Microbial Arsenic Methylation in Soil and Rice Rhizosphere

Methylated arsenic (As) species are a common constituent of rice grains accounting for 10–90% of the total As. Recent studies have shown that higher plants are unlikely to methylate As in vivo suggesting that As methylation is a microbial mediated process that occurs in soils prior to plant uptake. In this study, we designed primers according to the conserved essential amino acids and structural motifs of arsenite <i>S</i>-adenosylmethionine methyltransferase (ArsM). We report for the first time the successful amplification of the prokaryotic <i>arsM</i> gene in 14 tested soils with wide ranging As concentrations. The abundance and diversity of the <i>arsM</i> gene in the rice rhizosphere soil and roots were analyzed using the designed primers. Results showed that microbes containing <i>arsM</i> genes were phylogenetically diverse, as revealed by the clone library and terminal restriction fragment length polymorphism (T-RFLP) analysis, and were branched into various phyla. Concentration of methylated As species in the soil solution was elevated in the rhizosphere soil and also by the addition of rice straw into the paddy soil, corresponding to the elevated abundance of the <i>arsM</i> gene in the soil. These results, together with evidence of horizontal gene transfer (HGT) of the <i>arsM</i> gene, suggest the genes encoding ArsM in soils are widespread. These findings demonstrate why most rice, when compared with other cereals, contains unusually high concentrations of methylated As species

Overall survival rates for patients who achieved CR or PR after chemotherapy of metastatic lesions (a), for patients who achieved SD after chemotherapy of metastatic lesions (b).

<p>Overall survival rates for patients who achieved CR or PR after chemotherapy of metastatic lesions (a), for patients who achieved SD after chemotherapy of metastatic lesions (b).</p

Multivariate analysis of variables correlated with overall survival.

<p>HR: hazard ration; CI: confidence interval; CT: Chemotherapy CRT: Chemoradiotherapy; PD: Progression of disease; SD: Stable disease; PR: Partial remission; CR: Complete remission;</p>a<p> Statistically significant.</p><p>Multivariate analysis of variables correlated with overall survival.</p

Overall survival rates according to KPS (a), liver metastasis (b), number of metastatic site (c), radiotherapy of primary tumor (d), response to chemotherapy (e), number of cycles of chemotherapy (f) and LDH (g).

<p>Overall survival rates according to KPS (a), liver metastasis (b), number of metastatic site (c), radiotherapy of primary tumor (d), response to chemotherapy (e), number of cycles of chemotherapy (f) and LDH (g).</p

Treatment characteristics.

<p>*52 patients received RT to primary lesions and 27 patients did not received RT;</p>†<p>88 patients received RT to primary lesions and 43 patients did not received RT.</p><p>Treatment characteristics.</p

Laboratory characteristics.

<p>Laboratory characteristics.</p

Relationships between serum HER2 ECD levels and clinicopathological variables.

<p>Relationships between serum HER2 ECD levels and clinicopathological variables.</p

Kaplan–Meier estimates for overall survival according to serum HER 2 ECD levels and tissue HER 2 status.

<p>Serum HER 2 ECD levels showed no association with overall survival. Whereas positive tissue HER 2 status was significantly associated with worse overall survival.</p

ROC curve for selection of the best cut-off value of serum HER 2 ECD to predict tissue HER 2 status.

<p>A cut-off of 16.35 ng/mL has a sensitivity of 51.4% and a specificity of 97.3% in discriminating HER 2-positive and HER 2-negative tumours.</p

Serum HER 2 ECD levels stratified by different levels of tissue HER 2 amplification or expression.

<p>The median HER 2 ECD level was significantly higher in patients with high levels of HER 2 amplification than in patients with low to moderate levels of amplification or no amplification (A). The median HER 2 ECD level was significantly higher in patients with HER 2 IHC 3+ than in patients with HER 0–2+ (B).</p