AbstractBackground N-methyl-D-aspartate (NMDA) receptors play a major role in central nociceptive transmission. Recent studies identified \{NMDA\} receptors peripherally. Magnesium (Mg) has antinociceptive effects due to its antagonistic effect of \{NMDA\} receptors. The aim of this randomized, double-blinded, placebo-controlled study was to assess the potential analgesic effect of Mg when directly applied on the peripheral nerves, as well as to evaluate the efficacy of Mg to facilitate the local anesthetic effect of Bupivacaine during peripheral nerve block. Methods Sixty patients, \{ASA\} physical status I, İI\} & III, undergoing laser photocoagulation were randomly divided into 2 equal groups. Both groups received femoral nerve block using nerve stimulator. Patients of group A were given Bupivacaine and Magnesium sulfate, while patients of group B were given Bupivacaine and saline. Pain was assessed using Visual analogue scale (VAS). The duration of action of Bupivacaine was determined by assessing the duration of sensory block, as well as, assessing the motor block of the quadriceps muscle in both groups. 75 mg of Diclofenac sodium was administered İM\} as a rescue analgesic. The total dose of the Diclofenac sodium used was recorded. Results The current study showed a significantly shorter duration of action of Bupivacaine, with a significantly lower pain scores among patients of group A. On the other hand, bearable pain period was significantly shorter, and the total consumption of Diclofenac sodium in the 24 h postoperatively was significantly higher in group B. Conclusion The current study concluded that the admixture of magnesium to bupivacaine provides a profound prolongation of the femoral nerve block, in addition to a significant decrease in postoperative pain scores and total dose of rescue analgesia, with a longer bearable pain periods in the first postoperative day.

Multiple sclerosis (MS) is a chronic disease and one of the leading causes of disability in young adults. The current study aims to investigate the pathogenesis of MS via studying the regulatory role of novel lncRNA MAGI2-AS3 in miR-374b-5p and their downstream targets PTEN/AKT/IRF-3/IFN-β and the relationship of this pathway with disease severity. Moreover, it aims to assess the role of MAGI2-AS3/miR-374b-5p as diagnostic and/or prognostic biomarkers for MS. Overall, 150 contributors were recruited: 100 patients with MS and 50 healthy volunteers. Gene expression of MAGI2-AS3, miR-374b-5p, PTEN, AKT, and IRF-3 were assessed using RT-qPCR, and IFN-β was measured by ELISA. Compared with the healthy control group, serum MAGI2-AS3 and PTEN were downregulated in MS patients, whereas miR-374b-5p, PI3K, AKT, IRF-3, and IFN-β were upregulated in MS patients. Furthermore, MAGI2-AS3 was downregulated, while miR-374b-5p was upregulated in MS patients with an expanded disability status scale (EDSS) ≥3.5, compared to patients with an EDSS <3.5. Receiver-operating-characteristic curve analysis revealed that MAGI2-AS3 and miR-374b-5p can be used in the diagnosis of MS. Remarkably, multivariate logistic analysis revealed that MAGI2-AS3, miR-374b-5p, PTEN, and AKT act as independent variables in MS. Moreover, MAGI2-AS3 was directly correlated with PTEN and inversely correlated with miR-374b-5p, AKT, and EDSS. Regarding miR-374b-5p, it was positively correlated with AKT and EDSS. In conclusion, the study showed for the first time that the crosstalk between MAGI2-AS3 and miR-374b-5p could affect the AKT/IRF3/IFN-β axis in MS. Interestingly, MAGI2-AS3 and miR-374b-5p could be genetic noninvasive biomarkers for MS.

BACKGROUND: The World Health Organization (WHO) set a goal to eliminate hepatitis C (HCV) infection globally by 2030, with specific targets to reduce new viral hepatitis infections by 80% and reduce related deaths by 65%. However, an overlooked aspect that may hinder these efforts is the impact other liver diseases could have by continuing to drive liver disease progression and offset the beneficial impact of DAAs on end-stage liver disease and hepatocellular carcinoma (HCC). In particular, the decrease in HCV prevalence has been countered by a marked increase in the prevalence of metabolic-associated fatty liver disease (MAFLD).

AIMS: To review the potential interaction of HCV and MAFLD.

METHODS: We have reviewed the literature relating to an arrange of interaction of HCV, metabolic dysfunction and MAFLD.

RESULTS: In this viewpoint, international experts suggest a holistic and multidisciplinary approach for the management of the growing number of treated HCV patients who achieved SVR, taking into consideration the overlooked impact of MAFLD for reducing morbidity and mortality in people who have had HCV.

CONCLUSIONS: This will strengthen and improve the continuum of care cascade for patients with liver disease(s) and holds the potential to alleviate the cost burden of disease; and increase quality of life for patients following DAAs treatment.