Cytokines play a prominent role in etiology and pathogenesis of rheumatoid arthritis (RA), and one of these cytokines is interleukin-1β (IL-1β). The association between IL1B gene single nucleotide polymorphism (SNP: rs16944) and rheumatoid arthritis (RA) in a sample of Iraqi patients was investigated. Fifty-one RA patients (21 males and 30 females) were enrolled and their age range was 20 - 63 years (44.9 ± 1.5 years). In addition to patients, 45 apparently healthy control subjects were also enrolled in the study. They matched patients for ethnicity (Iraqis), gender (14 males and 31 females) and age (41.3 ± 1.3 years). Analysis of Hardy-Weinberg equilibrium (HWE) in RA patients and controls revealed that the IL1B genotypes were consistent with the equilibrium, and no significant differences (p > 0.05) were observed between the observed and expected genotype frequencies. Inspecting IL1B genotype and allele frequencies in RA patients and controls revealed that there were no significant variations between these frequencies, although a decreased frequency of T allele (67.7 vs. 73.3%) and an increased frequency of C allele (32.3vs. 26.7%) were observed in patients compared to controls. In conclusion, the results are in favor of no association between IL1B gene SNP (rs16944) and RA in Iraqi population.
Rheumatoid arthritis (RA) was a chronic inflammatory autoimmune disease for long-term that primarily affects small joints and leads to chronic inflammation in synovial. The aimed of the study to identify the relationships among some serological markers (antibodies to citrullinated protein/peptide antigens (ACPAs), anti-mutated citrullinated vimentin (anti-MCV), anti-carbamylated protein (Anti-Carp), anti- heterogeneous nuclear ribonucleoproteins (anti-hnRNP) and Glucose-6-phosphate isomerase (GPI)) and early diagnosis of RA. The study involved (60) Patients of newly diagnosis with RA that divided in to two subgroups (30 RF positive and 30 RF negative) groups and 30 subjects as healthy control group. The serological data from serum
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Background Type two diabetes (T2DM) is characterized by insufficient insulin production and secretion. Additionally, the body develops insulin resistance which affects 90–95% of diabetics. Complex cytokines, receptors, genetic pathways, and the immune system are involved in T2DM. Interleukin-18 (IL-18) is one of the inflammatory cytokines associated with Type 2 diabetes. Environmental and genetic variables, including genetic polymorphisms, can increase T2DM risk and its consequences. Single nucleotide gene polymorphisms (SNPs) are important risk factors for diabetes that can be used to find the disease early and treat it better. Objective This study aimed to determine the levels of IL-18 in the serum of Iraqi patients with Type 2 diabetes
... Show MoreToll-like receptors (TLRs) play a key role in innate immune response activation against viruses. TLR7, one of the TLRs family, is potentially important in controlling viral infection and the production of vaccines against the virus. The wide spectrum of discrepancy in response to antiviral drugs among different populations which is emerged by some pandemics like COVID-19 might be due to their different TLR7 single nucleotide polymorphisms (SNPs). The present study aimed to investigate the consequences of 401 non-synonymous missense SNPs (nsSNPs) within TLR7 on its protein structure, stability, and function by using specific bioinformatics tools. Seven bioinformatics tools were used to investigate 401
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The objective review is to inspect the involvement of Interleukin-6 (IL-6) in rheumatoid arthritis (RA) and to highlight the role of IL-6 and its variants in the pathogenesis of RA and response to anti-IL-6 agents. Several genetic and environmental risk factors and infectious agents contributed to the development of RA. Interleukin-6 is engaged in self-targeted immunity by modifying the equilibrium between T regulatory (T-reg) and T helper-17 (Th-17) cells. The evidences reported that IL-6 parti
Colorectal cancer (CRC) is the most common gastrointestinal malignancy and one of the top ten common cancers worldwide with approximately 2 million cases. There are multiple risk factors that could lead to CRC emergence; of which are genetic polymorphisms. Excision repair cross-complementing group 2 (ERCC2) gene encodes for ERCC2 enzyme which plays a crucial role in maintaining genomic integrity by removing DNA adducts. Several studies suggested that there could be a link between genetic polymorphisms of ERCC2 gene and the risk of CRC development. Hence the present study aims to validate the relationship between the following ERCC2 single nucleotide polymorphisms (rs13181, rs149943175, rs530662943, and rs1799790) and CRC susceptibility. A t
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Interleukin-33 [IL-33] is a specific ligand for the ST2 receptor, and a member of the
IL-1 family. It is a dual-function protein that acts both as an extracellular alarmin cytokine,
and an as an intracellular nuclear factor participates in maintaining barrier function by
regulating gene expression of IL-33 modulating tumor growth and anti-tumor immunity in
cancer patients. The present study aimed to investigate the role of IL-33 serum level and gene
polymorphism in Iraqi women with breast cancer. Materials and methods: Blood samples
were collected from 66 Iraqi patient women diagnosed with breast cancer, which were divided
into two groups: pre-treatment [PT] and under treatment with chemotherapy [UTC] patients in
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Rheumatoid arthritis (RA) is a systematic autoimmune disorder with chronic inflammation changes of unknown etiology. Various synovial inflammatory and proliferative alterations may contribute to the cartilaginous tissues and invasive bony tissues, leading to destructive joints and malformed bones. This disease is mostly due to infective microorganisms or genetic susceptibility causing immune system disturbances through triggering both T-cells and B-cells. Furthermore, different immune cells may secret cytokines, which are responsible for some RA pathogenesis activity. From ninety individuals, serum sample was collected; thirty of them were normal and sixty cases were patients with RA attended a privet medical clin
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Osteoporosis (OP)is one of the most important metabolic disorder also affected by interaction of genetic and environmental factors by almost 70% and 30% respectively. Genetic components are identified to strongly effect bone mineral density, bone building and turnover, so they play an important role in determining risk of OP and fragility fractures. This study consists of patient and control group; Group A: (70) postmenopausal women with OP and osteopenia, Group B: (20) control group. five milliliters of blood sample were divided into three tubes; one tube (1ml) contain gel for obtain serum to measure glucose level, the others tubes containing ethylene-diamine-tetra-acetic acid (EDTA), in 2 tube 2ml stored in deep freeze at (–40
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Background: Osteoporosis is an extra-articular complication of rheumatoid arthritis that results in increased risk of fractures and associated morbidity, mortality, and healthcare costs. Objective: To evaluate changes in bone mineral density in a sample of rheumatoid arthritis (RA) patients on biological (anti tumor necrosis factor (TNF) alpha) and non-biological agent disease modifying antirheumatic drugs (DMARDs). Patients and Methods: A cross sectional study enrolled 60 RA patients diagnosed by rheumatologist according to the 2010 American College of Rheumatology/European League Against Rheumatism (2010 ACR/EULAR) classification criteria for RA. Thirty patient on biological agent (anti TNF alpha) and 30 patient on non-biological agent (D
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