A total of 66 326 adult patients (age ≥20 years; 30.3% women) who underwent a first major cardiac surgery (isolated coronary artery bypass graft (CABG), isolated valve or concomitant bypass/valve) from 2000 to 2013 were identified via Taiwan NHIRD. Main outcome measures Outcomes of primary interest were in-hospital death and all-cause mortality during follow-up period. Propensity score matching was conducted as a secondary analysis for the sensitivity test. Results Women who underwent isolated CABG tended to have greater risks of both in-hospital (OR 1.37; 95% CI 1.26 to 1.49) and late outcomes (HR 1.26; 95% CI 1.22 to 1.31). Women after concomitant CABG/valve also had a greater in-hospital (OR 1.19; 95% CI 1.01 to 1.40) and long-term mortality (HR 1.14; 95% CI 1.05 to 1.24). Women after isolated mitral valve repair have a non-favourable outcome of in-hospital mortality (OR 1.70; 95% CI 1.01 to 2.87). Women who did not receive an isolated aortic valve replacement had more favourable all-cause mortality outcome (HR 0.90; 95% CI 0.84 to 0.96). Secondary analysis in the propensity score-matching cohort demonstrated results similar to the primary analysis. Conclusions Female patients who underwent procedures involving CABG (with or without concurrent valvular intervention) had generally worse outcomes. However, the results of isolated valve surgery were variable on the basis of the type of intervened valve.

Acetaminophen (APAP) overdose causes acute liver injury via oxidative stress, uncontrolled inflammatory response, and subsequent hepatocyte death. Nicotinamide adenine dinucleotide phosphate oxidase (NOX) is a potent source of cellular reactive oxygen species (ROS) and may contribute to oxidative stress in many inflammatory processes. Corilagin, a component of Phyllanthus urinaria, possesses antioxidant, anti-inflammatory, and hepatoprotective effects. We evaluated the mechanisms underlying the protective effect of corilagin against acetaminophen-induced liver injury. Mice were intraperitoneally administrated 300 mg/kg APAP or equal volume of saline (control), with or without various concentrations of corilagin (0, 1, 5, or 10 mg/kg) administered after 30 min. All animals were sacrificed 16 h after APAP administration, and serum and liver tissue assays including histology, immunohistochemistry, and Western blot assay were performed. Corilagin post-treatment significantly attenuated APAP-induced liver injury (p < 0.005), inflammatory cell infiltration, hepatic proinflammatory cytokine levels, and hepatic oxidative stress. Furthermore, corilagin attenuated the protein levels of NOX1, NOX2, signal transducer and activator of transcription 3 (STAT3), and nuclear factor kappa B (NF-κB) in APAP-induced liver injury. These results indicated that the antioxidant, anti-inflammatory, and protective effects of corilagin in APAP-induced liver injury might involve the regulation of interleukin (IL)-6/STAT3 and mitogen-activated protein kinase (MAPK)/NF-κB signaling pathways through NOX-derived ROS.