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SUMMARYThe participation of the cardiovascular and the pulmonary system is crucial for the significance of the clinical manifestation of a sickle cell patient. The activation of the endothelium and the vascular occlusion in conditions of high cardiac output further aggravate the clinical manifestation. The presence of a particular myocardial damage controversial. The aim of this review is to identify the role of the cardio-pulmonary participation in the sickle cell anemia.

1. Groves BM, Brondage BH, Elliott CG: Pulmonary hypertension associated with hepatic cirrosis. In FishmanAP(ed):The pulmonary circulation: Normal and abnormal. University of Pensylvania Press, Philadelphia ,1990:pp359-69.

2. Lindsay J, Meshel J, Patterson R. The cardiovascular manifestations of sickle cell disease. ArchInternMed 1974;133:643-651.

3. Faller DV . Endothelial cell responses to hypoxic stress. Clin Exp Pharmacol Physiol. 1999 ;26(1):74-84.

4. Haque AK, Gokhale S, Rampy BA, et al. Pulmonary hypertension in sickle cell hemoglobinopathy: a clinicopathologic study of 20 cases. Hum Pathol. 2002:,33(10):1037-43.

5. Aessopos A, Farmakis D, Loukopoulos D. Elastic tissue abnormalities resembling pseudoxanthoma elasticum in beta thalassemia and the sickling syndromes. Blood. 2002;99(1):30-5..

6. Mansi IA, Rosner F. Myocardial infarction in sickle cell disease. J Natl Med Assoc 2002;94(6):448-52.

7. Cipolotti R, Costa GB, Lima WH, et al. Echocardiographic characteristics of patients with sickle cell anaemia in Sergipe, Brazil. J Trop Pediatr. 2001;47(2):73-6.

8. Moyssakis I, Tzanetea R, Tsaftaridis P, et al. Systolic and diastolic function in middle aged patients with sickle beta thalassaemia. An echocardiographic study. Postgrad Med J. 2005 Nov;81(961):711-4.

9. Batra AS, Acherman RJ, Wong WY, Wood JC, Chan LS, Ramicone E, Ebrahimi M, Wong PC. Cardiac abnormalities in children with sickle cell anemia. Am J Hematol 2002;70(4):306-12.

10. Aessopos A, Farmakis D, Trompoukis C, et al. Cardiac involvement in sickle beta-thalassemia. Ann Hematol. 2009 Jun;88(6):557-64. Epub 2008 Dec 24.

11. Manno B, Burka E, Hakki A, et al. Biventricular function in sickle-cell anemia: radionuclide angiographic and thallium-201 scintigraphic evaluation. Am J Cardiol 1983;52:584-587.

12. Covitz W, Eubig C, Balfour I, et al. Exercise-induced cardiac dysfunction in sickle-cell anemia. A radionuclide

study. Am J Cardiol 1983;51:570-575. 13. Norris S, Johnson C, Hayward J. Sickle cell anemia:

Does myocardial ischemia occur during crisis? J Natl Med Assoc 1991;83:209-213.

14. Aessopos A., Tsironi M., Vassiliadis I., et al.: Exercise-induced myocardial perfusion abnormalities in sickle b-thalassemia:Tc-99m Tetrofosmin Gated SPECT Imaging study. AmJMed 2001;111:355-359.

15. Acar P, Maunoury C, de Montalembert M, Dulac Y. Abnormalities of myocardial perfusion in sickle cell disease in childhood: a study of myocardial scintigraphy Arch Mal Coeur Vaiss 2003;96(5):507-10.

16. Manci EA, Culberson DE, Yang YM, et al. Investigators of the Cooperative Study of Sickle Cell Disease.: Causes of death in sickle cell disease: an autopsy study. Br. J Haematol. 2003;123(2):359-65.

17. Castro O.,Hoque M.,Brown B.: Pulmonary hypertension in sickle cell disease: cardiac catheterization results and survival. Blood 2003;101(4) :1257-61.

18. Gladwin MT, Sachdev V, Jison ML, et al.: Pulmonary hypertension as a risk factor for death in patients with sickle cell disease. N Engl J Med. 2004 ;350(9):886-95.

19. Perez-Penate G, Julia-Serda G, Pulido-Duque JM,. One-year continuous inhaled nitric oxide for primary pulmonary hypertension. Chest. 2001;119:970-973

20. Channick RN, Simonneau G, Sitbon O, et al. Effects of the dual endothelin-receptor antagonist bosentan in patients with pulmonary hypertension: a randomised placebo-controlled study. Lancet. 2001;359:1119-1123.

21. Nagaya N, Uematsu M, Oya H, et al. Short-term oral administration of L-arginine improves hemodynamics and exercise capacity in patients with precapillary pulmonary hypertension. Am J Respir Crit Care Med. 2001;163:887-891

22. Morris CR, Morris SM Jr, Hagar W, et al. Arginine therapy: a new treatment for pulmonary hypertension in sickle cell disease? Am J Respir Crit Care Med 2003;168:63-69.

73

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80 , 10-50%. , . , , , . , , , . , , . , . , . . , . [8] , 30-60 . / 0.3 0.9 : , , , . [8,10,11] , 0.1.[10,11] Nation RL., 1980,[10] . , , ( 20% ), . ( 96% ),

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SUMMARY The absorption of the medications through the gastro-intestinal tract during pregnancy has not been studied enough. According to the data until now there is no difference between the absorption of the medications before pregnancy and during this period of time. The passage of the medications though the placenta is mainly done by the simple diffusion and depends on chemical qualities and the concentration of the free molecule of the drug. The pharmaceutical substances that go through the placenta reach the embryo on levels between 50 and 100% of those of the mother. The drugs role in the embryo dysplasias is not clear. It is believed today that drugs as a causal factor cover around 5% of the abnormalities. Generally speaking, we have to stress the fact that all antibiotics are ejaculated in milk, although in different concentrations. However, few side-effects have been reported in embryo, since the quantity of the drug is usually small within the total day nursing.. 1. Juchau MR, Dyer DC. Pharmacology of the

placenta. Pediatr Clin North Am. 1972 Feb;19(1):65-79.

2. Clayton-Smith J, Donnai D: Human malfor- mations. In Rimoin DL, Connor JM, Pyeritz RE. (eds): Emery and Rimoins Prin- ciples ans Practice of Medical Genetics, 3rd ed. New York, Churchill Livingston, 1996, p. 383.

3. Fitzgerald M. Sick and pregnant: treatment of common episodic illness. Program and abstracts of the National Conference for Nurse Practitioners 2001; November 7-10, 2001; Washington, DC.

4. Hale T.: Medications and Mothers Milk. 9th ed. Amarillo, Texas: Pharmasoft Publishing;2000.

5. Heinonen OP, Slone D., and Shapiro S.: Birth Defects and Drugs in pregnancy. Publishing Sciences Group Inc., Littleton, Mass. 1977.

6. Briggs GG, Freeman RK, Yaffe SJ ed. Drugs in pregnancy and Lactation. Lippincott Williams and Wilkins, 6th ed.,2002.

7. Physicians Desk Reference. Medical Econo- mics, Thomson Health Care 56ed.,2002

8. Landers DV, Green JR, Sweet RL: Antibiotic

use during pregnancy and the postpartum period. Clin Obstet Gynecol 26:391-406, 1983.

9. Chow AW, Jewesson PJ: Pharmacokinetics and safety of antimicrobial agents during pregnancy.Rev Infect Dis 7:287-313, 1985.

10. Nation RL: Drug kinetics in childbirth. Clin Pharmacokinet 5:340-364, 1980.

11. Philipson A: Pharmacokinetics of antibiotics in the pregnant woman. In Ledger .WJ (ed): Antibioticsin Obstetrics and Gynecology. The Hague, Martinus Nyhoff, 1982, pp 37-60.

12. Schwarz RH: Considerations of antibiotic therapy during pregnancy. Obstet Gynecol 58 (suppl) :95-99, 1981.

13. Stewart KS, Shaf M., Andrews JD., et al: Distribution of parenteral ampicillin and cephalosporins in late pregnancy. J Obstet. Gynec. Brit. 1973, 80, 902.

14. Beeley L: Drugs and breast feeding. Clin Obstet Gynecol 8:291-295, 1981.

15. Bowes WA Jr: The effect of medications on the lactating mother and her infant. Clln Obstet Gynecol 23:1073-1080, 1983.

82

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83

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84

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- , . , . , , , , .. SUMMARY Diabetes mellitus is a chronic metabolic disease which is caused by the in insufficient excretion of insulin or increased resistance of tissues in its action and has as a result the disturbances of metabolism of glucose. It is estimated that approximately 200 million people are affected worldwide and the number is expected to be double by 2030. It is calculated that the 1/5 of them will present ulcer their feet some time in their life. Perhaps, nowhere else in the human body can we observe, so clearly and to such extent the devastating consequences of the complications that diabetes causes as these are observed on the feet of people who suffer from diabetes. In all countries, the management of care on the diabetic foot requires the presence of a specialized nurse. The main role of the nurse is it to evaluate and offer specialized care in the diabetic ulcers, which includes cicatrisation of ulcers and use of suitable compresses. Another responsibility of the nurse is to be able to discharge the sensitive areas of the limbs. The specialized nurse is also in charge of the more general care and the suitable education of the patient and his/her family. Keywords: Diabetic foot, diabetes mellitus, diabetic ulcer, care, prevention, therapy, specialized nurse.

86

1. Bowker JH, San Giovanni TP. Amputations in

Diabetes Mellitus:Toes to above knee in The foot in Diabetes 3rd edn, Eds A J M Bounton, H connor and P.R. Cavanagh, 2000, John Wilcy and Sons Ldt.

2. Centers for Disease Control and Prevention. National diabetes fact sheet: Prevalence of diabetes in the United States. Atlanta, GA: US Department of Health and Human Services; 1997.

3. . . .2001;14,2:202-204.

4. Pham HT. Wound Care in diabetic foot ulceration, Wounds 2000; 12(Suppl. B):82B-89B.

5. , , Boulton AJM. . . .1992;5:1-8.

6. . . . 2001;14,2 :205-207.

7. . . . . 2000.

8. . . .. . 2008.

9.

. 2007.(): :8.

10. Young M. Managing infection in the diabetic Foot. The Diabetic Foot Journal 2007; 10 (1):10-16.

11. . - . 2008: 469-470.

12. Bell et al. Diabetes foot self-care practices in a rural. Triethnic Population. The Diabetes Educator.2005; 31:75-82.

13. Uccioli L, Fanglia G, Monticome G et al. Manufactured shoes for the prevention of diabetic foot ulcers. Diabetes Care 1995; 45 (10):28-34.

14. Inlow S, Kallia TP, Rahman J. Downloading plantar foot pressures in the diabetic patients. Ostomy Wound Manage 1999; 45 (10):28-34.

15. Consensus Development Conference on Diabetic Foot Wound Care. American Diabetes Association. Diabetes Care 1999; 22:1354-1360.

16. , . . . 3 2007;43..

87

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.,,.,I.,.,.,.,.,.,..,

: P 450 : : 588 . , ( , n = 340) ( , n = 248) . . : . 58 (9,9%) 20 (3,4%) 38 (6,5%) . [(10% vs 9,7% ), HR = 1,1 (95%CI: 0,6-1,8), p = 0.89]. : , .

[1]. . [2] [3].

[4-6]. To P450 .[7-9].

88

P450 2C19 [10] [11] , . H . , , [11]. 2003 2005 612 . ( 100mg 325mg) (300mg 600mg 75mg ) 12 . . , , . ( 2 ). ,

. 1,3,6,9,12 . . . , 7 .( ) ( ). t test Mann-Whitney U test. Kaplan-Meier . Cox . SPSS ( release 11.0,SPSS Inc, USA ). A : A 612 , 24 (3,9%) . 588 (96,1%) . 588 340 (57,8%) 248(42,2%) . 237 (69,7%) 103 (30,3%) . 210 (61,7%) . 130 (38,2%) 229 ( 7 362 ). , . 98,4%, 96,2% 91,9% , .

89

, , 9,3%, 1,3%, 7,1%, 1,1% . . : 100%. , . 20 (3,4%) 38 (6,5%) . ( 10% 9,7% hazard ratio(HR) 1,1[95%CI 0,6-1,8%];P=0,9) (3,5% 3,2%,R 1,1 [95%CI0,4-2,7];P=o,84) (6,5% 6,5%,R 1 [95% CI 0,5-1,9];P=,99). Academic Research Consortium (8,8% 8,5%, HR 1,1 [95% CI ,7-1,8%];P=0,88) ( 9,4% 8,9%, R [95%CI 0,6-1,9];P=0,82] . (9,7% 10%HR 0,9 [95%CI 0,4-2,1];P=0,91) ( 9% 11,5%, HR 0,8 [95% CI 0,4-1,6];P=0,46).

. . Gilard [10] 124 . . , , [12,13] , . . , . . , P450, , ; . 450 2C19 Gilard 10 [7-9,14,15]. .

90

, 450 34[16]. [17-19]. . , .

SUMMARYBACKGROUND: Because clopidogrel is converted to its active metabolite by P450 isoenzymes, which are also involved in the metabolism of omeprazole, there is concern regarding whether the action of clopidogrel would be reduced in patients also taking omeprazole. OBJECTIVE: To evaluate the impact of omeprazole administration on the effectiveness of clopidogrel drug therapy during the first year following successful coronary stenting (CS). METHODS: A total of 588 consecutive patients who underwent successful CS for stable or unstable coronary artery disease were studied. Patients were classified into those who were treated (group A, n=340) or not treated (group B, n=248) with omeprazole for seven or more consecutive days during the entire observation period. The composite of cardiac death or rehospitalization for nonfatal myocardial infarction during the first year was the prespecified primarystudyendpoint. RESULTS: Baseline characteristics, and dual clopidogrel and acetylsalicylic acid drug therapy were well balanced between the study groups. By one year, the primary end point was reached by 58 (9.9%) patients, including 20 (3.4%) who died due to cardiac reasons and 38 (6.5%) who were rehospitalized because of a nonfatal myocardial infarction. Patients in groups A and B, respectively, were at similar risk of the primary composite end point (10% versus 9.7%, hazard ratio1.1[95%CI0.6to1.8];P=0.89). CONCLUSIONS: According to the results of the present study, treatment with omeprazole had no impact on the clinical efficacy of clopidogrel drug therapy during the first year after successful CS.

1A

1B

1C

91

1. Bassand JP, Hamm C, Ardissino D, et al. The

Task Force for the Diagnosis and Treatment of Non-ST-Segment Elevation Acute Coronary Syndromes of the European Society of Cardiology. Guidelines for the diagnosis and treatment of non-ST-segment elevation acute coronary syndromes. Eur Heart J 2007;28:1598-660.

2. Schreiner GC, Laine L, Murphy SA, et al. Evaluation of proton pump inhibitor use in patients with acute coronary syndromes based on risk factors for gastrointestinal bleed. Crit Pathw Cardiol 2007;6:169-72.

3. Bhatt DL, Scheiman J, Abraham NS, et al. ACCF/ACG/AHA 2008 expert consensus document on reducing the gastrointestinal risks of antiplatelet therapy and NSAID use: a report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents. Circulation 2008;118:1894909.

4. Grossmann R, Sokolova O, Schnurr A, et al. Variable extent of clopidogrel responsiveness in patients after coronary stenting. Thromb Haemost 2004;92:1201-6.

5. Gurbel PA, Tantry US. Drug insight: clopidogrel nonresponsiveness. Nat Clin Pract Cardiovasc Med 2006;3:387-95.

6. Lev EI, Patel RT, Maresh KJ, et al. Aspirin and clopidogrel drug response in patients undergoing percutaneous coronary intervention: the role of dual drug resistance. J Am Coll Cardiol 2006;47:27-33.

7. Lau WC, Gurbel PA, Watkins PB, et al. Contribution of hepatic cytochrome P450 3A4 metabolic activity to the phenomenon of clopidogrel resistance. Circulation 2004;109:166-71.

8. Farid NA, Payne CD, Small DS, et al.

Cytochrome P450 3A inhibition by ketoconazole affects prasugrel and clopidogrel pharmacokinetics and pharmacodynamics differently. Clin Pharmacol Ther 2007;81:735-41.

9. Suh JW, Koo BK, Zhang SY, et al. Increased risk of atherothrombotic events associated with cytochrome P450 3A5 polymorphism in patients taking clopidogrel. Can Med Assoc J 2006;174:1715-22.

10. Gilard M, Arnaud B, Cornily J-C, et al. Influence of omeprazole on the antiplatelet action of clopidogrel associated with aspirin: the randomized, double-blind OCLA (Omeprazole CLopidogrel Aspirin) study. J Am Coll Cardiol 2008;51:256-60.

11. Foussas SG, Zairis MN, Patsourakos NG, et al. The impact of oral antiplatelet responsiveness on the long-term prognosis after coronary stenting. Am Heart J 2007;154:676-81.

12. Juurlink DN, Gomes T, Ko DT, et al. A population-based study of the drug interaction between proton pump inhibitors and clopidogrel. CMAJ 2009;180:713-8.

13. Ho PM, Maddox TM, Wang L, et al. Risk of adverse outcomes associated with concomitant use of clopidogrel and proton pump inhibitors following acute coronary syndrome. JAMA 2009;301:937-44.

14. Savi P, Combalbert J, Gaich C, et al. The antiaggregating activity of clopidogrel is due to a metabolic activation by the hepatic cytochrome P450-1A. Thromb Haemost 1994;72:313-7.

15. Hulot J, Bura A, Villard E, et al. Cytochrome P450 2C19 loss-of-function polymorphism is a major determinant of clopidogrel responsiveness in healthy subjects. Blood 2006;108:2244-7.

16. Lau WC, Waskell LA, Watkins PB, et al. Atorvastatin reduces the ability of clopidogrel to inhibit platelet aggregation: a new drug-drug interaction. Circulation 2003;107:32-7.

17. Lotfi A, Schweiger MJ, Giugliano GR, et al; TIMI 22 Investigators. High-dose atorvastatin does not negatively influence clinical outcomes among clopidogrel treated acute coronary syndrome patients-a Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis in Myocardial Infarction 22 (PROVE IT-TIMI 22) analysis. Am Heart J

2008;155:954-8. 18. Trenk D, Hochholzer W, Frundi D, et al. Impact

of cytochrome P450 3A4-metabolized statins on the antiplatelet effect of a 600-mg loading dose clopidogrel and on clinical outcome in patients undergoing elective coronary stent placement. Thromb Haemost 2008;99:174-81.

19. Saw J, Brennan DM, Steinhubl SR, et al; CHARISMA Investigators. Lack of evidence of a clopidogrel-statin interaction in the CHARISMA trial. J Am Coll Cardiol 2007;50:291-5.

92

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: : 212 30 98 2002- 2004. - : . () . AAH (xact Sig = 0,013 0.006). A AAH (xact Sig. = 0,907 0,770). , (xact Sig. = 0,92 0,25). AAH (xact Sig. = 0,01 0,006). : . , , , , AAH BPH. : , , . , (AAH), .

. 212 , 30 98 , 2002 2004, .

93

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(index tumor). (occular grid). ( ) ( ) H AAH , , . , . . , . : , , 15.5% . 65,5% 18,8%, . ( 1). 1.

AAH

1 >90 16 9 (56.2%) 13 (87.5%) 3 (18.7%) 2 80 -89 30 12 (40%) 29 (90.6%) 6 (20%) 3 70-79 36 11 (30.5%) 31 (86%) 9 (25%) 4 60-69 36 5 (13.8%) 25 (65.8%) 7 (19%) 5 50-59 38 2 (5.2%) 20 (58.8%) 4 (10.5%) 6 40-49 38 1(2.6%) 18 (47.3%) 3 (7.8%) 7 30-39 18 0 5 (27.7%) 1 (5.5%) Total 212 40 139 33

94

: 25% 50cc AAH AAH AAH (Exact Sig. = 0,013 0.006). ( 2) 2.

& & BPH

1 >90 9 2 (22.2%) 7 (77.7%) 2 80 -89 12 2 (16.6%) 10 (71.4%) 3 70-79 11 3 (27.7%) 7 (58.3%) 4 60-69 5 2 (33.3%) 2 (66. 6%) 5 50-59 2 0 1 6 40-49 1 0 0 7 30-39 0 0 0

. AAH, AAH (xact Sig. = 0,01 0,006). (50cc) (25-50cc) (< 25cc) . ( 3): 3.

N AAH & AAH

< 25cc 65 5 (7.7%) 2 (3%) 0 (0%) 25 -50 cc 69 12 (17.4%) 11 (15.9%) 0(0%) > 50cc 78 23 (24.5%) 20 (25,64%) 2 (100%) Total 212 40 33 2

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AAH ( ) AAH , , [10]. AAH 70-79 , , AAH (, ) . , AAH : AAH , . AAH [11] Kastendieck, [9]. , AAH [6]. AAH . , AAH . AAH , AAH

-- : Bostwick AAH - BPH. ( AAH) [12]. AAH ( 0.05) AAH . AH : [13], [14] DNA[15]. AAH . AAH , AAH .

SUMMARYCORRELATIONS AMONG ATYPICAL ADENOMATOUS HYPERPLASIA, BENIGN PROSTATE HYPERTROPHY AND HISTOLOGICAL LATENT CARCINOMA OF THE PROSTATE. Objective: To investigate the correlations among atypical adenomatous hyperplasia, latent carcinoma of the prostate, and benign prostate hyperplasia Material and Method: Data were obtained from 212 consecutive autopsy specimens of prostate gland of men above 30 and less 98 years of age who died, between August 2002 and August 2004, of diseases other than carcinoma of the prostate as clinically diagnosed. All specimens underwent whole-mount processing and complete sectioning. Results: All entities were more frequent in elderly men. Most latent cancers and AAH lesions were found in

96

large prostates; however no statistically significant relation was found between BPH and LCP (Exact Sig.= 0.92 in parametric and 0.25 in non parametric study). In contrary parametric and non parametric cross-correlations between prostate volume and AAH showed the tendency of AAH lesions to develop in larger prostates (Exact Sig. =0.013 and 0.006). No statistically significant relation was found between AAH and LCP (Exact Sig.= 0.907 and 0,770). The correlation between histological chronicle infection and atypical adenomatous hyperplasia was important but not statistically significant (Exact Sig. =0.013 in parametric and 0.006 in not parametric study) Conclusion: According to the results from our study, there doesnt seem to be any causative aetiopathogenetical or topographical relation between AAH lesions and prostate adenocarcinoma. Although well-differentiated low volume carcinomas of the TZ have been previously correlated with AAH lesions, we did not observe such relation in our relatively small sample of TZ carcinomas (12.5%). AAH lesion is a well defined mimicker of prostatic adenocarcinoma, while the reported association of AAH with carcinoma is probably an epiphenomenon. In addition, it seems that from the perspective of the practicing urologist, currently, there is not enough evidence in supporting the validity of a repeated biopsy protocol in patients with AAH lesions, although further studies are required in order to assess the need of similar recommendations. Keywords: Atypical adenomatous hyperplasia, Latent prostate cancer, Benign prostate hypertrophy, Autopsy study 1. Foster C. S., Sakr W: Exclusion f Prostate

Cancer by Pathological Assessment f Prostatic Biopsy Specimens. n: Chatelain C, Denis L, Foo K, Khoury S. Mc Connel J (editors). Benign prostatic hyperplasia. Plumdridge ltd. (distributors) Plymouth UK 2000.

2. Gleason DF. Atypical hyperplasia, benign hyperplasia and well differentiated carcinoma of the prostate Am. J. Clin Path 1985; 9: 53-67

3. Bostwick D., Srigley J., Grignon D., et al: Atypical adenomatous hyperplasia of prostate: Morphologic criteria for its distinction from well-differentiated carcinoma. Human Pathology 1993; 24: 818-832.

4. Grignon DJ, Sakr WA. Atypical adenomatous hyperplasia of prostate: a critical review. European Urology 1996;30:206-211

5. McNeal J. Morfogenesis of prostate carcinoma. Cancer 1965; 18: 1659-1666.

6. Thorson P, Humphrey PA. Minimal adenocarcinoma in prostate needle biopsy tissue. Am J Clin Pathol. 2000 Dec;114(6):896-909.

7. Cheng L, Shan A, Cheville JC, et al: Atypical adenomatous hyperplasia of the prostate: a premalignant lesion? Cancer Res 1998, 58:389-391

8. Brawn PN: Adenosis of the prostate: a dysplastic lesion that can be confused with prostate adenocarcinoma. Cancer 1982,

49:826-833 9. Kastendieck H. Correlations between atypical

primary hyperplasia and carcinoma of the prostate. Path. Res. Pract. 1980: 169; 366-387

10. Bostwick DG, Cooner WH, et al.The association of benign prostatic hyperplasia and cancer of the prostate. Cancer. 1992 1;70(1 Suppl):291-301.

11. McNeal JE. Cancer volume and site of origin of adenocarcinoma in the prostate: relationship to local and distant spread. Hum Pathol. 1992 Mar; 23(3):258-66

12. Bostwick DG: Prospective origins of prostate carcinoma: prostatic intraepithelial neoplasia and atypical adenomatous hyperplasia. Cancer 1996, 78:330-336

13. Hoda SA, Reed RJ: Morphologic characteristics of nucleoli in the differential diagnosis of well-differentiated prostatic adenocarcinoma (abstract). Am J Clin Pathol 1991, 95:271

14. Lopez-Bettran A, Pacelli A, Qian J, et al: Atypical adenomatous hyperplasia of the prostate: immunophenotype, genotype and DNA ploidy analysis. Mod Pathol 1996, 9:77A (abstract)

15. Humphrey PA, Zhu X, Crouch EC, et al: Mass-formative atypical adenomatous hyperplasia of prostate. J Urol Pathol 1998, 9:73-81

97

3.,2. , , , , , , ,.,..: , . , , . : M 2 110 , . 4 (: 75 ) . . , Doppler , . B. A, , . , . : 2 , - . , (). (), , . , , , , , [1]. Doppler [2]. , (),

, . (radial) , [3]. , , , , . , . ,

98

, [4-9]. ( , , , ) , . , , , . , 2, . ( 2004 2007), 270 . 160 2, 110 , , . (: 75 ). , . : KE > 50%, () . (< 50%) , , , . , , .

, . , . . [10]. -

140 / 90 mmHg . > 200 mg/dL > 150 mg/dL. , , DL-, - (HbA1C) , . , HbA1C, (Roche Modular Autoanalyzer, Roche Diagnostics, Milan, Italy). H bA1C (Bio-Rad, Richmond, CA, USA). . HDL- - , LDL- Friedewald. H . (..) SONOS 7500 (Philips Medical Systems, Andover, MA, USA), 1,7-3,5 MHz. Doppler (TDI). , .

99

, , . , , , [11]: () -, , , , ( ), . Simpson. : M = 0,8[ 1,04 ( + + ) 3 ( )3 ] + 0,6 g. Doppler Doppler . . Doppler : ( ) ( ) . Doppler (MPI) . [12]. . Doppler . Doppler, , , . (> 120 frames/s), . TDI

> 20, . (strain) (strain rate) RR . TDI . (off-line) (Q-Lab, Philips Medical Systems). H (Sm), (Em) (Am) , strain , (SSR) strain rate (EDSR) 12 . , . 4 mm 5 mm , 20 mm , strain strain rate. To Sm, strain SSR ( cm/s), ( %) ( s-1), , . Em EDSR ( cm/s) ( s-1) , . m ( cm/s), P . (SD). ANOVA, Students unpaired t-test Bonferroni Wilcoxon, - . 2 test Fishers test , . Moo

100

Pearson (r) Sm, . . P 0,70. SPSS 11.5, SPSS Inc., Chicago, IL, USA. P

101

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3. .

(75)

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102

, Sm, ( ) . ( Sm) . (r=-0.461, P < 0.001), (r=-0.424, P < 0.001), HbA1C (r=-0.380, P < 0.001) (r=-0.320, P < 0.001)

. , LDL (r=-0.181, P< 0.05 r=-0.158, P < 0.05, ). , HDL , , , . ,

4. .

(75)

P-value||

(+) 38 61 43 18 (-) 24 39 31 16 (mm) (+) 46,94,4 46,54,9 45,14,0 45,13,7 0,198 (-) 464,5 46,44,5 44,82,8 44,03,9 0,151 (mm)

(+) 9,71,4 10,11,4* 10,61,2 11,10,7

103

, (=-0.377, P < 0.001), HbA1C (=-0.307, P < 0.001) (=-0.244, P < 0.001) . 2 . TDI , . . , , , . -, m , . , Em . . , . , 13. . , Doppler, .

, , [13-19]. Wachter . 19 ( -, ) . U - . , . . , . . [20-23]. - TDI [24,25]. 1 . , . ,

104

. . . , . , . . . , .

, [26,27]. , . E , , . , , Doppler, 2, . , , , .

SUMMARYAbstract Aims. Previous studies indicate that diabetic patients show evidence of coexisting systolic and diastolic myocardial dysfunction when examined by new echocardiographic techniques. Yet, there is no systematic investigation of the serial age-related changes of left ventricular anatomy and function in this patient population. Methods and results. One hundred and sixty type 2 diabetic patients and 110 non-diabetic controls, all with no evidence of heart disease, were studied. The participants were stratified into four distinct agegroups (A: ,46, B: 4660, C: 6175, and D: .75 years) and underwent full echocardiographic examination. Conventional systolic and diastolic parameters were similar between the study groups. However, tissue Doppler imaging examination revealed an impaired systolic and diastolic longitudinal myocardial function in diabetic patients vs. controls, although these differences were not noticed within the youngest age-group. Diastolic dysfunction was established concomitantly in both diabetic and control subjects in age-group B. In contrast, diabetic patients showed an earlier induction of myocardial systolic dysfunction, evidenced by significantly lower average systolic longitudinal myocardial velocity in age-group B. Independent predictors of systolic myocardial dysfunction were age, glycated haemoglobin, and systemic blood pressure. Conclusion. Type 2 diabetic patients demonstrate an early and concomitant induction of systolic and diastolic myocardial dysfunction as a preclinical manifestation of diabetic cardiomyopathy.

105

1. Fang Z, Prins J, Marwick T. Diabetic

cardiomyopathy: evidence, mechanisms, and therapeutic implications. Endocr Rev 2004;25:54367.

2. Schannwell C, Schneppenheim N, Perings S, Plehn G, Strauer B. Left ventricular diastolic dysfunction as an early manifestation of diabetic cardiomyopathy. Cardiology 2002;98:339.

3. Vinereanu D, Nicolaides E, Tweddel A, Fraser A. Pure diastolic dysfunction is associated with long-axis systolic dysfunction: implications for the diagnosis and classification of heart failure. Eur J Heart Fail 2005;7: 8208.

4. Friedman N, Levitsky L, Edidin D, Vitullo D, Lacina S, Chiemmongkoltip P. Echocardiographic evidence for impaired myocardial performance in children with type I diabetes mellitus. Am J Med 1982;73:84650.

5. Mbanya JC, Sobngwi E, Mbanya D, Ngu K. Left ventricular mass and systolic function in African diabetic patients: association with microalbuminuria. Diabetes Metab 2001;27:37882.

6. Fang Z, Yuda S, Anderson V, Short L, Case C, Marwick T. Echocardiographic detection of early diabetic myocardial disease. J Am Coll Cardiol 2003;41:6117.

7. Scognamiglio R, Casara D, Avogaro A. Myocardial dysfunction and adrenergic innervation in patients with type 1 diabetes mellitus. Diabetes Nutr Metab 2000;13:3469.

8. Baum V, Levitsky L, Englander R. Abnormal cardiac function after exercise in insulin-dependent diabetic children and adolescents. Diabetes Care 1987;10:31923.

9. Zola B, Kahn J, Juni J, Vinik A. Abnormal cardiac function in diabetic patients with autonomic neuropathy in the absence of ischemic heart disease. J Clin Endocrinol Metab 1986;63:20814.

10. WHO Expert Committee on Diabetes Mellitus: second report. WHO Technical Report Series, Vol. 646. Geneva: World Health Organization; 1980. p180.

11. Schiller N, Shah P, Crawford M, De Maria A, Devereux R, Feigenbaum H et al. Recommendations for quantitation of the left ventricle by twodimensional echocardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms. J Am Soc Echocardiogr 1989;2:35867.

12. Tei C, Nishimura R, Seward J, Tajik A. Noninvasive Doppler derived myocardial performance index: correlation with simultaneous measurements of cardiac catheterization measurements. J Am Soc Echocardiogr 1997; 10:16978.

13. Liu J, Palmieri V, Roman M, Fabsitz R, Howard B, Welty T et al. The impact of diabetes on left ventricular filling pattern in normotensive and hypertensive adults: the Strong Heart Study. J Am Coll Cardiol 2001;37:19439.

14. Boyer J, Thanigaraj S, Schechtman K, Perez J. Prevalence of ventricular diastolic dysfunction in asymptomatic, normotensive patients with diabetes mellitus. Am J Cardiol 2004;93:8705.

15. Zabalgoitia M, Ismaeil M, Anderson L, Maklady F. Prevalence of diastolic dysfunction in normotensive, asymptomatic patients with well-controlled type 2

diabetes mellitus. Am J Cardiol 2001;87:3203. 16. Jain A, Avendano G, Dharamsey S, Dasmahapatra

A, Agarwal R, Reddi A et al. Left ventricular diastolic function in hypertension and role of plasma glucose and insulin. Comparison with diabetic heart. Circulation 1996;93:1396402.

17. Lee M, Gardin J, Lynch J, Smith V, Tracy R, Savage P et al. Diabetes mellitus and echocardiographic left ventricular function in free-living elderly men and women: the Cardiovascular Health Study. Am Heart J 1997;133: 3643.

18. Celentano A, Vaccaro O, Tammaro P, Galderisi M, Crivaro M, Oliviero M et al. Early abnormalities of cardiac function in non-insulin-dependent diabetes mellitus and impaired glucose tolerance. Am J Cardiol 1995; 76:1736.

19. Wachter R, Luers C, Kleta S, Griebel K, Herrmann-Lingen C, Binder L et al. Impact of diabetes on left ventricular diastolic function in patients with arterial hypertension. Eur J Heart Fail 2007;9:46976.

20. Vinereanu D, Nicolaides E, Tweddel A, Madler C, Holst B, Boden L et al. Subclinical left ventricular dysfunction in asymptomatic patients with Type II diabetes mellitus, related to serum lipids and glycated haemoglobin. Clin Sci (Lond) 2003;105:5919.

21. Andersen N, Poulsen S, Eiskjaer H, Poulsen P, Mogensen C. Decreased left ventricular longitudinal contraction in normotensive and normoalbuminuric patients with Type II diabetes mellitus: a Doppler tissue tracking and strain rate echocardiography study. Clin Sci (Lond) 2003;105:5966.

22. Fang Z, Yuda A, Anderson V, Short L, Case C, Marwick T. Echocardiographic detection of early diabetic myocardial disease. J Am Coll Cardiol 2003;41:6117.

23. Andersen N, Poulsen A, Poulsen P, Knudsen A, Helleberg K, Hansen K et al. Left ventricular dysfunction in hypertensive patients with Type 2 diabetes mellitus. Diabet Med 2005;22:121825.

24. Karamitsos T, Karvounis H, Dalamanga E, Papadopoulos C, Didangellos T, Karamitsos D et al. Early diastolic impairment of diabetic heart: the significance of right ventricle. Int J Cardiol 2007;114:21823.

25. Palmieri V, Capaldo B, Russo C, Iaccarino M, Pezzullo S, Quintavalle G. Uncomplicated type 1 diabetes and preclinical left ventricular myocardial dysfunction: insights from echocardiography and exercise cardiac performance evaluation. Diabetes Res Clin Pract 2008;79:2628.

26. Zellwegera M, Hachamovitcha R, Kanga X, Hayesa S, Friedmana J, Germanoa G et al. Prognostic relevance of symptoms versus objective evidence of coronary artery disease in diabetic patients. Eur Heart J 2004;25:54350.

27. Rajagopalan N, Miller T, Hodge D, Frye R, Gibbons R. Identifying high-risk asymptomatic diabetic patients who are candidates for screening stress single-photon emission computed tomography imaging. J Am Coll Cardiol 2005;45:439.

106

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112

SUMMARY Preoperative preparation for surgical correction of adolescent idiopathic scoliosis. Review on the occasion of the first adolescent idiopathic scoliosis surgically treated in G.H.P. Tzaneio. The indications for surgical treatment of adolescent idiopathic scoliosis are based on the natural history of the deformity and its consequences for the patient in adult life. The preoperative preparation should include a thorough history, full physical examination, imaging studies with roentgenographic computed tomography and magnetic resonance imaging of the spine, selection of the spinal levels to be fused, cardiopulmonary evaluation, autologous blood preoperative donations of the patient and peri-operative neurophysiological monitoring of his spinal cord. The aim of the treatment is correct the deformity. Key words: adolescent idiopathic scoliosis, preoperative evaluation 1. Campbells Operative Orthopaedics. Volume

two, Tenth Edition, S. Terry Canale 2003: 1757-1759, 1774-1775.

2. Dubousset J., Machida M.: melatonin: a possible role in the pathogenesis of human idiopathic scoliosis. In proceedings of the Tenth International Philip Zorab Symposium on Scoliosis, abstract 3.19, Oxford, 1998, Oxford University Press.

3. Weinstein SL., Ponseti IV.: curve progression in idiopathic scoliosis, J Bone Joint Surg 65A: 447, 1983.

4. . - , 2 . 1997: 241-248, 338-344.

5. Zaina F, Negrini S, Atanasio S: Trace (Trunk Aesthetic Clinical Evaluation), a routine clinical tool to evaluate aesthetics in scoliosis patients: development from the Aesthetic Index (AI) and repeatability, Scoliosis 2009, 4:3.

6. Grivas TB, Vasiliadis ES, Koufopoulos G, et al: Study of trunk asymmetry in normal children and adolescents, Scoliosis 2006, 1:19.

7. Cobb JR: Outline for the study of scoliosis in instructional course lectures. In The American Academy of Orthopaedic Surgeons: Instructional course lectures, vol.5, Ann Arbor, Mich, 1948, JW Edwards.

8. Nash C., Moe J.: A study of vertebral rotation, J Bone Joint Surg 51A: 223, 1969.

9. Lam GC, Hill DL, Le LH, et al: Vertebral rotation measurement: a summary and comparison of common radiographic and CT methods, Scoliosis 2008, 3:16.

10. Risser JC: The iliac apophysis: an invaluable sign in the management of scoliosis, Clin Orthop 11: 111, 1958.

11. Gelb DE, Lenke LG, Bridwell KH, et al: Spine 20: 1351, 1995.

12. . , 1994: 246, 361-365.

13. Ozturk C, Karadereler S, Ornek I, et al: The role of routine magnetic resonance imaging in

the preoperative evaluation of adolescent idiopathic scoliosis, abstract International Orthopaedics 2009.

14. Hausmann ON, Boni T, Pfirrmann CW, et al: Preoperative radiological and electrophysiological evaluation in 100 adolescent scoliosis patients, abstract, Eur Spine J. 2003 Oct;12(5):501-6.

15. Vialle R, Mary P, Harding I, et al: Surgical treatment of severe thoracic scoliosis in skeletally mature patients, abstract, Orthopedics. 2008 Mar;31(3):218.

16. Vedantam R, Lenke LG, Bridwell KH, et al: A prospective evaluation of pulmonary function in patients with adolescent idiopathic scoliosis relative to the surgical approach used for spinal arthrodesis, abstract, Spine J 2000, Vol 25, Issue 1: 82.

17. Nash CL JR, Lorig RA, Schatzinger LA, et al: Spinal cord monitoring during operative treatment of the spine, Clin Orthop 126: 100, 1977.

18. Laureau E, Marciniak B, Hebrard A, et al: Neuromonitoring and anesthesia in surgery of the spine, abstract, Neurophysiol Clin 1998 Sep;28(4):299-320.

19. Lenke LG, Betz RR, Harris J, et al: Curve typer and the criteria for structural curver and location of apex, J Bone Joint Surg 83A: 1169, 2001.

113

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114

E 2: . Melan A(x200).

3: . CKHMW (x200). , , . . ( superficial spreading melanoma), (nodular melanoma) () (acral lentiginous melanoma).5 T , , .6 3%

0,3%-0,8% .7 ( 65,5 ). , , . , , .8 .6,8 (58% ) (45% ). , . , . . , S100, HMB45, Melan A . , .6,9,10 , - . . / .11,12. , (thickness). 6,13 Li & , 2. 9,7 . , , , , FIGO.

115

, , , .6 , . , . Chung & . , , ,

. / . 5- 6,14. , , . , .

SUMMARYThe primary melanoma of the vagina is a very rare tumor associated with high risk of recurrence distant metastasis and short survival time. An 85 years old postmenopausal female patient presented with painless mass coming out of the vagina with occasional bleeding for the last 4 weeks. On vaginal examination there was a firm polypoid growth of size 5cm., attached to the left lateral wall and coming out of the introitus. Histological examination of the mass showed features of malignant melanoma . At the time of the diagnosis there was no evidence of nodal or distant metastasis. The patient was treated with colpectomy in term sept and local wide excision only. Adjuvant radio or chemotherapy did not seem to be justifiable. Key words : Female genital tract ,vagina ,malignant melanoma. 1. Churg A.F, Casey M.J, Flannery J.T, et.al :

Malignant melanoma of the vagina Report of 19 cases Obstet.Gynecol. 55:720, 1980

2. Liu L.Y,Hou Y.J, and Li J.Z : Primary malignant melanoma of the vagina. A report of seven cases Obstet. Gynecol. 70:569, 1987

3. Lee R.B , Buttoni I Jc. ,Dhru K.et.al.: Malignant melanoma of the vagina;A case report of progression from preexisting melanosis.Gynecol.Oncol,19:238, 1984: 385-387

4. Moros ML, Ferrer FP, Mitchelli MJ,et.al : Primary malignant melanoma of the vagina : poor response to radical surgery and abjuvant therapy. Eur.J Obstet.Gynecol. Reprod. Biol. 2004; 113: 248-50

5. Levers Histopathology of the skin: Malignant melanoma ,Eighth edition, Lippincott-Raven 1997,p654-679

6. Tayfun Gungor, Sunduz Ozlem Altikaya, Mustafa Ozat,et.al.: Primary Malignant Melanoma of the Femele Genital Tract.Taiwan J. Obstet. Gynecol. June 2009 Vol 48 No 2: 169-175

7. Reid GC, Schmidt RW, Robert JA, et.al.: Primary melanoma of the vagina a clinicopathologic analysis.Obstet. Gynecol. 1989;74:190-9

8. Gokaslan H, Sismanoglu A,Pekin T,et.al. :

Primary malignant melanoma of the vagina : a case report and review of the current tratament options Eur.J. Obstet. Gynecol. Reprod. Biol. 2005; 121; 243-8

9. Li Y, Li M, Wu Q, Clinical analysis of 25 cases of primary vaginal malignant melanoma Zhonghua Fu Chan Ke Za Zh, 1999;34:162-4

10. Liu L, Li X, Hong W. Primary malignant melanoma of the vagina : a report of 22 cases Zhonghua Zhong Liu Za Zh 1996;18:385-7

11. Petru E, Nagela F, Czewenka K, et al.: Primary malignant melanoma of the vagina:Long-term remission following radiation therapy.Gynecol.Oncol. 1998;70:23-6

12. Cobellis L, Calabrese E, Stefanoon B,et.al.: Malignant melanoma of the vagina : a report of 15 cases. Eur.J. Gynecol. Oncol. 2000;21:295-297

13. Miner TJ, Delgado R, Zeisler J,et.al.: Primary vaginal melanoma :a critical analysis of therapy. Ann. Surg. Oncol.

14. 2004;11:34-9 15. 14. Coleman RL. Primary vaginal melanoma : a

rare and problematic clinical entity Ann. Surg. Oncol. 2004;11:4-

16. Primary malignant melanoma of the vagina a case report.

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, - (1C). 3.1.5. 3-5D, Ca P , (Ca x P) (2D). 3.1.6. : 3-5D , ( ) (1). 3.2: -: 3.2.1. 3-5D , ( ): , , , , - ( ). 3.2.2. : 3-5D - (2). 3.2.3. : 3-5D (2). 3.2.4. :

123

( : procollagen type I C-terminal prope- ptide) ( : type I collagen cross-linked telopeptide, cross-laps, pyridinoline, deoxypyridinoline) - 3-5D (2C). 3.2.5. : 2-5D , 2-5D (1). 3.3: -: 3.3.1. , 3-5D, (2C). 3.3.2. 3-5D / (2). - ( ). 4.1: - 4.1.1. : P 3-5 (2C). 5D, P (2C). 4.1.2. : Ca 3-5D (2D). 4.1.3. : 1,25 1,50 mmol/l (2,5 3,0 mEq/l) 5D (2D). 4.1.4. : 3-5 (2D) 5D (2B). , -, ( ). 4.1.5. 3-5D , / D (1). 3-5D - , (2C) / (2C) / (2C). 4.1.6. :

3-5D. 5D, , (1C). 4.1.7. : 3-5D (2D). 4.1.8. : 3-5D (2C). 4.2: - 4.2.1. 3-5 . , (iPTH) , D (2C). : , , / D( ). 4.2.2. : D 3-5 , (2C). 4.2.3. 5D iPTH 9 (2C). , , (2C). 4.2.4. 5D , D - D - (2). - ( ). ( ). D (1). - D (2D).

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, , - (2D). iPTH , , D / (2C). 4.2.5. 3-5D () (2). 4.3: 4.3.1. 1-2 / , , (1). 4.3.2. 3 / , , (2). 4.3.3. 3 - / , (2D). 4.3.4. 4-5D - / , - - (2C). 4.3.5. 2-5D , , , (1). 5: 5.1. : Ca, P , , ( ) (1). 5.2. Ca, P ( ). : 1-3: Ca, P 6-12 , . 4: Ca, P 3-6 , 6-12 .

5: Ca, P 1-3 , 3-6 . 3-5: (. 3.2). - , ( ). 3-5 ( )(. 4.1 4.2). 5.3. 1-5, 25() D() (2C). 5.4. 1-5, D (2C). 5.5. 30 ml/min/1,73 m2, 3 (2D). 5.6. , 12 30 ml/min/1,73 m2 , D, / (2D). : -, , , , 25() D (2C). , , ( ). - 12 . 5.7. : 4-5, (2). 5.8. 4-5 , 4-5 , 4.1 4.2 (2C).

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16 2 - 5 2010, : : : 210-3244932, fax: 210-3250660, e-mail: info@16psn.gr , www.16psn.gr 3o 3 - 5 2010 Club Hotel Loutraki, : : : 210-6107213, fax: 210-6107864, e-mail: info@themateam.gr , www.themateam.gr 2 : Blood Pressure Monitoring in Cardiovascular Medicine and Therapeutics II 4 - 5 2010 "Makedonia Palace", : Praxicon : : 2310-460682, 460652, fax: 2310-435064, e-mail: info@praxicon.gr 13 4 - 6 2010 , : 2 " " 10 - 13 2010, : : PCO-Convin, . 210-6833600, email: congress@pco-convin.gr 10 - 13 2010, : - : . 2310-257128, 243588, email: info@forumcongress.com , www.forumcongress.com/6lungcancer 6th Congress of the European Association of Dermatologic Oncology 16 - 19 2010 : : 210-7257693, fax: 210-7257532, e-mail: info@eado2010.org , www.eado2010.org 12 16 - 19 2010 "Makedonia Palace", : : : 2310-889244-5, fax: 2310-889246, e-mail: diastasi@diastasitravel.gr , www.diastasitravel.com 8th International Conference of Adjuvant Therapy on Malignant Melanoma & 6th European Association of Dermato-Oncology 17 - 19 2010, : : 210-7257693, fax: 210-725732, e-mail: info@erasmus.gr , www.erasmus.gr 17 - 20 2010 "Porto Carras", : ... : E.T.S. Events & Travel Solutions, : 210-9880032, fax: 210-9881303, e-mail: ets@events.gr www.events.gr 3rd International Conference on Osteoimmunology: Interactions of the Immune and Skeletal Systems 20 - 25 2010, : http://www.aegeanconferences.org/

25 - 27 2010, : & : : 210-7210052, 7210001, fax: 210-7210051, e-mail: reception@congressworld.gr , www.congressworld.gr 26 2010 Rodos Palace : : 210-6889100, fax: 210-6844777

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3o . 1 - 3 2010 Stratos Vassilikos : : : 210-9311004-6, fax: 210-9370207 - 208, e-mail: congress@eventmakers.gr , www.eventmakers.gr 1st International Summit for Nail Diseases 2 - 4 2010, : info@nail2010.gr www.nail2010.gr 15 -18 2010, : : . 210-9311004-6, email: spapadopoulou@eventmakers.gr

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Presentation1.pdf 2 2010