Inhibitory effects of Sage extract on the growth of enteric bacteria.

Antibacterial activity of Sage extract at concentrations of 0.1, 0.05, 0.025, 0.0125, 0.00625, 0.003125, 0.00156, 0.0005 and 0.00025 g dL(-1) against Salmonella typhi, Shigella sonnei, S. flexneri, Proteus vulgaris, Staphylococcus aureus, ETEC Escherichia coli and Pseudomonas aeruginosa was evaluated. Susceptibility testing of bacterial strains against 18 antibiotics was also performed for comparison. The results showed that P. aeruginosa and ETEC E. coli were completely resistant to Sage extract even at concentration of 0.1 g dL(-1). Its antibacterial activity (0.1 g dL(-1)) against P. vulgaris, S. flexneri and S. sonnei was the same as nitrofurantoin and ampicilline respectively. Sage extract (0.1 and 0.05 g dL(-1)) exhibited the same effects as ampicilline and streptomycin against S. typhi. Its antibacterial activity (0.1, 0.05 and 0.25 g dL(-1)) against S. aureus was the same as ceftazidim, chloramphenicol, gentamycin, neomycin and nitrofurantoin and was more significant compared to streptomycin and vancomycin. The results suggest Sage can be considered as an alternative herbal in the treatment of infections caused by the above-mentioned bacteria.

Insulin does not disrupt actin microfilaments, microtubules, and in vitro aortic endothelial wound repair.

In the face of small denuding injuries, the endothelium undergoes a process of rapid repair involving actin microfilaments, microtubules, and centrosomes to reestablish an intact monolayer. Failure to maintain an intact endothelial monolayer is an important factor in the pathogenesis of the atherosclerotic plaque. It was hypothesized that increased susceptibility to atherosclerosis in diabetes mellitus may be, in part, due to delayed reendothelialization following endothelial injury. To test this, the effects of high insulin concentrations on the reendothelialization of small wounds were examined using an in vitro porcine aortic endothelial cell wound model. Elevated concentrations of insulin did not disrupt the confluent endothelial monolayer or alter endothelial cell shape. Insulin also did not induce detectable alterations in the distribution of microtubules and microfilaments in the confluent monolayer. High insulin did not reduce the extent of reendothelialization of a linear wound made in the confluent monolayer. Centrosomal reorientation was similar to that of control wounded cultures as was the reorganization of the microfilaments and microtubules. The data suggest that the atherogenic effects of hyperinsulinemia are not due to disruption of endothelial repair.