The goal of this study was to collect and analyse information on the prevalence of childhood migraine and disability due to migraine in primary school children of 4th to 8th grades (ages ranging from 9 to 17 years) in the Aydin urban area. A cross-sectional school-based study was conducted between March and June 2004. There were 76 333 children of 4th to 8th grades in primary schools in Aydin. Nearly 10% of this population (7721 out of 76 333) was evaluated by a multistage clustered sampling procedure. Four questionnaire forms were applied to each child by a study neurologist during class time. Questionnaire A consisted of a single question, 'Have you ever had a headache?'. To those who responded 'yes', questionnaire B was applied as a second step, which consisted of eight questions. Diagnosis of migraine headache was made according to International Classification of Headache Disorders 2004. Migraine disability was measured with questionnaire C, which was originally the Pediatric Migraine Disability Assessment (PedMIDAS). Migraine history, previous migraine diagnosis and pain intensity were measured with questionnaire D. According to questionnaire A, 79.6% of boys and 87.1% of girls suffered from headaches. The prevalence of migraine was 9.7% (7.8% in boys, 11.7% in girls) according to questionnaire B. The male:female ratio was 1:1.5. Total PedMIDAS score was 9.94 +/- 8.41 days in boys and 11.50 +/- 12.28 days in girls. Only 1.9% of the children had previously been diagnosed with migraine. The average migraine headache history was 2.48 +/- 1.18 years in girls and 2.57 +/- 1.18 years in boys. Although migraine is a common health problem among school children in Aydin, it is mostly still under-recognized.

IntroductionBoth hepatitis B virus (HBV) and hepatitis D virus (HDV) infection play an increasingly important role in liver diseases. The main objective of this study was to investigate the socio-epidemiological, laboratory and radiological aspects of both HBV and HDV infection near the Iranian border of Turkey.Material and methodsThe study included 3352 patients with HBV and HDV infection. Socioepidemiological, laboratory and radiological aspects of the study subjects were retrospectively examined. Comorbid metabolic diseases were not assessed due to the retrospective design of the study.ResultsMost of the study subjects were HBe antigen negative. No significant difference in terms of HBV-DNA levels or HBe antigen seropositivity was detected between the city centre and rural areas (p > 0.005). The mean HBV-DNA level in the anti-HDV-positive group was significantly lower than in the anti-HDV-negative group (p < 0.001). The rate of HDV-RNA positivity in women was higher than in their male counterparts (p = 0.017). Anti-HDV-IgG was detected in 18.4% of tested subjects who came from an urban area. In contrast, 12.5% of subjects of the rural group had a positive result for anti-HDV-IgG. Among 134 ultrasonographically evaluated delta hepatitis patients, 37.3% had liver cirrhosis. On the other hand, in 1244 patients with hepatitis B monoinfection, there were 90 patients with liver cirrhosis. Radiologically, the rate of hepatic steatosis in delta hepatitis patients was lower than in those with HBV monoinfection.ConclusionsHepatitis D virus infection was particularly prevalent among the urban population as well as in female subjects. More broadly, the current observations are the first to suggest an inverse correlation between delta hepatitis and ultrasonography-proven hepatic steatosis.

The transcription factor KLF6 gene has been identified as a tumor suppressor because of its inactivation in several types of cancers by different mechanisms. However, there are no data in the literature investigating the KLF6 mutation rate and expression levels in breast cancer. Therefore, the present study was conducted in order to investigate whether genetic alterations of KLF6 in association with the KLF6 mRNA expression levels may play a role in breast carcinogenesis. For this purpose, we analyzed alterations of the KLF6 gene by direct sequencing and the mRNA levels by reverse transcription-PCR (RT-PCR). In addition to four different non-coding alterations, one missense and two silent alterations were identified in the coding sequence. Reduced KLF6 expression was observed in 41 (83.67 %) of the 49 breast cancer tumors. These findings suggest that the mutation profile of the KLF6 gene in breast tumors is similar to other cancer types. However, these mutations do not exert any effect on the gene expression rate. Downregulation of KLF6 during the progression of breast cancer is independent of the mutations and occurs by a different mechanism.

ABSTRACT. Genetic and epigenetic factors affecting DNA methylation and gene expression are known to be involved in the development of colon cancer, but the full range of genetic alterations and many key genes involved in the pathogenesis of colon cancer remain to be identified. NPRL2 is a candidate tumor suppressor gene identified in the human chromosome 3p21.3 region. We evaluated the role of this gene in the pathogenesis of colorectal cancer by investigating NPRL2 mRNA expression in 55 matched normal and tumor colon tissue samples using quantitative RT-PCR analysis. There was significantly decreased NPRL2 expression in 45% of the patients. Lower NPRL2 expression was observed significantly more frequently in poorly differentiated tumor samples than in highly or moderately differentiated tumors. We conclude that expression of NPRL2 contributes to progression of colon cancer.

Coinfection with GBV-C/HGV in patients with chronic hepatitis C (CHC) may influence clinical course and response rates of antiviral therapy. Aim of the study was to investigate the prevalence of GBV-C/HGV/HCV coinfection and its influence on outcome of interferon/ribavirin combination therapy. Three hundred and four patients with CHC [m/f = 211/93, age: 42 (18-65)] were investigated. HGV RNA detection was performed by polymerase chain reaction prior to and 6 months after the end of antiviral therapy. HGV/HCV coinfection could be identified in 37/304 (12.2%) patients with intravenous drug abuse as the most common source of infection (N = 21, (56.8%)). The predominant HCV genotype in coinfected individuals was HCV-3a (HCV-3a: 51.4%, HCV-1: 37.8%, HCV-4: 10.8%). HGV coinfection was more prevalent in patients infected with HCV-3 compared to HCV-1 or HCV-4 [19/45 (42.2%) vs. 14/185 (7.6%) vs. 4/52 (7.7%), P < 0.01]. Patients with HGV/HCV coinfection were younger [35 (18-56) vs. 43 (19-65), years; P < 0.01], and advanced fibrosis (F3-F4) was less frequent (22.2% vs. 42.9%, P < 0.05). A sustained virological response was achieved more frequently in HGV/HCV coinfected patients [26/37 (70.3%)] than in monoinfected patients [120/267 (44.9%), P < 0.01]. HGV RNA was undetectable in 65.7% of the coinfected patients at the end of follow-up. Intravenous drug abuse seems to be a major risk factor for HGV coinfection in patients with chronic hepatitis C. Coinfection with HGV does not worsen the clinical course of chronic hepatitis C or diminish response of HCV to antiviral therapy. Interferon/ribavirin combination therapy also clears HGV infection in a high proportion of cases.