Background and objectives: Echinococcus granulosus exists as a complex of different strains that differ in a wide variety of criteria that impact on the epidemiology, immunology, pathology and control of hydatid disease. This study was undertaken to investigate both humoral and cellular immune responses that are developed against hydatid cysts in Erbil.

Methods: Thirty patients (9 males and 21 female) with surgically confirmed cystic echinococcosis and 10 apparently healthy individuals were included in this study. IgG ELISA was performed to asses humoral immune responses. CD4/ CD8 ratio, eosinophil count and lymphocyte transformation response were done to asses the cellular immune responses. The level of IFN-γ and TNF-α was also assayed.

Results: The sensitivity of ELISA to detect anti-hydatid antibodies was shown to be 83.33%. CD4 / CD8 ratio was significantly (P< 0.001) decreased in patients with cystic echinococcosis as compared to normal control group, while eosinophil count (P< 0.001), lymphocyte transformation response (P< 0.001) and IFN-γ level (P< 0.01) were significantly increased. In contrast the level of TNFα was non- significantly changed in echinococcosis patients.

Conclusion: The current study showed that the local strain of Echinococcus granulosus induces both cellular and humoral immune responses, and the number of peripheral blood CD8 T cells was significantly increased in cystic echinococcosis patients. However, hyporesponsivness to hydatid specific antigens has not been induced.

Background and Objectives: Toxic injury occurs in the liver more often than other organ, this can be attributed to the fact that virtually all ingested substances that are absorbed are first presented to the liver & that the liver is responsible for the metabolism and elimination of many substances. Carbon tetrachloride (CCl4) is very well known to cause hepatotoxicity that may be associated with impaired calcium and trace element homeostasis. This study was designed to evaluate the protective effect of benfotiamine against CCl4-induced disturbances in calcium, iron, copper and zinc homeostasis in liver tissue of rats.

Methods: Liver tissue homogenate from normal controls, CCl4-treated and benfotiamine (70 mg/kg) pre-treated before induction of hepatic damage with CCl4 in rats were obtained, and processed for estimation of levels of free forms of calcium, iron, copper and zinc using atomic absorption spectrophotometry.

Results: Analysis of data revealed significant elevation in calcium, iron and copper levels in hepatic tissue due to exposure to CCl4 compared to controls, while zinc levels not significantly affected. Pretreatment with benfotiamine results in significant decrease in calcium, iron and copper levels compared to non-treated group, while zinc levels found to be significantly elevated.

Conclusions: Benfotiamine has a protective effect against CCl4-induced hepatic tissue damage which may be, in part, attributed to restoration of calcium and other trace elements homeostasis.

Key words: benfotiamine, CCl4, hepatotoxicity, calcium, trace elements.

1. Hartmut J. Toxic responses of the liver. In: Casarett and Doull's Toxicology: The basic science of poisons. 7^th edition, 2008:557-582.

2. Poli G, Parola M. Oxidative damage and fibrogenesis. Free Radic Biol Med 1997; 22:287-305.

3. John MC. Mechanistic Classification of Liver Injury. Toxicol Pathol 2005; 33:6-8.

4. Lemaster JJ. Mechanisms of hepatic toxicity. Necraptosis and the mitochondrial permeability transition: Shared pathways to necrosis and apoptosis. Am J Physiol 1999; 276: G1-G6.

5. Berridge MJ, Bootman MD, Lipp P. Calcium: A life and death signal. Nature 1998; 395:645-648.

6. Weber LW, Boll M, Stampfl A. Hepatotoxicity and mechanism of action of haloalkanes: Carbon tetrachloride as a toxicological model. Crit Rev Toxicol 2003; 33(2):105-136.

7. Johnston DE, Kroening C. Mechanism of early CCl₄-toxicity in cultured rat hepatocytes. Pharmacol Toxicol 1998; 39:231-239.

8. Dani C, Pasquali MA, Oliveira MR, Umezu FM, et al. Protective Effects of Purple Grape Juice on Carbon Tetrachloride-Induced Oxidative Stress in Brains of Adult Wistar Rats. J Med Food 2008; 11(1):55-61.

9. Halliwell B, Gutteridge JMC. Free Radicals in Biology and Medicine, 3^rd ed. Clarendon, Oxford, 1999.

10. Tapiaro H, Towensend DM, Tevv KD. Trace elements in human physiology and pathology. Biomed pharmacother 2003; 57(9):386-398.

11. Marchetti V, Menghini R, Rizza S, Vivanti A, et al. Benfotiamine counteracts glucose toxicity effects on endothelial progenitor cell differentiation via Akt/FoxO signaling. Diabetes, 2006; 55: 2231-2237.

12. Wu S, Ren J. Benfotiamine alleviates diabetes-induced cerebral oxidative damage independent of advanced glycation end-product, tissue factor and TNF-alpha. Neurosci Lett 2006; 394: 158-162.

13. Gadau S, Emanueli C, Van Linthout S, Graiani G, et al.. Benfotiamine accelerates the healing of ischaemic diabetic limbs in mice through protein kinase B/Akt-mediated potentiation of angiogenesis and inhibition of apoptosis. Diabetologia 2006; 49: 405-420.

14. Ceylan-Isik AF, Wu S, Li Q, Li SY, Ren J. High-dose benfotiamine rescues cardiomyocyte contractile dysfunction in streptozotocin-induced diabetes mellitus. J Appl Physiol 2006; 100: 150-156.                                                                                      

15. Bruce AM, Milnen A, Peter JW. Introduction to atomic spectrophotometry. Clinical Lab Methods. The C.V. Mosby Company, Saint Louis. 1984, 78-80.

16. Abdollahi M, Ranjbar A, Shadnia S, Nikfar S, Rezaie A. Pesticides and oxidative stress. Med Sci Monit 2004; 10:141–147.

17. Brette F, Leroy J, Le Guennec JY, Salle L. Ca²⁺ currents in cardiac myocytes: old story, new insights. Prog Biophys Mol Biol 2006; 91:1-82.

18. Xiao YH, Liu DW, Li Q. Effects of drug serum of anti-fibrosis I herbal compound on calcium in hepatic stellate cell and its molecular mechanism. J Gastroenterol 2005; 11:1515-20.

19. Nakamura T, Arii S, Monden K, Furutani M, Takeda Y, Imamura M, et al. Expression of the Na⁺/Ca²⁺ exchanger emerges in hepatic stellate cells after activation in association with liver fibrosis. Proc Natl Acad Sci USA 1998; 95:5389-94.

20. Gressner AM, Weiskirchen R, Breitkopf K, Dooley S. Roles of TGF-beta in liver fibrosis. Front Biosci 2002; 7:793-807.

21. Elisabetta M, Gioacchino S. Copper-induced changes of non-protein thiols and antioxidant enzymes in the marine microalga Phaeodactylum tricornutum. Plant Sci 2004; 167: 289-296.

22. Liu J, Goyer RA, Waalker MP. Toxic Effect of Metals. In Casarett and Doull's toxicology: The basic science of poisons. 7^th edition, 2008, 931-979.

23. Knauer K, Behra R, Sigg L. Effects of free Cu²⁺ and Zn²⁺ ions on growth and metal accumulation in fresh-water algae. Environ Toxicol Chem 1997; 16(2):220-229.

24. Deitmer JW, Ivens I, Pernberg J. Changes in voltage-dependent calcium currents during the cell cycle of the ciliate Stylonychia. Exp Cell Res 1986; 162:549-54.

25. Gutteridge JM, Halliwell B. Free radicals and antioxidants in the year 2000: a historical look to the future. Ann N Y Acad Sci 2000; 899; 136–147.

26. Arezzini B, Lunghi B, Lungarella G, Gardi C. Iron overload enhances the development of experimental liver cirrhosis in mice.  Int J Biochem  Cell Biol 2003; 35:486-495.

27. Sidhu P, Garg ML, Morgenstern P, Vogt J, et al. Role of zinc in regulating the levels of hepatic elements following nickel toxicity in rats. Biol Trace Elem Res 2004; 102:161–172.  

28. Arezzini B, Lunghi B, Lungarella G, Gardi C. Iron overload enhances the development of experimental liver cirrhosis in mice. Int J Biochem Cell Biol 2003; 35:486–495.

29. Hammes H, Du X, Edelstein D, Taguchi T, et al. Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nature Med 2003; 9(3):294-300.

30. Stirban A, Negrean M, Stratmann B, Gawlowski T, et al. Benfotiamine prevents macro- and microvascular endothelial dysfunction and oxidative stress following a meal rich in advanced glycation end products in individuals with type 2 diabetes. Diabetes Care 2006; 29:2064–2071.

31. Aziz TA, Ahmed ZA, Juma'a KM, Abdulrazzaq MH, Hussain SA. Study of the protective effects of benfotiamine against CCl4-induced hepatotoxicity in rats. Iraqi J Pham Sci 2009; 18:47-53.

32. Stracke H, Hammes HP, Werkmann D, Mavrakis K, et al. Efficacy of benfotiamine versus thiamine on function and glycation products of peripheral nerves in diabetic rats. Exp Clin Endocrinol Diab 2001; 109:330-336.

33. Karachalias N, Babaei-Jadidi R, Ahmed N, Thornalley PJ. Accumulation of fructosyl-lysine and advanced glycation end products in the kidney, retina and peripheral nerve of streptozotocin-induced diabetic rats. Biochem Soc Trans 2003; 31:1423-1425.

34. Balakumar P, Ramica Sharma R, Singh M. Benfotiamine attenuates nicotine, uric acid-induced vascular endothelial dysfunction in the rat. Pharmacological Research 2008; 101: 210-214.

35. Babaei-Jadidi R, Karachalias N, Ahmed N, Battah S, Thornalley PJ. Prevention of incipient diabetic nephropathy by high-dose thiamine and benfotiamine. Diabetes 2003; 52:2110-212.

Background and objectives: Schizophrenia is the heartland of psychiatry and the core of its clinical practice. The onsets of schizophrenia characteristically occur between the ages of 15 and 45. There are minor sex differences in age of onset. Schizophrenia is over presented among people of lower social class. The relationship of birth order to schizophrenia has been controversial.

Methods: Eighty six schizophrenic patients who were admitted to psychiatric unit of Basra General Hospital, who met DSM-1V criteria for schizophrenia were included in this study. The data was obtained by personal interview from the patients and their accompanied relatives, after taking their consent, according to the following: age, sex, marital status, social class, season of birth and birth order.

Results: This study shows high male to female ratio. Two third of the patients were single and in younger age group. The study also shows high percentage of schizophrenic patients in upper and middle social class.  The season of birth of schizophrenic patients were in spring and there is no much difference between first and last born.

1.       Penick E. The endodontic management of root resorption. Oral Surgery, Oral Medicine, Oral Pathology 1963; 16: 344-352. Abs.

2.       Bellizzi R., Ciao W. Endodontic management of extensive internal root resorption Report of a case. Oral Surgery, Oral Medicine, Oral Pathology 1980; 49(2): 162-165. Abs.

3.       Skaljac-Staudt G., Katunaric M., Kardum M. Internal Resorption, Therapy and Filling.  Acta Stomat Croat 2000; 34(4): 431-433.

4.       Goldberg F., Massone E., Esmoris M., Alfie D. Comparison of different techniques for obturating experimental internal resorptive cavities. Dental Traumatology 2000; 16(3):116-121. Abs.

5.       Wilson P., Barnes I. Treatment of internal root resorption with thermo-plasticized gutta-percha. A case report. Int. Endod. J. 1987; 20: 94-7.

6.       Sonntag D., Delschen S., Stachniss V. Root-canal shaping with manual and rotary Ni-Ti files performed by students. Int Endod J 2003; 36: 715-723.

7.       Glossen C., Haller R., Dove S., del Rio C. A comparison of root canal preparations using Ni-Ti hand, Ni-Ti engine-driven, and K-flex endodontic instruments. J Endod 1995; 21: 146–51.

8.       Shabahang S. State of the art and science of endodontics. JADA 2005; 136: 41-52.

9.       Cohen S., Burns R. Pathways of the pulp. 8^th ed. Mosby. 2002.

10.    Shetty K., Chandra S. An In-vitro Evaluation of Volumetric Dye Penetration Observed with Quick Fil, Lateral condensation, Modifiedtrifecta, Single Cone, and No Obturation Preceded by Sodium Hypochlorite and E.D.T.A. Endodontology 2006; 18:5-10.

11.     Gutmann J. Adaptation of injected thermo-plasticized gutta-percha in the absence of smear layer. Int Endod J. 1993; 26(2):87-92. 

12.     Kqiku L., Weiglein A., Städtler P. A Comparative Study of Five Different Obturation Techniques. Acta Stomatol Croat. 2006; 40(1):3-11.

Background and objectives: Hyperlipidemia is characterized by increased concentrations of lipids including triglycerides, total cholesterol, low density lipoproteins, very low density lipoproteins in the blood and some times decreased high density lipoproteins .

Many drugs have been used for treatment of this disorder. The present study was designed to estimate the effects of simvastatin on lipid profile, atherogenic index,  transaminases,  creatinine, uric acid and alkaline phosphatase.

Methods: This study covered 70 subjects, they were divided into two groups, the first group included 45 hyperlipidaemic patients which were treated with 20mg simvastatin and second group included 25 normal  subjects. After 12 hours fasting, serum lipid profile, transaminases; alkaline phosphatase, uric acid and creatinine were measured for the patients in 3 intervals before treatment, after 8 weeks and 16 weeks of treatment, and one time for normal  subjects.

Results: : After therapy, simvastatin showed a significant reduction in serum (TC, TG, LDL, VLDL and atherogenic index) and also, significant rise in HDL noticed, by performing a comparison between the group before treatment, and groups after treatment.Serum ALT, AST and ALP were significantly increased but  were still within normal levels.Insignificant effect was observed from serum creatinine, uric acid and also body mass index by performing a comparison between group before treatment and groups after  treatment.

Conclusions:Simvastatin was effective in controlling lipid profile and atherogenic index, with no significant abnormality in liver functions.

Key words: Hyperlipidaemia , simvastatin, lipid profile , atherogenic index. 

1- Farnier M, Davignon J. Current and future treatment of hyperlipidemia: the role of statins. Am J  Cardiol 1998;82(4B):3J-10J.

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9. Ballantyne CM: Low-density lipoproteins and risk for coronary artery disease. Am J Cardiol 1998;82:3Q-12Q.

10. Bilheimer D, Grundy S, Brown M, Goldstein J. Mevinolin and colestipol stimulate receptor-mediated clearance of low-density lipoprotein from plasma in familial hypercholesterolemia heterozygotes. Proc  Natl  Acad  Sci  1983;80: 4124–8 .

11. Schaefer E, McNamara JR, Tayler T,Daly J, Gleason J. Comparisons of effects of statins (atorvastatin, fluvastatin, lovastatin, pravastatin, and simvastatin) on fasting and postprandial lipoproteins in patients with coronary heart disease versus control subjects. Am J Cardiol 2004;93:31-9.

12. Wierzbicki A, Lumb P, Semra Y, Chik G, Christ E . Atorvastatin compared with simvastatin-based therapies in the management of severe familial hyperlipidaemias.  Q J Med 1999;92: 387-94.

13. Santosh S, Pawan K . Effect of simvastatin and atorvastatin on coenzyme Q10.  The Internet Journal of Cardiology 2007; 4 (1).

14. Antti J, Jukka M, Risto H, Arja V, Merja R . Effects of diet and simvastatin on serum lipids,  insulin, and antioxidants in hypercholesterolemic men. JAMA 2002; 287: 598-605.

15. Osamu N, Masatoshi M, Motoshige M, Takahiro N, Iwao N . Effect of simvastatin on the lipid profile of hemodialysis patients. Kidney Int 1999;56: 219–21.

16. William L, John M, Bruce W, William S. The effect of high dose simvastatin on triglyceride rich lipoprotein metabolism in patients with type 2 diabetes        mellitus. J Lipid Res 2006;47: 193-200.

17. Peter J, Stephanie K, Irene L, Donald H. Comparative dose efficacy study of atorvastatin versus simvastatin, paravastatin, lovastatin and fluvastatin in patients with hypercholesterolemia( The curves study).Am J Cardiol 1998;81:582-7 .

18. Branchi A, Fiorenza A, Torri A, Muzio F, Rovellini A. Effects of atorvastatin 10mg and simvastatin 20mg on serum triglyceride levels in patients with hypercholesterolemia. Curr Therap Res 2001;8: 405-15.

19. Fernando C, Ana C, Juan F, Jose P, Garcia O. Comparison of the hypolipidemic effect of gimfibrozil versus simvavtatin in patients with type III hyperlipoproteinemia. Medscape Am J 1999; 138 (1):156-62. 

20. Abdul-Basit A, Humaira R, Zafar H, Rubina H,Yakoob A. The effect of simvastatin on diabetic dyslipidemia. Journal of Baqai Medical University. 2001; 2 :6-8.

21. Emel A, Banu N,  Canan O, Sema G and Sezer C. The Effect of simvastatin treatment on plasma ubiquinone, blood ATP concentrations, total antioxidant capacity and muscle related markers. Turk J Med Sci 2002;32:323-8.

22. Kubota T, Fujisaki K, Itoh Y, Yano T, Sendo T. Apoptotic injury in cultured human hepatocytes induced by HMG-CoA reductase inhibitors. Biochem. Pharmacol.2004; 67:2175-86.

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25. Zena A.,  Isam M .Comparative effects of lovastatin and simvastatin on liver function tests in hyperlipidemic patients. The Medical Journal of Basrah University  2007;25(1):20-4.

26. Jyh-Gang L, Mei-Mei H, Wey-Wen J and Jung-Kuei P. Efficacy and safety of 20 mg/day simvastatin in patients with renal impairment and combined hyperlipidemia. FJJM 2005; 3(1):51-5

27. Haralampos J, Anna I, Sofia G, Vasilios G, Eleni T. Effects of statin treatment on uric acid homeostasis in patients with primary hyperlipidemia. Medscape Am Heart J 2004; 148(4):635-40.

Background and objectives: Male Infertility is often caused by problems with sperm production or motility. Zinc in human semen seems to play an important role in the physiology of spermatozoa .This study was designed to demonstrate the relationships between concentrations of zinc and testosterone in serum and seminal plasma and sperm quality among infertile men.

Methods: One hundred four infertile males, aged (19-44) years, were selected from Infertile Clinic-Azadi Teaching Hospital- Kirkuk Province. Forty known fertile males were selected as normospermic control group. Semen samples were analyzed according to WHO criteria. Serum and seminal plasma zinc concentrations were estimated by atomic absorption technique. Serum testosterone was measured by MiniVIDAS apparatus.

Results: The mean value of serum testosterone was significantly lower in infertile males (4.87±0.15 ng/ml) as compared to control group (6.41±0.16 ng/ml); (P< 0.01), significant correlations were observed between serum testosterone with seminal plasma zinc level in oligospermic subjects (r=0.44) and with serum zinc level in azoospermic subjects (r=0.37), (P< 0.01); (P< 0.05) respectively. Serum and seminal plasma zinc levels were lower in infertile men (7.75±0.18 µmol/L); (0.83±0.02 mmol/L) when compared with normospermic control group (14.09±0.27 µmol/L); (1.41±0.01 mmol/L) respectively (p<0.01),

Conclusion: Zinc may contribute to fertility through its positive effect on spermatogenesis. Also there was significant decrease in serum and seminal plasma zinc levels in oligospermic and azoospermic infertile males with significantly low androgen. It indicates that the zinc may have a role for steroidogenesis.

Background and Objectives: Since 1950s, phototherapy had been the treatment of choice for neonatal jaundice. Continuous phototherapy was the pattern used for many years; however intermittent phototherapy was also used with conflicting and controversial results. This work aim is to assess intermittent phototherapy for the treatment of neonatal jaundice in comparison with continuous phototherapy.

Methods: In a prospective clinical study all newborns with neonatal jaundice admitted to neonatology department of Raperin hospital in Erbil, between August 2009 and February 2010, for phototherapy were included in the study. The patients were randomly divided into 2 groups. In the control group continuous phototherapy defined as two hours on and half an hour off was used while in the study group intermittent phototherapy defined as one hour on and one hour off was used. Mean total serum bilirubin level in both continuous and intermittent phototherapy groups were compared after each12, 24, 36, 48, and 72 hours of commencing phototherapy. The effect of biodemographic characteristics (gender, gestational age, birth weight, age in hours, and bilirubin levels at admission) were also studied.

Results: There was no any significant difference between the two groups regarding mean total serum bilirubin measured at every 12 hours. There was no any significant difference between the 2 groups regarding biodemographic characteristics (p> 0.05).

Conclusion: Intermittent phototherapy is as effective as continuous one in the treatment of indirect hyperbilirubinemia in full term infants and in the absence of hemolytic causes.   

Key words: Neonatal jaundice; indirect hyperbilirubinemia; Phototherapy.

Background and objectives: Urinary tract infections are amongst the most common infections, Hospital-acquired urinary tract infection increases not only morbidity and mortality but also hospital costs. The objectives of this study were to determine bacteria responsible for hospital-acquired urinary tract infection, their antibiotic sensitivities and to describe the risk factors of the infection.

Methods: All urine samples fulfilling the criteria for significant bacteriuria were included in the study. Isolation and identification of bacteria was performed by standard method and susceptibility testing was determined by disk diffusion method.

Results: Out of 290 patients, 133 (45.86%) have acquired hospital-acquired urinary tract infection. Older age, hospitalization and catheterization were risk factors of the infection. Escherichia coli (51.70%) and Klebsiella pneumoniae (16.33%) represented the most common isolates. The most bacteria isolates were sensitive to ciprofloxacin, rifampin and trimethoprim + sulphamethoxazole.

Conclusions: To prevent hospital-acquired urinary tract infections, important factors must be taken into consideration, for example: avoid unnecessary urethral catheterization, choose narrow spectrum antibiotics according to antibiotic sensitivities, and investigate regularly the causative bacteria and their susceptibility patterns

1. Melzack R, Wall PD. Pain mechanisms; a new theory. Science 1965;150 (699):971-9. Available from: http://www.medscape.com/medline/abstract/5320816. 

2.  Jensen JE, Conn RR, Hazelrigg G, Hewett JE. "The use of transcutaneous neural stimulation and isokinetic testing in arthroscopic knee surgery". Am J Sports Med 1985; 13 (1):2733. Available from: http://ajs.sagepub.com/cgi/content/abstract/13/1/27. 

3.  Johnson M, Martinson, M. "Efficacy of electrical nerve stimulation for chronic musculoskeletal pain: A meta-analysis of randomized controlled trials". Pain 2007; 130 (1): 157–65. Available from: http://www.painjournalonline.com3959(07)00073-5/abstract. 

4. Nnoaham KE, Kumbang J. Transcutaneous electrical nerve stimulation (TENS) for chronic pain. Cochrane Database Syst Rev. 2008;7:16. Available from: http://www.medscape.com/medline/abstract/18646088. 

5. Fernandez-Del-Olmo M, Alvarez-Sauco M, Koch G, et al. How repeatable are the physiological effects of TENS?. Clin Neurophysiol. 2008;119 (8):1834-9.

6.       Robertson V, Ward A, Low J, Reed A. Electrotherapy Explained: Principles and Practice, 4^th ed. Philadelphia: Butterworth-Heinemann (Elsevier); 2006.  Available from http://www.us.elsevierhealth.com/product.jsp?isbn=9780750688437. 

7.       Robinson AJ, Snyder-Mackler  L. Clinical Electrophysiology: Electrotherapy and Electrophysiologic Testing.  3^rd ed. USA: Lippincott Williams & Wilkins; 2007.

8.        Duggan A W. Foong FW. Bicuculine and spinal inhibition produced by dorsal column stimulation in the cat. Pain 1985; 22; 249-59.

9.       Johnson MI, Ashton CH, Thompson JW, An in-depth study on long term users of transcutaneous electrical nerve stimulation (TENS). Implications for clinical use of TENS. Pain 1991; 44; 221- 29.

10.   Hughes G., Lichstein P., Whitlock D., harker C. Response of plasma beta-endorphins to trancutaneous electrical nerve stimulation in healthy subjects; Physical Therapy 1984; 64 (7): 1062-6.

11. Garrison. DW and Foreman R. D. Effect of prolonged transcutaneous electrical nerve stimulation (TENS) and variation of stimulation variable on dorsal horn cell activity. Pain. 1996; 6: 87-94. 

12.   Sandkühler J. Long-lasting analgesia following TENS and acupuncture: Spinal mechanisms beyond gate control. In: Proceedings of the 9th World Congress on Pain, Progress in Pain Research and Management, Vol.16. Devor M, Rowbotham MC, Wiesenfeld-Hallin Z, eds. Seattle: IASP Press; 2000. P. 359–369.

13. Johnson MI, Ashton CH, Thompson JW. An in-depth study of long-term users of transcutaneous electrical nerve stimulation (TENS). Implications for clinical use of TENS. Pain. 1991; 44(3):221-9. 

14. Cheing GL, Hui-Chan CW. Transcutaneous electrical nerve stimulation: nonparallel antinociceptive effects on chronic clinical pain and acute experimental pain. Arch Phys Med Rehabil. 1999; 80(3): 305-12. 

15. Bjordal JM, Johnson MI, Ljunggreen AE. "Transcutaneous electrical nerve stimulation (TENS) can reduce postoperative analgesic consumption. A meta-analysis with assessment of optimal treatment parameters for postoperative pain". Eur J Pain 2003; 7 (2): 181–8.

16. Rakel B, Frantz R. "Effectiveness of transcutaneous electrical nerve stimulation on postoperative pain with movement". J Pain 2003; 4 (8): 455–64.

17. Thorsen SW, Lumsden SG, Trigeminal neuralgia; sudden and long term remission with transcutaneous electrical nerve stimulation. Physiol Ther 1997; 20: 415-9.

Background and objectives: Over the last 35 years electrical nerve stimulation has been employed increasingly in the treatment of chronic pain. This study was carried out to compare the analgesic effect that produced by applying a fixed frequency (50 Hz) high intensity tolerably painful transcutaneous electrical nerve stimulation (TENS) with the conventional low intensity TENS.

Results: Patients who received high intensity TENS; 94% of them got immediate pain relief and 17% got long lasting pain relief more than three months, while with the conventional TENS only  33% got immediate pain relief and no one got long lasting pain relief.

Conclusion: The tolerably painful high intensity TENS gives better analgesic effect than the conventional TENS, and in some patients it may leads to long lasting analgesic effect(this may be attributed to the pan stimulation involving a variety of afferent fibers; Aa/β, Ad & C).

Key words: transcutaneous electrical nerve stimulation, analgesia.

1.  Melzack R, Wall PD. Pain mechanisms; a new theory. Science 1965;150 (699):971-9. Available from: http://www.medscape.com/medline/abstract/5320816. 

2. Jensen JE, Conn RR, Hazelrigg G, Hewett JE. "The use of transcutaneous neural stimulation and isokinetic testing in arthroscopic knee surgery". Am J Sports Med 1985; 13 (1):2733.

3.  Johnson M, Martinson, M. "Efficacy of electrical nerve stimulation for chronic musculoskeletal pain: A meta-analysis of randomized controlled trials". Pain 2007; 130 (1): 157–65.  

4. Nnoaham KE, Kumbang J. Transcutaneous electrical nerve stimulation (TENS) for chronic pain. Cochrane Database Syst Rev. 2008;7:16.  

5. Fernandez-Del-Olmo M, Alvarez-Sauco M, Koch G, et al. How repeatable are the physiological effects of TENS?. Clin Neurophysiol. 2008;119 (8):1834-9.

6. Robertson V, Ward A, Low J, Reed A. Electrotherapy Explained: Principles and Practice, 4^th ed. Philadelphia: Butterworth-Heinemann (Elsevier); 2006.

7. Robinson AJ, Snyder-Mackler  L. Clinical Electrophysiology: Electrotherapy and Electrophysiologic Testing.  3^rd ed. USA: Lippincott Williams & Wilkins; 2007.

8.  Duggan A W. Foong FW. Bicuculine and spinal inhibition produced by dorsal column stimulation in the cat. Pain 1985; 22; 249-59.

9. Johnson MI, Ashton CH, Thompson JW, An in-depth study on long term users of transcutaneous electrical nerve stimulation (TENS). Implications for clinical use of TENS. Pain 1991; 44; 221- 29

10. Hughes G., Lichstein P., Whitlock D., harker C. Response of plasma beta-endorphins to trancutaneous electrical nerve stimulation in healthy subjects; Physical Therapy 1984; 64 (7): 1062-6.

11. Garrison. DW and Foreman R. D. Effect of prolonged transcutaneous electrical nerve stimulation(TENS) and variation of stimulation variable on dorsal horn cell activity. Pain. 1996; 6: 87-94. 

12. Sandkühler J. Long-lasting analgesia following TENS and acupuncture: Spinal mechanisms beyond gate control. In: Proceedings of the 9th World Congress on Pain, Progress in Pain Research and Management, Vol.16. Devor M, Rowbotham MC, Wiesenfeld-Hallin Z, eds. Seattle: IASP Press; 2000. P. 359–369.

13. Cheing GL, Hui-Chan CW. Transcutaneous   electrical nerve stimulation: nonparallel antinociceptive effects on chronic clinical pain and acute experimental pain. Arch Phys Med Rehabil. 1999; 80(3): 305-12. 

14. Bjordal JM, Johnson MI, Ljunggreen AE. "Transcutaneous electrical nerve stimulation (TENS) can reduce postoperative analgesic consumption. A meta-analysis with assessment of optimal treatment parameters for postoperative pain". Eur J Pain 2003; 7 (2): 181–8. 

15. Rakel B, Frantz R. "Effectiveness of transcutaneous electrical nerve stimulation on postoperative pain with movement". J Pain 2003; 4 (8): 455–64.

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Background and objectives: Otitis media with effusion is collection of fluid behind intact tympanic membrane. Otitis media with effusion usually coexists with the adenoid hypertrophy. The adenoid is a part of Waldeyer's ring; its basic function is thought to be antibody production. The aim is to identify the incidence of otitis media with effusion in children with adenoid hypertrophy.

Methods: A prospective descriptive cohort study had been employed at Rizgari Teaching Hospital/ Erbil from January 2008 to July 2008. Summation of total 120 Child aged 3-12 years old were being conducted in the survey. All patients subjected for history, local physical examination, Information's recorded on a specially designed Questionnaire and proper investigations were done including lateral X ray of post nasal space, and audiological examination.

Results: Among 120 patients age (3-12) years old with adenoid hypertrophy, 44 patients (36.7%) had OME, mean age was 6.5 years. Most common age group was (5-6) years (21) (47%).

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