Search PubMed⌕ Search

Biomedical subjects

N Kara

Publications and source records attributed to N Kara.

6 recordsLinked to original sources
PubMed2007

Lack of association between leptin G2548A gene polymorphism and Behçet's disease.

BACKGROUND: Behçet's disease is a chronic, multisystem, inflammatory disease characterized by the predominance of T-helper 1 cytokines. The disease is also characterized by infiltration of lymphocytes and neutrophils into the affected tissues. Because cytokines are involved in the regulation of lymphocyte and phagocyte functions, they may play an important role in the pathogenesis of Behçet's disease. Leptin, a member of the gp 130 family of cytokines, induces a strong T-helper 1 response and is regarded as a proinflammatory inducer. Recent studies have shown that serum leptin concentration was increased in patients with Behçet's disease and correlated with disease activity. OBJECTIVES: We aimed to investigate the role of G2548A polymorphism of leptin gene in patients with Behçet's disease and compare the results with healthy controls. PATIENTS AND METHODS: A total of 93 subjects with Behçet's disease and 125 healthy controls were included in this study. Analyses of G-2548A polymorphism of the LEP gene were performed using the PCR-restriction fragment length polymorphism technique. The genotypes (GG, GA, and AA of leptin G2548A) and alleles (G and A of leptin 2548) were scored and the frequency was estimated. The frequencies of the alleles and genotypes in patients and controls were compared. We analysed the correlation between leptin gene polymorphism and the clinical features of BD. RESULTS: Both genotype and allele frequencies were not significantly different between controls and Behçet's disease patients [OR=0.67, 95% CI (0.35-1.29), P=0.197 and OR=0.77, 95% CI (0.52-1.15), P=0.184]. We did not find any significant relationship between leptin gene polymorphism and the clinical features of BD (P>0.05). CONCLUSION: In the present case-control study, we found no evidence of an association between the G-2548A variant of the leptin gene and BD among Turks. Further studies are needed to investigate serum leptin level to explain the mechanisms behind the lack of association between leptin G2548A gene polymorphism and BD.

Base Sequence↗
PubMed1999

Blood pressure nomograms for children and adolescents in Turkey.

In order to obtain data on blood pressure (BP) distribution in Turkish children, a total of 5,599 Turkish children from birth to 18 years were studied. BP rises with age, and both systolic and diastolic BP showed a positive correlation with height and weight in both sexes. As the sampling was representative of Turkish children at different ages, the mean systolic and diastolic BP levels were compared for each age with the results reported in the study of the Second Task Force. The mean systolic and diastolic BP of Turkish children and the increase with growth and development were different from the Second Task Force study. Genetic, ethnic, and environmental factors were suggested to be responsible for this variation. In conclusion, normal BP curves should be applied with caution in childhood, and every population should use their own normal standards to define a measured BP level in children.

Adolescent↗
PubMed1999

Implications of certain genetic polymorphisms in scarring in vesicoureteric reflux: importance of ACE polymorphism.

Polymorphisms of the renin-angiotensin system (RAS) have been shown to affect renal prognosis in a number of diseases. We examined the influence of deletion (D) and insertion (I) polymorphism in the angiotensin I-converting enzyme (ACE) gene and the other polymorphic markers of RAS, and that of plasminogen-activator inhibitor-1 (PAI-1) on renal scarring in reflux nephropathy. Ninety-four children with third- or fourth-degree reflux were the subject of the study. They were stratified into two groups according to the technetium-99m-dimercaptosuccinic acid (DMSA) findings: the first group consisted of 41 patients with no scar formation. In the second group (n = 53), there was significant scar formation in the refluxing units. ACE levels, ACE gene, angiotensin-1 receptor (AT1) A1166C, angiotensinogen (ATG) M235T, and PAI-1 4G/5G polymorphisms were studied. In the second group with scarred kidneys, 18 patients had decreased renal function. The frequency of patients homozygous for the D allele was significantly greater in the second group with scar formation in the refluxing units compared with the first group of patients (P < 0.005). On multivariate analysis, the DD genotype was the only factor that had a significant impact on renal scar formation, introducing a 4.9-fold risk (P < 0.05, 95% confidence interval). We were unable to find any correlation with the presence ofDD genotype and hypertension, decreased renal function, proteinuria, or sex of the patient. DDgenotype correlated with the serum ACE levels (P < 0.005). AT1and ATGpolymorphisms and PAI-1 polymorphism did not correlate with scar formation or any of the parameters. This study provides evidence that the DDgenotype of ACE may be a genetic susceptibility factor contributing to adverse renal prognosis in reflux nephropathy; namely, scar formation. The role of the synergism between the aforementioned genetic polymorphisms can be enlightened with larger patient groups, possibly through multicenter studies.

Angiotensinogen↗
PubMed1997

Cardiac involvement in childhood polyarteritis nodosa.

In this report, we evaluated the cardiac findings of 15 children with polyarteritis nodosa. The age range of the patients was 4-14 years; with a mean of 10 years. All have had systemic involvement of the disease. The most common findings in cardiac evaluation were diminished left ventricular systolic functions and mild mitral and/or tricuspid valve regurgitation. One patient had pericardial thickening with no effusion. One had sinus tachycardia. There were no signs of myocardial infarction or ischemia clinically or electro-cardiographically. In conclusion, we did not find cardiac complications, such as pericarditis or myocardial infarction, to be as frequent as in previous reports. However, even in asymptomatic patients, systolic dysfunction or valvular involvement were common findings in patients with polyarteritis nodosa, which were not reported previously. These findings may be due to the histological changes of the myocardium or atrioventricular valves. Although these were not severe and fatal lesions, long-term follow-up of these patients with echocardiography may help to determine the course of cardiac involvement.

Adolescent↗
PubMedDate not supplied

Partial trisomy 18q.

Explore the source record for details and available documents.

Abnormalities, Multiple↗