Publications by authors named "Rezvan Khajavi"

3 Publications

  • Page 1 of 1

Multidrug and co-resistance patterns of non-fermenting Gram-negative bacilli involved in ventilator-associated pneumonia carrying class 1 integron in the North of Iran.

Germs 2017 Sep 1;7(3):123-131. Epub 2017 Sep 1.

MSc, Molecular and Cell Biology Research Center, Faculty of Medicine, Mazandaran, University of Medical Sciences, Km 18 Khazarabad road, Sari, Iran.

Introduction: Ventilator-associated pneumonia (VAP) due to non-fermenting Gram-negative bacilli (NFGNB), especially and spp., is one of the main hospital-acquired infections leading to mortality and morbidity, especially in intensive care units (ICUs). This study seeks to determine the multidrug and co-resistance (MDR) patterns of NFGNB that are agents of VAP, and assess the presence of class 1 integron in these bacteria.

Methods: This cross-sectional study involved VAP patients admitted in the ICUs of 18 hospitals in the Mazandaran province, located in the North of Iran. The antibiotic susceptibility pattern was determined by the minimum inhibitory concentration (MIC) test by using broth microdilution method. Presence of class 1 integron was evaluated by the polymerase chain reaction (PCR) assay.

Results: Out of a total of 83 patients who were microbiologically diagnosed as VAP, 52 non-duplicated NFGNBs (24 and 28 ) were causative of VAP, out of which MDR NFGNBs were responsible for 48 (57.83%) cases. The frequencies of MDR NFGNBs were as follows: 27 (56.25%) and 21 (43.75%) . isolates were resistant to all aminoglycoside antibiotics (50%), ciprofloxacin (45.8%), ceftazidime (70.8%), cefepime (87.5%), colistin (62.5%), and imipenem (29.2%). isolates were resistant to aminoglycosides (53.6%), ciprofloxacin (85.7%), ceftazidime (92. 9%), cefepime (92.9%), colistin (35.7%), and imipenem (57.1%). Twelve isolates were resistant to all 10 tested antibiotics. The number of rates of class 1 integron, positive for MDR and MDR , were 20 (95.23%) and 21 (77.78%), respectively.

Conclusion: The high prevalence of multidrug resistance and incidence of class 1 integron is a therapeutic concern. Employing antibiotic stewardship in hospitals could prevent the dissemination of MDR bacteria.
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http://dx.doi.org/10.18683/germs.2017.1117DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5601095PMC
September 2017

Association between interleukin-32 polymorphism and multiple sclerosis.

J Neurol Sci 2017 Aug 23;379:144-150. Epub 2017 May 23.

Molecular and Cell Biology Research Center, Department of Immunology, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran.

Background And Aim: Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). Environmental and genetic factors play a key role in the development of the disease. Interleukin-32 (IL-32) is a cytokine inducing crucial inflammatory cytokines such as TNF-α, IL-6, IL-1β, and MIP-2. The present study was an attempt to reveal any association between IL-32 levels and C/T promoter SNP with susceptibility to MS.

Methods: This case control study recruited a total of 304 subjects including 132 MS patients and 172 sex- and age-matched healthy controls. Clinical and epidemiological characteristics of the RRMS, PPMS, and PPMS populations were assessed. Serum levels and C/T polymorphism of IL-32 were determined by ELISA and RFLP-PCR methods, respectively.

Results: Serum levels of IL-32 were significantly different between MS patients and controls. IL-32 was dramatically higher in the patients than that healthy controls (2297.4±280.2 ver. 712.9±90.2, p=0.001). C allele was prominent in MS patients than the controls and might increase the risk of MS up to 1.6 fold (95% CI; 1.02-2.4, p=0.038). In addition, the presence of C allele enhanced IL-32 production drastically.

Conclusion: This is the first study in which IL-32 gene promoter C/T polymorphism and its serum levels were investigated. The increase in serum levels of IL-32 in accordance with additive effect of the presence of C allele in MS patients might introduce IL-32 as a key player in MS pathogenesis or immunedysregulation.
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http://dx.doi.org/10.1016/j.jns.2017.05.045DOI Listing
August 2017

Association between ghrelin gene (Leu72Met) polymorphism and ghrelin serum level with coronary artery diseases.

DNA Cell Biol 2014 Feb 17;33(2):95-101. Epub 2013 Dec 17.

1 Molecular and Cell Biology Research Center, Mazandaran University of Medical Sciences , Sari, Iran .

Research shows that ghrelin gene polymorphism has some association with coronary artery diseases (CAD). Due to genetic differences among nations and the high prevalence of CAD, we conducted this study to examine the possible association between the polymorphism of ghrelin gene Leu72Met and CAD among an Iranian population. This case-control study was undertaken with patients who were referred to referral heart center, in 2011, with chest pain or a positive exercise test. Patients with risk factors for heart disease or who were surgery candidates, who underwent angiography and echocardiography, were also included. DNA extractions were performed using a modified salting out method, and the ghrelin region was amplified using polymerase chain reaction. The presence of the Leu72Met polymorphism and the serum levels of ghrelin were determined using the restriction fragment length polymorphism method and the enzyme-linked immunosorbent assay, respectively. The results indicated that in CAD patients, the incidence of heart failure was significantly different between the groups with genotypes CC or AA+CA (p=0.041). Mean serum level of ghrelin in the CAD group was significantly higher than that in the control group (p<0.0001). Additionally, there was a significant relationship between the distribution of ghrelin genotypes and serum levels of ghrelin in both the CAD and control groups (p<0.0001). This study indicates that there was a significant association between heart failure in CAD patients and the presence of the polymorphism, as well as an increase in serum levels of ghrelin associated with genotype distribution such that ghrelin levels have an inverse relationship with the frequency of the CC genotype.
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http://dx.doi.org/10.1089/dna.2013.2218DOI Listing
February 2014