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Biomedical subjects

Ibrahim Pirim

Publications and source records attributed to Ibrahim Pirim.

8 recordsLinked to original sources

Association of HLA class I and class II alleles with psoriasis vulgaris in Turkish population. Influence of type I and II psoriasis.

OBJECTIVE: To investigate the role of human leukocyte antigen (HLA) in susceptibility to psoriasis vulgaris in the Northeast region of Turkey and to contribute to the data related to HLA and psoriasis. METHODS: The study included 72 unrelated psoriatic patients (43 men and 29 women; aged 11-76 years) admitted to the Dermatology Department, University Research Hospital, Erzurum, Turkey between April 2002 and November 2003. We studied the distribution of HLA class I and II antigens in patients with psoriasis: 72 patients were divided into 2 groups according to the onset of psoriasis before age 40 years with family history (type I) and onset after age 40 without family history (type II). The HLA class I and II antigens were analyzed using the PCR-SSP method in 72 patients and in 104 controls. RESULTS: We found an increase in HLA-A*30 and A*68, B*7, B*13, B*57, Cw6, and DRB1*07 antigens in psoriatic patients compared with controls. As we compared type I and type II psoriasis with control group, B*57, Cw6 and DRB1*07 alleles were more significant in patients with type I psoriasis. Our patients with type II psoriasis represented a significant association with the HLA-B*13. CONCLUSION: Our findings along with previous HLA studies on psoriasis vulgaris patients from different racial groups showed that HLA-B*57 and DRB1*07 alleles are associated with the disease.

Adolescent↗

Association between alopecia areata and HLA Class I and II in Turkey.

HLA class I and II alleles have been described in patients with alopecia areata (AA). As in other immune mediated diseases, the HLA alleles associated with AA may influence the patient's ability to respond to immune challenges from both self and non-self antigens and can offer clues to the cause, prognosis, and potential therapy for the disease. The aim of this study was to determine which HLA class I and II alleles are associated with Turkish alopecia areata patients. Sixty-three patients with AA, alopecia totalis, or alopecia universalis were included in this study and compared with seventy-six healthy transplant donors. HLA DNA typing was performed by the PCR/SSP method. The frequency of HLA-B62 was significantly higher in patients than in controls. HLA-A2, HLA-A24, HLA-B35, HLA-DRB1*11, and HLA-DRB1*15 were significantly less common in patients than in the control group.

Alleles↗

Familial Mediterranean fever in a childhood population in eastern Turkey.

BACKGROUND: Familial Mediterranean fever (FMF) is an autosomal recessive disease characterized by recurrent attacks of inflammation of serosal membranes. Amyloidosis is the most severe complication of the disease The aim of this study was to explore the magnitude of the FMF problem and to describe clinical phenotypic and genotypic profile in the childhood population in Eastern Turkey. METHODS: In this study, 52 patients who were diagnosed as FMF between January 2000 and January 2003 in Department of Pediatrics, Ataturk University Hospital, were included. The diagnosis of FMF was based on typical clinical and laboratory features. The 12 FMF mutations were investigated in the patients. RESULTS: Of the 52 patients, 30 (57.7%) were girls, 22 (42.3%) were boys, and the age ranged from 9 months to 15 years (8.5 +/- 3.2 years). A positive family history for FMF was noted in 33 (63.5%) patients. The mean onset age was 6 +/- 3.4 (from 8 months to 14 years). Nineteen children (36.5%) were symptomatic below the age of 5 years. Abdominal pain was observed in 50 (96.2%), fever in 42 (80.8%), arthralgia in 29 (55.8%), arthritis in 18 (34.6%), splenomegaly in 11 (21.2), hepatomegaly in 15 (28.8%), myalgia in 11 (26.2%), erysipelas-like erythema in 10 (19.2%), thoracic pain in four (7.7%), protracted febrile myalgia in three (5.8%), and seizures in two (3.8%). The most frequent mutation was the M694V/M694V. Clinical presentation of the patients was not different in respect with genotypes (P > 0.05). Two patients had chronic renal disease suggestive of amyloidosis. CONCLUSION: It was noted that the FMF patients in this study had a broad spectrum of mutation combination, which might reflect the intercultural interactions of ancient ethnic groups that lived in Anatolia, and these mutations were not significantly different in respect to clinical presentations.

Adolescent↗

Genotoxicity of thallium-201 in patients with angina pectoris undergoing myocardial perfusion study.

Thallium-201 (201Tl) has been widely used as a nuclear reagent for myocardial blood flow imaging. The purpose of this study was to investigate genotoxic effects of 201Tl in patients with angina pectoris (n = 21), who had undergone myocardial perfusion imaging. Lymphocytes were isolated from each patient before, and 3, 30 and 90 days after 201Tl administration (111 MBq, 3 mCi) and were analyzed for chromosomal aberrations, sister chromatid exchanges, mitotic index and replicative index. There were significant increases in chromosomal aberrations and sister chromatid exchanges 3 days after 201Tl administration (p < 0.001), although no difference was noted in these values after 30 and 90 days (p > 0.05). Moreover, decreased mitotic index and replicative index were noted after 3 days of 201Tl administration (p < 0.001). These results suggest that the administration of 201Tl for myocardial blood flow imaging may induce genetic damage.

Angina Pectoris↗

The assessment of genotoxic effects in lymphocyte cultures of infants treated with chloral hydrate.

Chloral hydrate is a sedative commonly used in pediatric medicine. It was evaluated for genotoxicity in cultured peripheral blood lymphocytes of infants who were given chloral hydrate for sedation. Sister chromatid exchange and micronucleus frequencies were determined before and after chloral hydrate administration. After treatment, the frequencies of sister chromatid exchange and micronuclei were significantly increased, suggesting that chloral hydrate has moderate genotoxic potential in infants.

Bromodeoxyuridine↗

N-terminal heterogenicity of amyloid protein examined in Alzheimer's disease.

Alzheimer's disease is the major cause of dementia in humans. The affected brain shows characteristic abnormal filamentous proteins that accumulate intracellularly as neurofibrillary tangles, and extracellularly as senile plaques, as well as in cerebral blood vessels. The extracellular deposits are an amyloid protein, which is highly insoluble. In our study, we intended to show that the N-terminus of amyloid A4 protein can change in length and sequence in Alzheimer's disease, and possibly in other dementias.

Alzheimer Disease↗

Apolipoprotein E polymorphism and stroke in a population from eastern Turkey.

Human apolipoprotein E (apo E) alleles are polymorphic with significantly different frequencies among different ethnic groups and have been associated with increased risk of coronary heart disease, and postulated as a major genetic susceptibility locus for Alzheimer's disease. Studies undertaken in different populations have shown different association patterns between apo E genotype and stroke. The aim of this study was to determine the risk of apo E genotype in stroke patients living in the eastern part of Turkey. The apo E genotypes and allele frequencies of 229 individuals from the same geographic area were determined by polymerase chain reaction and restriction fragment length polymorphism, of which 103 were patients with a documented history of stroke without other apparent dementia and 126 age-matched healthy subjects as a control group. A reduced E3/4 genotype frequency was found in subjects with stroke and the E2/3 genotype frequency was elevated in patients with previous stroke. There was no association between apo E epsilon4 allele and stroke. The APOE alleles had divergent effects in this population. Association between APOE (the gene) alleles and stroke in this population may be altered due to interaction with other genetic effects. The effects of APOE alleles and genotypes require further study in different populations.

Aged↗

Serum ubiquitin levels in patients with nonalcoholic steatohepatitis.

BACKGROUND/AIMS: Nonalcoholic steatohepatitis is increasingly recognized as the most common liver disease in patients with elevated liver enzymes. In the pathophysiology of nonalcoholic steatohepatitis, the first step is the lipid accumulation in the liver causing steatosis, the second step involves the endotoxins, cytokines and environmental toxins causing oxidative stress and lipid peroxidation, in time leading to steatohepatitis. Ubiquitin is a molecular chaperone that plays a major role in the degradation of intracellular proteins. Ubiquitin proteasome system is also considered as a cellular defense mechanism that removes damaged proteins generated by oxidative stress. In order to search for the role of ubiquitin in the pathogenesis of nonalcoholic steatohepatitis, serum levels of ubiquitin were studied in patients with nonalcoholic steatohepatitis for the first time in the literature, to our knowledge. METHODOLOGY: Eighteen patients with biopsy proven nonalcoholic steatohepatitis diagnosis (13 males and 5 females with a mean age of 41) and 16 healthy volunteers as a control group (11 males and 5 females, with a mean age of 38) were included in the study. Serum ubiquitin levels were studied by ELISA method. RESULTS: The mean serum ubiquitin level (14.13 +/- 1.46 micrograms/mL) in patients with nonalcoholic steatohepatitis was significantly elevated compared to that of the control group (7.66 +/- 0.40 micrograms/mL) (p < 0.001). No correlation was found among serum ubiquitin levels and hepatic steatosis, inflammation and fibrosis. CONCLUSIONS: Increased serum ubiquitin levels may show that the ubiquitin proteasome pathway actively participates in defending against oxidative stress in nonalcoholic steatohepatitis. Serum ubiquitin concentration may be a marker predicting the intracellular cytoprotective response against oxidative stress rather than the degree of liver damage in pathogenesis of nonalcoholic steatohepatitis. Ubiquitin proteasome system based therapies may have a place in the treatment of patients with nonalcoholic steatohepatitis in the future.

Adult↗