Besides, the ligustrazine-induced cell apoptosis and cell cycle arrest were markedly reversed by pifithrin-α (p53 inhibitor), which suggested that ligustrazine-induced cell apoptosis was achieved by regulating p53-dependent mitochondrial pathway and cell cycle arrest at the G0/G1 phase.
 
  These findings demonstrated that ligustrazine could induce SW480 and CT26 cells apoptosis via a p53-dependent mitochondrial pathway and cell cycle arrest at the G0/G1 phase. Ligustrazine may serve as a potential anti-cancer agent for CRC.
 These findings demonstrated that ligustrazine could induce SW480 and CT26 cells apoptosis via a p53-dependent mitochondrial pathway and cell cycle arrest at the G0/G1 phase. Ligustrazine may serve as a potential anti-cancer agent for CRC.
  An increasing number of jurisdictions around the world are legalizing assisted dying. This creates a particular challenge for the field of palliative care, which often precludes producing premature death by the injection or self-administration of lethal medications upon a patient's voluntary request. A 2019 systematic scoping review of the literature about the relationship between palliative care and assisted dying in contexts where assisted dying is lawful, found just 16 relevant studies that included varied and combined stances ranging from complete opposition, to collaboration and integration. Building on that review, the present study was conducted in Quebec (Canada), Flanders (Belgium), and Oregon (USA), with the objective of exploring the relationship between palliative care and assisted dying in these settings, from the perspective of clinicians and other professionals involved in the practice.
 
  Semi-structured in-depth qualitative interviews were conducted with 29 professionals from Oregon [10], Qua better understanding of whether and in what ways assisted dying presents a threat to palliative care.
 No clear and uniform relationship between palliative care and assisted dying can be identified in any of the three locations. The context and practicalities of how assisted dying is being implemented alongside access to palliative care need to be considered to inform future laws. We seek a better understanding of whether and in what ways assisted dying presents a threat to palliative care.
  Oxidative stress is one of the possible mechanisms in vancomycin (VCM) induced nephrotoxicity.  https://www.selleckchem.com/products/Eloxatin.html  Some studies suggested that high dose Vitamin C (VC) has protective effect against the nephrotoxicity in mice, but the underlying molecular mechanism is not mentioned. We investigated the potential targets of high dose VC against oxidative stress and inflammation induced by VCM in renal tubular epithelial cells.
 
  We conducted an in vitro study using an immortalized proximal tubule epithelial cell line from a normal adult human kidney (HK-2).
 
  VCM added to HK-2 cells caused an increase of cell death, oxidative stress and expression of inflammatory cytokines. Co-treatment with 0.5 and 1 mM VC attenuated 4-8 mM VCM induced cell death and increased the cell viability to 58-90%. VC significantly decreased lipid peroxidation and increased superoxide dismutase activity. The upregulations of NF-κB, TNF-α and IL-6 in HK-2 cells under 4 mM VCM were also reversed by 0.5 mM VC through the inhibition of oxidative stress.
 
  This study showed for the first time that VC can attenuate the VCM induced nephrotoxicity by decreasing lipid peroxidation and expression of inflammatory cytokines, and increasing superoxide dismutase 2 (SOD2) activity, this effect may relate to the regulation of ROS/NF-κB pathway.
 This study showed for the first time that VC can attenuate the VCM induced nephrotoxicity by decreasing lipid peroxidation and expression of inflammatory cytokines, and increasing superoxide dismutase 2 (SOD2) activity, this effect may relate to the regulation of ROS/NF-κB pathway.
  It is important to identify candidates who would benefit from target agent chemotherapy in advanced NSCLC patients. The purpose of this study is to evaluate the feasibility of DCE-MRI for early response evaluation in epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) treatment in patients with NSCLC.
 
  Seven patients were prospectively enrolled who have pathologically-proven NSCLC with EGFR mutations or at least 2 of the following factors; adenocarcinoma, female, or never-smokers. Patients were treated with gefitinib or erlotinib and the start of chemotherapy was denoted day 0. DCE-MRI was performed at day-1, day+7, and day+28. Longitudinal changes of perfusion parameters were quantified and compared to Response Evaluation Criteria in Solid Tumors (RECIST) results.
 
  Quantitative perfusion parameters; Ktrans, ve and vp of the lung cancer showed a significant decrease at day+7 (P=0.016), but no further significant decrease between day+7 and day+28 (P>0.05). Semiquantitative markers for tumor enhancement curve pattern; EA (enhancement amplitude), MS (maximum slope), and AUC (area under the curve) also showed a significant decrease at day+7 (P=0.016, 0.031, and 0.016, respectively), but no further significant decrease between day+7 and day+28 (P>0.05). When RECIST applied, all patient was in the stable disease at day+7 and three patients showed partial response (PR) at day+28. All seven patients showed PR by the 3-month follow-up.
 
  Perfusion parameters may be used as an early non-invasive imaging biomarker for the response evaluation of target agent treatment in NSCLC.
 Perfusion parameters may be used as an early non-invasive imaging biomarker for the response evaluation of target agent treatment in NSCLC.
  Chronic myelogenous leukemia (CML) is a malignant tumor formed by the clonal proliferation of bone marrow hematopoietic stem cells. CML is a relatively rare disease, mainly affecting elderly patients, but the prevalence of CML is expected to increase dramatically. The tyrosine kinase inhibitors (TKIs) have changed the CML patients' treatment patterns and improved its treatment effect, but drug resistance still remains a significant problem to be solved. Therefore, the identification of biomarkers of CML resistance involved therein is essential for treatment and prognosis prediction.
 
  Bioinformatics was used to analyze and construct a lncRNA-miRNA-mRNA network of CML resistance to dasatinib and predict key lncRNAs.
 
  By screening differentially expressed genes in CML resistant to dasatinib and comprehensively analyzing their functions and signal pathways, the core genes in these differential genes were found, and by predictive analysis of the upstream targets of these core genes. Finally, a network diagram containing lncRNA, miRNA, and mRNA was constructed.