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Home » News » Beware rogue Forces Charities
Beware rogue Forces Charities
Murray Hammick
Charities, News, UK, Veterans
Bogus Charities, Charities Commision, Forces Charities
The recent revelations about an organisation called 1st Knight Military Charity, registered number 1158701, highlight the problems of what you might call "pop-up" charities that have appeared on the back of the recent campaigns in Iraq and Afghanistan.
1st Knight was investigated in 2016 by the Charities Commission after the airing of a TV documentary called "The Great Military Charity Scandal', and found to be potentially in breach of regulations on a number of counts. The programme made much of the fact that various items likely to be offensive in nature were being sold in the shop and also that views expressed by charity staff were unacceptable. The scope of the investigation – in more official terms, was to look at the following issues:
– administration, governance and management of the charity by the trustees
– conduct of the trustees
– financial controls and management of the charity
– whether or not the trustees have and continue to comply with and fulfilled their duties and responsibilities as trustees under charity law
Depending upon your personal views, some – or all – of what was shown in the BBC programme would be deemed offensive. This included the sale of Nazi-themed items, about which the CEO of the Fundraising Regulator commented: "That is not respectful and ethical fundraising. We would not expect a professional fundraiser to engage in that sort of thing and would certainly be ready to investigate." That said, it should be noted that the sale of Nazi regalia as such is not illegal in this country. What also attracted the wrath of the Charity Commission were the Islamaphobic comments made by members of the charity's staff.
However, the Commission also uncovered wider issues that are perhaps more relevant to the huge expansion of military charities that has taken place over the last ten or so years. Namely, the problems of governance and financial management. The BBC documentary featured another charity called "Support the Heroes" whose staff claimed they were unpaid volunteers when caught on camera at a market stall. The managers of the charity later confirmed that they were in fact on commission. However, Support the Heroes was just one of a series of "forces" charities that attracted attention for all the wrong reasons.
Afghan Heroes, also called True Heroes, was supposed to be raising money to support returning soldiers and Army families. It managed to raise well over half a million pounds, but, according to the Charities Commission, only spent £15k of that on good works – that is to say, 3% of its revenues. Another charity, Our Local Heroes Foundation, was also able to raise £500k, but again only spent about £10k – or just 2% of donations. In both cases the charities used "management companies" in the background which took out huge amounts of cash for their work. Both charities were investigated by the Charities Commission.
In the case of Our Local Heroes Foundation, the Charities Commission findings, published on 30th March 2016, included the following statement:
"We identified serious regulatory concerns including a very low level of charitable expenditure, substantial spending outside the charity's objects, poor governance, conflicts of interest and an insufficient focus on providing grants to beneficiaries. The charity had entered into contracts and agreements without due diligence or proper records and there were poor financial controls. The charity's income in 2015 was £500,000, but only £10,000 had been used in to further the charity's objects by providing grants. There were 8 employees, with wages and office costs of £155,000.
The charity had signed a fundraising agreement with Targeted Management Ltd (TML) for a 5 year term which stipulated that the charity would be invoiced for 80% of all the funds they raised. TML managed the charity's fundraising and claimed that this arrangement did not bring them within the regulations that cover commercial participators and fundraisers. At the time of the visit, the average income was £20,000 a week with a potential income of £1,000,000 a year. There was no evidence of fraud or theft in the charity.
We stated that this was not acceptable and that there was likely to be justifiable public concern and damage to the charity's reputation if the ratio of income to charitable expenditure remained so low."
(The Commission allowed the charity to continue on condition it complied with specific requirements regarding cost control and management – but later that year it was again found to have engaged in questionable practises and was eventually shut down.)
Not all fundraising is done under the auspices of a charitable registration – which might make it harder to for the "system" to monitor. In 2015 Marvin Trussell set up a collection-scam called "Army of Heroes", posing as a charity when none existed; luckily, he was picked up by Trading Standards officials. He also tried to con the public by claiming he was in the process of registering a Community Interest Company (CIC). However, the judge at his trial made it clear he had no intention of actually completing the registration and that none of the money collected had gone to help troops. The judge sent him to prison for three years, saying:
"The organisation was entirely dishonest. You never kept a single record and there has never been any contact with any individual charity. You never had any intention that the money would go to those with life changing injuries as a result of serving in the armed forces."
One serious concern about these scams is that the public might be put-off giving to genuine good causes that really do help former service personnel and their families. So how do you know whether your money is going to the people and causes you wish to support? The answer is that it is not that easy when faced by a collection box in the street. TMT has contacted some of the larger charities and it is clear that, given the current state of law and technology (the inability in the UK to check a personal ID, etc.), there is very little an individual can realistically do to check whether either the charity or the collector is genuine.
It is not for TMT to advise on which charities anyone should support, but logic says that it might be safest to either contribute to a well-known national charity via their official sites or collections points, or to contribute to a local charity that you know to be genuine. However, even if you meet someone in the street with a collection bucket for a well-known charity, what should you look for if you have any doubts? The Police "ActionFraud" website has some useful advice:
Charity donation fraud
When fake charity collectors prey on your sympathy by asking you to make a donation to a worthy cause.
Charities always need to be registered and have a license if they're collecting in a public place. Check they're authentic with the Charity Commission.
If the charity is genuine, check the collection is authorised, too. Call the charity directly or look them up using a phone book or a website (don't accept websites or numbers provided by a collector).
If in doubt, tell the collector you'll donate directly to the charity yourself .
Spot the signs
Their promotional material or website is badly written or has spelling mistakes.
The collector is aggressive or intimidating, or uses excuses to explain why their collection is legitimate, such as showing fake ID or falsified documents.
They're using topical events, such as a natural disaster, to make it look like their charity has been created only recently in response.
How it happens
A fraudster will either pose as a collector for a charity they've made up, or they misuse the name of a genuine, often well-known, charity. They may be collecting sponsorship money for an event that they won't take part in or doesn't even exist. In any of these cases, the money you donate doesn't go to charity; the fraudsters keep it for themselves.
You may be given the address of a fake website, where the fraudsters record your credit or bank account details when you go to a donation page.
Alternatively you may be asked to call a phone number. It could be a premium rate number, taking even more of your money on top of your donation.
If you're asked to donate clothing or household items, fraudsters sell them on but keep the money rather than giving it to people in need.
How to report it
Report it to us online or call 0300 123 2040.
As a result of contacting some of the main charitable organisations, TMT has been invited to follow-up talks to see what can be done to publicise and avert the risks associated with fraudulent Forces Charites, as well as look at the way in which charitable support for Veterans might be more sensibly co-ordinated and presented to the most important people in the whole equation – those in need on the ground. We will of course publish the result of any such talks – but invite you, our readers, to send in any comments you might have on the whole topic of charitable support to Forces Veterans.
Comments on Beware rogue Forces Charities
There are 2 comments on Beware rogue Forces Charities
Comment by David Rischmiller
David Rischmiller
A common tactic is for individuals or organisations to sell a 'veterans' magazine in the street, this usually means they do not need a street trading licence and neither are they conducting a charity collection, it is usually very hard for the well-meaning public to tell the difference however when told its 'for veterans'. In reality there is no way of telling how much, if any, of the money handed over actually goes to veterans!
Comment by Janet Willis
Janet Willis
Hello, I think we came across a man in
Bowness in Winderemere today selling a magazine today for veterans . He said it was to help veterans and by donating £3 we would be helping. I was suspicious of his manner and his ID was sketchy and partly handwritten. He was putting the cash in a man bag and not a plastic collector. We declined . I took photos in case something further could be done ?


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TAEKWONDO CLUB IS FIGHTING FIT FOR THE FUTURE
Anyone who has enjoyed watching Welsh double Olympic gold medallist Jade Jones will know that Taekwondo is very much a contact sport. It is no surprise then that Covid-19 has posed some obvious problems for community clubs across the country.
Yet the Taekwondo Cymru – Little Mill club in Monmouthshire has overcome this challenge by finding innovative ways of delivering their sessions. And they have successfully applied for a grant from Sport Wales' Be Active Wales Fund to put these ideas into action.
Sarah Farthing, who runs the club based in the Little Mill Village Hall, explains: "We teach Olympic-style Taekwondo. It's a full contact sport which focuses predominantly on sparring and is very interactive, so social distancing has made this impossible! Our members have been amazing and have been working really hard on their fitness but without the contact they've found the experience disheartening and repetitive. It's basically not been a true reflection of the sport.
"We applied to the Be Active Wales Fund to enable us to invest in brand new kit, including punch bags, reaction light training and jump boxes. Using these training aids, we can design exciting, dynamic sessions with lots of variation. We can be really creative with them. For example, we can make mini training stations where members can do drills and timed rounds. The training aids are excellent for resistance too - it feels far more realistic to kick a punch bag rather than the air, and it is safer too."
The training aids will be available for all members to use. The club also plans to introduce 'sport bubbles' for the under-tens, once they are permitted to mix together again, so they can invite children from the waiting list to start training.
Once they are able to resume, the club is also hoping to attract more girls to the sport. They plan to showcase the new training aids on social media and on flyers to demonstrate how they are used and to get girls excited about having a go. The next Jade Jones could be just around the corner!
The £3,064 funding awarded to Taekwondo Cymru – Little Mill came from the 'Progress' element of the Be Active Wales Fund which provides grants of between £300 and £50,000 to support sports clubs and organisations with their future plans so that they can offer even better opportunities for the nation to be active beyond the Covid-19 crisis.
Since the pandemic began, more than 800 sports clubs and organisations have benefited from a share of over £2.1m through the Be Active Wales Fund, and more is still available for Sport Wales to distribute thanks to money from Welsh Government and re-purposed funding from the National Lottery.
Be Active Wales Fund
Grant funding to help you grow participation.

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The Business table arrangements comprise two armchairs, one sofa and a table. The setting can be black or white. The business club table is branded with your company logo and is reserved exclusively for your company through the entire trade show.
The setting of the trade show ensures that the distance between your business meetings is as small as possible. We believe as well, that doing business in a nice and relaxed atmosphere. We believe that doing business in a pleasant form means also, that good food and drinks should always be available. We therefore serve breakfast at the show and have lunch and coffee break during the day, to make sure that your brain will never suffer from hyperglycaemia. We always serve drinks and coffee to maintain the necessary caffeine level.
It is another USP of the European Electronic HomeShopping Conference that it is the conference of "short distance" between your meetings. We encourage therefore all attending companies to avoid to present their products in their suites and rather reserve one of the extra meeting spaces next to the show floor that we can provide. The Vienna 2014 electronic HomeShopping conference offered 5 meeting spaces for companies, who wanted to have more privacy during their business encounters. In 2014 we had reached our limits regarding available space. The Hotel Rey Juan Carlos I in Barcelona will give us in 2015 more space, more flexibility and opportunities to serve the needs of our attendees.


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Kent Place Middle School Presents "Mary Poppins" on January 24 and 25
Mary Poppins is set to fly over the rooftops of London and into the Hyde & Watson Theater at Kent Place School on Friday, January 24, and Saturday, January 25! Tickets will go on sale on Monday, January 6, via https://kpspoppins.bpt.me.
Carlo D'Anselmi: "The Deep End" at the Kent Place Gallery
The Kent Place Gallery is pleased to present an exhibition of artworks by Carlo D'Anselmi now through Friday, December 20, 2019.
Kent Place School Announces New Director of the Upper School
It's with great excitement that we introduce Nicole Hager, who has been unanimously selected by the search committee to be the next Director of the Upper School, effective July 1.
Cross Country Wins School's First Ever NJISAA Class A State Championship
Linda Flanagan
The Kent Place cross country team raced their way into the history books on Wednesday, when the girls captured the New Jersey Independent School Athletic Association's (NJISAA) Class A Prep Championship for the first time in the school's history.
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Bobbi Moran
The Kent Place varsity volleyball team kept spectators on the edge of their seats on Thursday, November 7, as the Dragons squared off against a talented squad from St. John Vianney in Holmdel at the New Jersey State (NJSIAA) Non-Public A second round.
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It's one of the "conversation norms" we have at Kent Place, and it's always resonated with me. Everyone has a different and equally valid perspective to bring to the table—so put yourself out there. –Mary, senior
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There are no jocks here at Kent Place, no science geeks, no theater nerds. Last month a varsity athlete went to sing at the Vatican. Everyone here has some unique quality — and they're amazing at what they do. –Claire, senior
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And multiple extracurricular activities. Busy days, and a few late nights. But through it all, don't lose your sense of fun. –Alessandra, junior
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KPS alumnae are amazing. I met one alumna after a math and science panel who works in retail architecture. That made me think about a cool way to combine two of my interests — math and fashion. –Amber, junior
YOUR TIME AT KPS IS GOING TO OPEN UP OPTIONS YOU HADN'T EVEN THOUGHT ABOUT.
And when it's time to choose, you're going to know yourself so well, you'll pick the college that's the best fit for you—academically, socially, personally. So don't get tunnel vision. This is your process. Just know that you'll be ready! –Jennifer Simpson, Director of College Advising
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In the Middle School we do a Science Expo—either two or four people work on a science project for a couple of months and then present it to the entire class. We go into some in-depth projects and it's incredible what we learn along the way, and how willing our teachers are to help us through the tough parts. –Toni Ann, eighth grade
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We Are Proud...
A season highlight, ArtsCentric will present a powerful play by African American Female playwright Jackie Sibblies Drury.
BaltimorePlay
This production takes place in Baltimore, MD.
About We Are Proud...
Six black and white American actors attempt to make their own play about the imperial German genocide of the Herero people of South West Africa in the late nineteenth, early twentieth century. "We Are Proud..." is a hilariously tragic story that forces the audience to examine the stereotypes we all see in other races and, at times, even in our own cultures.
ArtsCentric
2600 N. Howard Street, Baltimore, MD 21218
We Are Proud... tickets on TodayTix


The Anthony Cumia non-apology tour landed at the late-night satirical talk show Red Eye on FNC in the shock jock's first TV appearance since he lost his radio gig.
Satellite radio provider SiriusXM last week fired the outspoken Cumia, the co-host of the Opie & Anthony Show, after a racist and obscenity filled Twitter rant following what he claims was a mugging. The tweets have since been deleted.
In defense of what went down on social media, Anthony Cumia told the Red Eye panel that he was in Times Square taking photographs at 4 am when an altercation with a woman occurred. He admitted that in retrospect that he should have cooled off first before sending out the tweets. "I defy anyone to be that angry, especially after an assault, and come off reasonable," he added.
Levy pointed out that many Twitter users may have been unfamiliar with his radio show and were just reading the tweets in isolation.
In response to why he never called 911, Cuma said, "I'm not going to use up the police resources in the pinnacle of the free world to say that a girl hit me." The woman in question has yet to come forward.
Anthony Cumia is launching a podcast starting August 4. Opie is likely to continue broadcasting Opie without Anthony with show fixture and popular comic Jim Norton taking over the co-hosting duties.


Intimate embryo-maternal interaction is paramount for pregnancy success post-implantation. The embryo follows a specific developmental timeline starting with neural system, dependent on endogenous and decidual factors. Beyond altered genetics/epigenetics, post-natal diseases may initiate at prenatal/neonatal, post-natal period, or through a continuum. Preimplantation factor (PIF) secreted by viable embryos promotes implantation and trophoblast invasion. Synthetic PIF reverses neuroinflammation in non-pregnant models. PIF targets embryo proteins that protect against oxidative stress and protein misfolding. We report of PIF's embryotrophic role and potential to prevent developmental disorders by regulating uterine milieu at implantation and first trimester.
PIF's effect on human implantation (human endometrial stromal cells (HESC)) and first-trimester decidua cultures (FTDC) was examined, by global gene expression (Affymetrix), disease-biomarkers ranking (GeneGo), neuro-specific genes (Ingenuity) and proteins (mass-spectrometry). PIF co-cultured epidermal growth factor (EGF) in both HESC and FTDC (Affymetrix) was evaluated.
In HESC, PIF promotes neural differentiation and transmission genes (TLX2, EPHA10) while inhibiting retinoic acid receptor gene, which arrests growth. PIF promotes axon guidance and downregulates EGF-dependent neuroregulin signaling. In FTDC, PIF promotes bone morphogenetic protein pathway (SMAD1, 53-fold) and axonal guidance genes (EPH5) while inhibiting PPP2R2C, negative cell-growth regulator, involved in Alzheimer's and amyotrophic lateral sclerosis. In HESC, PIF affects angiotensin via beta-arrestin, transforming growth factor-beta (TGF-β), notch, BMP, and wingless-int (WNT) signaling pathways that promote neurogenesis involved in childhood neurodevelopmental diseases—autism and also affected epithelial-mesenchymal transition involved in neuromuscular disorders. In FTDC, PIF upregulates neural development and hormone signaling, while downregulating genes protecting against xenobiotic response leading to connective tissue disorders.
In both HESC and FTDC, PIF affects neural development and transmission pathways. In HESC interactome, PIF promotes FUS gene, which controls genome integrity, while in FTDC, PIF upregulates STAT3 critical transcription signal. EGF abolished PIF's effect on HESC, decreasing metalloproteinase and prolactin receptor genes, thereby interfering with decidualization, while in FTDC, EGF co-cultured with PIF reduced ZHX2, gene that regulates neural AFP secretion.
PIF promotes decidual trophic genes and proteins to regulate neural development. By regulating the uterine milieu, PIF may decrease embryo vulnerability to post-natal neurodevelopmental disorders. Examination of PIF-based intervention strategies used during embryogenesis to improve pregnancy prognosis and reduce post-natal vulnerability is clearly in order.
A rapid and critical period of embryogenesis ensues post-embryo hatching and post-implantation; embryogenesis is then completed by 6 weeks post-implantation. During this period, the embryo mainly relies on itself for development, though this paradigm shifts radically towards placenta and mother later in gestation. The intimate contact established by the trophoblast with the maternal decidua enables effective exchange of nutrients and trophic agents. Since trophoblastic cells do not create a true barrier, the embryo benefits from the surrounding uterine milieu.
The earliest structure formed in the embryo post-implantation is the neural plate, with the spinal cord fold fusing by 6 weeks. The genes for proteins such as sonic hedgehog (SHH), wingless-int (WNTs), notch, bone morphogenetic proteins (BMPs), transforming growth factor beta (TGF-β), EPH, and others are implicated in cerebral cortical function and formation [1–3], as chick embryo and rat studies have revealed. Whether all of these regulatory factors are endogenous to embryonic cells, derived from the uterine milieu, or derived from a combination of both sources is not yet fully established. Moreover, it is important to determine whether the embryo itself (by regulating the maternal decidua) is an active participant in directing the flow of trophic compounds or is a passive participant in this process. Finally, embryo-derived secretory products acting on the uterine milieu may provide protection during gestation and possibly prevent disorders that can manifest long after birth. Evidence for such a protective effect derives from experimental observations that trophoblastic cells, and the embryo, effectively inactivate xenobiotics [4–9].
To understand the embryo's role, examining embryo-specific compounds' effect on the intrauterine milieu provides crucial information on embryo-induced conditioning involved in successful implantation and ensuing embryogenesis. Preimplantation factor (PIF) is a specific, post-fertilization peptide signal secreted by viable embryos. PIF is expressed both by the embryo/fetus and the placenta and is present in the maternal circulation throughout viable pregnancy [10–12]. PIF exerts four major complementary effects that are essential for pregnancy initiation and maintenance: 1) promoting the development of cultured embryos and acting as a rescue factor negating toxic-serum-induced embryo demise ; 2) promoting endometrial receptivity by regulating genes that are involved in inflammation, adhesion, and apoptosis and promoting the secretion of immune regulatory ligands and modulation of kinase phosphorylation, which actively condition the uterine environment [14, 15]; 3) enhancing trophoblastic invasion, which provides effective oxygen and nutrient exchange for the fetus, an effect that is not synergized with epidermal growth factor (EGF) ; and 4) regulating systemic immunity to promote embryo tolerance while preserving the maternal ability to fight pathogens/disease and negating NK cell-induced toxicity [17, 18].
As recently reported, PIF plays a determining role in the embryo's neural development and neuroprotection by targeting the embryo proteins involved in oxidative stress, protein misfolding, and neural development. Specifically binding to protein-di-isomerase/thioredoxin (PDI/TRX) and heat shock proteins (HSPs) was noted. These major targets share a common binding site for PIF, enabling multi-targeting. In addition, PIF also targets tubulins, backbone of neurons . PIF also upregulates decidual proteins that play a major role in neural function: agrin (a component of the neuromuscular junction), Calpain1 (a cytoskeleton component), NDUFS3 (modulator of oxidative stress), and PPF1BP1 (involved in axon guidance), in human implantation models .
PIF reverses advanced brain damage induced by hypoxia and inflammation in newborn rat models [20–22]. In chronic neuro-inflammation models, PIF reverses severe paralysis by reducing oxidative stress and protein misfolding while promoting and facilitating neural repair (by increasing neuron assembly and transmission) via local and systemic effects . In a clinically relevant model for multiple sclerosis, subcutaneous administration of PIF led to reduced brain inflammation and reversal of paralysis. Notably, observations have demonstrated that PIF directly targets microglia, the major immune element within the CNS . In this and other models, the primary PIF targets are insulin degrading enzyme (IDE) and potassium channel Kv1.3b, both of which play a prominent role in neural diseases and are targets for neuroprotective drugs .
The aim of the current study is to assess the impact and perform a more complete characterization of PIF's effect on the maternal decidua, both at implantation and during the first trimester, in order to establish its embryotrophic and specifically neurotrophic roles in early gestation. For this, PIF's impact on gene expression was examined in relation to 1) genes involved in trophic effects on the embryo with an emphasis on the neural system and 2) genes involved in potentially protecting against development of diseases in childhood and throughout adult life. In addition, 3) PIF's specificity of action was examined by using EGF (a growth factor) as an antagonist. The data generated implies that the embryo, through PIF signaling, can condition the uterine milieu to regulate and mitigate the environmental impact on its own neural development. Thus, PIF, in addition to supporting embryo development, could play a role in decreasing the risk of developing post-natal disorders.
The method was already described . Briefly, synthetic PIF analog (MVRIKPGSANKPSDD) was produced using solid-phase peptide synthesis (Peptide Synthesizer, Applied Biosystems, Foster City, CA, USA) employing 9-fluorenylmethoxycarbonyl (Fmoc) chemistry. Final purification was carried out by reversed-phase high-pressure liquid chromatography, and peptide identity was verified by mass spectrometry as previously described .
Yale University School of Medicine review board approval was obtained for this study. Using our previously established cell culture method [14, 15], non-pregnant human endometrial stromal cells (HESC) and cells collected from healthy first trimester of pregnancy deciduas were studied. Discarded endometrial tissue from premenopausal women undergoing hysterectomies due to benign indications was used. Decidual specimens from the first trimester were obtained from women undergoing elective termination in weeks 6–12 of normal pregnancy. Endometrial and decidual cells were isolated and re-suspended in Roswell Park Memorial Institute (RPMI)-1640 medium, grown to confluence, and found to be leukocyte free (<1%). After reaching confluence, the cells were decidualized using 10-8 mol/L estradiol and 10-7 mol/L synthetic progestin analog (R5020) (DuPont/NEN, Boston, MA, USA), in both cases for 7 days. The cells were switched to a serum-free medium containing insulin, transferrin, and selenium (Collaborative Research Inc., Waltham, MA, USA); 5 μmol/L trace elements (GIBCO, Carlsbad, CA, USA); and 50 μg/mL ascorbic acid (Sigma-Aldrich, St. Louis, MO, USA), and treated for 24 h with or without synthetic PIF (100 ng/mL). In other experiments, 50 ng EGF was cultured together with 100 ng/mL PIF for 24 h in HESC and first-trimester decidua cultures (FTDC). The tissue culture was collected and frozen at -80°C The samples were tested in triplicate.
Total RNA was extracted from each cell culture. Analysis of HESC or FTDC with and without PIF 100 ng/mL (n = 3/group) or +/- EGF was examined using Affymetrix (Santa Clara, CA, USA) U133 Plus 2.0 Array (>38,500 human genes), followed by fluorescence labeling and hybridization with Fluidics Station 450 and optical scanning with GeneChip Scanner 3000 (Affymetrix) at W. M. Keck Foundation Biotechnology Resource Laboratory, Yale University, New Haven, CT, USA. Raw data were analyzed by GeneSpring software (Agilent, Santa Clara, CA, USA), normalized for inter-chip and intra-chip variations to eliminate false-positive results.
Genes that were significantly changed in expression by PIF (p < 0.05) using Student t test followed by a greater than twofold change were reported. Further results were divided into upregulated or downregulated lists and underwent new gene pathway analysis. MetaCore from GeneGo Inc., a Thomson Reuters business (Carlsbad, CA, USA), was used to identify and visualize the involvement of differentially expressed genes in specific cellular pathways. Enrichment analysis algorithms across several GeneGo ontologies were used to rank pathways, process, and diseases. To determine possible key regulators that may contribute to PIF-induced changes in gene expression to the human interactome (manually annotated interactions from peer-reviewed published experiments), the interactome tool in the MetaCore platform was used. To further understand the mechanisms and processes represented by the top connected hubs, networks were built using the shortest path algorithm followed by enrichment analysis using the disease and gene ontology processes.
Pathway analysis was performed using the Ingenuity Systems Inc. (Redwood, CA, USA) software, ranking by greatest number of genes in a given pathway and associated statistical significance.
HESC protein lysates (n = 3/group) from an independent experiment as compared to those of an mRNA study were homogenized in retinoic acid receptor alpha (RARA) buffer (100 mM Tris 250 mM NaCl, 0.1% Triton X-100, 0.1% sodium dodecyl sulfate (SDS)) and assayed for protein concentration. Twenty micrograms of each lysate was loaded in duplicate onto an SDS-poly-acrylamide gel Novex 4%–12% (Invitrogen, Carlsbad, CA, USA) followed by electrophoresis. Each lane was excised into 40 equal slices, digested with trypsin, and analyzed by nano-liquid chromatography/mass spectrometry (nano-LC/MS/MS) on an LTQ-Orbitrap XL™ tandem mass spectrometer (ThermoFisher, San Jose, CA, USA) carried out at NextGen Sciences (Ann Arbor, MI, USA). Data were searched against the Mascot concatenated forward-and-reversed v3.38 International Protein Index (IPI) database (Matrix Science Ltd., London, UK) and collated into non-redundant lists using Scaffold software (Proteome Software Inc., Portland, OR, USA). Using these combined forms of software creating ion identity score, and using the PeptideProphet provide high accuracy by determining true probabilities of proteins identified. Spectral counting was employed for relative quantitation, and a t test was utilized to show significant differences.
Neural development initiates shortly post-implantation, and therefore, PIF's effect on pathways that lead to the secretion of neurotrophic factors for the embryo by the decidua was examined (Table 1). The highest ranking gene (13.8-fold increase) is TLX2—a nuclear receptor subfamily 2 group E that binds DNA. This protein plays a major role in anterior brain differentiation and vision development . Also, highly ranking is EPHA10 (9 fold) whose protein encodes a receptor for tyrosine kinase targeted by ephrin-A family members . This protein is important for cell-to-cell communication and neural cell mobility. On the other hand, RARA gene expression decreased (-9 fold) . This gene encodes a receptor for retinoic acid which is involved in growth arrest.
In FTDC, the major upregulated gene was SMAD1 (53.4-fold increase) (Table 1) . Its encoded protein is TGFβ signaling protein, a major modulator of the bone morphogenetic protein—highly relevant for embryo neural development . There is also an increase in SMAD6 and SMAD2 (2.7-fold and 2.5-fold, respectively). EPHA5 increased by 7.8-fold; this protein is a receptor tyrosine kinase that binds ephrin-A family ligands, which are highly relevant to neural development, especially axonal guidance and synaptogenesis . On the other hand, PIF downregulates PPP2R2C, which is involved in negative control of cell growth and division . Collectively, this set of data indicates that PIF is involved in pathways that are critical for neural development.
PIF also appears to affect several neural-related pathways that could contribute to neurotrophic effects on the embryo. The highest correlation was found with axon guidance signaling followed by neuroregulin, which is involved in EGF signaling; the specific genes involved are listed in Table 2. Effective synaptic transmission is recognized to be critical for effective neural development. The regulatory effect of PIF in this pathway reflects the peptide's significant protective role against altered neural development. The lowest ranking—but still relevant—gene pathway affected by PIF is the oxidative phosphorylation pathway, which is also critical for embryo survival.
Upon analyzing the FTDC data (Table 3), an interesting pattern emerged since the data showed that the highest ranking neural pathways affected by PIF are actually related to adult neurological disorders. Among them are amyloid processing genes that can lead to Alzheimer's disease, amyotrophic lateral sclerosis, and Huntington's chorea. This is followed by effects on neural signaling pathways. PIF's effect on individual genes and their expression in the different pathways is shown in Table 3. This correlation with adult disease implies an evolution in PIF targeting of the maternal milieu with advancing gestation which is different from earlier development phases which appear to be more involved in early childhood diseases.
Since PIF exhibits trophic effects mainly on neural development, it was of interest to further examine the genes involved in embryo development as well, possibly a long-term protective strategy to prevent adverse post-natal disorders. The MetaCore program enabled such analysis. The full description of the role of PIF in multiple cellular signaling pathways is however beyond the scope of this manuscript. Hence, this information is available in detail in Additional file 1 (pages 1–42), and only key findings are referenced herein. For such a comprehensive analysis, the data had to be analyzed as pathway maps, process networks, followed by the specific physiologic processes involved, and finally the disease association, when these processes are perturbed which lead to disease during childhood or in adulthood (Table 4). Data was analyzed as the highest association in each category, with associated statistical significance.
PIF's highest ranking pathway in HESC is the angiotensin signaling via beta-arrestin, which is coupled with neural transmission or nerve impulse associated with nervous system development and, when affected, leads to autism. The second ranking pathway affected by PIF was genes involved in the epithelial-mesenchymal transition (EMT), which is associated with muscle contraction, is needed for neural functionality, and if affected, can lead to child development disorders. Interestingly, PIF was found to have significant associations with pathways relating to mood disorders and stress, TGFβ, WNT, CDK5, and BMP.
Among the significantly upregulated processes for which PIF increased the gene expression more than twofold are (Table 5) angiotensin—via beta arrestin, G-protein signaling RhoA/B, and CDC42, showing that the effects on neurogenesis and immune response are dominant. In contrast, the processes downregulated by PIF are EMT, EGF activation, and axon growth repulsion. The balance among upregulated and downregulated processes implies a dynamic adaptive effect on these pathways.
Listed are the top ten results from the Analyze Single Experiment Workflow across two ontologies. This table shows the upregulated and downregulated processes where the same processes between the two time points are italicized.
In FTDC (Table 6), on the other hand, different maps to diseases were identified. PIF's highest ranking pathway was acetaminophen metabolism (i.e., xenobiotics) which relates to reproduction/hormone signaling and, when affected, can lead to autoimmune connective tissue disorders (Table 5). The second ranking pathway was steroid metabolism related to vasculogenesis and, when altered, leads to development of skin disorders. Of note, connective tissue disorders and neoplasms occur mostly in adults. The associated upregulated processes are cell cycle role in 14-3-3, ERK5, and mitosis, and neuronal survival and development. The downregulated processes are xenobiotics related to acetaminophen, 2-napthalamine, benzo (a) pyrene, and steroid metabolism. The emphasis on protection against xenobiotics is critical for PIF's protective role during embryogenesis.
To document the dynamic gestational age-dependent effect of PIF in early pregnancy, similarities and differences between those critical time periods were examined. Common pathways affected by PIF include muscle contraction and angiotensin signaling via four independent pathways: STATs, ERK, PYK2, and CREB pathways. Neurophysiologic processes affected were melatonin signaling and receptor-mediated growth axon repulsion. Global processes were transmission of nerve impulses, axonal guidance, and cell adhesion. The similarity between the two time periods with respect to neural development illustrates PIF's continuing role in this critical process.
To better delineate a network of genes associated with PIF activity, an interactome analysis was carried out. This enables us to relate a large number of genes that are linked in a network. The hub enables to define the number of interactions among genes. Table 7 illustrates the leading genes and their interaction. In HESC, FUS was dominant . This gene controls genome integrity and RNA processing and has the highest (n = 68) interactions, followed by HIPK2, whose protein is a kinase involved in p53-regulated cellular apoptosis .
In FTDC, the number of interactions was much higher.
The FTDC interactions were much more extensive (Table 7). The highest ranking was STAT3 (n = 603) . The protein plays a central role in JAK/STAT signaling of several cytokines. The next ranking was CDK1 (n = 389), a kinase that controls cell cycle regulation . Of note, the decidua genes are more connected through two signaling steps than the genes found in HESC, in which three steps are involved.
Table 8 illustrates the top biological processes affected by PIF in HESC. The highly prominent DNA-dependent regulation is required during rapid cellular development. In contrast, the top process in FTDC is the response to chemical stimulus, i.e., protection against adverse environment during embryogenesis. This further substantiated the evolving role of PIF from supporting neural development to protection against xenobiotics.
Using an independent experiment, the effect of PIF on a number of protein levels was determined by using semi-quantitative mass spectrometry (14). To provide a more detailed analysis, we have analyzed, in addition, the effect of PIF on a total of >1,300 HESC proteins demonstrating that several of them were affected by PIF (Additional file 2). We found that PIF affected several proteins involved in the control of oxidative stress and protection against abnormal protein synthesis: PDIA3, P4HB (PDI), TXND, PRD6, HSPB1, SDHA, and BAG1. This was clearly in line with the microarray data. In addition, specifically focusing on proteins involved in neural function, the data revealed that PIF affects several additional proteins among them. PPIC is affected in ataxia and in degeneration of Purkinje cells . OCRL is affected in Lowe syndrome oculo-cerebral defects . AP3D1 is involved in budding vesicle transmission to neurons . SLC25A1 and SLC16A1 are proteins involved in mitochondrial transport widely expressed in the central nervous system . LDHA is involved in substania nigra development and is deregulated in glioma tumors . Thus, PIF also affects not only genes but also decidual proteins.
EGF is reported to block decidua formation, and PIF was shown to regulate EGF-related pathways, promoting amphiregulin and epiregulin while inhibiting betacellulin . Therefore, whether EGF can affect PIF's action was examined. Addition of EGF abolished PIF's effect on the global genome. Only a limited number of genes (N = 15) were affected, mostly of which were downregulated. The EGF treatment-related pathway is shown (Figure 1). The decrease noted in MMP metalloproteinase expression may interfere with decidual function . This is further amplified by the decrease in prolactin receptor (Figure 2), where the ligand is crucial for decidua formation. The most downregulated gene was BMPER, an inhibitor of BMP (-10 fold) followed by NIF3LBP1 (-7.4 fold), which binds NIF3 (an amyotrophic lateral sclerosis candidate gene), MCC1 (-7.4 fold) (a tumor suppressor), and PRLR (-4.2) (a prolactin receptor important for decidua function) [42–46]. The gene polymorphism is associated with multiple sclerosis. The only gene which was increased is Nov (2 fold), which is a negative regulator of cell growth in choriocarcinoma cells .
Pathway analysis as it relates to EGF signaling in HESC.
Pathway analysis as it relates to prolactin receptor gene in HESC.
PIF significantly reduces EGF receptor (-25.6 fold) in FTDC, therefore blocks the ligand's activity . Whether EGF interferes with PIF's action on the decidua was analyzed. The most downregulated gene was ZHX2 (-8.4 fold), which was shown to promote AFP secretion leading to activation in liver cancer . Figure 3 shows that EGF reduced IL8 expression and decreased PDE3A (-5.6 fold), involved in learning and memory . There was also a decrease in PEG3, which blocks inflammation-induced apoptosis and is a tumor suppressor in glioma cells (-6.3 fold). Interestingly, PIF alone on FTDC negated both PEG3 (-5 fold) and PDE7B (-5.7 fold) [50, 51]. These observations document the negative relationship between PIF, a promoter of decidual function, and EGF, which acts as a pro-proliferative agent with anti-decidual properties.
Pathway analysis as it relates to PEG3 gene in FTDC.
After hatching but before being protected by the placenta, the embryo is highly vulnerable to maternal adversity. However, the embryo has developed efficient protective mechanisms. It is herein demonstrated that PIF, an embryo-secreted peptide, differentially conditions the maternal uterine environment during implantation and the first trimester. By regulating the uterine milieu, PIF provides crucial embryotrophic support for the neural system, which is of central importance to the early embryo's development and has deep consequences throughout early as well as throughout adult life. During implantation, PIF's major effect is exerted on neurotrophic genes that are involved in regulating signaling involved in neurodevelopmental disorders. PIF, in the first trimester decidua during embryogenesis, affects signaling pathways that are involved in protecting against xenobiotic exposure and regulates pathways involved adult neurodegenerative and autoimmune connective tissue disorders. In contrast, EGF, a potent growth factor, is a PIF antagonist and abolishes its protective effects on the decidua. This demonstrates that PIF's embryotrophic and protective effect is dynamic and dependent on the conditioning of the maternal milieu.
Numerous decidual genes related to neural function and development affected by exposure to PIF are herein characterized and analyzed. This complements and expands observations of PIF's effect on genes associated with secreted products and phosphorylated kinases that can aid in embryo development [14, 15]. The observation that post-implantation PIF is present in the maternal circulation and is expressed by the placenta creates an intimate link between this embryo/trophoblast-secreted peptide and the maternal uterine environment . The use of two advanced modes of gene analysis (Ingenuity and MetaCore) reveals complex mechanisms involved in PIF's action.
PIF's gene/pathway regulation was examined as it is related to embryotrophic effects. Post-implantation, the neural plate forms via migration of primary cells, with fusion of the neural folds within 30 days post-conception; the upper segment then forms the brain, while the lower segment forms the spinal cord. Several trophic factors are involved in neural formation, including the TGFβ, BMP-2, EPH-1, and WNT-3 pathways [1–3]. Some trophic factors are endogenous to the embryo (which has a very small surface area for synthesis/secretion), while other trophic factors are of decidual origin which has a larger surface area and are likely to be dominant.
PIF upregulates decidual trophic genes, several of which promote neural system development. Specifically, during the implantation period, increases are noted in TLX2 and EPHA10 (a brain trophic agent and an agent that improves neural transmission, respectively). Conversely, PIF lowers RARA expression, preventing growth arrest. This was further emphasized in PIF's neural pathway ranking where the top ranking was in genes promoting axonal guidance and synaptic potentiation. Remarkably, in FTDC, in which the embryo/maternal relationship has already been well established, PIF significantly promotes SMAD1, which is involved in the BMP pathway and is critical for embryo neural development. With regard to pathway ranking in FTDC, PIF's more prominent effects are on genes relating to post-natal diseases since the embryo's neural fold has already been closed at this stage.
The MetaCore program provides a unique insight into gene regulation, pathways, and association with possible diseases. Analyzing in detail PIF's effects on disease-related pathways in the two different gestational times identifies a complex picture, since the number of genes affected is very large. This indicates that PIF's effect is robust, especially with respect to the angiotensins (mainly angiotensin II), which serve as brain modulatory factors implicated in stress response and vulnerability to cerebrovascular ischemia and inflammation. Angiotensin receptor blockers may protect neurons . Angiotensin IV and its receptor are implicated in cognitive processing and memory impairment . Specific downstream pathways via CREB and Akt are neural progenitor regulators  and targeted by using rapamycin against neonatal hypoxia and ischemia . Additionally, the angiotensin family (1–7) increases neuronal voltage-gated potassium current through nitric oxide pathway [14, 56]. Furthermore, viral infections cause, in the prenatal period, activation of the inOS pathway in murine models . We demonstrated that PIF controls the inflammatory response in macrophages by blocking this specific pathway . Therefore, the novel association found between PIF and angiotensin warrants further examination in targeting neurological diseases.
PIF also had a significant effect on genes involved in the EMT . This implies that PIF can affect cells that are involved in enabling transformation of one cell type to another, reversibly critical for proper embryo development. On the other hand, under inflammatory conditions, EMT can also be effectively activated, harming the host. The major factors involved are BMP7 and Wilms tumor 1 genes. As a consequence of this regulation, PIF affects genes involved in post-natal neurologic diseases such as autism and later onset neurodegenerative diseases like multiple sclerosis. Thus, altered embryo-maternal communication may increase the susceptibility for such disorders.
Endometrial inflammation is a frequent pathologic environment. When subtle, there may be no clear embryo rejection leading to spontaneous abortion; however, there may still be long-term adverse consequences that can manifest post-partum. PIF may play a role in averting such adverse events. As expected in the decidua, PIF's effect on xenobiotic metabolism and hormonal control are prominent; however, the more subtle effect on neurodevelopmental diseases is still evident, mostly their expression in adult diseases.
Our interactome analysis provided further insight into PIF's gene network, identifying those specifically involved. Interestingly, the linkage between genes was more tightly regulated in the FTDC. Perhaps this is related to the fact that the decidual cells were primary, as compared to HESC, which were steroid-activated stromal cells. Overall, the reciprocal relationship between the embryo through PIF and the maternal decidua appears to play an important role in the earliest stages of development. As the genes affected at implantation and FTDC are different, this is a further confirmation of PIF's selective and targeted effect on the maternal environment.
Further substantiating observations made on PIF regulatory effects on HESC proteins (14), we have examined PIF's effect on the global proteome. PIF affects proteins PDI and HSPs that reduce oxidative stress and protein misfolding. Remarkably, PDI and HSP are also PIF-binding targets (19). Therefore, we further document that PIF not only regulates HESC but also identifies through which proteins such a targeting most likely such effect takes place. Therefore, such data creates an intimate integration between effect and site of action.
The highly ranking neuroregulin pathway in HESC is EGF related. PIF inhibits this pathway by downregulating ERB03, ERBB2IP, and PRKCB-, pro-proliferative genes further amplified by the increase in PTEN, a tumor suppressor. Conversely, EGF completely blocked PIF's effect on both HESC and FTDC, confirming the antagonistic effect of the growth factor. This is expected since EGF promotes decidual cell proliferation and has anti-decidual effects . It is of note that decidual heparin-binding epidermal growth factor-like growth factor (HB-EGF) has distinct properties as compared with EGF . Such inhibitory action indicated also that PIF's effect is dynamic and is dependent on a given decidual environment.
From a clinical perspective, genetic defects and epigenetic modifications are major contributors to post-natal disease. Development of invasive and non-invasive diagnostic tests has led to a significant decrease in the birth of affected children. Despite these advances, in utero identification of more subtle neurodevelopmental disorders is still lacking. In autism, a condition whose incidence continues to rise, recent reports indicate that two complementary brain pathologies co-exist; immune over-activity and reduced neural interaction . Thus, the syndrome may initiate in the prenatal period, as supported by murine models . Consequently, it is important to address how early such defects initiate and whether they are preventable or treatable if identified early. Neural tube defects, and possibly other neurodevelopmental disorders, may also develop during early embryogenesis. Evidently, major neurologic disorders such as anencephaly will be self-limiting or diagnosed and eliminated, whereas more subtle forms might persist. Insight into these processes could move forward the field of neurodevelopment, with significant implications for post-natal life.
The current study supports the view that the embryo, through PIF, conditions the uterine environment to reduce the impact of adverse maternal environment. In addition to structural imaging, several serum markers (hCG, PAPP-A, estriol, and AFP) can identify neurodevelopmental disorders such as Down's syndrome and neural damage. Recently, metabolites related to oxidative stress were found to be increased in the serum of patients with Down's syndrome . These observations imply that maternal conditioning may play a significant role in regulating embryonic neural development. It is suggested here that PIF could improve such maternal conditioning.
The study is limited since PIF's effects were assessed in culture and therefore cannot directly reflect the in vivo environment. However, the two time-point models used are well established to provide important insight into the biology of early pregnancy. A further strength is the use of two complementary, advanced methods of data analysis which independently confirm the observation that PIF plays a central role in neural control both at implantation and in the first trimester. Finally, the use of EGF in both cell types demonstrated that PIF's effect is specific and can be blocked by the growth factor.
Overall, the current investigation reveals that the embryo, through PIF, conditions the maternal environment, specifically by targeting elements critical for survival (principally, the neural system). Hence, protection observed in both the newborn and the adult may be related to PIF's role in neural development and protection that initiates in the earliest stages of pregnancy. Such beneficial maternal conditioning may have long-term ramifications in protecting against childhood and adult neurologic diseases.
Dr. Graciela Krikun, Roxana Pickering and other members of the Yale University Reproductive Science for technical help. Dr. Richard Jones for the proteomic analysis (NexGen Sciences Inc., MI, USA). We thank Stephanie Zinn and Amy Carter for editorial assistance.
This work was supported through an unrestricted grant by BioIncept, LLC (MJP) and National Institutes of Health (grant number 5R01HD056123-02) (SJH). All other authors declare no competing interests.
CMD, MJP, and JSH carried out the experiments and helped in data analysis. LJ analyzed the MetaCore program. ERB discovered and developed the PIF technology, helped in data analysis, and wrote the manuscript with CMD, MJP, and LJ. All authors read and approved the final manuscript.


Sylvia Izzo Hunter was born in Calgary, Alberta, back in the days before Star Wars, and started making up stories at approximately the time she learned to talk. A couple of decades ago she moved to Toronto, Ontario, where she now lives with her husband and daughter and their slightly out-of-control collections of books, comics, and DVDs. She studied English and French literature (with a particular focus on medieval and Renaissance poetry and drama) at York University; she has since discovered that her mom was right: in order to be a functioning grown-up, you really do need to know how to do math. Over the course of her working life Sylvia has been a slinger of tacos, a filer of patient charts and answerer of phones, a freelance looker-up of unconsidered trifles, an Orff-singing stage monk, and an exam tutor, but has mostly worked in not-for-profit scholarly publishing, where she started out making lots of photocopies and now gets to make XML and EPUB files (which is more fun). She also sings in two choirs (including the Orpheus Choir of Toronto), reads as much as possible, knits (mostly hats), and engages in experimental baking.
Graham "Gray" Marshall is a gifted magician, studying magic at Oxford's Merlin College, when some of his classmates insist he come along on a midnight adventure. In no time, things go bad. Gray is blamed for the misadventure and sent away from Oxford to the Breton estate of his tutor, the small-minded, petty and envious Professor Appius Callender. Sophie Callender is the ignored middle daughter of the professor. Her father has told her, repeatedly, that she has no magical ability, but she thirsts for knowledge and reads magical texts in secret. There is a mystery about Sophie's mother, who died when Sophie was eight, and the housekeeper, Mrs. Wallis, knows more than she is telling.


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1. JEAN1 MARTEL was born Abt. 1587 in Dauphine, France. He married ANNE MARIZY January 11, 1611/12 in St. Eustache, Paris France, daughter of CHARLES MARIZY and MARIE PROURIANT. She was born Abt. 1590.
2. i. JEAN2 MARTEL, b. 1615, St. Eustache,Paris France; d. WFT Est. 1635-1695.
2. JEAN2 MARTEL (JEAN1) was born 1615 in St. Eustache,Paris France, and died WFT Est. 1635-1695. He married (1) BARBE MARIE DUSCHESNE Abt. 1630 in Saint-Eustache, Paris France. She was born Abt. 1615 in St. Eustache, Paris France, and died WFT Est. 1635-1701. He married (2) FRANCOISE PERROT July 28, 1652 in Seine, Paris France.
3. i. HONORE3 MARTEL, b. 1632, St-Eustache de Paris, France; d. July 28, 1710, L'Hotel-Dieu de Quebec, Canada.
3. HONORE3 MARTEL (JEAN2, JEAN1) was born 1632 in St-Eustache de Paris, France, and died July 28, 1710 in L'Hotel-Dieu de Quebec, Canada. He married (1) MARGUERITE L'AMIRAULT November 26, 1668 in Notre Dame de Quebec, daughter of FRANCOIS L'AMIRAULT and JEANNE GLAUSE. She was born Abt. 1645 in St.-Germain L'Auxerrois de Paris, France, and died October 17, 1706 in L'Hotel-Dieu de Quebec, Canada. He married (2) MARIE MARCHAND November 03, 1707 in Quebec, Canada. She was born Abt. 1630 in Notre Dame, Montreal Quebec Canada.
i. CHARLES4 MARTEL, b. October 04, 1669, Quebec, Canada; d. October 27, 1669, Quebec, Canada.
4. ii. JEAN-FRANCOIS MARTEL, b. November 04, 1671, Quebec, PQ, Canada; d. March 14, 1714/15, Hotel-Dieu, Quebec, PQ. Canada.
iii. JOSEPH-ALPHONSE MARTEL, b. May 12, 1672, Quebec, Canada; d. December 31, 1741, Longue Pointe, Quebec, Canada.
iv. MARIE-MADELEINE MARTEL, b. July 29, 1674, Notre Dame de Quebec, Canada; d. January 02, 1702/03, Quebec, Canada; m. LOUIS LOISEL, June 12, 1696, Quebec, Canada; b. 1650; d. March 17, 1743/44, Charlesbourg, Quebec Canada.
v. MARGUERITE MARTEL, b. July 29, 1676, Neuville, Quebec, Canada; d. July 27, 1762, Notre Dame, Montreal Quebec Canada; m. (1) LOUIS COURAULT DIT COULON, January 10, 1694/95, Quebec, Canada; b. 1673; d. 1699; m. (2) JEAN FRANCOIS DOUAULT DIT SAINT JEAN, January 28, 1703/04, Varennes, Quebec Canada.
vi. PAUL MARTEL, b. May 24, 1678, Neuville, Quebec, Canada; d. May 27, 1724, St. Antoine,Tilly, PQ. Canada.
vii. HONORE MARTEL, b. February 06, 1679/80, Neuville, Quebec, Canada; d. February 16, 1679/80, Pointe Aux Trembles, PQ, Canada.
viii. ANTOINE MARTEL, b. January 08, 1680/81, Neuville, Quebec, Canada; d. March 19, 1759, St. Pierre Ile Orleans, PQ, Canada.
ix. ISABELLE MARTEL, b. November 25, 1682, Neuville, Quebec, Canada; d. November 28, 1682, Neuville, Quebec, Canada.
x. ANNE-MARIE MARTEL, b. November 08, 1683, Neuville, Quebec, Canada; d. February 21, 1702/03, Saint Antoine-de-Tilly; m. CHARLES ROGNON DIT LAROCHE, November 09, 1698, Quebec, Canada; b. 1673; d. 1718.
xi. JEAN BAPTISTE MARTEL, b. November 13, 1685, St. Francois De Salles, Neuville, Quebec, Canada; d. September 22, 1762, Quebec, Canada.
xii. LOUIS MARTEL, b. September 01, 1687, Neuville, Quebec, Canada; d. December 04, 1720, Notre Dame, Montreal Quebec Canada.
xiii. MARIE-ANNE MARTEL, b. August 28, 1689, Neuville, Quebec, Canada; d. December 06, 1782, Ile Aux Coudres, Quebec, Canada; m. (1) THOMAS FERRET, August 29, 1708, Quebec, Canada; b. 1668; d. 1725; m. (2) FRANCOIS BOUCHER, July 10, 1727, Charlesbourg, Quebec; b. 1699.
xiv. MARIE-THERESE MARTEL, b. September 04, 1691, Neuville, Quebec, Canada; m. GUILLAUME HOGUENET DIT ARGENCOURT, September 03, 1714, Neuville, Quebec, Canada.
4. JEAN-FRANCOIS4 MARTEL (HONORE3, JEAN2, JEAN1) was born November 04, 1671 in Quebec, PQ, Canada, and died March 14, 1714/15 in Hotel-Dieu, Quebec, PQ. Canada. He married MARIE-MADELEINE VANIER February 14, 1694/95 in Charlesbourg, Porneuf Co., PQ, Canada, daughter of GUILLAUME VANNIER and MARGUERITE BAILLY. She was born January 03, 1674/75 in Quebec, and died Abt. 1759.
i. CHARLES5 MARTEL, b. May 07, 1696, Charlesbourg, Quebec, Canada.
ii. JEAN-FRANCOIS MARTEL, b. June 15, 1698, Charlesbourg, Quebec; d. June 15, 1760, Ste. Genevieve, Ile de Montreal, Quebec Canada.
iii. PIERRE MARTEL, b. January 16, 1700/01, Charlesbourg, Quebec; d. WFT Est. 1743-1797.
iv. JOSEPH MARTEL, b. May 12, 1706, Quebec, Canada; d. Longue Pointe, P.Q., Canada; m. (1) AGNES PAQUET, July 03, 1730, Charlesbourg; b. WFT Est. 1686-1713; d. WFT Est. 1735-1803; m. (2) M-ANNE GAUVIN, February 04, 1777, Charlesbourg; b. WFT Est. 1733-1760; d. WFT Est. 1782-1850.
v. CATHERINE MARTEL, b. April 09, 1708, Charlesbourg, Quebec; m. (1) JACQUES BOITEAU; m. (2) JEAN BAPTISTE BEDARD, January 11, 1733/34; b. September 07, 1695, Petit Auvergne, Charlesbourg, Quebec; d. January 21, 1741/42, Charlesbourg, Quebec.
5. vi. JEAN-BAPTISTE MARTEL, b. August 03, 1710, Quebec City, Quebec, Canada; d. June 03, 1770, L'Ardoise, Richmond Co..
vii. GENEVIEVE MARTEL, b. April 24, 1712, Charlesbourg, Quebec, Canada.
viii. MARIE MADELEINE MARTEL, b. July 17, 1714; d. April 28, 1759; m. JOSEPH RENAULT, November 11, 1737.
5. JEAN-BAPTISTE5 MARTEL (JEAN-FRANCOIS4, HONORE3, JEAN2, JEAN1) was born August 03, 1710 in Quebec City, Quebec, Canada, and died June 03, 1770 in L'Ardoise, Richmond Co.. He married MARIE-JOSEPHE POUJET Abt. 1733 in Port Toulouse (St. Peters) Nova Scotia, daughter of PIERRE POUJET and FRANCOISE MOYSE. She was born February 20, 1707/08 in Port Royal, Annapolis, Nova Scotia.
6. ii. JEAN-CHARLES MARTEL, b. Abt. 1734.
iii. JOSEPH MARTEL, b. Abt. 1735, St. Peters (Port Toulouse), Richmond Co, Nova Scotia, Canada; d. WFT Est. 1761-1827.
iv. JEAN-BAPTISTE MARTEL, b. Abt. 1738, Port Toulouse, Richmond, Nova Scotia; d. Aft. 1811, Petit-de-Grat, Richmond, Nova Scotia.
v. MADELEINE MARTEL, b. Abt. 1741, St. Peters (Port Toulouse), Richmond Co, Nova Scotia, Canada; d. Bet. 1776 - 1833.
vi. APOLLINIE MARTEL, b. Abt. 1743, Petit de Grat, Nova Scotia; d. Abt. 1839.
vii. HYPOLITE MARTEL, b. Abt. 1744.
6. JEAN-CHARLES6 MARTEL (JEAN-BAPTISTE5, JEAN-FRANCOIS4, HONORE3, JEAN2, JEAN1) was born Abt. 1734. He married (1) MARIE-MADELEINE BOIS Abt. 1754. She was born Abt. 1738, and died June 03, 1768 in L'Ardoise Harbour, Cape Breton, Nova Scotia. He married (2) ANNE LANDRY October 03, 1771 in L'Ardoise Harbour, Richmond Co., Nova Scotia, Canada, daughter of JOSEPH LANDRY and MARIE-MARGUERITE BREAU. She was born Abt. 1738 in St. Peters (Port Toulouse), Richmond Co, Nova Scotia, Canada.
i. CHARLES7 MARTEL, b. Abt. 1755, L' Ardoise, Richmond County, Nova Scotia; d. L' Ardoise, Richmond County, Nova Scotia.
ii. MATTHIAS MARTEL, b. Abt. 1758, Quebec, Canada; d. Abt. 1828, L' Ardoise, Richmond County, Nova Scotia.
iii. MARGUERITE URSULE MARTELL, b. June 03, 1763, L'Ardoise, Richmond Co., NS,Canada; d. May 10, 1847, L'Ardoise, Richmond Co., NS,Canada.
iv. JEAN MARTEL, b. April 23, 1765, Gabarus Bay, Cape Breton Co., NS,Canada; d. Abt. 1839.
7. v. AUGUSTINE PAUL MARTEL, b. February 18, 1761, L'Ardoise, Richmond Co., NS,Canada; d. May 08, 1849, L'Ardoise, Richmond Co., NS,Canada.
7. AUGUSTINE PAUL7 MARTEL (JEAN-CHARLES6, JEAN-BAPTISTE5, JEAN-FRANCOIS4, HONORE3, JEAN2, JEAN1) was born February 18, 1761 in L'Ardoise, Richmond Co., NS,Canada, and died May 08, 1849 in L'Ardoise, Richmond Co., NS,Canada. He married AGATHE PATE Abt. 1792 in L'Ardoise, Richmond Co., NS,Canada, daughter of JEAN PATE and FRANCOISE SAMSON. She was born October 15, 1767 in Quebec, Canada, and died May 08, 1849 in L' Ardoise, Richmond County, Nova Scotia.
8. i. JULIEN8 MARTEL-8, b. 1794, L' Ardoise, Richmond County, Nova Scotia; d. 1853, L' Ardoise, Richmond County, Nova Scotia.
ii. SUZANNE MARTEL, b. 1796, L' Ardoise, Richmond County, Nova Scotia.
iii. JUDITH MARTEL, b. 1793, L' Ardoise, Richmond County, Nova Scotia; d. 1863, L' Ardoise, Richmond County, Nova Scotia; m. CASIMIR PITRE; b. 1790, L' Ardoise, Richmond County, Nova Scotia; d. 1862, L' Ardoise, Richmond County, Nova Scotia.
iv. HONORE MARTEL, b. 1800, L' Ardoise, Richmond County, Nova Scotia; d. 1845, L' Ardoise, Richmond County, Nova Scotia.
9. v. ALEXIS MARTEL, b. L' Ardoise, Richmond County, Nova Scotia; d. L' Ardoise, Richmond County, Nova Scotia.
vi. MARIE MARTEL, b. 1806, L' Ardoise, Richmond County, Nova Scotia; d. 1871, L' Ardoise, Richmond County, Nova Scotia; m. MATTHIAS BRIAND; b. 1809, L' Ardoise, Richmond County, Nova Scotia.
8. JULIEN8 MARTEL (AUGUSTINE PAUL7, JEAN-CHARLES6, JEAN-BAPTISTE5, JEAN-FRANCOIS4, HONORE3, JEAN2, JEAN1) was born 1794 in L' Ardoise, Richmond County, Nova Scotia, and died 1853 in L' Ardoise, Richmond County, Nova Scotia. He married PELEGIE PITRE. She was born 1793 in L' Ardoise, Richmond County, Nova Scotia, and died 1872 in L' Ardoise, Richmond County, Nova Scotia.
i. AMELIA/EMELIA9 MARTEL, b. August 1818, L'Ardoise, Richmond County, Nova Scotia; d. 1921.
ii. PATIENT MARTEL, b. 1821, L' Ardoise, Richmond County, Nova Scotia; d. 1907, L' Ardoise, Richmond County, Nova Scotia.
iii. MARIE MARTEL, b. 1824, L' Ardoise, Richmond County, Nova Scotia; d. 1831, L' Ardoise, Richmond County, Nova Scotia.
10. iv. HONORE MARTEL, b. July 21, 1826, L' Ardoise, Richmond County, Nova Scotia.
v. SEVERIN MARTEL, b. 1828.
vi. SOPHIE MARTEL, b. 1831, L' Ardoise, Richmond County, Nova Scotia; d. 1930, L' Ardoise, Richmond County, Nova Scotia; m. PLACIDE RANCON; b. 1827, L' Ardoise, Richmond County, Nova Scotia.
vii. NATHALIE MARTEL, b. 1835, L' Ardoise, Richmond County, Nova Scotia; d. 1894, L' Ardoise, Richmond County, Nova Scotia.
viii. SEVERIN MARTEL, b. 1841, Petit de Grat, Richmond County, Nova Scotia; d. 1877, L' Ardoise, Richmond County, Nova Scotia.
ix. DOCITHE MARTEL, b. 1816, L' Ardoise, Richmond County, Nova Scotia; d. L' Ardoise, Richmond County, Nova Scotia.
9. ALEXIS8 MARTEL (AUGUSTINE PAUL7, JEAN-CHARLES6, JEAN-BAPTISTE5, JEAN-FRANCOIS4, HONORE3, JEAN2, JEAN1) was born in L' Ardoise, Richmond County, Nova Scotia, and died in L' Ardoise, Richmond County, Nova Scotia. He married JUSTINE MARTEL, daughter of JEAN MARTEL and URSULE SAMSON. She was born Abt. 1806 in L' Ardoise, Richmond County, Nova Scotia, and died 1896 in L' Ardoise, Richmond County, Nova Scotia.
i. MARINE9 MARTEL, b. 1837, L' Ardoise, Richmond County, Nova Scotia; d. 1883, L' Ardoise, Richmond County, Nova Scotia.
ii. MARIN MARTEL, b. 1838, L' Ardoise, Richmond County, Nova Scotia; d. 1915, L' Ardoise, Richmond County, Nova Scotia.
iii. ALEXIS MARTEL, b. 1841, L' Ardoise, Richmond County, Nova Scotia; d. 1924, L' Ardoise, Richmond County, Nova Scotia.
iv. VIRGINE MARTEL, b. 1842, L' Ardoise, Richmond County, Nova Scotia; d. 1902, L' Ardoise, Richmond County, Nova Scotia.
v. JEAN LOUISE MARTEL, b. 1845, L' Ardoise, Richmond County, Nova Scotia; d. 1864, L' Ardoise, Richmond County, Nova Scotia.
11. vi. GEORGE BONAVENTURE MARTEL, b. 1852, L' Ardoise, Richmond County, Nova Scotia; d. Georgetown, P.E. I. Canada.
10. HONORE9 MARTEL (JULIEN8, AUGUSTINE PAUL7, JEAN-CHARLES6, JEAN-BAPTISTE5, JEAN-FRANCOIS4, HONORE3, JEAN2, JEAN1) was born July 21, 1826 in L' Ardoise, Richmond County, Nova Scotia. He married APPOLINE MAILLET Bef. 1859. She was born 1835 in L' Ardoise, Richmond County, Nova Scotia, and died 1881 in L' Ardoise, Richmond County, Nova Scotia.
i. DANIEL-VITALIEN10 MARTEL, b. 1859, L' Ardoise, Richmond County, Nova Scotia; d. 1859, L' Ardoise, Richmond County, Nova Scotia.
ii. TIMOTHEE LAURENT MARTEL, b. 1862, L' Ardoise, Richmond County, Nova Scotia.
iii. MARIE MARTEL, b. 1864, L' Ardoise, Richmond County, Nova Scotia; d. 1908, L' Ardoise, Richmond County, Nova Scotia; m. SIMON-LAURENT LANDRY; b. 1853, L' Ardoise, Richmond County, Nova Scotia; d. 1930, L' Ardoise, Richmond County, Nova Scotia.
iv. DANIEL MARTEL, b. 1866, L' Ardoise, Richmond County, Nova Scotia; d. 1866, L' Ardoise, Richmond County, Nova Scotia.
12. v. MICHEL-REMI MARTELL, b. 1867, Georgetown, P.E. I. Canada; d. 1964, Georgetown, P.E. I. Canada; m. PRICILLA DOUCETTE; b. 1878, Georgetown, P.E. I. Canada; d. 1966, Georgetown, P.E. I. Canada.
13. vi. WILLIAM MARTELL, b. Dec 17, 1869, Georgetown, P.E. I. Canada; m. ELIZABETH BOURQUE; b. Georgetown, P.E. I. Canada.
vii. ALEXANDRE MARTELL, b. 1872, L' Ardoise, Richmond County, Nova Scotia.
14. viii. DANIEL MARTELL, b. Sept. 21, 1875, Georgetown, P.E. I. Canada, d. Jan. 10, 1959 in Georgetown, PEI; m. SOPHIE BOUCHARD; b. 1879; d. Nov. 2, 1919.
11. GEORGE BONAVENTURE MARTEL (ALEXIS8 , AUGUSTINE PAUL7, JEAN-CHARLES6, JEAN-BAPTISTE5, JEAN-FRANCOIS4, HONORE3, JEAN2, JEAN1) was born in 1852 in L' Ardoise, Richmond County, Nova Scotia; d. Georgetown, P.E. I. Canada. He married Melinda Dugas, b. 1854.
ii.GEORGES AIMI MARTEL, b. 1883, d. ?
12. MICHEL-REMI MARTELL , (HONORE9 , JULIEN8, AUGUSTINE PAUL7, JEAN-CHARLES6, JEAN-BAPTISTE5, JEAN-FRANCOIS4, HONORE3, JEAN2, JEAN1) b. 1867, Georgetown, P.E. I. Canada; d. 1964, Georgetown, P.E. I. Canada; m. PRICILLA DOUCETTE; b. 1878, Georgetown, P.E. I. Canada; d. 1966, Georgetown, P.E. I. Canada.
13. WILLIAM MARTELL (HONORE9 , JULIEN8, AUGUSTINE PAUL7, JEAN-CHARLES6, JEAN-BAPTISTE5, JEAN-FRANCOIS4, HONORE3, JEAN2, JEAN1) was born Dec 17, 1869, Georgetown, P.E. I. Canada; m. ELIZABETH BOURQUE; b. Georgetown, P.E. I. Canada.
i.WILLIAM MARTELL, b. July 31, 1896, d. Mar 3, 1969; m. JOSEPHINE GALLANT, b. Jan 27, 1912, d. May 1, 1973.
iii.PETER MARTELL, b. 1900, d.?; m. BETTY ?
14. DANIEL MARTELL, (HONORE9 , JULIEN8, AUGUSTINE PAUL7, JEAN-CHARLES6, JEAN-BAPTISTE5, JEAN-FRANCOIS4, HONORE3, JEAN2, JEAN1) was born Sept 21, 1875 in Georgetown, PEI. He married SOPHIE BOUCHARD before 1898. She was born in 1879; and died Nov 2, 1919.
i.PAULINE-11, b. 1898, Georgetown, P.E.I; d. 1917, Georgetown, P.E.I.
v.PRISCILLA, b. 1911; d. ?


text:
Take a first look at Disney's 'Raya and the Last Dragon'
By Silas Lesnick | Aug 27, 2020
Walt Disney Animation Studios is set to follow last year's record breaking Frozen 2 with an all new animated adventure, Raya and the Last Dragon. Today, the studio has debuted a first still from the March 2021 release, also announcing that Star Wars: The Last Jedi star Kelly Marie Tran will lend her voice to the title character Raya. As previously announced, Awkwafina will voice the other title character, a dragon named Sisu.
RAYA AND THE LAST DRAGON – As an evil force threatens the kingdom of Kumandra, it is up to warrior Raya, and her trusty steed Tuk Tuk, to leave their Heart Lands home and track down the last dragon to help stop the villainous Druun. © 2020 Disney. All Rights Reserved.
Long ago, in the fantasy world of Kumandra, humans and dragons lived together in harmony. But when sinister monsters known as the Druun threatened the land, the dragons sacrificed themselves to save humanity. Now, 500 years later, those same monsters have returned and it's up to a lone warrior, Raya, to track down the last dragon in order to finally stop the Druun for good. However, along her journey, she'll learn that it'll take more than dragon magic to save the world—it's going to take trust as well.
From directors Don Hall and Carlos López Estrada, co-directors Paul Briggs and John Ripa, producers Osnat Shurer and Peter Del Vecho, Raya and the Last Dragon opens in theaters March 12, 2021.


Out of the 100, only 5 make the grade. When we say about 5% achieved success, we have to define success. And here's the definition: Success is the progressive realization of a worthy ideal.
Conformity – people acting like everyone else, without knowing why, without knowing where they're going.
A success is anyone who is doing deliberately a pre-determined job, because that's what he decided to do – deliberately.
Selling is the world's highest paid profession – if we're good at it, and if we know where we're going.
Now it stands to reason that a person who is thinking about a concrete and worthwhile goal is going to reach it, because, that's what he thinking about; and, we become what we think about. Conversely, the man who has no goal, who doesn't know where he's going and whose thoughts of confusion and anxiety and fear and worry, becomes what he thinks about. His life becomes one of frustration, fear, anxiety and worry; and if he thinks about nothing, he becomes nothing.
Because the mind, like the land, doesn't care what you plant, but it doesn't care what you plant.
You see the human mind is the last, great, unexplored continent on the earth. It contains riches beyond our wildest dreams.
Familiarity breeds contempt. It can do any kind of job we assign to it but generally speaking, we use it for little jobs instead of big, important ones.
We are operating on about 10% of our ability.
You want to be an outstanding salesman, a better worker at your particular job, you want to go places in your company, in your community? All you've got to do is plant that seed in your mind; care for it, work steadily toward your goal – and it will become a reality. It not only will…There's no way that it cannot.
Every one of us is the sum total of his own thoughts. He is where he is, because that is exactly where he really wants to be, whether he'll admit that, or not.
Each of must live off the fruit of his thoughts and the future, because what you think today and tomorrow, next month and next year, will mold your life and determine your future. You're guided by your mind.
Are you going to keep both hands firmly on the wheel and control and direct its power to a specific, worthwhile purpose? It's up to you: You're in the driver's seat.
We must control our thinking. The same rule that can lead a man to a life of success, wealth, happiness and all the things he's ever dreamed of for himself and his family – that very same law can lead him into the gutter. It's all in how he uses it: for good, or for bad.
People are basically good, and that we came from some place and we're going someplace – so we should make our time here an exciting adventure. The architect of the universe didn't build a stairway leading nowhere.
Secondly, it's cutting away all the fetters from the mind and permitting it to soar, as it was divinely designed to do. It's the realization that your limitations are self-imposed and that the opportunities for you today are enormous beyond belief. It's rising above narrow-minded pettiness and prejudice.
Thirdly, to use all your courage to force yourself to think positively on your own problem; to set a definite, and clearly-defined goal for yourself; to let your marvellous mind think about your goal from all possible angles; to let your imagination speculate freely upon many different, possible solutions; to refuse to believe there are any circumstances sufficiently strong to defeat you in the accomplishment of your purpose. To act promptly and decisively when your course is clear, and to keep constantly aware of the fact that you are, at this moment, standing in the middle of your own acre of diamonds.
It's easier for a human being to think negatively than positively – that's why only 5% is successful.
Positive outlook, give of yourself more than you've ever done before.
Ask and it shall be given you, Seek and ye shall be find. Knock, and it shall be opened unto you. For everyone that asketh, receiveth; And he that seeketh, findeth; And to him that knocketh, it shall be opened.
Persistence is simply another word for faith. If you didn't have faith, you would never persist.
The only way to earn money is by providing people with services or products which are needed and useful.
If he wants more, he must be of more service to those from whom he receives and returns; if he wants less, he has only to reduce this service. This is the price you must pay for what you want.
An outstanding medical doctor recently pointed out six steps that will help you realize success: 1) Set yourself a definite goal. 2) Quit running yourself down. 3) Stop thinking of all the reasons why you cannot be successful, and instead think of all the reasons why you can. 4) Trace your attitudes back through your childhood and try to discover where you first got the idea you couldn't be successful. 5) Change the image you have of yourself by writing out a description of the person you would like to be. 6) Act the part of the successful person you have decided to become.


Bamboo body pillow goes to great lengths to support you while you sleep. Whether you're a side, back or stomach sleeper, the bamboo pillow conforms to your every curve for custom comfort from head to toe. Hypoallergenic, antimicrobial bamboo infused with aloe vera is softer than cotton and wicks away moisture to help keep you cool and dry. Removable zip cover is machine washable in cold water; tumble dry low heat. Spot clean pillow. Hypoallergenic pillow measures 53" long x 16" wide. Shredded polyurethane foam cushion; 40% bamboo/60% polyester cover.
Hypoallergenic, antimicrobial bamboo infused with aloe vera.
53" long x 16" wide.


Identify and eliminate root-cause problems to improve quality.
Organize management structure for better leadership and results.
Improve customer satisfaction and reduce complaints by identifying and implementing better and faster service.
Identify and remove roadblocks to efficient order processing, manufacturing, distribution and billing.
Communications with internal and external audiences for plan development, implementation, monitoring and feedback.
(2) React to Unanticipated Events and Opportunities.
For either choice, timely and accurate research, analysis and planning deliver guidance for effective action. Whether strategic or tactical decisions are required, we bring a broad range of experience, knowledge and resources to your conference table.
Whether advising, researching, avoiding (preferred) or supporting litigation (we are not attorneys), plan building or project managing, ComAd delivers tangible results, on your schedule and within your budget.


StarTech 24-port 0.5U Cat6a Patch Panel - Network Patch Panels - Memory Express Inc.
The compact patch panel condenses 24 network ports into a 0.5U panel that's ideal for installations inside 19" server racks. It's constructed out of heavy-gauge steel and includes an easy-access cover that protects the terminated cables and helps to keep them organized at the back of the rack. The back of the panel also features a C-shaped cable-management system to provide strain relief.
The 24-port patch panel is color coded for both T568A and T568B universal wiring and offers straight ports with 110-type and Krone termination. The panel is shielded to protect against electromagnetic interference (EMI), when used with shielded cables. The panel will also support unshielded cables, but with no EMI protection.
The Ethernet patch panel is fully rated to support 10 Gigabit networks and is compatible with 26-23 AWG solid or stranded cables. It is also backward compatible with Cat6 and Cat5e cables.
The panel offers a quick and easy way to identify your cable runs. It has port numbers clearly marked on the front of each RJ45 port, and has a writeable/erasable marking surface for efficient system management.
C6APANLHU24 meets or exceeds Cat6a specifications and is backed by a StarTech.com 2-year warranty.
Note: IDC Contact - Phosphor Bronze with Tin Plating.


Why was Aisha Tyler so cranky at the Critics' Choice Awards?
Aisha Tyler was at the helm of the Critics' Choice Awards Thursday night, to the delight of the audience. But as the night went on, she seemed to tell everyone how she really felt.
Aisha Tyler may have seemed like an unlikely host for the Critics' Choice Awards, but her comedic background made her the perfect choice. She worked well with the crowd and joked about many of the movies or actors without ever actually bad-mouthing any of them.
Tyler seems to keep the crowd upbeat all night, appearing every now and then, as hosts do. But each time she appeared, she seemed to slam the critics one more time.
Tyler made her critics jokes not in a playful way, but as if she really had something against the people who were putting on the show.
Winfrey didn't exactly seem to appreciate it, but seemed good-natured. Throughout the night, Tyler was playful and joking about many of the actors and films, but always going back to the critics.


text:
Leptomiza parableta is een vlinder uit de familie van de spanners (Geometridae). De wetenschappelijke naam van de soort is voor het eerst geldig gepubliceerd in 1926 door Prout.

parableta

redpajama_set_name: RedPajamaWikipedia


text:
Q: Which preposition should I use: BY or WITH I'm writing a text and I'm not sure which preposition I should use in the following sentence:

I should get married by 30

or

I should get married with 30

A:
I should get married by 30 -is correct.

You use 'by' when showing the limit of age there.

I should get married with 30 - is incorrect.

Additionally, when you want to say someone whom are you married to...you use 'to'.

I'm married to a doctor.

redpajama_set_name: RedPajamaStackExchange


Editor's Note: This is part 3 of a multi-part series. Read part 1 and part 2.
How does the value of the humanities find application in the classroom? How can outcomes be assessed? In the emoji and meme era, our student's abilities to communicate serious content have weakened. Critical thinking today? Anemic. Deep understanding of history and culture rarely appear among students. We could lament and complain of these faults until midnight, but how can we help students? In my three-semester sequence of History of Ideas courses, students learn the great ideas that built our civilization from fifty influential authors in history, from Gilgamesh to Camus. This vigorous reading program instills cultural depth. Equally important, students learn to communicate in these writing intensive classes. Students orally present each research paper while the others critique the papers with five separate sets of criteria. When students finish the courses, they communicate better, combining classical learning with contemporary challenges. The reading content and the writing exercise many humanities disciplines. Students discuss the weighty ideas they discover and assist each other to learn new perspectives. Lectures are rare in these discussion classes where articulation matters. Students should emerge able to clearly communicate complex ideas with sound arguments and application. We assess outcomes yearly.
What great commission impact do the humanities provide? The gospel can only be conveyed through language, either written or spoken. In addition to acts of love, service, and concern, the gospel proclaims a set of propositional truths. There's a reason John called Jesus the Logos, the Word. Observed acts of service convey the gospel, but language translates the exact meaning of these acts. The humanities disciplines prove essential in the propagation of the gospel cross-culturally or at home, enabling us to communicate clearly in any culture. Cross-cultural missionaries undergo extensive new language and cultural acquisition and must hone these skills daily. They must study the history, music, culture, stories, and literature of their target group to understand them. The study of missiology heavily draws on the humanities as much as the soft sciences of sociology and anthropology.
We often hear about "cultural engagement" in Christian circles. Cultural engagement without cultural understanding is like marital engagement to an unknown fiancé. No disciplines embody and embrace culture like the humanities. They incubate and nurture culture. Yet, in cultural retreat for over a century, Christians have largely ignored them. Rudely awakened to the haunting reality that Christians no longer drive any key part of our culture, they scramble to catch up. How? To engage anything, you fully commit to move it along, such as a relationship headed toward marriage or a clutch grabbing the engine to move a vehicle. Contact must occur; a grab, a capture happens. To engage culture, Christians must tango with it. So, you really want to engage culture huh? Which part of it you fully commit to move?
Cultural engagement without cultural understanding is like marital engagement to an unknown fiancé.
The humanities offer contact points for engagement. The door stands wide-open because the secular universities have zombified the humanities unto apocalypse. Christians must actively reclaim the humanities and express the Christian worldview through doing them with excellence. Reclaiming our lost humanities is mission, a massive global platform to reach the lost. In the past thirty years, Christian philosophers have started this, going to great lengths to interact with our culture through philosophy, setting forth profound works that proclaim Christianity. Other humanities disciplines equally need a fresh infusion of Christian scholars. Secularists fumble the ball too. Will Christians recover it and score? Young students need to know that scholarship in the humanities serves God and promotes the gospel. The university is a lost mission field with few Christian scholars in the classroom, few validating the Christian worldview. If more would return to humanities scholarship as a service to God, they could prevent many students from falling away in the precarious years where their faith falls prey to ambush on university campuses. An intellectual trap ensnares millions of unwary victims every fall. Erosion and barrenness sets in where Christians relinquish influence. A secular kudzu chokes our children, our schools—our souls. There's an eternal price (hell) to pay. Christians must realize that the university, once an asset to Christianity, is now extremely hostile, actively seeking to assassinate our youth's faith and civilization as we know it. We surrendered the university, so we have only ourselves to blame for the secular annexation.
Looking at other world challenges that will soon come, we must brace ourselves for the automation revolution. By most assessments our society and economy will soon undergo a rapid technological revolution of automation, driven by socio-economic forces of great momentum. This robotic and automation revolution will transform the global economy quickly, much like the internet and smartphone, which is barely ten years old. Robust benefits, profits, and rapid adoption will fuel automation. While we can see it coming, we can't quite predict its full consequences. Some (Zuckerberg) call for guaranteed basic incomes to give people money to replace income lost to automation. What is my economic value if I can provide no value to others due to machines? Others (Gates) call for robots to pay taxes.
The consequences of automation will affect the humanities exactly where it overlaps faith, work, and economics. My assessment may prove wrong, but those who possess the finer skills of the humanities need not fear this technological revolution initially. The soft skills people learn in the humanities remain impossible for us to reproduce or recreate in computer simulations. Just think of how easily Siri gets confused with language. We are a long way off from the average computer passing the famous Turin test. Perhaps AI will rival humans in the future and raise unimaginable existential questions. Until then, humans will excel in creativity and imagination. Our global thinking and ability to ask cosmic questions will push us to understand. Human compassion, empathy, and judgment will outstrip automation. The highest traits we value, including mercy and grace, will give us social skills that AI will not be able to possess.
Dr. Ivan Spencer is Professor of History and Philosophy at Southeastern Seminary. He educates Christians to understand the world of ideas in which they live, so that they can engage, challenge, and transform culture with the realities and truths of an informed and thoughtful Christianity. He is the author of Tweetable Nietzsche: His Essential Ideas Revealed and Explained.


igloo ? also see dream dictionary: buildings sometimes we perceive that others are cold hearted or emotional distant, but like the igloo, such people are warm inside. this can also apply to the dreamer personally in an effort to show them how they are perceived by others. additional dream interpretation… the igloo, with regard to femininity, can often represent frigidity. conversely, it can also be symbolic of relaxation ? either needed or acquired ? to engage sexually.