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Immunological aspects of cystic echinococcosis in ERBIL
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Hadi M. A. Al-Sakee
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.
Key
words: Echinococcosis, Immune response, CD4/CD8 ratio,
ELISA
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Immunodiagnosis of Echinococcus granulosus and a comparison of techniques for diagnosis of canine
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Effect of benfotiamine on hepatic tissue levels of free calcium, copper, iron and zinc during CCl4-induced hepatotoxicity in rats
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Tavga Ahmed Aziz
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.
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Hepatotoxicity and mechanism of action of haloalkanes: Carbon tetrachloride as
a toxicological model. Crit Rev Toxicol 2003;
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1998; 39:231-239.
8. Dani C, Pasquali MA, Oliveira MR,
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Towensend DM, Tevv KD. Trace elements in human physiology and pathology. Biomed
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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.
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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.
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Copper-induced changes of non-protein thiols and antioxidant enzymes in the
marine microalga Phaeodactylum tricornutum. Plant Sci 2004; 167:
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RA, Waalker MP. Toxic Effect of Metals. In Casarett and Doull's toxicology:
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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
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31. Aziz TA,
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32. Stracke H, Hammes HP, Werkmann D,
Mavrakis K, et al. Efficacy of benfotiamine versus thiamine on function
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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
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34. Balakumar P, Ramica Sharma R, Singh
M. Benfotiamine attenuates nicotine, uric acid-induced vascular endothelial
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35. Babaei-Jadidi R, Karachalias N, Ahmed
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Sociodemographic factors of schizophrenia in Basra
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Akeel Ibrahim Saleh
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.
Conclusion: There is certain factor, the young, single, season of birth … etc have
special risk in developing schizophrenia and these should provide basis for
further studies.
Key words: Sociology, schizophrenia, Demographic
factors, Basra.
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Maastricht University Library. 29 June 2010
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global prevalence of schizophrenia". PLoS Medicine 2005, 2 (5): e151; quiz e175.
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R, Chong SA . "Psychiatric co morbidity in first episode
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of the excess mortality of schizophrenia". British
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"The lifetime risk of
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Psychical , Scand 1985, 52,320-329.
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of schizophrenia. Epidemiol Rev1995, 7, 105-156.
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equatorial study. Acta psychiat – Scand 1997, 56,143-146
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births in U.S. Arch Gen psychiatry 1997, 43, 1065-70.
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schizophrenia in Tokyo. Japan. Acta
psychiat. Scand 1997, 55, 225-232
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control study. Social psychiatry 1995 , 7, 167-179
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D.J, kaklamni, E.P. et al. Birth order,
sib ship size and Socio – Economic Factors in risk of schizophrenia in Greece.
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J.S. Birth Rank in Schizophrenia
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Obturation of internally prepared cavities (simulating internal resorption) with three different techniques
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Media A. Saeed & Raid F. Salman
Background and objectives:There is controversy as to which instrumentation and/or obturation
techniques to choose for the treatment of the internal resorption defects. This
in vitro study compared the instrumentation and obturation quality of simulated
internal resorption cavities (IRC) with 3 different techniques.
Methods:Ninety extracted human roots were used and sectioned transversely 5 mm
from the apex and hemi-circular cavities were prepared in both sections. The
sections were glued back together using superglue and embedded in plaster mold,
thus obtaining root canals with cavities simulating internal resorption. The
samples were randomly divided into 3 groups of 30 roots and instrumented by
pro-taper rotary files, hybrid technique, or step-back technique, then each
group subdivided into three subgroups of 10 roots and obturated with cold
lateral condensation, warm vertical compaction, or injectable
thermo-plasticized technique. After obturation, the samples were radio-graphed
in Bucco-lingual and Mesio-distal view. After that, the plaster molds were
removed, and the samples were then sectioned at the previous level and the
quality of the obturation of the IRC were viewed under stereomicroscope.
Results: There was
highly significant difference between pro-taper rotary files compared with
hybrid and step-back techniques. The results of obturation techniques
radiographically and by stereomicroscope showed that there was highly
significant difference in between injectable thermo-plasticized compared with
other two techniques.
Conclusion:The pro-taper rotary
files and injectable thermo-plasticized technique gave the best results for
treatment of simulated internal resorption cavities (IRC).
Key words: Dental caries, salivary flow rate, pH, saliva, microorganisms, oral
hygiene.
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. 8th 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.
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Effects of simvastatin on lipid profile, atherogenic index and serum transaminases in hyperlipidemic patients
PDF
29-33
Showan D. Husain & Ari Aziz Salih
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.
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J, Harvey A, Champe C, Fisher D. Lippincott's illustrated reviews: Pharmacology
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8. Daniel W.W. Biostatistics: A foundation for analysis in the health
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9. Ballantyne
CM: Low-density lipoproteins and risk for coronary artery disease. Am J Cardiol
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Bilheimer D, Grundy S, Brown M, Goldstein J. Mevinolin and colestipol stimulate
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11.
Schaefer E, McNamara JR, Tayler T,Daly J, Gleason J. Comparisons of effects of
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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.
23. Scott R,
Lintott C, Wilson M. Simvastatin and side effects. N Z Med 1991; 104:493-5.
24. Darioli R,
Bovet P, Brunner HR, Bercher L. Evaluation of tolerance, efficacy and safety of
3-year simvastatin use in the treatment of primary hypercholesterolaemia.
Schweiz. Med. Wochenschr 1990; 120:85-91.
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
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148(4):635-40.
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Evaluation of testosterone hormone and zinc Levels among infertile males in Kirkuk province/ Iraq
PDF
34-39
Kamaran Y. Muhammadamin & Omeed O. Darweesh & Muhammad A. Alshawni
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.
Key words: Male infertility, testosterone, serum and seminal plasma zinc.
1.
Puttemans P., Ombelet W., Brosens I.:
Reflections on the way to conduct
an investigation of subfertility. Human reproduction, 1995; 10(suppl. 1):80–9. 2.
Tielemans E, Burdorf A., Velde E, Weber R, van Kooij R and
Heederik D.: Sources of bias in studies among infertility clients. Am J Epidemiol; 2002; 156: 86. 3. Zhu JL,
Basso O, Obel C, Bille C, and Olsen J.: Infertility, infertility treatment and
congenital malformations: Danish national birth
cohort. BMJ.
2006; 30; 333(7570):679. 4.
Pizzorno J.E. (): Textbook of Natural Medicine, 1999; 2nd
edition: 1377-1387. 5.
Grahn BH, Paterson PG, Gottschall-Pass KT, Zhang
Z: Zinc and the
eye. J Am Coll Nutr; 2001; 20:106–118. 6.
Silverberg
K.M and Turner T.: Evaluation of sperm. In: Text book of reproductive
techniques, laboratory and clinical perspective. Gardner, D.K; Weissman, A.; Howles, C.M;
and Shoham, Z. Martin Dunitz
Ltd; London, 2001; 61-74. 7.
World health Organization: WHO laboratory manual for
the examination
of human semen and sperm cervical mucus interaction. 4th ed.; New York; Cambridge University
Press; 1999; 4-59. 8. Jarow JP. : Endocrine
causes of male infertility. Urol Clin North Am; 2003; 30(1):83-90. 9.
Vaidya D.: The hormonal assessment of the
infertile male. In: A Publication of the Hope Infertility Clinic. 2006; Available
at: education. vsnl.com/hic/hic.html. 10.
Idrisa A and Ojiyi E.: Pattern of infertility in
North-Eastern
Nigeria; 2000;
23:261-5. 11.
Yeboah ED, Wadhwani JM, Wilson JB.: Etiological
factors of male infertility in Africa. Int J Fertil; 1992; 37:300-7. 12.
Subhan F., Tahir F., Ahmad R. and Khan, Z.D.: Oligospermia
and its relation with hormonal profile. Pak. Med. Assoc. 1995; 45 (9), 246.
13.
Saaranen
M, Suitomaa U, Kantola M, et al. : Azoospermia and Oligozoospermia: Semen and Hormonal analysis of
patients. Professional. 2005; 12: 80-84. 14. Ali H., Baig M., Rana M.F.,
Ali M., Qasim R.,
Khem A.K. : Relationship of serum and
seminal plasma zinc levels and serum testosterone in oligospermic and azoospermic infertile
men. J Coll Physicians Surg Pak.
2005; 15(11):671-3. 15.
Mubashir
A., Bilquees B., Muhammad Sh., et al: Azoospermia &Oligospermia; semen and hormonal
analysis of patients. Professional Med J; 2005; 12(1):80-4. 16.
Bedwal R.S. and Bahuguna A.: Zinc, copper and
selenium in reproduction.
Experientia; 1994; 50:626–640. 17.
Hunt CD, Johnson PE, Herbel J, Mullen LK. : Effects
of dietary zinc depletion on
seminal volume and zinc loss, serum testosterone concentrations, and sperm morphology in young
men. Am J Clin. Nut. 1992; 56:148–157. 18.
Chia S.E., Ong C.N., Chua L.H., et al.: Comparison
of zinc concentrations in blood and seminal plasma and the various sperm parameters between
fertile and infertile men. J Androl; 2000; 21:53-7. 19.
Henkel R, Bittner J, Weber R, et al.: Relevance
of zinc in human sperm flagella and
its relation to motility. Fertil Steril; 1999; 71: 1138–1143. 20.
Mohan H, Verma J, Singh I, Mohan P, Marwah S, Singh P.: Inte-relationship
of zinc levels in serum and semen in oligospermic infertile patients and fertile males.
Indian J Pathol Microbia; 1997; 40:451-5. 21.
Koca Y, Ozdal OL, Celik M, Unal S, Balaban N. :Antioxidant
activity of seminal plasma in fertile and infertile men. Arch Androl; 2003; 49:355-9. 22. Abasalt
H. C., Eisa T. M., Mohammad
J. C.: Zinc levels in seminal plasma are associated with sperm quality
in fertile and infertile
men, Nutrition
Research, 2009; 29(2):
82-88. 23.
Tikkiwal M, Ajmera RL, Mathur NK. : Effect of zinc administration on seminal zinc and fertility
of oligospermic males. Indian
J Physiol Pharmacology; 1987; 31:30–34. 24.
Kynaston HG, Lewis-Jones DI, Lynch RV, Desmond
AD. : Changes in seminal quality following oral zinc therapy. Andrologia; 1988; 20:21-22. 25.
Omu AE, Dashti H, AlOthman S.: Treatment of
asthenospermia with
zinc sulphate: andrological, immunological and obstetric outcome. Eur J Obstet
Gynecol Reprod
Biol; 1998; 79:179–184. 26.
Aitken RJ and Clarkson JS. : Cellular basis of
defective sperm function and
its association with genesis of reactive oxygen species by human
spermatozoa. J Reprod Fertil; 1987; 81:459–469. 27.
Gavella M and Lipovac V.: In vitro effect
of zinc on oxidative changes in human semen.
Andrologia; 1998; 30:317–323. 28.
Carreras A. and Mendoza C.: Zinc levels in seminal plasma of fertile and infertile men. Andrologia; 1990; 22:279-83. 29. Minal Mankad
N. G. Sathawara, Haresh H. N., Sunil K.: Seminal plasma
zinc concentration and α-
glucosidase activity with respect to semen quality. Biological Trace Element Research,
2006; 110(2): 97-106. 30.
Fuse H, Kazama T, Ohta S, Fujiuchi Y.: Relationship between zinc concentration in seminal plasma and
various sperm parameters.
In Urol
Nephrol; 1999; 31:401-8. 12. Chia SE, Ong CN. 31.
Eggert-Kruse W, Zwick EM, Batshulat K, et al.: Are
Zinc Levels in seminal plasma associated with seminal
leukocytes and others determinants of semen quality? Fertil steril; 2002; 77:260-9. 32.
Lin YC, Chang TC, Tseng YJ, Huang FJ, Kung FT,
Chang SY. : Seminal plasma zinc levels and sperm
motion characteristics in infertile samples.
Changgeng Yi Xue Za Zhi; 2000; 23:260-6.
33. Wong
WY, Merkus HM, Thomas CM, et al.: Effects of folic acid and zinc sulfate on male factor subfertility:
a double-blind, randomized,
placebo-controlled trial. Fertil Steril.; 2002; 77:491-498.
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Comparison between continuous and intermittent phototherapy in the management of neonatal jaundice
PDF
40-44
Muyesser Abdul-Kareem
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.
1. Cremer
RJ, Perryman PW, Richards DH. Influence of light on the hyperbilirubinemia of
infants .Lancet 1958; 1:1094-1097. 2. Van Kaam AH, Van Beek RH , Vergust –van Keuleu JG ,van der Heijden J
,lutz- Dettinger N , Hop W. Fiberoptic versus conventional phototherapy for
hyperbilirubinemia in preterm infants. Eur J Peditr. 1998;157: 132-137. 3. Silva
I , Luco M , Tapia J ,Perez ME , Salinas JA , Flores J ,Villaroell. Single vs.
double phototherapy in the treatment of full –term newborn with non hemolytic
hyperbilirubinemia.J Pediatr. 2009; 85(5): 455- 458. 4. Niknafs
P. , Mortazavi AA , Torabinejad MH , Bijari BB , Niknafs N. Intermittent versus
continuous phototherapy for reducing Neonatal hyperbilirubinemia. Iran j
Pediatr 2008; 18(3): 251-256. 5. Ronald
RJ , Desandre GH , Sibley E ,et al : Neonatal jaundice and liver diseases, In
martin RJ, Fanaroff AA, Walsh MCC(ed), Fanaroff and Martin's Neonatal
–Perinatal Madicine: Disesaes of the fetus and infant. 8th ed. Philadelphia, Mosby, 2006; Pp:1419-1463. 6. Maisels
MJ ,McDonagh AF, phototherapy for neonatal jaundice. N Engl J Med. 2008;
358(9): 920-928. 7. Stanley
IP , Chung M , Kulig J. An evidence- based
review of important issues concerning
neonatal hyperbilirubinemia. Pediatr. 2004; 114(1): 130-153. 8. Maisels
MJ . Jaundice : In Avery GB ,Fletcher MA, macDonald (ed). Neonatology:
Pathology and management of the newborn .6th ed.
Philadelphia, JB Lippincott 2005; Pp: 768-835. 9. Maisels
MJ . Jaundice in a newborn contempor Pedtiatr 2005; 229(5) : 34-54. 10.
Tan KL . Phototherapy for neonatal jaundice .Clin Perinatal 1991; 18(3): 423-439. 11.
Volg TP , Hegyi T , Hiatt IM .Intermittent phototherapy in the treatment of
jaundice in the premature infant. J Pediatr 1978; 92(4): 627-630. 12.
Maurer HM.controlled trail comparing agar, intermittent phototherapy and
continuous phototherapy for reducing neonatal hyperbilirubinemia . J Pediatr
1973; 82 (1) : 73 -76. 13.
Lau SP , Fung KP. Serum bilirubin Kinetics in intermittent phototherapy of
physiological jaundice .Arch Dis Child 1984; 50 (9): 892-894. 14.
Lazar L ,Litwin A , phototherapy for neonatal non hemolytic hyperbilirubinemia:
analysis of and indication for
discontinuing therapy .Clin Pediatr 1993; 32: 264-267. 15.Bhatta
BK, Shrestha PS .A comparative study of rate of fall of total serum bilirubin
in jaundiced babies following continuous and intermittent phototherapy.Journal
of Nepal Medical Association 2003 ; 40 (2) : 260-264.
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Bacteriological study of Hospital-acquired urinary tract infections in Erbil city
PDF
45-50
Aza Bahadeen Taha
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
Key words: Urinary tract infections; Hospital-acquired; Bacteria; Susceptibility.
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, 4th 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. 3rd 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.
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A comparison of high versus low intensity transcutaneous electrical nerve stimulation for chronic pain
PDF
51-56
Diyar Hussein Tahir
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.
Methods: Thirty six patients (26 Females and 10 males with age 18 – 54 years)
were selected from patients consulting a private psychiatric clinic in Erbil
city from March 2009 to march 2010. They had chronic pain in head and neck for
more than 2 years. The cases were allocated randomly into two groups; group A
treated by the conventional TENS of high frequency 100 Hz with low intensity
current, by applying the electrical electrodes on the nucheal region (back of
neck) for 20 minutes once daily for six days, and once weekly for one month
then follow up the patients after 3 months, while in group B; the same
procedure was applied but with fixed frequency 50 Hz and high intensity current
adjusted to a tolerably painful level. The pain measured by verbal scale ranged
from 0 to 4.
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, 4th ed. Philadelphia: Butterworth-Heinemann (Elsevier); 2006.
7. Robinson AJ, Snyder-Mackler L. Clinical Electrophysiology: Electrotherapy
and Electrophysiologic Testing. 3rd 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.
16.
Thorsen SW, Lumsden SG, Trigeminal
neuralgia; sudden and long term remission with transcutaneous electrical nerve
stimulation. Physiol Ther 1997; 20: 415-9.
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Incidence of otitis media with effusion in children with adenoid hypertrophy
PDF
57-63
Farhad J. Khayat & Lana Sh. Dabbagh
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%).
Conclusion: Adenoid Hypertrophy
(AH) can be relevant in the pathogenesis of otitis media with effusion (OME)
due to its anatomic position.
Key words: Otitis media
with effusion, adenoid hypertrophy, deafness.
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