ORIGINAL_ARTICLE
Publication Ethics: A Case Series with Recommendations According to Committee on Publication Ethics (COPE)
Ethical misconduct is not a new issue in the history of science and literature. However, ethical misconducts in science have grown considerably in the modern era which is due to emphasis on the scientific proliferation in research institutes and gauging scientists according to their publications. In the current case series, several misconducts occurring over the previous years in Mashhad University of Medical Sciences (Mashhad, Iran) either for Journals or Faculty members were gathered and specific recommendations were provided to avoid similar events in the future. All recommendations are according to Committee on Publication Ethics (COPE).
https://ijbms.mums.ac.ir/article_4905_3431673e71a3bf36e201c1ef74bc798b.pdf
2012-09-01
1003
1007
10.22038/ijbms.2012.4905
Authorship criteria
Copyright transfer
Data fabrication
Plagiarism
Publication Ethics
Bibi Seddigheh
Fazly Bazzaz
1
Biotechnology Research Centre, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Ramin
Sadeghi
sadeghir@mums.ac.ir
2
Nuclear Medicine Research Centre, Imam Reza Hospital, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
1. Siroos S. Style of Persian prose. Mitra publication.
1
2. Committee On Publication Ethics (COPE) website. Available at: http://publicationethics.org/.
2
3. http://publicationethics.org/files/u2/04D_Author_Remove_Published.pdf.
3
4. http://publicationethics.org/files/u2/04C_Author_Add_Published.pdf.
4
5. http://publicationethics.org/files/u2/04E_Author_Ghost_Guest_Gift.pdf.
5
6. Aldhous P. Hwang's forgotten crime: the exploitation of women is a far worse offence than data fabrication. New Sci 2006; 189:22.
6
7. http://publicationethics.org/files/u7140/Flowchart%20Fabricated%20B%20revised.pdf.
7
8. http://publicationethics.org/case/massaging-impact-factor.
8
9. http://publicationethics.org/files/u2/06_Ethics_Submitted.pdf.
9
10.http://publicationethics.org/files/Code%20of%20conduct%20for%20journal%20editors_0.pdf11. http://publicationethics.org/files/u2/01A_Redundant_Submitted.pdf.
10
12. http://publicationethics.org/files/u2/01B_Redundant_Published.pdf.
11
13. http://publicationethics.org/files/u2/02B_Plagiarism_Published.pdf.
12
ORIGINAL_ARTICLE
Chronic Low-grade Inflammation after Exercise: Controversies
https://ijbms.mums.ac.ir/article_4906_be2da992f2185f75b7604ea8916bd621.pdf
2012-09-01
1008
1009
10.22038/ijbms.2012.4906
Majid
Khazaei
khazaei@med.mui.ac.ir
1
Department of Physiology, Isfahan University of Medical Sciences, Isfahan, Iran
LEAD_AUTHOR
1. Kazeem A, Olubayo A, Ganiyu A. Plasma nitric oxide and acute phase proteins after moderate and prolonged exercises. Iran J Basic Med Sci 2012; 15:602-607.
1
2. Ribeiro F, Alves AJ, Duarte JA, Oliveira J. Is exercise training an effective therapy targeting endothelial dysfunction and vascular wall inflammation? Int J Cardiol 2010; 141:214-221.
2
3. Pearson TA, Mensah GA, Alexander RW, Anderson JL, Cannon RO, III, Criqui M, et al. Markers of inflammation and cardiovascular disease: application to clinical and public health practice: A statement for healthcare professionals from the Centers for Disease Control and Prevention and the American Heart Association. Circulation 2003; 28;107:499-511.
3
4. Gielen S, Schuler G, Hambrecht R. Exercise training in coronary artery disease and coronary vasomotion. Circulation 2001; 2;103:E1-E6.
4
5. Andersson J, Jansson JH, Hellsten G, Nilsson TK, Hallmans G, Boman K. Effects of heavy endurance physical exercise on inflammatory markers in non-athletes. Atherosclerosis 2010; 209:601-605.
5
6. Nicklas BJ, Ambrosius W, Messier SP, Miller GD, Penninx BW, Loeser RF, et al. Diet-induced weight loss, exercise, and chronic inflammation in older, obese adults: a randomized controlled clinical trial. Am J Clin Nutr 2004; 79:544-551.
6
7. Petersen AM, Pedersen BK. The anti-inflammatory effect of exercise. J Appl Physiol 2005; 98:1154-1162.
7
8. Wilund KR. Is the anti-inflammatory effect of regular exercise responsible for reduced cardiovascular disease? Clin Sci (Lond) 2007; 112:543-555.
8
9. Teixeira-Lemos E, Nunes S, Teixeira F, Reis F. Regular physical exercise training assists in preventing type 2 diabetes development: focus on its antioxidant and anti-inflammatory properties. Cardiovasc Diabetol 2011; 10:12.
9
10. Yudkin JS, Stehouwer CD, Emeis JJ, Coppack SW. C-reactive protein in healthy subjects: associations with obesity, insulin resistance, and endothelial dysfunction: a potential role for cytokines originating from adipose tissue? Arterioscler Thromb Vasc Biol 1999; 19:972-978.
10
11. Fischer CP, Berntsen A, Perstrup LB, Eskildsen P, Pedersen BK. Plasma levels of interleukin-6 and C-reactive protein are associated with physical inactivity independent of obesity. Scand J Med Sci Sports 2007; 17:580-587.
11
12. Niebauer J, Clark AL, Webb-Peploe KM, Coats AJ. Exercise training in chronic heart failure: effects on pro-inflammatory markers. Eur J Heart Fail 2005; 7:189-193.
12
13. Sallam N, Khazaei M, Laher I. Effect of moderate-intensity exercise on plasma C-reactive protein and aortic endothelial function in type 2 diabetic mice. Mediators Inflamm 2010: 149678.
13
14. Ploeger HE, Takken T, de Greef MH, Timmons BW. The effects of acute and chronic exercise on inflammatory markers in children and adults with a chronic inflammatory disease: a systematic review. Exerc Immunol Rev 2009; 15:6-41.
14
15. Zhang H, Zhang C. Vasoprotection by dietary supplements and exercise: role of TNFalpha signaling. Exp Diabetes Res 2012; 972679.
15
ORIGINAL_ARTICLE
Epidemiology of mecA-Methicillin Resistant Staphylococcus aureus in Iran: A Systematic Review and Meta-analysis
Objective(s)Staphylococcus aureus is a prevalent pathogen worldwide. Methicillin resistant S. aureus (MRSA), which is usually multi-resistant in hospitals, has been a daunting challenge for clinicians for more than half a century. The aim of this systematic review and meta-analysis is to determine the relative frequency (RF) of MRSA in different regions of Iran.Materials and MethodsSearch terms “Staphylococcus aureus”, “Methicillin”, “mecA” and “Iran” were used in PubMed, Scirus and Google Scholar. Two Persian scientific search engines and ten recent national congresses were also explored. Articles/abstracts, which used clinical specimens and had done PCR to detect the mecA gene, were included in this review. Comprehensive Meta-Analysis and Meta-Analyst software were used for statistical analysis.ResultsOut of 2690 results found in the mentioned databases, 48 articles were included in the final analysis. These studies were done in Ahvaz, Falavarjan, Fasa, Gorgan, Hamedan, Isfahan, Kashan, Mashhad, Sanandaj, Shahrekord, Shiraz, Tabriz, Tehran and Tonekabon. Pooled estimation of 7464 S. aureus samples showed that 52.7%±4.7 (95% confidence interval [CI]) of strains were mecA positive. MRSA RF in different studies varied from 20.48% to 90% in Isfahan and Tehran, respectively. We found a moderate heterogeneity (I2= 48.5%) of MRSA RF among studies conducted in Tehran (ranging from 28.88% to 90%, mean 52.7% [95% CI: 46.6%±58.8%]).ConclusionAccording to the results of this study, MRSA RF in Iran is in the high range. Thus, measures should be taken to keep the emergence and transmission of these strains to a minimum.
https://ijbms.mums.ac.ir/article_4907_9c7e0b6b23ef142fb5d3809af857d534.pdf
2012-09-01
1010
1019
10.22038/ijbms.2012.4907
Iran
Methicillin-Resistant Staphylococcus aureus
Systematic review
Emran
Askari
1
Mashhad Medical Microbiology Student Research Group, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Fatemeh
Soleymani
2
Mashhad Medical Microbiology Student Research Group, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Arash
Arianpoor
3
Mashhad Medical Microbiology Student Research Group, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Seyed Meghdad
Tabatabai
4
Mashhad Medical Microbiology Student Research Group, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Aminreza
Amini
aminiar901@mums.ac.ir
5
Department of Biostatistics, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Mahboobeh
Naderi Nasab
naderinasabm@mums.ac.ir
6
Mashhad Medical Microbiology Student Research Group, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
1. Deleo FR, Otto M, Kreiswirth BN, Chambers HF. Community-associated meticillin-resistant Staphylococcus aureus. Lancet 2010; 375:1557-1568.
1
2. Grundmann H, Aires-de-Sousa M, Boyce J, Tiemersma E. Emergence and resurgence of meticillin-resistant Staphylococcus aureus as a public-health threat. Lancet 2006; 368:874-885.
2
3. Cookson B. Five decades of MRSA: controversy and uncertainty continues. Lancet 2011; 378:1291-1292.
3
4. Köck R, Becker K, Cookson B, van Gemert-Pijnen JE, Harbarth S, Kluytmans J, et al. Methicillin-resistant Staphylococcus aureus (MRSA): burden of disease and control challenges in Europe. Euro Surveill 2010; 15:1-9.
4
5. Cosgrove SE, Sakoulas G, Perencevich EN, Schwaber MJ, Karchmer AW, Carmeli Y. Comparison of mortality associated with methicillin-resistant and methicillin-susceptible Staphylococcus aureus bacteremia: a meta-analysis. Clin Infect Dis 2003; 36:53-59.
5
6. Moellering RC. Why has methicillin-resistant Staphylococcus aureus become such a successful pathogen in adults? Infect Dis Clin Pract 2010;18:286-291.
6
7. Stefani S, Chung DR, Lindsay JA, Friedrich AW, Kearns AM, Westh H, et al. Meticillin-resistant Staphylococcus aureus (MRSA): global epidemiology and harmonisation of typing methods. Int J Antimicrob Agents 2012; 39:273-282.
7
8. Graveland H, Duim B, van Duijkeren E, Heederik D, Wagenaar JA. Livestock-associated methicillin-resistant Staphylococcus aureus in animals and humans. Int J Med Microbiol 2011; 301:630-634.
8
9. Forbes BA. Issues in the identification and susceptibility testing of Staphylococci. In: Crossley KB, Jefferson KK, Archer GL, Fowler VG, editors. Staphylococci in Human Disease. 2nd ed. Oxford, UK: Wiley-Blackwell; 2009. p. 235-252.
9
10. Karami S, Rahbar M, Vand Yousefi J. Evaluation of five phenotypic methods for detection of methicillin resistant Staphylococcus aureus (MRSA). Iran J Pathol 2011; 6:27-31.
10
11. Radlberger P, Zechmeister I. Innovative framework for evidence-based decision making in healthcare – standardised working in HTA (WP1.2): HTA- Projektbericht. 2011. Available at: http://eprints.hta.lbg.ac.at/932/1/HTA-Projektbericht_Nr.44a.pdf.
11
12. Clinical and Laboratory Standards Institute/NCCLS. 2007. Performance standards for antimicrobial susceptibility testing; 17th informational supplement. CLSI document M100-S17. Clinical and Laboratory Standards Institute, Wayne, PA.
12
13. Clinical and Laboratory Standards Institute/NCCLS. 2008. Performance standards for antimicrobial susceptibility testing; 18th informational supplement. CLSI document M100-S18. Clinical and Laboratory Standards Institute, Wayne, PA.
13
14. Ekrami A, Samarbafzadeh A, Alavi M, Kalantar E, Hamzeloi F. Prevalence of methicillin resistant Staphylococcus species isolated from burn patients in a burn center, Ahvaz, Iran. Jundishapur J Microbiol 2010; 3:84-91.
14
15. Moosavian M, Torabipour M. Identification of mecA gene in phenotypic methicillin-resistant Staphylococcus aureus strains isolated from clinical specimens.The First Iranian International Congress of Medical Bacteriology; 4-7 sep; Tabriz, Iran2011. p. 255.
15
16. Khosravi AD, Hoveizavi H, Farshadzadeh Z. The prevalence of genes encoding leukocidins in Staphylococcus aureus strains resistant and sensitive to methicillin isolated from burn patients in Taleghani hospital, Ahvaz, Iran. Burns 2012; 38:247-251.
16
17. Heidari M, Momtaz H, Madani M. Detection of the antibiotic resistance genes in Staphylococcus aureus isolated from human infections and bovine mastitis. Afr J Microbiol Res 2011; 5:5132-5136.
17
18. Abdollahi A, Koohpayeh A, Najafipour S, Mansouri Y, Abdollahi S, Jafari S. Evaluation of drug esistance and SCCmec genotype in MRSA strains. Behdad 2012; 1:47-52.
18
19. Vaez H, Tabaraei A, Moradi A,Ghaemi EA. Evaluation of methicillin resistance Staphylococcus aureus isolated from patients in Golestan province-north of Iran. Afr J Microbiol Res 2011; 5:432-436.
19
20. Zamani A, Sadeghian S, Ghaderkhani J, Alikhani MY, Najafimosleh M, Taghi Goodarzi M, et al. Detection of methicillin-resistance (mec-A) gene in Staphylococcus aureus strains by PCR and determination of antibiotic susceptibility. Ann Microbiol 2007; 57:273-276.
20
21. Alizargar J, Moravveji A. Prevalence of methicillin resistant Staphylococcus in Kashan. First International and 12th Iranian Congress of Microbiology; 23-26 May; Kermanshah, Iran:2011. p. 1328.
21
22. Havaei SA, Vidovic S, Tahmineh N, Mohammad K, Mohsen K, Starnino S, et al. Epidemic methicillin-susceptible Staphylococcus aureus lineages are the main cause of infections at an Iranian university hospital. J Clin Microbiol 2011; 49:3990-3993.
22
23. Zeinali E, Moniri R, Safari M, Mousavi GA. Molecular characterization and SCCmec typing in meticillin-resistant Staphylococcus aureus isolated from clinical samples. Feyz, J Kashan Univ Med Sci 2011; 14:439-446.
23
24. Naderi Nasab M, Tavakolafshar J, Nazem M, Fatehnasab P, Faramarzi P, Khodadoost M. Detection of methicillin-resistant Staphylococcus aureus by phenotypic methods. Med J Mashhad Univ Med Sci 2005; 48:7-16.
24
25. Vaiseh P, Ramezanzadeh R, Deilami Z. Identification of class I integron and mecA in Staphylococcus strains typed by REP-PCR method. The Congress of Infections and Antibiotic Resistance; 2-3 May; Gilan, Iran: 2012.p.101.
25
26. Shariati L, Validi M, Tabatabaiefar MA, Karimi A, Nafisi MR. Comparison of real-time PCR with disk diffusion, agar screen and E-test methods for detection of methicillin-resistant Staphylococcus aureus. Curr Microbiol 2010; 61:520-524.
26
27. Japoni A, Alborzi A, Orafa F, Rasouli M, Farshad S. Distribution patterns of methicillin resistance genes (mecA) in Staphylococcus aureusisolated from clinical specimens. Iran Biomed J 2004; 8:173-178.
27
28. Nikbakht M, Nahaei MR, Akhi MT, Asgharzadeh M, Nikvash S. Molecular fingerprinting of meticillin-resistant Staphylococcus aureus strains isolated from patients and staff of two Iranian hospitals. J Hosp Infect 2008; 69:46-55.
28
29. Zarrini G, Aein F, Bahari Delgosha Z. Study of nosocomial methicillin resistant Staphylococcus aureus (MRSA) using disc diffusion, MASTAScreen MRSA + kit and PCR methods.The Second Iranian Congress of Clinical Microbiology; 7-9 October; Shiraz, Iran:2008. p. 149.
29
30. Esfandyari Kalajahi A, Hasani A, Riyazi A, Abbasian S, Pourmohammad A, Hasani A. Detection of virulence genes of Staphylococcus aureus isolated from nasal specimens of patients admitted in high risk wards of University teaching hospital, Tabriz. 4th Congress of Laboratory and Clinic; 21-23 December; Tehran, Iran: 2011. p. 491.
30
31. Kiani nia M. Development of Multiplex PCR for the detection of aph(3)-IIIa and aac(6′)/aph(2′′) genes in methicillin-resistant Staphylococcus aureus (MRSA) isolates from Northwest, Iran. 4th Congress of Laboratory and Clinic; 21-23 December; Tehran, Iran: 2011. p. 996.
31
32. Kiani nia M, Hasani A, Hasani A, Mirza Ahmadi S, Sadeghifard M, Deghani L. Nasal colonization of high risk group patients of northwest Iran by MRSA Predictability of resistance and concern about prevention. 4th Congress of Laboratory and Clinic; 21-23 December; Tehran, Iran: 2011. p. 853.
32
33. Mirsalehian A, Jebelameli F, Kazemi B, Alizadeh SA. Comparison of disc diffusion method withpolymerase chain reaction for detectingmethicillin resistancein clinical isolates of Staphylococci. Tehran Univ Med J 2003; 61:420-425.
33
34. Aligholi M, Emaneini M, Hashemi FB, Shahsavan S, Jabalameli F, Kazemi B. Determination of antimicrobial resistance pattern of Staphylococcus aureus isolated from clinical specimens. Tehran Univ Med J 2006; 64:26-32.
34
35. Mostafaee M, Behzadian-Nejad G, Najar-peerayeh S, Rezaei Yazdi H, Tohidpoor A. Prevalence of mecA gene in Staphylococcus aureus strains isolated from Tehran hospitals, 1385.The First Iranian Congress of Clinical Microbiology; 8-10 May; Shiraz, Iran:2007.p.16.
35
36. Aligholi M, Emaneini M, Jabalameli F, Shahsavan S, Dabiri H, Sedaght H. Emergence of high-level vancomycin-resistant Staphylococcus aureus in the Imam Khomeini Hospital in Tehran. Med Princ Pract 2008; 17:432-434.
36
37. Fatholahzadeh B, Emaneini M, Gilbert G, Udo E, Aligholi M, Modarressi MH, et al. Staphylococcal cassette chromosome mec (SCCmec) analysis and antimicrobial susceptibility patterns of methicillin-resistant Staphylococcus aureus (MRSA) isolates in Tehran, Iran. Microb Drug Resist 2008; 14:217-220.
37
38. Habibi M, Saderi H, Owlia P, Asadi Karam M. Detection of methicillin resistance in Staphylococcus aureus by disk diffusion and PCR methods. Iran J Pathol 2008; 3:11-14.
38
39. Azimian A, Najar-peerayeh S, Farshchian M, Naderi M, Salehipoor Z, Mostafaee M. Occurrence of the methicillin-resistant Staphylococcus aureus (MRSA) among clinical samples in Tehran and its correlation with the site of infection.The Second Iranian Congress of Clinical Microbiology; 7-9 October; Shiraz, Iran:2008.p.1101.
39
40. Bagherzadeh Yazdchi S, Pourmand MR, Zaeimi Yazdi J. Anbiotic susceptibility patterns and detection of coa and mecA genes in the Iranian isolates of Staphylococcus aureus.13th International Congress on Infectious Diseases;19-22 June; Kuala Lumpur, Malaysia 2008. p. e271.
40
41. Dadaei T, Eftekhar F. Correlation of biofilm formation in clinical isolates of Staphylococcus aureus by colony morphology and microplate measurement of biofilm formation.The Second Iranian Congress of Clinical Microbiology; 7-9 October; Shiraz, Iran:2008. p.107.
41
42. Salehipour Z, Azimian A, Ghazvini K. Phenotypic and genotypic study of drug resistance in Staphylococcus aureus strains isolated from blood culture of septicemia pateints in selected hospitals of Tehran.The Second Iranian Congress of Clinical Microbiology; 7-9 October; Shiraz, Iran:2008. p.172.
42
43. Aligholi M, Emaneini M, Jabalameli F, Shahsavan S, Abdolmaleki Z, Sedaghat H, et al. Antibiotic susceptibility pattern of gram-positive cocci cultured from patients in three university hospitals in Tehran, Iran during 2001-2005. Acta Med Iran 2009;47:329-334.
43
44. Emaneini M, Taherikalani M, Eslampour MA, Sedaghat H, Aligholi M, Jabalameli F, et al. Phenotypic and genotypic evaluation of aminoglycoside resistance in clinical isolates of Staphylococci in Tehran, Iran. Microb Drug Resist 2009; 15:129-132.
44
45. Najar-Peerayeh S, Azimian A, Mostafaee M, Siadat SD. Identification of methicillin-resistant Staphylococcus aureus by disk diffusion method, determination of MIC, and PCR for mecA Gene. Modares Med Sci J: Pathobiol 2009; 12:61-69.
45
46. Rahimi F, Bouzari M, Maleki Z, Rahimi F. Antibiotic susceptibility pattern among Staphylococcus spp. with emphasis on detection of mecA gene in methicillin resistant Staphylococcus aureus isolates. Iran J Clin Infect Dis 2009; 4:143-150.
46
47. Yadegar A, Sattari M, Mozafari NA, Goudarzi GR. Prevalence of the genes encoding aminoglycoside-modifying enzymes and methicillin resistance among clinical isolates of Staphylococcus aureus in Tehran, Iran. Microb Drug Resist 2009; 15:109-113.
47
48. Farhadian A, Behzadian Nejad, Najar-peerayeh S, Farhadian A, Vaziri. Determination of vancomycin and methicillin resistant in isolates of S.aureus in hospitals in the Iran.Third Iranian Congress of Clinical Microbiology; 6-8 October; Shiraz, Iran:2009.p.21.
48
49. Javan E, Falahati H, Seifi M, Talebi M, Ebrahimpoor G, Poorshafi M. Detection of mecA gene in oxacillin resistant Staphylococcus aureus strains isolated from Tehran hospitals. Iran J Infect Dis Trop Med 2010; 49:17-22.
49
50. Faghri J, Azimian A, Sadighian H, Khosrojerdi M. Occurrence of the methicillin-resistant Staphylococcus aureus (MRSA)among respiratory tract samples in patients of selected Tehran hospitals.4th Iranian Congress of Clinical Microbiology; 9-11 November; Isfahan, Iran:2010.p.75.
50
51. Aligholi M, Mirsalehian A, Halimi S, Imaneini H, Taherikalani M, Jabalameli F, et al. Phenotypic and genotypic evaluation of fluoroquinolone resistance in clinical isolates of Staphylococcus aureus in Tehran. Med Sci Monit 2011; 17:PH71-74.
51
52. Nowroozi J, Pakzad P, Ebrahimi E, Razavipour R. Detection of biocide resistance genes, qac A/B and smr, among isolated Staphylococcus aureus from clinical and non-clinical sources. Pejouhandeh 2011; 16:83-91.
52
53. Saderi H, Emadi B, Owlia P. Phenotypic and genotypic study of macrolide, lincosamide and streptogramin B (MLSB) resistance in clinical isolates of Staphylococcus aureus in Tehran, Iran. Med Sci Monit 2011; 17:BR48-53.
53
54. Shahsavan S, Emaneini M, Noorazar Khoshgnab B, Khoramian B, Asadollahi P, Aligholi M, et al. A high prevalence of mupirocin and macrolide resistance determinant among Staphylococcus aureus strains isolated from burnt patients. Burns 2012; 38:378-382.
54
55. Ghorbani S, Imani Fooladi AA, Nourani MR. Prevalence of methicillin-resistance (mec-A) gene in Staphylococcus aureus strains from scar by PCR and determination of antibiotic susceptibility. 4th Congress of Laboratory and Clinic; 21-23 December; Tehran, Iran:2011.p.540.
55
56. Mobaiyen H, Molaabaszadeh H, Modirrousta S, Reza Soltani S. Surveying of Staphylococcus aureus methicillin resistant (mec-A) and determine its antibiotic susceptibility with PCR method in Tehran in 2010.International Union of Microbiological Societies 2011 Congress;Sapporo, Japan:2011. P-BA25-11.
56
57. Sahebnasagh R, Saderi H, Owlia P. Detection of methicillin-resistant Staphylococcus aureus strains from clinical samples in Tehran by detection of the mecA and nuc genes. The First Iranian International Congress of Medical Bacteriology; 4-7 September; Tabriz, Iran; 2011. p. 195.
57
58. Sepehriseresht S, Boroumand MA, Pourgholi L, Sotoudeh Anvari M, Habibi E, Sattarzadeh Tabrizi M, et al. Emergence of mupirocin-resistant MRSA among Iranian clinical isolates.Comp Clin Pathol 2012. doi: 10.1007/s00580-012-1472-z.
58
59. Razavi Davoodi N, Vand Yousefi A, Harzandi N, Hahrafi A, Rajaei B, Gerayeshnejad S, et al.Molecular detection of methicillin resistantStaphylococcus aureus (MRSA) and methicillinresistant coagulase-negative Staphylococcus (CoNS) inIran. Afr J Microbiol Res 2012; 6:3716-3721.
59
60. Azizi Barjini K, Mousazadeh M, Amani J, Asadi A, Khalili S. Detection of MRSA by Disk diffusion and PCR method and detection of resistance pattern. The Congress of Rational Usage of Antibiotics; 27-28 February; Sari, Iran :2012. p. 38.
60
61. Forghani F, Alipourfard I, Ghayyomi M, Mahmudi S, Heydari N. Comparative study of methicillin resistant Staphylococcus aureus (MRSA) molecular detection by PCR, with bacteriological methods. First International and 12th Iranian Congress of Microbiology; 23-26 May; Kermanshah, Iran:2011. p. 1194.
61
62. Dezfulian A, Aslani MM, Oskoui M, Farrokh P, Azimirad M, Dabiri H, et al. Identification and characterization of a high vancomycin-resistant Staphylococcus aureusharboring vanAgene cluster isolated from diabetic foot ulcer. Iran J Basic Med Sci 2012; 15:803-806.
62
63. Song JH, Hsueh PR, Chung DR, Ko KS, Kang CI, Peck KR, et al. Spread of methicillin-resistant Staphylococcus aureus between the community and the hospitals in Asian countries: an ANSORP study. J Antimicrob Chemother 2011; 66:1061-1069.
63
64. Guzmán-Blanco M, Hsueh PR, Isturiz R, Alvarez C, Bavestrello L, Gotuzzo E, et al. Epidemiology of methicillin-resistant Staphylococcus aureus (MRSA) in Latin America. Int J Antimicrob Agents 2009; 34:304-308.
64
65. Nimmo GR, Pearson JC, Collignon PJ, Christiansen KJ, Coombs GW, Bell JM, et al. Antimicrobial susceptibility of Staphylococcus aureus isolated from hospital inpatients, 2009: Report from the Australian Group on Antimicrobial Resistance. Commun Dis Intell 2011; 35:237–243.
65
66. Styers D, Sheehan DJ, Hogan P, Sahm DF. Laboratory-based surveillance of current antimicrobial resistance patterns and trends among Staphylococcus aureus: 2005 status in the United States. Ann Clin Microbiol Antimicrob 2006; 5:1-9.
66
67. Klevens RM, Morrison MA, Nadle J, Petit S, Gershman K, Ray S, et al. Invasive methicillin-resistant Staphylococcus aureus infections in the United States. JAMA 2007; 298:1763-1771.
67
68. Ray GT, Morrison MA, Baxter R. Trends and characteristics of culture-confirmed Staphylococcus aureusinfections in a large U.S. integrated health care organization. J Clin Microbiol 2012; 50:1950-1957.
68
69. Simor AE, Loeb M. Epidemiology of healthcare-associated Staphylococcus aureus infections. In: Crossley KB, Jefferson KK, Archer GL, Fowler VG, editors. Staphylococci in Human Disease. 2nded. Oxford, UK: Wiley-Blackwell; 2009. p. 290-309.
69
ORIGINAL_ARTICLE
Informative STR Markers for Marfan Syndrome in Birjand, Iran
Objective(s)Marfan syndrome (MFS) is a severe connective tissue disorder withan autosomal dominant inheritance pattern. Early diagnosis is critical in MFS. Because of the large size of fibrillin-1 gene (FBN1), the uniqueness of mutations, and the absence of genotype-to-phenotype correlations linkage analysis can be very helpful for early diagnosis of MFS. In this study, eight polymorphic markers were evaluated among families related to an affected pedigree.Materials and MethodsAn extended family in Birjand, Iran, with numerous cases of Marfan Syndrome in three consecutive generations, is being reported. From all consented members of these families, peripheral blood samples were collected in tubes containing EDTA. DNA extraction was performed by the conventional salting-out method. Eight STR markers were selected for linkage analysis, including four intragenic markers (MTS1, MTS2, MTS3, and MTS4) and another four flanking FBN1 markers (D15S119, D15S126, D15S1028, and D15S143). PCR-amplified fragments were evaluated on 15% polyacrylamide gel.ResultsMTS1, MTS2, and MTS3 were informative in the extended pedigree. D5S1028 was the only non-MTS marker which showed an informative diagnostic capability.ConclusionMTS markers were informative and useful in the molecular diagnosis of Marfan Syndrome in an extended pedigree. MTS1, MTS2, and MTS3 can be used as a prenatal or presymptomatic diagnosis for all members of the extended pedigree.
https://ijbms.mums.ac.ir/article_4908_882ec2c01db5eb31c76343f283ca33bf.pdf
2012-09-01
1020
1025
10.22038/ijbms.2012.4908
Linkage analysis
Marfan syndrome
Microsatellite
MTS
Ezzat
Dadkhah
dadkhah_k@yahoo.com
1
Department of Human Genetics, Immunology Research Centre, Avicenna Research Institute, Mashhad University of Medical Science, Mashhad, Iran
AUTHOR
Masood
Ziaee
2
Birjand Hepatitis Research Centre, Birjand University of Medical Sciences, Birjand, Iran
AUTHOR
Mohammad Hossein
Davari
3
Ophthalmology Department, Vali-e-Asr Hospital, Birjand University of Medical Sciences, Iran
AUTHOR
Toba
Kazemi
tkazemi911@yahoo.com
4
Birjand Atherosclerosis and Coronary Artery Research Centre, Birjand University of Medical Sciences, Birjand, Iran
AUTHOR
Mohammad Reza
Abbaszadegan
abbaszadeganmr@mums.ac.ir
5
Department of Human Genetics, Immunology Research Centre, Avicenna Research Institute, Mashhad University of Medical Science, Mashhad, Iran
LEAD_AUTHOR
1. Dietz HC, Loeys B, Carta L, Ramirez F. Recent progress towards a molecular understanding of Marfan syndrome. Am J Med Genet C Semin Med Genet 2005; 139C:4-9.
1
2. Judge DP, Dietz HC. Marfan's syndrome. Lancet 2005 ; 366:1965-1976.
2
3. Gao LG, Luo F, Hui RT, Zhou XL. Recent molecular biological progress in Marfan syndrome and Marfan-associated disorders. Ageing Res Rev 2009; 9:363-368.
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4. Dietz HC, Cutting GR, Pyeritz RE, Maslen CL, Sakai LY, Corson GM, et al. Marfan syndrome caused by a recurrent de novo missense mutation in the fibrillin gene. Nature 1991; 352:337-339.
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5. Sakai LY, Keene DR, Engvall E. Fibrillin, a new 350-kD glycoprotein, is a component of extracellular microfibrils. J Cell Biol 1986; 103:2499-2509.
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6. Judge DP, Dietz HC. Therapy of Marfan syndrome. Annu Rev Med 2008; 59:43-59.
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7. Mizuguchi T, Matsumoto N. Recent progress in genetics of Marfan syndrome and Marfan-associated disorders. J Hum Genet 2007; 52:1-12.
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8. Boileau C, Jondeau G, Mizuguchi T, Matsumoto N. Molecular genetics of Marfan syndrome. Curr Opin Cardiol 2005; 20:194-200.
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9. Nollen GJ, Mulder BJ. What is new in the Marfan syndrome? Int J Cardiol. 2004 Dec; 97 Suppl 1:103-8.
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10. Revencu N, Quenum G, Detaille T, Verellen G, De Paepe A, Verellen-Dumoulin C. Congenital diaphragmatic eventration and bilateral uretero-hydronephrosis in a patient with neonatal Marfan syndrome caused by a mutation in exon 25 of the FBN1 gene and review of the literature. Eur J Pediatr 2004; 163:33-37.
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11. Davari M, Kazemi T, Alimirzaei H, Rezvani M. Cardiovascular Manifestation of a Family with Marfan’s Syndrome. J Teh Univ Heart Ctr? 2011; 6:37-40.
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12. Judge DP, Biery NJ, Dietz HC. Characterization of microsatellite markers flanking FBN1: utility in the diagnostic evaluation for Marfan syndrome. Am J Med Genet 2001; 99:39-47.
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13. Lee NC, Hwang B, Chen CH, Niu DM. Intrafamilial phenotype variation in Marfan syndrome ascertained by intragenic linkage analysis. J Formos Med Assoc 2005; 104:964-967.
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14. Van Karnebeek CD, Naeff MS, Mulder BJ, Hennekam RC, Offringa M. Natural history of cardiovascular manifestations in Marfan syndrome. Arch Dis Child 2001; 84:129-137.
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15. Gonzales EA. Marfan syndrome. J Am Acad Nurse Pract 2009; 21:663-670.
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16. Hasan A, Poloniecki J, Child A. Ageing in Marfan syndrome. Int J Clin Pract 2007; 61:1308-1320.
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17. Loeys B, De Backer J, Van Acker P, Wettinck K, Pals G, Nuytinck L, et al. Comprehensive molecular screening of the FBN1 gene favors locus homogeneity of classical Marfan syndrome. Hum Mutat 2004; 24:140-146.
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18. Loeys B, Nuytinck L, Delvaux I, De Bie S, De Paepe A. Genotype and phenotype analysis of 171 patients referred for molecular study of the fibrillin-1 gene FBN1 because of suspected Marfan syndrome. Arch Intern Med 2001; 161:2447-2454.
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19. Collod-Beroud G, Le Bourdelles S, Ades L, Ala-Kokko L, Booms P, Boxer M, et al. Update of the UMD-FBN1 mutation database and creation of an FBN1 polymorphism database. Hum Mutat 2003; 22:199-208.
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20. Pereira L, Levran O, Ramirez F, Lynch JR, Sykes B, Pyeritz RE, et al. A molecular approach to the stratification of cardiovascular risk in families with Marfan's syndrome. N Engl J Med 1994; 331:148-153.
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21. Mottes M, Mirandola S, Rigatelli F, Zolezzi F, Lisi V, Gordon D, et al. Allelic frequencies of FBN1 gene polymorphisms and genetic analysis of italian families with Marfan syndrome. Hum Hered 2000; 50:175-179.
21
ORIGINAL_ARTICLE
Study of Radioprotective Effect of Green Tea against Gamma Irradiation Using Micronucleus Assay on Binucleated Human Lymphocytes
Objective(s)The aim of this study was to investigate the radioprotective effect of green tea against genotoxicity induced by gamma irradiation in cultured blood lymphocytes from 5 human volunteers.Materials and MethodsPeripheral blood samples were collected from volunteers before and 1, 3 and 5 hr after drinking a decoction 4 g green tea in 280 ml boiling water for 5 constitutive days with the same quantity. At each time point, the whole blood samples were exposed to 200 cGy of 60 Co gamma irradiation and then were cultured with mitogenic stimulation to determine the chromosomal aberration in micronucleus assay on cytokinesis-blocked binucleated cells.ResultsAs expected, for each volunteer, the results showed a significant increase in the incidence of micronuclei after exposure to gamma irradiation as compared to non-irradiated control samples. Only lymphocytes blood sample collected 3 hr after drinking green tea exhibited a significant decrease in incidence of micronuclei compared to non-treated irradiated samples.ConclusionThese results suggest the radioprotective ability of green tea against ionizing radiation in human lymphocytes, at specified time after consumptior.
https://ijbms.mums.ac.ir/article_4910_45e1dcff27a5de4843bfac814d3f2ce5.pdf
2012-09-01
1026
1031
10.22038/ijbms.2012.4910
Gamma irradiation
green tea
Lymphocytes
Micronucleus
Natural radioprotective
Hafezeh
Davari
1
Department of Biology, Faculty of Sciences, Ferdowsi University of Mashhad, Iran
AUTHOR
Farhang
Haddad
haddad@um.ac.ir
2
Department of Biology, Faculty of Sciences, Ferdowsi University of Mashhad, Iran
LEAD_AUTHOR
Ali
Moghimi
moghimi@um.ac.ir
3
Department of Biology, Faculty of Sciences, Ferdowsi University of Mashhad, Iran
AUTHOR
Mohammad Farhad
Rahimi
4
Department of Physics, Faculty of Sciences, Ferdowsi University of Mashhad, Iran
AUTHOR
Mohammad Reza
Ghavamnasiri
5
Cancer Research Centre (CRC), Department of Radiation Oncology, Omid Hospital, Mashhad University of Medical Science, Mashhad, Iran
AUTHOR
1. Goodhead DT. Initial events in the cellular effects of ionizing radiations: clustered damage in DNA. Int J Radiat Biol 1994; 65:7-17.
1
2. Iyer R, Lehnert BE. Effects of ionizing radiation in targeted and nontargeted cells. Arch Biochem Biophys 2000; 376:14-25.
2
3. Reily PA. Free radicals in biology: oxidative stress and the effect of ionizing radiation. Int J Radiat Biol 1994; 65:27–33.
3
4. Hosseinimehr SJ. Trends in the development of radioprotective agents. Drug Discov Today 2007; 12:794–805.
4
5. Kouvaris JR, Koulouias VE,Vlahos LJ. Amifostine: The First selective-yrtget and broad-spectrum radioprotector. Oncologist 2007; 12:738-747.
5
6. Van der Vijgh WJ, Peters GJ. Protection of normal tissues from the cytotoxic effects of chemotherapy and radiation by amifostine (Ethyol): preclinical aspects. Semin Oncol 1994; 21:2-7.
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7. Maurya DK, Devasagayam TP, Nair CK. Some novel approaches for radioprotection and the beneficial effect of natural products. Indian J Exp Biol 2006; 44:93-114.
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8. Hosseinimehr SJ, Mahmoudzadeh A, Ahmadi A, Mohamadifar S, Akhlaghpoor Sh. Radioprotective effects of hesperidin against genotoxicity induced by gamma-irradiation in human lymphocytes. Mutagenesis 2008; 24:233–235.
8
9. Hosseinimehr SJ, Mahmoudzadeh A, Azadbakht M, Akhlagpoor Sh. Radioprotective effects of hawthorn against genotoxicity induced by gamma-irradiation in human blood lymphocytes. Radiat Environm Biophys 2009; 48:95–98.
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10. Shimoi K, Masuda S, Furugori M, Esaki S, Kinae N. Radioprotective effects of antioxidative flavonoids in γ-ray irradiated mice. Carcinogen 1994; 15:2669-2672.
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11. Shimoi K, Masuda S, Furugori M, Esaki S, Kinae N. Radioprotective effects of antioxidative plant flavonoids in mice. Mutat Res 1996; 350:153-161.
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12. Tiwari AK. Imbalance in antioxidant defense and human diseases: multiple approach of natural antioxidants therapy. Current Sciences? 2001; 81:1179–1187.
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13. Hertog MGL, Hollman PCH, Vanderputte B. Content of potentially anticarcinogenic flavonoids of tea infusions, wines and friut juices. J Agric Food Chem 1993; 41:1242-1246.
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14. Cabrera C, Artacho R, Gime´nez R. Beneficial effects of green tea-a review. J Am Coll Nutr 2006; 25:79–99.
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15. Fenech M, Morley AA. Measurement of micronuclei in lymphocytes. Mutat Res 1985; 147:29-36.
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16. Fenech M. The in vitro micronucleus technique. Mutat Res 2000; 455:81–95.
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17. Durakovic CA. Radioprotective agents in medicine. Arh Hig Rada Toksilokol 1993; 44:331-354.
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18. Butt MS, Sultan MT. Green Tea: nature’s defense against malignancies. Critl Rev Food Sci Nutr 2009; 49:463–473.
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19. Velayutham P, Babu A, Liu D. Green Tea catechins and cardiovascular health: an update. Curr Med Chem 2008; 15:1840–1850.
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20. Wang Y, Ho CT. Polyphenolicc Chemistry of tea and coffee: a century of progress. J Agric Food Chem 2009; 57:8109–8114.
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21. Elbling L, Herbacek I, Weiss RM, Jantschitsch C, Micksche M, Gerner C, et al. Hydrogen peroxide mediates EGCG-induced antioxidant protection in human keratinocytes. Free Radic Biol Med 2010; 15:49:1444-1452.
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22. Li Q, Zhao H, Zhao M, Zhang Z, Li Y. Chronic green tea catechins administration prevents oxidative stress-related brain aging in C57BL/6J mice. Brain Res 2010; 24:1353:28-35.
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23. Itoh T, Imano M, Nishida S, Tsubaki M, Hashimoto S, Ito A, Satou T. (-)-Epigallocatechin-3-gallate protects against neural cell death and improves cerebral function after traumatic brain injury in rats. Neuromolecular Med 2011; 13:300-309.
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24. Yoo KM, Hwang IK, Moon B. Comparative flavonoids contents of selected herbs and associations of their radical scavenging activity with antiproliferative actions in V79-4 cells. J Food Sci 2009; 74:419-425.
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25. Alcaraz M, Armero D, Martínez-Beneyto Y, Castillo J, Benavente-García O, Fernandez H, et al. Chemical genoprotection: reducing biological damage to as low as reasonably achievable levels. Dentomaxillofac Radiol 2011; 40:310-314.
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26. Hu Y, Guo D, Liu P, Cao J, Wang Y, Yin J, et al. Bioactive components from the tea polyphenols influence on endogenous antioxidant defense system and modulate inflammatory cytokines after total-body irradiation in mice. Phytomedicine 2011; 18:970-975.
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27. Stalmach A, Troufflard S, Serafini M, Crozier A. Absorption, metabolism and excretion of choladi green tea flavan-3-ols by humans. Mol Nutr Food Res 2009; 53:S44 –S53.
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28. Stalmach A, Mullen W, Steiling H, Williamson G, Lean MEJ, Crozier A. Absorption, metabolism, and excretion of green tea flavan-3-ols in humans with an ileostomy. Mol Nutr Food Res 2010; 54:323–334.
28
ORIGINAL_ARTICLE
Comparison of in vivo Adjuvanticity of Liposomal PO CpG ODN with Liposomal PS CpG ODN: Soluble Leishmania Antigens as a Model
Objective(s)CpG oligodeoxynucleotides (CpG ODNs) have been shown to have potent immunostimulatory adjuvant activity for a wide range of antigens. Due to susceptibility of phosphodiester CpG ODNs (PO CpG) to nuclease degradation, nuclease-resistant phosphorothioate CpG ODNs (PS CpG) were currently utilized in an in vivo model. In this study, according to some recently reported drawbacks with PS CpG, the adjuvant potential of liposomal PO CpG as a substitute for PS CpG was evaluated.Materials and MethodsSoluble Leishmania antigens (SLA) as a model antigen and distearoylphosphatidylcoline (DSPC) as a neutral lipid were employed to prepare liposomes. Susceptible BALB/c mice received buffer, SLA, Lip-SLA, Lip-SLA-PS CpG, Lip-SLA-PO CpG, SLA+PS CpG, or SLA+PO CpG subcutaneously 3 times with 3 weeks intervals and then were challenged with Leishmania major’s live promastigotes. Blood and spleen samples were analyzed to determine the level and type of antibodies and cytokines. The number of live parasites in the spleen of immunized mice was determined. Moreover, the lesion size progress was assessed weekly by footpad swelling measurement.ResultsThe results showed that mice immunized with Lip-SLA-PS CpG or Lip-SLA-PO CpG developed a significantly smaller footpad swelling, higher level of anti SLA IgG antibodies before and after challenge, and lower spleen parasite burden compared with the control groups. However, there was no significant difference between mice received Lip-SLA-PS CpG and those received Lip-SLA-PO CpG.ConclusionThe results demonstrated that liposomal PO CpG ODN could be used instead of PS CpG ODN to overcome the possible drawbacks.
https://ijbms.mums.ac.ir/article_4912_5257c88bdfd98d3366903b8b51cd1fe6.pdf
2012-09-01
1032
1045
10.22038/ijbms.2012.4912
CpG ODNs
Leishmaniasis
Liposome
SLA
Vaccine
Ensieh
Golali
1
Nanotechnology Research Centre, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Mahmoud Reza
Jaafari
jafarimr@mums.ac.ir
2
Nanotechnology Research Centre, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Ali
Khamesipour
3
Centre for Research and Training in Skin Diseases and Leprosy, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Azam
Abbasi
abbasia2@mums.ac.ir
4
Nanotechnology Research Centre, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Zahra
Saberi
5
Nanotechnology Research Centre, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Ali
Badiee
badieea@mums.ac.ir
6
Nanotechnology Research Centre, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
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2. Klinman DM, Currie D, Gursel I, Verthelyi D. Use of CpG oligodeoxynucleotides as immune adjuvants. Immunol Rev 2004; 199:201-216.
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3
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67
ORIGINAL_ARTICLE
The Effects of Progesterone on Glial Cell Line-derived Neurotrophic Factor Secretion from C6 Glioma Cells
Objective(s)Progesterone is a steroid hormone whose biology has been greatly studied within the confines of reproductive function. In recent years, the neuroprotective effects of progesterone have attracted growing interest. Glial cell line-derived neurotrophic factor (GDNF), is a neurotrophic factor which plays a crucial role in the development and maintenance of distinct sets of central and peripheral neurons. In the present study, we investigated the potential implication of GDNF in the neuroprotective action of progesterone.Materials and MethodsCultured rat C6 glioma cells were treated with progesterone (100 nm, 1 μM, and 10 μM) or its vehicle. After 24, 36, 48 and 72 hr, GDNF protein levels were measured in the cell-conditioned media and cell lysates using a GDNF ELISA kit. Cell numbers were determined by a cell-counting assay kit.ResultsForty-eight hr treatment with progesterone (10 μM) resulted in a significant elevation of GDNF secretion from C6 glioma cells that remained elevated up to 72 hr. The intracellular content of GDNF and cell numbers were not affected by progesterone treatment.ConclusionStimulation of GDNF release from glial cells appears as a potential mechanism through which progesterone exerts its neuroprotective effects.
https://ijbms.mums.ac.ir/article_4913_d775837a0d11019390e8a92798451be3.pdf
2012-09-01
1046
1052
10.22038/ijbms.2012.4913
C6 glioma cells
GDNF
Progesterone
Parichehr
Hassanzadeh
pari_has@yahoo.com
1
Research Centre for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
Elham
Arbabi
elham_arbabi@yahoo.com
2
Research Centre for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
1. Di Cosmo A, Paolucci M, Di Cristo C, Botte V, Ciarcia G. Progesterone receptor in the reproductive system of the female of Octopus vulgaris: characterization and immunolocalization. Mol Reprod Dev 1998; 50:451–460.
1
2. Inoue T, Akahira J, Suzuki T, Darnel AD, Kaneko C, Takahashi K, et al. Progesterone production and actions in the human central nervous system and neurogenic tumors. J Clin Endocrinol Metab 2002; 87:5325–5331.
2
3. Meffre D, Delespierre B, Gouezou M, Leclerc P, Vinson GP, Schumacher M, et al. The membrane-associated progesterone-binding protein 25-Dx is expressed in brain regions involved in water homeostasis and is up-regulated after traumatic brain injury. J Neurochem 2005; 93:1314–1326.
3
4. Sakamoto H, Shikimi H, Ukena K, Tsutsui K. Neonatal expression of progesterone receptor isoforms in the cerebellar Purkinje cell in rats. Neurosci Lett 2003; 343:163–166.
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15. Sayeed I, Wali B, Stein DG. Progesterone inhibits ischemic brain injury in a rat model of permanent middle cerebral artery occlusion. Res Neurol Neurosci 2007; 25:151–159.
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16. Coughlan T, Gibson C, Murphy S. Progesterone, BDNF and neuroprotection in the injured CNS. Int J Neurosci 2009; 119:1718-1740.
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17. Akan P, Kızıldag S, Ormen M, Genc S, Öktem MA, Fadıloglu M. Pregnenolone protects the PC-12 cell line against amyloid beta peptide toxicity but its sulfate ester does not. Chem Biol Interact 2009; 177:65-70.
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63
ORIGINAL_ARTICLE
Calretinin Immunohistochemistery: An Aid in the Diagnosis of Hirschsprung’s Disease
Objective(s)
Definite diagnosis of Hirschsprung’s disease (HD) is based on histopathological study, but there are limitations associated with standard histology and histochemistry in this regard. The aim of this study was to investigate calretinin immunostaining patterns in both ganglionic and aganglionic HD intestinal specimens and to compare them with control specimens.
Materials and Methods
Specimens included 30 patients with histopathologic diagnosis of HD and 20 patients that underwent colectomy for other reasons (as control group). Eighty paraffin wax blocks of full thickness intestinal specimens (30 blocks of ganglionic segments, 30 blocks of aganglionic segments and 20 blocks of control group) were studied. Calretinin immunoreactivity and pattern of staining for ganglion cells (nuclear and cytoplasmic) and also nerve fibers in different layers of bowel were evaluated in IHC stained slides.
Results
There were positive immunostaining of nerve fibers in the lamina propria, submucosa and muscularis propria in control and patient group. There were also nuclear and cytoplasmic staining of ganglion cells in submucosa and muscularis propria in all specimens of both control group (100%) and ganglionic segments (100%). Calretinin immunoexpression of nerve fibers in muscularis propria of the aganglionic segments was negative in all but two cases (6.7%). This method had sensitivity of 93.3% and specificity of 100% for diagnosis of HD in full thickness specimens of intestinal wall. The positive predictive value was 100% and negative predictive value was 93.8%.
Conclusion
Calretinin immunohistochemistry can be used on suction rectal biopsies as a reliable and adjunctive method to diagnose HD.
https://ijbms.mums.ac.ir/article_4918_2f0f7ae20731e3978a41b4f6d77057b3.pdf
2012-09-01
1053
1059
10.22038/ijbms.2012.4918
Calretinin
Hirschsprung Disease
immunohistochemistry
Mehran
Hiradfar
1
Department of Pediatric Surgery, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Nourieh
Sharifi
nourieh_sharifi@yahoo.com
2
Department of Pathology, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Mohammad
Khajedaluee
khajedalueem@mums.ac.ir
3
Department of Community Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Nona
Zabolinejad
zabolinejadn@mums.ac.ir
4
Department of Pathology, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
Shirin
Taraz Jamshidi
5
Department of Pathology, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
1. Haricharan RN, Georgeson KE. Hirschsprung disease. Semin Pediatr Surg 2008; 17:266-275.
1
2. Roberts DJ, Goldstein AM, Greame-Cook F, Dahms BB. Gastrointestinal tract and pancreas. In: Gilbert-Barness E, Kapur RP, Oligny LL, editors. Potter’s Pathology of the fetus, infant and child. 2nd ed. Philadelphia: Mosby; 2007. p. 1176-1178.
2
3. Martucciello G, Pini Prato A, Puri P, Holschneider AM, Meier-Ruge W, Jasonni V, et al. Controversies concerning diagnostic guidelines for anomalies of the enteric nervous system: a report from the fourth International Symposium on Hirschsprung's disease and related neurocristopathies. J Pediatr Surg 2005; 40:1527-1531.
3
4. Noviello C, Cobellis G, Romano M, Amici G, Martino A. Diagnosis of Hirschsprung's Disease: an age-related approach in children below or above one year. Colorectal Dis 2010; 12:1044-1048.
4
5. De Lorijn F, Kremer LC, Reitsma JB, Benninga MA. Diagnostic tests in Hirschsprung disease: a systematic review. J Pediatr Gastroenterol Nutr 2006; 42:496-505.
5
6. Rahman N, Chouhan J, Gould S, Joseph V, Grant H, Hitchcock R, et al. Rectal biopsy for Hirschsprung's disease--are we performing too many? Eur J Pediatr Surg 2010; 20:95-97.
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7. Meier-Ruge WA, Bruder E. Current concepts of enzyme histochemistry in modern pathology. Pathobiology 2008; 75:233-243.
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8. Nakao M, Suita S, Taguchi T, Hirose R, Shima Y. Fourteen-year experience of acetylcholinesterase staining for rectal mucosal biopsy in neonatal Hirschsprung's disease. J Pediatr Surg 2001; 36:1357-1363.
8
9. Kapur RP. Practical pathology and genetics of Hirschsprung's disease. Semin Pediatr Surg 2009; 18:212-223.
9
10. Kapur RP. Can we stop looking? Immunohistochemistry and the diagnosis of Hirschsprung disease. Am J Clin Pathol 2006; 126:9-12.
10
11. Baimbridge KG, Celio MR, Rogers JH. Calcium-binding proteins in the nervous system. Trends Neurosci 1992; 15:303-308.
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12. McConalogue K, Low AM, Williamson S, Bornstein JC, Furness JB. Calretinin-immunoreactive neurons and their projections in the guinea-pig colon. Cell Tissue Res 1994; 276:359-365.
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13. Barshack I, Fridman E, Goldberg I, Chowers Y, Kopolovic J. The loss of calretinin expression indicates aganglionosis in Hirschsprung's disease. J Clin Pathol 2004; 57:712-716.
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14. Kapur RP, Reed RC, Finn LS, Patterson K, Johanson J, Rutledge JC. Calretinin immunohistochemistry versus acetylcholinesterase histochemistry in the evaluation of suction rectal biopsies for Hirschsprung Disease. Pediatr Dev Pathol 2009; 12:6-15.
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15. Guinard-Samuel V, Bonnard A, De Lagausie P, Philippe-Chomette P, Alberti C, El Ghoneimi A, et al. Calretinin immunohistochemistry: a simple and efficient tool to diagnose Hirschsprung disease. Mod Pathol 2009; 22:1379-1384.
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16. Pacheco MC, Bove KE. Variability of acetylcholinesterase hyperinnervation patterns in distal rectal suction biopsy specimens in Hirschsprung disease. Pediatr Dev Pathol 2008; 11:274-282.
16
ORIGINAL_ARTICLE
The Effect of Prenatal Exposure to Restraint Stress on Hippocampal Granule Neurons of Adult Rat Offspring
Objective(s)
It is well known that prenatal stresses (PS) induce a variety of neurobiological and behavioral alterations, some of them involving the hippocampal formation. This study aimed to determine whether restraint stress influences the neuronal volume and number of granule cells in the hippocampus of adult rat offspring.
Materials and Methods
Ten Wistar pregnant rats were randomly divided: stressed and control groups. Pregnant dams in the stressed group were placed in a Plexiglas restraint tube for 1 hr daily from days 15-21 of gestation. Neuroendocrinological consequences of prenatal stress exposure were evaluated in the male offspring on postnatal day 60. The total numbers and the individual volume of granule cells in the hippocampus were also estimated with the optical fractionator and the rotator methods, respectively.
Results
Prenatally stressed rats exhibited prolonged elevation in plasma glucocorticoid levels following acute exposure to restraint stress. Data also indicated that there is a decrease in neuronal volume of hippocampal granule cells in prenatally stressed compared with their controls (625±64.1 µm3 vs. 741±80.6 µm3). There was no significant difference in the total number of granule cells between prenatally stressed and control animals.
Conclusion
The present study indicated that exposure of pregnant female during last week of pregnancy leads to a decline in neuronal size in hippocampus of adult male rats without neuronal loss. The present results may provide a basis for the understanding of the reported disturbances in behavior and learning of PS offspring.
https://ijbms.mums.ac.ir/article_4919_322e55e6007e7c286fc645eb8f85479b.pdf
2012-09-01
1060
1067
10.22038/ijbms.2012.4919
Dentate gyrus
Hippocampus
Neuron
Number
Prenatal stress
Volume
Mohammad
Hosseini-sharifabad
m_hosseini@ ssu.ac.ir
1
Department of Cell Biology and Anatomy, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
LEAD_AUTHOR
Ebrahim
Esfandiari
2
Department of Biomedical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
Ali
Hosseini-sharifabad
3
Department of Pharmacology and Toxicology, Pharmacy Faculty, Shahid Sadoughi University of Medical Sciences, yazd, Iran
AUTHOR
1. Weinstock M. The long-term behavioural consequences of prenatal stress. Neurosci Biobehav Rev-2008; 32:1073-1086.
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2. Maccari S, Darnaudery M, Morley-Fletcher S, Zuena AR, Cinque C, Van Reeth O. Prenatal stress and long-term consequences: implications of glucocorticoid hormones. Neurosci Biobehav Rev 2003; 27:119-127.
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3. Brunton PJ, Russell JA. Prenatal social stress in the rat programmes neuroendocrine and behavioural responses to stress in the adult offspring: sex specific effects. J Neuroendocrinol 2010; 22:258-271.
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4. Szymańska M, Budziszewska B, Jaworska-Feil, L, Basta-Kaim A, Kubera, M, Leśkiewicz M, et al. The effect of antidepressant drugs on the HPA axis activity, glucocorticoid receptor level and FKBP51 concentration in prenatally stressed rats. Psychoneuroendocrinology 2009; 34:822-832.
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5. Szuran TF, Pliska V, Pokorny J, Welzl H. Prenatal stress in rats: effects on plasma corticosterone, hippocampal glucocorticoid receptors, and maze performance. Physiol Behav 2000; 71:353-362.
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6. Koehl M, Darnaudery M, Dulluc J, Van Reeth O, Le Moal M, Maccari S. Prenatal stress alters circadian activity of hypothalamo-pituitary-adrenal axis and hippocampal corticosteroid receptors in adult rats of both gender. J Neurobiol 1999; 40:302-315.
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10. Van den Hove DL, Steinbusch HW, Scheepens A, Van de Berg WD, Kooiman LA, Boosten BJ, et al. Prenatal stress and neonatal rat brain development. Neuroscience 2006; 137:145-155.
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11. Coe CL, Kramer M, Czeh B, Gould E, Reeves AJ, Kirschbaum C, et al. Prenatal stress diminishes neurogenesis in the dentate gyrus of juvenile rhesus monkeys. Biol Psychiatry 2003; 54:1025-1034.
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12. Koo JW, Park CH, Choi SH, Kim NJ, Kim HS, Choe JC, et al. The postnatal environment can counteract prenatal effects on cognitive ability, cell proliferation, and synaptic protein expression. FASEB J 2003: 17:1556-1558.
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45
ORIGINAL_ARTICLE
Preventive Effect of Novel Bacterial Polysaccharide and Animal Splenic Protein as Natural Adjuvants on Animal Model of Asthma
Objective(s)
Two new adjuvants from natural animal lipids (G2) and bacterial polysaccharide extracts (PC) were previously prepared by our group and showed a reduction in tracheal responsiveness. The aim of this study was to evaluate the preventive effect of recently introduced natural products (G2 and PC) on the development of asthma.
Materials and Methods
Asthma was induced using a standard method in four groups of BALB/c mice. A non-sensitized control group was also included in order to be compared with treated groups. Three groups were premedicated with novel agents named G2, PC, and a combination of these two for 20 days before starting the induction of asthma. Bronchoalveolar lavage fluid (BALF) was collected and analyzed for inflammatory cells. Interferon-γ, and IL-4 and the histopathological of both lungs were also evaluated.
Results
In all pretreated groups, the inflammatory cells infiltration especially eosinophils and smooth muscle hyperplasia decreased significantly. BALF cytology also showed significant decrease in eosinophil count in all pretreated groups. There was a significant increase in the BALF and serum INF-γ in all pretreated groups but the combination of G2/PC was more effective. BALF IL-4 decreased significantly in the group pretreated with a combination of G2 and G2/PC (4.11±0.86 and 4.02±0.52 pg/ml in G2 and G2/PC, respectively). Serum IL-4 in the PC group was significantly higher than the sensitized control.
Conclusion
G2 and PC may effectively prevent asthma development by activation of the type 1 T helper system.
https://ijbms.mums.ac.ir/article_4920_f16a8018ec3a5e49cdd4c3fba880cb3c.pdf
2012-09-01
1068
1075
10.22038/ijbms.2012.4920
Asthma
Interleukin-4
Immunomodulation
Interferon-gamma
prevention and control
Adjuvants
Immunologic
Majid
Mirsadraee
majidmirsadraee@mshdiau.ac.ir
1
Department of Internal Medicine, Medical School of Islamic Azad University- Mashhad Branch, Mashhad, Iran
LEAD_AUTHOR
Saleh
Mohaghegh Hazrati
2
Mohaghagh Hazreati Immunology and Biotechnology Researches Centre, Tehran Iran
AUTHOR
Mohammad Reza
Khakzad
3
Department of Immunology, Medical School of Islamic Azad University, Mashhad Branch, Mashhad, Iran
AUTHOR
Kamran
Ghafarzadegan
4
Department of Pathology Razavi Hospital, Mashhad, Iran
AUTHOR
Mohhamad Hosein
Boskabady
5
Mashhad University of Medical Science, Mashhad, Iran
AUTHOR
1. Cohn L, Elias JA, Chupp GL. Asthma: Mechanisms of disease persistence and progression. Annu Rev Immunol 2004; 22:789–815.
1
2. Randolph DA, Stephens R, Carruthers CJ, Chaplin DD. Cooperation between Th1 and Th2 cells in a murine model of eosinophilic airway inflammation. J Clin Invest 1999; 104:1021–1029.
2
3. del Giudice MM, Rocco A, Capristo C. Probiotics in the atopic march: highlights and new insights. Dig Liver Dis 2006; 38:S288-290.
3
4. Mohaghegh HS, Khanbaba CR, Mazaheri B, Gharagozlo MJ. A novel and invasive metastatic adenocarcinoma of breast cancer (HAZ-1) in small laboratory mice. 14th Iranian congress of Physiology and Pharmacology 1999; p.262.
4
5. Mohaghegh HS, Nasiri Khalaji S, Mohtarami F, Rahimi A. G2, PC and G2F in allergic asthma. Iran J Pediatr 2004; 13:30-33.
5
6. Neamati A, Boskabady MH, Afshari JT, Mohaghegh Hazrati S, Rohani A. The effect of natural adjuvants on tracheal responsiveness on cell count in lung lavage of sensitized guinea pigs. Respirology 2009; 14:877-884.
6
7. Annesi-Maesano I. Asthma epidemiology. Rev Prat 2005; 55:1295-1298.
7
8.Tarlo SM. Prevention of occupational asthma in Ontario. Can J Physiol Pharmacol 2007; 85:167-172.
8
9. Arshad SH. Primary prevention of asthma and allergy. J Allergy Clin Immunol 2005; 116:3-14.
9
10.Devereux G. Early life events in asthma--diet. Pediatr Pulmonol 2007; 42:663-673.
10
11.Sullivan SD, Melyzer EO. Emerging therapeutic strategies for asthma anagement. J Manag Care Pharm 2003; 9:14-21.
11
12.Tsitoura DC, Tassios Y. Immunomodulation: the future cure for allergic diseases. Ann N Y Acad Sci 2006; 1088:100-115.
12
13.Prescott SL, Björkstén DB. Probiotics for the prevention or treatment of allergic diseases. J Allergy Clin Immunol 2007; 120:255-262.
13
14.Platts-Mills T, Leung DYM, Schatz M. The Role of Allergens in Asthma. Am Fam Physician 2007; 76:675-680.
14
15.Bloebaum RM, Grant JA, Sur S. Immunomodulation: the future of allergy and asthma treatment. Curr Opin Allergy Clin Immunol 2004; 4:63-67.
15
16.Sharma S, Jaffe A, Dixon G. Immunomodulatory effects of macrolide antibiotics in respiratory disease: therapeutic implications for asthma and cystic fibrosis. Paediatr Drugs 2007; 9:107-118.
16
17.Van Rijt LS, Kuipers H, Vos N, Hijdra D, Hoogstenden HC, Lambrecht BN. A rapid flow cytometric method for determining the composition of bronchoalveolar lavage fluid cells of mouse models of asthma. J Immunol Methods 2004; 288:111-121.
17
18.Yoo J, Tcheurekdjian H, Lynch SV, Cabana M, Boushey HA. Microbial manipulation of immune function for asthma prevention; inferences from clinical trials. Proc Am Thorac Soc 2007; 4:277-282.
18
ORIGINAL_ARTICLE
Identification of Nontuberculous Mycobacteria Species Isolated from Water Samples Using Phenotypic and Molecular Methods and Determination of their Antibiotic Resistance Patterns by E- Test Method, in Isfahan, Iran
Introduction
Many studies have shown epidemiological links between strains isolated in tap water, and those isolated from patients. Molecular methods linked to PCR are more reliable and faster for identification of non- tuberculous mycobacteria(NTM). In this study molecular methods were used for identification and typing of NTM.
Materials and Methods
Five hundred ml of 85 water samples was passed through 0.45 μm filters. The filters were transferred directly onto 7H10 Middle Brook solid media, containing 15% OADC. PCR for 16S rRNA was done and the PCR product (1500 bp) was sequenced. PRA of the hsp65 gene was investigated to identify the species of isolates. For evaluation of susceptibility of NTM to antimycobacterial agents, E-test method was used.
Result
The genus of 26 isolated NTM was confirmed by 16s rRNA sequence based method. Nineteen isolates of Mycobacteria were differentiated using hsp65genes PRA. The dominant isolates were M. fortuitum (26.7%), M. chelonae like organism(13.3%) and M. mucogenicum (13.3%). Seventy one percent of NTM species were resistant to isoniazid, 64% to rifampin, 57% to ethambutol, 35% to tetracycline, 14 % to azithromycin and 7.1 % to amikacin.
Conclusion
The results showed that E-test method is not a proper technique for antimycobacterial assay because some NTM species are slow in growing and have no growth on Muller Hinton agar. Regarding the 16S rRNA sequence analysis, the identification of isolates was restricted to the genus level, because 99% similarity within 16S rRNA of two isolates may or may not determine the same species.
https://ijbms.mums.ac.ir/article_4922_ecc380cff8a5c2f4fa5ba1f93cf17d80.pdf
2012-09-01
1076
1082
10.22038/ijbms.2012.4922
Antibiotic resistance patterns
E-test
hsp65
NTM
Water samples
16S rRNA
Sharareh
Moghim
moghim@med.mui.ac.ir
1
Department of Microbiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
LEAD_AUTHOR
Ensieh
Sarikhani
2
Department of Microbiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
Bahram
Nasr Esfahani
3
Department of Microbiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
Jamshid
Faghri
faghri@med.mui.ac.ir
4
Department of Microbiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
1. Koning B, Amer Ina, Sollich V, Koning W. Intra and interpatient variability of the hsp65 and 16S-23S intergenic gene region in Mycohaterium abscessus strains from patients with cystic fibrosis. J Clin Microbiol 2005;43:3500-3503.
1
2. Groote MAD, Huitt G. Infections due to rapidly growing Mycobacteria. Clin Infect Dis 2006; 42: 1756 –1763.
2
3. Khan IUH, Yadav JS. Development of a single – tube, cell lysis – based, genus – specific PCR method for rapid identification of mycobacteria: optimization of cell lysis, PCR primers and conditions and restriction pattern analysis. J Clin Microbiol 2004; 42:453–457.
3
4. Kotoch VM. Infections due to non– tuberculous mycobacteria (NTM). Indian J Med Res 2004; 120: 290–304.
4
5. Covert TC, Rodgers MR, Reyes AL, Stelma GN. Occurrence of nontoberculous mycobacteria in environmental sample. Appl Environ Microbiol 1999; 68:3159–3161.
5
6. Park H, Jang H, kim C, Byungseon C, Chang CL, park SK, et al. Detection and identification of mycobacteria by amplification of the internal transcribed spacer regions with genus and species specific PCR primers. J Clin Microbiol 2000; 38:4080–4085.
6
7. Harmsen D, Dostal S, Roth A, Niemann S, Rothgänger J, Sammeth M, et al. Ridom comprehensive and public sequence database for identification of mycobacterium species. BMC Infect Dis 2003; 3:1-10.
7
8. Hafner B, Haag H, Geiss HK, Noite O. Different molecular methods for the identification of rarely isolated nontuberculous mycobacteria and description of new hsp65 restriction fragment length polymorphism patterns. Mol Cell Probes 2004; 18:59-65.
8
9. Lenor SC, Arnold EG, Andrew DE. Standard methods for the examination of water and wastewater. 20th ed.American Public Health Association, American Water Works Association, Water Environment Federation; United Book Press Inc; 1998. p.1-37.
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10. DPD: National drinking water standards.5th ed. Tehran: Iranian industrial research and standards organization publications; 1997; standard no .1053.
10
11. Cooper C, Revised by Jovell B. Isolation and quantification of genomic DNA from Mycobacterium tuberculosis. 1999.Available at: WWW. Wadsworth. Org / rflp/ tutorials/ DNA isolation.html.
11
12. Telenti A, Marcehesi F, Marianne Balz. Rapid identification of mycobacteria to the species level by polymerase chain reaction and restriction enzyme analysis. J Clin Microbiol 1993; 31:175-178.
12
13. Chang CT, Wang LY, Liao CY, Hvang SP. Identification of nontuberculous mycobacteria existing in tap water by PCR restriction fragment length polymorphism. Appl Environ Microbiol 2002; 68:3159–3161.
13
14. Steingrube VA, Gibson JL, Brown BA, Zhang Y, Wilson RW, Rajagopalan M, et al. PCR amplification and restriction endonuclease analysis of a 65-kilodalton heat shock protein gene asquence for taxonomic separation of rapidly growing mycobacteria. J Clin Microbiol 2003; 33: 149–153.
14
15. Brunello F, Ligozzi M. Identification of 54 mycobacterial species by PCR-restriction fragment length polymorphism analysis of the hsp65 gene. J Clin Microbiol 2001; 39:2799–2806.
15
16. Turenne C, Tschetter L, Wolfe J, Kabani A. Necessity of quality-controlled 16S rRNA gene sequence databases: identifying nontuberculous mycobacterium species. J Clin Microbiol 2001; 39:3637–3648.
16
17. Nasr-Esfahani B, Sarikhani E, Moghim S, Faghri J, Fazeli H, Hoseini N, et al. Molecular characterization of environmental non-tuberculous mycobacteria using PCR- RFLP analysis of 441 Bp heat shock protein 65 fragments. Iran J Publ Health? 2012; 41:108-114.
17
18. lin C, Xue C, Ting ZC, Huan DB, Zhong ZJ. Identification of Mycobacterium marinum 65 ka heat shock protein gene by polymerase chain reaction restriction analysis from lesion of swimming pool granuloma. Chin Med J 2006; 119:43–48.
18
19. Derek A, Wong PC,YIP W.Simple and Rational Approach to the Identification of Mycobacterium tuberculosis, Mycobacterium avium complex species, and other commonly isolated mycobacteria. J Clin Microbiol 2001; 39:3768–3771.
19
20. Argueta C, Yoder S, Holtzman AE, Aronson TW, Glover N, Berlin OG, et al. Isolation and identification of nontuberculous mycobacteria. J Food Prot2000; 63:930-933.
20
21. Wong DA, Yip PC, Tse DL, Tung VW, Cheung DT, Kam KM. Routine use of a simple low-cost genotypic assay for the identification of mycobacteria in a high throughput laboratory. Diagn Microbiol Infect Dis 2003; 47:421-426.
21
22. Shin JH, Lee EJ, Lee HR, Ryu SM, Kim RH, Chang CL, et al. Prevalence of non tuberculosis mycobacteria in a hospital environment. J Hosp Infect 2007; 65:143-148.
22
ORIGINAL_ARTICLE
Effect of Pentoxifylline on Ischemia- induced Brain Damage and Spatial Memory Impairment in Rat
Objective(s)
The brief interruption of cerebral blood flow causes permanent brain damage and behavioral dysfunction. The hippocampus is highly vulnerable to ischemic insults, particularly the CA1 pyramidal cell layer. There is no effective pharmacological strategy for improving brain tissue damage induced by cerebral ischemia. Previous studies reported that pentoxifylline (PTX) has a neuroprotective effect on brain trauma. The possible neuroprotector effects of PTX on behavioral deficit were studied in male Wistar rats subjected to a model of transient global brain ischemia.
Materials and Methods
Animals (n= 32) were assigned to control, sham-operated, vehicle, and PTX- treated (200 mg/kg IP) groups. PTX administered at 1hr before and 3 hr after ischemia. Global cerebral ischemia was induced by bilateral common carotid artery occlusion, followed by reperfusion.
Results
Morris Water maze testing revealed that PTX administration in cerebral ischemia significantly improved hippocampal-dependent memory and cognitive spatial abilities after reperfusion as compared to sham-operated and vehicle-treated animals. After the behavioral test, the rats were sacrificed and brain sections were stained with Nissl staining. There were no significant differences between number of pyramidal cells in both control and PTX groups.
Conclusion
Our study demonstrated that pentoxifylline had a protective effect on rats with transient global ischemia and could reduce cognitive impairment.
https://ijbms.mums.ac.ir/article_4923_3473fff9d569e5561529a974269cbc20.pdf
2012-09-01
1083
1090
10.22038/ijbms.2012.4923
Neuroprotective
Pentoxifylline
Spatial Memory
Transient Ischemia
Shabnam
Movassaghi
sm_movassaghi@yahoo.com
1
Anatomy Department, Tehran Medical Branch, Islamic Azad University, Tehran, Iran
AUTHOR
Zahra
Nadia Sharifi
2
Anatomy Department, Tehran Medical Branch, Islamic Azad University, Tehran, Iran
AUTHOR
Mansooreh
Soleimani
mansoorehsoleimani@gmail.com
3
Anatomy Department, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Mohammad Taghi
Joghataei
joghataei@uswr.ac.ir
4
Anatomy Department, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Mehrdad
Hashemi
hashemi_mehrdad@yahoo.com
5
Genetic Department, Tehran Medical Branch, Islamic Azad University, Tehran, Iran
AUTHOR
Hamed
Shafaroodi
shafarodi@yahoo.com
6
Pharmaceutical Science Branch & Pharmaceutical Science Research Centre, Islamic Azad University, Tehran, Iran
AUTHOR
Mehdi
Mehdizadeh
mehdizadehm@tums.ac.ir
7
Cellular & Molecular Research Centre, Tehran University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
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45.Radfar M, Larijani B, Hadjibabaie M, Rajabipour B, Mojtahedi A, Abdollahi M. Effects of pentoxifylline on oxidative stress and levels of EGF and NO in blood of diabetic type-2 patients: a randomized, double-blind placebo-controlled clinical trial. Biomed Pharmacother 2005; 59:302–306.
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46.Myers SI, Horton JW, Hernandez R, Walker PB, Vaughan WG. Pentoxifylline protects splanchnic prostacyclin synthesis during mesenteric ischemia/reperfusion. Prostaglandins 1994; 47:137–150.
46
47.Schermuly RT, Roehl A, Weissmann N, Ghofrani HA, Leuchte H, Grimminger F, et al. Combination of nonspecific PDE inhibitors with inhaled prostacyclin in experimental pulmonary hypertension. Am J Physiol Lung Cell Mol Physiol 2001; 281: L1361–L1368.
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48. Strieter RM, Remick DG, Ward PA, Spengler RN, Lynch JP, 3rd Larrick J, et al. Cellular and molecular regulation of tumor necrosis factor-alpha production by pentoxifylline. Biochem Biophys Res Commun 1988; 155:1230–1236.
48
49.Guggilam A, Haque M, Kerut EK, McIlwain E, Lucchesi P, Seghal I, et al. TNF-alpha blockade decreases oxidative stress in the paraventricular nucleus and attenuates sympathoexcitation in heart failure rats. Am J Physiol Heart Circ Physiol 2007; 293:H599-609.
49
50.Sirin BH, Yilik L, Coskun E, Ortac R, Sirin H. Pentoxifylline reduces injury of the brain in transient ischemia. Acta Cardiol 1998; 53:89–95.
50
51.Bruno Rde B, Marques TF, Batista TM, Lima JC, de Arruda KG, Lima PF, et al. Pentoxifylline treatment improves neurological and neurochemical deficits in rats subjected to transient brain ischemia. Brain Res 2009; 1260:55-64.
51
ORIGINAL_ARTICLE
Evaluation of Pinopodes Expression on the Mouse Endometrium Immediately before Implantation by Treatment with HMG/HCG and Sildenafil Citrate Administration
Objective(s)
Sildenafil citrate is a new drug and has special properties that bring about nitric oxide effects on vascular smooth muscle. The aim of this study was to assess the effects of ovarian stimulation and sildenafil citrate injection on pinopode expression in mice.
Materials and Methods
Thirty adult female mice were randomly divided into three groups: control, hyperstimulated and hyperstimulated +sildenafil citrate injection. In experimental groups mice received 7.5 IU human menopausal gonadotropin (HMG) and then after 48 hr received 7.5 IU human chorionic gonadotropic (HCG) hormones. After that every two females were put with one male in one cage for mating. Hyperstimulated +sildenafil citrate group were injected with sildenafil citrate (3 mg/mouse) every 24 hr for three days, after HMG injection. The animals were sacrificed by cervical dislocation 96 hr after HMG injection, and their uterine specimens (the middle one-third) were prepared for transmission electron microscope studies.
Result
Electron microscopy observations showed that in the control group there were long and short microvilli while no developed pinopodes were observed, however, in the two other groups, well developed pinopodes were expressed 4 days after HMG injection.
Conclusion
The results showed that hyperstimulation of mice with sildenafil citrate may be more helpful in formation of pinopodes and implantation.
https://ijbms.mums.ac.ir/article_4924_0e8c97774e716575493ad659cbd570b7.pdf
2012-09-01
1091
1096
10.22038/ijbms.2012.4924
Ovarian stimulation
Pinopode
Sildenafil citrate
Transmission electron microscopy
Bahman
Rashidi
b_rashidi:@med.mui.ac.ir
1
Department of Anatomical Sciences and Molecular Biology, School of Medicine, Isfahan University of Medical Science, Isfahan, Iran
LEAD_AUTHOR
Jafar
Soleimani Rad
2
Departments of Anatomy and Histology, School of Medicine, Tabriz University of Medical Science, Tabriz, Iran
AUTHOR
Leila
Roshangar
3
Departments of Anatomy and Histology, School of Medicine, Tabriz University of Medical Science, Tabriz, Iran
AUTHOR
Rafie
Alizadeh Miran
4
Department of Anatomical Sciences, School of Medicine, Tehran University of Medical Science, Tehran, Iran
AUTHOR
1.Oborná I, Novotný R, Brezinová J, Petrová P, Lichnovský V, Fingerová H. Changes in the development of uterine pinopodes in steroid hormone supplemented cycles. Physiol Res 2004; 53:423-429.
1
2. Bentin-Ley U, Sjögren A, Nilsson L, Hamberger L, Larsen JF, Horn T. Presence of uterine pinopodes at the embryo-endometrial interface during human implantation in vitro. Hum Reprod 1999; 14:515-520.
2
3.Quinn C, Ryan E, Claessens EA, Greenblatt E, Hawrylyshyn P, Cruickshank B, et al. The presence of pinopodes in the human endometrium does not delineate the implantation window. Fertil Steril 2007; 87:1015-1021. Epub 2007 Jan 16.
3
4. Salehnia M. Different pattern of pinopodes expression in stimulated mouse endometrium. Exp Anim 2005; 54:349-352.
4
5. Salehnia M. Progesterone shifts the pinopodes expression of mouse endometrium to pre-implantation time after ovarian hyperstimulation. Iran J Reproductive Med? 2003; 1:20-23.
5
6. Kolb BA, Najmabadi S, Paulson RJ. Ultrastructural characteristics of the luteal phase endometrium in patients undergoing controlled ovarian hyperstimulation. Fertil Steril 1997; 67:625-630.
6
7. Stavreus-Evers A, Nikas G, Sahlin L, Eriksson H, Landgren BM. Formation of pinopodes in human endometrium is associated with the concentrations of progesterone and progesterone receptors. Fertil Steril 2001; 76:782-791.
7
8. Achache H, Revel A. Endometrial receptivity markers, the journey to successful embryo implantation. Hum Reprod Update 2006 ; 12:731-46. Epub 2006 Sep 18.
8
9. Paulus WE, Strehler E, Zhang M, Jelinkova L, El-Danasouri I, Sterzik K. Benefit of vaginal sildenafil in assisted reproduction therapy. Fertil Steril 2002; 77:846-847.
9
10. Sher G, Fisch JD. Vaginal sildenafil (Viagra): a preliminary report of a novel method to improve uterine artery blood flow and endometrial development in patients undergoing IVF. Hum Reprod 2000; 15:806-809.
10
12. Boolell M, Gepi-Attee S, Gingell JC, Allen MJ. Sildenafil, a novel effective oral therapy for male erectile dysfunction. Br J Urol 1996; 78:257-261.
11
12. Khan RN, Hamoud H, Warren A, Wong LF, Arulkumaran S. Relaxant action of sildenafil citrate (Viagra) on human myometrium of pregnancy: Am J Obstet Gynecol 2004; 191:315-321.
12
13. Lundkvist O, Nilsson BO. Ultrastructural changes of the trophoblast-epithelial complex in mice subjected to implantation blocking treatment with indomethacin. Biol Reprod 1980; 22:719-726.
13
14. Ertzeid G, Storeng R. The impact of ovarion stimulation on implantation and fetal development in mice. Hum Reprod 2001; 16:221-225.
14
15. Emadi M, Salehnia M. The morphological expression of endometrial pinopodes during implantation in mice after ovarian stimulation and progesterone injection. Yakhteh Med J 2004; 5: 140-145.
15
15. Nikas G, Develioglu OH, Toner JP, Jones HW Jr. Endometrial pinopodes indicate a shift in the window of receptivity in IVF cycles. Hum Reprod 1999; 14:787-792.
16
17. Nikas G, Drakakis P, Loutradis D, Mara-Skoufari C, Koumantakis E, Michalas S, et al. Uterine pinopodes as markers of the nidation window in cycling women receiving exogenous oestradiol and progesterone. Hum Reprod 1995; 10:1208-1213.
17
18. Singh MM, Chauhan SC, Trivedi RN, Maitra SC, Kamboj VP. Correlation of pinopode development on uterine luminal epithelial surface with hormonal events and endometrial sensitivity in rat. Eur Endocrinol 1996; 135:107-117.
18
19. Salehnia M, Arianmanesh M, Beigi M. The impact of ovarian stimulation on mouse endometrium: a morphometrical study. Iran J Reproductive Med 2006; 4:7-11.
19
20. Ozgunen KT, Erdogan S, Mazmanoglu N, Pamuk I, Logoglu G, Ozgunen T. Effect of gonadotrophin dose on oocyte retrieval in superovulated BALB/c mice. Theriogenology 2001; 56:435-445.
20
21. Barroso RP, Osuamkpe C, Nagamani M, Yallampalli C. Nitric oxide inhibits development of embryo and implantation in mice. Mol Hum Reprod 1998; 4:503-507.
21
ORIGINAL_ARTICLE
Quantitative Analysis of GABAA Gamma Receptor Subunits in the Developing Embryonic Chick Forebrain
Objective(s)
In this study we investigated the expression of GABAA receptor subunits during brain development. These receptors may change in the embryonic chick forebrain.
Materials and Methodes
The expression levels of four types of GABAA receptor gamma subunits (γ1, γ2, γ3 and γ4) were quantified in the embryonic chick forebrain at 32 hr, 3, 7, 14, and 20 days of incubation and day one after hatching. The expression level of mRNA in the forebrain of embryonic chicken was measured using real-time RT-PCR. Results
The expression level of each subunit increased gradually with development and reached a plateau on 20th day of embryonic development. A reduction was observed on day one after hatching in all gamma subunits. Conclusion
This may explain the different physiological and pharmacological function of GABA receptor gamma subunits before and after hatching.
https://ijbms.mums.ac.ir/article_4925_a28581934838343da3af8046d1ab010d.pdf
2012-09-01
1097
1101
10.22038/ijbms.2012.4925
Developmental expression
Embryonic forebrain
GABAA Receptor subunit
Real-time RT-PCR
Sayed Rasul
Zaker
1
Department of Biology, Faculty of Sciences, University of Isfahan, Isfahan, Iran
AUTHOR
Abolghasem
Esmaeili
aesmaeili@sci.ui.ac.ir
2
Department of Biology, Faculty of Sciences, University of Isfahan, Isfahan, Iran
LEAD_AUTHOR
Majid
Bouzari
bouzari@yahoo.com
3
Department of Biology, Faculty of Sciences, University of Isfahan, Isfahan, Iran
AUTHOR
Elham
Shirani
4
Department of Biology, Faculty of Sciences, University of Isfahan, Isfahan, Iran
AUTHOR
1. Schousboe A, Waagepetersen HS. Gamma-aminobutyric acid (GABA). Encyclopedia of neuroscience. Oxford: Academic Press; 2009. p.511–515.
1
2. Snyder SH, Ferris CD. Novel neurotransmitters and their neuropsychiatric relevance. Am J Psychiatr 2000; 157:1738.
2
3. Macdonald RL, OlsenR. GABA receptor channels. Physiology and Pathology of Chloride Transporters and Channels in the Nervous System: From Molecules to Diseases, 2009: p. 257.
3
4. Davies M, Bateson AN, Dunn SMJ. Molecular biology of the GABA A receptor: functional domains implicated by mutational analysis. Front Biosci 1996; 1:214-233.
4
5. Sarto-Jackson I, Sieghart W. Assembly of GABAA receptors (Review). Mol Mem Biol 2008; 25:302-310.
5
6. Florey E. GABA: history and perspectives.Can J Physiol Pharmacol 1991; 69:1049.
6
7. Olsen RW, Sieghart W. GABAA receptors: subtypes provide diversity of function and pharmacology. Neuropharmacology 2009; 56:141-148.
7
8. Möhler H, Fritschy JM. GABAB receptors make it to the top--as dimers. Trends Pharmacol Sci 1999; 20:87.
8
9. Rodríguez Gil DJ, Vacotto M, Rapacioli M, Scicolone G, Flores V, Fiszer de Plazas. Development and localisation of GABAA receptor 1, 2, 2 and 2 subunit mRNA in the chick optic tectum. J Neurosci Res 2005; 81:469-480.
9
10. Burd GD, Rubel EW. Development of GABA immunoreactivity in brainstem auditory nuclei of the chick: ontogeny of gradients in terminal staining. J Comp Neurol 1989; 284:504-518.
10
11. Enomoto K, Kataoka H, Hirota A. Semiquantitative Analysis of the erpression of GABA-A receptor subunits in the developing embryonic Chick Brain Stem. Japan J Physiol 2001; 51: 53-61.
11
12. Mehta AK, Ticku MK. An update on GABAA receptors. Brain Res Rev 1999; 29:196-217.
12
13. Ben-Ari Y. Excitatory actions of GABA during development: the nature of the nurture. Nat Rev Neurosci 2002; 3:728-739.
13
14. Laurie D, Wisden W, Seeburg P. The distribution of thirteen GABAA receptor subunit mRNAs in the rat brain. III. Embryonic and postnatal development. J Neurosci 1992; 12:4151.
14
ORIGINAL_ARTICLE
The Effects of Cyclooxygenase Inhibitors on the Brain Inflammatory Response Following Traumatic Brain Injury in Rats
Objective(s)
Cytokines such as IL-1β are involved in inflammatory responses. This study evaluated the role of two different kinds of drugs (ibuprofen and celecoxib) on brain IL-10 and IL-1β after traumatic brain injury (TBI) in male rats.
Materials and Methods
Rats were assigned into 6 groups: intact, sham, TBI, and treated rats with vehicle, celecoxib or iboprophen. Cytokine concentrations were quantified by ELISA kits.
Results
Groups showed no significant difference in brain IL-10 either after TBI induction or after treatment with ibuprofen or celecoxib. Serum IL-10 in vehicle or ibuprofen treated animals was lower than in sham groups (P< 0.01). Brain IL-1β decreased after treatment by ibuprofen or celecoxib (P< 0.001). There was no statistical difference in serum IL-1β in TBI and intact. Serum IL-1β significantly decreased in rats that received celecoxib compared to TBI group (P< 0.01).
Conclusion
Based on our study IL-1β can decrease through both cyclooxygenase 1 (COX-1) and COX-2 pathway but serum IL-1β can decrease only by COX-2 pathway.
https://ijbms.mums.ac.ir/article_4926_8463413b5faeecbd381ae254b416cf59.pdf
2012-09-01
1102
1105
10.22038/ijbms.2012.4926
Brain injury
Celecoxib
Ibuprofen
Interleukin-10
Zakieh
keshavarzi
zakieh_keshavarzi@yahoo.com
1
North Khorasan University of Medical Sciences, Bojnord, Iran
LEAD_AUTHOR
Mohammad
Khaksari
m_khaksari@yahoo.com
2
Physiology Research Centre, Kerman University of Medical Sciences, Kerman, Iran
AUTHOR
Zohre
Razmi
3
Kerman University of Medical Sciences, Kerman, Iran
AUTHOR
Ava
Soltani Hekmat
4
Physiology Research Centre, Kerman University of Medical Sciences, Kerman, Iran
AUTHOR
Vida
Naderi
5
Kerman University of Medical Sciences, Kerman, Iran
AUTHOR
Sima
Rostami
6
Kerman University of Medical Sciences, Kerman, Iran
AUTHOR
1.Wang KK, Larner SF, Robinson G, Hayes RLet. Neuroprotection targets after traumatic brain injury. Curr Opin Neurol 2006; 19:514-519.
1
2. Sirotaa L, Shachama I, Punskyb H. Ibuprofen affects pro- and anti-inflammatory cytokine production by mononuclear cells of preterm newborns. Biol Neonate 2001; 79:103–108.
2
3. Warner TD, Giluliano F, Vojnovic I, Bukasa A, Mitchell JA, Vane JR. Nonsteroidal drug selectivities for cyclooxygenase-1 rather than cyclooxygenase-2 are associated with human gastrointestinal toxicity: a full in vitro analysis. Proc Natl Acad Sci USA 1999; 96:7563–7568.
3
4. Zhao SZ, Reynolds MW, Lejkowith J, Whelton A, Arellano FM. A comparison of renal-related adverse drug reactions between rofecoxib and celecoxib, based on the World Health Organisation/Uppsala Monitoring Centre safety database. Clin Ther 2001; 23: 1478–1491.
4
5. Marmarou A, Foda MA, van den Brink W, Campbell J, Kita H, Demetriadou K. A new model of diffuse brain injury in rats. J Neurosurg 1994; 80:291-300.
5
6. Soltani, Z, Khasksari M, Shahrokhi N,? et al. Effect of combined administration of estrogen and opogesterone on brain edema and neurological outcome after traumatic brain injury in female rats. Iran J Endocrinol Metabol 2009; 10:629-638.
6
7. Gopez JJ, Yue H, Vasudevan R, Malik AS, Fogelsanger LN, Lewis S, et al. Cyclooxygenase-2-specific inhibitor improves functional outcomes, provides neuroprotection, and reduces inflammation in a rat model of traumatic brain injury. Neurosurgery 2005; 56:590-604.
7
8. Scali C, Giovannini MG, Prosperi C, Bellucci A, Pepeu G, Casamenti F. The selective cyclooxygenase-2 inhibitor rofecoxib suppresses brain inflammation and protects cholinergic neurons from excitotoxic degeneration in vivo. Neuroscience 2003; 117: 909–919.
8
9.Chu K, Jeong SW, Jung KH, Han SY, Lee ST, Kim M, et al. Celecoxib induces functional recovery after intracerebral hemorrhage with reduction of brain edema and perihematomal cell death. J Cereb Blood Flow Metab 2004; 24:926-933.
9
10.Yamasaki Y, Matsuura N, Shozuhara H, Onodera H, Itoyama Y, Kogure K. Interleukin-1 as a pathogenetic mediator of ischemic brain damage in rats. Stroke 1995; 26:676-680.
10
11.Stolina M, Sharma S, Lin Y, Dohadwala M, Gardner B, Luo J, et al. Specific Inhibition of Cyclooxygenase 2 Restores Antitumor Reactivity by Altering the Balance of IL-10 and IL-12 Synthesis. J Immunol 2000; 164:361-370.
11
12. Blais V, Turrin NP, Rivest S. Cyclooxygenase 2 (COX-2) inhibition increases the inflammatory response in the brain during systemic immune stimuli. J Neurochem 2005; 95:1563-1574.
12
ORIGINAL_ARTICLE
AM281, Cannabinoid Antagonist/Inverse agonist, Ameliorates Scopolamine-Induced Cognitive Deficit
Objective(s)
Cannabinoids have been implicated in memory deficit. We examined the effect of AM281, cannabinoid antagonist/inverse agonist in prevention of scopolamine-induced cognitive deficit.
Materials and Methods
Object recognition task was used to evaluate memory in mice. Exploration time in the first and the second trial was recorded. The differences in exploration between a previously seen object and a novel object in second trial were taken as an index of memory. Scopolamine and AM281 were administrated at the same time, 40 min before second trial in the treatment group.
Results
Object discrimination was impaired after scopolamine (2 mg/kg; IP) administration. AM281 (2.5, 5 mg/kg; IP) significantly restored object recognition ability in mice treated with scopolamine by 75%.
Conclusion
This study extends earlier findings, suggesting the interaction of cannabinoid and cholinergic system in memory. Additionally cannabinoid antagonists seem to show variable pharmacological properties.
https://ijbms.mums.ac.ir/article_4927_0cc42d0fe9ecee0c43729cb023c9fae1.pdf
2012-09-01
1106
1110
10.22038/ijbms.2012.4927
AM281
Cannabinoid antagonist
Cognitive deficit
Mice
Scopolamine
Mohammed
Rabbani
1
Department of Pharmacology, Isfahan Pharmaceutical Sciences Research Centre, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
Golnaz
Vaseghi
golnazvaseghi@yahoo.com
2
Department of Pharmacology, Isfahan Pharmaceutical Sciences Research Centre, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran
LEAD_AUTHOR
Valiollah
Hajhashemi
hajhashemi@ pharm.mui.ac.ir
3
Department of Pharmacology, Isfahan Pharmaceutical Sciences Research Centre, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
1.Bartus RT, Dean RL, Beer B, Lippa AS. The cholinergic hypothesis of geriatric memory dysfunction. Science 1982; 217:408–414.
1
2.Roloff E, Harbaran D, Micheau J,Platt B, Riedel G. Dissociation of cholinergic function in spatial and procedural learning in rats. Neurosci 2007; 146:875-889.
2
3.Carlini EA, Hamaoui A, Bieniek D, Korte F. Effects of (−) delta-9-trans-tetrahydrocannabinol and a synthetic derivative on maze performance of rats. Pharmacol 1970; 4:359–368.
3
4.Terranova JP, Storme JJ, Lafon N, Perio A, Rinaldi-Carmona M, Le Fu G, et al. Improvement of memory in rodents by the selective CB1 cannabinoid antagonist, SR141716. Psychopharmacology 2007; 126:165–172.
4
5.Thiel CM. Cholinergic modulation of learning and memory in the human brain as detected with functional neuroimaging. Neurobiol Learn Mem 2003; 80:234–244.
5
6. Mazzola M, Micale V, Drago F. Amnesia induced by beta-amyloid fragments is counteracted by cannabinoid CB1 receptor blockade. Eur J Pharmacol 2003; 477:219–225.
6
7.Naoto R, Takahashi RN, Pamplona FL, Fernandes MS. The cannabinoid antagonist SR141716A facilitates memory acquisition and consolidation in the mouse elevated T-maze. Neuroscie Lett 2005; 380:270-275.
7
8. Bruin NM, Prickaerts J, Lange JH, Akkerman S, Andriambeloson E, Haan M, et al. SLV330, a cannabinoid CB1 receptor antagonist, ameliorates deficits in the T-maze, object recognition and social recognition tasks in rodents. Neurobiol Learn Mem 2010; 934:522-531.
8
9. Cosenza M, Gifford AN, Gatley SJ, Pyatt B, Liu Q, Makriyannis A, et al. Locomotor activity and occupancy of brain cannabinoid CB1 receptors by the antagonist/inverse agonist AM281. Synapse 2000; 38:477-482.
9
10.Bertaina-Anglade V, Enjuanes E, Morillon D, Drieu la Rochelle C. The object recognition task in rats and mice: simple and rapid modelin safety pharmacology to detect amnesic properties of a new chemical entity. J Pharmacol Toxicol Methods 2006; 54:99-105.
10
11.Van Meer P, Raber J. Mouse behavioral analysis in systems biology. Biochem J 2005; 389:593-610.
11
12.Okuda S, Roozendaal B, McGaugh JL. Glucocorticoid effects on object recognition memory require training-associated emotional arousal. Proc Natl Acad Sci 2004; 101:853-857.
12
13.Reibaud M, Obinu MC, Ledent C, Parmentier M, Bohme GA, Imperato A. Enhancement of memory in cannabinoid CB1 receptor knockout mice. Eur J Pharmacol 1999; 379:1-2.
13
14. Dillona GM, Lubbersb LS, Fergusona MT, Laoc JZ, Huang RC, Xiao JC, et al. MK-7128, a novel CB1 receptor inverse agonist, improves scopolamine-induced learning and memory deficits in mice. Behav Pharmacol 2011; 22:92-100.
14
15.Gifford AN, Tang Y, Gatley SJ, Volkow ND, Lan R, Makriyannis A. Effect of the cannabinoid receptor SPECT agent, AM 281, on hippocampal acetylcholine release from rat brain slices. Neurosci Lett 1997; 238:84-86.
15