Occurrence and Identification of a New Vector of Rice Orange Leaf Phytoplasma in South China.

Rice orange leaf disease (ROLD) is caused by rice orange leaf phytoplasma (ROLP) and occurs sporadically in rice-growing areas in countries of eastern and southeastern Asia. ROLD caused severe damage to rice production in South China in the 1980s. Although its impact subsequently declined in South China, it has reemerged as a serious threat recently. Our study showed that ROLD occurrence varies in different seasons and fields. It was more severe in summer-grown crops (from July to October) than in spring-grown crops (from March to July). In most fields, the incidence was less than 10%, and diseased plants were scattered throughout the fields. In 20% of fields, the incidence was between 10 and 30%. In some fields, over 90% of plants were affected, causing crop failure. Typical symptoms of ROLD include orange-colored leaves and poor growth. Diseased plants were determined as positive for ROLP but negative for Rice tungro bacilliform virus, Rice tungro spherical virus, and Rice transitory yellowing virus through polymerase chain reaction and reverse-transcription polymerase chain reaction. Phytoplasma bodies but not virus-like particles were observed by electron microscopy in phloem tissue of diseased leaves. The leafhopper Inazuma dorsalis, previously identified as the unique vector for ROLP, was rare in the affected fields. Another leafhopper, Nephotettix cincticeps, previously considered a nonvector for this phytoplasma, was very common. Transmission tests revealed that this insect could also transmit ROLP; therefore, it might represent a new vector responsible for the recent incidence of ROLD.

In vitro inhibition of fatty acid synthase by 1,2,3,4,6-penta-O-galloyl-ß-D-glucose plays a vital role in anti-tumour activity.

1,2,3,4,6-Penta-O-galloyl-ß-D-glucose (PGG) inhibits glioma cancer U251 cells, more strongly than MDA-MB-231 and U87 cells. In addition, PGG is transported across cancer cell membrane to further down-regulate FAS and activate caspase-3 in MDA-MB-231 cells. Compared with other FAS inhibitors, including catechin gallate and morin, PGG involves a higher reversible fast-binding inhibition with half-inhibitory concentration value (IC50) of 1.16 µM and an irreversible slow-binding inhibition, i.e. saturation kinetics with a dissociation constant of 0.59 µM and a limiting rate constant of 0.16 min(-l). The major reacting site of PGG is on the ß-ketoacyl reduction domain of FAS. PGG exhibits different types of inhibitions against the three substrates in the FAS overall reaction. The higher concentrations of PGG tested (higher than 20 µM) clearly altered the secondary structure of FAS by increasing the α-helix and induced a redshift in the FAS spectra. In addition, only PGG concentrations higher than 20 µM resulted in FAS precipitation.

Preparative isolation and purification of urolithins from the intestinal metabolites of pomegranate ellagitannins by high-speed counter-current chromatography.

Urolithins were separated from the intestinal metabolites of pomegranate ellagitannins by high-speed counter current chromatography in two steps using two solvent systems composed of n-hexane-ethyl acetate-methanol-acetic acid-water (2.5:2:0.25:5, v/v/v/v/v) and n-hexane-ethyl acetate-methanol-acetic acid-water (2.5:0. 8:0.25:5, v/v/v/v/v) for the first time. Each injection of 100mg extract yielded 21mg of pure urolithin A and 10mg of pure urolithin B. High-performance liquid chromatography analyses revealed that the purity of urolithin A and urolihtin B was over 98.5%. The structures of urolithin A and urolitihn B were identified by high resolution-MS, NMR and single crystal x-ray analysis. Urolithins reduced the oxidative stress status in colon cancer by decreasing the intracellular ROS and malondialdehyde levels, and increasing SOD activity in H2O2 treated Caco-2 cells.