Brood Pheromone Foraging

Foraging experiments conducted as described in Ma et al 2018 during Summer 2015. Camera indicates the recording equipment used to record foraging. Colony ID identifies each unique colony, that were randomly assigned Screen treatments. Repeated measures were conducted for 3 different pheromone treatments on 3 different Days. Foraging was recorded at 3 time points following pheromone treatment. The number of foaragers carrying pollen or not carrying pollen were recorded

EAG_2016

Electroantennography (EAG) data associated with Ma et al 2018. Colony represents the source colony from which individual nurses and foragers were taken. Behavior categorizes individual bees as nurses or foragers. Four concentrations for each of two pheromones were used for the analysis. Raw values were divided by eag response to average of hexane controls to produce standardized responses. Hexane responses were taken before and after pheromone exposure

BPO Forage May2018

R code in Rmarkdown format used to analyze foraging data

EAG May 2018

R code in Rmarkdown format used to anlayze EAG data

CHIP-induced AKT activation directly inhibited FoxO proteins, an occurrence closely correlated with apoptosis resistance.

<p>(A) MCF7 and MCF10A cells were transfected with Myc-CHIP or Myc empty vectors as negative control. AKT inhibition with LY294002 (20 µmol/L, 1h) led to the activation of FoxO proteins. (B) Cells transfected with CHIP siRNA or negative control siRNA were treated with LY294002 (20 µmol/L, 1h) and immunoblotted for p-AKT (T308), p-FoxO1 (S256), p-FoxO3 (S253), and p-FoxO4 (S193). (C) AKT activation induced by CHIP overexpression led to the decrease in Bim, cleaved caspase 9, and cleaved PARP. Treatment with LY294002 (20 µmol/L, 1h) could reverse this effect. (D) Knockdown of FoxO1, FoxO3, and FoxO4 led to the decrease in Bim, cleaved caspase 9, and cleaved PARP. Treatment with LY294002 (20 µmol/L, 1h) could not reverse this effect.</p

A model described how CHIP regulated PTEN protein level.

<p>Overexpression of CHIP promoted degeneration of PTEN, which can increase the activation of PI3K pathway to promote the phosphorylation of FoxO3. FoxO3 binding to bim and pten promoters was inhibited and Bim and PTEN protein levels were decreased. Cells demonstrated apoptosis resistance, and the phosphorylation of AKT increased significantly. It formed a loop to reduce the PTEN protein level constantly.</p

Sensitivity, specificity, and areas under the curves for CEA, CA153 and combinations of these markers in nipple discharge with breast cancer.

<p>Sensitivity, specificity, and areas under the curves for CEA, CA153 and combinations of these markers in nipple discharge with breast cancer.</p

CHIP regulated FoxO3 binding to <i>bim</i> and overexpression of CHIP induced apoptosis resistance.

<p>(A) CHIP inhibited FoxO3 binding to the <i>bim</i> promoter. MCF7 and MCF10A cells were transfected with or without Myc-CHIP, followed by ChIP assay. The relative band intensity of PCR products revealed the binding of FoxO3 to the <i>bim</i> promoter. RT-PCR was performed for <i>bim</i> promoter (* <i>P</i><0.05). (B) Knockdown of CHIP increased <i>bim</i> transcription in both MCF7 and MCF10A cells. Cells were transfected with CHIP siRNA or negative control siRNA, followed by ChIP assay. The relative band intensity of PCR products revealed the binding of FoxO3 to the <i>bim</i> promoter. RT-PCR was performed for <i>bim</i> promoter (* <i>P</i><0.05). (C) Overexpression of CHIP attenuated apoptosis in cisplatin-treated MCF7 and MCF10A cells. Myc-CHIP was overexpressed in MCF7 and MCF10A cells that were subsequently treated with cisplatin for 24 h. All groups of cells were analyzed by flow cytometry (* <i>P</i><0.05).</p

CHIP overexpression activated PI3K/AKT and inhibition of FoxO proteins.

<p>(A) CHIP overexpression activated the PI3K/AKT signaling pathway. MCF7 and MCF10A cells were transfected with Myc-CHIP or Myc empty vectors as negative control. The cells were harvested and blotted after 48 h. (B) CHIP overexpression increased the phosphorylation of FoxO family proteins.</p

Receiver operating characteristic (ROC) curve analyses.

<p>The ROC plots for CEA (A), CA153 (B), CA125 (C) and the combination of CEA and CA153 (D) were used to differentiate breast cancer from benign disease. AUC, area under the receiver operating characteristic curve; CI, confidence interval.</p