Objective: To assess possibility of polyphenol-enriched oolong tea to reduce dietary lipid absorption in humans. Design: Twelve healthy adult subjects, three males and nine females, aged (mean7s.d.) 22.071.8 years, respectively, were randomly divided into two groups. The participants were followed a double-blind placebo-controlled crossover design, including 7-day washout periods and 10-day treatment periods. During the treatment periods, subjects were given about 38 g of lipids from potato chips (19 g each within 30 min after lunch and dinner) and total 750 ml beverages (placebo-or polyphenolenriched oolong tea) at three meals. Blood samples were collected for biochemical examination at days 8, 18, 25 and 35 of the study period. On the last 3 days of each treatment period, feces were collected to measure the excretion of lipids. Results: Lipid excretion into feces was significantly higher in the polyphenol-enriched oolong tea period (19.3712.9 g/3day) than in the placebo period (9.477.3 g/3day) (Po0.01). Cholesterol excretion tended to increase in polyphenol-enriched oolong tea period (1.871.2 g/3day) compared with that of placebo (1.270.6 g/3day) (P ¼ 0.056). Conclusions:The results of this study indicated that polyphenol-enriched oolong tea could increase lipid excretion into feces when subjects took high-lipid diet.

These two new vascular indexes might be useful in actual clinical settings to evaluate cardiovascular risks with various clinical backgrounds.

Interferon-beta (IFN-β) is a critical antiviral cytokine and is essential for innate and acquired immune responses to pathogens. Treatment with polyinosinic:polycytidylic acid (poly(I:C)) induces transient accumulation of IFN-β mRNA, which involves an increase and a decrease of IFN-β mRNA. This phenomenon has been extensively analyzed as a model for understanding the mechanisms of gene induction in response to external stimuli. Using a new RNA metabolic labeling method with ethynyluridine to directly measure de novo RNA synthesis and RNA stability, we reassessed both de novo synthesis and degradation of IFN-β mRNA. We found that transcriptional activity is maintained after the maximum accumulation of IFN-β mRNA following poly(I:C) treatment on immortalized human bronchial epithelial cells. We also observed an unexpected change in the stability of IFN-β mRNA before and after the maximum accumulation. The results indicate that this method of RNA metabolic labeling provides a general approach for the simultaneous analysis of transcriptional activity and mRNA stability coupled with transcriptional timing.

Abstract-Renin belongs to a family of aspartyl proteases and is the rate-limiting enzyme in the synthesis of the potent vasoactive peptide angiotensin II. Processing of renal renin has been extensively investigated in juxtaglomerular granular cells, in which prorenin and active renin are present in secretory condensed granules. Previous studies demonstrated alternative renin transcription in rat adrenal glands. Different studies reported novel intracellular forms of renin deduced from novel 5′ variants derived from renin mRNA in both mice and humans. Comprehensive detailed studies in genetically engineered mice showed that both a secreted and an intracellular form of renin plays divergent mechanism regulating fluid intake and metabolism by the brain renin-angiotensin system; however, the presence, regulation, and functions of these renin isoforms in kidney and adrenal gland are not fully understood in mice. To investigate the characteristics of renin isoforms in mice, we performed a systematic inventory of renin transcripts of mice with and without a duplication of the renin gene alternatively from previous studies. We discovered a novel isoform of renin of the Ren2 gene, which conserved functionally important residues of the prosegment and incomplete isoforms of the Ren1C/D gene lacking a pre-pro segment. In situ hybridization assays revealed alternative renin isoforms expressed along cortical tubules. Newly generated transgenic mice with systemic overexpression of alternative renin transcript showed enhanced local angiotensin II generation without elevation of plasma renin activity and systemic insulin resistance in vivo, providing new pathophysiological insights into insulin resistance exaggerated by bona fide renin isoform. Correspondence to Tomoaki Ishigami, Department of Medical Science and Cardio-Renal Medicine, Yokohama City University, Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, Kanagawa, Japan. E-mail tommmish@hotmail.com Identification of Bona Fide Alternative Renin Transcripts Expressed Along Cortical Tubules and Potential Roles in Promoting Insulin Resistance In Vivo Without Significant Plasma Renin Activity ElevationTomoaki Ishigami, Tabito Kino,* Lin Chen,* Shintaro Minegishi, Naomi Araki, Masanari Umemura, Kaito Abe, Rie Sasaki, Hisako Yamana, Satoshi Umemura © 2014 American Heart Association, Inc. Materials and Methods Cloning and Identification of Alternative Renin Transcripts AnimalsAll animals were purchased from Oriental Yeast Company (Mihama, Chiba, Japan) and were housed and maintained under conditions approved by the Institution Animal Care and Use Committee of Yokohama City University. Rapid Amplification of cDNA Ends ProtocolTo investigate whether alternative renin expression is found in mouse adrenal glands, we performed 5′ rapid amplification of cDNA ends (RACE) analysis in adrenal tissue from 129 mice that endogenously have both Ren1D and Ren2 renin 6 and C57BL/6J mice with Ren1C renin. RNA was isolated from the mice with the use of Trizol reagent (Invitrogen, C...

We propose that API may be a new vascular index useful for monitoring and assessing the severity and complexity of atherosclerosis in subjects with coronary artery disease and for evaluating atherosclerotic diseases.

Atherosclerotic diseases, such as coronary artery disease and peripheral artery disease, are systemic disorders and among the leading causes of mortality and morbidity throughout the world. However, the exact pathophysiological mechanisms underlying the development of atherosclerosis remain unknown; currently, atherosclerosis is thought to involve an inflammatory process. Systemic inflammatory reactions and accumulation of immune cells in atherosclerotic lesions in situ are considered essential. We have comprehensively analyzed autoantibodies in patients with atherosclerosis by means of a newly developed high-throughput autoantibody analysis system. A wide range of autoantibodies was found in sera from patients with atherosclerosis. After we statistically analyzed the titers of each autoantibody with conventional techniques, the results underwent text-mining analyses based on natural language processing. Combinatory analysis revealed a close association between anti-interleukin (IL)-5 antibody and atherosclerosis. Titers of anti-IL-5 antibodies and serum IL-5 concentrations were also closely associated with other risk factors, such as low-density lipoprotein cholesterol, serum creatinine, fasting plasma glucose, gender, and age, suggesting that suppressed IL-5 function mediated by autoantibodies in patients with atherosclerosis plays an important role in the disease process. To validate the clinical significance of these findings, we computed the specificity and sensitivity of titers of anti-IL-5 autoantibodies for human atherosclerosis. When antibody titers of 1.49 were assumed to predict the presence of atherosclerosis, the sensitivity was 95.0% and the specificity 91.0%, with an area under the curve of 0.940. Our results provide important clues to understanding the role of autoantibody-mediated immune reactions in human atherosclerosis and suggest novel therapeutic opportunities for management of the disease.

are a certain number of RMI patients whose prognosis has not improved. Accordingly, the purpose of the present study was to clarify characteristics, treatment strategy, and in-hospital outcomes of RMI patients in the Tokyo CCU network database within the contemporary real-world setting. Methods Study DesignThis study was performed using data from the Tokyo CCU network database, collected between January 2013 and December 2016. Only the data of patients with MI were selected. Diagnoses of AMI were based on the univer-

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