The relationship of minerals and trace elements with inflammatory bowel disease (IBD) is complex. Alterations in their metabolism can be induced by the diseases and their complications. To study the role of trace elements in IBD patients' serum zinc and copper and their related enzymes, including superoxide dismutase (SOD), activity were measured in patients with IBD patients as well as in healthy subjects. In addition, the correlation between serum trace element levels, albumin, total protein, urea level, copper/zinc ratio, and disease activity (DA) was determined in these subjects. Serum samples were obtained from 35 patients (19 ulcerative colitis (UC) and 16 Crohn's disease (CD)) in the active phase of the disease and 30 healthy control subjects. Serum levels of zinc, copper, SOD activity, albumin, total protein, and urea were measured. The results were compared between the two groups using independent Student's t test in statistical analysis. Serum levels of zinc, SOD activity, albumin, and total protein were significantly lower (P < 0.05) in patients than controls, while serum urea level was significantly higher in patients compared to controls. Copper concentrations did not differ between patients with IBD (mean ± SD, 58.8 ± 20.7 μg/d) and controls (55.57 ± 12.6 μg/d). Decreased levels of zinc and SOD activity are associated with increased inflammatory processes indicating inappropriate antioxidant system in patients with IBD. Additionally, lower levels of albumin and total protein with higher level of urea reflect metabolic problems in liver system.

The human adenovirus E4 ORF 6 34 kDa oncoprotein (E4 34k), in concert with the 55 kDa product of E1b, prevents concatenation of viral genomes in infected cells, inhibits the repair of double strand breaks (DSBs) in the viral genome, and inhibits V(D)J recombination in a plasmid transfection assay. These activities are consistent with a general inhibition by the E4 34k and E1b 55k proteins of DSB repair by non-homologous end joining (NHEJ) on extrachromosomal substrates. To determine whether inhibition of NHEJ extends to repair of DSBs in the cell chromosome, we have examined the effects of E4 34k on repair of chromosomal DSBs induced by ionizing radiation in a cell line in which E4 34k expression and biological activity is inducible and E1b 55k is produced constitutively. We demonstrate that in this cell line, induction of E4 34k inhibits chromosomal DSB repair. Recently, it has been shown that in infected cells, E4 34k and the adenovirus E1b 55k proteins cooperate to destabilize Mre11 and Rad50, components of mammalian NHEJ systems. Consistent with this, induction of expression of E4 34k in the inducible cell line also reduces the steady state level of Mre11 protein.

Introduction:The interaction between angiotensin-converting enzyme 2 (ACE2) and SARS-CoV-2 is a crucial factor in the viral infections leading to the release of inflammatory proteins, such as TNF-a. Thus, it is hypothesized that TNF-a blockers can prevent either COVID-19 incidence or its serious symptoms. TNF-a blockers are prescribed to treat various autoimmune disorders, including rheumatoid arthritis (RA) and seronegative spondyloarthropathies (SpA). Therefore, the objective of this work was to examine this hypothesis that TNF-a blockers can prevent COVID-19 incidence in patients with RA or SpA.Methods: A case-control study was conducted through interviews based on a structured questionnaire to investigate the frequency of COVID-19 incidence in 254 eligible patients with RA or SpA about whom 45% were under treatment with one type of TNF-a blockers including infliximab, adalimumab, and etanercept at least for 3 months during the COVID-19 pandemic. Interviews were carried out twice, at the beginning and the end of the study (June-December 2020). Patients with COVID-19 during the study or before that were considered as cases. The control group was patients without COVID-19 experience. Data were analyzed using descriptive statistics, and logistic regression was used to determine the relationships between COVID-19 incidence and independent variables. Results: A small percentage of patients treated with TNF-a blockers (5.22%, 6/115) experienced COVID-19, while a large percentage of patients with COVID-19 did not receive TNF-a blockers (27.34%, 38/139). According to odds ratio, adalimumab, infliximab, and etanercept decreased significantly the risk of developing 95, and 80.3% (p \ 0.05), respectively. Therefore, TNF-a blockers could probably decrease the chances of the COVID-19 incidence in patients with RA or SpA. Conclusions: A direct and positive correlation between the use of TNF-a blockers and a reduction in the incidence of COVID-19 could suggest the prophylactic role of these drugs in

No abstract

No abstract

Long non‐coding RNAs (lncRNAs) have received particular attention in the last decade due to its engaging in carcinogenesis and tumorigenesis. Metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) is a lncRNA that plays physiological and pathological roles in many aspects of genome function as well as biological processes involved in cell development, differentiation, proliferation, invasion, and migration. In this article, we will review the effects of lncRNA MALAT1 on the progression of six prevalent human cancers by focusing on MALAT1 ability to regulate post‐transcriptional modification and signaling pathways.

No abstract

No abstract