Serum Cystatin C Level as a Biomarker of Aortic Plaque in Patients with an Aortic Arch Aneurysm.

AIM: During surgery for an aortic arch aneurysm, aortic plaque in the descending aorta should be evaluated, but there are currently no suitable biomarkers for it. Surgeons should be especially aware of cerebral embolism from femoral perfusion and of peripheral embolism from stent graft deployment. Cystatin C is a known useful marker of renal dysfunction with a role as a biomarker for severity of coronary artery disease. In the absence of a suitable biomarker for aortic plaque in the descending aorta, we examine cystatin C as a candidate. METHODS: In all, 75 patients who underwent surgery for an aortic arch aneurysm were enrolled. They were divided into two groups, depending on whether they had chronic kidney disease or not. The serum cystatin C value and creatinine value were evaluated preoperatively. The aortic plaque volume ratio and components in the descending aorta were calculated from preoperative enhanced computed tomography. RESULTS: The soft plaque volume ratio was higher in patients with chronic kidney disease than in patients without it. Cystatin C positively correlated with the total aortic plaque volume ratio in all cases, and it positively correlated with the soft plaque volume ratio in both groups. Creatinine had no correlation with any type of plaque volume ratio in either group. In patients without chronic kidney disease, the soft plaque volume ratio was higher in patients with higher cystatin C levels than in patients with normal levels. CONCLUSION: The preoperative serum cystatin C level could be a biomarker of aortic plaque in the descending aorta in patients with an aortic arch aneurysm.

Inhibitory effects of a novel cationic dodecapeptide [CL(14-25)] derived from cyanate lyase of rice on endotoxic activities of LPSs from Escherichia coli and periodontopathic Aggregatibacter actinomycetemcomitans.

OBJECTIVE: CL(14-25), a dodecapeptide of cyanate lyase from rice, is a novel cationic α-helical antimicrobial peptide. In this study, we examined inhibitory ability of CL(14-25) against endotoxic activities of lipopolysaccharides (LPSs) from Escherichia coli and periodontal pathogenic Aggregatibacter actinomycetemcomitans. METHODS: Endotoxin-neutralizing activity of CL(14-25) was evaluated by inhibition to induction of cytokine and nitric oxide in human aortic endothelial cells (HAECs) and RAW264 mouse macrophage cells, respectively. Protective effect of CL(14-25) was determined in mice against lethal toxicity of LPS. RESULTS: IL-6 in HAECs was induced by stimulation with LPS preparations of A. actinomycetemcomitans and E. coli tested in this study, and addition of CL(14-25) to the medium caused inhibition of their induction in a dose-dependent manner. CL(14-25) inhibited NO induction in RAW264 cells by a smooth type LPS of E. coli O55:B5 and an Rc type LPS of E. coli J5 as well as lipid A of E. coli R515 in a dose-dependent manner. Simultaneous injection of E. coli O55:B5 LPS and CL(14-25) in BALB/c mice resulted in prevention of lethal toxicity of the former. The results of a Limulus amebocyte lysate assay and surface plasmon resonance analysis of interaction between CL(14-25) and E. coli LPS or lipid A showed that CL(14-25) specifically binds to a lipid A moiety of LPS. CONCLUSION: The results of present study suggest that CL(14-25) has a potential to be used as a nutraceutical agent for periodontal therapy.