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Updated: England Hockey statement in relation to COVID-19 virus
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As elsewhere in society, the Coronavirus is impacting the current and future activities of England Hockey. Below details England Hockey's position in relation to community hockey, the England Hockey AGM, international fixtures and England Hockey offices.
Community hockey
Community hockey will continue to take place unless we are advised otherwise by government, and we will continue to update the Hockey Family on the situation. Please check with your local league if you are unsure if the game is going to take place. We would encourage all players to follow the widely available guidance of public health with regards to people maintaining good hygiene to avoid spreading of the Covid-19 virus.
In a hockey context, we would advise clubs and other hockey venues to ensure washing facilities have appropriate provision of hygiene products and urge players to follow the public health guidance in environments where they are in close proximity to others. If any players, officials or coaches are feeling unwell, please follow the government's advice to self-isolate and therefore do not take part in hockey-related activities. We also recommend our more elderly players and officials consider whether they should take part in hockey activity.
All players and officials are responsible for their own safety equipment (goalkeeping kit, facemasks, mouth guards, whistles, shin pads etc) and we would encourage everyone to ensure they are clean and not shared amongst team-mates.
Instead of the traditional handshake at the start and end of the game, we are encouraging players to tap sticks: https://twitter.com/Xenioshockey/status/1235819830562832384. A warm smile and thanks of appreciation to officials may be more appropriate at this current time.
England Hockey AGM - Tuesday 17 March
The AGM will take place as planned unless circumstances change. The meeting at Bisham Abbey begins at 7:30pm. If you are uncomfortable attending in the circumstances then duly authorised representatives are advised that you can instruct a proxy to cast your votes until 7:30pm on Sunday 15 March. Please click here for more information.
FIH Hockey Pro League & England Hockey domestic Finals
England Hockey is continuing to monitor government advice in relation to the hosting of events. At this juncture, there are no changes to our advertised programme. We will keep participants, ticket buyers and other stakeholders informed if this position changes.
International teams' tour to South Africa
The GB men's and women's squads were both due to travel to South Africa on Sat 13 Mar for warm weather training camps (with match play for the women) as part of their Tokyo preparations. After due consideration, it has been concluded that this is not in the best interest of players and staff, and they will not be travelling. With no international programme activity over the weekend of 13 and 14 Mar, players are available for selection for the final Men's and Investec Women's Hockey League matches of the season.
England Hockey Offices
England Hockey offices remain open for business. In the event the situation escalates and we need to close the offices, we are confident we have the capability to continue to provide services to our customers, through home working and mobile applications.
Updated: Answers to additional questions from clubs
Can umpires allow additional time at penalty corners for facemasks etc to be cleaned?
Yes, this is a sensible approach.
I am not attending the umpiring course I'm booked onto because of COVID-19, what happens next?
Our standard terms and conditions still apply, if cancelled on short notice, we will offer a transfer to another course.
We have a school games fixture and a pupil from both teams who have symptoms and are being tested so we have agreed to postpone our fixture.
Where possible, and if both teams agree, we will try to accommodate in the current climate. However, unless the government advise otherwise, games will go ahead as planned and if a fixture is not played on the correct date or at least before the 'slip' date, it will result in a forfeiture.
Should we still attend training camps and events?
As long as you are following PHE advice and you don't present with any symptoms, or you have not been in contact with someone who has presented with symptoms, all events will continue as normal.
You've mentioned elderly players, is there specific advice for them?
Not as such, no. It is just worth noting that there is slightly different government advice for the over 70s.
Should our team still travel abroad for matches?
Please follow advice and be aware of the countries that are listed on the FCO website: https://www.gov.uk/guidance/travel-advice-novel-coronavirus


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Biological effects of 17β-estradiol (17βE2) and other synthetic estrogens result from the activation and subsequent interaction of nuclear estrogen receptors (ER)α and ERβ with the genome. This classic or genomic mode of ER action is slow compared with rapid or nongenomic estrogen responses that can occur within minutes ( 1, 2). Several studies suggest that nongenomic responses to estrogen are mediated by two distinct mechanisms involving membrane ERs. The first invokes localization of nuclear ER at the plasma membrane ( 3– 5), whereas the second incorporates the seven-transmembrane (7TM) receptor GPR30 (GPER; refs. 6, 7). Similar to ER, GPR30 is not only activated by a wide variety of estrogenic compounds including ER agonists, but also by partial antagonists such as tamoxifen ( 7– 10). Although the potential contribution of GPR30 in breast cancer remains unclear ( 11), activation of GPR30 promotes proliferation of both uterine ( 12) and thyroid ( 9) cancer cells. Indeed, breast cancer cell lines including ER-positive (MCF-7) and ER-negative (SKBR3) lines strongly express GPR30 ( 7, 13). Moreover, a National Cancer Institute–sponsored survey of breast carcinomas reported that correlation between receptor expression and clinical outcomes are distinct for GPR30 and ER, with GPR30 expression strongly associated with HER2 expression and tumor progression ( 14).
Despite the lingering controversies surrounding the contribution of GPR30 to breast cancer, recent analyses of GPR30 knockout mouse firmly establish this 7TM receptor as an important player in mediating estrogen responses in vivo. Indeed, estrogen-induced thymic atrophy is severely compromised in GPR30 null mice ( 15). Other phenotypes, especially those involving reproduction, have yet to be reported in mice lacking GPR30. Regardless, the sum of these in vivo and in vitro data suggests strongly that physiologic responses initiated by natural and synthetic estrogens extend beyond the nucleus to include the 7TM receptor, GPR30.
Estrogenic ligand signaling through GPR30 is shown to have a number of rapid effects, including activation of the phosphatidylinositol 3-kinase (PI3K) and mitogen activated protein kinase (MAPK) pathways ( 7, 10, 16). Activation of these proliferative pathways by GPR30 is proposed to be propagated by trans-activation of the plasma membrane tyrosine kinase receptor epidermal growth factor (EGF) receptor ( 13). However, the fact that the GPR30-specific agonist G-1 ( 17) and EGF ( 18) stimulate proliferation in ER-negative SKBR3 breast cancer cells whereas E2 does not ( 18) suggests that GPR30 signaling may involve other mechanisms. Nonetheless, stimulation of MAPK and PI3K signaling pathways by GPR30 coincides with mechanisms proposed to activate NR5A nuclear receptors including steroidogenic factor 1 (SF-1) and liver receptor homologue 1 (LRH-1). Both of these transcription factors are important during development and in the adult due to their regulation of steroidogenesis and bile acid synthesis ( 19). Similar to other nuclear receptors, activation of the MAPK pathway and receptor phosphorylation by extracellular signal-regulated kinase (ERK) increases NR5A receptor activity ( 20). However, structural analyses of SF-1 and LRH-1 also revealed phosphatidylinositols including phosphatidylinositol-3,4,5-trisphosphate (PIP3) as a potentially unique class of ligands for this subfamily of nuclear receptors ( 21, 22).
Based on these collective findings, we hypothesized that GPR30 stimulation of PI3K- and MAPK pathways would increase the activity of SF-1/LRH-1. Unfortunately, distinguishing GPR30- from ER-specific effects is difficult in many cells. Therefore, synthetic compounds selective for GPR30, but not ERs, are useful tools for dissecting these signaling pathways. Two agonists proposed to activate membrane ERs include the GPR30-selective agonist G-1 ( 23), and the biphenylacrylamide compound STX that resembles 4-hydroxytamoxifen (OHT; ref. 24); no binding to nuclear ERs is exhibited by either compound. Although direct binding of STX to GPR30 has yet to be shown, primary hypothalamic neurons isolated from ERα and ERβ double knockout mice elicit a rapid and specific response to STX that mimics the response to a bovine serum albumin (BSA)–estradiol conjugate, suggesting that the biological response to STX is mediated through an estrogen membrane receptor such as GPR30 ( 25, 26).
To test the hypothesis that GPR30 mediates NR5A activation via estrogens, primary human endometriotic and immortalized uterine cancer cell lines were assayed with STX. Our results suggest a novel cellular signaling paradigm that is initiated by estrogen activation of the 7TM receptor GPR30, with signal transduction cascades (PI3K and MAPK) converging on nuclear hormone receptors (SF-1/LRH-1) to modulate their transcriptional output. Based on our findings, we speculate that such a pathway might contribute to the known proliferative effects of tamoxifen and other natural estrogens in the female reproductive tract.
Plasmids and reagents. Full-length human GPR30 (hGPR30) was isolated and expressed from a pIRESneo expression vector (Clontech Laboratories) harboring an NH2-terminal 3X-FLAG- or HA-epitope tag (FLAG-hGPR30/pIRESneo). Double-stranded RNAi oligonucleotides for GPR30, LRH-1, and GFP were cloned into the pSUPERneo vector (DNAengine). Full-length mouse SF-1 (mSF-1) was expressed from as either HA or 3X FLAG tagged version in pCIneo or pcDNA3, respectively. 3X FLAG-mSF-1 S203A and A270W mutants were created using the QuikChange Site-Directed Mutagenesis kit (Stratagene). Full-length human LRH-1 was obtained from human ductal carcinoma T47-D cDNA and subcloned into a 3X-FLAG epitope-tagged pcDNA3 vector. ERs, and ERE TATA-Luc vectors, were generous gifts from S. Kato (University of Tokyo, Tokyo, Japan). Antibodies, chemicals, and oligonucleotides used are specified in Supplementary Tables S1 and S2.
Cell culture and luciferase assays. Ishikawa and JEG3 cells were maintained in DME/H-21, 4.5 g/L glucose supplemented with 10% fetal bovine serum (FBS), and 1X penicillin/streptomycin. Endometriotic stromal H-38 cells were maintained in DME high glucose 50%/F-12 50% mixed with 10% FBS and 1X penicillin/streptomycin. Ishikawa cells stably expressing HA-hGPR30 were grown in selective medium containing 300 μg/mL of geneticin (Invitrogen). Cells were seeded in phenol red–free medium with 5% charcoal-dextran–stripped (CDS) FBS and cotransfected in serum-free medium with indicated receptor or siRNA construct using FuGENE 6 (Roche). Drugs were added to cells 4 to 8 h before harvesting to achieve maximal stimulation. All luciferase assays were normalized to β-galactosidase activity and results expressed as relative luciferase units or fold activation with all data representing the mean ± SD from three independent experiments performed in triplicate.
Proliferation studies. For quantitative fluorescence-activated cell sorting (FACS) analysis, Ishikawa cells were cultured in phenol red–free medium containing 5% CDS FBS for 48 h. Cells were treated with drugs as indicated for 16 h, collected, permeabilized with 40% ethanol in PBS, and resuspended in staining solution (50 μM propidium iodide, 3.8 mM sodium citrate in PBS RNase solution). Cell-cycle data were collected with a Becton Dickinson FACScan Immunocytochemistry system and analyzed with ModFit LT (Verity Software House).
For cell proliferation assays, Ishikawa cells were seeded in six-well plates with phenol red–free medium containing 5% CDS FBS. Cells were washed and the medium changed to 1% CDS and drug, as indicated. Medium and drugs were renewed every 2 d. Cell number was counted in a hemocytometer.
Immunocytochemistry and immunoblot analyses. For phospho-Akt and phospho-ERK1/2 analyses, Ishikawa cells were transfected with hGPR30. For phospho-SF-1 analysis, JEG3 cells were transfected with 3X-FLAG-mSF-1. Following transfection, cells were serum starved in phenol red–free medium, except for endometriosis H-38 cells where 2% CDS FBS was added. Cells were treated with drugs as indicated, washed, and lysed in ice cold 20 mM Tris-HCl (pH 7.4), 150 mM NaCl, 1 mM EDTA, 1 mM EGTA, 1% NaDeoxycholate, 1% Triton X-100, 0.1% SDS, Complete Protease Inhibitor Cocktail (Roche), 1 mM phenylmethylsulfonyl fluoride, 1X Phosphatase Inhibitor Cocktail I, and II (Sigma-Aldrich). Equal amounts of total protein were probed with antibodies directed against phospho-Akt (Ser473; 1:1,000), Akt (1:1,000), phospho-ERK1/2 (1:1,000), ERK1/2 (1:1,000), pSF-1 (1:2,500), or M2-Flag (1:5,000). Signal was detected using SuperSignal West Femto Maximum Sensitivity Substrate (Pierce). For all Western blots, equivalent levels of protein were added to each lane, as determined by a Bradford protein assay.
H-38 cells were fixed in 4% paraformaldehyde before being permeabilized with PBS containing 0.1% Triton X-100. Cells were incubated with primary antibodies overnight at 4°C in PBS containing 5% BSA. Primary antibodies were as follows: anti-GPR30 (Lifespan Biosciences; 1:250) and anti-calnexin (Abcam; 1:250). Images were collected using a Zeiss Pascal confocal microscope.
(32P) orthophosphate in vivo labeling and high performance liquid chromatography analysis of PIP3. Ishikawa cells containing empty vector or stably overexpressing GPR30 were starved in serum- and phosphate-free medium for 2 h, were labeled with 500 μCi of (32P)-orthophosphate (Amersham Biosciences) for 2 h at 37°C in 5% CO2 and then treated with DMSO or drug for 15 min. Total lipids were extracted into chloroform, deacylated in 750 μL of methylamine/methanol/n-butanol/H2O (26:45:11:16) at 53°C for 50 min, and polar head groups extracted into 10 mM NH4H2PO4. Anion exchange high performance liquid chromatography was used to separate soluble glycero-inositol head groups over a gradient of NH4H2PO4, and monitored using a Packard flow scintillation detector and compared with 32P-labeled standards (Amersham Biosciences, Sigma). All peaks were integrated using Pro-Star Varian Software, and PI(4)P levels or total radioactivity served as internal controls to quantify, both giving similar results.
Human ectopic endometrial cells express GPR30 and SF-1, but not ERs. We initially examined GPR30 expression in primary human stromal endometriotic H-38 cells obtained from patients with endometriosis, because GPR30 is amplified in endometrial cancer, is associated with advanced tumors and a poorer predicted survival rate ( 27), and seems to be enriched in the endometrium during the proliferative phase ( 28). We also used normal primary human endometrial cells (Endo), and several human cancer cell lines including MCF-7 breast, Ishikawa endometrial, and JEG3 placental cells for these studies. H-38 cells clearly express GPR30 as measured by quantitative PCR, with only MCF-7 cancer cells expressing higher levels ( Fig. 1A ). By contrast, neither ERα nor ERβ transcripts were detected in H-38 primary endometriotic cells ( Fig. 1A), suggesting that any estrogenic ligand effects would likely be mediated by GPR30. Immunocytochemistry confirmed that GPR30 is expressed in the H-38 cells and colocalized with calnexin, a marker of the endoplasmic reticulum ( Fig. 1B), consistent with GPR30 localization on intracellular membranes ( 7).
Primary human ectopic H-38 endometrial cells express GPR30, SF-1, and CYP19A1, but no ERs. A, relative expression of GPR30 and nuclear ERs in primary H-38 endometrial cancer cells, and other cell lines including breast carcinoma cell lines: MCF-7, MDA-MB-231 (MDA), and T47-D; endometrial cancer cell line: Ishikawa; choriocarcinoma placental cell line: JEG3; primary endometrial cells: normal endometrium (Endo) and endometriotic cells (H-38). B, localization of endogenous GPR30 (calnexin, endoplasmic reticulum membrane marker) in H-38 cells, determined by immunocytochemistry and confocal microscopy. C, relative expression of SF-1 and Cyp19a1 in T47-D, Ishikawa, normal endometrium, and H-38 cells.
Estrogen synthesis is markedly elevated in H-38 endometriotic cells compared with normal endometrial cells due to elevation in transcript levels encoding cytochrome p450 enzyme aromatase (Cyp19a1; ref. 29). Higher estrogen output by these cells is proposed to maintain endometrial cells in an ectopic location and contribute to endometrial cancer ( 30). Consistent with increased estrogen production in H-38 cells and the fact that Cyp19a1 is a known target of SF-1 ( 31), both Cyp19a1 and SF-1 transcripts are significantly elevated compared with primary endometrial cells ( Fig. 1C).
To examine how H-38 endometriotic cells respond to estrogens in the absence of ERs, we used a variety of estrogens including STX and OHT. Although OHT is proposed to act as a partial estrogen agonist in the uterus ( 32, 33), STX is a novel diphenylacrylamide tamoxifen analogue ( Fig. 2A ) that has previously been linked to estrogen activation of a GPCR ( 25, 26). Indeed, gene profiling in Ishikawa cells suggests that STX activates a distinct subset of genes from the cluster of genes induced by both OHT and 17βE2 (Supplementary Fig. S1). Both OHT and STX induce rapid phosphorylation of Akt and ERK1/2, ( Fig. 2B), showing that estrogen signaling is present in the apparent absence of any detectable ERα or ERβ ( Fig. 1A). Interestingly, OHT and STX activated the MAPK and PI3K pathways significantly more than 17β estradiol (17βE2; Fig. 2B), possibly reflecting more robust activation of GPR30 in this cellular context, as noted by others ( 12, 17). Taken together, these data show that human endometriotic cells express high levels of GPR30 and activate proliferative signals in response to OHT and STX.
Tamoxifen and the tamoxifen analogue STX activate PI3K and MAPK pathways in H-38 cells. A, chemical structures of STX and OHT. B, phospho-ERK1/2 (pERK1/2) and phospho-Akt (pAkt) were detected by immunoblotting using serum-depleted H-38 primary cells treated with negative control inhibitors [1 μM; 100 nM wortmannin (W) or 10 μM U0126 (U), 30 min pretreatment before adding STX], or with positive control drugs (EGF or insulin); total ERK1/2 and Akt show loading controls.
STX fails to bind, antagonize, or activate ERα and ERβ. To determine the GPR30-dependent effects of STX, we used other relevant cell lines that could be more easily manipulated, and did not exhibit the low transfection efficiency and extremely high levels of SF-1 and Cyp19a as observed for H-38 cells. Given that the affinity of STX for ERα and ERβ is several logs lower (106) compared with 17βE2 ( Fig. 3A ; ref. 24), it is not surprising that STX was unable to activate or repress a classic estrogen response element luciferase reporter (ERE TATA-Luc). No activation was observed in human placental choriocarcinoma cells JEG3 cells transiently overexpressing ERα; these cells are ERα/β negative and GPR30 positive. A similar observation was observed in human endometrial cancer Ishikawa cells, which express endogenous ERβ ( Fig. 3B). Consistent with data obtained in primary endometriotic H-38 cells, these results establish that STX signaling is independent of ERs and unlike OHT, STX neither activates nor antagonizes classic ERE-reporter constructs. Thus, although STX and OHT share similar structural features, STX fails to activate ERα/ERβ.
STX fails to bind, activate, or antagonize nuclear ERs. A, 17βE2 (open symbols) or STX (filled symbols) binding to hERα (top) or hERβ (bottom) was measured by competition binding assays; fluorescence polarization readout using fluorescently labeled E2. B, JEG3 (ER negative) cells transfected with hERα (top) or Ishikawa (ERβ positive) cells (bottom) were assayed for ERE TATA-luciferase reporter activity following 24 h off drug treatment (drug and dose indicated). Gen, genistein.
SF-1 transcriptional activation via estrogen stimulation of GPR30. We next assessed the potential link between GPR30 stimulation and activation of SF-1 or LRH-1. Ligand-stimulated GPR30 triggers activation of the MAPK pathway, which is then predicted to activate SF-1 by direct phosphorylation. GPR30 also stimulates the PI3K pathway, elevating cellular PIP3 levels ( Fig. 2B; ref. 2), which is also predicted to activate NR5A receptors by direct binding of PIP3 to the ligand binding domain ( 21). Using JEG3 cells that express endogenous GPR30, but very low levels of SF-1 and no ER, we found that both 17βE2 and STX produced dose- and time-dependent activation of an aromatase promoter luciferase reporter (Aro-Luc), after addition of mSF-1 and human LRH-1 (Supplementary Figs. S2 and S3; Fig. 4A ). STX failed to enhance the activity of estrogen-related receptor (ERRα; data not shown). Similar to other studies ( 9), we found that the estrogen antagonist, ICI182,780, failed to mimic STX (data not shown), despite the fact that ICI is reported to bind GPR30 directly ( 34). SF-1 mutants defective for phosphorylation (S203A) or with a disrupted ligand binding pocket (A270W) decreased or eliminated estrogen and STX stimulation of SF-1 transcriptional activity compared with wild-type SF-1, establishing the requirement for both Ser203 phosphorylation and a fully accessible ligand binding pocket for these estrogenic compounds to activate SF-1 (see Fig. 4B; ref. 21).
STX stimulates SF-1 transcriptional activity and increases SF-1 phosphorylation in a GPR30-dependent manner. A, drug-dependent stimulation of the aromatase promoter II luciferase reporter (Aro-Luc) in JEG3 cells transfected with mSF-1 with expression confirmed (inset). B, aro-Luc reporter activation by SF-1 or SF-1 variants (S203A or A270W) after treating cells with 1 μM of the indicated drug. C, effects of MAP/ERK kinase (10 μM U0126) or PI3K [100 nM wortmannin (WM)] inhibitors (30 min pretreatment) on 1 μM STX stimulation of SF-1 transactivation (left). Following a 10-min STX treatment, phospho-SF-1 and phospho-ERK1/2 (pSF-1 and pERK1/2) were detected (right) with vehicle (−) and EGF (positive control), also shown. D, effects of siRNA on 1 μM drug-stimulated SF-1 activity (left) and phosphorylation (right) with duplicate independent experiments (+) shown. Control, no siRNA added; sicRNA, control siRNA; si-GPR30, siRNA against GPR30; SF-1, total SF-1 loading control. Representative data from three independent experiments are shown. In A, B, C (left), and D (left), cells were treated with indicated drugs for 4 h, 16 h following transfection; luciferase activity is mean values ± SD. In C (right) and D (right), cells were treated with the indicated drugs for 1 h.
Inhibiting MAPK and PI3K signaling attenuates STX activation of SF-1 in JEG3 cells. Consistent with known effects of MAPK signaling on SF-1 and LRH-1, pharmacologic inhibitors of either MAPK/ERK kinase or PI3K (U0126 or wortmannin, respectively) effectively blocked 17βE2 and STX activation of SF-1 ( Fig. 4C, left). Furthermore, STX treatment increased ERK activation (phospho-ERK1/2) and SF-1 phosphorylation to equivalent levels as observed with EGF ( Fig. 4C, right). Importantly, siRNA directed against GPR30 abolished the ability of 17βE2 or STX to induce SF-1–dependent transcription ( Fig. 4D, left), as well as the ability of STX to induce SF-1 phosphorylation ( Fig. 4D, right). Interestingly, knocking down GPR30 consistently lowered basal levels of SF-1 phosphorylation, as shown in the DMSO control (−). Collectively, these data establish that SF-1 activation via estrogen and STX signaling is GPR30-dependent in JEG3 cells. Furthermore, receptor activation by STX and 17βE2 required phosphorylation of SF-1 and an accessible ligand-binding pocket.
STX activates SF-1 and increases PIP3 accumulation in Ishikawa cells. We next asked if STX stimulation of GPR30 is linked to NR5A receptor activation in Ishikawa endometrial cancer cells, where both GPR30 and nuclear ER signaling are suggested to promote proliferation ( 10, 12). In these cells, STX stimulation of SF-1 was amplified after increasing GPR30 expression transiently (Supplementary Fig. S3). Given this fact, we created a stable Ishikawa cell line expressing GPR30 comparable with levels observed in MCF-7 cells to fully characterize the pharmacologic effects of STX ( Figs. 5A, right , and 1A). These cells exhibited SF-1–dependent activation of the Aro-Luc reporter after 17βE2, OHT, and STX treatment, but not with the inactive 17αE2 ( Fig. 5A, left). Consistent with effects in endometriotic H-38 cells, we observed robust activation of the MAPK and PI3K pathways after treatment with OHT and STX in Ishikawa cells expressing GPR30 (Supplementary Fig. S4; Fig. 5B). Ishikawa cells are ERβ positive and express lower levels of GPR30 and ERα than MCF-7 cells (refer back to Fig. 1A).
STX increases PI3K/MAPK activity and PIP3 accumulation in Ishikawa cells stably expressing GPR30. A, drug-stimulated (4 h) Aro-Luc reporter activity in GPR30 stable Ishikawa cells with mSF-1 added was measured (left). Percent activation is normalized to activity observed with mSF-1 added and no drug treatment (100%). GPR30 mRNA expression was measured in GPR30 expressing stable Ishikawa cells (+ GPR30) and control cells (+ vector; right) B, phospho-Akt time course (1 μM drug) and dose response (15 min treatment) were detected by immunoblotting using cells transiently expressing GPR30. The inhibitor (100 nM WM) was added 30 min before 1 μM drug treatment for 15 min; total Akt shows loading controls and with negative controls as time (0) or vehicle (−). C, levels of [32P]PI(3,4,5)P3 measured by high performance liquid chromatography in stable GPR30-expressing Ishikawa cells after vehicle or STX treatment (dose indicated, 15 min) after [32P] orthophosphate labeling; peak shown confirmed to be glycero-inositol(1,3,4,5)P by de-acylated standard. D, dose response of STX or negative control vehicle (−) induced [32P]PI(3,4,5)P3 peak accumulation normalized to total radioactivity (columns, mean of three independent experiments; bars, SD).
Previous descriptive studies using a fluorescent-tagged pleckstrin homology domain of Akt suggested that stimulation of GPR30 results in nuclear PIP3 accumulation ( 7, 23). To determine if STX similarly increased cellular pools of PIP3, we measured levels of this very scarce phospholipid after STX stimulation of Ishikawa cells stably expressing GPR30 (see Materials and Methods). A dose-dependent STX-induced increase in PIP3 accumulation was observed with a maximal response occurring at 1 μM drug ( Fig. 5C and D); this same dose corresponded to the maximal stimulation of SF-1–dependent activation of the Aro-Luc reporter (refer to Figs. 4A and 5D). No accumulation of PIP3 was detected in cells treated with the inactive 17αE2 epimer, or with DMSO vehicle (data not shown). Taken together, these data show that estrogen signaling via GPR30 increases cellular levels of PIP3. Our ability to detect STX-induced increases in cellular PIP3, the least abundant cellular phosphatidylinositol, most likely reflects the fact that Ishikawa cells are negative for the lipid phosphatase PTEN, which removes the 3′ phosphate. Although others report that estrogen acting via ERα increases endogenous PIP3 in endothelial cells ( 35), our data using the selective compound STX suggest strongly that this effect on PI3K signaling might also be mediated by GPR30.
Effects of STX on cellular proliferation and aromatase (Cyp19a1) expression. Increased Ishikawa cell proliferation after 17βE2 or OHT treatment is attributed to the combined actions of both nuclear ERs and GPR30 ( 12). This prompted us to measure endogenous Cyp19a1 (aromatase) expression after STX treatment, given that both SF-1/LRH-1 are known to control expression of promoter II of Cyp19a1 ( 36). Indeed, we found that STX, OHT, and genistein, but not 17αE2, elevate endogenous Cyp19a1 transcripts in Ishikawa cells with induction greatly enhanced by GPR30 expression ( Fig. 6A ). Knockdown experiments using siRNA show that STX activation of Cyp19a1 depends on both GPR30 and LRH-1 (Supplementary Fig. S5; Fig. 6B). Finally, we observed a marked increase in Ishikawa cell proliferation as measured in two independent assays after treatment with STX, OHT, or the dietary estrogen genistein, but not with 17αE2 (Supplementary Fig. S6; Fig. 6C). Overexpressing GPR30 amplified this response ( Fig. 6C, right), although stimulation by 17βE2 was less robust than observed with STX. That STX elevates endogenous levels of the NR5A target aromatase and increases cell proliferation in a GPR30-dependent manner suggests that estrogen signaling via GPR30 might be an important pathway for increasing local levels of estrogen, and for promoting cellular proliferation in endometrial cells.
STX stimulation increases endogenous aromatase expression and proliferation in Ishikawa cells stably overexpressing GPR30 and Model. A, endogenous Cyp19a1 expression measured after drug treatment (1 μM 17αE2, genistein, OHT, STX, or 100 nM 17βE2 for 16 h) in Ishikawa cells stably expressing GPR30. B, effects of GPR30 siRNA (si-GPR30) on Cyp19a1 expression in drug-stimulated (1 μM for 16 h) Ishikawa cells stably expressing GPR30; control, untransfected; si-GFP, control siRNA. C, following serum depletion and drug treatment (1 μM 17αE2, genistein, OHT, STX, or 100 nM 17βE2 for 16 h), cell proliferation was analyzed by FACS for control (stable vector) and GPR30 stably expressing (stable GPR30) Ishikawa cells. A to B, expression measured by quantitative PCR; columns, mean values; bars, SD; A to C, vehicle negative control (−) is indicated. D, proposed model of GPR30 and NR5A receptor signaling by estrogens. STX and estrogens bind and activate GPR30. GPR30 is reported to reside on either the plasma membrane ( 49) and/or on intracellular membranes ( 7), as depicted in the model. GPR30 activation by STX or OHT increases ERK1/2 and PI3K phosphorylation and elevates the cellular pools of PIP3. Collectively, these events activate NR5A nuclear receptor activity to promote increased expression of target genes such as aromatase.
Here, we provide data supporting a novel pathway linking estrogen stimulation of the membrane receptor GPR30 with activation of NR5A nuclear receptors and the target gene aromatase ( Fig. 6D). Using human Ishikawa endometrial cancer cells or human primary endometriotic H-38 cells, we report that the GPR30-dependent tamoxifen-analogue STX rapidly activates both the PI3K and MAPK signaling pathways, and increases levels of cellular PIP3 in a dose-dependent manner. In Ishikawa cells, STX as well as OHT elevated endogenous levels of aromatase (Cyp19a1) and increased proliferation in a GPR30-dependent manner. These data suggest that STX activation of NR5A receptors depends on GPR30, but not nuclear ER signaling. Our study is now one of several suggesting that the physiologic effect of estrogen signaling in normal and disease states can be expanded beyond nuclear ER signaling to include a 7TM receptor. Using human primary H-38 cells, we provide further evidence that GPR30 alone is sufficient for estrogen signaling ( Figs. 1A and 6D). Moreover, this novel GPR30/SF-1 pathway shows how synthetic estrogen analogues such as OHT and STX increase local concentrations of estrogen, thereby amplifying estrogen signaling.
The link between estrogens and NR5A receptor activity is especially intriguing given that both SF-1 and LRH-1 are involved in steroid and estrogen production ( 37). When placed in the context of prior studies, our findings imply that GPR30 activation and up-regulation of SF-1 set up a feed-forward autocrine pathway for continuous synthesis of estradiol in tissues such as ectopic endometrium. Indeed, profiling studies comparing human ectopic and eutopic endometrium confirm that SF-1 and estradiol biosynthesis are amplified in ectopic disease tissue ( 38, 39). Mendelson and colleagues ( 40) found that immortalized human endometrial cells readily convert exogenously applied androstenedione to estradiol, with this androgen also promoting SF-1 recruitment to the CYP19A1 promoter. Regardless of whether androstenedione is supplied exogenously from the peritoneal cavity ( 41) or is synthesized de novo by ectopic endometrium, amplification of SF-1 ensures that local estrogen signaling increases dramatically in endometriosis.
Our model depicted in Fig. 6D also predicts that many dietary and environmental xenoestrogens could bind to GPR30, stimulate the PI3K/MAPK pathways, and ultimately activate SF-1. Indeed, in cellular assays, we find that the dietary estrogen genistein mimics STX, consistent with studies showing genistein to be the best competitive inhibitor of E2 binding to GPR30 ( 34). Given the crucial role of NR5A receptors in regulating early gonadal development, steroidogenesis, and peptide hormone signaling, genistein activation of GPR30 might be predicted to disturb genetic programs targeted by SF-1, and as a result alter reproductive and endocrine tissue development. Interestingly, although GPR30 is expressed in many endocrine tissues including the uterus, loss of GPR30 in mice does not impair reproduction, suggesting that GPR30 is not an essential gene for urogenital development ( 15).
STX is similar to other synthetic and environmental estrogens that activate the PI3K and MAPK signaling pathways in a GPR30-dependent manner ( 42, 43). The activation of PI3K by STX is of particular interest given that phospholipids seem to be integrally associated with purified human SF-1 ( 44) and that phosphatidylinositols such as PIP3 are hypothesized to modulate SF-1 activity ( 19, 22). Indeed, we show that STX increased cellular PIP3 and that STX stimulation of Cyp19a depends on an intact ligand-binding pocket mutant. Taken together, it is tempting to speculate that STX activation of GPR30 increases PIP3 cellular pools to then activate SF-1 with additional receptor activation arising from MAPK signaling and increased SF-1 phosphorylation. That STX elevated cellular PIP3 pools and activated the PI3K pathway might also be relevant to the increased risk of endometrioid ovarian cancer associated with endometriosis ( 45). Given that PTEN mutations are common in both uterine and ovarian cancers, as well as in endometriosis ( 45, 46), we speculate that activation of GPR30 in a PTEN-deficient genetic background would further amplify PIP3 signaling and promote tumor proliferation.
The role of GPR30 in endometrial cancer is now worth considering as cellular studies such as ours, and those surveying human cancer tissues are being reported. Initial studies linking GPR30 to endometrial proliferation showed that knockdown of GPR30 reduced estradiol and OHT-induced growth of Ishikawa and HEC1A endometrial cell lines, as well as induction of c-fos and ERK1/2 phosphorylation ( 10). Similarly, we find that both STX and genistein increase Ishikawa endometrial cell proliferation in a GPR30-dependent manner. More importantly, GPR30 is prominently expressed in primary human endometriotic H-38 cells. Thus, activation of GPR30 may underlie the higher risk of endometrium hyperplasia and/or cancer in postmenopausal women observed with chronic OHT treatment, but not with aromatase inhibitor therapy ( 47, 48). As such, development of drugs that specifically target this GPR30/SF-1 signaling axis might offer additional therapies in treating reproductive cancers in the future.
Grant support: Susan B. Komen Fellowship (M. Suzawa), a National Institute of General Medical Sciences ISIS UCSF Postdoctoral Fellowship (R.D. Blind), NIHCHD (S.E. Bulun), and National Institutes of Diabetes, Digestive and Kidney Diseases RO1 (T.S. Scanian and H.A. Ingraham).
We thank members of the Scanlan and Julius labs for experimental advice, Dr. M. Feldman for technical assistance, and Drs. E. Faivre and F. Lee for critical reading of the manuscript.
B.C. Lin, M. Suzawa, and R.D. Blind contributed equally to this work.
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Filardo EJ, Quinn JA, Bland KI, Frackelton AR, Jr. Estrogen-induced activation of Erk-1 and Erk-2 requires the G protein-coupled receptor homolog, GPR30, and occurs via trans-activation of the epidermal growth factor receptor through release of HB-EGF. Mol Endocrinol 2000; 14: 1649–60.
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Hammer GD, Krylova I, Zhang Y, et al. Phosphorylation of the nuclear receptor SF-1 modulates cofactor recruitment: integration of hormone signaling in reproduction and stress. Mol Cell 1999; 3: 521–6.
Krylova IN, Sablin EP, Moore J, et al. Structural analyses reveal phosphatidyl inositols as ligands for the NR5 orphan receptors SF-1 and LRH-1. Cell 2005; 120: 343–55.
Sablin EP, Blind RD, Krylova IN, et al. Structure of SF-1 bound by different phospholipids: evidence for regulatory ligands. Mol Endocrinol 2009; 23: 25–34.
Bologa CG, Revankar CM, Young SM, et al. Virtual and biomolecular screening converge on a selective agonist for GPR30. Nat Chem Biol 2006; 2: 175–6.
Tobias SC, Qiu J, Kelly MJ, Scanlan TS. Synthesis and biological evaluation of SERMs with potent nongenomic estrogenic activity. Chem Med Chem 2006; 1: 565–71.
Qiu J, Bosch MA, Tobias SC, et al. A G-protein-coupled estrogen receptor is involved in hypothalamic control of energy homeostasis. J Neurosci 2006; 26: 5649–55.
Qiu J, Bosch MA, Tobias SC, et al. Rapid signaling of estrogen in hypothalamic neurons involves a novel G-protein-coupled estrogen receptor that activates protein kinase C. J Neurosci 2003; 23: 9529–40.
Smith HO, Leslie KK, Singh M, et al. GPR30: a novel indicator of poor survival for endometrial carcinoma. Am J Obstet Gynecol 2007; 196: 386e1–9; discussion e9–11.
Burney RO, Talbi S, Hamilton AE, et al. Gene expression analysis of endometrium reveals progesterone resistance and candidate susceptibility genes in women with endometriosis. Endocrinology 2007; 148: 3814–26.
Zeitoun K, Takayama K, Michael MD, Bulun SE. Stimulation of aromatase P450 promoter (II) activity in endometriosis and its inhibition in endometrium are regulated by competitive binding of steroidogenic factor-1 and chicken ovalbumin upstream promoter transcription factor to the same cis-acting element. Mol Endocrinol 1999; 13: 239–53.
Bulun SE, Zeitoun KM, Takayama K, Simpson E, Sasano H. Aromatase as a therapeutic target in endometriosis. Trends Endocrinol Metabol 2000; 11: 22–7.
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Clyne CD, Speed CJ, Zhou J, Simpson ER. Liver receptor homologue-1 (LRH-1) regulates expression of aromatase in preadipocytes. J Biol Chem 2002; 277: 20591–7.
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Attar E, Tokunaga H, Imir G, et al. Prostaglandin E2 via steroidogenic factor-1 coordinately regulates transcription of steroidogenic genes necessary for estrogen synthesis in endometriosis. J Clin Endocrinol Metabol 2008; 94: 623–31.
Borghese B, Mondon F, Noel JC, et al. Gene expression profile for ectopic versus eutopic endometrium provides new insights into endometriosis oncogenic potential. Mol Endocrinol 2008; 22: 2557–62.
Bukulmez O, Hardy DB, Carr BR, et al. Androstenedione up-regulation of endometrial aromatase expression via local conversion to estrogen: potential relevance to the pathogenesis of endometriosis. J Clin Endocrinol Metabol 2008; 93: 3471–7.
Koninckx PR, Heyns W, Verhoeven G, et al. Biochemical characterization of peritoneal fluid in women during the menstrual cycle. J Clin Endocrinol Metabol 1980; 51: 1239–44.
Thomas P, Dong J. Binding and activation of the seven-transmembrane estrogen receptor GPR30 by environmental estrogens: a potential novel mechanism of endocrine disruption. J Steroid Biochem Mol Biol 2006; 102: 175–9.
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The skycoin project has been organizing a lot of conferences, meetups and promoting seminars to educate the members of the public about the project.
The skycoin project is the most advanced blockchain project that has focused its attention on product development and innovation in the last 7 years.
In the cryptocurrency world where 90 per cent of the projects are expected to fail, Skycoin has consistently delivered and executed their vision and purpose because they have probably the best technical know-how and experienced team in the blockchain industry.
To enhance the status of the project more, Skycoin recently appointed some new marketing officers for the project for South East Asia and Europe and the sole purpose is to educate people about the benefits of skycoin.
In recent Months, the skycoin project has been involved in a lot of conferences seminars, events and meetups.
In this write-up, I am going to review some of these events and give an update on the upcoming events skycoin will be partaking in.
In Mid July, Synth the founder of the project presented Skycoin to attendees of the International Blockchain Application & Strategic Development Summit Forum in Rome, Italy.
He educated the crowd on his vision to provide a new decentralized Internet with the skywire and skyminer. He explained in clear details how Skywire is a groundbreaking; novel technology wrestles the control from large Internet service providers (ISPs) and gives it back to the users. Its peer-to-peer model promotes net neutrality and sharing of content without blocking, slowdowns, or censorship. Skywire's open-access network preserves privacy and encourages free speech and promotes net neutrality.
The theme of the presentation was how Bandwidth backed, environmentally friendly skycoin will fuel the new Internet.
The skycoin team used the opportunity provide training in helping programmers to develop, expand and consolidate the local golang communities throughout the country, the collaborators living in Havana, in turn, volunteered their time to prepare each of the activities.
Skycoin was also making a lot of in route in Europe with Matt Oksa spearheading it.
He attended the Blockstars conference in Paraleni Polis in Prague.
The theme of the conference was "The business of blockchain". This was organized by the Institute of Cryptoanarchy or the Ztohoven.
This community my opinion this is the most decentralized community in the world. People talk about blockchain and decentralization a lot but if one is looking for a case study and a perfect example, the cryptoanarchy community is the one to study.
In one week, the cryptoanarchy community will teach you the basics of cryptocurrencies, the blockchain, digital security, darknet, 3D printing and electronics. They will equip you with the knowledge and tools to engage in an independent society and protect your liberty.
Craael displayed the skyminer at the conference and the community was fascinated with it.
The term cryptoanarchy indicates the growing environment of the unregulated Internet, where unlimited data sharing and the development of the free market became possible by using anonymous tools such as decentralised currencies like bitcoin, and antispyware encrypting tools.
From the intervention of a live broadcast of Czech Television to the virtual interaction with politician's mobile phones, members of the Ztohoven group are associated with hacking. The inspiration of technological innovation and its potential impact on society led them to a tight interaction with the hacker's scene.
The aim of the Institute of Cryptoanarchy is to make available tools for unlimited dissemination of information on the Internet and encouraging a parallel-decentralized economy, cryptocurrencies and other conditions for the development of a free society in the 21st century.
The main motive for them is the belief that censorship is not a phenomenon only in "the distant dictatorial world".
With a fast Internet connection, reliable anonymity and decentralized currency, you preserve freedom, which we have been loosing as a society. Sounds familiar ?
The three-day ChainXChange conference, which begins next week on August 13, is touted as serving as a gathering place where both "long-time industry titans and eager newcomers meet" to discuss this maturing market and how it will evolve in the months and years to come.
This conference will feature a line-up of entrepreneurs, blockchain experts, artificial intelligence (AI) specialists and well-known economic and business figures including Apple co-founder Steve Wozniak, Social Media's Gary Vaynerchuk, three-time Grammy Winner and Microsoft AI Spokesperson, Common, and Nobel Prize Winner Paul Krugman, to name a few.
In addition, everyone attending the conference will be wearing skycoin branded lanyard.
Skycoin will be giving away a lot of skycoin memorabilia like hats, tee shirts and of course the sky miner machine will be on display.
Skycoin will also be attending the US-China blockchain Digital currency conference scheduled for the 22nd of August 2018 in Los Angeles, California.
The one-day event is hosted by Blockchain China Connect and Artisan Business Group, Inc., and in partnership with FundingPost.com and WONO. It is the only Sino-US investment and funding focused business event for blockchain and cryptocurrency industry. As Chinese government has recently banned ICOs and cryptocurrency trading platforms in China, more tech investors, blockchain startups and bitcoin mining companies are seeking alternative solutions overseas; the U.S. is one of the top considerations and destinations.
Andrew Zapotochnyinorth American representative for cointraffic .
For more details check the link below .
The BLOCKCHANCE Conference 2018 'The future of economics' creates a platform for the exchange of knowledge, experience and success. It shows deep insights into the blockchain and cryptocurrency universe. The conference will open its doors to corporate partners, innovators, developers, future customers, investors and media for two days on August 24th and 25th.
The Platform will provide an inspiring mix of expert talks, panel discussions, breakout sessions, expo and networking breaks.
With the industry developing at a rapid pace, blockchain technology is starting to capture the attention not just of the financial and banking spheres. It has started to spread its roots in communication, medicine, and document circulation, energy, amongst almost all other industries.
This event teaches beginners in blockchain about the socio-economic impact of the coming blockchain revolution and also will allow for advanced crypto enthusiasts to have a platform for community building, meeting like-minded people, and making new friends. Collaborate, connect and learn from successful blockchain entrepreneurs who aim to build a decentralized future.
• Skycoin Fiber projects like solar bankers, MDL, KittyCash, Distributed Blocks and many more will speak and present their projects.
The Global Assets and Wealth Forum in Singapore will gather more than 400 decision makers over 2 days. The institutional themes on Day One and consumer agendas on Day Two are designed to benefit government leaders, top executives, investment managers, fund managers, bankers, business owners, professionals, technologists, wealthy families and high net worth individuals. An international team of experts will share insights into market trends, asset classes, strategies, investment models, risks, challenges, opportunities and returns.
The Global Assets and Wealth Forum 2018 will be attended by participants from the Platinum Circle community worldwide and invited guests. They include CEOs, policymakers, investors, business owners, family offices, fund managers, entrepreneurs, technologists and high net worth individuals from industry, governments and intergovernmental organizations in Asia, North America, Europe, Africa, Middle East and Latin America.
You can get more details about this conference by following the link below .
Skycoin will be attending and be presenting at the Tech Crunch Disrupt conference in San Francisco between the 5th and 7th of September 2018.
Disrupt is headlined by leaders of the startup and technology space. From tech luminaries and business moguls to headline-making founders and leading investors, the roster is packed with arbiters of great startups sharing their knowledge, providing perspective and showing the rest of us what it takes.
Also, more details will be released on the skycoin's telegram as they unveil .
This whole idea of attending and presenting in these seminars these seminars is to give the skycoin project a marketing push.
It is undeniable that the technology is groundbreaking in the crypto space but at the same time, we must come to the realization that Benjamin Franklin may have discovered Electricity but it was Oliver B. Shallenberger who made all the money after discovered the electric meter.
This is calling on all skyfleet members to their best in promoting skycoin as much as they can.


On June 19, 2018, the U.S. Department of Labor (DOL) issued an updated definition of "Employer" under Section 3(5) of ERISA (Association Health Plans), which was finalized in the final rule on July 10th, 2018.
The year-end is coming up and planning for 2018 should be underway at most companies. If you haven't started yet, or if you have, I think one quick story might be instructive about why it's a good idea to include your general counsel in the process.
With the end of the year fast approaching, now is the time to fine tune your estate plan before you get caught up in the chaos of the holiday season. One area that married couples should revisit is their estate planning documents.
Bonus E-Book: "20 Productivity boosting methods for the positive mind"
Excerpt: "Without a clear focus, it's too easy to buckle under to distractions. Set targets for every day beforehand. Decide what you'll do; then do it.
We often discuss our goals as if they're nothing but dreams. Actually, we can accomplish goals on a daily basis. Daily goals contribute to weekly goals. Weekly goals add to monthly goals. Monthly goals add to--you guessed it--yearly goals. With some preparation and planning, our goals can be something we accomplish day in and day out. Here's how to begin"
ESOPs...is it time to look?
Our main clients are closely held businesses (and their owners), so business and individual planning are often tied at the hip in our office. Often that means a business sale isn't the ideal exit or retirement solution for our clients, so we look hard for tax advantaged strategies that (at a minimum) won't hurt the underlying business operations and ESOPs have been a regular part of that analysis.
Ralph Waldo Emerson once said, "Speech is power: speech is to persuade, to convert, to compel. It is to bring another out of his bad sense into your good sense."
For quite some time I have suggested a plan (see below) of communication to clients and BAN participants. It's not anything ground breaking, but it is a programmatic way for a company to facilitate orderly communication. Nonetheless, it is amazing how few of them really follow it (or any other) systematic plan of communication and I think it ends up hurting them...potentially a lot.
Legal Checkup: "An ounce of prevention is worth a pound of cure"
A company legal checkup is similar to one that you would have with your personal physician. It's evaluating the status of your business's legal matters currently and prioritizing areas for improvement.


text:
// Copyright 2010-2014 RethinkDB, all rights reserved.
#include "rdb_protocol/artificial_table/artificial_table.hpp"

#include "clustering/administration/admin_op_exc.hpp"
#include "rdb_protocol/artificial_table/backend.hpp"
#include "rdb_protocol/env.hpp"
#include "rdb_protocol/func.hpp"
#include "rdb_protocol/table_common.hpp"
#include "rdb_protocol/datum_stream/readers.hpp"

/* Determines how many coroutines we spawn for a batched replace or insert. */
static const int max_parallel_ops = 10;

/* This is a wrapper around `backend->read_row()` that also performs sanity checking, to
help catch bugs in the backend. */
bool checked_read_row_from_backend(
        auth::user_context_t const &user_context,
        artificial_table_backend_t *backend,
        const ql::datum_t &pval,
        signal_t *interruptor,
        ql::datum_t *row_out,
        admin_err_t *error_out) {
    // Note that we'll catch the `auth::permission_error_t` that this may throw in the
    // calling function, as that's what we want in `do_single_update` below.
    if (!backend->read_row(user_context, pval, interruptor, row_out, error_out)) {
        return false;
    }

#ifndef NDEBUG
    if (row_out->has()) {
        ql::datum_t pval2 = row_out->get_field(
            datum_string_t(backend->get_primary_key_name()), ql::NOTHROW);
        rassert(pval2.has());
        rassert(pval2 == pval);
    }
#endif

    return true;
}

artificial_table_t::artificial_table_t(
        rdb_context_t *rdb_context,
        database_id_t const &database_id,
        artificial_table_backend_t *backend)
    : m_rdb_context(rdb_context),
      m_database_id(database_id),
      m_backend(backend),
      m_primary_key_name(backend->get_primary_key_name()) {
}

namespace_id_t artificial_table_t::get_id() const {
    return m_backend->get_table_id();
}

const std::string &artificial_table_t::get_pkey() const {
    return m_primary_key_name;
}

ql::datum_t artificial_table_t::read_row(ql::env_t *env,
        ql::datum_t pval, UNUSED read_mode_t read_mode) {
    ql::datum_t row;

    try {
        env->get_user_context().require_read_permission(
            m_rdb_context, m_database_id, m_backend->get_table_id());

        admin_err_t error;
        if (!checked_read_row_from_backend(
                env->get_user_context(),
                m_backend,
                pval,
                env->interruptor,
                &row,
                &error)) {
            REQL_RETHROW_DATUM(error);
        }
    } catch (auth::permission_error_t const &permission_error) {
        rfail_datum(ql::base_exc_t::PERMISSION_ERROR, "%s", permission_error.what());
    }

    return row.has() ? row : ql::datum_t::null();
}

counted_t<ql::datum_stream_t> artificial_table_t::read_all(
        ql::env_t *env,
        const std::string &get_all_sindex_id,
        ql::backtrace_id_t bt,
        const std::string &table_name,
        const ql::datumspec_t &datumspec,
        sorting_t sorting,
        UNUSED read_mode_t read_mode) {
    counted_t<ql::datum_stream_t> stream;

    try {
        env->get_user_context().require_read_permission(
            m_rdb_context, m_database_id, m_backend->get_table_id());

        if (get_all_sindex_id != m_primary_key_name) {
            rfail_datum(ql::base_exc_t::OP_FAILED, "%s",
                error_message_index_not_found(get_all_sindex_id, table_name).c_str());
        }

        admin_err_t error;
        if (!m_backend->read_all_rows_filtered_as_stream(
                env->get_user_context(),
                bt,
                datumspec,
                sorting,
                env->interruptor,
                &stream,
                &error)) {
            REQL_RETHROW_DATUM(error);
        }
    } catch (auth::permission_error_t const &permission_error) {
        rfail_datum(ql::base_exc_t::PERMISSION_ERROR, "%s", permission_error.what());
    }

    return stream;
}

scoped_ptr_t<ql::reader_t> artificial_table_t::read_all_with_sindexes(
        ql::env_t *env,
        const std::string &sindex,
        ql::backtrace_id_t bt,
        const std::string &table_name,
        const ql::datumspec_t &datumspec,
        sorting_t sorting,
        read_mode_t read_mode) {
    // This is just a read_all for an artificial table, because sindex is always
    // the primary index. We still need to return a reader_t, this is needed for
    // eq_join.
    r_sanity_check(sindex == get_pkey());
    counted_t<ql::datum_stream_t> datum_stream =
        read_all(env, sindex, bt, table_name, datumspec, sorting, read_mode);

    scoped_ptr_t<ql::eager_acc_t> to_array = ql::make_to_array();
    datum_stream->accumulate_all(env, to_array.get());
    ql::datum_t items = to_array->finish_eager(
        bt,
        false,
        ql::configured_limits_t::unlimited)->as_datum();

    std::vector<ql::datum_t> items_vector;

    guarantee(items.get_type() == ql::datum_t::type_t::R_ARRAY);
    for (size_t i = 0; i < items.arr_size(); ++i) {
        items_vector.push_back(items.get(i));
    }

    return make_scoped<ql::vector_reader_t>(std::move(items_vector));
}

counted_t<ql::datum_stream_t> artificial_table_t::read_changes(
        ql::env_t *env,
        const ql::changefeed::streamspec_t &ss,
        ql::backtrace_id_t bt) {
    counted_t<ql::datum_stream_t> stream;

    try {
        env->get_user_context().require_read_permission(
            m_rdb_context, m_database_id, m_backend->get_table_id());

        admin_err_t error;
        if (!m_backend->read_changes(
                env, ss, bt, env->interruptor, &stream, &error)) {
            REQL_RETHROW_DATUM(error);
        }
    } catch (auth::permission_error_t const &permission_error) {
        rfail_datum(ql::base_exc_t::PERMISSION_ERROR, "%s", permission_error.what());
    }

    return stream;
}

counted_t<ql::datum_stream_t> artificial_table_t::read_intersecting(
        ql::env_t *env,
        const std::string &sindex,
        UNUSED ql::backtrace_id_t bt,
        const std::string &table_name,
        UNUSED read_mode_t read_mode,
        UNUSED const ql::datum_t &query_geometry) {
    try {
        env->get_user_context().require_read_permission(
            m_rdb_context, m_database_id, m_backend->get_table_id());
    } catch (auth::permission_error_t const &permission_error) {
        rfail_datum(ql::base_exc_t::PERMISSION_ERROR, "%s", permission_error.what());
    }

    guarantee(
        sindex != m_primary_key_name,
        "read_intersecting() should never be called with the primary index");
    rfail_datum(ql::base_exc_t::OP_FAILED, "%s",
        error_message_index_not_found(sindex, table_name).c_str());
}

ql::datum_t artificial_table_t::read_nearest(
        ql::env_t *env,
        const std::string &sindex,
        const std::string &table_name,
        UNUSED read_mode_t read_mode,
        UNUSED lon_lat_point_t center,
        UNUSED double max_dist,
        UNUSED uint64_t max_results,
        UNUSED const ellipsoid_spec_t &geo_system,
        UNUSED dist_unit_t dist_unit,
        UNUSED const ql::configured_limits_t &limits) {
    try {
        env->get_user_context().require_read_permission(
            m_rdb_context, m_database_id, m_backend->get_table_id());
    } catch (auth::permission_error_t const &permission_error) {
        rfail_datum(ql::base_exc_t::PERMISSION_ERROR, "%s", permission_error.what());
    }

    guarantee(
        sindex != m_primary_key_name,
        "read_nearest() should never be called with the primary index");
    rfail_datum(ql::base_exc_t::OP_FAILED, "%s",
        error_message_index_not_found(sindex, table_name).c_str());
}

ql::datum_t artificial_table_t::write_batched_replace(
        ql::env_t *env,
        const std::vector<ql::datum_t> &keys,
        const counted_t<const ql::func_t> &func,
        return_changes_t return_changes,
        UNUSED durability_requirement_t durability,
        UNUSED ignore_write_hook_t ignore_write_hook) {
    try {
        env->get_user_context().require_read_permission(
            m_rdb_context, m_database_id, m_backend->get_table_id());
        env->get_user_context().require_write_permission(
            m_rdb_context, m_database_id, m_backend->get_table_id());
    } catch (auth::permission_error_t const &permission_error) {
        rfail_datum(ql::base_exc_t::PERMISSION_ERROR, "%s", permission_error.what());
    }

    /* Note that we ignore the `durability` optarg. In theory we could assert that it's
    unspecified or specified to be "soft", since durability is irrelevant or effectively
    soft for system tables anyway. But this might lead to some confusing errors if the
    user passes `durability="hard"` as a global optarg. So we silently ignore it. */

    ql::datum_t stats = ql::datum_t::empty_object();
    std::set<std::string> conditions;
    optional<std::string> permission_error_what;
    throttled_pmap(keys.size(), [&] (int i) {
        try {
            do_single_update(env, keys[i], false,
                [&] (ql::datum_t old_row) {
                    return func->call(env, old_row, ql::LITERAL_OK)->as_datum();
                },
                return_changes, env->interruptor, &stats, &conditions);
        } catch (auth::permission_error_t const &permission_error) {
            if (!static_cast<bool>(permission_error_what)) {
                permission_error_what.set(permission_error.what());
            }
        } catch (interrupted_exc_t) {
            /* don't throw since we're in throttled_pmap() */
        }
    }, max_parallel_ops);

    if (static_cast<bool>(permission_error_what)) {
        rfail_datum(
            ql::base_exc_t::PERMISSION_ERROR, "%s", permission_error_what->c_str());
    } else if (env->interruptor->is_pulsed()) {
        throw interrupted_exc_t();
    }

    ql::datum_object_builder_t obj_builder(stats);
    obj_builder.add_warnings(conditions, env->limits());
    return std::move(obj_builder).to_datum();
}

ql::datum_t artificial_table_t::write_batched_insert(
        ql::env_t *env,
        std::vector<ql::datum_t> &&inserts,
        std::vector<bool> &&pkey_was_autogenerated,
        conflict_behavior_t conflict_behavior,
        optional<counted_t<const ql::func_t> > conflict_func,
        return_changes_t return_changes,
        UNUSED durability_requirement_t durability,
        UNUSED ignore_write_hook_t ignore_write_hook) {
    try {
        env->get_user_context().require_read_permission(
            m_rdb_context, m_database_id, m_backend->get_table_id());
        env->get_user_context().require_write_permission(
            m_rdb_context, m_database_id, m_backend->get_table_id());
    } catch (auth::permission_error_t const &permission_error) {
        rfail_datum(ql::base_exc_t::PERMISSION_ERROR, "%s", permission_error.what());
    }

    ql::datum_t stats = ql::datum_t::empty_object();
    std::set<std::string> conditions;
    optional<std::string> permission_error_what;
    throttled_pmap(inserts.size(), [&] (int i) {
        try {
            ql::datum_t insert_row = inserts[i];
            ql::datum_t key = insert_row.get_field(
                datum_string_t(m_primary_key_name), ql::NOTHROW);
            guarantee(key.has(), "write_batched_insert() shouldn't ever be called with "
                "documents that lack a primary key.");

            do_single_update(
                env,
                key,
                pkey_was_autogenerated[i],
                [&](ql::datum_t old_row) {
                    return resolve_insert_conflict(
                        env,
                        m_primary_key_name,
                        old_row,
                        insert_row,
                        conflict_behavior,
                        conflict_func);
                },
                return_changes,
                env->interruptor,
                &stats,
                &conditions);
        } catch (auth::permission_error_t const &permission_error) {
            if (!static_cast<bool>(permission_error_what)) {
                permission_error_what.set(permission_error.what());
            }
        } catch (interrupted_exc_t) {
            /* don't throw since we're in throttled_pmap() */
        }
    }, max_parallel_ops);

    if (static_cast<bool>(permission_error_what)) {
        rfail_datum(
            ql::base_exc_t::PERMISSION_ERROR, "%s", permission_error_what->c_str());
    } else if (env->interruptor->is_pulsed()) {
        throw interrupted_exc_t();
    }

    ql::datum_object_builder_t obj_builder(stats);
    obj_builder.add_warnings(conditions, env->limits());
    return std::move(obj_builder).to_datum();
}

bool artificial_table_t::write_sync_depending_on_durability(
        ql::env_t *env,
        UNUSED durability_requirement_t durability) {
    try {
        env->get_user_context().require_write_permission(
            m_rdb_context, m_database_id, m_backend->get_table_id());
    } catch (auth::permission_error_t const &permission_error) {
        rfail_datum(ql::base_exc_t::PERMISSION_ERROR, "%s", permission_error.what());
    }

    /* Calling `sync()` on an artificial table is a meaningful operation; it would mean
    to flush the metadata to disk. But it would be a lot of trouble to implement in
    practice, so we don't. */
    rfail_datum(ql::base_exc_t::OP_FAILED,
        "Artificial tables don't support `sync()`.");
}

void artificial_table_t::do_single_update(
        ql::env_t *env,
        ql::datum_t pval,
        bool pkey_was_autogenerated,
        const std::function<ql::datum_t(ql::datum_t)>
            &function,
        return_changes_t return_changes,
        signal_t *interruptor,
        ql::datum_t *stats_inout,
        std::set<std::string> *conditions_inout) {
    cross_thread_mutex_t::acq_t txn = m_backend->aquire_transaction_mutex();

    admin_err_t error;
    ql::datum_t old_row;
    if (!checked_read_row_from_backend(
            env->get_user_context(), m_backend, pval, interruptor, &old_row, &error)) {
        ql::datum_object_builder_t builder;
        builder.add_error(error.msg.c_str());
        *stats_inout = (*stats_inout).merge(
            std::move(builder).to_datum(), ql::stats_merge, env->limits(),
            conditions_inout);
        return;
    }
    if (!old_row.has()) {
        old_row = ql::datum_t::null();
    }

    ql::datum_t resp;
    ql::datum_t new_row;
    try {
        new_row = function(old_row);
        rcheck_row_replacement(
            datum_string_t(m_primary_key_name),
            store_key_t(pval.print_primary()),
            old_row,
            new_row);
        if (new_row.get_type() == ql::datum_t::R_NULL) {
            new_row.reset();
        }

        if (!m_backend->write_row(
                env->get_user_context(),
                pval,
                pkey_was_autogenerated,
                &new_row,
                interruptor,
                &error)) {
            REQL_RETHROW_DATUM(error);
        }
        if (!new_row.has()) {
            new_row = ql::datum_t::null();
        }
        bool dummy_was_changed;
        resp = make_row_replacement_stats(
            datum_string_t(m_primary_key_name),
            store_key_t(pval.print_primary()),
            old_row,
            new_row,
            return_changes,
            &dummy_was_changed);
    } catch (const ql::base_exc_t &e) {
        resp = make_row_replacement_error_stats(
            old_row, new_row, return_changes, e.what());
    }
    *stats_inout = (*stats_inout).merge(
        resp, ql::stats_merge, env->limits(), conditions_inout);
}


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text:
A Spessarti szép napok 1967-ben készült  NSZK-beli filmvígjáték, Kurt Hoffman Spessart-sorozatának harmadik része, a Kísértetkastély Spessartban közvetlen folytatása. A kísértetek az előző film végén megkezdett, de félresikerült űrutazás kapcsán Spessart történetének néhány szép, vagy talán nem is annyira szép korszakába jutnak el. Utuk során eljutnak a múltba és a jövőbe, az út minden állomásán  meg kell állapítaniuk, hogy a szeretet és a szerelem ugyanúgy örök, mint a gyűlölet és a háború. A filmet az előző két résszel ellentétben magyarországi mozikban nem vetítették. Németországban több megvásárolható formában, a három filmet tartalmazó díszdobozban is megjelent.

Cselekmény

1967. A kísértetek hét évvel ezelőtt kezdődött Hold-utazása sikertelen volt, egy fúvóka hibája miatt az űrben ragadtak. Az átok alóli feloldozást jelentő jócselekedet a sikertelenség miatt elmaradt, így továbbra is kárhozott kísértetek maradtak. A láthatóvá tévő varázsszer hatása módosult, így folyamatosan láthatók, ám alkohol hatására ismét láthatatlanná válnak. Ahogy az előző filmben, beszédre és emberi cselekvésre képesek, ám csak a varázsszernek köszönhetően láthatók, és mivel egyszer már az 1820-ban történt befalazásuk alkalmával meghaltak, szellemként már halhatatlanok.

Miután hét év alvás után rájönnek, hogyan lehet az elromlott fúvókát megjavítani, sikeresen landolnak egy szálloda tetején, mely pontosan egykori bűneik helyszínén, a hírhedt rablótanya, a rossz hírű spessarti erdei fogadó helyén áll. Anneliese, a szálloda tulajdonosának a lánya, az első részben megismert Franziska von Sandau grófnő azonos küllemű dédunokája éppen esküvőjére készül német származású amerikai katonatiszt vőlegényével, akit azonban a rendkívül militáns, még egy katonai megbeszélésen, vagy egy kisvárosi terepjárós áthaladáson is rohamsisakot viselő, parancsolgatáshoz szokott Teckel tábornok egy kémügy miatt Amerikába küld, emiatt az esküvő elmarad.

A fiatal nőről a szellemek azonnal látják, hogy a rabló korukban megismert Franziska grófnő leszármazottja, eleinte alaposan ráijesztenek, de gyorsan összebarátkoznak vele. Felajánlják, hogy az űrhajóval percek alatt Amerikába viszik a vőlegényéhez, majd mindkettőjüket vissza is hozzák. Az utazás azonban ismét rossz irányba fordul, a tér helyett az időbe hatolnak be. Időutazásaik során a helyszín marad Spessart, de annak négy korszaka.

Első állomásuk a barbár germán törzsek korszaka, utána a harmincéves háborúban, majd a lovagok és trubadúrok korában, végül a közeljövőben, az éppen darabjaira hulló Németországban kötnek ki, ahol Anneliese saját időskori önmagát, megöregedett férjét, felnőtt gyerekeit is láthatja. Anneliese a múlt minden egyes állomásán találkozik szerelmének akkori inkarnációjával, akitől azonban a harc, a gyűlölet és a háború  elszakítja, így átéli a szeretet és a szerelem történelmen átívelő végtelenségét, de azt is tapasztalnia kell, hogy minden korszaknak meg vannak a maguk Teckel tábornokai, a háború, a harag és a szenvedés is örök.

Végül szerencsésen visszaérnek a jelenbe, autón elindul a násznép az esküvőre. Anneliese egy virágot dob a terepjárójában a menet elhaladtát váró Teckelnek, aki a történet során első alkalommal elmosolyodik, a mogorva katonatiszt álarca mögött mélyen elrejtve mégiscsak érző ember rejtőzik.

Szereplők

 Liselotte Pulver: Anneliese, Franziska von Sandau grófnő dédunokája
 Harald Leipnitz : Frank Green, Anneliese vőlegénye, amerikai katonatiszt a jelenben, Martin, Archibald von der Vogelwies, Willi Green a többi korszakban
 Hubert von Meyerinck: Teckel tábornok a jelenben, germán törzsfőnök, birodalmi tábornok, középkori lovag, meghatalmazott a békéért a többi korszakban
 Willy Millowitsch: Mümmelmann konzul
 Hannelore Elsner: Johanna
 Vivi Bach: Rosalinde, a lovagkorban
 Tatjana Sais: Mümmelmannné
 Hans Richter: Toni, kísértet
 Joachim Teege: Hugo, kísértet
 Rudolf Rhomberg: Max bácsi, kísértet
 Kathrin Ackermann: Katrin, kísértethölgy
 Klaus Schwarzkopf: Roland
 Gila von Weitershausen: Gundel
 Peter Capell : polgármester
 Paul Esser: fanatikus szerzetes

Humoros stáblista

Az alkotókat a film elején bemutató stáblista egy piaci séta során készült, minden felsorolt nevet egy piaci áruhoz, annak tulajdonságához vagy árához kapcsolnak:

 Liselotte Pulver: valódi svájci termék
 Vivi Bach: pikáns áru Dániából
 Rudolf Rhomberg: 60% zsírtartalom
 Katrin Ackermann: ropogósan friss
 Klaus Schwatzkopf, Peter Capel, Paul Esser: hármat kap egy márkáért, satöbbi.

Eltérések az előző két filmhez képest

 A második részben látott Charlotte grófnő, aki szintén Franziska dédunokája és hasonmása, a grófi cím és a kastély örököse, a szellemek jóbarátja, aki köré az előző film felépült, ebben a részben említés szintjén sem tűnik fel. Mindhárom szerepben Liselotte Pulver látható.
 A második részben látott von Teckel kormányhivatalnok, aki azonos küllemű dédunokája az első részben látott von Teckel ezredesnek, ebben a részben Teckel tábornok néven tűnik fel. Mindhárom szerepet Hubert von Meyerinck alakította.
 Az előző részben négy férfi kísértet szállt fel az űrhajóra, ebben a részben viszont Katrinon kívül csak hárman vannak rajta, Jockel kísértet nem szerepel.
 Katrin szellemet  mindhárom részben más alakítja.

Megítélése

 A film az elődeinél jóval kisebb sikert aratott és komoly negatív kritikákat kapott, eszerint az előző két film eredetiségével, kedvességével, humorosságával a harmadik rész nem vetekedhet annak ellenére, hogy jóval magasabb költségvetésből, két azonos és igen jónevű szereplővel forgatták. Az előzménnyel egyébként sem következetes űrhajósjelenetet leszámítva érthetetlenül kevés a kapcsolódás az előző filmhez, noha annak közvetlen folytatása. A kísértetek jórészt elveszítették földöntúli és kísérteties jellegüket, az öt űrhajósból egy hiányzik, csak négyen vannak.

Forgatási helyszínek

 A belső jeleneteket a spandaui Central Cinema Company (CCC) filmstúdióban forgatták.
 Bécs, Ausztria
 Kreuzenstein-kastély, Korneuburg, Ausztria (a lovaglós-dalos jelenet a vár felé a lovagkorban csak külső forgatás)
 Heppenheim, Németország, a kisváros főtere és főutcája
 Odenwald, Németország

Az előző két filmmel ellentétben nem Miltenberg, hanem Heppenheim a kisváros forgatási helyszíne

Jegyzetek

Források
 https://www.shotinberlin.de/DE/katalog/film/3154/

További információk
 Eredeti mozielőzetes

1967 filmjei
Német filmvígjátékok
Német musicalfilmek

redpajama_set_name: RedPajamaWikipedia


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PR disasters happen all the time. Some companies handle them with great dignity and finesse and use them as a learning experience, others try to hide them and make the problem worse when it comes to light. Here is a selection of the best, worst and ugliest PR disasters.
What happened? Disney, working under their alias Touchstone Pictures, released Kundun, a story about the life of the 14th Dali Lama which portrayed Chinese human rights abuses in a negative light. The Chinese didn't like it, so in addition to issuing lifetime bans from China to various members of the production team, including writer Melissa Mathison and director Martin Scorsese, they also threatened to ban Disney from the entire Chinese market.
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Incorporating key stakeholder input (divisional business leaders and IT functional managers), evaluate and recommend strategic alliance/sourcing opportunities that will result in increased value to the organization. Utilize expert digital marketing and technology industry knowledge, current and emerging business models, an entrepreneurial mindset and a creative business approach to accomplish this goal.
Organize and lead cross-divisional sourcing teams; including preparing advanced sourcing strategies, detailed procurement plans, requests for proposals (RFPs), performing detailed analysis of proposals and vendor capabilities. Ensure robust process in RFP structuring, bid analysis and negotiation.
Develop and negotiate contracts with new suppliers and/or renegotiate existing contracts to accomplish lowest total system cost and savings objectives.
Lead development and implementation of annual supplier management plans, including detailed spend analytics, forecasted spend, saving expectations and performance objectives.
Lead or direct formal software supplier management programs with preferred vendors, including regular business reviews and support other technology vendor management programs as needed.
Plan, schedule and monitor procurement initiatives, ensuring proper resource allocation and on-time delivery of projects; exercise tight project management.
Recognize and advise on the implications of change to the business units and functions as part of the potential impact of procurement initiatives.
Lead or support best practice identification across RELX with the goal of deploying cost and quality improvements via product standardization or use of product/services.
Create and deploy enterprise-wide metrics, key performance indicators, tools, and processes to optimize software and other technology sourcing, vendor activities, efficiencies, and to work collaboratively with business unit/functional leaders to prioritize and drive implementation.
Monitor compliance to digital marketing, software, cloud and other technology contract commitments; monitor performance across a variety of metrics to meet contractual requirements.
Create and/or direct the creation of digital marketing, software, cloud and other technology sourcing project plans, objectives and goals; identify and resolve roadblocks in a diplomatic and productive manner.
Relationships with Business and IT Functional Managers and budget owners.
Peers within Global Procurement to promote cross-category collaboration and teamwork. Set an example of professional excellence.
IT stakeholders across the globe to serve as an IT Procurement liaison and align appropriate category owners within Global Procurement to stakeholders.
Legal department for contract drafting, negotiation and monitoring.
Finance department for budget and savings tracking.


Toronto, ON (Apr. 9, 2019) — The Co-operators is further expanding its InsurTech investment by introducing a fund to facilitate partnerships with InsurTech firms. The investment fund reflects the organization's commitment to address the unmet insurance and financial services needs of Canadians participating in a fast-paced and ever-changing digital economy.
In support of the organization's innovation strategy, the fund focuses on investment priorities aligned with three key themes: meeting emerging and underserved insurance needs, enriching the resiliency of Canadians, and adapting to the changing nature of transportation.
The Co-operators entered into its first InsurTech partnership in 2018, teaming up with Slice Labs Inc. (Slice) to launch a digital insurance brand – Duuo by Co-operators™, a market-leading solution leveraging the Slice Insurance Cloud Services™ (ICS) platform.
InsurTech companies interested in learning more about The Co-operators and its fund are encouraged to submit a high-level summary of their company and technology to Daniel Sinclair, Vice President of Corporate Development at [email protected].


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What We're Reading: Everyone Versus Racism – Patrick Hutchinson
What We're Reading is back! On the shelf this week is Everyone Versus Racism: A Letter to My Children by Patrick Hutchinson. Marketing Executive Becca Joyce tells us all about it.
On 13 June 2020, Patrick Hutchinson, a black man, was photographed carrying a white injured man to safety during a confrontation in London between Black Lives Matter demonstrators and counter-protestors. The powerful image was shared and discussed all around the world.
Everyone versus Racism is a poignant letter from Patrick to his children and grandchildren. Writing from the heart, he describes the realities of life as a black man today and why we must unite to inspire change for generations to come.
What did Becca think?
'Wow. In Everyone Versus Racism, Patrick Hutchinson tells his incredible story and in doing so educates and inspires the reader to make a necessary change. This is a beautiful, emotional and powerful book that offers an accessible take on a vitally important topic, and Patrick's personality shines through on every page. Put simply, this is an impassioned but very humble and personable call to arms and take action.'
If you liked this, keep an eye out for…
The Power of Privilege by June Sarpong
In The Power of Privilege, June Sarpong empowers those fortunate enough not to be 'otherised' by mainstream Western society to become effective allies against racism, both by helping them understand the roots of their privilege and the systemic societal inequities that perpetuates it. The Power of Privilege offers practical steps and action-driven solutions so that those who have been afforded privilege can begin undoing the limiting beliefs held by society, and help build a fairer future for all.
You can see June Sarpong and Patrick Hutchinson in conversation about their books here.
What We're Reading: Out of Love – Hazel Hayes
What We're Reading: Queenie – Candice Carty-Williams
What We're Reading: Exciting Times – Naoise Dolan
What We're Reading: Wolf Hall – Hilary Mantel
What We're Reading: The Street – Anne Petry
This week, we asked Katie Seaman (Senior Commissioning Editor at HQ Fiction) to join us for What We're Reading! She told us all about The Street by Ann Petry, a book originally published in 1946, which was widely praised and became the first book by an African American author… Read More
On the shelf this week is Hilary Mantel's Wolf Hall, currently being read by Commercial Manager, Conor Anderson! Read on to find out more about What We're Reading… What's it about? England, the 1520s. Henry VIII is on the… Read More
Today we are joined by Marketing Assistant Becky Lushey who is here to tell us about her latest read – Exciting Times by Naoise Dolan – for What We're Reading! What's it about? Set in the international circles of contemporary Hong Kong, Exciting Times follows Dublin-transplant and English… Read More

redpajama_set_name: RedPajamaCommonCrawl


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Forums JSJS Designs JSJS.L announce new website to the stock market.
JSJS.L announce new website to the stock market.
This was published this morning on the RNS news wire:
RNS Number : 6186T
LightwaveRF.com Launch
JSJS Designs Plc ("JSJS" or "the Company"), the home automation specialists, announces the successful introduction of its new LightwaveRF.com site aimed at heightening the awareness of products to consumers but also in the recruitment of registered and approved installers. During the first month of operation the site has registered and opened trade accounts for over 250 electricians the majority through organic searches but close to 100 as a result of its new direct mail campaign which will roll out to a wider audience in January.
The campaign entitled "Britain's Brightest Sparks" targets electricians giving them facility to host their own promotional site within the LightwaveRF.com domain. The electricians are further supported by the new LightwaveRF promotional brochures and DVDs to aid in explaining the product range to their customers.
In addition the business has started taking pre orders for its much awaited new boiler and remote heating control system. The order bank has exceeded 100 systems in just three days.
Commenting on the developments Mike Lord JSJS Chairman and CEO said "The response to the new site has been much better than we had expected. The ability of an electrician to have a such high quality promotional support and access to consumer leads generated by the site has caught their attention as much as our fantastic product range. This is a higher margin channel for us and we are targeting a team of up to 1000 electricians initially which we are well on the way to achieving."
Mike Lord, CEO
Marc Davies / Mike Coe
This topic was modified 6 years, 7 months ago by Chris.
Of course it'd be lovely if it actually worked…. lightwaverf.co.uk works, but .com doesn't.
… or rather there's an odd redirect that points 'lightwaverf.com' to https:\\www.lightwaverf.com (which does not work). Manually using http:// instead works, and it stays there for subsequenent attempts rather than trying the secure version.