Background and objective: Hyperlipidemia refers to elevated levels of lipids and cholesterol in the blood, and is also identified as dyslipidemia, to describe the manifestations of different disorders of lipoprotein metabolism. The aim of this study was to investigate the available and commonly distracted natural and synthetic antihyperlipidemic agents in herbal shops, pharmacies and prescribed by physicians in Erbil city, and to determine physicians' response for the use of natural products.
Methods: Between November 2013 to February 2014; 20 herbal shops and 40 pharmacies in Erbil city were visited randomly for asking on available and most commonly distracted natural and synthetic antihyperlipidemic agents. Forty doctors at private clinics were asked about the most frequently prescribed natural and synthetic antihyperlipidemic agents in Erbil city.
Results: Of eight synthetic drugs available in pharmacies, statins were considered the first line agents as antihyperlipidemic drugs particularly atorvastatin and rosuvastatin. Of 16 natural products available in Erbil herbal shops and pharmacies, garlic and omega 3 give positive response by patients and highly distracted by pharmacist and herbalist. Of 40 physicians, 27 (68%) prescribe both natural and synthetic agents while only 13 (32%) prescribe synthetic drugs as antihyperlipidemic agents for patients.
Conclusion: Statins used in first order as antihyperlipidemic drugs and uses of natural products, as lipid lowering agents in Erbil, is getting larger interest by people, herbalists, pharmacists and doctors. Of 40 doctors, 68% prescribe natural products along with synthetic drugs but also there is a need to educate the people on how to use these natural agents and choice suitable products for them.
1. Mahmood ZA, Ahmed SW, Sualeh M, Mahmood SBZ. Hyperlipidemia development and consequences. Med Channel 2009; 5:14-17.
2. Ducharme N, Radhamma R. Hyperlipidemia in the elderly. Clin Geriatr Med 2008; 24:471-87.
3. Reiner Z, Tedeschi-Reiner E. Atherosclerosis – a paradox of Eastern European countries. Atherosclerosis 2006; 7:461.
4. Simons LA. Additive effect of plant sterol-ester margarine and cerivastatin in lowering low density lipoprotein cholesterol in primary hypercholesterolemia. Am J Cardiol 2002; 90:737.
5. Yokozawa T, Ishida A, Cho E J, Nakagawa T. The effects of Coptidis rhizoma extract on a hypercholesterolemic animal model. Phytomedicine 2003; 10:17.
6. Soutar AK, Naoumova RP. Mechanisms of disease: genetic causes of familial hypercholesterolemia. Nat Clin Pract Cardiovasc Med 2007; 4:214-25.
7. Ibrahim SRM, Mohamed GA, Banjar ZM, Kamal HKM. Natural antihyperlipidemic agents: Current status and future perspectives. Phytopharmacology 2013; 4(3):492-531.
8. Durington P. Dyslipidaemia. Lancet 2003; 362:717-31.
9. Farnier M. Cerivastatin in the treatment of mixed hyperlipidemia: the right study. The Cerivastatin Study Group. Cerivastatin, Gemfibrozil, Hyperlipidemia Treatment. Am J Cardiol 1998; 82:47-51.
10. Trevor AJ, Katzung BG. Clipstone N. Drugs used to treat Hyperlipidemia I & II. Pharmacology: Examination and Board Review. 9ed. Anthony J 2012; 605-17.
11. Naples M, Federico LM, Xu E, Nelken J, Adeli K. Effect of rosuvastatin on insulin sensitivity in an animal model of insulin resistance: evidence for statin-induced hepatic insulin sensitization. Atherosclerosis 2008; 198(1):94-103.
12. Souza TD, Mengi SA, Hassarajani S, Chattopadhayay S. Efficacy study of the bioactive fraction (F-3) of Acorus calamus in hyperlipidemia. Indian J Pharmacol 2007; 39(4):196-200.
13. Moser A, Segars LW: Assessment of antihyperlipidemic therapy in US patients with coronary heart disease. J Am Osteopath Assoc 2010; 110(6):331-39.
14. Tsujita T, Takaichi H, Takaku T, Aoyama S, Hiraki J. Antiobesity action of -polylysine, a potent inhibitor of pancreatic lipase. J Lipid Res 2006; 47:1852-58.
15. Farnsworth NR, Akerels O, Bingel AS, Soejarto DD, Guo Bull Z. Medicinal plants in therapy. Bull World Health Organ 1985; 63:965.
16. Ibraheem DA. Comparative study between plant and animal sources of Omega-3 fatty acid in their potential role of regulating blood glucose and lipid profile in healthy volunteers. Yemeni J Med Sci 2011; 5:7-14.
17. Yeh Y, Liu L. Cholesterol-lowering effect of garlic extracts and organosulfur compounds: Human and animal studies. The Am Soc Nutr Sci 2001; 131(3):9895-935.
18. Vijaimohan K, Jainu M, Sabitha KE, Subramaniyam S, Anandhan C, Shyamala Devi CS. Beneficial effects of alpha linolenic acid rich flaxseed oil on growth performance and hepatic cholesterol metabolism in high fat diet fed rats. Life Sci 2006; 79(5):448-54.
19. Kaatabi H, Bamosa AO, Lebda FM, Abdulmohsen H, Al-Sultan AI. Favorable impact of Nigella sativa seeds on lipid profile in type 2 diabetic patients. J Fam Commun Med 2012; 19(3):155–61.
20. Asgary S, Rafieian-Kopaei M, Najafi S, Heidarian E, Sahebkar A. Antihyperlipidemic effects of Sesamum indicum L. in Rabbits Fed a High-Fat Diet. The Sci World J 2013; 5.
21. Fuhrman B, Rosenblat M, Hayek T, Coleman R, Aviram M. Ginger extract consumption reduces plasma cholesterol, inhibits LDL oxidation and attenuates development of atherosclerosis in atherosclerotic, apolipoprotein e-deficient mice. J Nutr 2000; 130(5):1124-31.
22. Yousaf MJ, Naveed AK, Ahmed T, Khan S, Azeem Z. Hypolipidemic effect of extra virgin olive oil in diabetic rats. J Rawal Med Col 2012; 16(1):70-72.
23. Jäger S, Trojan H, Kopp T, Laszczyk M, Scheffler A. Pentacyclic triterpene distribution in various plants - rich sources for a new group of multi-potent plant extracts. Molecules 2009; 14: 2016-31
24. Suriyamoorthy P, Mary MRF, Subrhamanian H, Kanagasapabathy D. Anti hyperlipidemic effect of aqueous extract of Aegle marmelos and camellia sinensis in oil fed hyperlipidemic rats. Int J Pharm Sci, 2014; 6(2):338-41.
25. Vuyyuru A, Kotagiri S, Vrushabendra Swamy BM, Archana Swamy P. Antihyperlipidemic activity of Ananas Comosus L. leaves extract in Albino rats. Res J Pharma Biol Chem Sci 2012; 3(3):1229.
26. Leontowicz H, Leontowicz M, Gorinstein S, Martin-belloso O, trakhtenberg S. apple peels and pulp as a source of bioactive compounds and their influence on digestibility and lipid profile in normal and atherogenic rats. J Med weter 2007; 63(11):1434-6.
27. Qin Y, Xia M, Ma J, Hao YT, Liu J, Mou HY et al. Anthocyanin supplementation improves serum LDL- and HDL-cholesterol concentrations associated with the inhibition of cholesteryl ester transfer protein in dyslipidemic subjects. Am J Clin Nutr 2009; 90:485-92.
28. Udani JK, Singh BB, Singh VJ, Barrett ML. Effects of Açai (Euterpe oleracea Mart.) berry preparation on metabolic parameters in a healthy overweight population: a pilot study. Nutr J 2011; 10:45.
Background and objective: Pertussis is one of the vaccine preventable diseases. Bordetella pertussis (B. Pertussis) continues to circulate even in countries with good childhood vaccination. The aim of this study was to evaluate patients suspected or confirmed to have pertussis in relation to certain clinical and laboratory data.
Methods: A prospective study was conducted in Rapareen Teaching Hospital from June 1st, to September 1st, 2010. The study enrolled 651 inpatients below five years of age with respiratory tract infection with 72 of them having initial suspicion of pertussis. Demographic and clinical data were obtained from them and nasopharyngeal swab were sent for culture for isolation of microorganisms as well as blood samples obtained for haematological assessment (white blood cell differential count and platelet count). Those confirmed to have pertussis and para-pertussis were considered as group A while other culture results were considered group B.
Results: Most of patients were below one year of age (56.9%) with large numbers were not properly vaccinated and they had positive family history of paroxysmal cough (68.1% and 58.3%, respectively). Twenty one patients confirmed to have pertussis and parapertussis by culture methods. There was no significant difference between patients with group A when compared to group B regarding gender, vaccination status, history of post-tussive vomiting or whoop and family history of chronic cough. Mean platelet count was significantly different between two groups, with pertussis and parap-pertussis cases had less platelet count.
Conclusion: Near half of patients with B. pertussis and parapertussis have a defect in their vaccination program.
1. Leber A, Salamon D, Prince H. Clinical microbiology newsletter 2011; 33 (15):111-5.
2. Howidi M, Nair R, Rajah J. The severity of pertussis in young infant in the United Arab Emirates Proceedings of the ESPID. Annual Conference. Brussels, Belgium 2009; June 9-13
3. Burr S, Jenkins T, Harrison R, Meert K, Anand K, Berger J, et al. The Collaborative Pediatric Critical Care Research Network (CPCCRN) Critical Pertussis Study: Collaborative Research in Pediatric Critical Care Medicine. Pediatr Crit Care Med 2011; 12(4):387-92.
4. Communicable disease toolkit, Iraq crisis. WHO, March 2003, available from: http://www.who.int/diseasecontrol_emergencies/toolkits/Iraq_profile_ok.pdf ( accessed on 17 of january 2013)
5. Al-Bargish K A. Outbreak of pertussis in Basra, Iraq. East Mediterr Health J 1999; 5(3):540-8.
6. Colorado Department of Public Health and Environment (homepage on internet) Summary of Pertussis Investigation and Control Guidelines [cited 2011 June 11, accessed at 17 of January 2013]. Available from: http://www.colorado.gov/cs/Satellite/CDPHE-Main/CBON/1251583470000
7. Crespo I, Cardenosa N, Godoy P, Carmona G, Sala M., Barrabeig I, et al. Epidemiology of pertussis in a country with high vaccination coverage. Vaccine 2011; 29(25):4244-8.
8. Al-Shammary M. The descriptive epidemiology of pertussis in Al Diwaniya governorate for the years 1990 through 2007, Kufa Med Journal 2010;13(2): 7-17.
9. Cardenosa N, Romero M, Quesada M, Oviedo M, Carmona G, Codina G, et al. Is the vaccination coverage established enough to control pertussis, or it is a re-emerging disease? Vaccine 2009; 27(25-26):3489-91.
10. Ferrer A, Moraga F, Olsina M, Campins M, Planells I. Culture-confirmed whooping cough in a tertiary center over a twelve-year period. An Pediatr (Barc) 2003; 58(4):309-15.
11. Muhsim M, Al-Tufaili Y,Shalan A. The epidemiological profiles of hospitalized pertussis patients in Babylon province. Kufa Med Journal 2009; 12(2):230-9.
12. Al-Tawfiq J, Abukhamsin A. Bordetella pertussis infection in highly vaccinated population in Saudi Arabia, 1996-2004. J infection 2007; 55(3):249-53.
13. Mughal A, Kazi Y, Bukhari H, Ali M. Pertussis resurgence among vaccinated children in Khairpur, Sindh, Pakistan. Public Health 2012; 126 (6):518-22.
14. Yildirim I, Ceyhan M, Kalayci O, Cengiz A, Secmeer G, Gur D, et al. Frequency of pertussis in children with prolongued cough. Scand J Infect Dis 2008; 40(4):314-9.
15. Baptista P, Magalhães V, Rodrigues L.Children with pertussis inform the investigation of other pertussis cases among contacts. BMC Pediatr 2007; 7:21.
16. Hochwald O, Bamberger ES, Rubin L, Gershtein R, Srugo I. A pertussis outbreak among daycare children in Northern Israel: who gets sick? Isr Med Assoc J 2010; 12(5):283-6.
17. Cengiz A, Yildirim I, Ceyhan M, Seçmeer G, Gür D, Kara A. Comparison of nasopharyngeal culture, polymerase chain reaction (PCR) and serological test for diagnosis of pertussis. Turk J Pediatr 2009; 51(4):309-16.
18. Zouari A, Smaoui H, Brun D, Njamkepo E, Sghaier S, Zouari E, et al. Prevalence of Bordetella pertussis and Bordetella parapertussis infections in Tunisian hospitalized infants: results of a 4 year prospective study. Diagn Microbiol Infect Dis 2012; 72(4):303-17.
21. Worthington Z, Van Roooijen N, Carbonetti N. Enhancement of Bordetella parapertussis infection by Bordetella pertussis in mixed infection of the respiratory tract. FEMS Immunol Med Microbiol 2011; 63:119-28.
22. Mattoo S, Cherry JD. Molecular pathogenesis, epidemiology, and clinical manifestations of respiratory infections due to Bordetella pertussis and other Bordetella subspecies. Clin Microbiol Rev 2005; 18:326-82.
23. Long S, Kleigman R, Stanton B, Geme J, Schor N, Behrman R. Pertussis. Nelson textbook of pediatrics.19th edition. Philadelphia: Elsevier Saunders; 2011. p 945.
Background and objective: Death of an infant in utero or at birth has always been a devastating experience for the mother and of concern in clinical practice. The aim of this study was to determine the prevalence, probable risk factors and association of stillbirth with different maternal variables in Erbil Maternity Teaching Hospital.
Methods: A cross-sectional design was used to determine the prevalence of stillbirth and a case control design was used to determine the probable risk factors and demographic characteristics of women with stillbirth in Maternity Teaching Hospital in Erbil city, Kurdistan region, Iraq, from April 1st, to December 31st, 2011.Three hundred seventy nine women having stillbirth were regarded as cases while 758 women delivering alive newborns were regarded as control group.
Results: The prevalence of stillbirth during the period of the study was 20.4 per1000 total births. Macerated stillbirth was about four times higher than the fresh stillbirth. There were statistically significant differences between the cases and controls in relation to: maternal age (≥ 35 years), level of education, history of antenatal care visits, parity, medical diseases of the mother, congenital anomalies of the newborn, and history of previous stillbirth. In 65.4% of cases the probable cause of death was unexplained.
Conclusion: The prevalence of stillbirth in the Maternity Teaching Hospital in Erbil is high in comparison to the rate in other countries. This could be due to high level of deliveries per day and lack of good follow up of patients during labour.
1. James D. Perinatal mortality. In: David M L, Philip N B editors. Obstetrics and Gynaecology an evidence-based text for MRCOG. Second edition. Great Britain: Edward Arnold publishers; 2010. 482-83.
2. Frøen JF, Gordijn SJ, Abdel-Aleem H, Bergsjø P, Betran A, Duke CW, et al . Making stillbirths count, making numbers talk - issues in data collection for stillbirths. BMC Pregnancy Childbirth. 2009; 9:58.
3. Neonatal and Perinatal Mortality: Country, Regional, and Global Estimates. World Health Organization; Geneva, Switzerland: 2006.
4. Abdou J, Siri V, Juhanne S. Stillbirth in rural hospitals in The Gambia:A cross-sectional retrospective study. ObstetGynecolInt 2010; (1):2
5. Feresu SA, Harlow SD, Welch K, Gillespie BW. Incidence of stillbirth and perinatal mortality and their associated factors among women delivering at Harare maternity hospital, Zimbabwe: a cross-sectional retrospective analysis. BMC Pregnancy Childbirth 2005; 5(1):9.
6. DI Mario S, Say L, Lincetto O. Risk of stillbirth in developing countries: a systematic review. ReprodCHealth2006; 3:1
7. Arun K A, Vanita J, Rajesh K. Validity of verbal autopsy for ascertaining the causes of stillbirth. Central Bulletin WHO, 2010.
8. Audu BM, Alhaji MA, Takai UI, Bukar M. Risk factors for stillbirths at university of Maiduguri teaching hospital.BMC pregnancy and childbirth2009; 50(2):42-6.
9. Kumar R, Singhi S. Risk factors for stillbirth in rural community medical education and research Chandigarh. Indian J Pediatr1992; 59(4):455-61.
10. Petersson K, Stray PB, Malm G, Forsgen E, Vengard B. Seroprevalence of Toxoplasmosis gonodi among pregnant women in Sweden. Acta Obstet Gynecol Scand 2000; 79:824-9.
11. Lyon JL, Sara M, Alder SC, Varner M W. Effects of grand multipara on intrapartum and newborn complications in young women. Obstet Gynecol 2005; 106:454-60.
12. Agudelo A, Belizan JM, Rossello JL. Epidemiology of fetal death in Latin America.ActaObstetGynecolScand 2000; 79:371-8.
13. Magaan E F, Winchester MJ, Carter DP, Mastin JN, Bass JD. Pregnancy outcome. AMJ1995; 12:462-6.
14. Humphrey MD. Is grand multiparity an independent predictor of pregnancy risk? A retrospective observational study. Med J Aust 2003; 179(6): 294-6
15. Rizk ED, Khalfan M, Ezimokhai M. Obstetrics outcome in grand multipara in the United Arab Emirates. A case control study. Arch Gynecol.Obstet2001; 264(4):194-8.
16. Hinkula M , Kauppila A, Nayha S, Pukkalaa E, Causes specific mortality of Grand multiparous women in Finland. Am J Epidemiol 2006; 163(4):367-73.
17. Aliyu MH, Jolly PE, Ehiri JE, Salihu HM. High parity and adverse birth outcomes: exploring the maze. Birth 2005; 32(1):45-59.
18. Surkan P, Stephansson O, Dickman P, Cnattingius S. Previous Preterm and Small for gestational ages Births and the Subsequent Risk of Stillbirth. NEJM 2004;350:777-85.
19. Samueloff A, Xenakis EM, Berkus MD, Huff RW, Langer O. Recurrent stillbirth Significance and Characteristics . J Reprod Med 1993; 38(11):88.
20. Huang DY, Usher RH, Kramer MS, Yang TT, Morin, Fretts RC. Determinants of unexplained antrpartum fetal deaths. ObstetGyneacol 2000; 95:215-21.
21. Petridon E, Kotsifakis G, Revinthi K, Polychronopoulou A, Trichopoulos D. Determinants of stillbirth mortality in Greece. Soz Preventiv Med 1996; 41(2):70-8.
22. Gadow EC, Lopez CJ, Queenan JT. Stillbirth rates and associated risk factors among 8699750 Latin American hospital births 1982-1986. IJOG1991; 35(3):209-14.
Background and objective: A dramatic rise in caesarean deliveries has been occurring over the past three decades. The old myth of “once a caesarean always a caesarean” is no longer acceptable as this increases maternal morbidity. The aim of this study was to evaluate the safety and success of vaginal birth after caesarean section performed before less than two years.
Methods: A cross-sectional study was conducted in the Maternity Teaching Hospital in Erbil, Iraq from May to October 2012. Ninety two patients meeting the inclusion criteria were included in this study and followed up during their labour. Patients monitored for vaginal bleeding, scar tenderness and tachycardia.
Results: Of 92 patients with single lower segment caesarean section that underwent trial of labour; 52 (56.5%) patients had successful trial of labour and 40 (43.5%) had a repeated caesarean section. Factors found to be significantly affecting trial of labour were parity (P = 0.01), inter-delivery interval (P <0.001) and cervical dilatation (P = 0.015).
Conclusion: Vaginal birth after caesarean section is a reasonable choice for women with single lower segment caesarean section with good monitoring of mother and baby during labour. Short inter-delivery period does not preclude vaginal delivery in a woman with single lower segment caesarean section providing that there is no contraindication for vaginal delivery.
1. Mehta SH, Bujold E, Blackwell SC, Sorokin Y, Sokol RJ. Is abnormal labor associated with shoulder dystocia in nulliparous women? Am J Obstet Gynecol 2004; 190(6):1604-9.
2. World Health Organization. Appropriate technology for birth. Lancet 1985. Available at www.blogs.scientificamerican.com (Accessed 1st may 2014).
3. Betran AP, Merialdi M, Lauer JA, Bing-Shun W, Thomas J, Van Look P et al. Rates of caesarean section: analysis of global, regional and national estimates. Paediatr Perinat Epidemiol 2007; 21(2):98-113.
4. Monitoring the situation of children and women findings from Iraq. Multiple indicator cluster survey 2006. Final report 2007 October, 1. 2010
5. C-section rates around globe at ‘epidemic’ levels". 2010
6. Guleria K, Dhall GI, Dhall K. Pattern of cervical dilatation in previous lower segment Caesarean section patients. J Indian Med Assoc 1997; 95:131-4.
7. Marie-Jocelyne M, Saskatoon SK , MacKinnon C J, Brantford ON. Guidelines for Vaginal Birth after Previous Caesarean Birth; JOGC No 155 (Replaces guideline No 147), February 2005.
8. Salih R A, Aldabbagh SR. Modes of delivery among women with previous single lower transverse caesarean section of birth interval less than 2 year and their fetal outcome in Erbil Maternity Teaching hospital; 2009
9. Srinivas SK, Stamilio DM, Sammel MD. Vaginal birth after caesarean delivery: does maternal age affect safety and success? Paediatr Perinat Epidemiol 2007; 21:11.
10. Al-Wazzan RM; Factors affecting success of trial of labour after previous one lower segment Caesarean section; Ann Coll Med Mosul 2010; 36(1&2):121-9.
11. Yamani TY. Vaginal birth after caesarean section in grand multiparous women; Arch Gynecol Obstet 2004; 270(1):21-4.
12. Landon MB, Leindecker S, Spong CY, Hauth JC, Bloom S, Varner MW, et al. National Institute of Child Health and Human Development Maternal Fetal Medicine Units Network; The Maternal Fetal Medicine Units Caesarean Registry: factors affecting the success of trial of labor after previous caesarean delivery. Am J Obstet Gynecol 2005; 193(3 Pt2):1016-23.
13.Gyamfi C, Juhasz G, Gyamfi P, Stone JL. Increased success of trial of labor after previous vaginal birth after caesarean. Obstet Gynecol 2004; 104(4):715
14. Kashif S, Mansoor M, Tariq R, Tahira T. Vaginal birth after caesarean section to evaluate factors for successful outcome. Professional Med J 2010; 17(4):665-9.
Background and objective: Chronic periodontitis is the destruction of the tooth supporting structures as a result of a complex interaction between bacteria colonizing the gingival crevice and host’s immune responses. Porphyromonas gingivalis is one of the main periodontopathogens with multiple virulence factors. The aim of this study was to investigate the detection rate of Porphyromonas gingivalis in chronic periodontitis patients versus healthy subjects using PCR assay, and its association with increased pocket depth and clinical attachment loss.
Methods: Seventy subjects (35 patients with chronic periodontitis and 35 healthy subjects) meeting the inclusion criteria of this study were selected. All the subjects were clinically assessed for probing pocket depth and clinical attachment loss then subgingival microbial samples were collected using sterile paper points and analyzed for the presence of Porphyromonas gingivalis using polymerase chain reaction assay.
Results: A significant difference in Porphyromonas gingivalis detection rate between chronic periodontitis and healthy groups was recorded. Porphyromonas gingivalis was significantly associated with deep pockets. The detection rate increased with the increase in the severity of the disease, although, this correlation was not statistically significant.
Conclusion: A positive association was observed between Porphyromonas gingivalis and increased pocket depth. The recovery rate was higher in severe cases.
1. Kumar PS, Griffen AL, Moeschloeger ML, Leys EJ. Identification of candidate periodontal pathogens and beneficial species by quantitative 16S clonal analysis. J Clin Microbiol 2005; 43: 3944-55.
2. Vajawat M, Kumar V, Rajeshwari KG, Deepika PC. Clinical, microbiological and molecular study of Porphyromonas gingivalis in patients with chronic periodontitis. Int J Basic Appl Med Sci 2013; 3:56-61.
3. Holt SC, Kesavalu L, Walker S, Genco CA. Virulence factors of Porphyromonas gingivalis. Periodontol 2000; 20:168-238.
4. Avila-Campos MJ. PCR detection of four periodontopathogens from subgingival clinical samples. Braz J Microbiol 2003; 34:81-4.
5. Herrera D, Contreras A, Gamonal J, Oteo A, Jaramillo A, Silva N, et al. Subgingival microbial profiles in chronic periodontitis patients from Chile, Colombia and Spain. J Clin Periodontol 2008; 35:106-13.
6. Lamont RJ, Jenkinson, HF. Life below the gum line: pathogenic mechanisms of Porphyromonas gingivalis. Microbiol Mol Biol R 1998; 62:1244-63.
7. Samaranayake L, Jones BM, Scully C. Essential microbiology for dentistry. 3rd ed. Edinburgh: Churchill Livingstone-Elsevier; 2012. p. 291-3.
8. Brochut PF, Marin I, Baehni P, Mombelli A. Predictive value of clinical and microbiological parameters for the treatment outcome of scaling and root planning. J Clin Periodontol 2005; 32: 695-701.
9. Suchett-Kaye G, Morrier JJ, Barsotti O. Clinical usefulness of microbiological diagnostic tools in the management of periodontal disease. Res Microbiol 2001; 152:631-9.
10. Listgarten MA, Loomer PM. Microbial identification in the management of periodontal disease. Ann Periodotol 2003; 8:182-92.
11. Dewhirst FE, Paster BJ, Tzellas N, Coleman B, Downes J, Spratt DA, et al. Characterization of novel human oral isolates and cloned 16S rDNA sequences that fall in the family Coriobacteriaceae: description of Olsenella gen. nov., reclassification of Lactobacillus uli as Olsenella uli comb. nov. and description of Olsenella profusa sp. nov. Int J Syst Evol Micr 2011; 51:1797-804.
12. Wade WG. Has the use of molecular methods for the characterisation of the human oral microbiome changed our understanding of the role of bacteria in the pathogenesis of periodontal disease? J Clin Periodontol 2011; 38(Suppl. 11):7-16.
13. Mahon CR, Tice D. Clinical laboratory immunology. New Jersey: Pearson Education; 2006.
14. Boutaga K, Winkelhoff AJ, Vandenbroucke-Grauls CMJE, Savelkoul PHM. Comparison of Real-Time PCR and Culture for Detection of Porphyromonas gingivalis in Subgingival Plaque Samples. J Microbiol 2003; 41:4950-4.
15. Fawzi MM, Fawzi MM, El-Amin HM, Elafandy MH. Detection and quantification of Porphyromonas gingivalis from saliva of Schizophrenia patients by culture and Taqman real-time PCR: a pilot study. Life Sci J 2011; 8: 65-74.
16. Al-Rawi AMM. Detection of Porphyromonas gingivalis from periodontal pocket infections by microbial cultivation and PCR. Rafidain Journal of Science 2012; 23:39-55.
17. Haffajee AD, Bogren A, Hasturk H, Feres M, Lopez NJ, Socransky SS. Subgingival microbiota of chronic periodontitis subjects from different geographic locations. J Clin Periodontol 2004; 31:996-1002.
18. Escalona LA, Brito A, Almon R, Bravo IM, Perrone M, Correnti M. Distribution of Prevotella intermedia, Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans in Venezuelan population with chronic periodontitis. Revista Venezolana de Investigacian Odontologica 2007; 7:29-37.
19. Carranza FA, Newman MG, Henry HT, Klokkevold PR. Carranza’s Clinical Periodontology. 10th edition. St. Louis: Saunders Elsevier; 2006.
20. Sambrook J, Russel DW. Molecular Cloning: a laboratory manual. 2nd ed. Cold Spring Harbor Laboratory Press; 2001. p. 5-14.
21. Griffen AL, Becker MR, Lyons SR, Moeschberger ML, Leys EJ. Prevalence of Porphyromonas gingivalis and periodontal health status. J Clin Microbiol 1998; 36:3239 - 42.
22. Boyanova L, Setchanova L, Gergova G, Kostyanev T, Yordanov D, Popova C, et al. Microbiological diagnosis of the sever chronic periodontitis. J IMAB -Annual Proceeding (Scientific Papers) 2009; book 2: 89-94.
23. Lamont R J, Gil S, Demuth DR, Malamud D, Rosan B Molecules of Streptococcus gordonii that bind to porphyromonas gingivalis. Microbiol 1994; 140 (Pt. 4):867-72.
24. Nelson KE, Fleischmann RD, DeBoy RT, Paulsen IT, Fouts DE, Eisen, JA. Complete genome sequence of the oral pathogenic bacterium Porphyromonas gingivalis strain W83. J Bacteriol 2003; 185:5591-601.
25. Kawada M, Yoshida A, Suzuki N, Nakano Y, Saito T, Oho T, et al. Prevalence of porphyromonas gingivalis in relation to periodontal status assessed by real-time PCR. Oral Microbiol Immun 2004; 19:289-92.
26. Tannner ACR, Paster BJ, Lu SC, Kanasi E, Kent R, Van Dyke T, et al. Subgingival and tongue microbiota during early periodontitis. JDR 2006; 85:318-23.
Background and objective: Evidence from research is underutilized in policy and practice in the majority of developing countries including Iraq. This aim of this study was to assess the role of research in health policy making in Iraqi Kurdistan context and identify the main barriers and facilitators for enhancing such role.
Methods: This cross-sectional survey was carried out between November 2013 and March 2014 in the three governorates of the Iraqi Kurdistan Region, Erbil, Duhok and Sulaimaniyah. The study participants included 10 key health informants and three health advisors. Two types of combined questionnaires for health policy makers and health advisors were used for data collection.
Results: Conferences and seminars were the main sources of scientific evidences identified by health policymakers (80%), followed by consultants (70%). Different jargons/discourse was the main obstacle in consulting researchers (90%), followed by lack of tradition in collaborating (70%). Collection of specialists/advisors, followed by professional associations, scientific committees and international organizations/UN agencies were the main groups identified by health advisors to build bridges between the scientific community and policymakers.
Conclusion: Policymakers very rarely consult researchers directly in their decision making. There is poor networking among researchers, policy-makers, practitioners and representatives from civil society which has its negative impact on evidence-based policymaking. There is obviously a lack of any sort of program of funded research that can inform policymaking.
1. Davies P. ‘Is evidence-based government possible?’ Jerry Lee Lecture, presented at the 4th Annual Campbell Collaboration Colloquium, Washington DC; 2004.
2. Sutcliffe S, Court J. A toolkit for progressive policymakers in developing countries. Research and Policy in Development Programme. 111 Westminster Bridge Road, London, SE1 7JD; 2006.
3. Swartz L, Tomlinson M, Landman M. Evidence, policies and practices: Continuities and discontinuities in mental health promotion in a developing country. Int J Ment Health Prom 2004; 6:33-7.
4. Kothari A, Birch S, Charles C. "Interaction" and research utilization in health policies and programs: does it work? Health Policy 2005; 71:117-25.
5. Innvaer S, Vist G, Trommald M, Oxman A. Health policy-makers' perceptions of their use of evidence: a systematic review. J Health Serv Res Policy 2002; 7:239-44.
6. Lavis J, Davies H, Oxman A, Denis J-L, Golden-Biddle K, Ferlie E. Towards systematic reviews that inform health care management and policy-making. J Health Serv Res Policy 2005; 10:35-48.
7. Lawis JN, Ross S, Hurley JE, Hohenadel JM, Stoddart JL, Woodward CA, et al. Examining the role of Health Services Research in Public Policymaking. Milbank Q 2002; 80(1):125-54.
8. Tawfik-Shukor A, Khoshnaw H. The impact of health system governance and policy processes on health services in Iraqi Kurdistan. BMC Int Health Hum Rights 2010; 10:14.
9. Abdulahad F, Shabila NP. A perception-based survey on evaluating the impact of locally published medical journals. Middle East J Fam Med 2009; 7(9):31-4.
10. Shabila NP, Al-Taweel N, Tahir R, Shwani FH, Salih AM, Al-Hadithi TS. Iraqi health system in Kurdistan region: medical professionals' perspectives on challenges and priorities for improvement. Confl Health 2010; 4:19.
11. Europea Commision. Scientific evidence for policy-making. European research area, socio-economic sciences and humanities 2008:25-7. Available from: http://ec.europa.eu/research/research-eu [Accessed on 17 March 2014]
12. Uneke CJ, Ezeoha AE. Development of Health Policy and Systems Research in Nigeria: Lessons for Developing countries ' Evidence-Based Health Policy Making Process and Practice. Healthcare Policy 2010; 6(1):109-26.
13. Feldman PH, Nadash P, Gursen M. Improving communication between researchers and policymakers in long-term care: or, Reesearchers are from Mars; Policymakers are from Venus. The Gerontologist 2001; 41(3):312-21
14. El-Jardali F, Lavis JN, Ataya N, Jamal D. Use of health systems and policy research evidence in the health policymaking in eastern Mediterranean countries: views and practices of researchers. Implementation Science 2012; 7:2.
15. Nutley S. ‘Bridging the Policy/Research Divide: Reflections and Lessons from the UK’, Keynote Paper at National Institute of Governance Conference ‘Facing the Future: Engaging stakeholders and citizens in developing public policy’, Canberra, Australia; 23–4 April 2003.
16. Hyder AA, Corluka A, Winch PJ, El-Shinnawy A, Ghassany H, Malekafzail H, et al. National policy-makers speak out: are researchers giving them what they need? Health Policy Plan 2011; 26:73-82
17. Mitton C, Adair CE, McKenzie E, Patten SB, Waye PB. Knowledge transfer and exchange: review and synthesis of the literature. The Milbank Quarterly 2007; 85(4):729–68.
Background and objective: Community medicine is an important discipline for medical students who are going to be future doctors and deal with different health problems. Community Medicine is taught in 3rd, 4th and 6th year of study at Hawler College of Medicine. The aim of the study was to explore students' perception about this subject because it plays an important role in determining educational outcome.
Methods: This study was carried out in Hawler College of Medicine, Erbil city, Iraqi Kurdistan Region in the academic year 2013-2014. It was based on a self-administered questionnaire survey of 4th year students. The questionnaire consisted of closed and open ended questions related to the attitude of students toward community medicine course, views on the positive and negative aspects and recommendations to improve the course. The quantitative data were analysed through using the statistical package for the social sciences (version 19), while qualitative data analysis comprised thematic analysis of open-ended questions using common coding techniques.
Results: The result of this study suggested that high percentage of the students had positive attitude toward the course. Sixty-six respondents (55.4%) mentioned that there are positive aspects in the course like research project (33.3.1%), having respectful and friendly teachers (31.8%) and participation of students in discussions in the classroom. Sixty-six respondents (55.4%) mentioned that there are negative aspects in the course like short duration of the course (27.2%) and some topics were repeated from other years. Fifty-seven respondents (47.8 %) have recommended a number of priorities for improving the quality of the course like: increasing practical sessions with more student participation (36.8%); decreasing theoretical lectures (22.8%) and the time for the research should be isolated without lectures (19.2%).
Conclusion: Community medicine course is well perceived by the students with some negative aspects. Some recommendations have been made for improving the quality of the course.
1. Navinan MR, Wijayaratne DR, Rajapakse S. Final year students’ perception regarding the curriculum in public health. Indian J community Med 2011; 36(4):268-74.
2. Dare AJ, Bullen C. Shifting perceptions and challenging the profession’s paradigms: Reflection from undergraduate week of population health. N Z Med J 2008; 121:45-50.
3. Hensel WA, Smith DD, Barry DR, Foreman R. Changes in medical education: the community perspective. Acad Med 1996; 71:441-6.
4. Gordon L. Public health is more important than health care. J Public Health Policy 1993; 14: 261-4.
5. Appleton DDR. What statistics should we teach medical undergraduates and graduates? Statistics in Medicine 1990; 9(9):1013-21.
6. Looney SW, Grady CS, Steiner RP. An update on biostatistics requirements in US medical schools. Acad Med 1998; 73(1):92-4.
7. Daher AM, Amin F. Assessing the perceptions of a biostatics and epidemiology module: View of Year 2 medical students from a Malaysian university. A cross-sectional survey. BMC Med Educ 2010; 10:34.
8. Ahmad F, Zehra N, Omair A, Anjum Q. Students' opinion regarding application of epidemiology, biostatistics and survey methodology courses in medical research. J Pak Med Assoc 2009; 59(5):307-10.
9. Dommisse J, Joubert G. Profile of research methodology and statistics training of undergraduate medical students at South African universities. SA Fam Pract 2009; 51(2):158-61.
10. Ercan I, Ozkaya G, Ocakoglu G, Yazici B, Sezer A, Ediz B. Determining Biostatistics Knowledge of Students and Physicians in Medical School. Inter Stat 2008; 3:1-17.
11. Harden RM. Developments in outcome-based education. Med Teach 2002; 24(2):117-20.
12. Harden RM, Crosby JR, Davis MH. An introduction to outcome-based education. Med Teach 1999; 21(1):7-14.
13. Hoat LN, Son NM, Wright EP. Perceptions of graduating students from eight medical schools in Vietnam on acquisition of key skills identified by teachers. BMC Med Educ 2008; 8(1):5.
14. Victor MN, Maria MM, Elsa CM. Perceptions on the importance of gerontological education by teachers and students of undergraduate health sciences. BMC Med Educ 2007; 7(1).
15. Lempp H, Seale C. The hidden curriculum in undergraduate medical education: qualitative study of medical students' perceptions of teaching. BMJ 2004; 329(7469):770-3.
16. Hawler College of Medicine: Self study report. Erbil: College of Medicine, Hawler Medical University. Unpublished report, 2011.
17. Darko H, Ivan K, Imir L, Ana M, Ivana V, Ana V, et al. Teaching research methodology in medical schools: students' attitudes towards and knowledge about science. Med Educ 2004; 38(1):81-6.
18. Sahai H. Teaching biostatistics to medical students and professionals: Problems and solutions. International Journal of Mathematical Education in Science and Technology 1999; 30(2):187-96.
19. Mostert P. Changing approaches and perceptions: biostatistics and its role in teaching the Stellenbosch doctor. In Proceedings of the Seventh International Conference on the Teaching of Statistics (ICOTS 7): 2006; Salvador, Brazil. Aukland: IASE; 2006.
20. Lam YM. Teaching statistics to medical students in the New Medical School. Journal of the Hong Kong Medical Association 1986; 38(4):196-8.
21. Altman DG, Bland JM. Improving doctors' understanding of statistics. Journal of the Royal Statistical Society Series A (Statistics in Society) 1991; 154(2)223-67.
Background and objective: Immunohistochemistry is the application of immunologic principles and techniques to demonstrate molecules in cells and tissues. Gene p53 is a tumor-suppressor gene. The product of this gene is a nuclear protein thought to be involved in the control of the cell cycle, apoptosis, and the maintenance of genomic stability. Gene p53 is the most frequently mutated tumor suppressor gene found in human cancer. The aim of this study was to investigate p53 protein over expression in skin cancer and compare it with benign skin lesion.
Methods: A retrospective study was conducted on paraffin block from skin biopsy of 36 patients with various skin lesions; eight benign cases and 28 malignant cases. The sample of patients was collected from the Pathology Laboratory in Rizgary Teaching Hospital in Erbil, Kurdistan region, Iraq from December 2011 to December 2012. The age of the patients ranged from 34 to 80 years. The p53 protein over expression was investigated by immunohistochemical staining. Sample sections were stained and scored.
Results: Nineteen out of 28 (76.8%) skin cancer showed over expression of p53 gene compared with benign skin lesion and there was a statistically significant difference. There was statistical significant difference in relation to the age group of patients with various skin cancers which was higher in patient above 40 years.
Conclusion: Increased expression of p53 a nuclear protein can be detected in human skin cancer compared with benign skin lesion and it may play an important role in pathogenesis of many types of skin cancers.
1. Chan J KC. P53 expression. Rosai and Ackerman's Surgical Pathology. 10th Edition. New York, SA: Mosby Elsever; 2011. PP 58.
2. Purdie CA, Grady J, Piris J, Wylie AH, Biral. P53 expression in colorectal cancer. AJP 1991; 138 (4):22-7.
3. Ghaderi R, Haghighi F. Immunohistochemistry assessment of p53 protein in basal cell carcinoma. Iran J Allergy Asthma Immunol 2005; 4(4):167-71.
4. Kricker A, Armstrong B K, English DR, Heenan PJ. Pigmentary and cutaneous risk factors for nonmelanocytic skin cancer a case control study. Int J Cancer 1991; 48(5):650-62.
5. Marisa RN, Christopher PC. In Mills SE, Carter D, Greenson JK, Reuter VE and stoler MH, Editors. Sternberg. Non melanocytic cutaneous tumor. Diagnostic Surgical Pathology. 5th Edition. Baltimore USA: Lippinvott Williams and Wilkins; 2010. PP46-60.
6. Dinehart SM, Nelson-Adesokan P, Cockerell C, Russell S, Brown R. Metastatic cutaneous squamous cell carcinoma derived from actinic keratosis. Cancer 1997; 79(38):920-3.
7. Johnson TM, Rowe DE, Nelson BR, Swanson NA. Squamous cell carcinoma of the skin (excluding lip and oral mucosa).Journal American Acad Dermatol 1992; 26(5):467-84.
8. Agar NS, Halliday GM, Bametson RS .The basal layer in human squamous tumors harbors more UVA than UVB fingerprint mutations: A role for UVA in human skin carcinogenesis. Proc Natl Acad Sci USA 2004; 101(16):4954-9.
9. Shea CR, McNutt NS, Volkenandt M, Lugo J, Prioleau PG, Albino AP. Overexpression of p53 protein in basal cell carcinomas of human skin. Am J Pathol 1992; 141(1):25-9.
10. SoiniY, Kamel D,Pääkkö PLethtoV-P,Oikarinen A, VähäkangasK. Aberrant accumulation of p53 associates with Ki67 and mitotic count in benign skin lesions. British J Dermatol 1994; 131(4): 514-20.
11. Brown DC, Gatter KC. Ki67 protein: The immaculate deception? Histopathol 2002; 40(1): 2-11.
12. Shimuzu T, Oga A, Murakami T, Muto M. Overexpression of p53 protein associated with proliferative activity and histological degree of malignancy in solar keratosis. Dermatol 1999; 28(6):113-8.
13. Hermeking H, Eick D. Mediation of c-Myc-induced apoptosis by p53. Science 1994; (26)5:2091-3.
14. Shimuitzu T, Muto M, Murakami T, Furumoto H, Mogami S, Asagami C. Over expression of p53 protein associated with proliterative activity as evaluated by Ki-67 immunostaining in well-differentiated squamous cell carcinoma of the skin. Dermatol 1997; 195(3):224-7.
15. Ringer DP, Schniper LE. Principles of cancer biology. Gene mutation that can lead to cancer. In: Lenhard RE, Osteen RT, Gansler T. Clinical Oncology. Atlanta, GA: American Cancer Society; 2001: 25– National Cancer Institute. Understanding Gene Testing. Accessed at http://www.cancer.gov/cancertopics/understandingcancer/genetesting on 12/13/2011.
16. Sidransky D, Hollstein M. Clinical implications of the p53 Gene. Annu Rev Med 1996; 47(3): 285-301.
17. Whiteman DC, Parsons PG, Green AC. p53 expression and risk factors for cutanous melanoma: A case control-study. Int J Cancer 1998; 77(6):843-8.
18. Jonason AS1, Kunala S, Price GJ, Restifo RJ, Spinelli HM, Persing JA, et al. Frequent clones of p53-mutated keratinocytes in normal human skin. Proc Natl Acad Sci USA 1996; 93(24):14025-9.
19. Batinac PT, Zamolo G, Jonjic N, Gruber F, Petroveckj M. P53 protein expression and cell proliferation in non neoplastic and neoplastic proliferative skin diseases. Tumori 2004; 90(6):120-7.
Background and objective: A thin central corneal thickness has been reported to be a risk factor for developing primary open-angle glaucoma. This has led to a hypothesis that thinning of the cornea may be an indication of generalized weakness of the ocular integument. This study was conducted to explore the relationship between central corneal thickness and axial length in a sample of Erbil population.
Methods: This is an observational cross sectional prospective study that was conducted from October 2012 to March 2013 and included 260 eyes of 130 patients. The mean age (± SD) was 37.8 ± 17.7 years for males and 35.4 ± 15.5 years for females. Axial length was measured with A-scan ultrasound biometry and central corneal thickness with ultrasonic Pachymeter.
Results: The mean central corneal thickness (± SD) was 542.8 ± 36 µm in male eyes and 530.1 ± 32.5 µm in female eyes. The mean axial length (± SD) was 23.38 ± 1.1 mm in male eyes, 23.15 ± 1.2 mm in female eyes. Central corneal thickness was not correlated with axial length (Pearson correlation coefficient r = 0.037, P = 0.558).
Conclusion: Central corneal thickness and axial length of the eye are two independent measurements. Thin corneas are not related to longer eye.
1. Shah S, Chatterjee A, Mathai M, Kelly SP, Kwartz J, Henson D, et al. Relationship between corneal thickness and measured intraocular pressure in a general ophthalmology clinic. Ophthalmology 1999; 106(11)2154-60.
2. Doughty MJ, Zaman ML. Human corneal thickness and its impact on intraocular pressure measures: a review and meta-analysis approach. Surv Ophthalmol 2000; 44(5)367-408.
3. Eysteinsson T, Jonasson F, Sasaki H, Arnarsson A, Sverrisson T, Sasaki K, et al. Central corneal thickness, radius of the corneal curvature and intraocular pressure in normal subjects using non-contact techniques: Reykjavik eye study. Acta Ophthalmol Scand 2002;80(1)11-15.
4. Millodot BH, Dictionary of Optometry and Visual Science, 7th edition. 2009; Butterworth-Heinemann.
5. Gregory L. Skuta, Louis B. Cantor, Jayne S. Weiss, Basic and Clinical Science Course. Clinical optics Section 3. San Francisco, USA: American Academy of Ophthalmology; 2010. 10-50.
6. Feltgen N, Leifert D, Funk J. Correlation between central corneal thickness, Applanation tonometry and direct intracameral intraocular pressure readings. Br J Ophthalmol 2001; 85:85-7.
7. Ehlers N, Bramsen T, Sperling S. Applanation tonometry and central corneal thickness. Acta Ophthalmol (Copenh) 1975; 53:34-43.
8. Louisa W, Beth E, Lan E, Murdoch. Central corneal thickness: will one measurement suffice? Ophthalmology 2005; 112:225-8.
9. Sora H, Stanley A, Mei Ying-Lai, Rohit V, Los Angeles Latino Eye Study Group. Central corneal thickness in Latinos. IVOS 2003; 44:1508-12.
10. Whitacre MM, Stein RA, Hassanein K. The effect of corneal thickness on Applanation tonometry. Am J Ophthalmol 1993; 115:592-6.
11. Orssengo GJ, Pye DA. Determination of the true intraocular pressure and modulus of elasticity of the human cornea in vivo. Bull Math Biol 1999; 61,551-72.
12. Mazhar UL, Aziz UR, Munawar A, Umar F, Nasir B, Ashraf D, et al. Central corneal thickness and Intraocular pressure in selected Pakistani Population. Pak J Ophthalmol 2010; 26:79-82.
13. Argus WA. Ocular hypertension and central corneal thickness. Ophthalmology 1995; 102: 1810-2.
14. Copt RP, Thomas R, Mermoud A. Corneal thickness in ocular hypertension, primary open-angle glaucoma, and normal tension glaucoma. Arch Ophthalmol 1999; 117:14-16.
15. Brandt JD, Beiser JA, Kass MA, Gordon MO, the Ocular Hypertension Treatment Study (OHTS) group. Central corneal thickness in the ocular hypertension treatment study (OHTS). Ophthalmology 2001; 108:1779-88.
16. Herndon LW, Choudhri SA, Cox T, Damji KF, MB Sheilds, RR Allingham. Central corneal thickness in normal, glaucomatous, and ocular hypertensive eyes. Arch Ophthalmol 1997; 115:1137-41
17. Kanski JJ. Clinical Ophthalmology. 5th edition. Edinburgh: Elsevier Science; 2003. 100-196.
18. Gupta JM, Deepak DS. Glaucoma diagnosis and management; risk factors 2005; 5-6
19. Gordon MO, Beiser JA, Brandt JD, Heuer DK, Higginbotham EJ, Johnson CA, et al. The ocular hypertension treatment study; baseline factors that predict the onset of primary open angle glaucoma. Arch ophthalmol 2002; 120(6);829-30.
20. Medeiros FA, Samples PA, Zangwill LM, Bowd C, Aihara M, Weinrob RN. Corneal thickness as a risk factor for visual field loss in patient with preperimetric glaucomatous optic neuropathy. Am J Ophthalmol 2003; 136(5):805-13.
21. Quigly HA, Habman RM, Addicks EM, Massof RW, Green RW. Morphologic changes in the lamina cribrosa correlated with the neural loss in open angle glaucoma. Am J Ophthalmol 1983; 95:673-91.
22. Brown KE, Gongdon NG. Corneal structure and biomechanics: impact on the diagnosis and management of glaucoma. Curr Opin Ophthalmol 2006; 17:338-43.
23. Shimmyo M, Orloff PN. Corneal thickness and axial length. Am J Ophthalmol 2005; 139:553-4.
24. Siu A, Herse PR. The effect of age on human corneal thickness: statistical implications of power analysis. Acta Ophthalmol Scand 1993; 71:51-6.
25. Foster PJ, Baasanhu J, Alsbirk PH, Munkhbayar D, Uranchimeg D, Johnson GJ. Central corneal thickness and intraocular pressure in a Mongolian population. Ophthalmology 1998; 15:969-73.
26. La Rosa FA, Gross RL, Orengo-Nania S. Central corneal thickness of Caucasians and African Americans in glaucomatous and nonglaucomatous populations. Arch Ophthalmol 2001; 119:123-7.
27. Alsbirk, PH. Corneal Thickness. I. Age variation, sex difference and oculometric correlations. Acta Ophthalmol Scand 1978; 56:95-104.
28. Dougthy MJ, Zaman ML. Human corneal thickness and its impact on intraocular pressure measures: a review and meta-analysis approach. Surv Ophthalmol 2000; 44,367-408.
29. Nemesure B, Barbados Eye Study Group. Corneal thickness and intraocular pressure in the Barbados eye studies. Arch Ophthalmol 2003; 121(2):240-4.
30. Wong AC, Wong CC, Yuen NS, Hui SP. Correlational study of central corneal thickness measurements on Hong Kong Chinese using optical coherence tomography, Orbscan and ultrasound pachymetry. Eye 2002; 16:715-21.
31. Suzuki S, Suzuki Y, Iwase A, Araie M. Corneal thickness in an ophthalmologically normal Japanese population. Ophthalmology 2005; 112:1327-36.
32. Hansen FK. A clinical study of the normal human central corneal thickness. Acta Ophthalmol (Copenh) 1971; 49:82–89.
33. Price FW Jr. Central corneal pachymetry in patients undergoing laser in situ keratomileusis. Ophthalmology 1999; 106:2216-20.
34. Xie R, Zhou XT, Lu F, chen M, Xue A, Chen S. Correlation between myopia and major biometric parameters of the eye: A retrospective clinical study. Optom Vis Sci 2009; 86(5):E503-8.
Background and objective: Malt beverage without alcohol (Barbican) is an energy beverage which is regularly consumed by Muslim countries and substantial quantities are exported to the Gulf States and Middle East countries. Barbican is used widely by people whom alcohol is forbidden either on medical grounds or on religious aspects. The aim of this study was to assess the effect of short-term drinking of Barbican on urinary excretion of calcium and uric acid in normal young males in Erbil city.
Methods: Thirty healthy male volunteer subjects of 21-23 years age consumed 330 ml of Barbican® beverage per day for two successive days after cross design. The urinary calcium and urinary uric acid were evaluated before and after consumption.
Results: There was no statistically significant increase in urinary uric acid before and after consumption of Barbican beverage (P = 0.071). Urinary calcium significantly decreased after consumption of Barbican drink (P = 0.037).
Conclusion: Although many extrinsic and intrinsic factors influence formation of kidney stones and bone resorption, this study suggests that drinking of Barbican beverage may be helpful to prevent bone resorption and also to reduce risk of stone formation.
1. EL-Naggar AY, Arida H, Montasser M, Hassan R. Measures affecting alcohol in malt beverages according to Islamic religion. J Am Sci 2012; 8(10):455-60.
2. Safreit D. Written communication from Brain Shrager, Midwest Research Institute, Cary, NC, to Dallas Safreit, U.S. Environmental Protection Agency, Research Triangle Park, NC; 1994.
3. Nutt D, King LA, Saulsbury W, Blakemore C. Development of a rational scale to assess the harm of drugs of potential misuse. The Lancet 2007; 369(9566):1047-53.
4. Meyer, Jerold S, Quenzer LF. Psychopharmacology: Drugs, the Brain, and Behavior. Sunderland, Massachusetts: Sinauer Associates, Inc; 2005; P. 228.
5. Oscar-Berman M, Marinkovic K. Alcoholism and the brain: an overview. Alcohol Res Health 2003; 27(2):125-33.
6. Klatsky AL, Friedman GD. Alcohol and longevity. Am J of Public Health 1995; 58(1):16-8.
7. Penniston KL, Nakada SY. Diet and alternative therapies in the management of stone disease. Urol Clin N Am 2013; 40:31-46.
8. Shimizu T, Kitada H, Umeyama M, Hori H, Takasaki N. Noval evaluation of nephrolithiasis as a complication of gout: A cross-sectional study using helical computerized tomography. J Urology 2013; 189:1747-52.
9. Copelovitch L. Urolithiasis in children. Pediatr Clin N Am 2012; 59:881-96.
10. Frassetto L, Kohlstadt I. Treatment and prevention of kidney stones: An update. Am Fam Physician 2011; 84(11):1234-42.
11. Tiwari R, Campfield T, Wittcopp C, Braden G, Visintainer P, Reiter EO, et al. Metabolic Syndrome in Obese Adolescents is Associated with Risk for Nephrolithiasis. J Pediatr 2012; 160:615-20.
12. Sweeney DD, Tomazewski JJ, Ricchiuti DP, Averch TD. Effect of carbohydrate-electrolyte sports beverages on urinary stone risk factors. J Urology 2009; 182:992-7.
13. Meschi T, Nouvenne A, Borghi L. Lifestyle recommendations to reduce the risk of kidney stones. Urol Clin N Am 2011; 38(3):313-20.
14. Bagga HS, Chi T, Miller J, Stoller ML. New insights into the pathogenesis of renal calculi. Urol Clin N Am 2013; 40:1-12.
15. Eisner BH, Goldfarb DS, Pareek G. Pharmacologic treatment of kidney stone disease. Urol Clin N Am 2013; 40:21-30.
16. He J, Reilly M, Yang W, Chen j, Go AS, Lash JP, et al. Risk factors for coronary artery calcium among patients with chronic kidney disease (from the chronic renal insufficiency cohort study). Am J Cardiol 2012; 110:1735-41.
17. Barger-Lux MJ, Heaney RP. Caffeine and the calcium economy revisited. Osteoporosis Int 1995; 5:97-102.
18. Ross AC, Taylor CL, Yaktine AL, Del HB Vitamin D and Calcium: updated dietary reference intakes. Available at (http://www.hc-sc.gc.ca/fn-an/nutrition/vitamin/vita-d-eng.php) in 25 June 2014.
19. Goldfarb DS, Arowojolu O. Metabolic Evaluation of First-time and Recurrent Stone Formers. Urol Clin N Am 2013; 40:13-20.
20. Tietz NW. Text book of clinical chemistry. 3rd Ed. USA: WB Saunders; 1999.
21. Moorehead WR, Briggs HG. Clinical chemistry. USA: WB Saunders; 1974.
22. Fossati P, Prencipe L, Berti G. Use of 3, 5-dichloro-2-hydroxybenzene sulfonic acid/ 4 amino phenazone chromogenic system in direct enzymatic assays of uric acid in serum and urine. Clin Chem 1980; 26:227-31.
23. Daniel WW. Biostatistics: A foundation for analysis in the health science. 3rd Edition. USA: John Wiley and Sons; 1983.
24. Taylor EN, Curhan GC. Fructose consumption and the risk of kidney stones. Kidney Int 2008; 73:207-12.
25. Kok DJ, Papapoulos SE, Bijvoet OL. Excessive crystal agglomeration with low citrate excretion in recurrent stone-formers. Lancet 1986; 1:1056-8.
26. Seltzer MA, Low RK, McDonald M, Shami GS, Stoller ML. Dietary manipulation with lemonade to treat hypocitraturic calcium nephrolithiasis. J Urol 1996; 156:907-9.
27. Kang DE, Sur RL, Haleblian GE, Fitzsimons NJ, Borawski KM, Preminger GM. Long-term lemonade based dietary manipulation in patients with hypocitraturic nephrolithiasis. J Urol 2007; 177:1358-62.
28. Heaney RP, Rafferty K. Carbonated beverages and urinary calcium excretion. Am J Clin Nutr 2001; 74(3):343-7.
29. Bhowmik D, Kumar S, Paswan S, Sirvastava S. Tomato - A natural medicine and its health benefits. Phyto J 2012: 1(1):33-43.
30. Knight J, Assimos DG, Easter L, Holms RP. Metabolism of fructose to oxalate and glycolate. Horm Metab Res 2010; 42(12):868-73.
31. Eisner BH, Asplin JR, Goldfarb DS, Ahmad A, Stoller ML. Citrate, malate and alkali content in commonly consumed diet sodas: Implications for Nephroliathiasis Treatment. J Urology 2010; 183:2419-23.
32. Kovacevic L, Christensen CW, Edwards L, Sadaps M, Lakshmanan Y. From hypercalciuria to hypocitraturia- A shifting trend in pediatric urolithiasis? J Urology 2012; 188:1623-7.
33. Zuckerman JM, Assimos DG. Hypocitraturia: pathophysiology and medical management. Rev Urol 2009; 11:134-44.
34. Baraf HM, Adamson HS, Basile TC, Cole L, Doghramaji B, Guadagnoli PP, et al. Recommendations for the diagnosis and management of gout and hyperurecemia. The physician and Sports Medicine 2011; 39(4): 98-123.
Background and objective: Evidence-based medicine, by guiding medical care towards meaningful outcomes to patients, has a significant worldwide impact on medical care and education. It is important that medical students, whom are the future physicians, keep themselves updated with recent advancement in medical knowledge and health care. The aim of this cross-sectional study was to determine the attitude, knowledge and barriers among students towards evidence-based medicine and making them familiar with the concept and advantage of evidence based medicine.
Methods: A cross-sectional study was conducted on 163 sixth year students of the College of Medicine at Hawler Medical University during the period from October 2012 to May 2013. The response rate was 86.5%. Knowledge towards evidence-based medicine, accessing and interpreting evidence and perceived barriers to practice evidence-based medicine among participants were the main outcome measures.
Results: Of 141 of participants that filled the questionnaire, only 69.5% had heard about evidence-based medicine. Around 82% stated that they had known evidence-based medicine and only 23.5% had known steps of evidence-based medicine. Around 65% of respondents welcomed the promotion of evidence-based medicine and 74.4% agreed with that finding from the current study in which it would be helpful in daily management of patients. Furthermore, 31.6% of students reported that standard textbook as a frequent source used for medical knowledge. Around 91% of students did not know the strongest evidence in the hierarchy of evidence and only small proportion of students reported that they understand the common epidemiological concepts that are used in evidence-based medicine.
Conclusion: Evidence-based medicine is relatively a new concept among students at the College of Medicine in Erbil. Although the students appeared interested in learning and implementing evidence-based medicine in clinical practice, they need more guidance and training to ensure the correct use of evidence-based medicine ideals.
1. Glasziou P, Del Mar C, Salisbury J. Evidence based medicine workbook. Finding and applying the best research evidence to improve patient care. 2nd ed. London: BMJ books; 2007.
2. Irshad A, Ramzan M, Iqbal M. Assessment of knowledge about evidence based medicine in medical students and doctors in a Pakistani health care setting. Pakistan J Ayub Med Coll Abbottabad 2010; 22(2):126-9.
3. Straus SE, Richardson WS, Glasziou P, Haynes RB. Evidence-based medicine how to practice and teach EBM. 3rded. London: Elsevier Churchill Livingstone; 2005.
4. Risahmawati, Emura S, Nishi T, Widodo DW, Ismail I, Sugioka T, Koizumi S. A comparative assessment of attitudes, knowledge and self-perceived barrier to the practice of evidence based medicine in Japan and Indonesia. J Med Med Sci 2012; 3(1):16-29.
5. McColl A, Smith H, White P, Field J. General partitions of the route to evidence based medicine: questionnaire survey. BMJ 1998; 316:361-5.
6. Khader YS, Batayha W, Al-Omari M. The effect of evidence-based medicine (EBM) training seminars on the knowledge and attitudes of medical students towards EBM. J Eval Clin Pract 2011; 17(4):640-3.
7. Hassanien MA. Introduction to Evidence-Based Medicine: a student-selected component at the Faculty of Medicine, King Abdulaziz University. J Adv Med Educ Pract 2011; 2:215-9.
8. Dawes MG. On the need for evidence-based general and family practice. EBM 1996; 1:68-9.
9. Al-Omari FK, Al-Asmary SM. Attitude, awareness and practice of evidence based medicine among consultant physicians in Western region of Saudi Arabia. Saudi Med J 2006; 27:1887-93.
10. Iqbal M, Zaidi Z. The ‘ripple effect’ of introducing Evidence based medicine into a curriculum. Med Educ J 2009; 43:475.
11. Evidence-based medicine working group. Evidence-based medicine. A new approach to teaching the practice of medicine. JAMA 1992; 268 (17):2420-5.
12. Aslam F, Qayyum MA, Mahmud H, Qasim R, Haque IU. Attitudes and practices of post graduate medical trainees towards research –a snapshot from Faisalabad. J Pak Med Assoc 2004; 54: 534-6.
13. Al-Ansary LA, Khoja TA. The place of evidence-based medicine among primary health care physicians in Riyadh region, Saudi Arabia. J Fam Pract 2002; 19(5):537-42.
14. Amin FA, Fedorowicz Z, Montgomery AJ. A study of knowledge and attitudes toward the use of evidence-based medicine among primary health care physicians in Bahrain. Saudi Med J 2006; 27(9):1394-6.
15. Al-Almaie SM, AL-Baghli N. Barriers facing physicians practicing evidence based medicine in Saudi Arabia. J Contin Educ Health Prof 2004; 24(3):163-70.
16. Scott I, Heyworth R, Fairweather P. The use of evidence-based medicine in the practice of consultant physicians. Results of a questionnaire survey. Aust NZ J 2000; 30(3):319-26.
17. Reilly B, Lemon M. Evidence-based morning report: a popular new format in a large teaching hospital. Am J Med 1997; 103:419-26.
18. Bazarian JJ, Davis CO, Spillane LL, Blumstein H, Schneider SM. Teaching emergency medicine residents evidence-based critical appraisal skills: a controlled trial. Ann Emerg Med 1999; 34:148-54.
19. Green ML, Ellis PJ. Impact of an evidence-based medicine curriculum based on adult learning theory. J Gen Intern Med 1997; 12:742-750.
Background and objective: Maternal deaths are still leading problems in many developing countries, including Iraq. Iraq is, in fact, far away to reach the Millennium Development Goal declared to reduce the maternal mortality ratio by three quarters between 1990 and 2015. The aim of this study was to highlight the main causes of avoidable deaths that lead to maternal mortality among those admitted to Maternity Teaching Hospital in Erbil.
Methods: This survey was carried out in the Maternity Teaching Hospital in Erbil city, Kurdistan region, Iraq. Variables included in this study were those related to patient’s age, number of parity and mode of delivery of the last baby. Data were collected from patient’s records. In addition, some clinical data were included related to causes leading to death and underlying condition of death.
Results: Of the total 75000 live birth recorded in the hospital during the study period (2011-2013), 33 maternal deaths were recorded which gives an overall maternal mortality ratio of 44 per 100,000 live births. Pre-eclampsia and eclampsia were among the top causes of maternal deaths in this study (42.4%) followed by obstetrical bleeding and rapture uterus (30.3%).
Conclusion: Maternal mortality rate in Maternity Teaching Hospital was 44/100,000 total live births. The main cause of the maternal deaths was pre-eclampsia and its complications. Most of those died were residents of rural areas and were illiterate women.
1. World Health Organization, UNICEF, UNFPA and The World Bank. Trends in maternal mortality: 1990 to 2010 WHO, UNICEF, UNFPA and The World Bank estimates, 2012.
2. Fikree FF, Gray RH, Berendes HW, Karim MS. A community-based nested case-control study of maternal Mortality. Int J Gynaecol Obstet 1994; 47:247-55.
3. World Health Organization. New estimates of Maternal Mortality. Wkly Epidemiol Rec 1996; 97-110.
4. Court C. WHO claims maternal mortality has been underestimated. BMJ 1996; 312:398-9.
5. Salanave B, Bouvier-Colle MH, Varnoux N. Classification differences and maternal mortality: European study. MOMS group. Mothers’ Severe morbidity. Int J Epidemiol 1999; 64-9.
6. Requejo JH, Merialdi M, Bustreo F .Improving global maternal health:progress, challenges, and promise. Curr Opin Obstet Gynecol 2011; 465-70.
7. Bueno de Mesquita J, Kismodi E .Maternal mortality and human rights: landmark decision by United Nations human rights body. Bull World Health Organ 2012; 90: 7.
8. Campbell OM, Graham WJ, Lancet Maternal Survival Series steering group .Strategies for reducing maternal mortality: getting on with what works. Lancet 2006; 1284-99.
9. WHO. Trends in Maternal Mortality: 1990 to 2008 Estimates developed by WHO, UNICEF, UNFPA and The World Bank. WHO Library Cataloguing-in- Publication Data. 2010.
10. UNHRC .The Millennium Development Goals report. New York: UN Human Rights Council; 2011.
11. WHO . World Health Statistics 2012. Geneva, Switzerland: World Health Organization.
12. Nawzad T. Draft of Regional Development Strategy- Kurdistan region 2013-2017. Ministry of Planning 2012;139-41.
13. Zahr CA, Wardlaw TM, Hill K, Choi Y. Maternal mortality in 2000: Estimates developed by WHO, UNICEF and UNFPA. Geneva: WHO; 2004.
14. Kilpatrick SJ, Prentice P, Jones RL, Geller S State Maternal Mortality Review: Process and Impact. J Womens Health (Larchmt). JCommunity Med Health Educ. 2012;
15. WHO, UNICEF, UNFPA ,The World Bank and United Nations population Division. Maternal mortality in Iraq 1990-2013. 2014.
16. Ahlam Saleh Bin-Berik1 and Amen Ahmed Bawazir. Trends in Maternal Mortality at the Mukalla City, Yemen, 2000–2010,
17. Al-Sumadi MD, Rami SM. Maternal mortality ratio at the Royal Medical services Hospitals: Hospital-based data. JRMS April 2009;16(1):26-9.
18. Al-Meshari A, Chattopadhyay SK, Younes B, Hassonah M. Trends in maternal mortality in Saudi Arabia. Int J Gynaecol Obstet 1996; 52(1):25-32.
19. Etard JF, Kodio B, Traore S. Assessment of maternal mortality and late maternal mortality among a cohort of pregnant women in Bamako, Mali. Br J Obstet Gynaecol 1999;106:60-5.
20. Ounsa MAAE, Mohamed EY .Maternal Mortality in Ribat University Hospital, Khartoum, Sudan: Seven years of experience. Sudan Med J.2011; 6.
21. Ikeako LC, Onah HE, Iloabachie GC. Influence of formal maternal education on the use of maternity services in Enugu, Nigeria. J Obstet Gynaecol. 2006; 26(1):30-4.
22. Chibber R1, Al-Hijji J, Al-Adwani AR, Rammah A, Fouda M, Al-Saleh E, Tasneem MA.Trends in maternal mortality over 29 years in a Kuwait Tertiary Teaching Hospital: signs of progress? Eur J Contracept Reprod Health Care. 2009;14(1):75-82.
23. François J , Kodio B , Traoré S. Assessment of maternal mortality and late maternal mortality among a cohort of pregnant women in Bamako, Mali. BJOG 1999 ; 106 (1):60-5.
24. WHO Reproductive Health Library, No. 2. Geneva, World Health Organization, 1999.
25. Report of Arab Conference on Safe Motherhood, Amman, Jordan, 1988; 1-34.
Background and objective: Estimation of C-reactive protein is a simple method and could be helpful in detecting cases at risk for pre-term delivery. In this study we examined the association of maternal C-reactive protein in second trimester with risk of occurrence of preterm delivery later on.
Methods: A prospective case-cohort study was conducted between June 2011 and July 2012 at Maternity Teaching Hospital Iraq- Erbil. The sample size was 205 women at gestational age of 20+0 weeks to 26+6 weeks and after exclusion of all risk factors for preterm delivery. High-sensitivity C-reactive protein assays were performed on serum samples.
Results: Median concentration of C-reactive protein was 4.7 mg/liter. No significant association was found between high level of C-reactive protein and occurrence of preterm delivery (P = 0.78).
Conclusion: Measurement of C-reactive protein in second trimester cannot be used as an indicator for pre-term delivery.
1. American College of Obstetricians and Gynecologist. ACOG Practice Bulletin. Assessment of risk factors for preterm birth. Clinical management guidelines for obstetrician-gynecologists. Number 31, October 2001.
2. ACOG practice bulletin. Management of preterm labor.Number 43, May2003. Int J Gynaecol Obstet 2003; 82(1):127-35.
3. Tucker J, McGuire W. Epidemiology of preterm birth. BMJ 2004 ; 329(7467):675-78.
4. Murphy DJ. Epidemiology and environmental factors in preterm labor. Best Pract Res Clin Obstet Gynaecol 2007; 21(5):773-89.
5. Eden RD, Penka A, Britt DW, Landsberger EJ, Evans MI. Re-evaluating the role of the MFM specialist: lead, follow, or get out of the way. J Matern Fetal Neonatal Med 2005; 18(4):253-58.
6. Bennet P. Pretermlabor, Chapter 28, part 6, in Keith Edmond (editor) Dewhurst's textbook of Obs & Gyn., 8th edition 2012; p338-43
7.Vrachnis N, Vitoratos N, Iliodromiti Z, Sifa K, Deligeoroglou E, Creatsas G. Intrauterine inflammation and preterm delivery. Ann NY Acad Sci 2010;1205:118-22.
8. Romero R, Mazor M. Infection and preterm labor. ClinObstetGynecol1988; 31: 553-84.
9. Luesly DM, Baker PN, Talor M. Late pregnancy/ intrapartum events. Preterm labor, Obstetrics and Gynecology, An evidence-based text for MRCOG second edition 2010;21:299-301.
10. McDonald HM, O′Loughlin JA, Jolley P, Vigneswaran R, McDonald PJ. Vaginal infection and preterm labor. Br J Obstet Gynecol 1991; 98(5):427-35.
11. Romero R., Mazor M., Wu YK, Infection in the pathogenesis of preterm labor. Semin Perinatol 1988;12(4):262-79.
12. Dortbudak O, Eberhardt R, Ulm M, Persson GR. Periodontitis, a marker of risk in pregnancy for preterm birth. J Clin Periodontol 2005; 32(1): 45-52.
13. Offenbacher S., Lieff S., Boggess KA. Maternal periodontitis and prematurity. Part I: Obstetric outcome of prematurity and growth restriction. Ann Periodontol 2001; 6(1):164-74.
14. Thompson D., Pepys MB., Wood, SP. The physiological structure of human C-reactive protein and its complex with phosphocholine. Structure1999; 7(2): 169–77.
15. Castell JV.,Gomez-Lechon MJ., David M., Fabra R., Trullenque R., Heinrich PC. Acute-phase response of human hepatocytes: regulation of acute-phase protein synthesis by interleukin-6. Hepatology1990; 12(5):1179–86.
16. Yap SH., Moshage HJ., Hazenberg BP. Tumor necrosis factor (TNF) inhibits interleukin (IL)-1 and/or IL-6 stimulated synthesis of C-reactive protein (CRP) and serum amyloid A (SAA) in primary cultures of human hepatocytes. Biochim Biophys Acta 1991; 1091(3):405–8.
17. Ford ES. Body mass index, diabetes, and C-reactive protein among U.S. adults. Diabetes Care,1999; 22(12):1971–7.
18. Pannacciulli N, Cantatore FP., Minenna A., Bellacicco M., Giorgino R., De Pergola G. C-reactive protein is independently associated with total body fat, central fat, and insulin resistance in adult women. Int J Obes Relat Metab Disord 2001; 25(10):1416-20.
19. Mazor M, Kassis A., Horowitz S. Relationship between C-reactive protein levels and intraamniotic infection in women with preterm labor. J Reprod Med 1993; 38(10):799-803.
20. Potkul RK, Moawad AH., Ponto KL. The association of subclinical infection with preterm labor: the role of C-reactive protein. Am J Obstet Gynecol 1985; 153(6):642-5.
21. Redman CW, Sacks GP., Sargent IL.. Preeclampsia: an excessive maternal inflammatory response to pregnancy. Am J Obstet Gynecol 1999; 180(2 Pt 1):499-506.
22. 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(4):972–8.
23. Hvilsom GB., Thorsen P., Jeune B, Bakketeig LS.. C-reactive protein: a serological marker for preterm delivery? Acta Obstet Gynecol Scand2002; 81(5):424-9.
24. Pitiphat W, Gillman MW,Joshipura KJ, Williams PL, Douglass CW, Rich-Edwards JW. Plasma C-reactive protein in early pregnancy and preterm delivery. Am J Epidemiol 2005; 162(11):1108-13.
25. Vogel I, Grove J, Thorsen P., Moestrup SK., Uldbjerg N., Moller HJ. Preterm delivery predicted by soluble CD163 and CRP in women with symptoms of preterm delivery. B J Obstet Gynecol 2005; 112(6):737-42.
26. Romero R, Gomez R, Ghezzi F. A fetal systemic inflammatory response is followed by the spontaneous onset of preterm parturition. Am J Obstet Gynecol1998; 179:186-93
27. Ghezzi F., Franchi M., Raio L. Elevated amniotic fluid C-reactive protein at the time of genetic amniocentesis is a marker for preterm delivery. Am J Obstet Gynecol 2002; 186(2):268-73.
28. Borna S, Mirzaei F, Abdollahi A, Sarbiaei A.Predictive value of mid-trimester amniotic fluid high-sensitive C-reactive protein, ferritin, and lactate dehydrogenase for fetal growth restriction. I J Pathol 2009; (1):5-8.
29. Ozer KT, Kavak ZN, Gokaslan H, Elter K, Pekin T. Predictive power of maternal serum and amniotic fluid CRP and PAPP-A concentrations at the time of genetic amniocentesis for the preterm delivery 2005; 122(2):187-90.
30. Cark S., Belfort M., Dildy G., Herbst M., Meyers J., Hankins G. Maternal death in the 21st century: causes, prevention, and relationship to cesarean delivery. Am J Obstet Gyn 2008; 199(1): 36e1-36e5.
Background and objective: An expectation of beautiful smiles at the end of orthodontic treatment is a primary concern to each patient, but is also equally concerned with appearance while undergoing treatment. The development of appliances that combine both acceptable aesthetics for the patient and adequate technical performance for the clinician is the ultimate goal. The aim of this study was to compare three different aesthetic orthodontic techniques with different biomechanics in order to quantify the efficiency of these techniques in alignment of displaced upper right central incisor and investigating the effects of these variables on alignment considering its tipping and rotation.
Methods: The sample consisted of three groups with each group including 15 samples; (1) conventional buccal technique group, (2) lingual technique group and (3) Inman Aligner group, all on a typodont simulation system (dentsply). Preoperative and postoperative digital images were taken and analyzed using Autodesk AutoCAD software.
Results: The conventional buccal technique gave rise to the highest mean of tooth tipping and rotation followed by the lingual technique. The Inman Aligner produced the least level of tooth tipping and rotation.
Conclusion: The best method of alignment is the conventional buccal technique followed by the lingual technique. The least favourable one is the Inman Aligner.
1. Jena AK, Duggal R, Mehrotra AK. Physical properties and clinical characteristics of ceramic brackets: A comprehensive review. Trends Biomater Artif Organs 2007; 20(2):1.
2. Winchester L. Bond strengths of five different ceramic brackets: an in vitro study. Eur J Orthod 1991; 13:293-305.
3. Harris A, Joseph V, Rossouw P. Shear peel bond strengths of esthetic orthodontic brackets. Am J Orthod Dentofac Orthop 1992; 102:215-9.
4. Angolkar P, Kapila S, Duncanson JMG, Nanda R. Evaluation of friction between ceramic brackets and orthodontic wires of four alloys. Am J Orthod Dentofac Orthop 1990; 98:499-506.
5. Pratten D, Popli K, Gemmane N, Gunsolley J. Frictional resistance of ceramic and stainless steel orthodontic brackets. Am J Orthod Dentofac Orthop 1990; 98:398-403.
6. Nimitpornusko C, Viwattanatipa N. Introduction to lingual orthodontics. KDJ 2000; 3(2):2.
7. Profﬁt WR, Fields HW, Ackerman JL. Mechanical principles in orthodontic force control. In: Profﬁt WR (ed.). Contemporary orthodontics. 2000: 326 – 62.
8. Qureshi A. The Inman Aligner for Anterior Tooth Alignment. Dent Update 2008; 35:377-84.
9. Huffman DJ, Way DC. A clinical evaluation of tooth movement along arch wires of two different sizes. Am J Orthod Dentofacial Orthop 1983; 83(6):453-9.
10. Rhee JN, Chun YS and Row J. A comparison between friction and frictionless mechanics with a new typodont simulation system. Am J Orthod Dentofacial Orthop 2001; 119(3):293-9.
11. Alshahery WG. Upper canine retraction by sliding technique using stainless steel and nickel titanium coil spring. M.Sc. thesis, College of Dentistry, university of Mosul; 2010; Pp: 64, 66-71.
12. Kircelli ND. Incorporating the forsus fatigue resistant device with the Incognito appliance system. Orthotown 2013; 17(2):38-41.
13. Yamada K, Kuroda Sh, Deghuchi T, Yamamoto TT, Yashiro T. Distal movement of maxillary molars using miniscrew anchorage in the buccal interradicular region. The Angle Orthodontist 2009; 79(1):78-84.
14. Geron S, Romano R, Brosh T. Vertical forces in labial and lingual orthodontics applied on maxillary incisors. Angle Orthodontist 2004; 74 (2):6-8.
15. Alexander CM, Alexander RG, Gorman JC. Lingual orthodontics: a status report. Part 5. Lingual mechanotherapy. J Clin Orthod 1983; 17(2):99-115.
16. Smith JR, Gorman JC, Kurz C. Keys to success in lingual therapy. Part 1. J Clin Orthod 1986; 20:252-61.
17. Nanda R, Kuhlberg A. Principles of biomechanics. In: Nanda R, ed. Biomechanics in Clinical Orthodontics. Philadelphia, Penn: WB. 1997; 1–22.
18. Stamm T, Wiechmann D, Heinecken A, Ehmer U. Relation between second and third order problems in lingual orthodontic treatment. J Lingual Orthod 2000;1:5–11.
19. Diamond M. Critical aspects of lingual bracket placement. J Clin Orthod 1983;17:688-91.
20. Diamond M. Improved vision and isolation for direct lingual bonding of the upper arch. J Clin Orthod 1984; 18:814-5.
21. Scholz RP, Swartz ML. Lingual orthodontics: a status report. Part 3. Indirect bonding. J Clin Orthod 1982; 16:812-20.
22. Liaw YC, Su YY , Lai YL, Lee SY. Stiffness and frictional resistance of a superelastic nickel-titanium orthodontic wire with low-stress hysteresis. Am J Orthod and Dentofac Orthop 2007; 131:578.e12-578.e18
23. Rinchuse DJ, Rinchuse DJ, Kapur-Wadhwa R. Orthodontic appliance design. Am J Orthod Dentofacial Orthop 2007; 131:76-82.
24. Bednar JR, Gruendeman GW. The inﬂuence of bracket design on moment production during axial rotation. Am J Orthod Dentofacial Orthop 1998; 104:254-61.