Baghdad Journal of Biochemistry and Applied Biological Sciences

Many reviews and studies have brought to light the varied nature of the causes of fluorosis, as well as the necessity of conducting an in-depth investigation to guide strategies for prevention and management. Overconsumption of fluoride over an extended period, particularly when teeth or bones are growing, causes fluorosis, whether it affects the bones or teeth. The amount, timing, and duration of fluoride treatment all influence how serious the illness is. Dental fluorosis rarely manifests in its more severe forms; most cases are extremely moderate to mild. It has also been investigated how fluoride affects the immune system, the intestinal mechanical barrier, and innate immunity. In addition, current research has concentrated on the global impacts of skeletal fluorosis and the role oxidative stress plays in its advancement. The reviews emphasize how important prevention is and draw attention to the lack of specific treatments for skeletal fluorosis. The comprehensive results of the study underscore the intricacy of fluorosis and the necessity for comprehensive approaches to prevention and treatment.

Cancer development is driven by uncontrolled cellular proliferation resulting from the accumulation of genetic mutations. One of the most well-studied mechanisms behind these mutations is DNA damage. Cellular DNA is under constant threat of damage by exogenous and endogenous sources. Microplastics are one of these exogenous sources and characterized by their small size and high surface-area-to-volume ratio, have the ability to interact strongly with biological systems, leading to cytotoxicity, cell damage, and DNA mutations that increase cancer risk. Microplastics uptake and subsequent bioaccumulation in the human body are increasingly considered to negatively impact the body’s usual mechanisms of damage repair, with resultant increases in apoptosis, necrosis, inflammation, oxidative stress, and aberrant immune responses. In this study we tried to Design a compound for the efficient absorption of microplastics by the use of PubChem, Avogadro, PyMOL, and SWISSADME. A general approach to designing such a compound include: 1. Targeting and Binding Microplastics. 2. Biocompatibility. 3. Efficient Elimination. 4. Delivery Mechanism. We found that modified chitosan could be the best compounds for microplastics adsorption from human body. PubChem was used to obtain the Chitosan chemical structure (C56H103N9O39) M.wt: 1526.5 g/mol. Avogadro was used for Chitosan fragmentation in to smaller pieces to increase solubility, permeability through cellular membrane and enhance activity. PyMOL was used to check out the 3D structure and its functional groups. SWISSADME was applied to analyze GI absorption, skin permeation, bioavailability, and the level of compliance with Lipinski rules of 5. This research highlights the potential of chitosan-based compounds as a prevention strategy for mitigating microplastic-induced carcinogenesis.

Disaster victim identification (DVI) is crucial in the aftermath of mass casualty events, necessitating rapid and precise identification methods. Single-nucleotide polymorphisms (SNPs) have gained significant prominence in forensic genetics due to their abundance, stability, and ease of analysis. SNPs are highly valuable genetic markers for DVI, particularly because they are insensitive to DNA degradation and possess high annotation potential, making their underlying biological information invaluable for human identification in molecular forensics. Unlike traditional methods, SNP typing offers a more powerful set of genetic markers, enabling complex analysis and profiling techniques suitable for various genotyping scenarios, from specialized forensic markers to expanded tiling arrays. The small differences in DNA due to polymorphisms, approximately 1 in 1,000 nucleotides, provide sufficient information to uniquely identify a person. SNP assays are particularly effective for analyzing severely damaged DNA samples, a common characteristic of disaster remains, as demonstrated in real-world applications such as the 2004 Indian Ocean tsunami, the 2010 Haiti earthquake, the 2015 Germanwings Flight 9525 crash, and the Yazidi Genocide in Iraq. These assays offer advantages including cost-effectiveness, multiplexing capabilities, and suitability for robotic automation. They also provide valuable information for ancestry inference and the prediction of externally visible characteristics. The ongoing development of SNP assay technologies and their use in DVI protocols highlight their important role in giving accurate identifications and helping families find closure.

Acute Coronary Syndrome (ACS) represents a spectrum of life-threatening cardiovascular conditions characterized by sudden myocardial ischemia. This review synthesizes current knowledge on the pathophysiological roles of 13-hydroxyoctadecadienoic acid (13-HODE), 15-lipoxygenase (15-LOX), and peroxisome proliferator-activated receptor alpha (PPAR-α) in ACS development, with particular emphasis on the PPAR-α rs1800206 (Leu162Val) polymorphism. Emerging evidence highlights the dual role of 13-HODE as both a pro-inflammatory mediator and angiogenic factor, while 15-LOX drives oxidative stress and contributes to plaque destabilization. The PPAR-α pathway emerges as a critical regulator of lipid metabolism and vascular inflammation, with the rs1800206 variant modifying disease susceptibility and therapeutic responses to fibrates. The authors further explore established and novel biomarkers, including high-sensitivity troponin, CK-MB, hs-CRP, and atherogenic lipid profiles, which collectively enhance ACS diagnosis and risk stratification. The integration of these molecular and genetic markers provides a framework for understanding the complex interplay between inflammation, oxidative stress, and metabolic dysregulation in ACS. Therefore, the findings have value in the clinic since they increase therapy choices for PPAR-α and draw attention to the potential for personalized medicine in ACS. This literature review endeavors to push precision medicine for ACS, by reviewing the specific mechanisms of 13-HODE, 15-LOX and PPAR-α polymorphisms and showing how this information can be applied to help patients.

Recent worldwide patterns suggest a possible resurgence of cases as the COVID-19 pandemic evolved, driven by the emergence of new variants, waning immunity, and adjustments to public health protocols. This academic review examines variables such as seasonal variations, vaccine effectiveness over time, and viral mutations that may contribute to the potential recurrence of COVID-19. It also examines the consequences for public health, including the preparedness of the healthcare system, the risks of reinfection, and the effectiveness of mitigation techniques. To regulate and mitigate the effects of a potential new wave of infections, this review summarizes the most recent COVID-19 variants, as well as their impact on healthcare providers and the public. It does this by combining epidemiological data and current research. The results demonstrate the value of ongoing monitoring, adaptable vaccination strategies, and evidence-based treatments in halting the spread of the disease.

Background:

Chelation therapy plays a crucial role in the management of beta-thalassemia major, a genetic disorder characterized by defective hemoglobin production, resulting in chronic anaemia and iron overload due to frequent blood transfusions. Over time, excess iron accumulates in vital organs, causing significant damage, which is why chelation therapy, aimed at removing excess iron, is a standard treatment approach. However, this therapy's impact extends beyond iron regulation, influencing various physiological processes, including the regulation of hepcidin, ferritin, and fertility hormones. Hepcidin is a key regulator of iron homeostasis, while ferritin serves as an iron storage protein that reflects the body’s iron levels. Understanding the complex interplay between chelation therapy and these biomarkers is critical for improving the management of beta-thalassemia major and mitigating potential long-term complications

OBJECTIVES: This study aims to evaluate the impact of chelation therapy on iron regulation and fertility hormones in females with beta thalassemia major.

Methods: A cross-sectional case–control study was conducted over 12 months from January to June 2024 involving 180 women (90 healthy controls and 90 patients) aged 16-40 years. Patients were randomly selected according to the specific inclusion and exclusion criteria. The serum levels of hepcidin hormone, ferritin, and fertility hormones were measured by Enzyme-Linked Immunosorbent Assay. SPSS Program was used to code, enter, and process the gathered data.

RESULTS: Serum hepcidin levels in patients with good compliance did not differ significantly from those with poor compliance while Ferritin levels were significantly lower in good compliance patients (769.16±176.36) vs. poor compliance (868.62±140.81), p=0.005. LH and prolactin showed non-significant increases in good compliance (1.40±0.77, 2.55±1.11) vs. poor compliance (1.39±0.86, 2.28±1.08). FSH and estradiol levels were significantly higher in good compliance patients (2.51±1.20, 11.65±0.95) compared to poor compliance (1.87±0.95, 11.20±1.04), p<0.05.

CONCLUSIONS: Patients with better compliance to iron chelation had higher hepcidin, lower ferritin, and improved FSH and E2 levels, emphasizing the importance of adherence to therapy.

Background: Alzheimer’s disease is characterized by progressive neurodegeneration and cognitive decline. Early diagnosis and monitoring are critical but remain challenging. Apelin-17 and Elabela, endogenous ligands of the apelin receptor (APJ), have emerged as neuroprotective peptides with potential biomarker utility. Objective: To evaluate circulating Apelin-17 and Elabela levels as predictive biomarkers of neurodegeneration and cognitive impairment in Alzheimer’s disease. Methods: We measured plasma Apelin-17 and Elabela in 60 Alzheimer’s disease patients and 60 cognitively normal controls. Correlations with cognitive scores, CSF AD biomarkers (Aβ42, total tau, phosphorylated tau), inflammatory markers (IL-6, TNF-α, CRP), and MRI volumetric data were assessed. A subset (n=30) was followed longitudinally for 12 months. Results: Alzheimer’s disease patients showed significantly reduced Apelin-17 (48.7 ± 15.3 pg/mL vs. 82.1 ± 20.4 pg/mL) and Elabela levels (31.5 ± 9.8 pg/mL vs. 57.3 ± 14.1 pg/mL; p < 0.001 for both). Peptide levels correlated positively with MMSE and specific cognitive domains and inversely with CSF tau, inflammatory markers, and brain atrophy (hippocampus, entorhinal, parietal cortex). Baseline peptides predicted 12-month cognitive decline and hippocampal volume loss. Combined biomarker models including Apelin-17, Elabela, and classical markers improved diagnostic accuracy (AUC=0.93). Conclusion: Circulating Apelin-17 and Elabela are promising predictive biomarkers for neurodegeneration and cognitive decline in Alzheimer’s disease, reflecting multiple pathological processes. They hold potential for early diagnosis, monitoring, and therapeutic targeting.

Catheter implantation is the main cause of neonatal thrombosis. We present two cases of neonatal intracardiac thrombus associated with central venous catheters, each managed with different therapeutic approaches based on specific risk factors. In the first case, a large intracardiac thrombus, secondary to an umbilical venous catheter, was successfully treated with low molecular-weight heparin and antiplatelet therapy. In contrast, the second case, despite resolution with alteplase and heparin infusion, demonstrated thrombus recurrence despite catheter replacement and ongoing anticoagulation therapy. Currently, no standardized treatment guidelines exist for neonatal thrombosis.