Background: Alopecia areata(AA) is a common autoimmune disease that causes hair loss without scarring. It occurs as a result of T-helper 1 (Th1) and Th17 cells attacking the anagen hair follicles. Genetic factors play a role in the occurrence of infection, which stimulates the production of pro and anti-inflammatory interleukins. Polymorphisms of IL-37 play a role in autoimmune diseases. However, IL37 single nucleotide polymorphisms(SNP) have not been identified in patients with AA. Therefore, this study aimed to reveal the IL37 gene SNP and its relationship to AA. Methods: Genotyping of IL-37 gene single nucleotide polymorphisms SNPs were detected using sequence-specific primer-polymerase chain reaction (SSP-PCR) method was done following

Background: Diabetic neuropathy can affect any peripheral nerve, including sensory neurons, motor neurons, and the autonomic nervous system. Therefore, diabetic neuropathy has the potential to affect essentially any organ and can affect parts of the nervous system like the optic nerve, spinal cord, and brain. In addition, chronic hyperglycemia affects Schwann cells, and more severe patterns of diabetic neuropathy in humans involve demyelization. Schwann cell destruction might cause a number of changes in the axon. study aims to evaluate serum myelin protein level as a predicting marker in the diagnosis of diabetic neuropathy and to prevent early neuropathy complications of type 2 diabetes.

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Dual-species biofilms of Pseudomonas aeruginosa and Staphylococcus aureus generate difficult-to-treat illnesses. Nutrition stress in biofilms affects physiology, microbial metabolism, and species interactions, impacting bacteria growth and survival. Furthermore, the function of alginate, which is encoded by the algD gene, in the production of biofilms has been established. The present study aimed at investigating the impact of starvation on algD gene expression in single-species biofilm of P. aeruginosa and dual-species biofilms of P. aeruginosa and S. aureus from hospital sewage. A total of six P. aeruginosa and six S. aureus isolates were obtained from the microbiology laboratory at the Department of Biology, College of Science, Universit

The objective of this study is to evaluate the level of cytokines IL-1?, IL-10 and IL-17A in the serum of patients with Alzheimer's disease (AD), vascular dementia (VD) and down syndrome (DS). The results showed that Serum level of IL-1? was significantly increased in AD patients (3.79 ± 0.26 pg/ml) as compared with DS patients (2.78 ± 0.39 pg/ml) or controls (2.78 ± 0.22 pg/ml), while no significant difference was observed between AD and VD (3.25 ± 0.20 pg/ml) patients or between VD patients, DS patients and controls. The serum level of IL-10 was approximated in VD and DS patients and controls (3.39 ± 0.24, 2.77 ± 0.39 and 3.41 ± 0.35 pg/ml, respectively), but was significantly (P ? 0.05) increased in AD patients (5.73 ± 0.55 pg/ml

Background: Bowel cancer is the most prevalent digestive system cancer and is the 4th largest cause of cancer-related death worldwide. In Iraq, colon and rectal cancer (CRC) is the 6th most common malignancy in males and the 5th in females. This cancer is sluggish in growth, which gives a window of opportunity to screen for both precursor lesions and early cancer. The Cluster of Differentiation 47 (CD47) protein is a type of transmembrane glycoproteins found on nearly all human cells, including non-hematopoietic and hematopoietic cells. CD47 promotes CRC growth by triggering angiogenesis and apoptosis of tumor cell. Objectives: To evaluate the immunohistochemical expression of (CD47) in various colorectal samples from Iraqi patients

Over the past decades, several studies have examined the subcellular localization of the cauliflower mosaic virus (CaMV) P6 protein by tagging it with GFP (P6-GFP). These investigations have been essential in the development of models for inclusion body formation, nuclear transport, and microfilament-associated intracellular movement of P6 inclusion bodies for delivery of virions to plasmodesmata. Although it was shown early on that the translational transactivation function of P6-GFP was comparable to wild type P6, it has not been possible to incorporate a P6-GFP gene into an infectious clone of CaMV. Consequently, it has not been possible to formally prove that a P6-GFP fusion is comparable in function to the unmodified P6 protein. Here w