Do social support and community engagement act as mechanisms in the association between neighbourhood income inequality and the mental health of mothers in Calgary,Canada? A mediation analysis

PurposeAccording to the social determinants of health framework, income inequality is a potential risk factor for adverse mental health. However, few studies have explored the mechanisms suspected to mediate this relationship. The current study addresses this gap through a mediation analysis to determine if social support and community engagement act as mediators linking neighbourhood income inequality to maternal anxiety and depressive symptoms within a cohort of new mothers living in the City of Calgary, Canada.MethodsData collected at three years postpartum from mothers belonging to the All Our Families (AOF) cohort were used in the current study. Maternal data were collected between 2012 and 2015 and linked to neighbourhood socioeconomic data from the 2006 Canadian Census. Income inequality was measured using Gini coefficients derived from 2006 after-tax census data. Generalized structural equation models were used to quantify the associations between income inequality and mental health symptoms, and to assess the potential direct and indirect mediating effects of maternal social support and community engagement.ResultsIncome inequality was not significantly associated with higher depressive symptoms (β = 0.32, 95%CI = −0.067, 0.70), anxiety symptoms (β = 0.11, 95%CI = −0.39, 0.60), or lower social support. Income inequality was not associated with community engagement. For the depression models, higher social support was significantly associated with lower depressive symptoms (β = −0.13, 95%CI = −0.15, −0.097), while community engagement was not significantly associated with depressive symptoms (β = 0.059, 95%CI = −0.15, 0.27). Similarly, for the anxiety models, lower anxiety symptoms were significantly associated with higher levels of social support (β = −0.17, 95%CI = −0.20, −0.13) but not with higher levels of community engagement (β = 0.14, 95%CI = −0.14, 0.41).ConclusionThe current study did not find clear evidence for social support or community engagement mediating the relationship between neighbourhood income inequality and maternal mental health. Future investigations should employ a broader longitudinal approach to capture changes in income inequality, potential mediators, and mental health symptomatology over time.     

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

75" alt="">

1. Download : Download high-res image (204KB)
2. Download : Download full-size image

     

SLC及其受体CCR7与Ⅰ期非小细胞肺癌淋巴结微转移的相关性

目的 探讨溶质载体蛋白（SLC）及其受体趋化因子受体7（CCR7）与I期非小细胞肺癌（NSCLC）淋巴结微转移的相关性。方法 选取2019年1月~2020年3月于我院就诊的I期NSCLC患者127例为研究对象，按照淋巴结微转移情况分为对照组92例和转移组35例，所有患者入院后均通过根治术切除病灶，通过免疫组化方式检测病灶中SLC7A11及CCR7含量，并收集患者临床资料、实验室检查资料及影像学检查资料。通过Logistic回归分析评价SLC7A11及CCR7与淋巴结微转移之间的关系。最后通过建立ROC曲线分析两者及其联合检测对NSCLC患者微淋巴结转移的预测价值。结果 两组患者SLC7A11及CCR7表达水平存在显著差异（P＜0.05）。转移组患者病灶直径、支气管受累及TLG显著高于对照组（P＜0.05）。病灶直径（OR=49.254,95%CI=11.062~507.604）是影响NSCLC淋巴结微转移的独立危险因素（P＜0.05）。SLC7A11（OR=8.622）及CCR7（OR=8.709）表达水平是影响NSCLC淋巴结微转移的独立因素（P＜0.05）。SLC7A11、CCR7及联合诊断对NSCLC淋巴结微转移具有较好的检测价值（均P＜0.05）。联合检测特异度显著高于 SLC7A11及CCR7单独检测（2=7.292，15.125；均P＜0.01）。结论 SLC家族的中SLC7A11及其受体CCR7与NSCLC患者微淋巴结转移显著相关。     

股骨转子间骨折的稳定性重建概念演化与研究进展

�76ee;�7684;总�7ed3;近^74;765;股骨转子间骨折728;�7a33;定؂7;重建方 762;�7684;概念演化与�7814;�7a76;进展。方法7e5;阅国内外�76f8;Q73;٘7;�732e;^76;�7ed3;合自身�7ecf;验，从股骨转子间骨折�7684;解剖�7279;�70b9;、�7a33;定78b;骨折与不�7a33;定78b;骨折分�7c7b;、�7a33;定؂7;复位与不�7a33;定؂7;复位、72f;中加压初始�7a33;定与72f;后滑动二次�7a33;定、内固定72f;后�7a33;定؂7;评估、早71f;下730;�7ad9;�7acb;负重�7b49;方 762;进行总�7ed3;分790;。�7ed3;79c;股骨转子间骨折发�751f;于股骨颈^72;骺�7aef;转换区，Q77;709;天�7136;�7684;内�7ffb;不�7a33;定倾向。骨折复位质量是_71;响后�7eed;内固定�7269;安放�7684;700;重要前提因�7d20;。判断骨折复位质量709;对�7ebf;和对位两方 762;，对�7ebf;ज7;�7528; Garden ذ7;e70;；728;对位方 762;，随�7740;�76ae;质对位�7406;念（正؂7;、中؂7;、负؂7;）�7684;提出，�7279;别强调前内Ӻ7;�76ae;质�7684;�76f8;互�7825;住支撑（解剖、正؂7;），是࠻7;׹7;骨折�7a33;定؂7;复位�7684;Q73;键，而不再强调后内Ӻ7;小转子骨757;�7684;作�7528;。72f;后_71;像学�7684;�7a33;定؂7;评分为早71f;下730;�7ad9;�7acb;负重提供了量化ذ7;ڀ7;。但72f;中�7684;前内Ӻ7;�76ae;质支撑复位，728;72f;后头颈骨757;滑动࠻7;׹7;二次�7a33;定�7684;ࣼ7;�7a0b;中，仍709;�76ae;质对位丢失�73b0;象， 700;�7814;�7a76;Q76;S71;险因�7d20;和防范措施。�7ed3;论股骨转子间骨折728;取׹7;良Y7d;对�7ebf;�7684;7fa;�7840;上，只要࠻7;׹7;了前内Ӻ7;�76ae;质�7684;�76f8;互�7825;住和支撑，^76;�7528;内固定器械�7ef4;持住，就࠻7;׹7;了72f;后�7a33;定؂7;。72f;后�7a33;定؂7;评分优良者，可以安全730;早71f;下730;负重、�7ad9;�7acb;行70;活动。     

Efeitos Terapêuticos da Tripla Antiagregação Plaquetária em Pacientes Femininas Idosas com Diabetes e Infarto Agudo do Miocárdio

BackgroundDual antiplatelet therapy (DAPT) is the cornerstone treatment of acute myocardial infarction (AMI).ObjectiveThe present study aimed to investigate the efficacy and safety of triple antiplatelet therapy (TAPT) in elderly female patients with diabetes and ST segment elevation myocardial infarction (STEMI), who had undergone percutaneous coronary intervention (PCI).MethodsWe designed a randomized, single-blind study. Control group A (97 elderly male patients with diabetes and STEMI, whose CRUSADE scores were < 30) received aspirin, ticagrelor, and tirofiban. A total of 162 elderly female patients with diabetes and STEMI were randomly divided into two groups according to CRUSADE score. Group B (69 patients with CRUSADE score > 31) received aspirin and ticagrelor. Group C (93 patients with CRUSADE score < 30) received aspirin, ticagrelor and tirofiban. P values < 0.05 were considered statistically significant.ResultsCompared to the findings in group A, post-PCI Thrombolysis in Myocardial Infarction (TIMI) grade 3 blood flow and TIMI myocardial perfusion grade 3 were significantly less prevalent in group B (p < 0.05). When compared to groups A and C, the incidence of major adverse complications was significantly higher in group B (p < 0.05).ConclusionTAPT could effectively reduce the incidence of major complications in elderly female patients with diabetes and STEMI. However, close attention should be paid to hemorrhage in patients receiving TAPT. (Arq Bras Cardiol. 2020; [online].ahead print, PP.0-0)     

PD-L1高表达晚期非小细胞肺癌患者单纯免疫治疗与免疫联合化疗疗效比较

背景与�76ee;�7684;以免�75ab;检7e5;�70b9;抑制剂（immune checkpoint inhibitors, ICIs）为代表�7684;免�75ab;治�7597;越765;越^7f;泛730;应�7528;于肺�764c;治�7597;。�7136;而，对于�7a0b;序؂7;k7b;亡Խ7;体配体1（programmed cell death-ligand 1, PD-L1）高表达，S73;肿�7624;比例评分（tumor proportion score, TPS）≥50%�7684;晚71f; 75e;小�7ec6;胞肺�764c;（non-small cell lung cancer, NSCLC）患者，ज7;�7528;单�7eaf;免�75ab;治�7597;还是免�75ab;联合化�7597;728;临床上仍存争议。72c;�7814;�7a76;旨728;评估PD-L1高表达�7684;晚71f;NSCLC患者接Խ7;单�7eaf;免�75ab;治�7597;与免�75ab;联合化�7597;�7684;�7597;效。方法72c;�7814;�7a76;回˜7e;؂7;分790;了49例PD-L1高表达晚71f;NSCLC患者�7684;临床资料。PD-L1表达ज7;�7528;22C3ة7;体行免�75ab;�7ec4;化7d3;‚72;，按TPS判读PD-L1表达水^73;。比较不同临床�7279;征分�7ec4;患者�7684;客观�7f13;解�7387;（objective response rate，ORR）和无进展�751f;存时间（progression free survival, PFS）。�7ed3;79c;免�75ab;单药与免�75ab;联合化�7597;�7ec4;�7684;ORR分别为47.1%（8/17）和43.8%（14/32），差异无�7edf;计学意义（P=0.825）。免�75ab;单药与免�75ab;联合化�7597;�7ec4;�7684;中位PFS分别为8.0个708;和6.8个708;，差异无�7edf;计学意义（P=0.502）。^76;对72c;�7ec4;PD-L1高表达患者免�75ab;治�7597;�7684;预测因�7d20;进行了分790;，�7ed3;79c;显�793a;，一�7ebf;免�75ab;治�7597;ORR（12/19, 63.2%）显ࡅ7;优于二�7ebf;及以上免�75ab;治�7597;（10/30, 33.3%），差异709;�7edf;计学意义（P=0.041），二者间PFS无差异。^74;龄、؂7;别、吸�70df;史、功能�72b6;态评分（performance status, PS）、�75c5;�7406;�7c7b;78b;、肿�7624;֒7;小、肿�7624;淋巴�7ed3;转�79fb;（tumor node metastasis, TNM）分71f;与ORR和PFS不�76f8;Q73;。�7ed3;论PD-L1高表达�7684;晚71f;NSCLC患者接Խ7;免�75ab;单药和免�75ab;联合化�7597;�7684;�7597;效�76f8;近。PD-L1高表达患者一�7ebf;免�75ab;治�7597;�7684;ORR更O73;。对此�7c7b;人�7fa4;�7684;700;O73;治�7597;方案709;待于前�77bb;؂7;临床�7814;�7a76;进一步探�7d22;。     

Redox active or thiol reactive? Optimization of rapid screens to identify less evident nuisance compounds

Compounds that exhibit assay interference or undesirable mechanisms of bioactivity are routinely encountered in assays at various stages of drug discovery. We observed that assays for the investigation of thiol-reactive and redox-active compounds have not been collected in a comprehensive review. Here, we review these assays and subject them to experimental optimization to improve their reliability. We demonstrate the usefulness of our assay cascade by assaying a library of bioactive compounds, chemical probes, and a set of approved drugs. These high-throughput assays should complement the array of wet-lab and in silico assays during the initial stages of hit discovery campaigns to pursue only hit compounds with tractable mechanisms of action.