Gorkem Mungan

The effect of Helicobacter pylori on insulin resistance.

Helicobacter pylori causes a lifelong infection in the stomach after exposure. H. pylorihas been shown to be associated with peptic ulcer and gastric cancer development. Moreover, it is held responsible for some other nongastric diseases. Among them, coronary heart disease attracts much debate. Many studies have demonstrated a close relationship between insulin resistance and atherosclerosis. Chronic inflammation and alterations in counter-regulatory hormones are deemed responsible for the etiology of insulin resistance. We aimed to examine the effect of H. pylori on insulin resistance. Sixty-three patients were enrolled in the study. Patients were divided into two groups according to H. pylori presence. HOMA-IR (homeostasis model assessment of insulin resistance) level was used to assess insülin resistance. Thirty-six patients were H. pylori positive and 27 were H. pylori negative. There was no difference between the two groups with regard to age, gender, or body mass index. HOMA-IR level was 1.73± 1.1 in the H. pylori-negative group, whereas it was 2.56 ± 1.54 in the H. pylori-positive group (P < 0.05). This study provides the first direct evidence for an association between chronic H. pylori infection and insulin resistance.

Effect of Dexmedetomidine on Testicular Torsion/Detorsion Damage in Rats

Background and Objective: We assessed the antioxidant activity of dexmedetomidine (DEX) during an ischemic period in a rat model of testicular torsion/detorsion (T/DT) by using biochemical and histopathological methods. Methods: Wistar Albino male rats weighing 250–300 g were divided into three groups: sham (group S, n = 7); torsion/detorsion (group T/DT, n = 7), and DEX treatment (group DEX, n = 7). In the T/DT group, right testes were rotated 720° for 1 h. Group S served for normal basal values. Rats in group T/DT were operated to make T/DT, this group served as a control group. Group DEX received intraperitoneal DEX 10 µg · kg–1 after the 30-min torsion period. For measurement of total antioxidant enzyme activities and malondialdehyde (MDA) levels, testes of 7 animals in each group were excised after 4 h of reperfusion. Germ cell apoptosis was evaluated using the apoptosis protease-activating factor 1 (APAF-1) antibody in all groups and also on the expressions of endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) were assessed within the bilateral testes. Results: Mean MDA levels in group T/DT were significantly higher than in groups S and DEX (p < 0.05). There were also significant decreases in mean total antioxidant activities in group T/DT when compared to groups S and DEX (p < 0.05). These values were significantly higher in group DEX than group T/DT. Germ cell apoptosis, eNOS and iNOS levels were significantly higher in group T/DT when compared to groups S and DEX (p < 0.05). Conclusions: DEX treatment has potential biochemical and histopathological benefits by preventing ischemia/reperfusion-related cellular damage in an experimental testicular torsion model. Preference of DEX for anesthesia during the detorsion procedure may attenuate ischemia-reperfusion injury.

Vardenafil Reduces Testicular Damage Following Ischemia/Reperfusion Injury in Rats

We investigated the effect of intraperitoneal vardenafil (1 mg/kg) administration during an ischemic period in a rat model of testicular torsion/detorsion (T/D). Twenty‐one adult Wistar rats were equally randomized into a control group, a T/D group and a vardenafil group. The control group was designed to collect basal values for biochemical and histopathological parameters. The T/D group underwent testicular torsion for 1 hour. The vardenafil group received vardenafil (1mg/kg) intraperitoneally at 30 minutes after torsion. All rats were sacrificed 4 hours after reperfusion to evaluate the tissue levels of malondialdehyde and total antioxidant status. Germ cell apoptosis was evaluated using the apoptosis protease activating factor 1 antibody in all groups. The expressions of endothelial nitric oxide synthase (NOS) and inducible NOS were also assessed in both testes of all rats. The malondialdehyde levels in the T/D group were significantly higher than in the control and vardenafil groups. There were also significant decreases in total antioxidant status in the T/D group compared with the control and vardenafil groups. Vardenafil treatment significantly reduced apoptosis protease activating factor 1, endothelial NOS and inducible NOS levels in the vardenafil group compared with the T/D group. Administration of 1 mg/kg vardenafil during testicular torsion decreased ischemia/reperfusion cellular damage. Our results indicate that the reduction in oxidative stress by vardenafil may play a major role in its cytoprotective effects.

Coenzyme Q10 treatment reduces lipid peroxidation, inducible and endothelial nitric oxide synthases, and germ cell–specific apoptosis in a rat model of testicular ischemia/reperfusion injury

In this experimental study, we assessed the preventive effects of coenzyme Q(10) (CoQ(10)) in a rat model of ischemia/reperfusion injury. The results of this study show that CoQ(10) administration before the reperfusion period of testicular torsion provides a significant decrease in testicular lipid peroxidation products and expressions of inducible nitric oxide synthase, endothelial nitric oxide synthase, and germ cell-specific apoptosis.

Angiotensin-converting enzyme insertion/deletion polymorphism has no effect on the risk of atherosclerotic stroke or hypertension

BACKGROUND AND PURPOSE Stroke is a heterogeneous multifactorial disease. Hence, a large number of candidate genes are involved in stroke pathophysiology, such as blood pressure regulation and atherosclerosis. Although angiotensin-converting enzyme insertion/deletion (ACE I/D) polymorphism is considered to have a role in hypertension, coronary artery disease, and myocardial infarction, its relationship with cerebrovascular disease and hypertension in stroke in different ethnic populations is still inconsistent. METHODS ACE I/D polymorphism, detected by polymerase chain reaction (PCR), was studied in 97 patients with large-vessel and 60 patients with small-vessel atherosclerotic stroke (44 asymptomatic, 16 symptomatic lacunes) and 85 healthy subjects with normal brain imaging. The demographic data, lipid profile and risk factors of patients and controls were obtained retrospectively. RESULTS ACE genotypes were in Hardy-Weinberg equilibrium in both patients and controls. Prevalences of DD, ID and II genotype were 41%, 40%, and 19%, respectively, in the stroke group. Differences in ACE I/D polymorphism distribution were statistically insignificant between the groups. This lack of association between stroke and ACE I/D polymorphism did not change in the presence of traditional risk factors (hypertension, diabetes mellitus, smoking, and dyslipidemia). Although hypertension was significantly more common in the patient groups, ACE I/D polymorphism showed no effect on hypertension risk. This lack of association also did not change according to groups or in the presence of diabetes mellitus, male gender or smoking. CONCLUSION ACE I/D polymorphism did not predict the risk of stroke or hypertension in our population living in the western Black Sea region of Turkey.

Comparison of angiotensin-converting enzyme, malonaldehyde, zinc, and copper levels in preeclampsia

Preeclampsia is a syndrome of unknown etiopathogenesis. Recent studies carried out on preeclampsia have focused on the increase in free radicals in the feto-placental unit with poor perfusion. It is believed that the renin-angiotensin system (RAS) has a role in the poor perfusion of the placenta. It is uncertain whether there is a pre-existing impairment in RAS in pre-eclamptic pregnant women or not. In the present study, we measured angiotensin-converting enzyme (ACE), malonaldehyde (MDA), zinc, and copper levels in the placental tissue of 16 pre-eclamptic pregnant women and compared them with those in 20 healthy pregnant women.Whereas ACE activity and MDA were found to be high in the placentas of pre-eclamptic patients, zinc and copper levels were low and there was a negative correlation between ACE activity and zinc concentration. These findings suggest that high ACE activity might play a role in the increase in tissue hypoxia and consequent lipid peroxidation through vasoconstriction; zinc deficiency in the placental tissue might cause insufficiency of superoxide dismutase, an antioxidant enzyme. Furthermore, deficiency in placental zinc also plays a role in the biosynthesis of connective tissue, maintaining its integrity, which might have an impact on the structure of the spiral arteries

Inflammatory markers in preeclamptic patients.

Abstract Background: Preeclampsia is characterized by hypertension and proteinuria that begins in the second half of pregnancy. Endothelial dysfunction and trophoblastic hypoperfusion seen in preeclampsia suggested to be part of an increased maternal inflammatory response to pregnancy. In this study, we aimed to evaluate some inflammatory markers in pre-eclamptic and normotensive pregnants. Methods: The study included 36 cases with mild preeclamp-sia, 36 cases with severe preeclampsia and 33 cases of normotensive pregnant. High sensitive C-reactive protein (hsCRP) and serum amyloid A (SAA) were measured by enzyme-linked immunosorbent assays, serum procalcitonin was measured by enzyme-linked fluorescent immunassay. Mean arterial pressure (MAP) was used as an indicator of the severity of the disease. Results: In severe preeclampsia group hsCRP, serum amyloid A and procalcitonin levels were significantly higher than mild preeclamptic and normotensive groups. SAA and hsCRP levels were higher in mild preeclamptic group when compared with normotensive pregnant but no significant difference was found in procalcitonin between these groups. There were significant correlations betweeen hsCRP, SAA, procalcitonin and MAP. Conclusions: The results confirm that inflammatory reactions are closely associated with preeclampsia.

Levels of Oxidized LDL, Estrogens, and Progesterone in Placenta Tissues and Serum Paraoxonase Activity in Preeclampsia

In vitro literature studies have suggested that atherosclerotic oxidized low density lipoprotein (OxLDL) inhibits trophoblast invasion. The objective of this study was to determine the levels of OxLDL and to examine the relationship between antioxidative estradiol, estriol, and prooxidative progestin in normal and preeclamptic placental tissues and measure the serum activity of antioxidative paraoxonase (PON1). The study included 30 preeclamptic and 32 normal pregnant women. OxLDL was determined with ELISA, estradiol, unconjugated estriol, and progesterone that were determined with chemiluminescence method in placental tissues. Serum PON1 activity was determined with spectrophotometric method. Levels of OxLDL (P = 0.027), estriol (P < 0.001), estradiol (P = 0.008), and progesterone (P = 0.009) were lower in the placental tissues of preeclamptic group compared to the normal pregnant women. Serum PON1 activity was higher in preeclamptic group (P = 0.040) and preeclamptic group without intrauterine growth restriction (P = 0.008) compared to normal pregnant women. Tissue estriol of preeclamptic group without/with IUGR (P < 0.001, P = 0.002) was lower than the normal group. Results of our study suggest that the events leading to fetoplacental insufficiency lead to a reduction in the levels of estriol limit deposition of OxLDL in placental tissues. The serum PON1 activity is probably important in the inhibition of OxLDL in preeclampsia.

Is direct method of low density lipoprotein cholesterol measurement appropriate for targeting lipid lowering therapy

OBJECTIVES The aim of this study was to compare the Friedewald Formula with direct homogeneous low density lipoprotein cholesterol (LDL-C) assay for the detection of LDL-C levels. METHODS Fasting serum samples were obtained for lipid analysis from 1001 patients. Total cholesterol (TC) and triglyceride (TG) levels were measured with enzymatic methods and the measurements of high density lipoprotein cholesterol (HDL-C) and LDL-C levels were detected using direct methods. RESULTS The mean levels of serum TC, TG, HDL-C and LDL-C were detected with in the reference range. The LDL-C estimated by the Friedewald formula was significantly correlated (P<0.01) with the direct method but there was a negative bias among them. CONCLUSION Laboratories cannot use direct method as a substitute for Friedewald formula because direct method has not been standardized in large populations and increase cholesterol assay costs.

The cutoff level of free/total prostate specific antigen (f/t PSA) ratios in the diagnosis of prostate cancer: A validation study on a Turkish patient population in different age categories

We investigated an optimal cutoff level of free/total PSA ratios (f/t PSA) in predicting prostate cancer in different age groups, focusing on the avoidance of unnecessary prostate biopsies. A total of 4955 men were enrolled into the study. Serum tPSA, fPSA, and f/t PSA ratios were determined for the study population. All males who had suspicious digital rectal examination and tPSA > 4 ng/mL underwent transrectal ultrasonography‐guided prostate biopsy. Receiver operating characteristic (ROC) curves for each group were generated by plotting the sensitivity versus 1‐specificity for the f/t PSA ratio. The sensitivity, specificity, positive likelihood ratio (PLR), and negative likelihood ratio (NLR) were obtained using various f/t PSA ratio cutoffs for different age groups. There were 657 patients with a PSA level of 4–10 ng/mL. According to sensitivity and specificity f/t% PSA cutoff points were determined to be 10%, 15%, 15%, and 10% in 50–59 years, 60–69 years, >70 years, and all ages categories, respectively, in patients with initial PSA level of 4–10 ng/mL. f/t PSA ratio had an area under the curve (AUC) value of 0.81 (95% confidence level: 0.80–0.82) for all age groups in detecting prostate cancer. f/t PSA ratio has an AUC value of 0.669 (0.632–0.705) in detecting prostate cancer among patients with a PSA level of 4–10 ng/mL. Ten percent of f/t PSA ratio had the highest specificity with PLR and 30% f/t PSA ratio had the highest sensitivity with lower NLR in the all‐age categories. The current study shows that the use of f/t PSA ratio in patients with PSA levels of 4–10 ng/mL should enhance the specificity of PSA screening and decrease the number of unnecessary biopsies. The age‐related changes warrant further investigation in a large, multicentric, and multinational population to improve the clinical use of f/t PSA cutoffs.