Iranian Journal of War and Public Health

eISSN (English): 2980-969X
eISSN (Persian): 2008-2630
pISSN (Persian): 2008-2622
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F. Parvizpour, T. Ghazanfari, H. Salimi, S. Faghihzadeh, R. Yaraee, Z. Sharifnia, M.r. Soroosh, M.m. Naghizadeh,
Volume 3, Issue 4 (9-2011)
Abstract

Background: Transcription factor NFκB is responsible for a large number of genes expression including inflammatory cytokines, chemokine, immune receptors, enzymes and other preinflammatory molecules. NFκB deviation is one of the mechanisms of some diseases especially those that are associated with inflammation or apoptosis. Sulfur mustard is an alkylating agent that can damage enzymes, DNA and other macromolecules, also induces oxidative stress responses. Results obtained from recent studies on Sardasht sulfur mustard victims 20 years after exposure showed alterations on immune and inflammatory responses. Regard to NFκB significance in inflammatory and its related cytokines in this research we assessed NFκB level in these victims. Purpose: NFκB gene expression assess in mustard victims 20 years after exposure.

Methods and materials: Population study was 189 people of Sardasht sulfur mustard victims and control group include 32 people of Rabat civil. Sampling procedure was systematic random. The result analyzed by SPSS and X2 and T-test static procedures. For nonparametric analysis Mann-Witney and Kruskall-Wallis were used. NFκB expression levels were evaluated by standard PCR in peripheral white blood cells.

Results: Result assessment in two groups showed that NFκB median in exposure group were 188.75 ngr/μl and in control group were 142.84 ngr/μl which NFκB expression level in exposure group was upregulated. This increasing was significant (P= 0.009).

Conclusion: NFκB factor involved in many cellular functions, so its increasing or decreasing has its own results. Due to reduction of inflammatory factors in these victims, its decline was expected but the results of this study showed its increment which likely was for compensates the reduction of inflammatory factors.


R.a. Mustafa, H.a. Jasim, S.kh. Al-Salait,
Volume 14, Issue 1 (1-2022)
Abstract

Aims: Acute lymphoblastic leukemia (ALL) is the most prevalent malignancy in children, accounting for up to 25% of all malignancies in children under the age of 15. TLRs are associated with the transduction of molecular signals in immune processes such as the production of cytokines, and recognition of specific molecular patterns on the surface of microorganisms, but they are also involved in cancer development. This study was trying to throw light on any possible association of gene expression of TLR4, TLR7, and TLR9 in pediatric patients with ALL.
Materials & Methods: A case-control study was conducted on pediatric patients with ALL who have been admitted to Al-Basra Children Teaching Specialty Hospital. Over a period from September 2020 through June 2021, 62 patients (42 newly diagnosed and 20 relapses) were enrolled, in addition to 60 matched normal control, aged 6 months to 16 years. Three ml of blood was collected from all participants in EDTA tubes used for RNA extraction and then molecular analysis. Gene expression of TLR4, TLR7, and TLR9 was done by Real Time-qPCR and the results were reported as ∆Ct (mean±SD).
Findings: The mean ∆Ct of TLR7 (-5.2200±3.29806) reflects the high expression of the gene being the most highly expressed gene (p<0.001). The mean ∆Ct±SD of TLR7 and TLR9 are high in a newly diagnosed group than relapsed one with no significant differences (p=0.686, and 0.400) respectively, while the mean ∆Ct of TLR4 is higher significantly (p<0.05) in a newly diagnosed group than relapsed one.
Conclusion: TLR4, TLR7, and TLR9 gene expression are higher in ALL patients, whether newly diagnosed or relapsed than in the control group. TLRs expression might be part of the immune-evasion mechanism developed by the malignant cells that play an important role in leukemogenicity and disease progression.
J.m. Mezban, B.a. Abbas, M.h. Khudor,
Volume 15, Issue 1 (1-2023)
Abstract

Aims: In recent years, the global incidence of infections caused by gram-negative bacteria resistant to antibiotics has increased. This study aimed to investigate the presence and frequency of coagulase-negative Staphylococci in contact between animals and people and determine the phenotypic antimicrobial resistance profiles of coagulase-negative Staphylococci isolates from these sources.
Materials & Methods: 80 samples were collected from humans in different areas of Basrah Province, including 40 samples from human hand swabs and 40 from nasal swabs. The samples were inoculated onto mannitol salt agar and blood agar and then incubated at 37ºC for 24 hrs. Antibiotic susceptibility testing was performed using the disc diffusion method. A molecular study was done using the PCR technique.
Findings: 37 samples (46.25%) were positive for staphylococcal infection. Five species, including S. sciuri, S. lentus, S. gallinarum, S. chromogen, and S. haemolyticus were identified, according to Vitek 2 kit. Staphylococci were resistant to several different antibiotics. Out of 20 amplification samples, only 12 positive samples were purified for the ermA gene region with a PCR product of 190 bp. The results also showed the presence of an ermC band with a size of 299 bp, which represents the correct expected band in 8 isolates out of all isolates.
Conclusion: Gram-positive organisms are increasingly identified as the source of acute clinical infection in animals and humans. Some isolates are resistant to several different antibiotics. The ermC gene, ermA gene, and both ermA and ermC genes are present in the genome of these bacteria.
W.n. Ibraheim,
Volume 15, Issue 2 (4-2023)
Abstract

Aims: Bronchial asthma is a life-threatening disease with a multifactorial etiology. It was shown that immunological dysregulations play an essential role in the exacerbation of the patient’s attacks. Toll-like receptors act as a bridge in the transmission of different signals associated with the regulation of immune responses. According to numerous research, TLR2 causes different outcomes in asthma. TLR2 and TLR4 overexpression seems to predispose to an increase in the frequency of dyspneic attacks. Therefore, this study aimed to learn more about the function of TLR2 and TLR4 and investigate their underlying association with allergic airway inflammation in asthmatic patients.
Materials & Methods: In this case-control study conducted at outpatient clinics in a Specialized Allergy Center in Basrah City, South of Iraq, 70 asthmatic patients and 70 healthy individuals were investigated. 4ml of venous blood was drawn and divided into two parts: 2ml was used for RNA extraction and qRT-PCR, and another 2ml was used for the serological tests. Data analysis was done by SPSS 26 software.
Findings: The mean serum levels of TLR2 and TLR4 were significantly higher in the asthmatic group (28.33±13.00ng/ml and 46.30±20.32ng/ml, respectively) than in the control group (7.33±3.73ng/ml and 26.28±14.32ng/ml, respectively). Also, the expression level of TLR2 and TLR4 was significantly higher in the asthmatic group (p<0.05).
Conclusion: TLR2 and TLR4 are increased in patients with bronchial asthma compared to healthy individuals. Elevated levels of both biomarkers may act as a trigger for increased secretion of other cytokines, leading to exacerbation of asthmatic signs and symptoms.

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