Pasteur Institute of Iran
Iranian Biomedical Journal
1028-852X
2008-823X
18
4
2014
10
1
MS14 Down-Regulates Lipocalin2 Expression in Spinal Cord Tissue in an Animal Model of Multiple Sclerosis in Female C57BL/6
196
202
EN
Abbas
Ebrahimi-Kalan
N
Jafar
Soleimani Rad
N
Laya
Kafami
N
Daryoush
Mohammadnejad
N
Mehryar
Habibi Roudkenar
N
Amir Afshin
Khaki
N
Zeynab
Aliyari Serej
N
Amaneh
Mohammadi Roushandeh
a.mohammadiroshandeh@umsha.ac.ir
Y
10.6091/ibj.1375.2014
Notice of the Full Retraction of the Above-Mentioned Article
Due to the redundant information presented in this paper and the paper published in the Iran Red Crescent Journal: "MS14, a Marine Herbal Medicine, an Immunosuppressive Drug in Experimental Autoimmune Encephalomyelitis. Iran Red Crescent Med J. 2014 July; 16(7): e16956, the editor/publisher primarily declared a notice of "partial retraction" (dated 26 August, 2020). But since the amount of redundant information was later found very significant (Figure-1 and the graph in Figure-2) and its omission would not leave a credible paper, IBJ was obliged to issue a notice of full retraction on 1 November 2020. The authors are not in agreement with this decision.
Notice of the Partial Retraction of the Above-Mentioned Article
The authors would like to retract Figure 1 from the paper entitled: “MS14 Down-regulates Lipocalin2 Expression in Spinal Cord Tissue in an Animal Model of Multiple Sclerosis in female C57BL/6”. The reason for this partial retraction is the duplicity of this Figure in the addressed paper and the paper entitled: “MS14, a Marine Herbal Medicine, an Immunosuppressive Drug in Experimental Autoimmune Encephalomyelitis” (Iran Red Crescent Med J, 2014 July; 16(7): e16956). The duplicity was inevitable, as the data was needed for the presentation of the rest of the data in the former paper, whereas the latter paper was not then published. However, considering both papers are published at this time, we would like to retract Figure 1 from the above-addressed paper.
http://ibj.pasteur.ac.ir/article-1-1490-en.html
http://ibj.pasteur.ac.ir/article-1-1490-en.pdf
Pasteur Institute of Iran
Iranian Biomedical Journal
1028-852X
2008-823X
18
4
2014
10
1
Effects of Coenzyme Q10 on the ratio of TH1/TH2 in Experimental Autoimmune Encephalomyelitis Model of Multiple Sclerosis in C57BL/6
203
211
EN
Maryam
Soleimani
N
Seyed Behnamedin
Jameie
behjame@gmai..com
Y
Mahmood
Barati
N
Mehdi
Mehdizadeh
N
Mahdieh
erdari
N
10.6091/ibj.13362.2014
Background: Multiple sclerosis (MS) is known as a progressive central nervous system inflammatory disease. Certain factors, such as interleukins, inflammatory cells, and oxidative stress are supposed to involve in MS etiology. Because of the important role of oxidative stress, antioxidant therapy for MS has received more attention. Although coenzyme Q10 (CoQ10) acts as an antioxidant, there is a lack of enough research on its effects on MS. Therefore, the present research was designed. Methods: C57BL/6 female adult mice (n = 30) were used in this study. The animals were randomly divided into trial and control groups. To induce MS, routine procedure for experimental autoimmune encephalomyelitis (EAE) was used, and scoring was performed based on clinical signs. By detecting score one, CoQ10 administration was started (10 mg/kg/three weeks). By using ELISA and real-time PCR, the brain levels of TNF-gamma, IL-10, IL-4, and IL-12 were studied. Statistical tests were used to analyze the data and the P value less than 0.05 was considered to be significant. Results: Clinical symptoms in EAE animals were significantly decreased (P<0.05) as compared to control ones. In addition, the level of the TNF-gamma was significantly decreased following CoQ10 administration versus IL-10. The ratio of TH1/TH2 interleukins in treated animals was significantly less than that in non-treated animals (P<0.01). Conclusion: Our findings showed that CoQ10 is capable of suppressing the inflammatory pathway of MS.
Experimental autoimmune encephalomyelitis (EAE), Multiple Sclerosis (MS), Coenzyme Q10 (CoQ10)
http://ibj.pasteur.ac.ir/article-1-1165-en.html
http://ibj.pasteur.ac.ir/article-1-1165-en.pdf
Pasteur Institute of Iran
Iranian Biomedical Journal
1028-852X
2008-823X
18
4
2014
10
1
Immunogenicity of a Fusion Protein Comprising Coli Surface Antigen 3 and Labile B Subunit of Enterotoxigenic Escherichia coli
212
218
EN
Masoome
Alerasol
N
Seyed Latif
Mousavi Gargari
slmousavi@shahed.ac.ir
Y
Shahram
Nazarian
N
Samane
Bagheri
N
10.6091/ibj.1344.2014
Background: Enterotoxigenic Escherichia coli (ETEC) strains are the major causes of diarrheal disease in humans and animals. Colonization factors and enterotoxins are the major virulence factors in ETEC pathogenesis. For the broad-spectrum protection against ETEC, one could focus on colonization factors and non-toxic heat labile as a vaccine candidate. Methods: A fusion protein is composed of a major fimbrial subunit of coli surface antigen 3, and the heat-labile B subunit (LTB) was constructed as a chimeric immunogen. For optimum level expression of protein, the gene was synthesized with codon bias of E. coli. Also, recombinant protein was expressed in E. coli BL21DE3. ELISA and Western tests were carried out for determination of antigen and specificity of antibody raised against recombinant protein in animals. The anti-toxicity and anti-adherence properties of the immune sera against ETEC were also evaluated. Results: Immunological analyses showed the production of high titer of specific antibody in immunized mice. The built-in LTB retains native toxin properties which were approved by GM1 binding assay. Pre-treatment of the ETEC cells with anti-sera significantly decreased their adhesion to Caco-2 cells. Conclusion: The results indicated the efficacy of the recombinant chimeric protein as an effective immunogen inducing strong humoral response. The designated chimer would be an interesting prototype for a vaccine and worthy of further investigation.
Recombinant vaccine, Enterotoxigenic Escherichia coli (ETEC), cstH, eltB
http://ibj.pasteur.ac.ir/article-1-1233-en.html
http://ibj.pasteur.ac.ir/article-1-1233-en.pdf
Pasteur Institute of Iran
Iranian Biomedical Journal
1028-852X
2008-823X
18
4
2014
10
1
Antibiotic Resistance Pattern of Different Escherichia coli Phylogenetic Groups Isolated from Human Urinary Tract Infection and Avian Colibacillosis
219
224
EN
Ali
Kazemnia
Kazemnia.ali@gmail.com
Y
Malahat
Ahmadi
N
Mahdi
Dilmaghani
N
10.6091/ibj.1394.2014
Background: The emergence and propagation of different phylogenetic groups of antimicrobial-resistant E. coli have become a worldwide health concern in human and veterinary medicine. Therefore, the evaluation of the phylogenetic distribution of antibiotic-resistant E. coli is important for therapeutic and economic purposes. The aims of this study were to determine phylogenetic groups and patterns of antibiotic resistance of E. coli strains isolated from human urinary tract infection and avian colibacillosis. Methods: A total of 50 E. coli isolates (25 from human urinary tract infection and 25 from avian colibacillosis) were characterized by culture and assigned as different phylogenetic groups (A, B1, B2, and D) by triplex PCR assay. Kirby-Bauer disk diffusion method was used to assess the susceptibility of all isolates to ten antibiotics. Results: Results showed that the majority of the human and poultry isolates belonged to phylogenetic groups A and B2 and phylogenetic group B1 of the avian pathogenic strain isolates were the most drug-resistant isolates. Most of the isolates were resistant to at least five antibiotics, and multiple drug resistance was observed in 98% of E. coli isolates. A high degree of resistance was seen against penicillin and erythromycin. Conclusion: According to the results of this study, multidrug-resistance among isolates and high relation between phylogenetic groups and resistance in both human and poultry isolates were observed.
Escherichia coli, Avian colibacillosis, Phylogenetic grouping
http://ibj.pasteur.ac.ir/article-1-1166-en.html
http://ibj.pasteur.ac.ir/article-1-1166-en.pdf
Pasteur Institute of Iran
Iranian Biomedical Journal
1028-852X
2008-823X
18
4
2014
10
1
Traumatic Brain Injury Has Not Prominent Effects on Cardiopulmonary Indices of Rat after 24 Hours: Hemodynamic, Histopathology, and Biochemical Evidence
225
231
EN
Hamid
Najafipour
najafipourh@ yahoo.co.uk
Y
Ali
Siahposht Khachaki
N
Mohammad
Khaksari
N
Beydolah
Shahouzehi
N
Siyavash
Joukar
N
Hamid Reza
Poursalehi
N
10.6091/ibj.13222.2014
Background: Accidents are the second reason for mortality and morbidity in Iran. Among them, brain injuries are the most important damage. Clarification of the effects of brain injuries on different body systems will help physicians to prioritize their treatment strategies. In this study, the effect of pure brain trauma on the cardiovascular system and lungs 24 hours post trauma was assessed. Methods: Male Wistar rats (n = 32) were divided into sham control and traumatic brain injury (TBI) groups. In TBI animals, under deep anesthesia, a blow to the head was induced by the fall of a 450 g weight from 2 m height. Twenty four hours later, heart electrocardiogram and functional indices, cardiac troponin I, IL-6, TNF-alpha, IL-Ibeta in tissue and serum, and the histopathology of heart and lung were assessed. Results: The results showed that none of the functional, biochemical, inflammatory, and histopathology indices was statistically different between the two groups at 24 hours post TBI. Indices of impulse conduction velocity in atrium (P wave duration and P-R interval) were significantly longer in the TBI group. Conclusion: Overall, no important functional and histopathologic disturbances were found in heart and lung of TBI group after 24 hours. If the data is reproduced in human studies, the medical team could allocate their priority to treatment of brain disorders of the victim in the first 24 hours of pure TBI and postpone extensive assessment of heart and lung health indices to later time, thus reducing patient and health system expenditures.
Brain injury (TBI), Cardiopulmonary, Myocardial contraction, Cytokines
http://ibj.pasteur.ac.ir/article-1-1167-en.html
http://ibj.pasteur.ac.ir/article-1-1167-en.pdf
Pasteur Institute of Iran
Iranian Biomedical Journal
1028-852X
2008-823X
18
4
2014
10
1
Candesartan Attenuates Ischemic Brain Edema and Protects the Blood–Brain Barrier Integrity from Ischemia/Reperfusion Injury in Rats
232
238
EN
Hamdollah
Panahpour
Y
Ali Akbar
Nekooeian
N
Gholam Abbas
Dehghani
h.panahpour@arums.ac.ir
N
10.6091/ibj.13672.2014
Background: Angiotensin II (Ang II) has an important role on cerebral microcirculation however, its direct roles in terms of ischemic brain edema need to be clarified. This study evaluated the role of central Ang II by using candesartan, as an AT1 receptor blocker, in the brain edema formation and blood-brain barrier (BBB) disruption caused by ischemia/reperfusion (I/R) injuries in rat. Methods: Rats were exposed to 60-min middle cerebral artery (MCA) occlusion. Vehicle and non-hypotensive doses of candesartan (0.1 mg/kg) were administered one hour before ischemia. Neurological dysfunction scoring was evaluated following 24 h of reperfusion. Animals were then decapitated under deep anesthesia for the assessments of cerebral infarct size, edema formation, and BBB permeability. Results: The outcomes of 24 h reperfusion after 60-min MCA occlusion were severe neurological disability, massive BBB disruption (Evans blue extravasation = 12.5 ± 1.94 µg/g tissue), 4.02% edema, and cerebral infarction (317 ± 21 mm3). Candesartan at a dose of 0.1 mg/kg, without changing arterial blood pressure, improved neurological dysfunction scoring together with significant reductions in BBB disruption (54.9%), edema (59.2%), and cerebral infarction (54.9%). Conclusions: Inactivation of central AT1 receptors, if not accompanied with arterial hypotension, protected cerebral micro-vasculatures from damaging effects of acute stroke.
Blood–brain barrier, Brain edema, AT1 receptor, Candesartan
http://ibj.pasteur.ac.ir/article-1-1168-en.html
http://ibj.pasteur.ac.ir/article-1-1168-en.pdf
Pasteur Institute of Iran
Iranian Biomedical Journal
1028-852X
2008-823X
18
4
2014
10
1
Effect of Combination Therapy Using Hypothermia and Granulocyte Colony-Stimulating Factor in a Rat Transient Middle Cerebral Artery Occlusion Model
239
244
EN
Laya
Ghahari
N
Manouchehr
Safari
N
Mohamad Taghi
Joghataei
N
Mehdi
Mehdizadeh
N
Mansoureh
Soleimani
mansourehsoleimani@gmail.com
Y
10.6091/ibj.13852.2014
Background: Stroke is the third leading cause of death. Hypothermia has been recognized as an effective method in reducing brain injury. In this study, we assessed the effects of granulocyte colony-stimulating factor (G-CSF) as a neuroprotective agent and mild hypothermia on mortality, behavioral function, infarct volume, and brain edema in Wistar rats. Methods: Forty male rats were used in five groups (eight rats in each group): control, hypothermy, G-CSF, combination hypothermy + CSF, and sham. Rats were anesthetized by injection of chloral hydrate (400 mg/kg) intraperitoneally. Transient cerebral ischemia was induced by 60-min intraluminal occlusion of left middle cerebral artery. Hypothermia, initiated at the time of reperfusion and G-CSF was started one hour after reperfusion at a dose of 15 mg/kg subcutaneously. The motor behavior was measured using Garcia’s index and animals were assigned for the assessments of infarction, brain swelling, and mortality rate. Results: The mortality was 38.46% (control group) and reduced in other groups. Neurological deficit score of control group (40.31 ± 1.56) was significantly lower than in treatment groups. The total cerebral infarct volume of treatment group was significantly lower than control group (43.96 ± 44.05 mm3). Treatment with hypothermy plus G-CSF (2.69 ± 0.24%) could significantly reduce brain swelling volume than other treatment groups. Conclusion: Our major finding is that mild hypothermic treatment plus G-CSF significantly reduced mortality rate and edema and improved neurological function. The results suggest that the combination of hypothermia and G-CSF is more effectively than other treatment groups being used alone.
Granulocyte colony-stimulating factor (G-CSF), Rats, Brain ischemia, Hypothermia
http://ibj.pasteur.ac.ir/article-1-1170-en.html
http://ibj.pasteur.ac.ir/article-1-1170-en.pdf
Pasteur Institute of Iran
Iranian Biomedical Journal
1028-852X
2008-823X
18
4
2014
10
1
A 40-bp Insertion/Deletion Polymorphism of Murine Double Minute2 (MDM2) Increased the Risk of Breast Cancer in Zahedan, Southeast Iran
245
249
EN
Mohammad
Hashemi
hashemim@zdmu.ac.ir
Y
Mohsen
Omrani
N
Ebrahim
Eskandari-Nasab
N
Seyed-Shahaboddin
Hasani
N
Mohammad Ali
Mashhadi
N
Mohsen
Taheri
N
10.6091/ibj.13332.2014
Background: MDM2 (Murine Double Minute2) is an oncoprotein that inhibits the P53 activity. Overexpression of MDM2 gene has been reported in several human tumors. In the present study, we aimed to evaluate the impact of 40-bp insertion/deletion (ins/del) polymorphism on the promoter of MDM2 and susceptibility to breast cancer in a sample of Iranian population. Methods: This case-control study was carried out on 236 patients with breast cancer and 203 healthy individuals. Genomic DNA was extracted from the whole blood by the salting-out method. The 40-bp ins/del polymorphism was determined by using polymerase chain reaction. Results: The findings indicated that MDM2 ins/del variant increased the risk of breast cancer in co-dominant- (odds ratio [OR] = 2.09, 95% CI = 1.14-3.85, P = 0.018, del/del vs. ins/ins), dominant- (OR = 1.49, 95% CI = 1.02-2.18, P = 0.038, ins/del + del/del vs. ins/ins), and recessive- (OR = 1.86, 95% CI = 1.03-3.34, P = 0.038, del/del vs. ins/ins + ins/del) tested inheritance models. The del allele increased the risk of breast cancer (OR= 1.48, 95% CI=1.11-1.98, P=0.008) compared with ins allele. Conclusions: Our result revealed that 40-bp ins/del polymorphism in the promoter of MDM2 increased the risk of breast cancer in an Iranian population. Further investigations with larger sample sizes and diverse ethnicities are needed to verify our findings.
Breast cancer, Murine Double Minute2 (MDM2), Polymorphism
http://ibj.pasteur.ac.ir/article-1-1171-en.html
http://ibj.pasteur.ac.ir/article-1-1171-en.pdf