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Biomedical subjects

T Isbir

Publications and source records attributed to T Isbir.

At least 19 recordsLinked to original sources
PubMed2006

Analysis of L-myc gene polymorphism in patients with renal failure outcome to renal transplant.

BACKGROUND: Abnormalities of cell numbers and apoptosis have been observed in renal failure. As uncontrolled expression of c-myc is known to induce apoptosis, we thought that polymorphism in the other myc gene, L-myc gene, which is structually similar to c-myc and reported to be expressed in the kidney, may have a role in the induction of apoptosis and thus have role in chronic renal failure. The aim of this study was to investigate the relationship between the distribution of L-myc genotypes and renal failure. METHODS: In the present study we examined 101 chronic renal failure patients who had either live or cadaveric renal transplants and 105 healthy individuals, for L-myc gene polymorphism by polymerase chain reactions and restriction fragment length polymorphism techniques. RESULTS: Among our patient group, the distribution of the LL, LS, and SS genotypes was 24% (n=25), 71% (n=71), and 5% (n=5), respectively, versus 41% (n=43), 47% (n=49), and 12% (n=13) in our control group. The distribution of genotypes was significantly different between our patients and the control group (chi2=12.281; P=.002). The frequency of the S allele was significantly higher in the patient group (chi2=6.122; P=.013). CONCLUSION: Our study showed that having an S allele in the L-myc gene may increase the risk of renal failure.

Genes, myc↗
PubMed2006

Effects of cholesteryl ester transfer protein TAQ1B polymorphism in renal transplant patients.

BACKGROUND: Dyslipidemia is an important complication in renal transplant patients. Cholesteryl ester transfer protein (CETP) mediates the exchange of cholesteryl ester between high density lipoproteins and low density lipoproteins. The aim of this study was to investigate CETP Taq1B gene polymorphism and lipid abnormalities in renal transplant patients. METHODS: We studied 29 renal transplant patients and 29 healthy controls. CETP Taq1B polymorphism was determined by polymerase chain reaction and restriction fragment length polymorphism techniques. Serum lipid levels were measured enzymatically. Statistical analyses was performed by SPSS for Windows version 7.5. RESULTS: The frequencies of CETP Taq1B B1B1, B1B2, and B2B2 genotypes in patients were 44.8%, 34.5%, and 20.7%; and in control subjects, 37.9%, 37.9%, and 24.2%, respectively. The patients with B1B1 genotype displayed higher levels of total cholesterol (TC), triglycerides, low density lipoprotein-cholesterol (LDL-C), very low density lipoprotein-cholesterol (VLDL-C), and diastolic blood pressure (DBP). (P<.05). Also, patients showing a B1 allele had higher levels of TC, LDL-C, VLDL-C, and DBP compared to healthy controls (P<.05). CONCLUSION: We observed that CETP Taq1B B1 allele and B1B1 genotype have effects on the serum lipid profile among renal transplant patients.

Carrier Proteins↗
PubMed2005

Paraoxonase (PON1) 55 and 192 polymorphism and its effects to oxidant-antioxidant system in turkish patients with type 2 diabetes mellitus.

Paraoxonase (PON1) is a serum enzyme with an antioxidant function, protecting the low density lipoproteins (LDL) from oxidative modifications. Because diabetic patients are at greater risk of oxidative stress, we investigated the effect of PON1 55 methione (M)/leucine (L) and PON1 192 glutamine (A)/arginine (B) polymorphisms on oxidant-antioxidant system in 213 individuals with type 2 diabetes mellitus and 116 non-diabetic control subjects from Turkish population were included in the study. Polymerase chain reaction (PCR), restriction fragment length polymorphism (RFLP), and agarose gel electrophoresis techniques were used to determine the PON1 genotypes. Thiobarbituric acid reactive substances (TBARS), conjugated dienes levels in the serum and glutathione (GSH) levels in whole blood were measured spectrophotometrically. In both groups PON1 192 AA and PON1 55 MM genotypes had higher TBARS, conjugated dienes levels and lower GSH levels, whereas PON1 192 BB and PON1 55 LL genotypes had lower TBARS, conjugated diene levels and higher GSH level than other genotypes. We thus conclude that PON1 192 BB and PON1 55 LL alleles have protective effect against oxidative stress.

Aryldialkylphosphatase↗
PubMed2004

Paraoxonase 192 polymorphism and its relationship to serum lipids in Turkish renal transplant recipients.

BACKGROUND: Cardiovascular disorders are the leading cause of death in patients with chronic renal insufficiency. Paraoxonase (PON1) gene variants have been identified as risk factors for cardiovascular disease (CVD). METHODS: We investigated the effect of PON1 192 polymorphisms on serum lipid profiles in 29 renal transplant recipients and 26 control subjects. Distribution of the PON1 192-gene polymorphism was determined by polymerase chain reaction-based restriction fragment length polymorphism. Serum lipid levels were measured enzymatically. RESULTS: Frequencies of PON1 192 AA, BB, and AB genotypes among the renal transplant recipients were 38.5%, 26.9%, and 34.6%, and among control subjects they were 35.75%, 17.9%, 46.4%, respectively. The genotype distribution for the PON1 192 polymorphism was not different between the two groups (P = NS, chi-square test). The PON1 192 polymorphisms failed to consistently influence the serum lipid profiles in renal transplant recipients. CONCLUSION: We have shown that the 192 polymorphism of the PON1 gene is not associated with increased cardiovascular risk in renal transplant recipients.

Adult↗
PubMed2003

Is there additional effect of MTHFR C677T mutation on lipid abnormalities in renal allograft recipients?

BACKGROUND: The MTHFR C677T mutation and elevated atherogenic lipoprotein levels are known as cardiovascular risk factors in patients with renal transplantation treated with cyclosporine (CsA). The aim of the present study was to eveluate the contribution of MTHFR C677T mutation to the risk of dyslipidemia in renal transplant recipients. We also studied the effect of the MTHFR-C677 T genotype on transplant survival. METHODS: The study included 29 nondiabetic renal transplant recipients and 27 healthy controls. MTHFR C677T genotypes were determined by PCR and RFLP techniques. Biochemical parameters were measured in a computerized autoanalyzer. RESULTS: In the patient group, the distribution of the CC, CT, and TT genotypes was 44.8% (n = 13), 37.9% (n = 11), and 17.2% (n = 5), respectively. The frequencies of the C and T alleles were 0.64 and 0.36, respectively. Subjects with the T allele had the highest levels of TC (P <.05) and LDL-C (P <.05); subjects with the CC genotype had the lowest. CONCLUSIONS: We observed that the MTHFR T allele has an unfavorable effect on serum lipid profile, leading to a rise in the total and LDL cholesterol concentrations. Thus, we believe that MTHFR C allele has a protective effect and MTHFR T allele has a detrimental effect on the serum lipid profile.

Arteriosclerosis↗
PubMed2003

Cholesterol ester transfer protein, apolipoprotein E and lipoprotein lipase genotypes in patients with coronary artery disease in the Turkish population.

The aim of this study was to compare patients with coronary artery disease (CAD) to healthy objects, in order to explore a possible association between CAD and the variants in the gene encoding cholesterol ester transfer protein (CETP), apolipoprotein E (Apo E) and lipoprotein lipase (LPL). The relationship between CETP MspI, apo E and LPL PvuII gene polymorphisms and serum lipids were investigated in 173 patients with CAD and 111 healthy controls. The frequency of Apo epsilon4 (p < 0.05) and CETP M1 (p < 0.01) alleles were higher in the CAD group than in the control group. In the CAD group, those with the Msp M1 allele had higher levels of total cholesterol (TC) (p = 0026) and low-density lipoprotein cholesterol (LDL-C) than those with the Msp M2 allele. Subjects with an epsilon2 allele had the lowest levels of TC and LDL-C, while subjects with the epsilon4 allele had the highest. In the control group, CETP, the Msp M2 allele was associated with a higher level of high-density lipoprotein cholesterol (HDL-C) (p = 0.012) than the Msp M1 allele. The distributions of LPL genotype and allele did not differ between the CAD and control groups. The present study demonstrates that the CETP Msp1 and Apo E gene polymorphisms are associated with variations in lipids in patients with CAD and healthy controls in Turkish population.

Adult↗
PubMed2001

Is epsilon4 allele of apolipoprotein E associated with more severe end-organ damage in essential hypertension?

The aim of the present study comparing patients with mild to moderate hypertension with controls, was to explore a possible association between hypertension-related target organ damage and evaluation found in the gene encoding apolipoprotein E (apo E) genotype. Detailed medical history was recorded and physical examination was performed for all patients in the study (88 hypertensives, 63 normotensive controls). PCR (Polymerase Chain Reaction), RFLP (Restriction Fragment Length Polymorphism), and agarose gel electrophoresis techniques were used to determine the apo E genotypes. The frequencies of apo epsilon2, apo epsilon3, and apo epsilon4 alleles were 3.97, 88.06, and 9.95%, respectively in the hypertensive group. The frequencies of apo epsilon2, apo epsilon3, and apo epsilon4 alleles were 5.5, 92.0, and 2.38%, respectively in the control group. There were about twice as many individuals in the heterozygote hypertensive group who had apo E3/4 as compared to the control group (7.30 vs. 2.38%) (p = 0.07). The hypertensive patients who were carriers of the apo epsilon4 had significantly higher organ damage (left ventricular hypertrophy (p < 0.001). dilated left atrium (p < 0.05), retinopathy (p < 0.05)) as compared to those who were not carriers of apo epsilon4. These results showed a trend for the epsilon4 allele to be associated with a higher prevalence of target organ damage in patients with mild to moderate hypertension.

Adult↗
PubMed2001

Increased plasma levels of interleukin-6 and interleukin-8 in beta-thalassaemia major.

Several immunological defects can be found in patients with beta-thalassaemia, among which the impairment of neurophil and macrophage phagocytic and killing functions and the production of some cytokines are the most important. It is known that interleukin-6 (IL-6) and interleukin-8 (IL-8) are important components of the pro-inflammatory response. The plasma levels of these cytokines may be relevant in the pathophysiology of beta-thalassaemia. To assess this hypothesis, the plasma IL-6 and IL-8 concentrations in patients with beta-thalassaemia, were investigated. Fourteen patients with thalassaemia major were studied by evaluating body iron status, iron supply for erythropoiesis, and plasma IL-6 and IL-8 levels, together with 12 age-matched healthy controls. The plasma levels of IL-6 and IL-8 were determined by enzyme-linked immunosorbent assay (ELISA). Patients with beta-thalassaemia were found to have higher IL-8 concentrations than normal controls (p < 0.001) and plasma IL-6 concentrations increased significantly in the beta-thalassaemic patients compared with control subjects (p = 0.01). Serum ferritin levels of beta-thalassaemic patients were significantly higher than those of control groups (p < 0.05). IL-8 levels correlated with ferritin levels (r = 0.694; p < 0.05) and the total number of transfusions (r = 0.64; p < 0.05). Plasma IL-6 levels in beta-thalassaemic patients did not correlate with any clinical, haematological or biochemical parameters. It was also found that plasma IL-8 levels in the patients who had blood transfusions over 100 times were significantly higher than those of under 100 times (p < 0.05), whereas there was no statistical difference for IL-6. Markedly increased plasma IL-6 and IL-8 levels were documented in patients with beta-thalassaemia. Increased production of IL-6 and IL-8 might have contributed to abnormalities in iron metabolism and it is probably due to overstimulation of macrophages. Before a clinical value can be ascribed to these changes in plasma cytokine levels in beta-thalassaemia, the follow-up samples of larger series of patients with 8-thalassaemia should be evaluated.

Adolescent↗
PubMed2001

The effects of the pre-treatment of intravenous nimodipine on Na(+)-K+/Mg+2 ATPase, Ca+2/Mg+2 ATPase, lipid peroxidation and early ultrastructural findings following middle cerebral artery occlusion in the rat.

Excessive calcium influx has been implicated in the pathophysiology of ischemic cerebral damage. The effects of nimodipine, a calcium antagonist, on the Na(+)-K+/MG+2 ATPase activity, Ca+2/Mg+2 ATPase, lipid peroxidation, and early ultrastructural findings were examined at the acute stage of ischemia in the rat brain. Ischemia was produced by permanent unilateral occlusion of the middle cerebral artery. In Group I, the rats which had no ischemia and not received medication were used for determining Na(+)-K+/Mg+2 ATPase, Ca+2/Mg+2 ATPase, the extent of lipid peroxidation by measuring the malondialdehyde content and normal ultrastructural findings. In Group II, the rats which had only subtemporal craniectomy without occlusion and received saline solution were used for determining the effect of the surgical procedure on the biochemical indices and ultrastructural findings. In Group III, the rats received saline solution following the occlusion in the same amount of nimodipine and in the same duration as used in Group IV. In Group IV, nimodipine pre-treatment 15 min before occlusion (microgram kg-1 min-1 over a 10 min period) was applied i.v. Na(+)-K+/Mg+2 ATPase and Ca+2/Mg+2 ATPase activities decreased significantly and promptly as early as 10 min and remained at a lower level than the contralateral hemisphere in the same group and at the normal level in Group I. Nimodipine pre-treatment immediately attenuated the inactivation of Na(+)-K+/Mg+2 ATPase (p < 0.05) but there was no change on Ca+2/Mg+2 ATPase activity (p < 0.05). Malondialdehyde content increased significantly in Group III following ischemia as early as 30 min. Nimodipine pre-treatment decreased the malondialdehyde level in Group IV (p < 0.05). This study supports the possibility that nimodipine pre-treatment effects the membrane stabilizing properties via inhibiting the lipid peroxidation and subsequently restoring some membrane bound and lipid dependent enzymes' activity such as Na(+)-K+/Mg+2 ATPase and the ultrastructural findings.

Animals↗
PubMed2000

Age-related changes in GM1, GD1a, GT1b components of gangliosides in Wistar albino rats.

In this study, age-related changes of GM1, GD1a, GT1b fractions of gangliosides were investigated in whole brain of male Wistar albino rats. Insignificant increases were detected in GM1 values from the third to the 24th month, whereas GD1a and GT1b concentrations of ganglioside in 24-month-old rats decreased significantly as compared to 6-month-old rats. Although there were no significant differences in the GD1a/GT1b ratio of any groups, GM1/GD1a and GM1/GT1b ratios were significantly increased as compared to 6-month-old rats. The increase in the ratios of gangliosides are not due to an increase of GM1 fractions; they result from a decrease of GD1a and GT1b fractions of gangliosides. In conclusion, the concentration of ganglioside decreased with ageing.

Age Factors↗
PubMed2000

Influence of antioxidants on blood-brain barrier permeability during adrenaline-induced hypertension.

We have examined the effect of antioxidants (vitamin E, and selenium) on the blood-brain barrier permeability during adreneline-induced acute hypertension in the female rats. The rats supplemented with nontoxic doses of sodium selenite in drinking water for three months or vitamin E was given intraperitoneally before adrenaline-induced acute hypertension. Evans-blue was used as a blood-brain barrier tracer. Mean values for Evans-blue dye were found to be 0.28 +/- 0.04 microg/g tissue in control animals and 1.0 +/- 0.2 microg tissue after adrenaline-induced acute hypertension (p < .01). Rats pretreated with selenium or vitamin E also showed macroscopic leakage of Evans-blue albumin after adrenaline injection i.e., there was no significant difference in protein extravasation between untreated and treated animals (p > .5). The mean value for Evans-blue dye was found to be 1.0 +/- 0.2 microg/g tissue in acute hypertension group, 0.9 +/- 0.2 microg/g tissue in selenium pretreated animals and 1.0 +/- 0.2 micrg/g tissue vitamin E injected animals after acute hypertension. The results show that antioxidants did not influence the blood-brain barrier breakdown during adrenaline-induced acute hypertension.

Animals↗
PubMed1999

Association between angiotensin-converting enzyme gene polymorphism and coronary artery disease.

An insertion/deletion (I/D) polymorphism in the gene for angiotensin-converting enzyme (ACE) is associated with myocardial infarction and other cardiac pathology. There is evidence for a role of the renin-angiotensin system in cell growth and in the repair of damaged arterial walls, so the ACE gene is postulated to be a candidate gene affecting the important clinical problem of coronary artery disease (CAD). In view of the clinical importance of the ACE as a major marker of cardiovascular diseases, we investigated the I/D polymorphism of the ACE gene in Turkish CAD patients in comparison with control subjects to evaluate a possible association between CAD and the gene encoding ACE. Polymerase chain reaction, restriction fragment length polymorphism, and agarose gel electrophoresis techniques were used to determine the ACE genotype in 58 subjects. The frequencies of ACE D and ACE I allele among the patients with CAD were 62.26% and 37.73 % and in the control subjects were 49.3% and 50.76%, respectively. The greater frequency of deletion allele (D) was in the CAD group than in the control subjects was significant (P < 0.01).

Adult↗
PubMed1996

The effects of the pretreatment of intravenous high dose methylprednisolone on Na(+)-K(+)/Mg(+2) ATPase and lipid peroxidation and early ultrastructural findings following middle cerebral artery occlusion in the rat.

The sodium-potassium activated and magnesium dependent adenosine-5'-triphosphatase (Na(+)-K(+)/Mg(+2) ATPase EC.3.6.1.3.) activity and lipid peroxidation and early ultrastructural findings were determined in rat brain at the acute stage of ischaemia produced by permanent unilateral occlusion of the middle cerebral artery (MCA). The effects of the pretreatment with intravenous high-dose methylprednisolone (MP) on these biochemical indices and ultrastructural findings were also evaluated in the same model. The rats were divided into four groups. In group I, 10 rats were used to determine Na(+)-K(+)/Mg(+2) ATPase activity and the extent of lipid peroxidation by measuring the malondialdehyde (MDA) content and normal ultrastructural findings. In group II on 20 rats, only subtemporal craniectomy was done in order to determine the effects of the surgical procedure on these indices and findings. This group was treated intravenously with saline solution before occlusion. In group III with MCA occlusion, saline solution was administered intravenously to 20 rats in the same amount of methylprednisolone used in group IV, ten minutes before the occlusion. In Group IV, a single high-dose (30 mg/kg) of methylprednisolone was administered intravenously, ten minutes before occlusion in 20 rats. After occlusion of the middle cerebral artery, Na(+)-K(+)/Mg(+2) ATPase activity was decreased promptly in the first ten minutes in the ischaemic hemisphere and remained at a lower level than the contralateral hemispheres in the same group and the normal levels in group I, during 120 minutes of ischaemia. A single dose methylprednisolone pretreatment prohibited the inactivation of Na(+)-K(+)/Mg(+2) ATPase. On the other hand, there was significant difference in malondialdehyde content between group I and group III. Malondialdehyde levels were significantly increased following ischaemia and a non-significant increase was observed in the contralateral hemisphere. Methylprednisolone treatment significantly decreased malondialdehyde content on the side of the ischaemic hemisphere. We conclude that there is a positive relationship between membrane-bound enzyme Na(+)-K(+)/Mg(+2) ATPase activity, malondialdehyde content and early ultrastructural changes in the treated group with MP. These data suggest that the pretreatment injection of high doses (30 mg/kg) methylprednisolone contribute to the protection of the brain from ischaemia with stabilization of the cell membrane by effecting the lipid peroxidation and the activation of Na(+)-K(+)/Mg(+2) ATPase.

Animals↗