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Background and Aims: The associations between dietary vitamin C (VC), vitamin E (VE) intake and aortic aneurysm and dissection (AAD) remain unclear. This study aimed to prospectively investigate the associations between dietary VC and VE with the incident risk of AAD., Methods and Results: A total of 139 477 participants of UK Biobank cohort were included in the analysis. Dietary VC and VE consumptions were acquired through a 24-h recall questionnaire. Cox proportional regression models were used to examine the associations between VC, VE intake and the risk of AAD. Incident AAD was ascertained through hospital inpatient records and death registers. During a median follow-up of 12.5 years, 962 incident AAD events were documented. Both dietary VC [adjusted hazard ratio (HR), 0.77; 95 % confidence intervals (CI), 0.63-0.93; P-trend = 0.008] and VE (adjusted HR, 0.70; 95 % CI, 0.57-0.87; P-trend = 0.002) were inversely associated with incident AAD when comparing the participants in the highest quartile with those in the lowest. In subgroup analyses, the associations were more pronounced in participants who were over 60 years old, participants with smoking history, hypertension or hyperlipidemia, who were under the high risk of AAD., Conclusion: Higher dietary VC and VE intakes are associated with reduced risk of AAD. Our study emphasizes the importance of diet adjustment strategies targeted on VC and VE to lower the incidence rate of AAD especially in the high-risk population., Competing Interests: Declaration of competing interest The authors declare that they have no conflict of interest., (Copyright © 2024 The Italian Diabetes Society, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition and the Department of Clinical Medicine and Surgery, Federico II University. Published by Elsevier B.V. All rights reserved.)

OK-432, a streptococcal preparation, has been shown as an effective activator to induce human monocyte-derived dendritic cells maturation. During this process, the activation of Toll-like receptor 4 plays an important role. However, the signaling pathway involved in has not been fully understood. In the present study, we investigated the underlying mechanisms, by which OK-432 induced maturation of human monocyte-derived DCs (MoDCs). We observed that exposure of immature MoDCs to OK-432 activated the p38 MAPK and NF-kappaB pathway, accompanied up-regulated the surface expression of maturation markers CD80, CD83, CD86 and HLA-DR, increased secretion of TNF-alpha, IL-12 and chemokine, IP-10. In addition, T cells stimulatory capacity was also enhanced. The maturation of MoDCs stimulated by OK-432 was inhibited by treatment with p38 pathway inhibitor, SB203580, or NF-kappaB pathway inhibitor, BAY-117082. Whereas, blocking of JNK pathway with SP600125 or ERK pathway with PD98059 did not influence OK-432-induced DCs maturation. Taken together, our data indicated that OK-432-induced DCs maturation was due, at least partly to the activation of p38 and NF-kappaB pathway.

Two representative spirostanol saponins that have the typical structure for the sugar moiety, diosgenyl alpha-L-rhamnopyranosyl-(1-->2)-[beta-D-glucopyranosyl-(1-->3)]-beta-D-glucopyranoside (gracillin) and diosgenyl alpha-L-rhamnopyranosyl-(1-->2)-[alpha-L-rhamnopyranosyl-(1-->4)]-beta-D-glucopyranoside (dioscin), were easily synthesized by a general approach. A procedure using guanidine for the selective deblocking of acetyl while retaining benzoyl protecting groups is described.

Three new triterpenoid saponins were isolated from the alcoholic extract of the bark of Nothopanax davidii. Their structures have been determined on the basis of spectral and chemical data as 3-O-alpha-(4'-O-acetyl)-L-arabinopyranosyl-3 beta-hydroxyolean-12-ene- 28,29-dioic acid-28-O-[alpha-L-rhamnopyranosyl(1-->4)-beta-D-glucopyranosyl (1-->6)-beta-D-glucopyranosyl]ester, named yiyeliangwanoside IX; 3-O-alpha-(2'-O-acetyl)-L-arabinopyranosyl-3 beta-hydroxyolean-12-ene-28,29- dioic acid-28-O-[alpha-L-rhamnopyranosyl(1-->4)-beta-D-glucopyranosyl(1-->6)- beta-D-glucopyranosyl] ester, named yiyeliangwanoside X; and 3-O-beta-d-xylopyranosyl-3 beta-hydroxyolean-12-ene-28,29-dioic acid-28-O-[alpha-L-rhamnopyranosyl(1-->4)-beta-D-glucopyranosyl(1-->6)-b eta-D - glucopyranosyl] ester, named yiyeliangwanoside XI.

13,17-Secodiacholestanes (6) were synthesized from cholesterol (1) in six steps. The key intermediates, (20R)- and (20S)-diacholest-13(17)-enes (3a and 3b), underwent ozonization and reduction to provide (20R)- and (20S)-13,17-secodiacholesta-13,17-dione (5a and 5b), respectively. On Clemmensen reduction, the diones (5a and 5b) yielded the target molecule 6. The structure of an unknown biomarker was shown to be different from the proposed 6 by gas chromatographic/mass spectrometric comparison.

5 alpha-(17R,20R)-14,15-Secocholestane (12) was synthesized from cholesterol (1) in 12 steps. The key intermediate, 5 alpha-cholest-14-en-3 beta-yl acetate (4), underwent ozonization, reduction, hydrolysis, and oxidation to provide 5 alpha-14,15-secocholesta-3,14,15-trione (8). One of the Clemmensen reduction products of 8 is 5 alpha(17R,20R)-14,15-secocholest-15-ol (11); treatment of the alcohol (11) with tosyl chloride and subsequent reduction with lithium aluminum hydride yielded the target molecule (12).