Corporate Culture and Empathy and Excitement Labor of Service Employees inService Company, Mainly at Tokyo Disneyland

東京ディズニーランド(ディズニーシーを含むパーク)の大成功(集客と驚異的リピート率)の要因は、①「夢と魔法の王国」にふさわしいアトラクション1、②接客従業員(主に、非正社員、キャラクターを含む)のホスピタリティ・サービスが、顧客に「素晴らしい思い出に残る感動経験」を与えていることである。望ましいサービス労働のあり方は「顧客・従業員インターラクティブの共感に基づく従業員の感動労働」であるという仮説をたて、その解明を研究目的とした。①先行研究の考察、②運営会社へのインタビュー、③現場でのキャストのサービス労働の実査と簡単な質問、④顧客へのヒストリカル・インタビュー・アンケート実施という研究方法によって、接客従業員の「共感・感動労働」を実証中である。共感・感動労働の視点で、東京ディズニーランドと日本マクドナルド、スターバックスコーヒーとを比較した

Expression of uPA and Caveolin-1 in endocrine-resistant versus sensitive cell lines.

<p>Assessment of mRNA relative expression of uPA and Caveolin-1 using qPCR in wt-MCF7, MCF7-LTED, 1%MCF7 and MCF7-TAMR cell lines. Bars represent ± SEM. *p<0.05, **p<0.01, ***p<0.001.</p

Analysis of src and downstream signalling in response to dasatinib combined with endocrine agents.

<p>Wt-MCF7, MCF7-LTED, 1%MCF7 and MCF7-TAMR cells were treated for 24-hours with the drug combinations mentioned above. Standard concentrations of dasatinib (100nM), E2 (0.01nM), 4-OHT (10nM) and fulvestrant (ICI) (10nM) were used. Whole-cell extracts were assessed for expression of various proteins indicated using immunoblotting. Figures below each panel represent semi-quantitave changes in protein expression relative to actin.</p

Dasatinib promotes nuclear shuttling of ER in the MCF7-TAMR cells but not the 1%MCF7.

<p>1%MCF7 and MCF7-TAMR cells were treated for 24-hours with 1%FBS, dasatinib (100nM), 4-OHT (10nM), or the combination and stained with ER, pSrc^tyr416 and DAPI; bars indicate 20μm <b>(A)</b>. Schematic diagram showing cross-talk between non-genomic ER and Src. ER associates with Src at the cell membrane via a non-genomic mechanism. This leads to an increase in both ERK1/2 and AKT providing a survival advantage. The reduced genomic activity of ER in this setting enhances resistance to tamoxifen. Inhibition of Src with dasatinib causes ER to shuttle to the nucleus where it is targeted by tamoxifen, leading to a decrease in proliferation and re-sensitization to the endocrine agent <b>(B)</b>.</p

Antiproliferative effects of dasatinib alone or in combination with endocrine agents.

<p>Cells were treated with increasing concentrations of dasatinib (<b>A,B</b>), or fixed concentration of dasatinib and increasing concentrations of 4-OHT (<b>C,D</b>) or fulvestrant (ICI) (<b>E,F</b>) for 6-days with a medium change at day 3. Cell viability was determined using CellTitre-Glo^® Luminescent Cell Viability Assay. The data are representative of three independent experiments (Error bars represent ± SEM).</p

Effects of dasatinib on ER-mediated transcription and ER signalling.

<p>Cell lines were co-transfected with EREIItkLuc and pCH110 and treated with the combinations mentioned (<b>A, B, C, D</b>). Standard concentrations of dasatinib (100nM), E2 (0.01nM), 4-OHT (10nM) and fulvestrant (ICI) (10nM), were used. Normalized luciferase activity from triplicate wells was expressed relative to the vehicle-treated control. Bars represent ± SEM. *p<0.05, **p<0.01, ***p<0.001. Effects were confirmed in three independent experiments. Wt-MCF7, MCF7-LTED, 1%MCF7 and MCF7-TAMR cells were treated as indicated for 24-hours, with the same amounts as stated above. Western blot was used to assess changes in total ER and PgR. Figures below each panel represent semi-quantitave changes in protein expression relative to actin.(<b>E</b>).</p

Additional file 8: Figure S2. of Cholesterol biosynthesis pathway as a novel mechanism of resistance to estrogen deprivation in estrogen receptor-positive breast cancer

A. Kaplan-Meier plots revealing the influence of high or low expression of MSMO1, LBR, SQLE and EBP in relapse-free survival of 496 ER- BC patients treated with chemotherapy, from publicly available data collected over 10 years. B. wt-MCF7, MCF7 LTED and ZR75.1 LTED were treated with siRNA targeting siMSMO1, siLBR, siSQLE and siEBP. Wt-MCF7 were treated with or without E2. Change in proliferation was expressed as fold change relative to sicontrol. Bars represent Âą SEM from eight replicates. The assessment was carried out in two independent experiments

Additional file 3: Table S2. of Cholesterol biosynthesis pathway as a novel mechanism of resistance to estrogen deprivation in estrogen receptor-positive breast cancer

Alteration in transcript levels for genes within the cholesterol biosynthesis pathway

Legislative Documents

Also, variously referred to as: House bills; House documents; House legislative documents; legislative documents; General Court documents

Additional file 4: of Targeting tumour re-wiring by triple blockade of mTORC1, epidermal growth factor, and oestrogen receptor signalling pathways in endocrine-resistant breast cancer

Figure S4. Anti-proliferative effect combination of RAD001 and neratinib together with endocrine agents (a) 4-OHT and (b) ICI. Endocrine-resistant and -sensitive BC cell lines were treated with a combination of RAD001 and neratinib and increasing concentrations of (a) 4-OHT or (b) ICI for 6 days with media change at day 3. Cell viability was analysed using a cell titer-glo assay. Data are expressed as fold-change relative to vehicle control. Error bars represent mean ± SEM. wt-MCF7 (1.5 nM RAD001; 200 nM neratinib); MCF7-LTED (1.5 nM RAD001; 300 nM neratinib); wt-SUM44 (0.37 nM RAD001; 450 nM neratinib); SUM44-LTED (0.37 nM RAD001; 250 nM neratinib); wt-HCC1428 (1.5 nM RAD001; 500 nM neratinib); HCC1428-LTED (3 nM RAD001; 250 nM neratinib). (PDF 208 kb