Dhafer Abdulmahdi Faisal Al-Koofee

Background: Diabetic nephropathy (DN) is a major cause of end-stage kidney disease, associated with severe complications. Numerous studies have found connections between variations in the ADIPOQ gene and both type two diabetes mellitus (DM) and DN. Objective: The objective of the present investigation is to evaluate the correlation between the ADIPOQ polymorphism (rs1501299) and the exposed to DN in the Iraqi patients. Materials and Methods: A case-control study involved 121 subjects divided into three groups: 45 type 2 diabetes (T2DM) patients with nephropathy, 39 T2DM patients without nephropathy, and 37 healthy subjects. Biochemical analysis was carried out on all participants and PCR method was utilized for genotyping the adiponectin polymorphism (rs1501229). Results: In the DN group, the genotype models frequencies were 22.2% for genotype (GG), 33.3% for heterozygous genotype (GT), and 44.4% for homozygous (TT), while the DM group had frequencies of 29.7% for GG, 51.3% for GT, and 23% for TT. When comparing the polymorphism between the control group and the DN group, T allele carriers had a high significant risk of DN under the codominant TT model ( P = 0.01), the dominant GT + TT model ( P = 0.04), and the recessive model ( P = 0.01). In the T2DM group, the risk of DN was notably higher among T allele carriers under the recessive model ( P = 0.04). Additionally, in the codominant model, the rs1501299 polymorphism genotypes were significantly associated with elevated levels of serum fasting blood sugar, HbA1c, urea, creatinine, and estimated glomerular filtration rate in the study participants. Conclusion: Our findings demonstrate a substantial association between the polymorphism (rs1501299) and an increased susceptibility to DN among individuals with T2DM in the Iraqi patient population.

Background End-stage chronic kidney disease (CKD) can lead to life-threatening complications and is caused primarily by CKD and cardiovascular issues. CKD is characterized by the inability of the kidneys to filter waste and excess fluids from the blood. This study investigated the associations of the genetic variants XRCC1 rs1799782 (C194T) and ERCC2/XPD rs25487 (Q399R) with CKD susceptibility in Iraqi patients and related biochemical changes. Methods The research was performed from 25/01/2023 to 30/06/2023, we analyzed the genetic associations of two SNPs of DNA repair genes (XRCC1 and ERCC2/XPD) in a case‒control study involving 219 CKD patients diagnosed by a nephrologist and 246 healthy controls. Data and blood samples were collected, and the genotype distribution frequency was determined via the PCR-based high-resolution melting (PCR-HRM) technique. Results This study included 465 participants, with 219 CKD patients and 246 healthy controls. XRCC1 and ERCC2/XPD gene polymorphisms were significantly associated with CKD susceptibility in Iraqi patients (p = 0.025 and p = 0.0001, respectively). Multivariate linear regression confirmed the associations of rs1799782 G/A and rs13181T/G with CKD, adjusting for sex, age, and BMI. Moderate and statistically significant linkage disequilibrium (0.43) between the two SNPs was observed, indicating nonrandom associations. Conclusion XRCC1 (rs1799782) and ERCC2/XPD (rs13181) polymorphisms are associated with an increased risk of CKD. The AG haplotype model is particularly related to increased CKD susceptibility in Iraqi patients, suggesting the importance of these DNA repair gene polymorphisms in CKD risk assessment.

Chronic kidney disease (CKD) is a progressive condition characterized by declining kidney function, ranging from mild damage to end‑stage renal disease. Its prevalence globally is estimated to be between 8 and 16%, with higher rates occurring in low‑ and middle‑income regions. Underlying factors include diabetes, hypertension and genetic predisposition. The multifactorial nature of CKD is influenced by genetics, renal function monitoring, anemia, electrolyte imbalances and other risk factors. The present study collected 465 samples from subjects aged 18‑65 years for a case‑control study. These included 219 patients with CKD (101 females and 118 males; mean ages, 46.56 and 46.84 years, respectively) and 246 healthy individuals (131 women and 115 men; mean ages, 37.16 and 41.23 years, respectively). Whole blood was drawn for serum analysis for the purpose of comparing various biochemical parameters between patients with CKD and the healthy subjects, including total protein, albumin, ferritin, unsaturated iron binding capacity, iron, alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), bilirubin, glucose, urea, serum creatinine, total calcium, free calcium, sodium, potassium, 8‑hydroxy‑2'‑deoxyguanosine (8‑OHdG) and phosphorus. The results obtained revealed a significant association between age and the occurrence of CKD (P<0.001), as well as between body mass index and the likelihood of developing CKD (P=0.031), indicating a connection between obesity and CKD. Biochemical analysis revealed disparities in several markers among patients with CKD, including glucose, urea, serum creatinine, iron, liver enzymes (ALP, AST and ALT), phosphorus, potassium, sodium, calcium and 8‑OHdG (P<0.05). However, no notable differences in terms of sex were observed when comparing each sex group separately for the patients and controls. On the whole, the present study underscores the multifactorial nature of CKD, and its significant association with age. The 8‑OHdG oxidative stress marker demonstrated potential in terms of distinguishing between CKD and healthy subjects. Further research is required, however, to explore additional CKD factors and to develop interventions for at‑risk populations.

Thank you for involving me in the revision of this article. I have an opposite opinion related to the suggested equation that relies only on the BMI, CRP, and IL-6. All these variables are flexible and not specific; that is to say, for example, IL-6...

Purpose Coronary artery disease (CAD) is a major cause of death worldwide. There is relatively little data available on the genetic susceptibility to CAD in the Iraqi population. We have therefore investigated the association between angiotensin II type 1 receptor gene polymorphism A1166C and the presence of CAD in a sample of the Iraqi population. Methods This case-control study enrolled 150 CAD patients, with CAD confirmed by coronary angiography, and 200 controls. The AT1R polymorphism A1166C was analyzed by the allele-specific polymerase chain reaction (AS-PCR) technique. Serum analyses, such as lipid concentrations, were measured and analyzed. Results The C allele and CC genotype frequencies were significantly higher in patients with CAD compared to the controls. Logistic regression analysis showed that the codominant, dominant, and recessive models were associated with risk of CAD of (OR = 1.32, 95% CI: 1.2-1.4, P = 0.000; OR = 1.25, 95% CI: 1.1-1.3, P = 0.000, OR = 1.27, 95% CI: 1.1-1.3, P = 0.000, OR = 1.18, 95% CI: 1.0-1.4), respectively. In the patient group, the presence of the mutant C allele was significantly associated with higher levels of CAD risk factors such as total cholesterol (TC) and low-density lipoprotein (LDL). Conclusion The study indicated that the A1166C polymorphism may be associated with the presence of CAD in the Iraqi population. The AT1R polymorphism may therefore be a useful marker of susceptibility to CAD.

The present study aimed to examine the polymorphism -938C > A of BCL-2 gene and promoter -248G>A in the Bax gene, as well as their relationship with specific clinical-pathological characteristics, in patients with breast cancer. Blood samples were obtained from 70 patients who had been diagnosed with breast cancer and 34 healthy women as the control group. Polymorphic analysis was performed using the polymerase chain reaction-restriction fragment length polymorphism assay. Anthropometric data were assessed. Estrogen receptor (ER), human epidermal growth factor receptor 2 (Her-2), and progesterone receptor (PR) were measured by immunohistochemistry. The data of age and body mass index (BMI) demonstrated no significant variations between the two groups (P>0.05). The results of HER-2 revealed that 42.86% of breast cancer patients reflected positively for Her-2/neu expression, while 24.29% reflected negative results of Her-2/neu. Moreover, the results of ER revealed that 42.86% and 28.57% of subjects were positive and negative ER, respectively; moreover, the missing data was 28.57%. In addition, the results of PR indicated that 35.71% of patients (25/70) were positive for PR, while 28.57% reflected negative results, and the missing results were 35.71%. The genotype and allele frequencies of BCL-2(-938C>A) were not statistically significant in women with breast cancer and the control group (P=0.574, P=0.533) for heterozygous and recessive models, respectively. The genotype of BCL-2(-938C>A) in control and patients in codominant, dominant, recessive, and additive models demonstrated no significant variations of all genotypes in all groups. Genotypes and allele frequencies for Bax (-248G>A) in patients with breast cancer and control indicated that the frequencies of GG, AG, and AA genotypes in cases were 16.67%, 3.33%, and 80 %, while in controls, these values were 3.23 %, 58.06 %, and 3.23 %, respectively. The heterozygous genotype (AG) in the codominant model was OR=36.00 (95% CI 4.5608 - 284.1608; P=0.0007). In comparison with the wild type (GG), there was a 36-fold increase in the risk of breast cancer. Furthermore, the findings of this study revealed a significant correlation between Bax (-248G>A) polymorphism and breast cancer risk under the dominant and overdominant (OR=6.33; 95% CI 2.2604 -17.7452; P=0.0004, and OR=40.154; 95% CI 5.1365 - 313.8949; P=0.0004, respectively. The recessive model revealed that there was a decreased risk of breast cancer (OR= 0.167; 95% CI 0.0303 to 0.9168; P=0.039). Based on the results, it can be concluded that there were no significant variations in BCL-2 (-938C>A) polymorphism of all genotypes models when breast cancer women are compared with healthy ones. In a similar vein, there was no significant association between the BCL-2 (-938C>A) polymorphism and breast cancer risk under dominant, codominant, or recessive models.

Purpose Colorectal cancer (CRC) is the third most common cancer in the world, with enhancing morbidity and mortality each year. Due to the drug resistance against CRC, the use of novel compounds besides chemotherapy is required. Natural seafood contains large amounts of biologically active substances with new chemical structures and new medicinal activities. The aim of this study was to evaluate the effects of hydroalcoholic extract of Sargassum oligocystom algae on SW742, HT-29, WiDr, and CT-26 CRC cell lines, and to evaluate the expression of P53 and APC genes using quantitative real-time PCR (RT-qPCR). Methods The cytotoxicity of S. oligocystom hydroalcoholic extract was determined by MTT and trypan blue methods in six different concentrations including 0.1, 0.2, 0.5, 1, 2, and 4 mg/mL on various CRC cell lines and a control group. The expression of P53 and APC genes in exposure to 2 mg/mL of the extract was also evaluated using RT-qPCR. Results The LD50 and LD90 of S. oligocystom included 0.5–1 and > 2 mg/mL, respectively mostly affecting SW742 and CT-26 cells. In the trypan blue test, 90% viability and death of cells were observed at 0.1 and 4 mg/mL of extract, respectively. The 2 mg/mL was a safe cytotoxic concentration. A significant viability decrease was observed at concentrations ≥ 1 mg/mL (p < 0.001). Sargassum oligocystom extract at 2 mg/mL significantly increased the expression of APC ranging 1.98–2.2-fold (p < 0.001) but not P53 gene which ranged 0.5–0.68-fold (p = 0.323) after 24 h. Conclusion These results indicated that the brown algae S. oligocystom extract had significant antitumor effects against the SW742, HT-29, WiDr, and CT-26 CRC cell lines and especially CT-26, suggesting that it may be a potential candidate for further studies and therefore designing drugs of natural anticancer origin. The S. oligocystom had an anticancer effect via an increase in the APC gene expression.

Objective: As part of the bioinformatics studies, we utilized National Cancer Institute (NCI)’s Breast Cancer Risk Assessment Tool to estimate the five-year period and lifetime risk of breast cancer development among Iraqi risky women. Methods: Totally, 110 risky women aged 21-67 (mean=36±7.4) years were interviewed by a series of questions regarding the risk of breast cancer development. Moreover, 100 cases with mutation in the BRCA1 or BRCA2 genes were included. Results: Our results demonstrated that the patient’s estimated risk of breast cancer development during the next five years and lifetime (until the age 90 years) included 0.96% (p=0.211) and 9.97% (p=0.002), respectively being relatively low. Accordingly, the lifetime risk for the breast cancer development was significantly higher (10.38%) than that of 5-year. However, the age of patients was not significantly associated to the breast cancer development as there was no significant difference among various age groups. Conclusion: It was concluded that long-term or lifetime period plays as a significant risk factor for developing breast cancer among female patients who had had a screening episode in Iraq.