نور محمود مجيد

Introduction: Umbilical cord–derived mesenchymal stem cells (UCMSCs) are widely utilized in regenerative medicine owing to their proliferative and secretory capabilities. However, the effects of alcohol- and tobacco-derived metabolites, specifically acetaldehyde and cotinine, on UCMSC viability and function remain poorly understood. This study aimed to compare the cytotoxic and secretory responses of rat UCMSCs following in vitro exposure to acetaldehyde and cotinine. Materials and Methods: Rat UCMSCs were cultured in DMEM/F12 and seeded at 5×10⁵ cells per T-25 flask. A total of 40 flasks were allocated to three groups: acetaldehyde (30 µM, n = 15), cotinine (14 µM, n = 15), and untreated controls (n = 10). Cells were incubated for 5 days under standard conditions. Cell counts were recorded daily, and the levels of VEGF, HGF, IGF-1, SDF-1/CXCL12, IL-6, TNF-α, and IL-1β were quantified using a multiplex immunoassay. Statistical analysis was performed using two-way ANOVA. Results: Acetaldehyde exposure resulted in a progressive decline in UCMSC numbers from 4.8×10⁵ to 2.8×10⁵ over 5 days, whereas cotinine increased cell numbers from 5.4×10⁵ to 9.0×10⁵. Acetaldehyde induced an early peak, followed by subsequent declines in VEGF, HGF, IGF-1, SDF-1/CXCL12, and IL-6, while TNF-α and IL-1β showed variable patterns. In contrast, cotinine led to significantly less expansion compared with untreated controls, although it did induce a modest increase from baseline. Conclusions: Acetaldehyde exerts a markedly more pronounced cytotoxic and suppressive effect on rat UCMSCs compared with cotinine, which induces a gradual increase in cell proliferation and secretory activity. However, cotinine's effect is less inhibitory than acetaldehyde, yet it still significantly reduces expansion relative to untreated cells. These findings underscore the differential biological impacts of alcohol- and tobacco-related metabolites on stem cell function in vitro.

Background. Cancer is caused by the accumulation of genetic and epigenetic changes in the oncogenes and tumor-substituting genes. The discovery of the epigenetic pathways that control gene expression has substantially progressed in understanding cancer biology. Purpose. Investigation of epigenetic effects of oxidative stress on the regulation of gene expression in intestinal cancer. Methods. DLD-1 colorectal adenocarcinoma cells were treated with the oxidant 2,2’-Azobis (2-amidinopropane) dihydrochloride (AAPH) and the antioxidant hydroxytyrosol. Cellular viability, apoptosis, reactive oxygen species (ROS) production, and expression of key genes (CDH17, CXCL12, TGFB1) were examined. Results. Hydroxytyrosol treatment improved DLD-1 cell viability in a time-dependent manner. AAPH-induced oxidative stress decreased cell viability and increased apoptosis and ROS production. Combination treatment with hydroxytyrosol and antioxidant enzymes enhanced these effects. Oxidative stress altered the expression of CDH17, CXCL12 and TGFB1, with TGFB1 showing a dose-dependent increase. Conclusion. Oxidative stress influences epigenetic regulation of gene expression in intestinal cancer cells. Combination therapies targeting both oxidative stress pathways and epigenetic mechanisms may be a promising approach for colorectal cancer treatment.

Psoriasis is a chronic disease caused by an overactive immune status, leading to the rapid multiplication of the skin cells and the formation of scaly, inflamed patches on various parts of the body. This study aims to determine the gene expression of ERAP1, RUNX3, and HLA-C in Iraqi patients with psoriasis. Seventy serum samples were collected from individuals attending Yarmouk Teaching Hospital in Baghdad, Iraq. The current study included two groups: Group 1 (G1) consisted of 50 patients with psoriasis, while Group 2 (G2) included 20 healthy individuals. Gene expression was assessed using quantitative polymerase chain reaction in both groups. Moreover, gene expression was analysed for both acute and chronic forms of psoriasis. The results showed that the expression of ERAP1 and HLA-C genes was increased in patients with psoriasis compared to G2. In contrast, the expression of RUNX3 gene was decreased in patients with psoriasis compared to G2. In addition, the expression of ERAP1 and HLA-C genes was significantly higher in the acute form of psoriasis compared to the chronic form and G2, while the expression of the RUNX3 gene was reduced in the acute form compared to the chronic form and G2. These findings suggest that the upregulation of ERAP1 and HLA-C genes and the downregulation of RUNX3 gene are indicative of psoriasis, particularly in its acute form. These evidence supports the potential involvement of these genes in the pathogenesis of psoriasis and highlights their distinct roles in acute and chronic cases of the disease