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Objective: Failure to rescue (FTR), defined as in-hospital death following a major complication, has been increasingly studied in patients who undergo cardiothoracic surgery. This study tested the hypothesis that elderly patients undergoing lung cancer resection have greater rates of FTR compared with younger patients. Methods: Patients who underwent surgery for primary lung cancer between 2011 and 2020 and had at least 1 major postoperative complication were identified using the National Surgical Quality Improvement Program database. Patients who died following complications (FTR) were compared with those who survived in an elderly (80+ years) and younger (

G protein-coupled receptor 120 (GPR120) and PPARγ agonists each have insulin sensitizing effects. But whether these two pathways functionally interact and can be leveraged together to markedly improve insulin resistance has not been explored. Here, we show that treatment with the PPARγ agonist rosiglitazone (Rosi) plus the GPR120 agonist Compound A leads to additive effects to improve glucose tolerance and insulin sensitivity, but at lower doses of Rosi, thus avoiding its known side effects. Mechanistically, we show that GPR120 is a PPARγ target gene in adipocytes, while GPR120 augments PPARγ activity by inducing the endogenous ligand 15d-PGJ2 and by blocking ERK-mediated inhibition of PPARγ. Further, we used macrophage- (MKO) or adipocyte-specific GPR120 KO (AKO) mice to show that GRP120 has anti-inflammatory effects via macrophages while working with PPARγ in adipocytes to increase insulin sensitivity. These results raise the prospect of a safer way to increase insulin sensitization in the clinic.

A microfluidic strategy has been used for the time- and labour-efficient evaluation of the relative efficiency and thermodynamic parameters of CO2 binding by three Lewis acid/base combinations, where efficiency is based on the amount of CO2 taken up per binding unit in solution. Neither tBu3P nor B(C6F5)3 were independently effective at CO2 capture, and the combination of the imidazolin-2-ylidenamino-substituted phosphine (NIiPr)3P and B(C6F5)3 was equally ineffective. Nonetheless, an archetypal frustrated Lewis pair (FLP) comprised of tBu3P and B(C6F5)3 was shown to bind CO2 more efficiently than either the FLP derived from tetramethylpiperidine (TMP) and B(C6F5)3 or the highly basic phosphine (NIiPr)3P. Moreover, the proposed microfluidic platform was used to elucidate the thermodynamic parameters for these reactions.

A microfluidic strategy has been used for the time- and labour-efficient evaluation of the relative efficiency and thermodynamic parameters of CO2 binding by three Lewis acid/base combinations, where efficiency is based on the amount of CO2 taken up per binding unit in solution. Neither tBu3P nor B(C6F5)3 were independently effective at CO2 capture, and the combination of the imidazolin-2-ylidenamino-substituted phosphine (NIiPr)3P and B(C6F5)3 was equally ineffective. Nonetheless, an archetypal frustrated Lewis pair (FLP) comprised of tBu3P and B(C6F5)3 was shown to bind CO2 more efficiently than either the FLP derived from tetramethylpiperidine (TMP) and B(C6F5)3 or the highly basic phosphine (NIiPr)3P. Moreover, the proposed microfluidic platform was used to elucidate the thermodynamic parameters for these reactions.

The current dogma is that obesity-associated hepatic inflammation is due to increased Kupffer cell (KC) activation. However, recruited hepatic macrophages (RHMs) were recently shown to represent a sizable liver macrophage population in the context of obesity. Therefore, we assessed whether KCs and RHMs, or both, represent the major liver inflammatory cell type in obesity. We used a combination of in vivo macrophage tracking methodologies and adoptive transfer techniques in which KCs and RHMs are differentially labeled with fluorescent markers. With these approaches, the inflammatory phenotype of these distinct macrophage populations was determined under lean and obese conditions. In vivo macrophage tracking revealed an approximately sixfold higher number of RHMs in obese mice than in lean mice, whereas the number of KCs was comparable. In addition, RHMs comprised smaller size and immature, monocyte-derived cells compared with KCs. Furthermore, RHMs from obese mice were more inflamed and expressed higher levels of tumor necrosis factor-α and interleukin-6 than RHMs from lean mice. A comparison of the MCP-1/C-C chemokine receptor type 2 (CCR2) chemokine system between the two cell types showed that the ligand (MCP-1) is more highly expressed in KCs than in RHMs, whereas CCR2 expression is approximately fivefold greater in RHMs. We conclude that KCs can participate in obesity-induced inflammation by causing the recruitment of RHMs, which are distinct from KCs and are not precursors to KCs. These RHMs then enhance the severity of obesity-induced inflammation and hepatic insulin resistance.

It is well known that the ω-3 fatty acids (ω-3-FAs; also known as n-3 fatty acids) can exert potent anti-inflammatory effects. Commonly consumed as fish products, dietary supplements and pharmaceuticals, ω-3-FAs have a number of health benefits ascribed to them, including reduced plasma triglyceride levels, amelioration of atherosclerosis and increased insulin sensitivity. We reported that Gpr120 is the functional receptor for these fatty acids and that ω-3-FAs produce robust anti-inflammatory, insulin-sensitizing effects, both in vivo and in vitro, in a Gpr120-dependent manner. Indeed, genetic variants that predispose to obesity and diabetes have been described in the gene encoding GPR120 in humans (FFAR4). However, the amount of fish oils that would have to be consumed to sustain chronic agonism of Gpr120 is too high to be practical, and, thus, a high-affinity small-molecule Gpr120 agonist would be of potential clinical benefit. Accordingly, Gpr120 is a widely studied drug discovery target within the pharmaceutical industry. Gpr40 is another lipid-sensing G protein-coupled receptor, and it has been difficult to identify compounds with a high degree of selectivity for Gpr120 over Gpr40 (ref. 11). Here we report that a selective high-affinity, orally available, small-molecule Gpr120 agonist (cpdA) exerts potent anti-inflammatory effects on macrophages in vitro and in obese mice in vivo. Gpr120 agonist treatment of high-fat diet-fed obese mice causes improved glucose tolerance, decreased hyperinsulinemia, increased insulin sensitivity and decreased hepatic steatosis. This suggests that Gpr120 agonists could become new insulin-sensitizing drugs for the treatment of type 2 diabetes and other human insulin-resistant states in the future.

Background: Taiwan has advocated health-promoting schools (HPS) since 2001 and established the Health-Promoting School Supporting Network (HPSSN) in 2005 to offer administrative support and consultation. Respondents' opinions about HPSSN and the relationship between these perceptions and HPS implementation were examined. Methods: In 2011, 800 primary and middle schools were selected through stratified random sampling. School staff members (N = 656) in charge of HPS programs reported their impressions of the HPSSN's support. Results:Respondents were most satisfied with consultants and schools' recognition of responsibilities and rules and their interactions with HPSSN administrators. They were least satisfied with the extent of their HPSSN consultant interaction and believed HPSSN provided insufficient resources to establish HPS. Respondents' consultant partnerships and satisfaction with HPSSN administration significantly predicted HPS implementation. Additionally, the predictive values of healthy policies and school-community relationships were greater than the other 6 HPS components. Conclusions: HPSSN positively influenced HPS implementation; however, consultant/school partnerships and school resource allocations must be improved.

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Background: We hypothesized that the ratio of positive lymph nodes to total assessed lymph nodes (LNR) is an indicator of cancer burden in esophageal adenocarcinoma and may identify patients who may most benefit from AC. Objective: The aim of this study was to discern whether there is a threshold LNR above which AC is associated with a survival benefit in this population. Methods: The 2004-2015 National Cancer Database was queried for patients who underwent upfront, complete resection of pT1-4N1-3M0 esophageal adenocarcinoma. The primary outcome, overall survival, was examined using multivariable Cox proportional hazards models employing an interaction term between LNR and AC. Results: A total of 1733 patients were included: 811 (47%) did not receive AC whereas 922 (53%) did. The median LNR was 20% (interquartile range 9-40). In a multivariable Cox model, the interaction term between LNR and receipt of AC was significant (P = 0.01). A plot of the interaction demonstrated that AC was associated with improved survival beyond a LNR of about 10%-12%. In a sensitivity analysis, the receipt of AC was not associated with improved survival in patients with LNR <12% (hazard ratio 1.02; 95% confidence interval 0.72-1.44) but was associated with improved survival in those with LNR >=12% (hazard ratio 0.65; 95% confidence interval 0.50-0.79). Conclusions: In this study of patients with upfront, complete resection of node-positive esophageal adenocarcinoma, AC was associated with improved survival for LNR >=12%. LNR may be used as an adjunct in multidisciplinary decision-making about adjuvant therapies in this patient population. [ABSTRACT FROM AUTHOR]

Introduction The spleen plays a role in the immune and coagulative responses, yet a splenectomy may be required during ovarian cancer surgery to achieve complete cytoreduction. The aim of the study was to correlate hematologic changes with the development of infection and venous thromboembolism in patients undergoing splenectomy. Methods This single-institution retrospective review includes all patients undergoing splenectomy during cytoreductive surgery for advanced ovarian cancer, March 2001 to December 2016. We compared postoperative hematologic changes (evaluated daily before discharge) in patients developing infection within 30 days' post-surgery (Infection group) with those who did not (No-Infection group). We also compared patients developing venous thromboembolism with those without. Results A total of 265 patients underwent splenectomy. Median age was 64 years (range 22-88): 146 (55%) patients had stage IIIC and 114 (43%) patients had stage IV. The majority, 201 (76%) patients underwent splenectomy during primary debulking. A total of 132 (50%) patients comprised the Infection group (most common: urinary tract infection, 54%). Median time from surgery to infection was 8 days (range, 0-29). After initial rise in white blood cell count in both groups, the Infection group had a second peak on postoperative day 10 (median 16.6K/mcL, IQR 12.5-21.2) not seen in the No-Infection group (median 12K/mcL, IQR 9.3-16.3). A total of 40 (15%) patients developed venous thromboembolism, median time of 6.5 days (range, 1-43). All patients demonstrated a continuous rise in platelets during postoperative days 0-15. Thrombocytosis was present in 38/40 (95%) patients with venous thromboembolism vs 183/225 (81%) patients without (P=0.036). Median days with thrombocytosis was higher in venous thromboembolism (8 days, range 1-15) vs non groups (6 days, range 1-16, P=0.049). Conclusion We identified initial leukocytosis after splenectomy in all patients. The Infection group had a second peak in white blood cell count on postoperative day 10, not present in the No-Infection group. Among patients with venous thromboembolism, thrombocytosis was more frequent and of longer duration. [ABSTRACT FROM AUTHOR]