Abdulkerim Bedir

Association between adiponectin, resistin, insulin resistance, and colorectal tumors

PurposeIn this study, we have examined the correlation between colorectal cancer (CRC) and serum adiponectin and resistin levels, body mass index and insulin resistance.MethodsThe relation between serum adiponectin and resistin levels, obesity and insulin resistance in 36 CRC patients and 37 controls was examined.ResultsInsulin and homeostasis model assessment insulin resistance index (HOMA-IR) levels were higher, and adiponectin levels were significantly decreased in patients versus controls, whereas, resistin levels were significantly increased. A negative correlation between adiponectin, HOMA-IR, and insulin and a positive correlation between HOMA-IR, insulin, and stage were detected. There was no correlation between the stage and resistin. Adiponectin level negatively correlated with the stage. Adiponectin and resistin could play a role in colon cancer carcinogenesis, and adiponectin could be responsible for poor prognosis in colorectal cancer.

Angiotensin converting enzyme gene polymorphism and activity in turkish patients with essential hypertension

Studies in various ethnic groups have shown contradictory evidence on the association of the angiotensin converting enzyme (ACE) insertion/ deletion (I/D) polymorphism with essential hypertension. We conducted a case-control study in Samsun, Turkey, to examine the association between ACE genotype, ACE serum activity, and blood pressure. Serum ACE activity was measured and ACE I/D polymorphism performed in 165 hypertensive and 143 normotensive subjects. Genomic DNA was extracted from blood samples and amplified by polymerase chain reaction (PCR). PCR primers were flanking the polymorphic region in intron 16 of the ACE gene. The distribution of the DD, ID, and II ACE genotypes was 65, 77, and 23 in hypertensive patients and 42, 82, and 19 in normotensive subjects (P > .05). The estimated frequency of the insertion allele was 0.37 in hypertensive and 0.42 in normotensive subjects. Nevertheless, sensitivity analysis, based on positive family history and severity of hypertension, suggested that significant associations existed between more homogeneous groups of hypertensives and normotensives (P < .05). ACE genotype influenced ACE activity and the highest level was in DD genotype, being the lowest in II genotype. ACE serum levels were significantly higher in hypertensives as compared with normotensives (P < .01). A modest correlation was observed between blood pressure and ACE among hypertensive persons (r = 0.25, P < .05) and this did persist in multivariate analysis (P < .05 for systolic blood pressure and P < .005 for diastolic blood pressure). These data suggest that ACE DD genotype may have predisposing effects on severe hypertensives and cases with positive family history, and that ACE may be one of the independent factors on hypertension.

SAA1 α/α alleles in Behçet’s disease related amyloidosis

Behçet’s disease (BD) related amyloidosis is relatively rare. Serum amyloid A protein (SAA) protein gene polymorphism is one of the factors implicated in the pathogenesis of AA type amyloidosis. The aim of this study is to investigate SAA1 gene polymorphism in different patient groups: (1) BD related amyloidosis, (2) BD without amyloidosis, and (3) healthy controls. One hundred eleven patients from three main groups were included in the study: (1) BD related amyloidosis (n = 9), (2) BD without amyloidosis (n = 39), and (3) healthy controls (n = 63). Homozygous α/α is present in 78% of patients with BD and amyloidosis. The SAA1 α/α genotype is significantly more common among patients with BD and amyloidosis. This study demonstrated increased frequency of α/α genotype in BD related amyloidosis. To our knowledge, the relationship between α/α genotype and BD related amyloidosis was not studied previously. In conclusion, the SAA1 α/α genotype is a risk factor for amyloidosis in BD.

Effect of Vitamin E and Pentoxifylline on Glycerol-Induced Acute Renal Failure

The pathogenesis of acute renal failure may involve, among other causes, ischemia, vascular congestion, arachidonic acid pathways, and reactive oxygen metabolites. The aim of this study is to evaluate the effects of pentoxifylline and vitamin E on the prevention of experimental acute renal failure induced by glycerol. Eighty-five Sprague-Dawley rats weighing 170–230 g were included in the study. The rats were randomly divided into four groups: group 1 was given 1 ml saline; group 2, glycerol; group 3, glycerol plus vitamin E, and group 4, glycerol plus pentoxifylline. Extent of histological renal tubular necrosis and regeneration in each animal were graded. Blood urea nitrogen, serum creatinine, and creatine kinase concentrations were measured. Mean blood urea nitrogen and serum creatinine concentrations and tubular injury scores were significantly lower in group 1 than in groups 2–4 (p < 0.001), but there were no significant differences among groups 2–4. We conclude that postinsult administration of vitamin E and pentoxifylline does not have a beneficial effect on prevention and severity of acute renal failure and that controlled, multicenter studies involving a large number of patients are needed to clarify this subject.

Is Vitamin D Deficiency a Risk Factor for Respiratory Distress Syndrome

BACKGROUND Previous studies have shown the relationship between in utero lung development and vitamin D [25(OH)D], but there have been no studies to investigate whether vitamin D deficiency is a risk factor for respiratory distress syndrome (RDS) in preterm babies. OBJECTIVES In this study, we investigated if 25(OH)D deficiency is a risk factor for RDS. METHODS One hundred fifty-two preterm newborns, born at 29 - 35 weeks gestational age, were included in the study following informed consent from the parents. Peripheral blood samples were collected within the first 24 hours of life and 25(OH)D levels were measured by liquid chromatography-tandem mass spectrometry. Demographic characteristics of the babies and the diagnosis of RDS were recorded. RESULTS In 64 % of preterm infants, 25(OH)D levels were compatible with severe deficiency (≤ 10 ng/mL), 33 % with moderate deficiency (10 - 20 ng/mL), and 3 % with mild deficiency (20 - 30 ng/mL). In none of the babies was a normal 25(OH)D level observed. Serum 25(OH)D levels were not correlated with gestational age. Respiratory distress syndrome was more common in preterm babies with severe (28 %) compared to mild-moderate 25(OH)D deficiency (14 %) (p < 0.05). CONCLUSIONS None of the preterm infants in this study had normal vitamin D level, which underlined the burden of vitamin D deficiency in pregnant women and their offspring. RDS was more common in severely vitamin D-deficient preterms. Determination of vitamin D status of the mothers and appropriate supplementation might be a valuable strategy to reduce RDS, in addition to antenatal steroids. Besides, since vitamin D is a regulatory factor in many organs during fetal development, long-term effects of in utero vitamin D deficiency warrant further studies.

Preventive and protective effects of turkish propolis on H2O2-induced DNA damage in foreskin fibroblast cell lines

The aim of the present study was to evaluate the potential of Turkish propolis extracts if they prevent or protect foreskin fibroblast cells against hydrogen peroxide (H₂O₂)-induced oxidative DNA damage. Hydrogen peroxide (40 μM) was used as an inducer of oxidative DNA damage. The damage of DNA was evaluated by using the alkaline single cell gel electrophoresis (comet) assay. Turkish propolis extracts at concentrations of 25, 50, 75 and 100 μg/ml were prepared by ethanol. Anti-genotoxicity was assessed before, simultaneously, and after treatment of propolis extract (50 μg/ml) with H₂O₂. The results showed a significant decrease in H₂O₂-induced DNA damage in cultures treated with propolis extract. The antioxidant activity of phenolic components found in propolis may contribute to reduce the DNA damage induced by H₂O₂. Our findings confirmed the chemopreventive activity of propolis and showed that this effect may occur under different mechanisms.

Assessment of Genotoxicity in Rats Treated With the Antidiabetic Agent, Pioglitazone

Pioglitazone (PIO), a member of the thiazolidinedione class of antidiabetic agents, specifically targets insulin resistance. Drugs of this class act as ligands for the gamma subtype of the peroxisome proliferator‐activated receptor. Although troglitazone, another drug in this class, displayed unacceptable hepatotoxicity, PIO was approved for human use by the U.S. Food and Drug Administration. To our knowledge, there are no published reports on the genotoxicity of PIO; however, the package insert indicates that it has minimal genotoxicity. In this study, we used the comet assay to investigate the DNA damage in the peripheral blood and liver cells of rats treated with PIO. Sixteen male Sprague‐Dawley rats were randomly distributed into four groups, and dosed daily for 14 days by oral gavage with 0, 10, 20, and 40 mg/kg/day PIO. A dose‐dependent increase in DNA damage, as assessed by % tail DNA, was observed in both hepatocytes and blood lymphocytes of the PIO‐treated groups, with significant increases detected between the rats treated with all the doses of PIO and the control, and between the rats treated with different PIO doses (P < 0.005 to P < 0.0001). Treating nuclei from the exposed animals with an enzyme cocktail containing Fpg and Endonuclease III prior to performing the comet assay increased the level of DNA damage, which reflects oxidized purine and pyrimidine. Taken together, our data indicate that PIO is able to dose‐dependently induce DNA damage in both the liver and blood lymphocytes of rats, which is partially due to the generation of oxidative lesions. Environ. Mol. Mutagen., 2008.

Low hair selenium and plasma glutathione peroxidase in children with chronic renal failure.

Selenium (Se) is a trace element that incorporates into the selenoenzyme glutathione peroxidase (GSH-Px). There are conflicting results regarding the Se levels and activity of GSH-Px in adult uremic patients. The aim of this study was to determine (1) the hair Se status, (2) the possible relation between the hair Se status and the antioxidant enzyme, GSH-Px, and (3) the influence of different treatment procedures on hair Se status and GSH-Px activity in children with CRI, those treated conservatively and those on HD and on CAPD. Ninety-three patients, including 32 patients with CRI, treated conservatively, 42 PD patients, 19 HD patients and 34 healthy children were enrolled in the study. The hair Se level was measured by the atomic absorption spectrophotometer method. Plasma GSH-Px activity was determined using a Randox test combination (RANSEL). Hair Se levels were significantly lower in the CRI, CAPD, and HD groups when compared to the control group (P=0.001, P=0.001, and P=0.001, respectively). Plasma GSH-Px activity was significantly lower in the CRI, CAPD, and HD groups when compared to the control group (P=0.001, P=0.001, and P=0.001, respectively). Plasma GSH-Px activity correlated with the GFR in patients with CRI and the control group (P=0.000; r2=0.60). There was no correlation between plasma GSH-Px and hair Se levels in the patient and control groups. These results revealed a decreased hair Se level and impaired antioxidative capacity in children with CRI on CAPD and HD. The lack of any relation between plasma GSH-Px and hair Se suggests that plasma GSH-Px is not a good marker of Se stores.

Urinary Leucine Aminopeptidase Is a More Sensitive Indicator of Early Renal Damage in Non-lnsulin-Dependent Diabetics than Microalbuminuria

We measured urinary activity of leucine aminopeptidase (EC 3.4.11.2) and creatinine concentrations (Cr, in mmol) in samples of second morning urine from 25 healthy subjects and 59 non-insulin-dependent diabetic (NIDD) subjects. If NIDD subjects are grouped according to their Alb/Cr ratio into normoalbuminuria (group A, Alb/Cr < 2.8 mg/mmol), microalbuminuria (group B, Alb/Cr 2.8-26.8 mg/mmol), and macroalbuminuria (group C, Alb/Cr > 26.8 mg/mmol), LAP/Cr ratios in all three groups exceeded those for healthy age-matched controls. Moreover, this ratio was higher in group B than in group A. The value for LAP/Cr was clearly abnormal (i.e., exceeded the upper limit of normal, log normal + 2 SD, found in healthy subjects) in 44% of group A. In the first 10-year period Of NIDD, prevalance of abnormal LAP/Cr ratio was 61.3%, whereas that of microalbuminuria was 35.5%. We have also found a LAP/Cr ratio abnormality of 91% in group B. Evidently, LAP/Cr may be increased early in NIDD subjects and be a more sensitive predictor of incipient nephropathy than microalbuminuria.

Plasma Cell-Free DNA Levels in Children on Peritoneal Dialysis

Background/Aims: Plasma levels of cell-free DNA (cfDNA) are elevated in various clinical conditions including cancer, stroke, trauma, myocardial infarction, autoimmune disorders, and pregnancy-associated complications. Previously, increased cfDNA levels were reported during hemodialysis. However, there is limited data regarding cfDNA levels in peritoneal dialysis (PD) patients. The aim of this study was to investigate the levels of cfDNA in children on PD. Methods: Twenty-one children on PD (median age: 12; range: 4–18 years) and 21 healthy children (median age: 10; range: 6–16 years) were enrolled into the study. Plasma cfDNA was measured using a real-time quantitative PCR for the beta-globin gene. Results: The median concentrations of cfDNA in the plasma of PD patients and healthy controls were 2,205 genome-equivalents/ml of plasma (range: 39–5,845) and 1,033 genome-equivalents/ml of plasma (range: 254–5,116), respectively (p = 0.026). A significant positive correlation was observed between C-reactive protein levels and plasma cfDNA levels (r: 0.52, p < 0.0001). Conclusion: Our data have demonstrated for the first time that cfDNA is increased in children on PD treatment. However, the mechanism by which the levels of cfDNA is increased and the clinical significance of this finding in PD patients is unclear. Further studies are warranted to clarify the precise mechanism and clinical significance of elevated cfDNA in children on PD.