Background: Rheumatoid Arthritis is a chronic joint synovial arthritic joint deterioration. The identification of novel biomarkers is crucial for improving diagnostic accuracy and understanding disease pathogenesis. Spexin, a recently discovered adipokine, has been implicated in metabolic and inflammatory processes, While Annexin A2 is recognized to have a pro-inflammatory function in the pathophysiology of RA, Spexin, a recently identified adipokine, has been linked to metabolic and inflammatory processes. Objective: The objective of this study was to investigate serum spexin levels and their correlation with Annexin A2 in males with rheumatoid arthritis compared to healthy controls, as well as to evaluate the diagnostic efficacy of these biomarker1s. Methods: A case-control study was undertaken including 42 male RA patients and 42 age- and BMI-matched healthy male controls (45-70 years). Serum concentrations of spexin, Annexin A2, anti-cyclic citrullinated peptide (ACCP), erythrocyte sedimentation rate (ESR), and uric acid were examined. Receiver operating characteristic (ROC) curve analysis, Pearson correlation, and independent t-tests were among the statistical methods used. Results: Results: The concentrations of serum spexin were significantly decreased in the RA group compared to the control group (4.201 ± 1.350 vs. 5.988 ± 1.666 ng/mL, p < 0.0001). On the other hand, the concentrations of serum Annexin A2 were significantly increased in the RA group (30.73 ± 6.543 vs. 21.21 ± 5.505 ng/mL, p < 0.001). Spexin had only poor analytical sensitivity (AUC = 0.221), whereas Annexin A2 had a good diagnostic value (AUC = 0.868). Conclusion: Lower serum levels of spexin and higher levels of Annexin A2 have been linked to RA in males. The inverse relationship between spexin and Annexin A2 levels implies possible interaction in the pathophysiology of RA. Annexin A2 can be used for diagnosing RA, whereas spexin may act as a treatment target.

Our bodies make molecules when they break down food and when they are stressed. These molecules are called radicals. Free radicals are important for our bodies to work properly like when we're fighting off sickness and our cells are talking to each other. When we have too many free radicals it can cause problems. Our brain cells are very sensitive to damage from radicals. This is because brain cells use a lot of oxygen they have a lot of fat they do not have things to protect them from damage and they do not fix themselves very well. Free radicals can hurt our brain cells. Cause oxidative stress. Our brain cells are very important. When free radicals hurt them it can cause big problems. Free radicals are a problem, for our brain cells. Oxidative stress causes a lot of problems like lipid peroxidation, protein oxidation, mitochondrial malfunction, DNA damage, compromised synaptic transmission and neuronal apoptosis. Oxidative stress is the reason for neurodegenerative diseases such as Alzheimers disease, Parkinsons disease, amyotrophic lateral sclerosis and Huntingtons disease. These diseases happen because of the changes that oxidative stress causes. This review talks about the production and metabolism of radicals the molecular processes that cause neuronal damage the endogenous antioxidant defense systems and the connection between oxidative stress and neurodegeneration from a thorough biochemical standpoint focusing on oxidative stress and neurodegeneration and how oxidative stress affects the body. The review covers stress and its effects on the body including neurodegeneration to understand how oxidative stress leads to neurodegenerative diseases, like Alzheimers disease, Parkinsons disease, amyotrophic lateral sclerosis and Huntingtons disease. New ways to reduce damage and keep neuronal function working are also talked about along with new ideas, for using antioxidants to treat people. If we understand the pathways that connect free radicals to neuronal deterioration better this can help us find more effective ways to prevent and treat neurological illnesses like these neurological illnesses. The more we know about the pathways that connect free radicals to neuronal deterioration the more we can do to stop neurological illnesses from happening in the first place and the more we can do to treat neurological illnesses when they do happen.

Azo dyes are really good at helping us detect heavy metal ions in a way. We have made a lot of progress in making Azo dyes in a natural way and using tiny particles, which is called nanotechnology. This has led to the creation of Nano-azo dye products that're easier to use and give faster results. The main points of this review talk about how we can make Nano-azo dyes using things like plant extracts and natural solvents and how we can use techniques like microwaves and sound waves to save energy. Nano-azo dyes are very good at finding metals like iron, copper and lead because they have a big surface area and can be adjusted to work well with light. This is very important. Even though we have gotten some results there are still some problems to solve like making sure the Nano-azo dyes are stable and do not get confused by other ions and finding a way to make them on a big scale so we can use them commercially. We need to make the sensors stronger and find ways to use them with tiny materials and we want to use them to monitor the environment and help people’s health. Using Nano-azo dyes that are made in a way is a great idea for the future because it will help us detect heavy metal ions in a way that is good, for the planet, efficient and affordable.

Background: Prostate cancer (PCa) is the second most prevalent cancer among men globally. Medicinal plants have emerged as a promising source of anticancer compounds. Aim: The aim of the present study was to evaluate the methanol extract from the Iraqi plant Cordia myxa as an anti-prostate cancer cell agent. Methodology: Fresh Cordia myxa leaves were collected and a methanolic extract was prepared. Phytochemical screening was performed on the extract. The MTT assay and calculation of IC50 values were used to assess the cytotoxic effects of the Cordia myxa methanolic extract on human prostate cancer cell lines (PC3). Acridine Orange staining, DNA fragmentation, and Annexin V-FITC/PI flow cytometry assays were also employed to identify the induction of apoptosis. Results: Phytochemical screening of the extract revealed the presence of flavonoids, alkaloids, tannins, saponins, terpenoids and phenolic compounds. The Cordia myxa methanolic extract exhibited dose- and time-dependent cytotoxicity against PC3 cells, with increased exposure time leading to enhanced cytotoxic effects. The findings also demonstrated that the treated prostate cancer cells underwent apoptosis. Flow cytometry confirmed that Cordia myxa extract induced significant apoptosis (48.2%) in human PC3 cells. Conclusion: The methanolic extract of Cordia myxa was observed to exert potent anticancer activity against prostate cancer cells, primarily through the induction of apoptosis. These findings represent a crucial step towards understanding the therapeutic potential of Cordia myxa as a natural treatment for prostate cancer, thereby paving the way for the development of novel, more effective, and less toxic therapies.

Based on the influence of estrogen deficiency, inflammatory markers related to heart remodeling were determined and corresponding telomere lengths compared with those in the chemically induced ovarian failure model (4-vinylcyclohexene diepoxide (VCD)) in female rats. Estrogen deficiency induces cardiovascular dysfunction by increased inflammation, oxidative stress and cellular senescence. Adult female albino rats were used in both groups: (a) controls (untreated) and VCD-treated (undergoing ovarian failure). Blood and cardiac tissue were obtained 6–8 weeks after 15 days of VCD (80 mg/kg) intraperitoneal administration to induce ovarian failure for biochemical, molecular and histopathological analyses. Serum levels of interleukin-6 (IL-6) and C-reactive protein (CRP), as well as telomere length, using quantitative real-time PCR. Moreover, oxidative stress markers were assessed and the expression of estrogen receptor genes were investigated. The results demonstrated a high and significant decrease in serum estrogen levels (indicating ovarian failure) in the sera of the VCD-treated group, which was confirmed by increased serum levels of IL-6 and CRP only. The length of telomeres was significantly reduced in cardiac tissues, which prompted to an enhanced cellular senescence. In addition, levels of oxidative stress were achieved higher due to elevated malondialdehyde (MDA) levels followed by reduced glutathione and nitric oxide. Histopathological examination showed signs of degeneration, inflammatory infiltration and fibrosis in the myocardium. In conclusion, estrogen deficiency-related cardiac remodeling involves a complex web of pathways (such as inflammation, oxidative stress, and telomere shortening) that can be integrated into molecular targets indicating their feasibility to serve as potential predictive biomarkers for cardiovascular disease.

Anemia is a physiological condition characterized by a decrease in hemoglobin levels or packed cell volume below normal. This study aimed to evaluate and compare the physiological impact of anemia on liver and kidney function and serum lipid levels in Salah al-Din Governorate, comparing the effects on both sexes. The study included 120 participants with anemia of both sexes. Packed cell volume (PCV), liver enzyme activity (ALT and AST), kidney function (urea and creatinine), and lipid profile levels (TC, TG, VLDL-c, HDL-c) were measured. The results showed a significant decrease (P ≤ 0.05) in PCV values among anemic individuals, along with a significantly higher urea and creatinine levels compared to healthy individuals, confirming impaired kidney function. No significant differences were found in liver enzyme levels (ALT and AST). The results also revealed a significant difference in lipid levels between the sexes. Males with anemia showed a significant decrease in TC, TG, and VLDL-c levels, while females with anemia showed a significant increase in these values compared to the control groups. The study concludes that anemia leads to significant kidney stress and changes in lipid profiles with sex-specific responses.

Background: Etoposide is a popular chemotherapeutic agent that causes a massive oxidative stress and reproductive toxicity effect in male patients. Objective: Examined the protective properties of cinnamon alcoholic extract (Cinnamomum zeylanicum) to etoposide-induced testicular damage in male Wistar rats. Methodology: Forty adult male rats were randomly separated into four groups namely control, cinnamon extract, etoposide extract, and etoposide extract combined with cinnamon extract. The parameters of the hormones studied were testosterone, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), testicular tissue histology, and molecular evidence of oxidative stress. Results: Findings revealed that cinnamon extract had an important ameliorative effect against etoposide induced hormonal imbalances, maintained testicular histoarchitecture, mitigated oxidative stress indicators as well as augmented antioxidant enzyme functions. Such findings imply cinnamon alcoholic extract has strong antioxidant and protective effect on chemotherapy-induced reproductive toxicity, and can be used as a potential therapy to preserve male fertility during cancer therapy. Conclusion: The alcoholic extract of cinnamon (Cinnamomum zeylanicum) offers great protection against the etoposide induced testicular damage in the male Wistar rats through intensive antioxidant action. These results propose cinnamon extract as a promising, safe adjuvant treatment in preserving male fertility in cases of chemotherapy.