No abstract

Background Cell-free DNA (cfDNA) has the potential to serve as a non-invasive prognostic biomarker in some types of neoplasia. The investigation of plasma concentration of cfDNA may reveal its use as a valuable biomarker for risk stratification of diffuse large B-cell lymphoma (DLBCL). The present prognostic value of plasma cfDNA has not been widely confirmed in DLBCL subjects. Here, we evaluated cfDNA plasma concentration and assessed its potential prognostic value as an early DLBCL diagnostic tool. Methods cfDNA concentrations in plasma samples from 40 patients with DLBCL during diagnosis and of 38 normal controls were determined with quantitative polymerase chain reaction (qPCR) for the multi-locus L1PA2 gene. Results Statistically significant elevation in plasma cfDNA concentrations was observed in patients with DLBCL as compared to that in normal controls ( P <0.05). A cutoff point of 2.071 ng/mL provided 82.5% sensitivity and 62.8% specificity and allowed successful discrimination of patients with DLBCL from normal controls (area under the curve=0.777; P =0.00003). Furthermore, patients with DLBCL showing higher concentrations of cfDNA had shorter overall survival (median, 9 mo; P =0.022) than those with lower cfDNA levels. In addition, elevated cfDNA concentration was significantly associated with age, B-symptoms, International Prognostic Index (IPI) score, and different stages of disease (all P <0.05). Conclusion Quantification of cfDNA with qPCR at the time of diagnosis may allow identification of patients with high cfDNA concentration, which correlates with aggressive clinical outcomes and adverse prognosis.

No abstract

Background: Emerging evidence indicates that metformin has anti-inflammatory effect; however, the results differ concerning randomized controlled trails of the effect of metformin on inflammatory markers in type 2 diabetes (T2D) patients. Objective: This study reassessed the data on the effect of metformin treatment on inflammatory markers in T2D patients through a systematic review and meta-analysis. Methods: A systematic search was performed in the PubMed, ISI Web of Science, EMBASE, Cochrane Library and Scopus databases to collect relevant published data up to September 2020. Data of each study was combined using random-effects model. Subgroup analysis was performed based on subgroups of the treatment duration, dose and target population. Results: Thirteen RCTs including 1776 participants with T2D were analyzed. Although CRP levels significantly decreased [SMD: –0.76 mg/L; 95% CI (–1.48, –0.049); P = 0.036] in patients with T2D following metformin treatment, circulating levels of TNF-α [SMD: –0.17 pg/mL; 95% CI (–0.55, 0.20); P = 0.37] and IL-6 [SMD: –0.06 pg/mL; 95% CI (–0.38, 0.25); P = 0.69] were insignificant after metformin treatment. Compared to treatment duration of less than 24 weeks, longer treatment duration (more than 24 weeks) was associated with reduced level of CRP. Relevance to Patient Care and Clinical Practice: Based on available evidence from RCTs in this meta-analysis, metformin decreased CRP level. However, strategies for the treatment of inflammation should focus on metformin in patients with T2D. Conclusion: The present study evidences that therapy with metformin can reduces CRP level significantly in T2D patients compared to other inflammatory markers.

Purpose: blood-brain barrier (BBB) is made of specialized cells that are responsible for the selective passage of substances directed to the brain. The integrated BBB is essential for precise controlling of the different substances passage as well as protecting the brain from various damages. In this article, we attempted to explain the role of liver X receptor (LXR) in maintaining BBB integrity as a possible drug target. Methods: In this study, various databases, including Pub Med, Google Scholar, and Scopus were searched using the following keywords: blood-brain barrier, BBB, liver X receptor, and LXR until July, 2020. Additionally, contents close to the subject of our study were surveyed. Results: LXR is a receptor the roles of which in various diseases have been investigated. LXR can affect maintaining BBB by affecting various ways such as ATP-binding cassette transporter A1 (ABCA1), matrix metalloproteinase-9 (MMP9), insulin-like growth factor1(IGF1), nuclear factor-kappa B (NF-κB) signaling, mitogen-activated protein kinase (MAPK), tight junction molecules, both signal transducer and activator of transcription 1 (STAT1), Wnt/β-catenin Signaling, transforming growth factor beta (TGF-β) signaling, and expressions of Smad 2/3 and Snail. Conclusion: LXR could possibly be used either as a target for drug delivery to brain tissue or as a target for maintaining the BBB integrity in different diseases; thereby the drug will be conducted to tissues, other than the brain. If it is verified that only LXRα is necessary for protecting BBB, some specific LXRα ligands must be found and then used in medication.