@article { author = {El Meligy, Salwa and El Batch, Manal and Abd El Alem, Ghada}, title = {Effect of Resveratrol on Dipeptidyl Peptidase-4 (DPP-4) and Phospho Enol Pyruvate Carboxy Kinase (PEPCK) in Streptozotocin -Induced Diabetic Rats}, journal = {Bulletin of Egyptian Society for Physiological Sciences}, volume = {31}, number = {1}, pages = {1-14}, year = {2011}, publisher = {Egyptian Society for Physiological Sciences}, issn = {1110-0842}, eissn = {2356-9514}, doi = {10.21608/besps.2011.35949}, abstract = {The aim of the present study was to determine the effect of resveratrol on dipeptidylpeptidase 4 (DPP-4) and phosphoenolpyruvate carboxykinase (PEPCK) enzymeactivities in streptozotocin (STZ) induced diabetic rats, trying to find an explanationfor its hypoglycemic effect. Sixty male Wistar Albino rats were included in the presentstudy and classified into three groups, group I (control,non-diabetic), group II(diabetic group),group ІІІ (diabetic rats treated with resveratrol, 5 mg/kg bodyweight/day) for 30 days. After 30 days, blood was collected for determination of;serum glucose, insulin and DPP-4 enzyme activity. The liver was excised forestimation of liver glycogen and PEPCK enzyme activity. Serum glucose, DPP-4activity, and liver PEPCK activity were significantly increased but serum insulinand liver glycogen were significantly decreased in STZ treated group, while uponresveratrol treatment , they were all reversed with no significant difference betweengroup I and group III ( except for final fasting serum glucose level). Conclusion theantihyperglycemic effect of resveratrol may be related to its stimulatory effect oninsulin ,its suppressive effect on :either DPP-4, so increases the level of incretins withsubsequent increase in insulin release followed by lowering blood glucose level ,or itsinhibitory effect on PEPCK enzyme activity and subsequent decrease ingluconeogenesis, or, finally its stimulation of glucose utilization by increasingglycogen formation.}, keywords = {}, url = {https://besps.journals.ekb.eg/article_35949.html}, eprint = {https://besps.journals.ekb.eg/article_35949_61a3e9e4564dddf5fe12cb1f7fb15e90.pdf} } @article { author = {Ali, Khitam and Sahib, Amany}, title = {Elevated Serum TNF – α and Decreased IL-6 levels in Iraqi Women with First Trimester Missed and Threatened Miscarriage Compared to Healthy Pregnancy}, journal = {Bulletin of Egyptian Society for Physiological Sciences}, volume = {31}, number = {1}, pages = {15-28}, year = {2011}, publisher = {Egyptian Society for Physiological Sciences}, issn = {1110-0842}, eissn = {2356-9514}, doi = {10.21608/besps.2011.35956}, abstract = {Objective: To measure serum tumor necrosis factor- alpha (TNF-α) and interleukin-6(IL-6) in Iraqi women with first trimester missed and threatened miscarriage andcompare their levels with those of normal pregnancy. Methods: A case control studywas conducted from November 2009 to March 2010 at Obstetric and GynecologyDepartment of Al-Yarmouk Teaching Hospital, Baghdad, Iraq. Samples wereobtained from 62 pregnant women in the first trimester: eighteen women withthreatened miscarriage (group A), 22 with missed miscarriage (group B), 22apparently healthy pregnant (group C) (positive controls) matched in age and bodymass index (BMI) and 23 non-pregnant women (group D) (negative controls). Theconcentrations of serum TNF-α and IL-6 were determined by an enzymeimmunometric assay (EIA). Results: Serum TNF-α levels in group B showed a highlysignificant increase compared to group A and D (17.68±2.90 pg/ml., 9.75±1.66pg/ml. and. 4.41±1.23 pg/ml., p=0.039 and p=0.0001 respectively). A significantdecrease in mean serum IL-6 in group B compared to group C (3.73±0.65 pg/ml.versus 6.99±1.02 pg/ml., p=0.014). No significant correlation was found betweenserum levels of TNF-α and IL-6 in all subjects. Conclusion: TNF-α might play animportant role in the process of missed and threatened miscarriage and IL-6 may bean important factor for healthy pregnancy.}, keywords = {Cytokines,TNF-α,IL-6,Missed Miscarriage,threatened miscarriage}, url = {https://besps.journals.ekb.eg/article_35956.html}, eprint = {https://besps.journals.ekb.eg/article_35956_decb61ef4fab08b1ea67052919d67064.pdf} } @article { author = {Saleem, Tahia and Abd EL-Aziz, Mohamed and El-Baz, Mona and Okda, Tarek and Abdel-Aziz, Hekmat}, title = {Galectin-3 in Repairing Damaged Mice Liver Induced By Ccl4: Role of Apoptosis and Oxidative Stress.}, journal = {Bulletin of Egyptian Society for Physiological Sciences}, volume = {31}, number = {1}, pages = {29-42}, year = {2011}, publisher = {Egyptian Society for Physiological Sciences}, issn = {1110-0842}, eissn = {2356-9514}, doi = {10.21608/besps.2011.35959}, abstract = {Background: Carbon tetrachloride (CCl4) causes hepatic injury. Galectin-3 is amember of the lectin family; several studies have suggested that Gal-3 could repairliver damage. Objective: To estimate Gal-3 expressions in different periods after CCl4administration and to explore the mechanism of repair of the injured liver by Gal-3either through modulation of apoptosis or oxidative stress. Materials and methods:Twenty male mice (age 6 weeks; weight 25-30 g) were divided into 4 groups of 5 miceeach in separate cages with free access to food and water. Group (I): Control group.Groups II, III and IV administered orally CCl4 as a single dose 50% (W/W); CCl4 inolive oil at 2 ml/kg of body weight and left for 48, 72 and 96 hours respectively. Theperiod of repair of hepatocytes injured by CCl4 and signaling proteins intrinsic tothese periods were examined. Results: A 30 kDa polypeptide was detected by bothRT-PCR and Western blot analysis using anti-galectin-3 antibody in livers from mice48 to 96 hours after administration of a single dose of CCl4 and was identified asgalectin-3 in hepatocytes. Levels of Gal-3 were significantly higher in liver of mice at48 to 72 hour after CCl4 treatment compared to the control. Its level was reduced at96 hours after CCl4 administration. Bcl-2 levels increased significantly during theexperimental period after administration of CCl4, where presented in low amount inthe control mice. Caspase-3 was detected in trace amount in control mice, increasedafter 48 and 72 hours from administration of CCl4 and then decreased gradually at96 hours. Both tissue homogenate levels of nitric oxide and lipid peroxidation showedmarked increase at 48 hours as compared to controls. Their levels decreasedgradually at 72 and 96 hours after CCl4 administration. The tissue homogenate levelsof antioxidants CAT, GSH and SOD activity of all groups were significantlydecreased at 48 hours and then increased gradually at 72 and 96 hours after CCl4administration but did not reach to normal level. Conclusion: Gal-3 plays animportant role in repairing the hepatocellular damage which occurred by CCl4through its role as anti-apoptotic agent and against free radical generation.}, keywords = {}, url = {https://besps.journals.ekb.eg/article_35959.html}, eprint = {https://besps.journals.ekb.eg/article_35959_9c9c956bbc544d6a5168148716bc375a.pdf} } @article { author = {Galal, Omyma and Awad, Effat and Taha, Amal and Mahmoud, Faten}, title = {Impact of IGF-1, GH and Oxidative Stress in the Experimental Model of Juvenile and Adult Hypothyroid Retinal Degeneration}, journal = {Bulletin of Egyptian Society for Physiological Sciences}, volume = {31}, number = {1}, pages = {43-62}, year = {2011}, publisher = {Egyptian Society for Physiological Sciences}, issn = {1110-0842}, eissn = {2356-9514}, doi = {10.21608/besps.2011.35963}, abstract = {Background: The pathophysiological mechanisms involved in hypothyroid retinaldamage are still debate. Materials and methods: To study these mechanisms, ninetysix pubs of albino rats were equally divided into three groups, control, hypothyroidmodel and thyroid supplement. Each group was separated into two juvenile and adultsubgroups that were sacrificed at day 20 and 60 postnatally respectively. Pubs inhypothyroid group their mother received 0.05mg carbimazole/day/pregnant femaleorally during gestation and 20 days of lactation in juvenile subgroup while adultsubgroup received the hypothyroid agent until day 60 postnatally. Thyroidsupplement group received antithyroid agent then treated with L-thyroxine (TH)orally (10 ug/ kg body weight) for one month. Results: A significant reduction in bodyweight, temperature, heart rate, levels of T3, T4, GH, IGF-1, and antioxidant enzymeswhile increased systolic pressure and LP products were evident in hypothyroidsubgroups associated with decreased in the thickness and degeneration of retinallayers. Thyroid supplementation group showed a partial normalization of themeasured mediators accompanied with recovery of structural changes especially injuvenile subgroup. Conclusions: Thyroid H has a vital role in normal retinal growth.Also, GH, IGF-1, oxidative stress are significant mediators of retinal degeneration.}, keywords = {}, url = {https://besps.journals.ekb.eg/article_35963.html}, eprint = {https://besps.journals.ekb.eg/article_35963_774a37c51b0f4dc318ea5f8a7e8f110d.pdf} } @article { author = {Shehata, Ahmed}, title = {Neuroprotective Effects of Methylene Blue on Scopolamine-Induced Amnesia via Anti-Cholinesterase and Anti-oxidative Activities in Adult Rat}, journal = {Bulletin of Egyptian Society for Physiological Sciences}, volume = {31}, number = {1}, pages = {63-74}, year = {2011}, publisher = {Egyptian Society for Physiological Sciences}, issn = {1110-0842}, eissn = {2356-9514}, doi = {10.21608/besps.2011.35966}, abstract = {Methylene blue (MB) is currently used to treat methemoglobinemia, a blood disorder.But because high concentrations of methylene blue were known to damage the brain,no one thought to experiment with low concentrations. The study aimed to evaluatethe possible protective effect of methylene blue against scopolamine induced- amnesiain adult rats. Methylene blue (2 and 5mg/kg, i.p.) was administered separately orconcurrently with scopolamine administration (1mg/kg, i.p). Results showed thatscopolamine induced amnesia in passive avoidance task, increased the catalyticactivity of total cholinesterase and decreased content of acetylcholine depressed thelevel of reduced glutathione (GSH) and total antioxidant activity in the hippocampusand brain cortex. Methylene blue dose-dependently inhibited the enzymatic activity oftotal cholinesterase and increased the acetylcholine content, increased GSH contentand total antioxidant activity in the hippocampus and brain cortex. Concurrenttreatment of MB dose-dependently minimized both amnesic and anti-cholinergiceffect of scopolamine. The study indicated that MB could protect against thescopolamine effects at low doses through its enhancing effect on cholinergicpathways and anti-oxidative activities. Methylene blue with its neuroprotective effectsand could thus act as disease modifiers in patients, slowing the progression ofbehavioral deterioration since acetylcholinesterases themselves could contribute tothe degenerative process.}, keywords = {Alzheimer- scopolamine- methylene blue- cholinergic system- oxidative,Stress}, url = {https://besps.journals.ekb.eg/article_35966.html}, eprint = {https://besps.journals.ekb.eg/article_35966_7ae3cf009160e4c4349351d7251088d3.pdf} } @article { author = {Hassan, Hosny and EL-Baz, Mona and Sobh, Mohammed and Abo Zaid, Hossam and Mostafa, Taha}, title = {Inflammation, Oxidative Stress and Atherosclerosis in Chronic Renal Failure Patients}, journal = {Bulletin of Egyptian Society for Physiological Sciences}, volume = {31}, number = {1}, pages = {75-91}, year = {2011}, publisher = {Egyptian Society for Physiological Sciences}, issn = {1110-0842}, eissn = {2356-9514}, doi = {10.21608/besps.2011.35970}, abstract = {Background: Accelerated atherosclerosis is the major cause of mortality in patientson chronic hemodialysis (HD). Inflammation, increased oxidative stress andendothelial activation or dysfunction might be the major factors leading to highcardiovascular mortality rate in HD patients. Also, C667T mutation ofmethylenetetrahydrofolate reductase (MTHFR) might be associated with acceleratedatherosclerosis. Aim: The present study was designed to clarify the role ofinflammation, oxidative stress parameters, endothelial activation or dysfunction andgenotyping of MTHFR enzyme which affect the level of homocysteine and theirrelation to carotid artery intima-media thickness (CIMT) as indicators ofatherosclerosis. Subjects & Methods: 44 chronic hemodialysis (HD) patients and 40healthy subjects were included in the study. Serum highly sensitive C reactive protein(hs-CRP) and IL-6 were measured as inflammatory markers, soluble vascular celladhesion molecule-1 (sVCAM-1) was measured as a marker of endothelial activationand dysfunction. Serum thiobarbituric acid reactive substances (TBARS), total nitricoxide (NO), total peroxides (TP), total antioxidant capacity (TAC) and oxidativestress index (OSI) levels were determined as oxidative stress markers. Commoncarotid intima media thickness (CC-IMT) was assessed by carotid arteryultrasonography, genotyping of MTHFR enzyme which affect the level ofhomocysteine was analyzed by PCR –RFLIP technique. Results: Chronic HD patientshad elevated levels of inflammatory markers (hs-CRP and IL-6), enhancedendothelial activation or dysfunction demonstrated by elevated VCAM-1 as comparedby healthy controls. Also, they had enhanced oxidative stress indicated by the higherlevels of NO, TBARS, TP, OSI and lower levels of TAC as compared to controls.Hemodialysis patients had significantly higher CC-IMT levels. There is a significantpositive correlation between inflammatory cytokines (hs-CRP and IL-6), and each ofTBARS, total NO, TP and OSI with CC-IMT Also, the previous parameters negativelycorrelated with TAC. There is no significant difference in the genotype of C667TMTHFR between patients and controls, but that mutation especially the TT genotypeis associated with development of atherosclerosis as indicated by the increase of CCIMT.}, keywords = {}, url = {https://besps.journals.ekb.eg/article_35970.html}, eprint = {https://besps.journals.ekb.eg/article_35970_2c7922fc6914dcdb2c90789698e5de2d.pdf} } @article { author = {Hussien, Yousry and Gharib, Amal and MD, Hanan and Karam, Rehab and Elsawy, Wael}, title = {Impact of DNA Repair Gene Polymorphisms (XPD and XRCC1) on the Risk of Breast Cancer in Egyptian Female Patients}, journal = {Bulletin of Egyptian Society for Physiological Sciences}, volume = {31}, number = {1}, pages = {91-106}, year = {2011}, publisher = {Egyptian Society for Physiological Sciences}, issn = {1110-0842}, eissn = {2356-9514}, doi = {10.21608/besps.2011.35973}, abstract = {The genes involved in DNA repair system play a crucial role in the protection againstmutations .It has been hypothesized that functional deficiencies in highly conservedDNA repair processes resulting from polymorphic variation may increase geneticsusceptibility to breast cancer. There are multiple pathways to repair the differenttypes of DNA damage and maintain genomic integrity among them is the nucleotideexcision repair (NER) and the base excision repair (BER) pathways. Aim & methods:The aim of the present study was to examine the relation between the DNA repairgene polymorphisms and breast cancer (BC) risk in Egyptian females and to analyzetheir relation to clinico-pathological parameters of BC and also to investigate thesynergistic effect of both genes on BC susceptibility . Both XPD and XRCC1polymorphisms were characterized in 100 BC Egyptian females and 100 healthywomen who had no history of any malignancy by amplification refractory mutationsystem -polymerase chain reaction (PCR) (ARMS) method and PCR with confrontingtwo-pair primers(PCR–CTPP) , using DNA from peripheral blood in a case controlstudy. RESULTS: our results revealed that the frequencies of AA genotype of XPDcodon 312 polymorphism were significantly higher in the breast cancer study patientsthan in the normal individuals(p≤0.003), and did not observe any associationbetween the XRCC1 Arg399Gln polymorphism and risk of developing breast cancerAlso, no association between both XPD Asp312Asn and XRCC1 A399Gpolymorphisms and the clinical characteristics of disease Finally ,the combinationof AA(XPD)+AG(XRCC1) were significantly associated with breast cancer risk. Inconclusion, the present results suggest that, XPD gene is an important candidategene for susceptibility to breast cancer. Also, gene–gene interaction betweenXPD(AA)+XRCC1(AG) polymorphism may be associated with increased risk ofbreast cancer in Egyptian women.}, keywords = {nucleotide excision repair,base excision repair,breast cancer,XPD,XRCC1}, url = {https://besps.journals.ekb.eg/article_35973.html}, eprint = {https://besps.journals.ekb.eg/article_35973_f6454b96a05f6441765e1b25baa6b6b0.pdf} } @article { author = {Hussien, Yousry and Gharib, Amal and Ibrahim, Hend and Abdel-Ghany, Mohamed and Elsawy, Wael}, title = {Analysis of BRCA1 and BRCA2 Mutations in Eastern Egyptian Breast Cancer Patients}, journal = {Bulletin of Egyptian Society for Physiological Sciences}, volume = {31}, number = {1}, pages = {107-116}, year = {2011}, publisher = {Egyptian Society for Physiological Sciences}, issn = {1110-0842}, eissn = {2356-9514}, doi = {10.21608/besps.2011.35974}, abstract = {Mutations in breast cancer susceptibility genes 1 and 2 (BRCA1 and BRCA2) havehigher frequency in breast cancer cases. Three founder mutations 185delAG and5382insC in BRCA1 and 6174delT in BRCA2 are frequently reported in breast cancerpatients from various ethnic backgrounds. The aim of the current study was toevaluate the frequency of the BRCA1 and BRCA2 mutations in Eastern Egyptiansporadic breast cancer patients and their relatives as possible diagnostic markers.One hundred women with sporadic breast cancer and one hundred healthy firstdegreerelatives were included in the study. Multiplex polymerase chain reactionmethod was used to analyze the DNA prepared from peripheral blood. Data analysisshowed that 185delAG mutation in BRCA1 was expressed at low frequency (3%),whereas the 5382insC in BRCA1 and 6174delT in BRCA2 were not detected withinthe Eastern Egyptian population. Conclusion: The low percentage of BRCA1 andBRCA2 mutations in apparently sporadic early- onset cancer and relatives suggestedthat mutation detection is insufficient to screen Egyptian population.}, keywords = {}, url = {https://besps.journals.ekb.eg/article_35974.html}, eprint = {https://besps.journals.ekb.eg/article_35974_69ea15d4aa27ddb3e4432c55f234d7ce.pdf} } @article { author = {Zakaria, Soha and Hamouda, Hala and Ismail, Saber and Mayah, Wael and Keder, Mahmoud}, title = {Role of Some Adipokines in Nonalcoholic Fatty Liver Diseases}, journal = {Bulletin of Egyptian Society for Physiological Sciences}, volume = {31}, number = {1}, pages = {117-134}, year = {2011}, publisher = {Egyptian Society for Physiological Sciences}, issn = {1110-0842}, eissn = {2356-9514}, doi = {10.21608/besps.2011.35975}, abstract = {Background: The prevalence of non-alcoholic fatty liver disease (NAFLD) isincreasing dramatically. It is unclear why some patients develop steatohepatitis,fibrosis and cirrhosis from steatosis, while others do not. A role for adipokines hasbeen claimed. Aim of the Study: Evaluation of serum levels of leptin, soluble leptinreceptor (sOB-R), TNF-, adiponectin and insulin resistance (IR) in cases of NAFLD,and to clarify their potential role in disease progression. Subjects and Methods: Thestudy included 60 individuals, who were divided into three equal groups; group I:Normal healthy volunteers (control subjects) with BMI (Kg/m2) of 25.2 ±2.6; groupII: Obese individuals with fatty infiltration of the liver and having normal liverfunctions and BMI of 31.8±1.1. Group III: Obese individuals with elevated liverfunctions and BMI of 32.7 ± 1.4. All groups were subjected to estimation of liverfunction tests, lipid profile, fasting blood glucose level, HBsAg, HCVAb andevaluation of body mass index (BMI). Serum levels of insulin, leptin, soluble leptinreceptor (sOB-R), TNF -, and adiponectin were measured in all groups using ELISAtechnique. IR was estimated by homeostasis model assessment index ratio (HOMAIR).Results: Serum triglycerides, insulin and HOMA-IR were significantly increasedin the patients’ groups, when compared to the control group. Serum levels of ALT,AST, leptin and TNF- were significantly increased, while sOB-R and serumadiponectin levels were significantly decreased in group III compared to groups I andII. Serum leptin and TNF- levels were positively correlated with BMI and HOMA-IRin groups II & III and with serum ALT and AST enzyme activity in group III, while,sOB-R levels were negatively correlated with serum leptin, TNF-, BMI and HOMAIRin both patients’ groups and with ALT and AST enzyme activity in group III. Onthe contrary, serum adiponectin levels were negatively correlated with BMI andHOMA-IR, serum leptin and TNF- levels in groups II & III and with both ALT andAST enzyme activity in group III. Conclusion: Measurement of serum TNF-, serumleptin and/or adiponectin may be helpful biochemical markers of NAFLD,particularly when serum AST and ALT are within normal limits.}, keywords = {Nonalcoholic fatty liver disease (NAFLD),soluble leptin receptor (sOBR),homeostasis model assessment index ratio (HOMA-IR)}, url = {https://besps.journals.ekb.eg/article_35975.html}, eprint = {https://besps.journals.ekb.eg/article_35975_a1cf810a34f986faf6dbe1baf2021487.pdf} } @article { author = {Shehata, Ahmed}, title = {Neurophysiological Studies on the Effect of Acetone on Pentylenetetrazole-Induced Seizure in Rats}, journal = {Bulletin of Egyptian Society for Physiological Sciences}, volume = {31}, number = {1}, pages = {135-146}, year = {2011}, publisher = {Egyptian Society for Physiological Sciences}, issn = {1110-0842}, eissn = {2356-9514}, doi = {10.21608/besps.2011.35976}, abstract = {Recent interest in the anticonvulsant effects of acetone has stemmed from studiesrelated to the ketogenic diet (KD). Despite knowledge of acetone's anticonvulsantproperties, the neurochemical basis for this effect is not well known. The presentstudy aimed to explore the neurochemical basis underlying the anticonvulsant effectof acetone in pentylenetetrazol (PTZ) - induced convulsions. This was achievedthrough determining the neurochemical changes of acetone in pentylenetetrazol(PTZ) – treated rats. Male adult rats received either saline, acetone (15 m mol/kgi.p.), PTZ (60 mg/kg, i.p.), or acetone 3 h before PTZ injection. Result showed that themaximum concentration of acetone reached about 3 h after acetone administration.Thus, the animals were administered pentylentetrazole three hours after acetonetreatment. Pentylenetetrazole treated rats exhibited epilepsy, increased brain levels ofexcitatory amino acids (glutamate and aspartic acids) and decreased levels ofinhibitory amino acid (γ-aminobutyric acid and glycine). In addition,pentylenetetrazole treatment decreased total antioxidant activity and reducedglutathione (GSH) in brain. Acetone pretreatment remarkably decreased seizureincidence rate and increased seizure latency. Moreover, acetone significantlyminimized the disturbing effect of pentylenetetrazole on the redox status and thebalance between excitatory and inhibitory amino acids. The study indicated that theepilepsy might be mediated, at least partially, through the disturbance in the redoxstatus and imbalance between excitatory and inhibitory amino acids in the brain.Moreover, the study indicated that the antiepileptic effect of acetone might be due toits antioxidant effect and sustaining the balance between excitatory and inhibitoryamino acids. Moreover, the study might recommend the concurrent intake ofketogenic diets with the conventional antiepileptic drugs. In addition, synthesizingnew chemical entities yielding acetone during its metabolism in the body mightprovide new candidates as antiepileptic drugs.}, keywords = {}, url = {https://besps.journals.ekb.eg/article_35976.html}, eprint = {https://besps.journals.ekb.eg/article_35976_b172bbf53d13f12bd0764a575afaff93.pdf} } @article { author = {Hamouda, Hala and Abd-Allah, Ahmed and Abd El Alem, Ghada and El-Deeb, Omnia and El-Desoky, Kareema}, title = {Effect of Melatonin on some Inflammatory Markers in L-arginine Induced acute Pancreatitis in Rats}, journal = {Bulletin of Egyptian Society for Physiological Sciences}, volume = {31}, number = {1}, pages = {147-164}, year = {2011}, publisher = {Egyptian Society for Physiological Sciences}, issn = {1110-0842}, eissn = {2356-9514}, doi = {10.21608/besps.2011.35978}, abstract = {Objective: Acute pancreatitis is an inflammatory disease of the pancreas resulting insignificant morbidity and mortality, due to distant organ failure. Melatonin exertscomplex physiological and pharmacological effects on multiple systems and organs.Aim of the study: The present study was designed to investigate the effects ofmelatonin pre- and post-treatment with L-arginine (L-Arg.) on some inflammatorymarkers in acute pancreatitis in rats. Materials and methods: The present study wascarried out on 75 white albino rats which were randomly classified into five equalgroups; group I (control group); group II (L-arginine injected group); group III(melatonin pre-treatment with L-arginine); group IV (melatonin post-treatment withL-arginine) and group V (melatonin injected group). All groups were subjected tomeasurements of serum amylase and lipase activities; total antioxidant capacity (TAC)levels, serum and tissue TNF α levels; MPO and PON1 enzymes activities, in additionto histopathological examination of all pancreatic specimens. Results: L-arginineinjected group showed severe necrotizing pancreatitis confirmed by histopathologicalchanges and significant elevations in serum amylase and lipase activities relative tothe control values. Also, significant increase of serum TAC, serum and tissue TNF-αlevels and MPO enzyme activity and significant decrease of PON-1 enzyme activitywere detected in L-arginine injected group as compared to control group. Inmelatonin injected groups, either pre- or post- treatment with L-arginine, serumamylase and lipase activities and both serum and tissue TNF-α levels, MPO activitywere significantly decreased in both groups with significantly lower levels in ratsgiven melatonin pre- treatment with L-arginine. Also, significant increase of bothserum and tissue PON-1 were found in both groups. Conclusion: These data mightconfirm the protective effect of melatonin as an antioxidant in acute pancreatitis.}, keywords = {Acute pancreatitis (AP),tissue tumor necrosis α (TNF α),myeloperoxidase (MPO),paraoxonase-1 (PON-1)}, url = {https://besps.journals.ekb.eg/article_35978.html}, eprint = {https://besps.journals.ekb.eg/article_35978_d0c581b6a8bb23c64968ac3467ed4b29.pdf} } @article { author = {Badr, Eman and Safan, Manal and Hadhoud, Mahmoud}, title = {A Study of Apolipoprotein E (Apo E) Gene Polymorphisms in Chronic Spinal Cord Compression and their Relation with Cervical Spondylotic Myelopathy}, journal = {Bulletin of Egyptian Society for Physiological Sciences}, volume = {31}, number = {1}, pages = {165-178}, year = {2011}, publisher = {Egyptian Society for Physiological Sciences}, issn = {1110-0842}, eissn = {2356-9514}, doi = {10.21608/besps.2011.35979}, abstract = {Object: Cervical spondylotic myelopathy is a common disease of multifactorial originin which neural and vascular processes contribute to the final neurological damage.Apolipoprotein (Apo) E is a multifunctional protein with central roles in lipidmetabolism and neurobiology. The aim of present study is to determine the possiblerelationship of polymorphisms of apolipoprotein E (Apo E) gene with occurrence ofcervical spondylotic myelopathy (CSM) in spinal cord compression patients.Methods: The present study was carried out on 60 consecutive patients (34 men, 26women), with spinal cord compression who underwent anterior microsurgicaldecompression. The studied subjects were classified into two groups: Group (I): Itincluded 32 patients with chronic spinal cord compression without cervicalspondylotic myelopathy (18 males and 14 females), Group (II): It included 28patients with chronic spinal cord compression with cervical spondylotic myelopathy(16 males and 12 females). Neurological deficits were classified according to themodified Japanese Orthopedic Association Scale. All studied persons were subjectedto full history taking, general clinical examination, MRI and laboratory investigationsincluding ApoE genotyping which was carried out by isolation of DNA from venousblood samples. The APOE genotypes were determined by polymerase chain reactionfollowed by restriction enzyme digestion (PCR-RFLP) analysis followed by agarosegel electrophoresis of digested fragments. Results: The results of the present studyshowed a significant increase in group II when compared to group I as regarding theage (P<0.05), duration of symptoms (P<0.001), number of affected segments(P<0.001) and a significant decrease in the diameter of spinal canal (P< 0.001),whereas no significant difference regarding gender. On comparing the two studiedgroups a significant difference was found as regards apolipoprotein E genotypedistribution with increased frequency of the E4 genotype in group II, the E4 allelewas significantly increased in patients with CSM when compared with the othergroup without CSM, whereas no significant differences in the distribution of E2 andE3 alleles. The odds ratio for E4 allele was 3.2 (95% CI: 1.3-9.8). Multiple regressionanalysis revealed that duration of symptoms, number of affected segments anddiameter of spinal canal are independent risk factors for CSM. Conclusions: It couldbe concluded that E4 polymorphism of the ApoE gene is associated with thesusceptibility to CSM in spinal cord compression and that, longer duration ofsymptoms, smaller diameter of spinal canal and more number of affected segments  are risk factors for such complication. The presence of the ApoE E4 allele is anindependent predictor for presence of CSM. Further studies are needed to evaluatethe type of ApoE polymorphism in patient with improvement or no improvement aftersurgery.}, keywords = {cervical spondylotic myelopathy,apolipoprotein E,apolipoprotein E polymorphism,spinal cord compression}, url = {https://besps.journals.ekb.eg/article_35979.html}, eprint = {https://besps.journals.ekb.eg/article_35979_1b8cbdc92cf9d0f09dfb54b937153e8a.pdf} } @article { author = {Mostafa, Samia and Obaia, Eman and Abd El Aziz, Ghada and Fathi, Marwa and laz, Nabila}, title = {Surfactant Protein D and C-Reactive Protein as serum biomarkers in Chronic Obstructive Pulmonary Disease}, journal = {Bulletin of Egyptian Society for Physiological Sciences}, volume = {31}, number = {1}, pages = {179-194}, year = {2011}, publisher = {Egyptian Society for Physiological Sciences}, issn = {1110-0842}, eissn = {2356-9514}, doi = {10.21608/besps.2011.35980}, abstract = {Introduction: With the growing awareness of COPD as a systemic disease, there hasbeen a shift in the focus of biomarker discovery away from lung sources and towardblood specimens. Aim of Work: The aim of the present work was to evaluate theutility of serum SP-D compared to serum CRP as biomarkers in tracking diseaseprogression of COPD and to assess the effect of smoking and inhaled steroid on theirlevels. Subjects and Methods: Seventy subjects were enrolled in this study dividedinto 2 main groups: healthy control group (30 subjects) and COPD patients' group(40 subjects).Serum SP-D and serum CRP were measured using enzyme linkedimmunsorpent assay method (ELISA). Results: revealed that COPD is associatedwith significant higher levels of both serum SP-D and CRP, while smoking isassociated with significant higher levels of SP-D only. On the other hand, inhaledsteroid is associated with significant lower serum levels of both SP-D and CRP. Inaddition, serum SP-D levels correlate positively with the severity of COPD diseasewhile CRP levels showed no significant correlation with severity of the disease.Conclusion: These results empower the sensitivity of both markers in diagnosis ofCOPD and in following the response of the patients to steroid therapy. On the otherhand, results suggest that SP-D is more accurate than CRP as serum biomarker intracking disease progression of COPD patients.}, keywords = {COPD,Surfactant protein D,C reactive protein,biomarker,Inhaled Steroid,Smoking}, url = {https://besps.journals.ekb.eg/article_35980.html}, eprint = {https://besps.journals.ekb.eg/article_35980_f0489c5d3c14a6a9b5eca2b2b0222dc9.pdf} } @article { author = {Salem, Dawlat and Obaia, Eman and Abd El Aziz, Ghada and El Abedeen, Eman}, title = {Oxidative Stress Increases Activin A Secretion in Pregnancy Hypertensive States}, journal = {Bulletin of Egyptian Society for Physiological Sciences}, volume = {31}, number = {1}, pages = {195-210}, year = {2011}, publisher = {Egyptian Society for Physiological Sciences}, issn = {1110-0842}, eissn = {2356-9514}, doi = {10.21608/besps.2011.35981}, abstract = {Introduction: Activin A is a glycoprotein hormone produced by many tissues. Duringnormal pregnancy the fetoplacental unit is the main source of activin A with theplacenta producing the majority of secreted activin A. Oxidative stress may be theunderlying mechanism for increased placental activin A production in preeclampsia.Aim of Work: To evaluate the levels of activin A and malondialdehyde (MDA) inpregnancy hypertensive states and to explore whether circulating levels of activin Aare correlated to MDA levels (marker of oxidative stress). Subjects and Methods:The study included 75 pregnant women divided into three groups: 25 pregnantwomen with normal blood pressure (group1 as control), 25 pregnant women withpregnancy induced hypertension (PIH) (groupII) and 25 pregnant women withpreeclampsia (groupIII). Serm levels of activin A and malondialdehyde (MDA) weremeasured by ELISA and by colorimetric methods respectively. Results: Serum levelsof activin A and malondialdehyde were higher in patients with preeclampsia than inpatients with pregnancy induced hypertension and that of control group. There was ahighly significant correlation between serum levels of activin A and each ofmalondialdehyde and blood pressure in preeclampsia group and PIH group.Conclusion: Serum levels of activin A might be used as a marker that reflects theseverity of pregnancy hypertensive states. Oxidative stress might be the mechanism ofincreased secretion of activin A.}, keywords = {preeclampsia,Oxidative Stress,Activin A}, url = {https://besps.journals.ekb.eg/article_35981.html}, eprint = {https://besps.journals.ekb.eg/article_35981_6191e1980bd46237f1d2ca0e856662c5.pdf} } @article { author = {Kamal, Manal and Hassan, Asmaa}, title = {Impact of Insulin - Induced Hypoglycemia on some Plasma Markers of Skeletal Muscles and Heart Damage in Adult Male Rats: Relation to Oxidative Stress and Plasma Epinephrine}, journal = {Bulletin of Egyptian Society for Physiological Sciences}, volume = {31}, number = {1}, pages = {211-224}, year = {2011}, publisher = {Egyptian Society for Physiological Sciences}, issn = {1110-0842}, eissn = {2356-9514}, doi = {10.21608/besps.2011.35983}, abstract = {Objective: Hypoglycemic damage to the central nervous system is well knowncomplication of insulin therapy. Little is known about the effect of insulin inducedhypoglycemia on peripheral tissues as skeletal muscles and heart. In the presentstudy the effect of acute and recurrent insulin- induced hypoglycemia on plasmacreatine kinase (CK) and Lactate dehydrogenase (LDH); markers of skeletal musclesand heart damage was studied. Oxidative stress in those tissues and plasmaepinephrine levels after hypoglycemia were also evaluated to elucidate themechanism of hypoglycemic effect on those tissues. Methods: The study consisted of50 adult male rats divided into three groups: (1) Control group. (2) Acute insulininducedhypoglycemia group (AHG): injected with human insulin (humulin)intraperitoneal (ip) in a dose of 10 U/kg, food was then withheld for 6 hours. (3)Recurrent insulin-induced hypoglycemia group (RHG): received recurrent ipinjection with 10 U/kg humulin once per day for three consecutive days, food is givenafter 2 hours and in the fourth day they received the same dose of insulin, then foodwas withheld for 6 hours. Blood glucose was measured before and 30, 60, 90 and 120min after the injection. Plasma levels of CK, LDH were estimated before and 6 hoursafter the injection. Epinephrine levels were measured before and 90 min after theinjection. Animals were sacrificed by decapitation 6 h after the injection formeasurement of malondialdehyde (MDA) and total antioxidant capacity (T-AOC) inskeletal muscle and heart tissue homogenate. Results: it was found that acute andrecurrent insulin induced hypoglycemia caused elevated levels of plasma CK, LDH,increase lipid peroxidations (MDA) together with decrease in T-AOC in skeletalmuscle and heart tissue homogenate. The plasma epinephrine levels in response tohypoglycemia were significantly more in AHG group and RHG group at day 1 thancontrol. It was also demonstrated that recurrent insulin induced hypoglycemiaresulted in more increase in the levels of plasma CK, LDH and MDA with moredecrease in T-AOC and blood glucose levels compared to acute insulin hypoglycemiarats. There was also revealed lower epinephrine levels in response to recurrenthypoglycemia at day 4 compared to control.Conclusions: our findings indicate that acute and recurrent insulin inducedhypoglycemia caused skeletal muscle and heart damage. This damage may beattributed to increased oxidative stress revealed in those tissues. This damaging effect  is more following recurrent hypoglycemia which may be related to the lowerepinephrine levels in response to recurrent hypoglycemia detected in this group. Thatresulted in more decrease in blood glucose and therefore more damaging effects tothose tissues.}, keywords = {}, url = {https://besps.journals.ekb.eg/article_35983.html}, eprint = {https://besps.journals.ekb.eg/article_35983_4a3e4e155f6bdc3388778669106784e3.pdf} } @article { author = {Ahmed, Marwa and ELosaily, Gehan}, title = {Role of Oxytocin in Deceleration of Early Atherosclerotic Inflammatory Processes in Adult Male Rats}, journal = {Bulletin of Egyptian Society for Physiological Sciences}, volume = {31}, number = {1}, pages = {225-238}, year = {2011}, publisher = {Egyptian Society for Physiological Sciences}, issn = {1110-0842}, eissn = {2356-9514}, doi = {10.21608/besps.2011.35984}, abstract = {Objective: The study aimed to examine the effect of exogenous OT administration onthe inflammation and atherosclerosis in adult male rats and its possible mechanisms.Thirty adult male rats equally divided into three groups .Control group fed regulardiet; group II fed control diet supplemented with L-methionine for 10 weeks. GroupIII received L-methionine and oxytocin treatment for 10 weeks. RT-PCR analysisshowed that OT administration increased oxytocin receptor mRNA (2 fold, P,0.05).Blood samples were evaluated for total homocysteine, interlukin-6(IL-6),monocytechemoatrratant protein-1 (MCP-1) and C-reactive protein (CRP) by ELIZA. lipidprofile, nitric oxide (NO), malondialdehyde (MDA) and reduced glutathione (GSH)were determined. Specimens from aorta were processed for immunohistochemicalstaining for Aorta nuclear factor _B (NF-_κB) p65 protein. Result showed that OTadministration to group III decreased the plasma levels IL-6, MCP-1and CRP levelswhich were elevated in group II. Moreover, there was decrease of the oxidative stressof group III in terms of increased plasma levels of NO and GSH and decreasedplasma levels of MDA in blood. In addition, rats of group II showed histologicalabnormalities manifested by thickening and ulceration of the aortic wall. Markedincreased expression of NF-_κB in aorta of in group II was detected. However, OTadministration restores the histological structure of the aorta and decreased theexpression of NF-_κB in aorta of group III similar to the control group.Conclusion: OT has anti inflammatory pathway in atherosclerosis as it deceleratesatherosclerosis by decreasing the proinflammatory responses through manymechanisms, mainly the up regulation of its receptors.}, keywords = {oxytocin – atherosclerosis – inflammation- methionine}, url = {https://besps.journals.ekb.eg/article_35984.html}, eprint = {https://besps.journals.ekb.eg/article_35984_92b753b3e2c11f73d25dc399bbded0af.pdf} } @article { author = {Bendary, M.}, title = {A study on the effect of Chromium Administration on the Altered Urinary Bladder Reactivity in Experimentally-induced Diabetic Rats}, journal = {Bulletin of Egyptian Society for Physiological Sciences}, volume = {31}, number = {1}, pages = {239-260}, year = {2011}, publisher = {Egyptian Society for Physiological Sciences}, issn = {1110-0842}, eissn = {2356-9514}, doi = {10.21608/besps.2011.35985}, abstract = {Diabetic-induced urinary bladder dysfunction (diabetic cystopathy) is among themost common complications of chronic uncontrolled diabetes mellitus. Thiscystopathy, involves altered urinary bladder contractility and reactivity, is suggestedto be due to the oxidative stress encountered in diabetes. Chromium, an antioxidantmicronutrient, is proposed nowadays as an adjuvant in some diabetic complications.Accordingly, this study was designed to evaluate the possible role of oral chromiumadministration on the altered urinary bladder reactivity in experimentally-induceddiabetic rats. In the present study, 36 adult male albino rats, weighing 150-180 gmeach, were used. They were divided into 6 equal groups. Group1 (Control group),Group2 (Cr-treated control group), Group3 (untreated diabetic group), Group4(Insulin-treated diabetic group), Group5 (Cr-treated diabetic group) and Group6(Concomitantly insulin & Cr-treated diabetic group). Fasting serum glucose, seruminsulin, homeostatic model assessment to detect insulin resistance (HOMA-IR index),lipid profile, urinary bladder tissue malondialdehyde (MDA) (a tissue marker ofoxidative stress and lipid peroxidation) and glutathione (GSH) (as an index of thetissue antioxidant enzyme defense activity) were measured. In addition, the total bodyweight, urinary bladder weight and the reactivity of isolated urinary bladder strips tocarbachol (Cch) were determined. The untreated diabetic group exhibited significantincrease of the serum glucose, HOMA-IR index, lipid profile, bladder tissue MDA andurinary bladder weight, (p<0.05) together with a significant decrease (p<0.05)ofserum insulin, total body weight and bladder tissue GSH level. In addition, thecontractile response of the isolated urinary bladder strips to Cch was significantlyhigher in untreated diabetic rats relative to the other tested groups, (p<0.05).Interestingly, when the diabetic rats were treated with subtherapeutic doses of insulinalone or oral chromium alone, a significant improvement (p<0.05) of all the alteredparameters was obtained. However, when the diabetic rats were administeredconcomitantly with insulin & chromium, a highly significant improvement (p<0.001)of the deteriorated parameters that have been returned nearly close to the controllevel. In conclusion, oral chromium administration has a beneficial effect inameliorating the changes in the urinary bladder reactivity in experimentally-induceddiabetic rats, probably through its antioxidant effect and its ability in increasinginsulin sensitivity.}, keywords = {}, url = {https://besps.journals.ekb.eg/article_35985.html}, eprint = {https://besps.journals.ekb.eg/article_35985_3822a4c2e2556e57a574b96d194e4b3f.pdf} } @article { author = {Shaker, Olfat and El-Demery, Ahmed and El Nemr, Mohamed and Desoky, Ahmed}, title = {Molecular Detection of Mutated Factor V (Leiden) and Factor XIII in Ischemic Heart Disease}, journal = {Bulletin of Egyptian Society for Physiological Sciences}, volume = {31}, number = {1}, pages = {261-270}, year = {2011}, publisher = {Egyptian Society for Physiological Sciences}, issn = {1110-0842}, eissn = {2356-9514}, doi = {10.21608/besps.2011.35987}, abstract = {The present work was performed to evaluate the incidence of gene mutation affectingfactor V Leiden (FVL) &factor XIII in cases of myocardial ischemia. Thirty cases ofmyocardial ischemia as well as ten age and sex matched healthy subjects wereincluded in the study. DNA was extracted from blood samples drawn from all subjectsincluded in the study and was subjected to PCR amplification for factors V (Leiden)and factor XIII genes, using biotinylated specific primers. The PCR products werehybridized using strip containing immobilized allele-specific oligonucliotide probe.The products of hybridization were visualized using striptavidin-alkaline pH andcolor substrate. LDL-c was significantly higher in heterozygous factor V leiden Theresults of the study showed that heterozygous mutations involving factor V Leidencases were in a positive correlation with LDL-c results and homozygous mutationsinvolving factor XIII cases showed a positive correlation with AST changes. Theseresults gave an idea about the mutational changes involving factors V Leiden andXIII and may be considered as risk factors for the incidence of myocardial infarction.}, keywords = {}, url = {https://besps.journals.ekb.eg/article_35987.html}, eprint = {https://besps.journals.ekb.eg/article_35987_9a20f5f85c9af59c77713e7799f1002c.pdf} } @article { author = {Abdel-Hafez, Mohamed and Ahmed, Hanan and Mostafa, Hebatallah and Marzouk, Samar and Ahmed, Marwa}, title = {Atrial Natriuretic Peptide and Leptin in Obesity-associated Hypertension in Middle-aged Egyptian Women}, journal = {Bulletin of Egyptian Society for Physiological Sciences}, volume = {31}, number = {1}, pages = {271-284}, year = {2011}, publisher = {Egyptian Society for Physiological Sciences}, issn = {1110-0842}, eissn = {2356-9514}, doi = {10.21608/besps.2011.35988}, abstract = {Obesity is a world-wide health problem, whose incidence and prevalence are risingsteadily; it may be combined with hypertension, diabetes, dyslipidemia,atherosclerosis, and/or chronic renal failure. Among these, hypertension has beenobserved in roughly 50% of obese individuals, which has led researchers to considerobesity as one of the most common causes of hypertension. The mechanisms linkingobesity to hypertension have not been fully cleared. The present study aimed to clarifythe interaction of leptin, soluble leptin receptors and the atrial natriuretic peptide inobese hypertensive patients. The study was performed on seventy five female subjectswho were classified into three groups: group I (n=15) healthy lean controls, group II(n=30) obese normotensive patients, and group III (n=30) obese hypertensivepatients. All participants were subjected to a thorough clinical assessment, andestimation of serum levels of glucose, creatinine, urea, cholesterol, leptin, solubleleptin receptors (sLR), and atrial natriuretic peptide (ANP). The serum levels of leptinand ANP were significantly higher in obese hypertensive and obese normotensivepatients than in the controls, also, these levels were significantly higher in obesehypertensive patients when compared to obese normotensive patients. The serum sLRlevel in obese hypertensive and obese normotensive patients was significantly lowerthan in the controls, while its level in obese hypertensive patients was significantlylower than in obese normotensive patients. In the whole studied groups, the serumleptin and ANP levels were positively correlated, significantly, with BMI, diastolicblood pressure, and systolic blood pressure, but their levels were negativelycorrelated significantly with sLR. The serum sLR level was, significantly, negativelycorrelated with BMI, diastolic blood pressure, systolic blood pressure, leptin andANP.}, keywords = {atrial natriuretic peptide,leptin,soluble leptin receptor,Obesity,Hypertension}, url = {https://besps.journals.ekb.eg/article_35988.html}, eprint = {https://besps.journals.ekb.eg/article_35988_d71c4e60701b65f20f32ef17731775cb.pdf} } @article { author = {Tahoon, Nahid and Zineldeen, Doaa and El-Desuky, Karima}, title = {Urotensin II in the Pathogenesis of Atherosclerosis in Cholesterol Fed Rats}, journal = {Bulletin of Egyptian Society for Physiological Sciences}, volume = {31}, number = {1}, pages = {285-296}, year = {2011}, publisher = {Egyptian Society for Physiological Sciences}, issn = {1110-0842}, eissn = {2356-9514}, doi = {10.21608/besps.2011.35990}, abstract = {Background: Atherosclerosis is the most common cause of ischemic heart diseases.Urotensin II is the most potent vasoactive peptide discovered to date with potencythat overcomes that of angiotensin II, endothelin-1, serotonin and thromboxan A2.Aim: This study was undertaken to evaluate the role of exogenous urotensin II in thepathogenesis of atherosclerosis and the effect of blocking the endogenous urotensinII. Material and Methods: 32 male wistar rat were divided into 2 groups, normalcontrol group (8 rats) and cholesterol rich diet group (24 rats).The latter is furtherlysubdivided into vehicle, urotensin II and palosuran groups (each is 8 rats). In allthese groups lipid profile, some inflammatory and atherosclerotic markers weremeasured. Histopathological examination of tissue samples from aorta andcoronaries for atheromatous changes was also done in all groups. Results: UrotensinII produced significant hyperlipidemia, increased CRP and SVACM-1 and decreasedNO. Foam cells and VSMC proliferation were evident histopathological findings. Theeffect of urotensin II was partially reversed by palosuran. Conclusion: urotensin II isan important mediator in the pathogenesis of atherosclerosis in hypercholesterolemicmodel. Urotensin receptor blocker may be considered as an important therapeutictarget in atherosclerosis.}, keywords = {}, url = {https://besps.journals.ekb.eg/article_35990.html}, eprint = {https://besps.journals.ekb.eg/article_35990_5c704dc61cab04aa4ddc3772cab5e575.pdf} }