Keap1-Nrf2 signaling pathway is one of the most important antioxidant signaling pathways, and its abnormal activation is related to cancer metastasis and drug resistance. Many studies have shown Keap1 and Nrf2 mutations are closely associated with cancer occurrence. However, few studies focus on Keap1-Nrf2 binding characteristics of cancer-associated mutations. The study investigated the molecular mechanism between Keap1/Nrf2 mutations and cancer. We have determined the crystal structure of the Keap1-Kelch domain with Nrf2 25-mer peptide. What's more, we clarified the molecular effects of Nrf2 and Nrf2 on the binding of Keap1 by the method isothermal titration calorimetry (ITC), differential scanning fluorimetry (DSF) and electrophoretic mobility shift assay (EMSA). Especially, we confirmed the effect of Thr80 and Pro85 mutations on Keap1/Nrf2 signaling pathway in HEK293T cells by RT-PCR and western blot (WB). Finally, we verified the effect of six cancer-related high-frequency somatic mutations Keap1 , Keap1 , Keap1 , Keap1 , Keap1 and Keap1 on binding with Nrf2 through ITC experiments. Nrf2 and Nrf2 play a vital role in the Keap1-Nrf2 interaction. Mutant or modification at position Thr80 will disrupt the interaction. Especially, Nrf2 and Nrf2 mutations activate the expression of cytoprotective genes in HEK293T cells. As for Keap1, except G364C, the binding affinity of other cancer-related mutants to Nrf2 hardly changed, which means that Keap1 mutants can activate Nrf2 without disrupting the binding to Nrf2. The study provides new insight into Keap1/Nrf2 signaling pathway and cancer.The study provides new insight into Keap1/Nrf2 signaling pathway and cancer.Severe liver diseases have been considered the most common causes of adult deaths worldwide. Until now, liver transplantation is known as the only effective treatment for end stage liver disease. However, it is associated with several problems, most importantly, the side effects of immunosuppressive drugs that should be used after transplantation, and the shortage of tissue donors compared to the increasing number of patients requiring liver transplantation. Currently, tissue/organ decellularization as a new approach in tissue engineering is becoming a valid substitute for managing these kinds of problems. Decellularization of a whole liver is an attractive procedure to create three-dimensional (3D) scaffolds that micro-architecturally and structurally are similar to the native one and could support the repair or replacement of damaged or injured tissue. In this review, the different methods used for decellularization of liver tissue have been reviewed. In addition, the current approaches to overcome the challenges in these techniques are discussed.Despite numerous studies on the mechanisms of cigarette smoking toxicity over the past three decades, some aspects remain obscure. Recent developments have drawn attention to some hopeful indicators that allow us to advance our awareness of cigarette-induced cell death. Ferroptosis is considered a type of governed death of cells distinguished by the iron-dependent lipid hydroperoxide deposition to fatal concentrations. Ferroptosis has been linked with pathological settings such as neurodegenerative diseases, cancer, heart attack, hemorrhagic stroke, traumatic brain injury, ischemia-reperfusion injury, and renal dysfunction. This review tries to explain the causal role of ferroptosis cascade in cigarette smoke-mediated toxicity and cell death, highlighting associations on potential action mechanisms and proposing suggestions for its detoxifying and therapeutic interventions. Exercise training increases circulating and tissue levels of angiotensin-(1-7) [Ang-(1-7)], which was shown to attenuate inflammation and fibrosis in different diseases. Here, we evaluated whether Ang-(1-7)/Mas receptor is involved in the beneficial effects of aerobic training in a chronic model of asthma. BALB/c mice were subjected to a protocol of asthma induced by ovalbumin sensitization (OVA; 4i.p. injections) and OVA challenge (3 times/week for 4weeks). Simultaneously to the challenge period, part of the animals was continuously treated with Mas receptor antagonist (A779, 1μg/h; for 28days) and trained in a treadmill (TRE; 60% of the maximal capacity, 1h/day, 5days/week during 4weeks). PGC1-α mRNA expression (qRT-PCR), plasma IgE and lung cytokines (ELISA), inflammatory cells infiltration (enzymatic activity assay) and airway remodeling (by histology) were evaluated. Blocking the Mas receptor with A779 increased IgE and IL-13 levels and prevented the reduction in extracellular matrix deposition in airways in OVA-TRE mice. Mas receptor blockade prevented the reduction of myeloperoxidase activity, as well as, prevented exercise-induced IL-10 increase. These data show that activation of Ang-(1-7)/Mas receptor pathway is involved in the anti-inflammatory and anti-fibrotic effects of aerobic training in an experimental model of chronic asthma. Our results support exercise training as a non-pharmacological tool to defeat lung remodeling induced by chronic pulmonary inflammation. Epacadostat mouse Further, our result also supports development of new therapy based on Ang-(1-7) or Mas agonists as important tool for asthma treatment in those patients that cannot perform aerobic training.Our results support exercise training as a non-pharmacological tool to defeat lung remodeling induced by chronic pulmonary inflammation. Further, our result also supports development of new therapy based on Ang-(1-7) or Mas agonists as important tool for asthma treatment in those patients that cannot perform aerobic training. To determine the association between diabetes status, glycemia, and cognitive function among a national U.S. sample of older adults in the 2011-2014 National Health and Nutrition Examinations Surveys. Among 1,552 adults age≥60years, linear and multivariable logistic regressions were used to determine the association between diabetes status (diabetes, prediabetes, normoglycemia) and cognitive function [Consortium to Establish a Registry for Alzheimer's Disease-Word Learning (CERAD W-L), Animal Fluency test, Digit Symbol Substitution Test (DSST)]. Overall, diabetes was associated with mild cognitive dysfunction. In age-adjusted models, adults with diabetes had significantly poorer performance on the delayed and total word recalls (CERAD W-L) compared to those with normoglycemia (5.8 vs. 6.8 words; p=0.002 and 24.5 vs. 27.6 words; p<0.001, respectively); the association was non-significant after adjusting for cardiovascular disease. Among all adults, cognitive function scores decreased with increasing HbA1c for all assessments, but remained significant in the fully adjusted model for the Animal Fluency and DSST [beta coefficient=-0.