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Colorectal cancer (CRC) is distinguished by epigenetic elements like DNA methylation, histone modification, histone acetylation and RNA remodeling which is related with genomic instability and tumor initiation. Correspondingly, as a main epigenetic regulation, DNA methylation has an impressive ability in order to be used in CRC targeted therapy. Meaningly, DNA methylation is identified as one of most important epigenetic regulators in gene expression and is considered as a notable potential driver in tumorigenesis and carcinogenesis through gene-silencing of tumor suppressors genes. Abnormal methylation situation, even in the level of promoter regions, does not essentially change the gene expression levels, particularly if the gene was become silenced, leaving the mechanisms of methylation without any response. According to the methylation situation which has a strong eagerness to be highly altered on CpG islands in carcinogenesis and tumorigenesis, considering its epigenetic fluctuations in finding new biomarkers is of great importance. Modifications in DNA methylation pattern and also enrichment of methylated histone signs in the promoter regions of some certain genes like MUTYH, KLF4/6 and WNT1 in different signaling pathways could be a notable key contributors to the upregulation of tumor initiation in CRC. These epigenetic alterations could be employed as a practical diagnostic biomarkers for colorectal cancer. In this review, we will be discuss these fluctuations of MUTYH, KLF4/6 and WNT1 genes in CRC.

Background: Strokes are among the major causes of disabilities worldwide. In recent years, there has been considerable interest in evaluating stroke prognoses. Objectives: In this investigation, we studied the association of lymphocyte-monocyte ratio (LMR), neutrophil-lymphocyte ratio (NLR), platelet-lymphocyte ratio (PLR), C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and ESR-CRP ratio (ECR) with 3 months outcomes among those with acute ischemic stroke (AIS). Materials & Methods: We carried out the present cross-sectional investigation among AIS patients at an academic hospital in northern Iran (from 2019 to 2021). Within 24 hours after the onset of symptoms, laboratory and clinical data of the patients were obtained. We assessed the results using the modified rankin scale (mRS) 90 days after the initial assessment. Statistical significance for comparing descriptive data was determined as P<0.05. Results: We entered 341 participants (Mean±SD age: 69.10±13.55 years, 53.1% female) into this investigation. Based on univariate analysis, there were poor correlations between NLR (r=0.361, P<0.001), PLR (r=0.215, P<0.05), CRP (r=0.234, P<0.001), LMR (r=-0.184, P<0.05), and ECR (r=-0.191, P<0.05) and a 3-month mRS. Also, after three months, the NLR, PLR, and CRP values were higher in the patients who died, but the LMR (P<0.001) and ECR (P<0.05) were lower. In multivariate comparison, only ECR was independently higher among the participants who died within 3 months (P<0.05). Conclusion: In this study, ECR within 24 hours of symptoms onset was related to functional outcomes and mortality at 3-month follow-up. Thus, ECR might provide valuable prognostic information at a relatively low cost. [ABSTRACT FROM AUTHOR]

Introduction: Neuroinflammation is a primary pathophysiological condition that is associated with cognitive impairment and neurodegenerative diseases. The present study was designed to evaluate the effects of enriched environment (EE) on passive avoidance (PA) memory impairment caused by lipopolysaccharide (LPS) induced neuroinflammation. Methods: Twenty-eight male Wistar rats were assigned into the following groups: 1, control; 2, control+ EE; 3, LPS and 4, LPS+ EE. LPS injection (1mg/kg/i.p.) was done on days 1, 3, 5 and 7 of experiment. Two different housing conditions were used in this experiment, including a standard environment house and an enriched environment house. The passive avoidance task was used to examine animals learning and memory performance. The hippocampal level of interleukin-6 (IL-6) and brain-derived neurotrophic factor (BDNF) was also measured using sandwich-ELISA method. Results: Obtained data indicated that LPS significantly impaired passive avoidance memory, decreased the step-through latency and increased the time spent in the dark compartment of the LPS treated group compared to the control group. On the other hand, EE housing could significantly ameliorate memory impairment. Hippocampal IL-6 level was increased and BDNF was decreased in the LPS group, whereas EE could decrease and increase IL-6 and BDNF levels in the LPS+EE group, respectively. Conclusion: EE should probably be considered as an alternative strategy in neuro-inflammatory diseases to minimize the memory impairment. [ABSTRACT FROM AUTHOR]

Background Recently, researchers have considered extremely low-frequency electromagnetic fields (ELFEMFs), as one of the non-invasive therapies, in the treatment of many severe neurological disorders, including Alzheimer Disease (AD). AD is a progressive neurodegenerative disease characterized by the deposition of amyloid plaques in the brain. However, the increase in microglial cells increases phagocytosis and the destruction of amyloid plaques. Therefore, the present study aimed to investigate the amount of β-amyloid precursor deposition and the number of microglia cells in the animal model of AD before and after exposure to ELF-EMFs. Objective The aim of this study was to investigate the deposition of beta ameloid precursor and the number of microglial cells in the Alzheimer's animal model before and after exposure to magnetic waves. Methods Fifty male adult rats were randomly grouped into 5: The control group, the ELF-EMFs group, the AD group, the treatment group 1, and the treatment group 2. After the study period, the animals were killed for immunohistochemistry assessment to detect and compare the deposition of β-amyloid and the production of allograft inflammatory factor 1 (Iba1) protein. Results Exposure to ELF reduced the deposition of β-amyloid and increased microglia cells. However, these changes were not different between the control and ELF-EMFs groups (P<0.001). Conclusion ELF-EMF can reduce the formation of β-amyloid plaques and induce the proliferation of microglia cells. Therefore, they can be used to treat brain damage caused by Alzheimer disease. [ABSTRACT FROM AUTHOR]