801some other Cg components, e.g., (Zl-6-nonenal or (2)-6nonenyl acetate, which were described by Buttery et al. (1982) to possess strong melon-like aroma far below the level of detection used in this study, seems probable.Registry No. , 95-16-9. LITERATURE CITEDAbd El-Baki, M. M.; A s h , A.; El-Samahy, S. K.; Abd El-Fadeel, M. G. Dtsch. Leben.sm.-Rundsch. Velluz, A.; Passerat, J.-P.; Ohloff, G. J. Sci. Food Renold, W.; Niif-Muller, R.; Keller, U.; Willhalm, B.; Ohloff, G. Schultz, T. H.; Flath, R. A.; Mon, T. R.; Eggling, S. B.; Teranishi, Tressl, R.; Engel, K.-H.; Kossa, M.; Koppler, H. J. Agric. Food Winter, M.; Kloti, R. Helv. Chim.p-Mentha-195-dien-8-01 (3a) and p-mentha-l(7),2-dien-8-01 (3b) were isolated from deteriorated citral as major components and were identified by IR, EI-MS, FI-MS, ' H NMR, and 13C NMR. When 3a or 3b was treated with aqueous citric acid, an equlibrium mixture of 3a-3b isomers (55:45) resulted and both isomers were subsequently converted to p-cymen-8-01(6) by disproportionation and redox reactions.

Background and objectives: Cardiac failure is directly affected by left ventricular (LV) dysfunction, and particularly LV systolic dysfunction is strongly associated with survival in ESRD patients. The aim of this study was to determine the prognostic value of reduced LV ejection fraction (LVEF) measured at the time of initiation of hemodialysis (HD) in incident HD patients.Design, setting, participants, & measurements: 1254 consecutive ESRD patients who electively started HD therapy were screened by echocardiography within 1 month after its inception. They were divided into five groups according to LVEF levels with a decrease of 0.1 each and were followed up for up to 7 years. Survival was examined with the Kaplan-Meier method and compared using the log-rank test.Results: Among the 1254 patients, LVEF levels >0. Conclusions: Reduced LVEF on starting HD therapy could stratify risk of cardiovascular and all-cause mortality in ESRD patients. Screening by echocardiography at start of HD therapy might be recommended to predict prognosis in patients with ESRD.

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IntroductionChemokines and their receptors are potential therapeutic targets in rheumatoid arthritis (RA). Among these, several studies suggested the involvement of CXC chemokine 4 (CXCR4) and its ligand CXC ligand 12 (SDF-1) in RA pathogenesis. However, the role of these molecules in T-cell function is not known completely because of embryonic lethality of Cxcr4- and Cxcl12-deficient mice. In this report, we generated T cell-specific Cxcr4-deficient mice and showed that the CXCR4 in T cells is important for the development of collagen-induced arthritis (CIA).MethodsT cell-specific Cxcr4-deficient mice were generated by using the Cre-loxP system. Mice harboring loxP sites flanking exon 2 of the Cxcr4gene (Cxcr4flox/flox) were generated by homologous recombination and crossed with Cre transgenic mice expressing Cre recombinase under the control of Lck promoter (Cxcr4+/+/Lck-Cremice) to generate T cell-specific Cxcr4-deficient mice (Cxcr4flox/flox/Lck-Cre mice). CIA was induced by immunization with chicken type II collagen and Complete Freund's Adjuvant (CFA).ResultsThe incidence, but not the severity, of CIA was significantly reduced in Cxcr4flox/flox/Lck-Cre mice compared with Cxcr4+/+/Lck-Cre mice. We found that the expression of CXCR4 was enhanced in activated T cells, and the migration of Cxcr4-deficient T cells toward SDF-1 was severely impaired. However, antibody production, cellular proliferative response, and cytokine production on treatment with type II collagen (IIC) were normal in these knockout mice, suggesting that CXCR4 is not involved in T-helper functions. Interestingly, the proportion of CXCR4-expressing T cells was much increased in affected joints compared with that in draining lymph nodes in CIA-induced mice, and distribution of Cxcr4flox/flox/Lck-Cre mouse-derived T cells into affected joints was suppressed compared with that in Cxcr4+/+/Lck-Cre T cells.ConclusionsThese results indicate that CXCR4 expression in T cells is important for the development of CIA, by recruiting activated T cells toward inflammatory sites, and suggest that CXCR4 is a good target for the treatment of RA in humans.