Publications by authors named "H Elyas"

Background: Non-communicable diseases emerge as major public health challenges with increasing prevalence and mortality. The armed conflict in Sudan has resulted in the displacement of 6.8 million people, putting a significant strain on the health sector in the displacement areas.

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Purpose: Transient receptor potential melastatin 2 (TRPM2), a calcium-permeable ion channel, is shown as a prognostic marker candidate in prostate cancer (PCa) and an important regulator of autophagy. We aimed to determine the changes in TRPM2 and autophagic-apoptotic gene expression levels in human prostate adenocarcinomas, and to investigate the affect of TRPM2 on autophagic pathways in PC-3 cell line.

Methods: Human prostate tissues were classified considering the grade levels and were divided into the control, BPH, and grade 1-5 groups.

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Depression is a common mental disorder characterized by the mood of deep sadness. Recent studies have demonstrated that microRNAs and ion channels have significant roles in the etiopathogenesis of depression. Therefore, we investigated the effects of the TREK1 ion channel inhibitor anandamide and the TRPC3/6 inhibitor norgestimate on microRNA expression and antidepressant effect in the mouse chronic mild stress (CMS) model of depression.

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In early April 2014, two South Sudanese refugees in the Gambella region of western Ethiopia experienced acute onset of jaundice, accompanied by fever. One patient was a pregnant woman aged 24 years evaluated at a routine prenatal clinic visit in Leitchour refugee camp. The second patient was a malnourished boy aged 1 year who resided in Tierkidi refugee camp.

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Rheumatoid arthritis (RA) is a major cause of adult chronic inflammatory arthritis and an autoimmune disease of unknown etiology in which the inflammatory pathology involves T cell activation. Genetic mutations in the Mediterranean fever (MEFV) gene, encoding pyrin, influence the severity of RA, but the underlying mechanisms are not completely understood. In this study, we investigated whether the full-length MEFV gene (MEFV-fl) and the exon 2-deleted splice isoform (MEFV-d2) expression are associated with or responsible for the clinical conditions of RA.

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