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Polymorphisms in the promoter region of the serotonin reuptake transporter (SERT) gene may underlie the disturbance in gut function in patients with irritable bowel syndrome (IBS). Association studies of SERT polymorphisms and IBS have shown diverse results among different countries, which might be due to racial and subject composition differences. The aim of this study was to assess the potential association between SERT polymorphisms and IBS in Koreans. A total of 190 IBS patients, who met the Rome II criteria, and 437 healthy controls were subjected to genotyping. SERT polymorphisms differed in the IBS and control groups (P = 0.014). The SERT deletion/deletion genotype occurred with greater frequency in the diarrhoea-predominant IBS group than in the controls. A strong genotypic association was observed between the SERT deletion/deletion genotype and diarrhoea-predominant IBS (P = 0.012). None of the clinical symptoms analysed was significantly associated with the SERT genotypes. The frequency of the SERT insertion/insertion genotype was much lower than that of the other two genotypes. A significant association was observed between the SERT polymorphism and IBS, especially diarrhoea-predominant IBS, suggesting that the SERT gene is a potential candidate gene involved in IBS in Korea.

Objective: Ghrelin is a recently discovered peptide, which is produced primarily in the stomach. This orexigenic peptide participates not only in the induction of mealtime hunger but also in long-term body weight regulation and energy homeostasis. Adiponectin is a protein secreted by adipocytes, and has been proposed to mediate obesity-related insulin resistance. Moreover, concentrations of adiponectin are reduced in individuals with obesity, insulin resistance and cardiovascular disease. However, human data are sparse about the direct relationship between adiponectin, ghrelin and cardiovascular risk factors including insulin resistance. Design: Three hundred and thirty-eight elderly Korean women (mean age^S.D., 72.3^5.5 years) were included in the present study. Methods: Plasma ghrelin and adiponectin levels were measured by RIA. Anthropometric measurements were taken and a 75 g oral glucose tolerance test performed. Fasting insulin and lipid profile were measured and insulin resistance was determined using the homeostasis model assessment insulin resistance index (HOMA-R) and the quantitative insulin sensitivity check index. Results: Plasma adiponectin levels were negatively correlated with central obesity indices such as waist circumference (r ¼ 20.27, P , 0.001) and waist-to-hip ratio (WHR) (r ¼ 20.32, P , 0.001), and with insulin resistance indices such as fasting insulin (r ¼ 20.17, P ¼ 0.004) and HOMA-R (r ¼ 2 0.13, P ¼ 0.035). Plasma ghrelin levels were negatively correlated with WHR (r ¼ 2 0.12, P ¼ 0.03), but plasma adiponectin and ghrelin levels were not correlated (r ¼ 0.03, P ¼ 0.66). Multiple regression analysis showed that adiponectin was associated with WHR, fasting insulin and fasting glucose levels. When ghrelin was used as a dependent variable, only WHR remained in the final fitted model. Conclusion: Fasting plasma adiponectin and ghrelin levels were found to be associated with central obesity or insulin resistance. However, plasma adiponectin and ghrelin concentrations were not associated with each other in elderly Korean women. 150 715-718 European Journal of Endocrinology

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Objectives: When we perform chest compression on a patient on a bed, the mattress and bed frame can be depressed together with the patient's chest. This study was conducted to assess whether bed frame deflection occurred during chest compressions. Methods: We designed a firm bed ("bed like the ground," BLG) to assess the bed frame deflection in the Stryker Trauma Stretcher (STS) and the ER stretcher cart (ER-SC). The STS included a soft mattress and the ER-SC a hard mattress. We performed 50 continuous chest compressions on the Resusci Anne Skill Reporter with CPRmeter in each experiment. The experiments were done in four settings. Test 1 included the BLG; test 2 included a mattress and backboard on each bed; test 3 included the mattress of each bed and a backboard on the BLG; and test 4 included the mattress of each bed on the BLG. We calculated the mattress and bed frame deflections using the gaps of compression depths between the values measured by Resusci Anne and CPRmeter. Results: The mattress deflections of the STS and ER-SC mattress were determined to be 11.2 and 0.67 mm, respectively. The bed frame deflection for the STS and ER-SC were 0.95 and 5.17 mm, respectively. Conclusion: The study confirms that bed frame deflection will occur when we perform chest compressions on the manikin lying on a bed. Additionally, the bed frame deflections differ depending on the type of bed. (Hong Kong j.