Ginsenoside Rg1 prevents acetaminophen-induced oxidative stress and apoptosis via Nrf2/ARE signaling pathway

Inappropriate use of acetaminophen (APAP) can lead to morbidity and mortality secondary to hepatic necrosis. Ginsenoside Rg1 is a major active ingredient in processed Panax ginseng, which is proved to elicit biological effects. We hypothesized the beneficial effect of Rg1 on APAP-mediated hepatotoxicity was through Nrf2/ARE pathway. The study was conducted in cells and mice, comparing the actions of Rg1. Rg1 significantly improved cell survival rates and promoted the expression of antioxidant proteins. Meanwhile, Rg1 reduced the excessive ROS and the occurrence of cell apoptosis, which were related to Nrf2/ARE pathway. Expression of Nrf2 has a certain cell specificity.

     

“Driven and Tense,Stressed Out and Anxious”: Clinicians’ Perceptions of Post-Traumatic Stress Disorder Symptom Expressions in Adults with Autism and Intellectual Disability

ABSTRACT

Introduction

Individuals with autism spectrum disorder (ASD) and intellectual disability (ID) seem to be at increased risk for post-traumatic stress disorder (PTSD), but knowledge is sparse regarding its identification in this population. Previous research indicates that certain symptoms of PTSD may be more easily recognized, and that identifying reexperiencing and avoidance is particularly challenging.     

脑卒中患者急性应激障碍及影响因素研究

目的探讨脑卒中患者急性应激障碍发生现状及影响因素。方法采用斯坦福急性应激反应问卷对349例脑卒中住院患者进行调查。结果共163例(46.70%)患者发生急性应激障碍;Logistic回归分析结果显示,患者性格、是否存在偏瘫及是否吞咽功能障碍是脑卒中患者发生急性应激障碍的主要影响因素(P0.05,P0.01)。结论脑卒中患者急性应激障碍发生率较高,内向性格及存在偏瘫和吞咽功能障碍的患者更容易发生急性应激障碍。医护人员应及时为高危患者提供个体化治疗及预见性护理,防止脑卒中患者发生急性应激障碍。     

Losing the uphill battle? Emergent harm reduction interventions and barriers during the opioid overdose crisis in Canada

Canada continues to experience an escalating opioid overdose crisis that has claimed more than 8000 lives in the country since 2016. The presence of the synthetic opioid fentanyl and its analogues is a central contributor to the increases in preventable opioid-related deaths. However, a number of converging social-structural factors (e.g., the continued criminalisation of drug use, political changes) and political barriers are also complicating and contributing to the current crisis. We briefly outline four harm reduction interventions (i.e., injectable opioid agonist treatment, naloxone distribution programs, overdose prevention sites, and drug checking services) as emerging and rapidly expanding responses to this crisis in Canada. These examples of innovation and expansion are encouraging but also occurring at the same time that the opioid overdose crisis shows few signs of abating. To truly address the crisis, Canada needs political environments at all government levels that are responsive and foster harm reduction innovation and drug policy experimentation.     

Synergism through combination of chemotherapy and oxidative stress-induced autophagy in A549 lung cancer cells using redox-responsive nanohybrids: A new strategy for cancer therapy

A combination of various therapeutic approaches has emerged as a promising strategy for cancer treatment. A safe and competent nano-delivery system is thus in urgent demand to facilitate the simultaneous transport of various therapeutic agents to cancer cells and a tumor region to achieve synergistic effect. Gold nanoparticles (GNPs) and mesoporous silica nanoparticle (MSNs) were fabricated herein as potential candidates for drug delivery. Serving as gatekeepers, GNPs (5 nm in diameter) were attached onto the amino-functionalized MSNs (denoted as NMSNs) via a relatively weak gold–nitrogen bonding. The resulting nanohybrids (denoted as GCMSNs) were uptaken by cells, and the detachment of GNPs and subsequent intracellular drug release from NMSNs were achieved by competitive binding of intracellular glutathione to GNPs. In addition to the function of gatekeeping, GNPs also play another role as the oxidative stress elicitor. Our in vitro studies revealed that GCMSNs induced higher oxidative stress in lung cancer cells (A549) than in normal cells (3T3-L1). This growth inhibitory effect found in the cancer cells was likely induced by mitochondria dysfunction originated from the GCMSN-induced, oxidative stress-triggered mitochondria-mediated autophagy. The redox-responsive nanohybrids were further loaded with camptothecin and the intensified synergistic therapeutic effects were observed associated with combined chemotherapy and oxidative stress strategy. The results clearly demonstrate that such unique nanohybrids hold great promise for selective and effective cancer treatments.