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Sleep disorders (SDs) are frequently seen in patients with liver cirrhosis. Polysomnography (PSG), actigraphy, and electroencephalogram (EEG) are the common objective methods to diagnose SDs. The most commonly used subjective methods are the Pittsburgh sleep quality index (PSQI) and Epworth sleepiness scale (ESS). We aimed to evaluate the effect of liver transplantation (LTx) on SDs using a combination of objective (PSG and EEG) and subjective (PSQI and ESS) methods.

A total of 18 patients with cirrhosis on an LTx waiting list were included in this study. Patient clinical status and biochemical parameters were evaluated. All patients completed the validated Turkish forms of the PSQI and ESS before and 9 months after LTx. All patients underwent EEG and PSG before and 9 months after LTx.

In total, 18 patients with liver cirrhosis (men 12; 66.7%, mean age 53.22±10.43 years) were included in this study. Pretransplant mean PSQI and ESS scores were 8.4±3.11 and 7.28±3.89, respectively; 9-month posttransplant mean PSQI and ESS scores were 4.5±2.8 and 4.72±2.91 (p<0.01), respectively. Before transplantation, metabolic encephalopathy was detected in 6 patients by EEG, whereas metabolic encephalopathy was detected in only 1 patient posttransplant. Posttransplantation PSG sleep duration (all stages) increased relative to pretransplant PSG values. Sleep latency and rapid eye movement latency were found to be reduced compared to the pretransplant values.

This pilot study compared SDs in patients with pre- and post-LTx by combining the subjective and objective methods. Significant SD improvements were found at the 9th month.

This pilot study compared SDs in patients with pre- and post-LTx by combining the subjective and objective methods. Significant SD improvements were found at the 9th month.

The importance of hyperplastic polyps during colorectal carcinogenesis is appreciated related to the understanding of serrated pathway. The morphologic subtypes of hyperplastic polyps in carcinogenesis and the nomenculature of lesions with both hyperplastic and adenomatous areas are controversial. We aimed to reveal the molecular properties of hyperplastic polyp subtypes and the molecular changes in polyps containing both hyperplastic and adenomatous areas. Matherial and Methods 49 hyperplastic polyps [19 microvesicular (MVHP), 19 goblet-rich (GRHP), 11 mucin-poor (MPHP)] and 10 mixed hyperplastic and adenomatous polyps were analysed for KRAS, BRAF mutations and MSI with real-time PCR.

68,4% of MVHPs and 81% of MPHPs which were localized in right colon had BRAF mutations. While none of the GRHPs showing a KRAS mutation with a rate of 73% was localized in the ascending colon, 63% of them were localized in the rectosigmoid area. In five (50%) of the mixed polyps, KRAS mutation was detected both in the hyperologist’s attention.

Inflammatory bowel diseases (IBD) impairs patients’ quality of life (QoL). Inflammatory bowel disease questionnaire (IBDQ) is created to measure the health-related QoL specific for IBD. We planned to investigate the validation and reliability of the Turkish translation of IBDQ.

Patients filled self-report questionnaires (Turkish Inflammatory bowel disease questionnaire (TrIBDQ) and Short Form-36 (SF-36)) themselves under a physician’s supervision, and they were free to ask questions about the questionnaires. The participants then filled the same questionnaire after at least two weeks. Construct validity, discriminant ability, reliability, and susceptibility to change were analyzed separately for the IBD patients. Intra-class correlation coefficient (ICC) was used to assess test-retest reliability. Cronbach’s alpha values were used to assess internal consistency.

A hundred patients enrolled in the study, 53 with Crohn’s disease (CD), 47 with ulcerative colitis (UC). We found a moderate to high positive correlation between the TrIBDQ domains and the SF-36 dimensions. In UC and CD, TrIBDQ was able to differentiate active disease and remission. We found Cronbach’s alpha for TrIBDQ domains ranged from 0.76-0.94 in CD and from 0.79-0.92 in UC. The total Cronbach’s alpha for TrIBDQ was 0.96 in CD and 0.95 in UC. Sensitivity-to-change analyses of the bowel, systemic, and emotional scores showed statistically significant differences between their baseline and follow-up values.

TrIBDQ is a valid and reliable tool for assessing the quality of life in Turkish speaking IBD patients. Thus it can be used in clinical research and practice.

TrIBDQ is a valid and reliable tool for assessing the quality of life in Turkish speaking IBD patients. Thus it can be used in clinical research and practice.

Fanconi anemia complement group F (FANCF) is known to be involved in DNA repair, and the overexpression of FANCF protein leads to cell proliferation and ultimately to cancer. The purpose of this study was to assess whether FANCF methylation was associated with colorectal cancer (CRC).

A case-control experiment was conducted to study the association between FANCF methylation and CRC. We used quantitative methylation-specific PCR to measure the FANCF promoter methylation, and the percentage of methylation reference (PMR) to quantify the FANCF promoter methylation level. To investigate the effect of the selected FANCF fragment on gene expression regulation, we also performed a dual-luciferase reporter gene assay.

The results indicated that FANCF methylation in CRC tumor tissues was significantly lower than that in the nontumor tissues (median PMR 44.86% vs. 65.77%, p=0.00001). Analysis of receiver-operating characteristic curves showed that FANCF hypomethylation had a diagnostic value for CRC (area under curve [AUC] 0.670, sensitivity 55.8%, specificity 71.7%, p=0.00001). The dual-luciferase reporter assay showed that the FANCF fragment upregulated gene expression (fold change 1.93, p=0.002).

Research demonstrates for the first time that FANCF hypomethylation is significantly associated with CRC risk. FANCF hypomethylation may ultimately increase the risk of CRC by upregulating the expression of FANCF.

Research demonstrates for the first time that FANCF hypomethylation is significantly associated with CRC risk. this website FANCF hypomethylation may ultimately increase the risk of CRC by upregulating the expression of FANCF.