Cigdem Yenisey

Adnan Menderes University, Güsel Hissar, Aydın, Turkey

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Publications (84)134.45 Total impact

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    ABSTRACT: The aim of this study was to investigate the antibacterial, anti-inflammatory, and antioxidant activities and probable toxic effects of Aloe vera (AV) in a rat peritonitis model.
    Indian journal of pharmacology. 05/2014; 46(3):322-7.
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    ABSTRACT: Lithium (Li) and lamotrigine (LTG) have neuroprotective properties. However, the exact therapeutic mechanisms of these drugs have not been well understood. We investigated the antioxidant properties of Li (40 and 80 mg/kg/day) and LTG (20 and 40 mg/kg/day) in a rat model of global cerebral ischemia based on permanent bilateral occlusion of the common carotid arteries (BCAO). Nitric oxide (NO), malondialdehyde (MDA), glutathione (GSH), glutathione reductase (GSH-R), catalase (CAT) and superoxide dismutase (SOD) levels were measured as an indicator of oxidative-nitrosative stress in both prefrontal cortex (PFC) and hippocampus after 28 days of treatment. The spatial learning disability was also assessed at the end of the study by Morris water maze (MWM) test. All oxidative-nitrosative parameters were found to be higher in the groups under treatment than in sham. Both drugs caused a decrease in PFC NO and MDA elevation, meanwhile the increase in GSH, GSH-R, CAT and SOD levels was significantly more evident in treated groups. We also found higher PFC GSH-R and hippocampal SOD levels in BCAO + Li (80 mg/day) treated group when compared with BCAO + LTG 40 mg/day. MWM test data showed a similar increase in spatial learning ability in all groups under treatment. We found no other statistical difference in comparison of treated groups with different dosages. Our findings suggested that Li and LTG treatments may decrease spatial learning memory deficits accompanied by lower oxidative-nitrosative stress in global cerebral ischemia. Both drugs may have potential benefits for the treatment of vascular dementia in clinical practice.
    Neurochemical Research 03/2014; · 2.13 Impact Factor
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    ABSTRACT: Background Bronchopulmonary dysplasia (BPD) is a chronic lung disease that causes significant morbidity and mortality in premature infants. Inflammation and oxidative injury play an important role in the pathogenesis of BPD. Resveratrol is an antioxidant and anti-inflammatory agent. In this study, the histopathological and biochemical effects of resveratrol on a hyperoxia-induced lung injury model in newborn rats were investigated. Methods The experiment was performed on newborn rat pups from the 3rd to 13th postnatal day and they were randomly divided into four groups: Group 1 (air-exposed + saline, n = 10), Group 2 (air-exposed + resveratrol, n = 11), Group 3 (hyperoxia-exposed + saline, n = 6) and Group 4 (hyperoxia-exposed + resveratrol, n = 7). Resveratrol was administered (30 mg/kg/day) intraperitoneally. The histopathological effects of resveratrol on lung tissue were assessed by alveolar surface area, fibrosis, and smooth muscle actin (SMA) score, and the biochemical effects on lung tissue were assessed by glutathione (GSH), superoxide dismutase (SOD), nitric oxide (NO), tumor necrosis factor-α (TNF-α), and nuclear factor kappa B (NF-κB) levels. Results The alveolar surface area, fibrosis, SMA score, and NO levels were found to be significantly higher in Group 3 compared with Group 1 (p < 0.05). In addition, it was found that resveratrol treatment significantly reduced the SMA score and the NO and TNF-α levels, and increased the GSH and SOD levels in the hyperoxia group (p < 0.05). Conclusion This experimental study showed that oxidative stress and NO contributed to the pathogenesis of hyperoxia-induced lung injury, and that resveratrol had a preventive effect on hyperoxic lung injury through its anti-inflammatory and antioxidant properties.
    Pediatrics & Neonatology 01/2014; · 0.93 Impact Factor
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    ABSTRACT: Background Cilostazol is a phosphodiesterase inhibitor that has anti-inflammatory potential in addition to vasodilator and antiplatelet effects. The aim of this study was to determine the influence of cilostazol on biochemical markers of oxidative damage, proinflammatory cytokine release, and spinal cord injury after transient aortic occlusion in rats. Methods Animals were randomized into 3 groups. Sham group rats were subjected to laparotomy without aortic occlusion. Control group rats were pretreated with intraperitoneal dimethyl sulfoxide, and cilostazol group rats received intraperitoneal cilostazol (20 mg/kg/day) for 3 days before the induction of ischemia. Ischemia was induced by clamping of the infrarenal aorta, and 48 hours after reperfusion, Tarlov grades were assessed and spinal cord conduction velocities (SCCVs) were measured using epidural electrical stimulation. Erythrocyte superoxide dismutase (SOD) and catalase activities and plasma malondialdehyde, serum tumor necrosis factor–α, interleukin-1β, and interleukin-6 levels were analyzed. Spinal cord histopathology was examined to determine neuronal damage and tissue inflammation. Results Aortic occlusion caused significant increases in SOD, catalase activities, and malondialdehyde and cytokine levels accompanied by spinal cord injury. Cilostazol significantly reduced malondialdehyde levels but did not significantly alter the activations of antioxidant enzymes, levels of proinflammatory cytokines, or histologic severity of inflammation. The differences regarding the results of Tarlov grading, SCCVs, and neuronal viability between the ischemic and cilostazol pretreated groups were statistically nonsignificant. Conclusion The present experimental study indicated that cilostazol pretreatment used in this study before aortic occlusion decreased lipid peroxidation, which may be related to the reduction of reactive oxygen species. Cilostazol did not significantly suppress systemic cytokine release and prevent spinal cord inflammation and injury; however, it did show some benefit. Additional investigations might be needed to determine the critical dose of cilostazol for clarifying the protective role of this drug in spinal cord ischemia/reperfusion injury.
    Annals of Vascular Surgery 01/2014; 28(2):479–488. · 0.99 Impact Factor
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    ABSTRACT: OBJECTIVE: Insulin resistance (IR) has effects on inflammation and oxidative stress which have importance in acute stroke. Our aim was to investigate the relationships between IR, inflammation, oxidative stress and stroke severity in acute ischemic stroke patients. METHODS: We examined the relationships between inflammation, oxidative stress and stroke severity in 75 acute stroke patients with and without IR. Serum levels of oxidative stress markers (nitric oxide (NO), malondialdehyde (MDA), glutathione (GSH)) were measured as well as the cytokines interleukin-6 (IL-6) and interleukin-10 (IL-10). RESULTS: The levels of IL-10 (13.7±19.11 vs 51.20±89.32 pg/ml, p<0.00) in IR group were significantly reduced. Patients with IR had higher levels of NO (30.26±17.63 vs 22.57±14.5 µmol/L, p=0.04) and IL6 (27.44±57.13 vs 8.68±11.8 pg/ml, p<0.00) and higher NIHSS scores (11.40±5.35 vs 8.81±5.76, p=0.04) when compared with noninsulin resistant group. IL-10 was found negatively correlated with HOMA. Additionally, the parameters with positive correlations with HOMA were NIHSS, IL-6 and NO. CONCLUSIONS: Inflammation and oxidative stress are more evident in acute stoke patients with insulin resistance which may cause worse stroke severity. Our data also suggest that IL-10 as an antiinflammatory cytokine can be much lower in insulin resistance in acute phase of ischemic stroke. However it can be elevated as an adaptive mechanism in metabolic syndrome as a chronic condition.
    Neuro endocrinology letters 02/2013; 34(4):52-57. · 0.93 Impact Factor
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    ABSTRACT: Eggs (n = 1,800) obtained from Ross broiler breeders at 32 and 48 wk of age were incubated at either a constant temperature of 37.6°C throughout (T1), or the temperature was reduced for 6 h to 36.6°C each day during embryonic age (EA) 10 to 18 (T2). Yolk sac, liver, and brain fatty acid profiles and oxidant and antioxidant status of liver and brain were measured at EA 14, 19, and day of hatch (DOH). Fatty acid profiles of yolk sac, liver, and brain were influenced by age of breeder with significant breeder hen age × incubation temperature interactions. At EA 14, higher levels of 20:4n-6 and 22:6n-3 had been transferred from the yolk sac to T2 embryos from younger than older breeders, whereas for T1 and T2 embryos, yolk sac 20:4n-6 and 22.6n-3 values were similar for older breeders. Accumulation of 20:4n-6 and 22:6n-3 fatty acids in the liver of T1 and T2 embryos from younger breeders was similar; however, T2 embryos from older breeders had higher liver levels of 20:4n-6 and 22:6n-3 than T1 embryos. At EA 19, liver nitric oxide levels were higher for T2 embryos from younger breeders than those from breeders incubated at T1. Brain catalase levels of T2 embryos from younger breeders were higher than those from older breeders at DOH. Thus, changes in fatty acid profiles and catalase and nitric oxide production of brain and liver tissues resulting from 1°C lower incubation temperature from EA 10 to 18 reflect adaptive changes.
    Poultry Science 12/2012; 91(12):3260-70. · 1.52 Impact Factor
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    ABSTRACT: ABSTRACT Purpose: We aimed to investigate the effects of caffeic acid phenethyl ester (CAPE) on intestinal mucosal injury induced by superior mesenteric occlusion. Methods: This experimental study was conducted on 48 male Wistar-albino rats. The animals were randomly allocated into four groups: (i) Sham-operated group, laparotomy without intestinal ischemia/reperfusion (IR) injury (n = 12); (ii) Sham + CAPE group, identical to group 1 except for CAPE treatment (10 μmol/kg, intravenously) (n = 12); (iii) Intestinal IR group, 60 min of superior mesenteric ischemia followed by 3 hr of reperfusion (n = 12); and (iv) (IR + CAPE)-treated group, 10 μmol/kg injection of CAPE intravenously 30 min before the reperfusion period (n = 12). We evaluated the degree of intestinal mucosal injury on a grading scale, histopathologically, and by measuring oxidative stress markers and antioxidant parameters, biochemically. Intestinal edema was estimated by using wet/dry weight ratios. The plasma proinflammatory cytokine levels were measured. Animal survival was observed up to one week. Results: Intestinal mucosal injury scores were significantly decreased with CAPE administration (p < .05). CAPE treatment significantly reduced oxidative stress markers in the intestinal tissues (p < .05) and the plasma proinflammatory cytokine levels (p < .05), and significantly increased antioxidant parameters in the intestinal tissues (p < .05). Intestinal edema was significantly alleviated by CAPE treatment (p < .05). The survival rates of CAPE-treated IR animals were significantly higher than IR-subjected rats (p < .05). Conclusion: This study clearly showed that CAPE treatment significantly alleviated the intestinal mucosal injury caused by superior mesenteric ischemia/reperfusion. Further clinical studies are required to clarify whether CAPE has a useful role in reperfusion injury during particular surgeries in which IR-induced organ injury occurs.
    Journal of Investigative Surgery 12/2012; 25(6):354-365. · 1.32 Impact Factor
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    ABSTRACT: ABSTRACT Purpose: We aimed to investigate the effects of caffeic acid phenethyl ester (CAPE) on wound healing in left colonic anastomoses in the presence of intraperitoneal sepsis induced by cecal ligation and puncture (CLP) in a rodent model. Methods: This experimental study was conducted on 48 male Wistar albino rats. The animals were randomly allocated into four groups and a left colonic anastomosis was performed on the day following sham operation or CLP in all rats: (i) sham-operated control group, laparatomy plus cecal mobilization (n = 12) (Group 1), (ii) sham + CAPE group, identical to Group 1 except for CAPE treatment (10 μmol/kg, intraperitoneally, 30 min before construction of the colonic anastomosis) (n = 12) (Group 2), (iii) CLP group, cecal ligation and puncture (n = 12) (Group 3), and (iv) CLP + CAPE-treated group, 10 μmol/kg, intraperitoneally, 30 min before the construction of colonic anastomosis (n = 12) (Group 4). On the postoperative day 7, the animals were subjected to relaparotomy for in-vivo measurement of the colonic anastomotic bursting pressure. A colonic segment including the anastomotic site was resected for histopathological evaluation and biochemical analyses of hydroxyproline (Hyp) contents, myeloperoxidase (MPO) acivity, malondialdehyde (MDA) levels, reduced glutathione (GSH) levels, and superoxide dismutase (SOD) activity. Body weight changes were examined. Results: CAPE treatment significantly increased colonic anastomotic bursting pressures (p < .05), colonic anastomotic tissue Hyp contents, and enzymatic and nonenzymatic antioxidant markers (p < .05), and significantly decreased oxidative stress parameters in colonic anastomotic tissues (p < .05). Histopathological scores were significantly better by CAPE administration (p < .05). Conclusion: This study clearly showed that CAPE treatment prevented the detrimental effects of intraperitoneal sepsis on colonic anastomotic wound healing. Further clinical studies are required to determine whether CAPE has a useful role in the enhancement of gastrointestinal anastomotic wound healing during particular surgeries in which sepsis-induced organ injury occurs.
    Journal of Investigative Surgery 10/2012; 25(5):301-10. · 1.32 Impact Factor
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    ABSTRACT: ABSTRACT Purpose: We aimed to investigate whether caffeic acid phenethyl ester (CAPE) prevents detrimental systemic effects of intestinal ischemia-reperfusion (IR) injury on colonic anastomotic wound healing. Methods: This experimental study was conducted on 48 male Wistar albino rats. The rats were randomly allocated into four groups and a left colonic anastomosis was performed in all rats: (i) sham-operated group (n = 12), laparatomy without intestinal IR injury; (ii) sham + CAPE group (n = 12), identical to Group 1 except for CAPE treatment (10 μmol/kg, intravenously); (iii) intestinal IR group (n = 12), 60 min of superior mesenteric ischemia followed by reperfusion; and (iv) IR + CAPE-treated group (n = 12) (10 μmol/kg, intravenously, 30 min before the construction of colonic anastomosis). On the postoperative day 7, the rats were subjected to relaparotomy for in vivo measurement of the colonic anastomotic bursting pressure. A colonic segment including the anastomotic site was resected for histopathological evaluation and biochemical analyses. The plasma proinflammatory cytokine levels were measured. Body weight changes were examined. Results: CAPE treatment significantly increased colonic anastomotic bursting pressures, and colonic anastomotic tissue hydroxyproline contents and antioxidant parameters (p < .05), and significantly decreased oxidative stress markers in colonic anastomotic tissues and plasma proinflammatory cytokine levels (p < .05). Histopathological scores were significantly better due to CAPE administration (p < .05). Conclusions: This study clearly showed that CAPE treatment prevented the delaying effects of remote IR injury on colonic anastomotic wound healing. Further clinical studies are required to determine whether CAPE has a useful role in the enhancement of gastrointestinal anastomotic wound healing during particular surgeries in which IR-induced organ injury occurs.
    Journal of Investigative Surgery 05/2012; · 1.32 Impact Factor
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    ABSTRACT: The aim of this study was to compare maternal and umbilical cord serum levels of the angiogenic and anti-angiogenic factors in early- and late-onset pre-eclamptic pregnancies as well as in normal pregnancies, which might have significant importance in the etiology of pre-eclampsia. This prospective case-control study was carried out with pre-eclamptic (early-onset, ≤ 34 weeks and late-onset, >34 weeks) and normal pregnant women. VEGF, PIGF, sFlt-1 and sEng levels in maternal and umbilical cord serum were measured before delivery and the findings were compared. The study was conducted with 15 early- and 15 late-onset pre-eclampsia patients, and 17 patients with normal pregnancies. It was found that sEng levels were higher in the umbilical cord serum in the early-onset and in the maternal serum in the late-onset pre-eclampsia group than the control group (p < 0.05). No significant difference in any factor was observed between the early- and late-onset pre-eclampsia groups. In this study, the results showed that angiogenic and anti-angiogenic factor levels in maternal serum and umbilical cord serum may not be related to the time of onset of pre-eclampsia.
    Gynecological Endocrinology 03/2012; 28(8):628-32. · 1.30 Impact Factor
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    ABSTRACT: Increased inflammatory response and cytokines are claimed to play a significant role in the etiology of preeclampsia. Interleukin-6 (IL-6) is a proinflammatory cytokine. Limited number of studies evaluating IL-6 levels in preeclamptic patients have produced conflicting results. Therefore, the present study sought to compare maternal and umbilical cord serum levels of IL-6 in early- and late-onset preeclamptic pregnancies as well as in normal pregnancies. A total of 69 participants were enrolled in the study. The control group consisted of 24 participants with normal pregnancies. Preeclampsia group consisted of 45 participants. The preeclampsia group was further classified into the subgroups of early- and late-onset preeclampsia. Late-onset preeclampsia group consisted of 24 women whereas early-onset preeclampsia group consisted of 21 women. Serum and umbilical cord samples of IL-6 were compared. There was no significant difference between maternal and umbilical cord serum IL-6 concentrations between the preeclampsia and control group. No significant difference was observed in maternal and umbilical cord serum IL-6 levels between early- and late-onset preeclampsia groups. Our results do not support an increase in IL-6 levels in patients with early- and late-onset preeclampsia. The clinical relevance of our findings needs to be further investigated.
    Gynecological Endocrinology 02/2012; 28(8):640-3. · 1.30 Impact Factor
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    ABSTRACT: Obesity is a chronic disease that is characterized by excessive accumulation of body fat. The physiological changes associated with estrogen deprivation in menopause have a significant impact on total body fat and adipose tissue distribution. Adipocytokines, such as adiponectin and leptin are related to adipose tissue, and their levels are affected by estrogen. The aim of the present study was to investigate the alteration of adipocytokine levels with estrogen therapy. Aged Wistar albino rats were divided into two main groups: control (C) and ovariectomized (OVX). Six months after ovariectomy, the ovariectomized group was divided into four subgroups: two ovariectomized groups received saline (OVX) and sesame oil (OVX+S.oil), and two groups received physiological dose (OVX+PhyE2) and pharmacological dose (OVX+PharmE2) estrogen (2 and 20µg/kg per day, respectively). Body weight was monitored weekly for 6weeks. Adiponectin, leptin and homocysteine levels were measured from blood samples before and after treatment. Body weight increased in OVX, OVX+S.oil and OVX+PhyE2 over 6weeks (P<0.001). Adiponectin levels were significantly decreased in the OVX+S.oil and OVX+PhyE2 groups (P=0.017 and P=0.008, respectively). Leptin level was significantly decreased in the OVX+PharmE2 group (P=0.042). Homocysteine level was decreased in the OVX+S.oil group (P=0.037).   Adipocytokines may play a role in the pathogenesis of cancer or obesity-related complications in menopause. Estrogen therapy may reduce these complications by changing the levels of adipocytokines.
    Journal of Obstetrics and Gynaecology Research 12/2011; 38(1):231-8. · 0.84 Impact Factor
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    ABSTRACT: The purpose of this study is to investigate the protective effects of Ginkgo biloba extract (EGb 761) in rat pups with hypoxia/reoxygenation (H/R)-induced bowel injury. One-day-old Wistar albino rat pups (n = 21) were randomly divided into 3 groups: group 1 (control, untreated and not exposed to H/R, n = 7), group 2 (untreated but exposed to H/R, n = 7), and group 3 (EGb 761 + H/R, n = 7). Ginkgo biloba extract was administered (100 mg/kg per day, subcutaneously) to group 3 for 3 days. On the fourth day, all animals except controls were exposed to H/R and were killed 6 hours after H/R. Histopathologic injury scores (HIS), malondialdehyde, glutathione (GSH), GSH-peroxidase (Px) activities, and nitric oxide (NO) levels were measured on intestinal samples. Although the control group had normal HIS, group 2 had grade 3 HIS. In contrast, group 3 had minimal HIS, and these results were significantly better than those of group 2 (P < .001). Malondialdehyde and NO levels of group 3 were significantly lower than those of group 2 (P < .01). Glutathione and GSH-Px activities of group 1 were higher than those of groups 2 and 3 (P < .05). However, there were no significant differences for GSH and GSH-Px activities between groups 2 and 3. This study showed that hypoxia and NO contributed to the pathogenesis of H/R-induced intestinal injury and that prophylactically administered EGb 761 had a protective effect on bowel injury.
    Journal of Pediatric Surgery 04/2011; 46(4):685-90. · 1.38 Impact Factor
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    ABSTRACT: Objective: In this study, we aimed to investigate the cytoprotective effect of L-carnitine against cisplatin-induced nephrotoxicity and to compare its efficacy with that of amifostin by quantitative renal Tc 99m DMSA uptake. Material and Methods: Male Wistar rats were randomly divided into six groups of six animals each. 1) Control (saline; 5 ml/kg intraperitoneally); 2) L-carnitine (CAR; 300 mg/kg intraperitoneally); 3) Amifostine (AMI; 200 mg /kg intraperitoneally); 4) Cisplatin (CIS;7 mg/kg intraperitoneally); 5) Cisplatin plus L-carnitine (CIS + CAR); 6) Cisplatin plus amifostine (CIS + AMI). L-carnitine and amifostine were injected 30 minutes before cisplatin in Group 5 and 6. Tc 99m DMSA, 7.4 MBq/0.2 ml, was injected through the tail vein 72 hours after the drug administration. Rats were killed and kidneys removed by dissection 2 hours after the injection of the radiopharmaceutical. The percentage of the injected dose per gram of kidney tissue (%ID/g) was calculated. Renal function was monitored by measuring BUN and plasma levels of creatinine. Lipid peroxidation and glutathione content were determined by measuring malondialdehyde (MDA) and reduced glutathione (GSH) in kidney tissue homogenates. Results: Tc 99m DMSA uptake per gram tissue of the kidney as %ID/g was 29.54±4.72, 29.86 ± 7.47 and 26.37 ± 4.54 in the control, CAR and AMI groups respectively. %ID/g was the lowest of all the groups, 11.60±3.59 (p<0.01), in the cisplatin group. Carnitine or amifostine administration 30 minutes before cisplatin injection resulted a significant increase in %ID/g, 21.28±7.73 and 18.97±3.24 respectively, compared to those of cisplatin-treated rats (p<0.002). A marked increase in plasma BUN and creatinine indicating nephrotoxicity and acute renal failure was observed in the cisplatin-treated group. MDA and GSH levels were concordant with cisplatin-induced oxidative stress in the kidney tissue. Conclusion: The results showed that L-carnitine significantly attenuates the cisplatin-induced nephrotoxicity as amifostin. Conflict of interest:None declared.
    Molecular imaging and radionuclide therapy. 04/2011; 20(1):1-6.
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    ABSTRACT: Routine use of transcutaneous bilirubin (TcB) measurement in the newborn nursery could reduce costs, readmission rates for hyperbilirubinemia and the need for total serum bilirubin (TSB) measurements. The aim of this study was to examine the correlation between TcB measurement, as performed using BiliCheck, and TSB, measured with high-pressure liquid chromatography (HPLC) and with standard laboratory methods, and to determine the TcB cutoff points with desirable sensitivity and specificity values for various clinically relevant TSB levels by HPLC. Fifty-four infants of > or = 30 weeks of gestational age were enrolled in the study. Near simultaneous blood collection for TSB analysis by three methods--bedside bilirubinometer, diazo method and HPLC--and TcB measurement were performed. There was good correlation between TcB and HPLC-bilirubin (B) (r = 0.85), TSB by bilirubinometer and HPLC-B (r = 0.91) and TSB by diazo method and HPLC-B (r = 0.91). The cut-off limits providing a sensitivity of 100% for TcB measurements were TcB > or = 9 mg/dl for HPLC-B > 17 mg/dl and TcB > or = 8 mg/dl for HPLC-B > 15 mg/dl and HPLC-B > 13 mg/dl. Despite having good correlation with HPLC, BiliCheck showed worse performance than bilirubinometer and diazo method at various clinically relevant cut-off values. Since BiliCheck required relatively lower thresholds with false-positive results for having a sensitivity of 100%, it cannot be recommended as a complete substitute for serum bilirubin measurements.
    The Turkish journal of pediatrics 01/2011; 53(1):67-74. · 0.56 Impact Factor
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    ABSTRACT: This study was designed to determine the role of oxidative stress, nitric oxide (NO), and glutathione-related antioxidant enzymes in rat pups with hypoxia/reoxygenation (H/R)-induced bowel injury and to evaluate the potential benefits of prophylactic clarithromycin. One-day-old Wistar albino rat pups (N = 21) were randomly divided into 3 groups: group I (control), group II (exposed to H/R), and group III (clarithromycin + H/R). Clarithromycin was administered (40 mg/kg) subcutaneously to group III for 3 days. On the fourth day, all rats except controls were exposed to H/R and were killed at 6 hours after H/R. Histopathologic injury scores (HIS), malonyldialdehyde, glutathione (GSH), glutathione-peroxidase (GSH-Px) activities, and NO levels were measured on intestinal samples. Whereas there was no difference for malonyldialdehyde levels among groups, HIS and NO levels were higher in group II than groups I and III (P < .05). However, GSH and GSH-Px activities were lower in group II than groups I and III (P < .05). Clarithromycin significantly increased GSH and GSH-Px activities and reduced HIS and NO levels in group III. This study showed that oxidative stress and NO contributed to the pathogenesis of H/R-induced bowel injury and that clarithromycin had a protective effect on bowel injury owing to anti-inflammatory and antioxidant effects.
    Journal of Pediatric Surgery 11/2010; 45(11):2169-74. · 1.38 Impact Factor
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    ABSTRACT: The aim of this study was to investigate the efficacy of ibuprofen on the healing of esophagus and the prevention of stricture development after esophageal caustic injuries in rats. Rats were divided into three groups as: group 1(sham), group 2(esophageal burn injury), group 3(injury + ibuprofen). In groups 2 and 3, a standard esophageal burn injury was created by applying 10% NaOH solution to distal esophagus of about 3 cm. To rats in the sham group, isotonic solution was given instead of NaOH. Ibuprofen (90 mg/kg/day) was given via oral route to group 3 rats. Normal saline as placebo was given via the same route to rats in groups 1 and 2. 28 days later, all the live rats were killed. The distal esophageal segments of all rats were removed and divided into two equal parts for biochemical and histopathologic examination. In the tissue samples, biochemically hydroxyproline and histopathologically collagen content and stenosis indices were evaluated for efficacy of treatment. The hydroxyproline level (microg/mg wet tissue) in the groups was 1.54 +/- 0.08, 4.82 +/- 0.60, and 3.28 +/- 0.27, respectively. The hydroxyproline level increased significantly in group 2 compared with group 1 (P < 0.01). Although the hydroxyproline level was significantly increased in group 3 compared with group 1, it decreased significantly in group 3 compared with group 2 (P < 0.05) by treatment of ibuprofen. In group 3, the collagen content score (1.50 +/- 0.26) was significantly lower than in group 2 (2.62 +/- 0.37) (P < 0.05). The stenosis index was found as 0.37 +/- 0.02 in group 1, 0.84 +/- 0.02 in group 2, and 0.67 +/- 0.03 in group 3. The stenosis index in group 2 was significantly higher than group 1 and group 3 (P < 0.01). Although the stenosis index was significantly higher than in group 1, a significant decrease in stenosis index was found in group 3 compared with group 2, by ibuprofen treatment (P < 0.01). Based on these results, we concluded that the treatment with ibuprofen in acute phase esophageal burn injury has beneficial effects on healing of esophagus and may decrease the stricture formation. For these reasons, ibuprofen may effectively be used in the acute phase treatment of caustic esophagus injury and after esophageal dilatation procedures.
    Pediatric Surgery International 07/2010; 26(7):721-7. · 1.22 Impact Factor
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    ABSTRACT: 1. The objective was to evaluate the effects of brooding temperature on intestinal development, oxidative organ damage, and performance of chicks acclimated to high temperature during incubation. The effects of acclimation and brooding temperatures on slaughter weights of broilers under heat stress were also investigated. 2. Eggs were incubated at either 378 degrees C (INC(Cont)) or heat-acclimated at 395 degrees C for 6 h daily from d 10 to d 18 of incubation (INC(H)). Brooding temperatures at floor level were set at 32, 335 and 35 degrees C (Bt(32), Bt(335), Bt(35), respectively) for the first 5 d. The temperature was reduced gradually to 30 degrees C from d 6 to d 10. From 21 to 42 d, broilers from INC(Cont) Bt(32) and INC(H) Bt(32) and Bt(35) were divided into two groups; half from each group was exposed to daily cyclic higher ambient temperatures, while the other half was reared at control temperature. 3. INC(H) chicks had lower jejunum, but greater liver and residual yolk sac weights than INC(Cont) chicks on the day of hatching. Although INC(H) chicks from Bt(335) and Bt(35) had lighter body weights than Bt(32) on d 5, no significant differences were observed in the body weight of broilers among treatments at 10 and 21 d. 4. Similar jejunum protein, alkaline phosphatase, maltase, glutathione, and malondialdehyde contents of chicks from INC(Cont) and INC(H) suggested that heat acclimation during incubation has no effect on jejunum enzyme activity or oxidative status of chicks. 5. Taking into account INC(H) Bt(35) chicks having lower T(3) levels on d 5, lower heterophil/lymphocyte (H/L) ratios and similar weights at 42 d under heat stress compared with control broilers, the results suggested that although higher brooding temperatures had no effect on body weights of INC(H) chicks during the brooding period, those broilers may able to cope better with heat stress.
    British Poultry Science 06/2010; 51(3):444-52. · 1.15 Impact Factor
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    ABSTRACT: Although the injury to the peripheral nervous system is a common clinical problem, understanding of the role of melatonin in nerve degeneration and regeneration is incomplete. The current study investigated the effects of neonatal pinealectomy on the sciatic nerve microarchitecture in the chicken. The chickens were divided into two equal groups: unpinealectomized controls and pinealectomized chickens. At the end of the study, biochemical examination of 10 sciatic nerve samples from both groups was performed and a quantitative stereological evaluation of 10 animals in each group was performed. The results were compared using Mann-Whitney test. In this study, the results of axon number and thickness of the myelin sheath of a nerve fiber in newly hatched pinealectomy group were higher than those in control group. Similarly, surgical pinealectomy group had significantly larger axonal cross-sectional area than the control group (p < 0.05). In addition, the average hydroxyproline content of the nerve tissue in neonatal pinealectomy group was higher than those found in control group. Our results suggest that melatonin may play a role on the morphologic features of the peripheral nerve tissue and that melatonin deficiency might be a pathophysiological mechanism in some degenerative diseases of peripheral nerves. The changes demonstrated by quantitative morphometric methods and biochemical analysis has been interpreted as a reflection of the effects of melatonin upon nerve tissue. In the light of these results from present animal study, changes in sciatic nerve morphometry may be indicative of neuroprotective feature of melatonin, but this suggestion need to be validated in the human setting.
    Journal of Brachial Plexus and Peripheral Nerve Injury 01/2010; 5:10.
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    ABSTRACT: Insulin resistance has effects on the coagulation system, which is important in the acute phase of infarct. We examined the relationships between insulin resistance, hemostatic markers and stroke severity in acute ischemic stroke patients. Protein C (PC), protein S (PS), fibrinogen, von Willebrand factor and antithrombin III (AT III) were studied in 75 acute ischemic stroke patients with and without insulin resistance. The PC and PS levels of insulin-resistant patients were significantly lower than those of non-insulin-resistant patients (PC: 87 ± 19.23 vs. 97.89 ± 13.3%, p = 0.007; PS: 84.75 ± 15.72 vs. 93.21 ± 15.02%, p = 0.02), and both of the anticoagulants were correlated with the homeostasis model assessment (HOMA; r = -0.339, p = 0.003 and r = -0.481, p = 0.000, respectively). Additionally, the NIH Stroke Scale (NIHSS) score correlated negatively with PS (r = -0.329, p = 0.004) and AT III levels (r = -0.235, p = 0.04). The parameters with positive correlations with NIHSS were fibrinogen (r = 0.270, p = 0.019), fasting glucose (r = 0.358, p = 0.008) and HOMA (r = 0.286, p = 0.013). The significant associations between insulin resistance and hemostatic markers may be relevant to stroke severity by causing a procoagulant tendency in acute ischemic stroke.
    European Neurology 01/2010; 64(4):201-6. · 1.50 Impact Factor

Publication Stats

483 Citations
134.45 Total Impact Points

Institutions

  • 1995–2014
    • Adnan Menderes University
      • • Department of Biochemistry
      • • Faculty of Medicine
      Güsel Hissar, Aydın, Turkey
  • 2009
    • Haydarpasa Numune Research and Teaching Hospital
      İstanbul, Istanbul, Turkey
  • 2006–2008
    • Pamukkale University
      • Department of General Surgery
      Denisli, Denizli, Turkey
  • 2007
    • Ege University
      • Department of General Surgery
      İzmir, Izmir, Turkey