20 research outputs found

    Leptin to high-molecular-weight adiponectin ratio is independently correlated with carotid intima-media thickness in men, but not in women.

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    BACKGROUND: The leptin:adiponectin ratio (L:A ratio) is an independent predictor of carotid intima-media thickness (CIMT). OBJECTIVE: To evaluate whether the leptin:high-molecular-weight adiponectin ratio (L:HA ratio) is associated with CIMT in the general population. METHODS: We investigated the relationship between the L:HA ratio and CIMT in 233 Japanese study participants (106 men and 127 women). RESULTS: After adjustment for confounding factors, CIMT was significantly correlated with the log L:HA ratio (beta = 0.11, p = 0.014) in men, whereas no correlation was observed in women (beta = 0.01, p = 0.50). Conclusion: The L:HA ratio is closely correlated with CIMT in men, but not in women

    Low educational level increases functional disability risk subsequent to heart failure in Japan: On behalf of the Iwate KENCO study group.

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    ObjectivesThe risk factors that contribute to future functional disability after heart failure (HF) are poorly understood. The aim of this study was to determine potential risk factors to future functional disability after HF in the general older adult population in Japan.MethodsThe subjects who were community-dwelling older adults aged 65 or older without a history of cardiovascular diseases and functional disability were followed in this prospective study for 11 years. Two case groups were determined from the 4,644 subjects: no long-term care insurance (LTCI) after HF (n = 52) and LTCI after HF (n = 44). We selected the controls by randomly matching each case of HF with three of the remaining 4,548 subjects who were event-free during the period: those with no LTCI and no HF with age +/-1 years and of the same sex, control for the no LTCI after HF group (n = 156), and control for the LTCI after HF group (n = 132). HF was diagnosed according to the Framingham diagnostic criteria. Individuals with a functional disability were those who had been newly certified by the LTCI during the observation period. Objective data including blood samples and several socioeconomic items in the baseline survey were assessed using a self-reported questionnaire.ResultsSignificantly associated risk factors were lower educational levels (odds ratio (OR) [95% confidence interval (CI)]: 3.72 [1.63-8.48]) in the LTCI after HF group and hypertension (2.20 [1.10-4.43]) in no LTCI after HF group. Regular alcohol consumption and unmarried status were marginally significantly associated with LTCI after HF (OR [95% CI]; drinker = 2.69 [0.95-7.66]; P = 0.063; unmarried status = 2.54 [0.91-7.15]; P = 0.076).ConclusionPreventive measures must be taken to protect older adults with unfavorable social factors from disability after HF via a multidisciplinary approach

    Truncated product of the bifunctional DLST gene involved in biogenesis of the respiratory chain

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    Dihydrolipoamide succinyltransferase (DLST) is a subunit enzyme of the α-ketoglutarate dehydrogenase complex of the Krebs cycle. While studying how the DLST genotype contributes to the pathogenesis of Alzheimer’s disease (AD), we found a novel mRNA that is transcribed starting from intron 7 in the DLST gene. The novel mRNA level in the brain of AD patients was significantly lower than that of controls. The truncated gene product (designated MIRTD) localized to the intermembrane space of mitochondria. To investigate the function of MIRTD, we established human neuroblastoma SH-SY5Y cells expressing a maxizyme, a kind of ribozyme, that specifically digests the MIRTD mRNA. The expression of the maxizyme specifically eliminated the MIRTD protein and the resultant MIRTD-deficient cells exhibited a marked decrease in the amounts of subunits of complexes I and IV of the mitochondrial respiratory chain, resulting in a decline of activity. A pulse-label experiment revealed that the loss of the subunits is a post-translational event. Thus, the DLST gene is bifunctional and MIRTD transcribed from the gene contributes to the biogenesis of the mitochondrial respiratory complexes
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