Multiple species of wild tree peonies gave rise to the 'king of flowers', Paeonia suffruticosa Andrews.

The origin of cultivated tree peonies, known as the 'king of flowers' in China for more than 1000 years, has attracted considerable interest, but remained unsolved. Here, we conducted phylogenetic analyses of explicitly sampled traditional cultivars of tree peonies and all wild species from the shrubby section Moutan of the genus Paeonia based on sequences of 14 fast-evolved chloroplast regions and 25 presumably single-copy nuclear markers identified from RNA-seq data. The phylogeny of the wild species inferred from the nuclear markers was fully resolved and largely congruent with morphology and classification. The incongruence between the nuclear and chloroplast trees suggested that there had been gene flow between the wild species. The comparison of nuclear and chloroplast phylogenies including cultivars showed that the cultivated tree peonies originated from homoploid hybridization among five wild species. Since the origin, thousands of cultivated varieties have spread worldwide, whereas four parental species are currently endangered or on the verge of extinction. The documentation of extensive homoploid hybridization involved in tree peony domestication provides new insights into the mechanisms underlying the origins of garden ornamentals and the way of preserving natural genetic resources through domestication.

[Mannose-binding lectin (MBL) inhibits human cytomegalovirus infection of human MD-DC].

OBJECTIVE: To explore the inhibitory effect of different sources, different concentrations of Mannose-binding lectin (MBL) on human cytomegalovirus infection of human MD-DC cells. METHODS: The recombinant MBL was acquired by vector construction, and the natural MBL was purified from human plamsa. MD-DC were pre-exposed to several dilutions of the hMBL/rMBL for 30 min, then HCMV suspensions were added to MD-DC for 2 h to compare the inhibitory effect of hMBL/rMBL on the HCMV infection of MD-DC. MD-DC infected by HCMV co-culture with hMBL/rMBL to compare the inhibitory effect of hMBL/rMBL on the HCMV diffusion between MD-DC. HCMV-DNA in MD-DC was detected by fluorescence quantitative PCR. HCMV-PP65 in MD-DC was analyzed with flow cytometry, the ability of MD-DC to capture HCMV was observed with immunofluorescence confocal microscope. RESULTS: In hMBL/rMBL inhibition the ability of MD-DC capture HCMV experiments, the fluorescent quantitative PCR demonstrated that the amount of HCMV-DNA in 1 microg/mL of hMBL/rMBL treated cells was not significantly different from that of control group (P < 0.05). But the HCMV-DNA in 5 microg/mL and 10 microg/mL hMBL/rMBL treated group were significantly lower than that of control group (P < 0.05). The significant inhibit effects of 10 microg/mL hMBL/rMBL on the ability of MD-DC capture HCMV were observed by immunofluorescence confocal microscopy and flow cytometry. The inhibit effects of hMBL/rMBL on HCMV diffusion between MD-DC were also observed in 5 microg/mL and 10 microg/mL hMBL/rMBL treated groups at 72 hours. CONCLUSION: The hMBL/rMBL in physiological concentration range (5-10 microg/mL) can significantly inhibit human cytomegalovirus infection of human MD-DC cells, and the hMBL is more effective than rMBL.

Inhibitive effects of anti-oxidative vitamins on mannitol-induced apoptosis of vascular endothelial cells.

OBJECTIVE: Study blood vessel injury and gene expression indicating vascular endothelial cell apoptosis induced by mannitol with and without administration of anti-oxidative vitamins. METHODS: Healthy rabbits were randomly divided into four groups. Mannitol was injected into the vein of the rabbit ear in each animal. Pre-treatment prior to mannitol injection was performed with normal saline (group B), vitamin C (group C) and vitamin E (group D). Blood vessel injury was assessed under electron and light microscopy. In a second experiment, cell culture specimen of human umbilical vein endothelial cells were treated with mannitol. Pre-treatment was done with normal saline (sample B), vitamin C (sample C) and vitamin E (sample D). Total RNA was extracted with the original single step procedure, followed by hybridisation and analysis of gene expression. RESULTS: In the animal experiment, serious blood vessel injury was seen in group A and group B. Group D showed light injury only, and normal tissue without pathological changes was seen in group C. Of all 330 apoptosis-related genes analysed in human cell culture specimen, no significant difference was seen after pre-treatment with normal saline, compared with the gene chip without pre-treatment. On the gene chip pre-treated with vitamin C, 45 apoptosis genes were down-regulated and 34 anti-apoptosis genes were up-regulated. Pre-treatment with vitamin E resulted in the down-regulation of 3 apoptosis genes. CONCLUSION: Vitamin C can protect vascular endothelial cells from mannitol-induced injury.