Introduction and Aim: Breast cancer is the most prevalent sex-based malignancy worldwide. Nolvadex is commonly used as first-line therapy for patients with breast cancer. However, studies have indicated that long-term usage of this medicine can result in nephrotoxicity, which can damage kidney tissues. So, the aim of this research was to examine what happened to the serum levels of urea, uric acid, and creatinine when the drug was given to rats in a range of different doses.   Materials and Methods: Male Wistar rats (n=40) were randomly divided into four groups (n=10 each). The physiological solution (normal saline, 0.9%) was given to the control group (G1). Rats in Groups 2, 3, and 4 received Nolvadex at dosages of 30, 40, and 50 mg/kg of body weight four times weekly for a total of 10 weeks. At the end of the experimental period blood drawn from these animals were checked for serum concentrations of urea, uric acid, and creatinine. The animals were sacrificed and their kidneys subjected to histopathological examination. Data obtained was subjected to statistical analysis.   Results: The levels of urea, uric acid, and creatinine that were discovered in the experimental groups were all determined to be significantly higher than the levels that were discovered in the control group. In the experimental group that was given Nolvadex, an infiltration of inflammatory cells, blood congestion, pyknic and necrotic nuclei in the glomerulus, substantial epithelial deterioration in the renal tubules, and an altered renal tissue architecture were detected.   Conclusion: Serum levels of urea, uric acid and creatinine levels increased when experimental rats were administered with varying concentration of the drug Nolvadex. Its administration caused alteration to the architecture of renal tissue.

Crohn's disease (CD) is one of the most common IBD types. CD necessitates an erratic immune response. Previous research has shown that inflammation of the intestines is elevated or continues due to inappropriate immune responses that result from the relationships between environmental factors, intestinal microbiota, and genetic factors. Induces intense transmural inflammation. This study aimed to investigate (i) CD detection by Histopathology and Immunohistochemistry (IHC) Markers that are Mycobacterium avium subspecies paratuberculosis MAP antibody and TWEAK/Fn14 antibody and their association with CD. (ii) Prove or disprove the hypothesis of MAP as a potential cause of CD. Tissue biopsies of 30 cases with a recognized diagnosis of CD and 20 cases as control presented without disease symptoms were collected. They are 20 males and 10 females for patients, and 13 males and 7 females for control with ages ranging from 9-55(±34.78) years. From 2019 - 2020, Biopsies were collected from Medical City Hospitals in Baghdad. One tissue section has been stained by the Hematoxylin & Eosin (H&E) for histopathology examinations. IHC stained the other two sections to the markers mentioned earlier in the IHC technique. The results of IHC for MAP showed a highly significant relationship in the ileal tissues of patients with disease CD with varying degrees according to the intensity of the immune reaction, which represents the intensity of the color, which is distributed between weak, moderate and strong, according to the (Aperio image Scope) program. Where it was 10% weak, 43.33% medium, and 46.67% strong. The P-value for patients vs. control was 0.0052 and 0.0001, respectively (P-value 0 ≤ 0.01). The result of IHC proves the hypothesis of MAP as a potential cause of CD. The other effects of IHC staining for TWEAK/Fn14 marker showed a highly significant relationship in the ileal tissues of patients with Crohn's Disease with varying degrees according to the intensity of the immune reaction, according to the Aperio image Scope program. It was 10% weak, 36.67% medium, and 53.33% strong. P-value for patients vs control were 0.0003 and 0.0001, respectively (P-value 0 ≤ 0.01).

Inflammatory bowel disease (IBD) applies to two main forms of chronic relapsing inflammatory intestinal disorders: Crohn's disease (CD), Ulcerative colitis (UC). CD requires an irregular immune reaction that induces intense inflammation. The cause of CD disease is not yet fully known; previous research, however, indicated inflammation of the intestines elevated or continues due to inappropriate immune responses due to associations between genetic factors, intestinal microbiota, and environmental factors contributing to the production of IBD. This study aimed to investigate predisposing genes, single nucleotide Polymorphisms (SNPs) NOD1/CARD4 and NOD2/CARD15) with CD in Iraqi patients. The common NOD1 (G796A) SNP and NOD2 SNPs R702W, G908R and L1007fsinC for NOD2 SNPs were selected. Thirty Iraqi citizens with a recognized diagnosis of CD and twenty apparently healthy controls were included in the study from November 2019 to December 2020; the common NOD1 and NOD2 polymorphisms have been screened by the polymerase chain reaction/restriction analysis length polymorphism (PCR/RFLP). The results of the current investigation for NOD1 polymorphism in studied patients and controls, the allelic and genotypic data show a highly significant association of G796A SNPs in the NOD1 with Crohn's disease, GA percentage was 56.67% in patients as compared to controls genotype was (0.00%). Furthermore, the G allele was more common in Crohn's patients than the A allele 0.72 vs. 0.28. Also, the allelic and genotypic frequency distribution of the studied NOD2 SNPs in the current study were (R702W, G908R, and L1007fs) in Iraqi patients, and controls revealed a highly significant connection between the G908R SNP with Crohn's disease susceptibility. The proportion of the genotype GC was 30% in patients while 0% in the control group, the frequency of the G allele was 0.85 vs 0.15 respectively, which was more than the frequency of the A allele. There were no significant changes in genotypic and allelic frequencies of the R702W and L1007fs SNPs in Iraqi Crohn's disease patients. The present study concluded that the NOD1 SNP of allelic and genotypic data show a highly significant association of G796A with a predisposition to Crohn's disease in Iraqi patients. And the NOD2 SNPs of G908R were also revealed to be highly effective. While the other studied SNPs were R702W and L1007fsinsC of NOD2, which showed no significant changes in the allelic and genotypic frequencies of the SNPs with Crohn's disease Iraqi patients. Keywords: Inflammatory bowel disease, Crohn's disease, NOD1/CARD4, NOD2/CARD15, polymorphisms.