Evaluating a Food Pantry–Based Intervention to Improve Food Security,Dietary Intake,and Quality in Midwestern Food Pantries

BackgroundVoices for Food was a longitudinal community, food pantry–based intervention informed by the social ecological model, and designed to improve food security, dietary intake, and quality among clients, which was carried out in 24 rural food pantries across 6 Midwestern states.ObjectiveOur objective was to evaluate changes in adult food security, dietary intake, and quality from baseline (2014) to follow-up (2016), and to assess the role of adult food security on dietary outcomes.DesignA multistate, longitudinal, quasi-experimental intervention with matched treatment and comparison design was used to evaluate treatment vs comparison group changes over time and changes in both groups over time.Participants/settingAdult food pantry clients (n = 617) completed a demographic food security survey, and up to three 24-hour dietary recalls at baseline (n = 590) and follow-up (n = 160).InterventionCommunity coaching served as the experimental component, which only “treatment” communities received, and a food council guide and food pantry toolkit were provided to both “treatment” and matched “comparison” communities.Main outcome measuresChange in adult food security status, mean usual intakes of nutrients and food groups, and Healthy Eating Index-2010 scores were the main outcome measures.Statistical analyses performedLinear mixed models estimated changes in outcomes by intervention group and by adult food security status over time.ResultsImprovements in adult food security score (–0.7 ± 0.3; P = .01), Healthy Eating Index-2010 total score (4.2 ± 1.1; P < .0001), and empty calories component score (3.4 ± 0.5; P <.0001) from baseline to follow-up were observed in treatment and comparison groups, but no statistically significant changes were found for adult food security status, dietary quality, and usual intakes of nutrients and food groups between the 2 groups over time. The intervention effect on dietary quality and usual intake changes over time by adult food security status were also not observed.ConclusionsFood pantry clients in treatment and comparison groups had higher food security and dietary quality at the follow-up evaluation of the Voices for Food intervention trial compared with baseline, despite the lack of difference among the groups as a result of the experimental coaching component.     

胆囊结石合并胆总管结石术后患者复发情况及危险因素分析

目的 探讨胆囊结石合并胆总管结石(CBDS)术后患者复发情况及危险因素。方法 纳入114例2019年1月~2020年12月在本院行ECRP联合LC治疗的胆囊结石合并CBDS患者,回顾性分析其临床资料,根据所选患者ECRP联合LC术后随访1年内是否复发(REC)将其分为REC组(32例)和未REC组(82例)。回顾性统计胆囊结石合并CBDS术后患者REC情况,比较REC组和未REC组的临床资料,并分析胆囊结石合并CBDS术后患者REC的危险因素。结果 114例胆囊结石合并CBDS术后患者REC32例,发生率28.07%。胆囊结石合并CBDS术后患者REC的危险因素为胆道感染、胆道口括约肌切开、术者经验≤3年、胆道括约肌功能障碍(OR=4.170、4.047、3.568、3.367,P<0.05)。结论 胆囊结石合并CBDS术后患者REC的危险因素与胆道感染、胆道口括约肌切开、术者经验≤3年、胆道括约肌功能障碍密切相关,可据此针对性制定临床治疗及护理干预措施方案,以降低胆囊结石合并CBDS术后患者REC率。     

PCI术后病人的体力活动水平及其影响因素分析研究

目的:探讨经皮冠状动脉介入(PCI)术后病人的体力活动水平及其影响因素。方法:选择常州市三级甲等综合医院心内科接受PCI治疗的冠心病病人,收集资料,分析PCI术后冠心病病人体力活动动机、体力活动和自我效能现状;冠心病病人自我效能、体力活动动机与体力活动的相关性,并分析影响PCI术后病人体力活动水平的相关危险因素。结果:共发放调查问卷400份,回收400份,有效率为94.75%(379/400);379例冠心病病人术后每周体力活动为(3570.85±314.19)MET-min,以低、中强度为主;冠心病病人术后自我效能总分、体力活动动机总分与体力活动呈正相关(P<0.05);体质指数(BMI)、PCI次数≥2次、年龄、PCI支架数量≥3枚、自我效能、体力活动动机是影响PCI术后冠心病病人体力活动水平的高危因素(OR>1且P<0.05)。结论:PCI术后病人体力活动水平处于较低的水平,PCI次数、BMI、年龄、PCI支架数量、自我效能、体力活动动机是影响PCI术后冠心病病人体力活动水平的高危因素,临床需针对各高危因素制定相应的干预措施,提高病人体力活动水平。     

PARP7 negatively regulates the type I interferon response in cancer cells and its inhibition triggers antitumor immunity

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Fluoxetine-induced hepatic lipid accumulation is mediated by prostaglandin endoperoxide synthase 1 and is linked to elevated 15-deoxy-Δ12,14PGJ2

Major depressive disorder and other neuropsychiatric disorders are often managed with long-term use of antidepressant medication. Fluoxetine, an SSRI antidepressant, is widely used as a first-line treatment for neuropsychiatric disorders. However, fluoxetine has also been shown to increase the risk of metabolic diseases such as non-alcoholic fatty liver disease. Fluoxetine has been shown to increase hepatic lipid accumulation in vivo and in vitro. In addition, fluoxetine has been shown to alter the production of prostaglandins which have also been implicated in the development of non-alcoholic fatty liver disease. The goal of this study was to assess the effect of fluoxetine exposure on the prostaglandin biosynthetic pathway and lipid accumulation in a hepatic cell line (H4-II-E-C3 cells). Fluoxetine treatment increased mRNA expression of prostaglandin biosynthetic enzymes (Ptgs1, Ptgs2, and Ptgds), PPAR gamma (Pparg), and PPAR gamma downstream targets involved in fatty acid uptake (Cd36, Fatp2, and Fatp5) as well as production of 15-deoxy-Δ^12,14PGJ₂ a PPAR gamma ligand. The effects of fluoxetine to induce lipid accumulation were attenuated with a PTGS1 specific inhibitor (SC-560), whereas inhibition of PTGS2 had no effect. Moreover, SC-560 attenuated 15-deoxy-Δ^12,14PGJ₂ production and expression of PPAR gamma downstream target genes. Taken together these results suggest that fluoxetine-induced lipid abnormalities appear to be mediated via PTGS1 and its downstream product 15d-PGJ₂ and suggest a novel therapeutic target to prevent some of the adverse effects of fluoxetine treatment.     

Hepatotoxicity of cantharidin is associated with the altered bile acid metabolism

Cantharidin (CTD) is an effective antitumor agent. However, it exhibits significant hepatotoxicity, the mechanism of which remains unclear. In this study, biochemical and histopathological analyses complemented with ultra-high-performance liquid chromatography–tandem mass spectrometry (UHPLC-MS/MS)-based targeted metabolomic analysis of bile acids (BAs) were employed to investigate CTD-induced hepatotoxicity in rats. Sixteen male and female Sprague–Dawley rats were randomly divided into two groups: control and CTD (1.0 mg/kg) groups. Serum and liver samples were collected after 28 days of intervention. Biochemical, histopathological, and BA metabolomic analyses were performed for all samples. Further, the key biomarkers of CTD-induced hepatotoxicity were identified via multivariate and metabolic pathway analyses. In addition, metabolite–gene–enzyme network and Kyoto Encyclopedia of Genes and Genomes pathway analyses were used to identify the signaling pathways related to CTD-induced hepatotoxicity. The results revealed significantly increased levels of biochemical indices (alanine aminotransferase, aspartate aminotransferase, and total bile acid). Histopathological analysis revealed that the hepatocytes were damaged. Further, 20 endogenous BAs were quantitated via UHPLC-MS/MS, and multivariate and metabolic pathway analyses of BAs revealed that hyocholic acid, cholic acid, and chenodeoxycholic acid were the key biomarkers of CTD-induced hepatotoxicity. Meanwhile, primary and secondary BA biosynthesis and taurine and hypotaurine metabolism were found to be associated with the mechanism by which CTD induced hepatotoxicity in rats. This study provides useful insights for research on the mechanism of CTD-induced hepatotoxicity.