AhIRT1 and AhNRAMP1 metal transporter expression correlates with Cd uptake in peanuts under iron deficiency - Fig 4

<p>Expression pattern of <i>AhNRAMP1</i> (a) and <i>AhIRT1</i> (b) in the roots of Luhua 8 and Zhenghong 3 grown in full nutrient solution (+Fe) or without Fe (−Fe) for 12 d. The expression levels of <i>AhNRAMP1</i> and <i>AhIRT1</i> were normalized to that of <i>Ahactin</i> gene. Different letters above error bars indicate values (mean ± SE, n = 3) are significantly different between treatments at the 0.05 level.</p

Growth of wild-type yeast cells transformed with empty vector pYES2, <i>AhIRT1</i> and <i>AhNRAMP1</i> in the presence of galactose.

<p>Serial dilutions of the transformed yeast cells with OD_600nm 0.5 to 0.0005 were spotted on SD-Ura plates containing 0 or 30 μM CdCl₂ in the presence of galactose. The yeast was grown on the plates at 30°C for 3 d for the comparison.</p

Parameters of the Michaelis-Menten plus linear model used to resolve the kinetic of influx curves in Fig 3.

<p>Data represent mean values ± SE.</p

KRS and KGS inhibited the expression of proinflammatory mediators in tMCAO rats.

<p>(A) Representative photomicrographs of the immunohistochemical expression of iNOS, MMP9, MPO, ICAM, TNF-α, and IL-1β (brown staining) in the cortical ischemic penumbra. (B, C) Immunoreactivity of proinflammatory mediators measured using the integrated optical density (IOD) of the immunostained-positive cells. The data are expressed as mean ± SEM (<i>n  = </i>6 each group). Treatment with KRS and KGS significantly reduced the expression of proinflammatory mediators. *<i>p<</i>0.05, **<i>p<</i>0.01, compared with the vehicle-treated group.</p

KRS and KGS inhibited the activation of NF-κB and STAT3 in tMCAO rats.

<p>(A) Representative photomicrographs of the immunohistochemical expression of p-NF-κB p65 and p-STAT3 (brown staining) in the cortical ischemic penumbra. (B) Immunoreactivity of p-NF-κB p65 and p-STAT3 measured using the integrated optical density (IOD) of the immunostained-positive cells (<i>n  = </i>6 each group). (C) Representative immunoblots of NF-κB p65, Lamin B, p-STAT3, and STAT3. The data are expressed as mean ± SEM. (D, E) Immunoblot expression measured using densitometry. The data are expressed as mean ± SEM (<i>n  = </i>3 each group). The loaded protein amount was normalized to Lamin B or STAT3, and the data are expressed as a percentage of the mean value in the sham-operated group. Treatment with KRS or KGS significantly reduced the phosphorylation of STAT3 at Tyr705, phosphorylation of NF-κB p65 at Ser536 and the nuclear content of NF-κB p65. *<i>p<</i>0.05, **<i>p<</i>0.01, compared with the vehicle-treated group.</p

KRS and KGS attenuated ischemic neuron and axon damage in tMCAO rats.

<p>(A) Representative photomicrographs of NeuN-immunopositive neurons (brown staining) in the cortical ischemic penumbra. The neurons injured by ischemia had altered morphology or died. (B) Representative photomicrographs of APP immunoreactivity (brown staining) in the ipsilateral corpus callosum and striatum. The damaged axons were intensely stained for APP. (C) Schematic representation of a coronal brain section shows the ischemic penumbra in cortex, corpus callosum and striatum. Three fields were selected at each indicated position for quantitative measurements of immunohistochemical staining. (D) Relative number of NeuN-positive neurons expressed as a percentage of the neurons in the sham-operated group. (E) APP immunoreactivity measured using the integrated optical density (IOD) of the immunostained-positive cells. Treatment with KRS or KGS significantly reduced neuron and axon damage compared with the vehicle-treated controls. The data are expressed as mean ± SEM (<i>n  = </i>6 each group). *<i>p<</i>0.05, **<i>p<</i>0.01, compared with the vehicle-treated group.</p

Chemical structures of kaempferol glycosides.

<p>Chemical structures of kaempferol glycosides.</p

Bioinformatic analyses of microRNA-targeted genes and microarray-identified genes correlated with Barrett's esophagus

<p>Barrett's esophagus (BE) is defined as a metaplasia condition in the distal esophagus, in which the native squamous epithelium lining is replaced by a columnar epithelium with or without intestinal metaplasia. It is commonly accepted that BE is a precancerous lesion for esophageal adenocarcinoma. The aim of this study was to investigate the aberrant microRNAs (miRNAs) and differentially expressed genes (DEGs) associated with BE based on online microarray datasets. One miRNA and five gene expression profiling datasets were retrieved from the Gene Expression Omnibus Database. Aberrant microRNAs and DEGs were obtained using R/Bioconductor statistical analysis language and software. 23 dysregulated miRNAs and 632 DEGs demonstrating consistent expression tendencies in the five gene microarrays were identified in BE. Moreover, 1962 target genes of aberrant miRNAs were predicted using three bioinformatic tools, namely TargetScan, RNA22-HSA and miRDB. Ultimately, 93 target DEGs were obtained, after which functional annotation was performed on DAVID Bioinformatics Resources. Among Gene Ontology (GO) biological processes, digestive tract development and epithelial cell differentiation have demonstrated significant associations with BE pathogenesis. In addition, analysis of the KEGG pathways has revealed associations with cancer. To enable further study, one miRNA-target DEGs regulatory network was constructed using Cytoscape. 6 target DEGs demonstrated higher-degree distributions in the network, and ROC analysis indicated that FNDC3B may be the best potential biomarker for BE diagnosis. The data presented herein may provide new perspectives for exploring BE pathogenesis and may offer hits with regard to potential biomarkers in BE diagnosis, prediction and therapeutic evaluation.</p

KRS and KGS improved neurological deficit in tMCAO rats.

<p>The neurological deficit scores evaluated after 2 h ischemia or 22 h reperfusion following 2 h ischemia, respectively. Post-ischemic treatment with an equimolar dose of KRS (10.0 mg/kg) or KGS (7.5 mg/kg) administrated i.v. significantly ameliorated the neurological deficit scores compared with the vehicle-treated controls. The data are expressed as mean ± SEM (<i>n</i> = 17 each group). *<i>p<</i>0.05, **<i>p<</i>0.01, compared with the vehicle-treated group.</p

KRS and KGS attenuated brain infarction in tMCAO rats.

<p>(A) Representative photographs of TTC-stained brain coronal sections. (B) Infarct volume expressed as a percentage of whole brain volume. Treatment with KRS or KGS greatly ameliorated the infarct volume compared with the vehicle-treated controls. The data are expressed as mean ± SEM (<i>n  = </i>8 each group). *<i>p<</i>0.05, **<i>p<</i>0.01, compared with the vehicle-treated group.</p