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1. Take a hayride through the woods to pick out that perfect pumpkin at the Stonycreek Farm Pumpkin Festival Thursday, October 1 - Saturday, October 31.
2. Get spooked by the Headless Horseman at Conner Prairie, then stick around for Ghost stories by the fire- Friday, October 23 - Saturday, October 24.
3. Have an Adventure in Archaeology at Strawtown Koteewi Park - Friday, October 23.
4. Come dressed up in costume and ready to party at PumpkinFest in Carmel's West Park Saturday, October 24.
5. Take the train and enjoy a pizza dinner during Pizza Train Saturday, October 24.
6. Get an early start on holiday shopping at one of our local Indiana shopping hot spots like Clay Terrace, Hamilton Town Center, Carmel Arts & Design District or Downtown Noblesville.
7. In need of a long weekend away? Enjoy the special that Springhill Suites in Carmel is offering - buy 2 nights and get 1 free!


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Voices from the Frontlines | Planet SOS | Al Jazeera English
Presenting Al Jazeera's environmental magazine programme from the studio in Qatar. I was instrumental in getting the series commissioned. The growing urgency of the climate and ecological crisis had made me determined to do all I could to get more environmental coverage onto the channel.
I'm grateful it came off and to have had the opportunity to highlight issues and stories that don't necessarily fit into earthrise's documentary remit.
Planet SOS launched in September 2019, as people across the world took to the streets calling for action against climate change.
In this opening programme, we speak to some of the protesters taking part including Vanessa Nakate, a Ugandan activist who has since been interviewed by Angelina Jolie for the cover of Time magazine. We follow her from her home on the outskirts of Kampala as she prepares to travel to New York for the Climate Summit called by UN Secretary-General Antonio Guterres, who we also interview for the show.
From the studio, I speak to environmental activist Severn Cullis-Suzuki who addressed the UN in 1992 when she was aged just 12. We talk about the comparisons with Greta Thunberg, what has changed, and whether protests by today's youth will make a difference.

redpajama_set_name: RedPajamaCommonCrawl


A newly published book by forester and Bushfire Front Chairman Roger Underwood is the first to undertake a thorough analysis of the event. What happened and why, what were the impacts and costs? What are the lessons for the future?
A highlight of the book is nearly 100 first-hand stories from people who were caught up in the storm and the bushfires. Many of the stories tell of fearsome experiences near Bridgetown, Manjimup, Nannup and Pemberton. As well as the terror and heartbreak, there were many amazing rescues and near-death experiences.
Roger Underwood was caught up in the event, as he was the Fire Controller at Manjimup during the crisis. But he still finds the stories in the book inspiring. "They tell of the courage, resilience, bushmanship, sheer guts and even the grim humour of rural West Australians who suddenly found themselves facing a chaos of storm and fire". He particularly valued the stories of the incredible bravery of the nurses, ambos, and vollies, but said that he had a special place in his memory for the forestry officers and crews who carried the brunt of the firefighting under near-impossible conditions.
Mr Underwood said that it is essential that events like Cyclone Alby are remembered and recorded and that personal memories are not forgotten. "Even more important" he said "is not to forget the lessons learned so that we can do better if another Cyclone Alby hits".


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Home / News & Reviews / News Wire / Rare New York Central electric locomotives still threatened
Rare New York Central electric locomotives still threatened
By Dan Cupper | November 22, 2022
NYC RS-3 and U25B diesels, 4 passenger cars will be scrapped
Badly vandalized but historically irreplaceable, the two New York Central electric locomotives it near a former power plant site south of Albany in April 2021. An effort to save the two electrics is running out of time; two diesels and four passenger cars are set to be scrapped. Jose Alves
GLENMONT, N.Y. — Red tape, a gas pipeline utility, and a lawsuit have combined to delay and further threaten the rescue of two historic New York Central electric locomotives stranded for three decades along the Hudson River south of Albany.
The Danbury Railway Museum of Danbury, Conn., has been working for nearly a year to remove the units from a power-plant site where they are standing in the way of plans to build a factory to manufacture offshore wind-turbine towers [see "Museum works to save two rare New York Central electric locomotives," Trains News Wire, March 18, 2022]. That $350 million project has faced delays because of a lawsuit by nearby homeowners.
According to project director Stan Madyda, the museum this week will investigate the feasibility and cost of placing panel track to clear the area for a roadway. Otherwise, the remaining option is to hire four sidewinder lifting devices at a cost at $150,000 to $225,000 to move the engines just 200 yards to a temporary staging area, before they can be trucked 120 miles to Danbury.
"We're running out of time," Madyda said. "Every time we think we have a solution on our end, we get blockaded by something else. The power plant agreed to allow access through the property with a truck, pending an engineering study. [It] came back that there is a high-pressure [natural] gas line buried 30 feet under the property that is not owned by the power plant, but there's an objection to anything going over the gas line with plating. Our trucking firm said it should be fine, but [the gas line owner] wanted a [costly temporary] bridge.
"It's the perfect storm of things working against us."
Once restored but now heavily vandalized, the locomotives — NYC Class S-1 (2-D-2 configuration) unit No. 100, built in 1904, and Class T-3a (B-B+B-B configuration) unit No. 278, built in 1926 — weigh 113 tons and 146 tons respectively. Dumping of fly ash aggravated the swampy-soil conditions on the area formerly called Beacon Island, which is no longer a separate landmass. The railroad bridge that once provided access has washed out, leaving the engines stranded and making trucking the only alternative for removal.
"We're going to keep trying until the very end," Madyda said. "We're up against the deadline right now."
Legal action caused delay
The site was reopened last week after an eight-month delay caused by a homeowners' lawsuit filed in March. It stopped all work to investigate the public-health implications of disturbing the 2 million tons of toxic fly ash dumped by the generating station of PSEG Power New York LLC (formerly Niagara Mohawk). Built as a coal-burning utility, the plant later converted to natural gas.
The S-1 electric the museum is trying to save is the prototype for the model that launched electrification in the New York City area. Danbury Railway Museum collection
The museum, Madyda said, got a "letter of exception" from the town, which allows the group to bring in tracked vehicles. During the legal-action pause, only rubber-tired vehicles were permitted.
"There's a staging area on the property where we can put the locomotives for 60 days or whatever," he said, "then they can be loaded by crane onto our trucking-company trailers and brought out that way. There's a new access road with a 6% grade, but our trucking company says it should be OK."
If the sidewinder option is the only solution, he added, the company owning them said the move would likely damage the locomotives and the firm will require a liability waiver.
These NYC units are among the last of their kind. Both were built by a consortium of American Locomotive Co. of Schenectady, N.Y., and General Electric Co. No. 100, built as No. 6000, served as the prototype of a 47-unit fleet that made possible NYC's 600-volt DC third-rail electrification program, including the opening of the 1913 Grand Central Terminal complex. No. 278 is one of 36 locomotives, and the only survivor, in a second generation of units on NYC electrified commuter and freight lines around New York City.
Diesels to be scrapped
Madyda said scrapping is set to begin next week on two diesel units, NYC Alco RS-3 No. 8254, later Amtrak 126, and NYC General Electric U25B No. 2510, along with four passenger cars also on site. Formel Auto Salvage of Great Barrington, Mass., he said, agreed to dismantle the six pieces in exchange for retaining the scrap metal, meaning no cost to the museum. "It was the only option that made it work for them," Madyda said.
Construction of the wind-turbine factory is being undertaken by the Port of Albany, with a U.S.-Canadian-Danish consortium, Marmen-Welcon LLC; a Belgian steel construction company, Smulders; and a Norwegian energy company, Equinor ASA. The wind turbines will be placed off Long Island.
T-3 locomotive No. 278 at Harmon, N.Y., in 1953. Danbury Railway Museum colleciton
In a statement released by Museum President Jose Alves and Madyda, the group further explained its plight: "Where the historic locos currently sit is where the new access road from River Road [State Route 144] onto Beacon Island is set to end. The consulting firm needs this area cleared of all rolling stock and rail infrastructure, so the new access road can be built and preparation to the ground started for construction of one of the buildings. Of the 80 acres of land that will be developed, our locomotives are right in the spot where the earliest stages of construction need to occur.
"At this time the cost of this project has ballooned to a point where existing donations simply can't cover it, especially if the consulting firm will also be charging us unknown storage fees. Funding this project through use of the museum surplus puts the future of our organization in great financial uncertainty. Our board's No. 1 responsibility is to keep our museum financially viable, and after we and many other organizations hemorrhaged money during the pandemic, this task has not been easy.
"While we didn't create the situation where the locomotives ended up where they are now, a small group of strong-willed volunteers, and a lot of money and resources has already been expended trying to undo mistakes of the past. We want to see these locomotives saved, if not by us, then so be it. Donations are still being accepted on our website."
For more on the topic, see this December 2021 Spotlight News article by John McIntyre.
9 thoughts on "Rare New York Central electric locomotives still threatened"
Michael Lampman says:
If 30 feet of soil isn't adequate cover for a pipeline made of eggshells, too bad for them. Tell them to untwist their panties and plate over it and get it done. A lit match will take care of any gas leak. [/sarcasm]
Talk with the adults (and not the lawyers) and see what can get done.
John Rice says:
Send them to IRM, they say no engine will be turned away.
Mark Shapp says:
Mr. Rice: Didn't you read the article? Obstacles have been put in the way that are preventing the engines from being sent ANYWHERE.
Yes, I read the article. I was being sarcastic.
Gerald McFarlane says:
It's funny, this is the exact time during a potential economic meltdown that businesses should be looking for ways of helping their local communities through public donations…such as the current power plant owner, PSEG Power New York LLC, just paying the cost of getting the equipment offsite as a goodwill gesture to quiet the NIMBY's…it works if you have smart people in PR and the cost isn't all that much for a power company.
Richard Kessler says:
What about Chuck Schumer? He seems to have his nose in everything these days.;
Not being directly involved it is hard to know the truth of the situation, but I get the impression that there is no one (outside of the Danbury Museum perhaps) that wants to bring solutions to the table. Without a project champion on the other side of the table, it is damn near impossible to move forward through the ongoing chorus of "this can't be done" and "you can't do that".
Thomas Engel says:
I'v already given $250 last spring. All gone, apparently.
Maynard Stowe says:
Sad as when Dick Jensen's pacific was scrapped. Hope it all works out.


Nearing the 500th anniversary of the Protestant Reformation, we're taking a few weeks to consider the 5 key slogans framing that amazing move of God reviving His church – the five "solas".
Last we looked at the slogan – Sola Scriptura. By it, the Reformers were calling the Church back to Scripture Alone as its final authority in faith and practice.
It was not a call to abandon common sense, logic, history, science or the Church fathers, instead to say: where the Bible speaks, it speaks with absolute and final authority for the Church. No council, no organization, no individual has the right to override, ignore, twist, add to or take away from – Scripture. As God-breathed it stands in a place of singular supreme authority, especially over the conscience.
When this fundamental concept the FORMAL concept is surrendered, then fallen men will inevitably seize that authority for themselves – and someone or something else takes the rightful place of God Himself.
So it is, the second watchword of the Reformation grows directly out of this first one.
Hence we encounter the very next phrase: Sola Gratia – by Grace Alone.
Here, the Reformers were addressing the fact that over time, the Church had begun to redefine Scripture words and terms without reference to how the Bible uses them. And in so doing created a doctrine of salvation that directly contradicts the Bible's own teaching.
If the Church, or an individual, takes the right to themselves to re-define the words the Bible uses, the Bible can be made to say anything you want to make it say. And nowhere was this more true than when it came to the concept of grace.
Sometimes, when Evangelicals critique the Romanist teaching on salvation, we oversimplify it and just say Rome teaches salvation by works apart from grace. This both inaccurate and unfair. By the time Luther and the others were calling for reform, the Church's teaching on salvation HAD become pretty distorted, but it was so because of this issue of definitions. This will play a major role in the 3rd Sola when we look at Sola Fide as well.
1. One must co-operate in order to OBTAIN the grace of justification.
2. Christ's satisfaction is not sufficient for our sin but guilt must still be met by temporal punishment either in this world or in Purgatory before the kingdom of Heaven can be opened to him.
3. And in both cases, the Roman Church said if one does not agree with them on this, they are not just wrong – but are "anathema" – under the judgment of God – cursed by Him and thus ex-communicated from the Church.
I took that directly from the Vatican Website, neither an ancient nor outside source.
In Luther's day, what grace was and how it worked had been so redefined, that it bore very little resemblance to grace the way the Bible speaks of it.
The bottom line issue is one of worthiness when it comes to salvation.
The Reformers insisted that the Bible teaches that an individual's worthiness could play no role in salvation, or salvation ceases to be a free gift. But the Roman view instead, if only in part, said and STILL says a person can MERIT for themselves and others – all the graces needed to attain eternal life. The worthiness of the individual to obtain eternal life is brought about by cooperating with the grace given at conversion.
Sola Gratia: [The] Latin phrase meaning "grace alone" that expresses the Reformation* doctrine that salvation* is all of divine grace at every stage, from election* to glorification.* Inherent in this phrase is the truth that no merit* of man either before, at, or after his regeneration* by the Holy Spirit* contributes to his salvation. The only merit by which a sinner is saved is Christ's merit. Thus, sola gratia is usually employed in conjunction with solo Christo, "in or by Christ alone," to denote that it is solely in Christ and by virtue of His atoning work that men receive the saving grace of God.
In other words, this comes down to the very Gospel we preach. A Gospel which announces the free gift of saving grace to all who will believe – versus a NON-Gospel, of entering into a man-made system of rites, rituals and regulations which help you become worthy. And just how worthy you have to be no one can tell you, because Purgatory is yet before you.
So why does this cooperative view of making ourselves worthy fail so miserably? I want to advance 7 Biblical arguments.
Because of how the Bible speaks of our lost condition. Our condition before we are saved is so dire, that God actually has to overcome our resistance to Him in order to save us – Not only are we not worthy, we are actually in opposition to His grace, until by grace, He overcomes it in us. Ephesians 2:1–22 "And you were dead in the trespasses and sin in which you once walked, following the course of this world, following the prince of the power of the air, the spirit that is now at work in the sons of disobedience— among whom we all once lived in the passions of our flesh, carrying out the desires of the body and the mind, and were by nature children of wrath, like the rest of mankind. 11 Therefore remember that at one time you Gentiles in the flesh, called "the uncircumcision" by what is called the circumcision, which is made in the flesh by hands— remember that you were at that time separated from Christ, alienated from the commonwealth of Israel and strangers to the covenants of promise, having no hope and without God in the world.
4 But God, being rich in mercy, because of the great love with which he loved us, even when we were dead in our trespasses, made us alive together with Christ—by grace you have been saved— and raised us up with him and seated us with him in the heavenly places in Christ Jesus, so that in the coming ages he might show the immeasurable riches of his grace in kindness toward us in Christ Jesus. For by grace you have been saved through faith. And this is not your own doing; it is the gift of God, not a result of works, so that no one may boast. For we are his workmanship, created in Christ Jesus for good works, which God prepared beforehand, that we should walk in them.
Because it slanders Christ and says His blood is not sufficient to cleanse all our sins. Hebrews 10:1–14 For since the law has but a shadow of the good things to come instead of the true form of these realities, it can never, by the same sacrifices that are continually offered every year, make perfect those who draw near. Otherwise, would they not have ceased to be offered, since the worshipers, having once been cleansed, would no longer have any consciousness of sins? But in these sacrifices there is a reminder of sins every year. For it is impossible for the blood of bulls and goats to take away sins. Consequently, when Christ came into the world, he said, "Sacrifices and offerings you have not desired, but a body have you prepared for me; in burnt offerings and sin offerings you have taken no pleasure. Then I said, 'Behold, I have come to do your will, O God, as it is written of me in the scroll of the book.' " When he said above, "You have neither desired nor taken pleasure in sacrifices and offerings and burnt offerings and sin offerings" (these are offered according to the law), then he added, "Behold, I have come to do your will." He does away with the first in order to establish the second. And by that will we have been sanctified through the offering of the body of Jesus Christ once for all. And every priest stands daily at his service, offering repeatedly the same sacrifices, which can never take away sins. But when Christ had offered for all time a single sacrifice for sins, he sat down at the right hand of God, waiting from that time until his enemies should be made a footstool for his feet. For by a single offering he has perfected for all time those who are being sanctified.
Because no one CAN make themselves worthy, therefore, no one is REQUIRED to make themselves worthy. We must receive salvation as it is, a free gift, with no attention to our own worthiness whatsoever. Christ does not save worthy people, He saves sinners, condemned and unclean and in no wise capable of making themselves worthy of His gift.
So the problem at the time of the Reformation was that people were brought into a slavish system of humanly invented rites, ceremonies, rules, regulations and requirements in order to finally help make themselves worthy of eternal justification. Which would still be followed by indeterminate periods of time in the afterlife in Purgatory, still paying for their own sins until the debt was fully discharged.
Today, the landscape is far different, but the need to be called back to Sola Gratia all the more necessary.
Not because people are so worried about making themselves fully worthy of final salvation – but because in our culture at least – people already judge themselves worthy – and so do not NEED to depend upon God's grace in Christ alone.
After all – we're all pretty good! We DESERVE nothing but the best.
God actually owes it to us in some respect. We DO merit it.
In this generation of self-esteem and the celebration of human accomplishment, the idea that we are very worthy beings is drilled into us from almost every corner and that from birth.
Believer – Once in Christ, and we fail and commit sin, our tendency still is to try in some way to redeem ourselves in God's eyes afterword.
It is a fool's errand. We cannot do it. If we've sinned against other people, we need to make it right with them as best we can. But in terms of having sinned against God – we must cast ourselves back on grace and grace alone, and rest there.
Of course we repent and turn away from our sin anew – but we cannot somehow make up for sin in God's eyes. Here, by faith, we look once again to the cross, and trust in His unmerited and free grace. We cannot merit forgiveness after we've come to Christ, any more than we could before we first came. We stand in this grace as Rom. 5 puts it – always.
Unbeliever – Beloved, there is only one way you can be saved from your sin – and that is to come to Christ guilty, condemned, unclean and in need of the free gift of His grace in Jesus Christ.
If you will not condemn yourself so as to receive His forgiveness and imputed righteousness today, then He will condemn you on the last day, and to an eternal condemnation from which there is no escape or hope of deliverance.
Come today to the Christ who justifies the wicked. He alone is sufficient for your sin.
If the Spirit is convicting you of your sin today, so that you long to be forgiven and reconciled to God – come and by His grace be justified by placing your entire trust in the finished work of Christ at Calvary – and not in any intrinsic merit you think you have, nor any you can somehow earn.
If this is you, any one of the elders here would be more than happy to spend some time with you right now to talk with you pray with you that you might be born again.
 Alan Cairns, Dictionary of Theological Terms (Belfast; Greenville, SC: Ambassador Emerald International, 2002), 422.


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Entertainment > Theatre, dance & other performing arts > Theatre
Poetry, Drama & Criticism > Literature: history & criticism > Literary studies > Literary studies: 1900 onwards
Poetry, Drama & Criticism > Literature: history & criticism > Plays & playwrights
Beckett: Waiting for Godot - Plays in Production (Paperback)
David Bradby (author)
Waiting for Godot is a byword in every major world language. No other twentieth-century play has achieved such global currency. His innovations have affected not only the writing of plays, but all aspects of their staging. In this book David Bradby explores the impact of the play and its influence on acting, directing, design, and the role of theatre in society. Bradby begins with an analysis of the play and its historical context. After discussing the first productions in France, Britain and America, he examines subsequent productions in Africa, Eastern Europe, Israel, America, China and Japan. The book assesses interpretations by actors such as Bert Lahr, David Warrilow, Georges Wilson, Barry McGovern and Ben Kingsley, and directors Roger Blin, Susan Sontag, Sir Peter Hall, Luc Bondy, Yukio Ninagawa and Beckett himself. It also contains an extensive production chronology, bibliography and illustrations from major productions.
'... an excellent historical account of Waiting for Godot in performance, covering an impressive range of productions ... Beckett: Waiting for Godot is certainly an invaluable source of information for anyone interested in staging the play.' Theatre Research International
'... this is a first-rate guide to the multiple ways this text has been made to work.' English Studies
'David Bradby's contribution to Cambridge University Press's fine series Plays In Production is a superb volume on Waiting for Godot ... a most welcome addition ... It is elegantly written, well presented, and immensely helpful through the wealth of information, insights, and analysis it presents in a very handy format.' Becket Circle Newsletter
'David Bradby provides the first comprehensive survey of the key production of Samuel Beckett's most renowned dramatic work and a refreshing assessment of the genesis of the play within its cultural contexts ... the book sits usefully on the shelf of anyone with an interest not only in Beckett's theatrical achievement, but in issues of play authorship and the interfaces between actors, directors, designers and a playscript or its author. The writing would attract and interest the general reader as well as the scholar, student, actor, director or designer and the work as a whole represents a useful sourcebook and a fascinating and readable account of the history of this most celebrated of plays.' Studies in Theatre and Performance
Theatre and Audience
Lois Weaver
How To Do Accents
Edda Sharpe
The Golden Rules of Acting
The Frantic Assembly Book of Devising Theatre
Contemporary Monologues for Women
Trilby James
The Complete Stanislavsky Toolkit
Bella Merlin
Acting Through Song
Paul Harvard
Shakespeare Monologues for Young Women
Luke Dixon
The Crafty Art of Playmaking
Shakespeare Monologues for Men
The Methuen Drama Book of Monologues for Young Actors
Anne Harvey
Actions: The Actors' Thesaurus
Marina Caldarone
An Actor Prepares
Respect for Acting
Not My Father's Son


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The template of the form is available in both PDF and word format. Make necessary changes in the format as per your needs and then print the form.
A family reunion survey form is made to identify that how often an individual joins his/her family.


Rapper Joe Budden's mom bailed him out of jail early Thursday after the rapper turned himself in to answer charges that he beat and robbed his ex-girlfriend.
The "Pump It Up" hip-hop star surrendered to cops at the 34th Precinct stationhouse in Inwood Wednesday, with his attorney in tow, at about 9 a.m., cops said.
He was arraigned late in the day on charges of assault, grand larceny and robbery in Manhattan criminal court but was released after his mother came to his rescue with $10,000 in cash for bail.
"It's good to be free," Budden told the Daily News as he left the courthouse. He also took a parting shot at his accuser.
"I've been portrayed worse by better," he said.
The rapper was ordered to sign an order of protection forbidding him from contacting his ex-girlfriend, who police said he assaulted on Aug. 18 after she posted a picture of herself with another man on Twitter.
On that day, an enraged Budden drove up to a restaurant near Nagle Ave. and Dyckman St. at 4:30 a.m., grabbed his ex's cell phone, pushed her in the head, twisted her arm and then choked her before slamming her head against the passenger-side window as he forced her into his car, according to the criminal complaint.
After driving back to the New Jersey home the two shared, Budden grabbed the woman's hair and dragged into their bedroom, where he punched her in the stomach, the court papers said.
He then said he needed to call a cab before he killed the woman, according to the complaint.
The beatdown has been compared to rapper Chris Brown's savage attack on megastar Rihanna in 2009.
Budden, 33, has mantained his innocence publicly on Twitter.
In court, Budden's lawyer, Nima Ameri, said the rapper's tweets, including those taunting the NYPD, were jokes.


text:
Minister meets Hollywood stars, visits movie set in resort city
Culture and Tourism Minister Mehmet Nuri Ersoy has visited the set of director Guy Ritchie's forthcoming international spy thriller film titled "Five Eyes," which is being shot in the Mediterranean province of Antalya.
Meeting with Ritchie and the world-famous actor Jason Statham, the leading actor of the film, Ersoy chatted with the duo and wished success to the production team. He then went to the set and watched the shooting of a scene from behind the camera.
The minister, who also visited sections created in an EXPO area for the film, then left the site.
The 121-acre fairground in Aksu district, which had been a topic of discussion on how to use it after EXPO 2016, was turned into a movie studio, after the production team started their official correspondence with officials regarding permits.
The shooting of the scenes is planned to be completed in three weeks and the open-air studio set up in the EXPO area will be dismantled in March.
The film marks the latest collaboration between Ritchie and Statham, who have previously worked together on "Lock, Stock and Two Smoking Barrels," "Snatch" and "Revolver" as well as the upcoming action thriller "Wrath of Man."


text:
Q: Is it possible to make agreements fields not required? is it possible to make agreements fields on checkout billing screen not required?
They are added from Stores -> Terms and Conditions in admin panel.

A: If you want to make checkout agreements field not required then its simplest solutions is disable the terms and condtions status.
If you can disable terms and condtions then its not display inside checkout billing.
if you want keep some terms and conditions, its mandotory required to choose at checkout step.Generally its useful when you have to some Terms and condtions for your site.

A: @Mateusz_Procner, did you find the solution to the issue raised?
I need some agreements to be obligatory(required) and others not, but all to be displayed to the user.

redpajama_set_name: RedPajamaStackExchange


Each session of psychological therapy, for self referred individuals is £90, which is payable prior to each session.
Cancellation or non attendance within 48 hours of the appointment incurs the full session fee.
I also accept referrals from clients registered with BUPA and other insurance company referrals. Please contact me to discuss the fee for this work.


If user don't want to include any logical operation on request and redirect to some resource then user used UrlFilenameViewController that's transform the virtual path of a URL into a view name and provide a view to display as a user interface.
If user don't want to include any logical operation on request and redirect to some resource then user used UrlFilenameViewController that's transform the virtual path of a URL into a view name and provide a view to display as a user interface. In this example we will discuss about UrlFileNameViewController.
Let's start developing the example program that uses UrlFileNameViewController class. Follow the steps mentioned below and develop the example program. You can also download source code of UrlFileNameViewController example discussed here from the download link provided at the end of this tutorial.
Now we will create two jsp file inside /WEB-INF/ folder that's name "MyAddress.jsp" and "MyOfficeAddress.jsp" for redirect the user on.


text:
"Our lovely daughter was diagnosed with autism..."
"Our lovely daughter was diagnosed with autism in October 2014, aged 3.5. After unsuccessfully trying our daughter in a familiar mainstream school to her – it only lasted a term when it became painfully apparent that neither party could cope – we had to find an alternative setting for our daughter in a special independent school.
By then, our local authority had already rejected our request for an EHCP assessment for our daughter (due to them submitting incorrect paperwork), so a state special school was also not an option.
We contacted Douglas Silas Solicitors in the summer of 2015. At that stage, we were privately funding our daughter's special school, at which she was much more settled, calmer and happier, but which was an unsustainable provision without the financial assistance of the LA.
We did not want to run the risk of upsetting our daughter by moving her out of her school. By then, we had (belatedly) just been granted our second request for an EHCP assessment, which was at an early stage in what became a drawn-out process.
Eventually, we got to a successful conclusion – namely that our daughter remains at her current school where we feel that she has the best chance to maximise her potential (whatever that may be), and that the educational provision is fully funded.
But, this outcome only came after many emotional conversations and meetings with our LA, detailed submissions from our daughter's school and us on her significant level of needs (sensory, speech, safety etc) etc. Nor was it quick, with many LA decisions only taken at the absolute last minute, which then pushed other timeframes back.
We have learnt that, much like a typical building project, there are substantial risks of over-run, and that patience is required. Courtesy is vital too – we were lucky that our case officer at the LA was co-operative and very knowledgeable, but at an emotional time, it's important to try and remain polite.
It's vital to have a clear game-plan, and seek external advice where needed to navigate through the SEN legal morass – we contacted Douglas because of his outstanding references, his superbly informative website etc – but our LA also had a very knowledgeable Parent Partnership team. Be flexible to at least considering other options, especially those that your LA may suggest.
Ultimately, each case is different, but some basic principles do remain. The process can be confusing, emotionally-draining and slow...parents naturally want clarity and help immediately, but this is unlikely and persistence will be needed. There are people out there who can help and advise, and many others who have been through your situation.
We wish you the best of luck, and, can thoroughly recommend Douglas and his team for their timely and always well-informed guidance."
A Parent's Story - S v Lambeth LA


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Das Solling-Projekt war das erste interdisziplinäre Programm Deutschlands zur Ökosystemforschung. Es wurde in den Sechzigerjahren im Rahmen des UNESCO-Programmes International Biological Programme (IBP), 1966 bis 1973, zur Erforschung von Ökosysteme durchgeführt, die vom Menschen unbeeinflusst sind.

Namensgebend war das deutsche Mittelgebirge Solling, wo die Probeflächen lagen. Wissenschaftlicher Hauptinitiator und langjähriger Projektleiter war der Ökosystemforscher Heinz Ellenberg.

Die Datenerhebung belegte einen erheblichen Einfluss menschlicher Tätigkeit auf das Gebiet.
Die langjährigen Auswertungen lieferten Erkenntnisse über die Wirkung von saurem Regen auf die Bodenfruchtbarkeit und weitere Ursachen und Zusammenhänge mit den heute als neuartige Waldschäden benannten Phänomenen.

Die Studien wurden in Folgeprojekten und Zeitreihenanalysen  fortgeführt und werden heute von der forstwissenschaftlichen Fakultät der Universität Göttingen betreut. Budgetprobleme in Niedersachsen gefährden jedoch die Fortführung.

Literatur
 Heinz Ellenberg (Hrsg.): Ökosystemforschung, Ergebnisse des Sollingprojekts. 1966 - 1986. Ulmer, Stuttgart 1986, 507 S., ISBN 3-8001-3431-4.
 Gerhard Seibt: Die Buchen- und Fichtenbestände der Probeflächen des Sollingprojektes der Deutschen Forschungsgemeinschaft. Schriften aus der Forstlichen Fakultät der Universität Göttingen und der Niedersächsischen Forstlichen Versuchsanstalt (Band 72). Sauerländer, Frankfurt am Main 1981, 109 S., ISBN 3-7939-5072-7.

Umwelt- und Naturschutz (Niedersachsen)
Umweltprojekt
Waldökologie
Solling
Forstwirtschaft und Holzeinschlag (Deutschland)

redpajama_set_name: RedPajamaWikipedia


The USDA is poised to eliminate the restrictions on seeds engineered to resist applications of 2,4-D, the chemical agent better known as one half of the recipe for Agent Orange—the potent defoliant used in the Vietnam War.
After farmers who bought into the genetically modified farming model started to notice pests and weeds becoming resistant to the chemicals commonly used in tandem with the seeds—mainly Monsanto's glyphosate herbicide called Roundup—the biotech industry began to look for stronger chemical killers, like 2,4-D.
Now, the USDA has released an Environmental Impact Statement recommending "full deregulation" for Dow AgroScience's corn and soybean traits that are resistant to 2,4-D. The products are branded under the "Enlist Weed Control System" label.
The Associated Press reports that it's a move "welcomed by many farmers but feared by scientists and environmentalists who worry it could invite growers to use more chemicals."
The nature of 2,4-D makes it toxic to plants early on in their growth cycles, but the modified seeds "would allow farmers to use the weed killer throughout the plants' lives."
But skeptics say that 2,4-D isn't an answer to anything—it's just creating another potential rise in resistant weeds. "It's just so clear. You can see that you have this pesticide treadmill effect," Bill Freese, a chemist with the Washington, D.C.-based Center For Food Safety, which promotes organic agriculture, told the AP. 2,4-D skeptics like Freese are also concerned over the human health risks that could arise with approval of the seeds. "Freese said he would rather see farmers use organic means to control weeds," reports the AP, "perhaps by using cover crops that go into the ground after the harvest to hold soil in place and deter weeds until the next growing season."
Agent Orange 2.0? Why Won't The EPA Ban Toxic 2,4-D?


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Character Size
Press Conference by Defense Minister Inada (08:25-08:29 A.M. November 25, 2016)
Press Conference by the Defense Minister
Time & Date: 08:25-08:29 A.M. November 25, 2016
Place: Entrance of the Prime Minister's Office
(This is a provisional translation of an announcement by the Defense Minister and the Q&A session at the subsequent press conference for reference purposes only.)
The original text is in Japanese.
In relation to the introduction of THAAD, I hear that a committee to consider this matter will be convened within the MOD. Could you tell me about the progress status?
Concerning the threat of ballistic missiles, it is important to develop Japan's own BMD system and to strive to enhance the deterrence and response capabilities based on the Japan-U.S. Alliance. As for the development of the BMD system, we are conducting various activities, including surveys and research on a future ballistic missile interception system. There is no concrete plan for introducing THAAD, but I expect that introducing new assets like this will lead to the enhancement of our own specific capabilities. We are considering what the MOD/SDF can do, but for the moment, I would like to refrain from commenting on the details.
There has been a media report that Chief of Staff Takei of the MSDF will be disciplined soon in connection with the next-generation multi-purpose helicopter. Could you share the facts?
At the moment, the Inspector General's Office of legal compliance is conducting a special defense inspection, so I would like to refrain from commenting on the specifics related to the inspection.
The other day, GSOMIA with the Republic of Korea (ROK) was signed and took effect immediately. Could you explain its significance?
Since the beginning of this year, North Korea has conducted two nuclear tests and launched more than 20 missiles, so the threat has grown considerably. In this situation, cooperation between Japan and the ROK is very important. The signing of GSOMIA has long been a pending matter. I am expecting that information exchanged between the governments of Japan and the ROK will be appropriately protected and more smooth and prompt information exchange between the two governments will be facilitated.
In relation to North Korea, next month will be the anniversary of Chairman Kim Jong-un's assumption of his post, so it is said that the threat may be ratcheted up again and the possibility of acts of provocations may rise. Could you share your comments on signs and the possibility of such a situation arising in the future?
We are constantly devoting efforts to information gathering and surveillance with a sense of alertness, including with respect to the point you mentioned just now.
Concerning the disciplining of the Chief of Staff of the MSDF, as his term of office is about to expire, will his disciplining be in effect a demotion?
Nothing has been decided with respect to the disciplining and the inspection is now ongoing, so I would like to refrain from commenting on matters like that.
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Japan Ministry of Defense
5-1 Honmura-cho, Ichigaya,
Shinjuku-ku, Tokyo 162-8801
Phone: 03-5366-3111 (switchboard)
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Gangapur City is a city, nagar parishad located, near Sawai Madhopur City in Gangapur City District  in the Indian State of Rajasthan.  Population-wise, it is the 18th largest city in Rajasthan.

History
King Kushaliram Haldiya established Gangapur and originally named it Kushalgarh (Hindi: कुशालगढ़). Gangapur took its current name from Kushaliram's brother, Gangaram. In older days, Gangapur City was the cultural capital of Jaipur State and was known as "The Jugad of the East". Today, Gangapur is primarily known for being an important part of the West Central Railway.
Gangapur City is now getting famous for Nazimwala Talab (kushalgarh Bird Sanctuary), where a number of migrating birds are coming in the winter season.

Geography
Gangapur City is located in the eastern part of Rajasthan in Sawai Madhopur; it is situated 75 km from district headquarters at Sawai Madhopur and 140 km from Jaipur. The city's area is about 12 km2.

Demographics
The 2011 Census of India considered Gangapur City as an urban agglomeration. The city has a population of 119,090; males constitute 53% of the population and females constitute 47%.

Literacy rates

The average literacy rate in Gangapur is 79.12%.

Religions

Hinduism is majority religion in Gangapur City, with 71.91% of the city as followers. Islam is the secondmost common religion, with 26.32% following it in the city.

Climate
Gangapur City is in a subtropical dry climate that experiences summer, winter, and the wet season. Temperature may rise above 40 °C in summers and can be low as 5 °C in winters. The average precipitation is 24.48 cm. Humidity is about 5–10% in summers and rises to about 75% in rainy seasons.

Gangapur City Wards Map
Before 2019 total 40 wards in Gangapur city.

Currently total 60 wards in Gangapur City.

Transportation

Railways
 is a railway station on the Delhi–Kota–Vadodara–Mumbai railway line and it is abbreviated as GGC. Many of the major trains on this route stop at the station. It is in the West Central Railway Zone under the Kota Division. Gangapur City is directly connected to major cities like Delhi, Mumbai, Jaipur, Kota, Agra, Indore, Mathura, Patna, Jammu, Amritsar, and Udaipur.

Station also serve as only railway source to places like Karauli, Sapotara, Bamanwas, Lalsot, Kailadevi, Piplai which did not have railway connectivity.

A new railway line is under construction which links  and  to connect Gangapur City to the Ahmedabad Junction railway station, in order to decrease travel time to cities like Jaipur, Jodhpur, and Ahmedabad and provide railway connectivity to areas like Lalsot, Piplai, and Bamanwas.को दौसा - गंगापुर सिटी रेलमार्ग से जोडा जा रहा है, यह कार्य वर्ष 2023 तक पूर्ण होने की आशंका है।

Another railway line has been proposed between Dholpur and Gangapur City to connect Gangapur City to the Delhi–Bhopal–Mumbai rail route and to provide connectivity to Karauli.

Roadways
Gangapur City has a Rajasthan roadways bus stand for Rajasthan government buses and a private bus stand for privately owned buses. Gangapur City has regular government and private buses to cities like Jaipur, Dausa, Karauli, Dholpur, Gwalior, Ajmer, Pushkar, Hindaun, Alwar,Bikaner, Bhilwara, sikarand Sawai Madhopur.

Major roads passing through Gangapur City are:
 National Highway 23: Dholpur–Karauli–Gangapur–Lalsot–Kothun
 Rajasthan SH-1: Jhalawar–Kota–Sawai Madhopur–Gangapur City–Bharatpur–Mathura
 Rajasthan SH-25: Gangapur City–Sikandra–Bandikui–Rajgarh–Alwar–Tijara–Bhiwadi–Daruhera

The distances of major cities from Gangapur City are:
 Jaipur: 141 km
 Sawai Madhopur: 75 km
 Bharatpur: 145 km
 Kota: 206 km
 New Delhi: 238 km
 Udaipur: 458 km
 Ajmer: 274 km
 Karauli: 34 km
 Gwalior: 203 km
 Alwar: 142 km

Airways
The nearest airports to the city are Jaipur International Airport in Jaipur and Indira Gandhi International Airport in New Delhi.

Medical facilities
Gangapur City has a government hospital situated in Sursagar, which has an operation theatre, post-mortem room, maternity ward, and laboratory. It also has more than 5 multi specialty hospitals. Riya hospital, garg hospital etc.

Banking
All major Indian banks have branches in Gangapur City.

 Allahabad Bank
 Axis Bank
 Bank of Baroda
 Baroda Rajasthan Kshetriya Gramin Bank
 Central Bank of India
 Canara Bank
 HDFC Bank
 ICICI Bank
 Indian Bank
 Indian Overseas Bank
 Oriental Bank of Commerce
 Punjab National Bank
 State Bank of India
 Union Bank of India
 UCO Bank
 United Bank of India
 Yes Bank

Media
 Dainik Bhaskar
 Dainik Jagran
 Dainik Navajyoti
 Rajasthan Patrika
 The Times of India

Dainik Bhaskar, Dainik Navajyoti and Rajasthan Patrika are the major newspapers read in Gangapur City, which are printed in the city. Other newspapers include The Times of India, Bajriya Ki Bhore, Badti Kalam,
Rashtradut, Kushalgarh Ka Suraj. Chamkti Aankhe and Dainik Jagran.

G News Portal is the mostly watched news portal of Gangapur City, which shows live news of local incidents.

Internet Service Provider
  Airtel
  BSNL
  Jio
  Radinet
  Railwire

External links
 https://www.gangapur.city
 https://www.bhaskar.com/local/rajasthan/sawai-madhopur/gangapur/
 https://geoiq.io/places/Gangapur-City-(M)/yQSgXcvBJm
 https://www.giveindia.org/all-ngos/rajasthan/gangapur-city/
 https://www.mapsofindia.com/maps/rajasthan/gangapur.html
 https://women.raftaar.in/ghumne-ki-jagah/rajasthan/gangapur_city

References

Cities and towns in Sawai Madhopur district


The change in biosynthetic capacity requires induction of a growth of location and volume and a wide array of secretory pathway genes of the ER. In plasma mobile differentiation, the transcription factor X box binding protein 1 was found to organize the changes in cellular structure and func-tion. Also for the biogenesis of the secretory equipment of exocrine glands such as salivary gland and exocrine pancreas, XBP 1 is necessary, and its erasure severely reduced growth of the ER and the appearance of certain ER chaperones. As signaled from the UPR xbp 1 has become considered as the central person of an integration mechanism between the level of protein processing and the demands for (-)-MK 801 ER membrane potential. XBP1 is formed downstream of ER stress triggered inositol necessitating enzyme 1 that cleaves XBP 1 mRNA by an unconventional splicing mechanism, which is needed for its protein expression. A vital position for XBP 1 in promoting ER development is supported by the observation that added retroviral expression of active XBP 1 led to increased activity of enzymes involved with phospholipid biosynthesis. That lipid reaction particularly is dependent upon IRE1 XBP 1, the UPR branch for adaptation to longterm or chronic ER stress. This means a model where development Endosymbiotic theory of the whole ER supplies a long term commitment to improved ER function, including it does occur in differentiating plasma cells and perhaps in other professional secretory cells. Lately, ATF6 was found to induce a second path distinct from XPB 1, relating UPR and ER development, further strengthening evidence for the connection betweenUPRpathways, fat production and ER biogenesis. Being an adaptive reaction in chronically infected airway epithelia a key role for that IRE1 XBP 1 part of the UPR has additionally become apparent. Airway epithelial infection/inflammation triggers an UPR because of ER stress resulting from a heightened need for epithelial re-pair proteins and newly synthesized inflammatory mediators. XBP 1 then mediates ER Ca2 store expansion and up regulation of the protein secretory pathway. The increased Ca2 response as a result of the store expansion is effective for infected/inflamed airways due to an up regulation ALK inhibitor of Ca2 mediated mucociliary clearance. The bigger Ca2 signals elicited by apical P2Y2 receptor activation in cystic fibrosis airway epithelia is due to the development of the apical ER Ca2 stores triggered by persistent infection/inflammation. An additional consequence of XBP 1 induced Ca2 shop extension is as seen in human cystic fibrosis airway epithelia a Ca2 mediated super irritation. Recent studies have linked XBP 1 mediated ER pressure responses to intestinal inflammation, suggesting its importance forhumaninflammatory bowel dis-ease.
Significantly more Ca2 entry through L typ-e Ca2 programs is situated in control cells in comparison with Bcl2 revealing cells, due to a lower depolarization created by 75mM external K. This keeps pace with the reduced Ca2 access elicited by K activation of Bcl2 cells. Hence, it appears that Bcl2 is making the cell more resistant to depolarizing stimuli, slowing, this way, the hiring of M type Ca2 channels and decreasing Ca2 entry and mitochondrial Ca2 excess. The results of this study might be highly appropriate in the context of Fingolimod distributor cell death evoked by M type Ca2 channel activator Bay K 8644 in E depolarized chromaffin cells; under these conditions, extra Ca2 access through the L type Ca2 channel causes mitochondrial dysfunction and apoptosis, and the L type Ca2 channel blocker nimodipine avoided such damaging effects. In our studies, the m was also enhanced by Bay K 8644 in get a handle on PC12 cells, and nimodipine blocked such increase. It was interesting that Bcl2, that also protected PC12 cells against cell death evoked by various stimuli including Ca2 overload, also mitigated Ca2 access, h increase, and m inside our present studies. Therefore, we believe that Bcl2 has a nimodipine like effect in preventing Ca2 overload, Ca2 entry, and cell death by indirectly down regulating the plasmalemmal M typ-e Ca2 channel. Caution should be applied when attempting to interpret data obtained Gene expression with stably transformed cells, as reviewed by Blum et al.. A priori, it is hard to discard a genetic stimulated phenotypic transformation of our Bcl2 cells, explaining the changes in Ca2 fluxes that we obtained in terms of unspecific cell changes rather than to Bcl2 overexpression it self. In principle, our findings with acutely transfected cells, that don't show genetic change, assist our idea that, certainly, Bcl2 is causing the disturbances observed in Ca2 access and it subsequent redistribution in-to mitochondria. In addition, tests conducted with shRNA, conjugating enzyme to knock down the expression of Bcl2, support-the proven fact that Bcl2 can be a vital player in the downregulation of Ca2 homeostasis in Bcl2 clones. Not surprisingly, in Fig. 8a and b we demonstrate that the interference with the phrase with the protein Bcl2 results in a restoration of the Ca2 signal as compared to control cells. However, as a way to be sure about the effects, we also performed a pharmacological approach. Once more, we show that the inhibition of Bcl2 reverts its effects on cell Ca2 homeostasis after E depolarization. On-the other hand, we have observed that nerve growth factor induces differentiation of Bcl2 and control cells equally well, suggesting that both cell types have an identical phenotype. To summarize, our results suggests that Bcl2 indirectly causes down regulation of M type Ca2 routes, ultimately causing the mitigation of K evoked increase of c and m.
the incorporation of taxane into induction chemotherapy further improves end result. Regardless of treatment method advances, recurrence and mortality charge of HNSCC stays large, reflecting the aggressiveness of disorder. Cetuximab, an anti epidermal growth issue antibody, in blend with chemotherapy JZL184 1101854-58-3 or radiation, demonstrates its exercise and has been approved for being the first molecular targeted therapy for HNSCC. Nonetheless, its clinical use is limited as a result of modest efficacy. Consequently, new therapies for HNSCC are needed. Bortezomib, a proteasome 20S inhibitor, is clinically authorized for your treatment method of many myeloma and mantle cell lymphoma. Amongst identified targets in myeloma and lymphoma, nuclear factor kB continues to be proposed a significant target of bortezomib. By blocking the degradation of IkB, bortezomib exhibits its exercise against hematological malignancies through sequestration of NF kB in cytoplasm and reduction of its transcriptional activity.
In strong tumors, bortezomib also demonstrates in vitro activities by means of NF kB inhibition. A numbers of clinical trials in reliable tumors are actually conducted, even so, the efficacy is constrained, suggesting the molecular targets of bortezomib in solid tumors may be various from those reported Metastatic carcinoma in hematological malignancies. Cancerous inhibitor of protein phosphatase 2A, initially named KIAA1524 or P90, has become cloned from hepatocellular carcinoma sufferers. By means of inhibiting protein phosphatase 2A activity toward phosphorylated c Myc serine 62, CIP2A is shown to promote anchorage independent cell growth and tumor formation by stopping c Myc degradation. In addition to HCC, CIP2A is more than expressed in other reliable tumors, which include gastric cancer, head and neck cancer, colon cancer, breast cancer, esophageal cancer, and non tiny cell lung cancer.
In our preceding review, bortezomib exhibited proteasome independent activity towards HCC cells in vitro via inhibition of Akt. Fingolimod manufacturer The mechanism of bortezomib induced Akt inhibition was even more explored and demonstrated that this inactivation depends on CIP2A mediated PP2A dephosphorylation of Akt. By disclosure of the new mechanism of bortezomib, we propose CIP2A might serve as being a new therapeutic target in solid tumors. Within this study, we aim to investigate the position of CIP2A inside the impact of bortezomib in HNSCC. Ca9 22 cell was kindly offered by Dr. Hsin Ming Chen, Graduate Institute of Oral biology, School of Medication, National Taiwan University. SAS was kindly supplied by Dr. Han Chung Wu, Institute of Cellular and Organismic Biology, Academia Sinica, Taiwan. SCC 25 was cultured in 50% Hams F twelve medium, 50% DMEM supplemented with 0. five lg/ml hydrocortisone, and 10% fetal bovine serum.
we demonstrate that Myc overexpression facilitates Bax conformational activation, resulting in enhanced apoptosis in response to histone deacetylase inhibitor SAHA, a promising new anticancer drug in clinical trials. We even more demonstrate that Bax Deubiquitinase inhibitors activation needs the transcriptional induction of professional apoptotic BH3 only protein Bim by SAHA. Importantly, we show that Myc is not demanded for your Bim induction by SAHA. Rather, Myc regulates Bimmediated Bax activation by way of its potential to modulate anti apoptotic Bcl two or Bcl xL expression. Consequently, the Myc Bcl 2/Bcl xL module appears to become central to Mycmediated sensitization to apoptosis induction by SAHA. As we demonstrate, in Rat 1a fibroblast cells undergoing SAHA induced apoptosis this module dictates the efficiency of Bim in triggering Bax activation and apoptosis induction. In rodent fibroblast cells which include MEFs Bax has been shown for being transcriptionally regulated by Myc.
In these cells, Myc overexpression results in enhanced susceptibility to apoptosis like a consequence of elevated Bax expression rather than activation. Contrary to what has become observed in MEFs, we identified that Myc overexpression Endosymbiotic theory in Rat 1a fibroblast cells didn't induce improved Bax expression, suggesting that Bax is just not a transcriptional target of Myc in Rat 1a cells. Consequently, Myc regulates Bax transcription in a contextdependent manner. Additionally, we determined that Bax was conformationally activated by Myc in a Bimdependent method, since Bim depletion significantly lowered Bax activation by SAHA in Myc expressing cells. Prior to this operate, no BH3 only proteins had been reported to become involved in Myc dependent apoptosis.
Though microinjection in the BH3 peptide or even the ecotopic expression of Bid is identified to cooperate with Myc to induce Bax dependent apoptosis, to date, there no experimental information demonstrates how the endogenous BH3 only proteins are engaged in Myc mediated Bax activation. Our experiments working with SAHA to induce the endogenous Bim ATP-competitive ALK inhibitor will be the initially evidence for a purpose of the BH3 only protein in Bax activation upon Myc overexpression. In Myc null Rat 1a cells, Bim induction by SAHA failed to induce Bax activation, this suggests that Bim induction per se is inadequate to activate Bax, and that it demands supplemental mechanisms that are Myc regulated. It's been previously reported that Myc negatively regulates Bcl 2 or Bcl xL expression. Indeed, we found that Myc null cells express elevated Bcl two or Bcl xL relative to Myc expressing cells.
Knockdown of Bcl 2/Bcl xL in Myc null cells efficiently restored both the Bax activation and apoptosis induction by SAHA. Depending on these results, we surmise that Myc facilitates the down regulation of Bcl2/Bcl xL in response to SAHA.
The present acquiring that expression of TIMP three was not improved in cortical neurons undergoing widespread necrosis right after publicity toNMDA or Fe2 supports a selective causal role of TIMP 3 in neuronal apoptosis. Expression of TIMP three mRNA and protein is elevated in ischemic cortical neurons Docetaxel molecular weight following transient occlusion of your middle cerebral artery. We identified that expression of TIMP three was elevated selectively in spinal motor neurons from the transgenic mouse model of ALS. TIMP three was also upregulated in degenerating TUNEL beneficial neurons in the brain ofADpatients. In light of your putative function of apoptosis in AD, animal versions of ischemia and ALS, and development, TIMP 3 might mediate neuronal apoptosis in acute and persistent neurodegenerative conditions including ischemia, ALS, and AD. TIMP 3 inhibits metalloproteinases, which can shed and stabilize death receptors including Fas and tumor necrosis component receptor one, resulting in extended activation of death receptors.
We identified that TIMP three and MMP 3 had been colocalized in cortical neurons deprived of serum and their interaction was enhanced as early as 2 h after serum deprivation. Interaction of TIMP three and MMP three was also greater in the spinal cord of G93A Chromoblastomycosis transgenic mice. Enhanced TIMP three expression and TIMP3?MMP 3 interaction were followed by concomitant maximize in Fas and FADD interaction, activated caspase eight, and caspasce 3 following serum deprivation and in G93A transgenic mice. Administration of your lively catalytic subunits of MMP three attenuated the interaction of Fas and FADD, activation of caspase 8 and caspase three, and neuronal death following serum deprivation. In addition, knock down of TIMP 3 expression by RNA interference blocked expression of TIMP 3 and inhibited SDIA.
This implies that MAPK activity TIMP three mediates SDIA probably by inhibition of MMP 3, which success in subsequent activation of the Fas mediated apoptosis pathway. Fas interacts with Daxx, a transcriptional repressor, receptorinteracting proteins with serine/threonine kinase action, and FADD. Interaction of Fas and its adaptor proteins triggers a number of cellular events. One example is, Fas stimulates the processing and release of inflammatory cytokines which include interleukin 1, interleukin 6, and interleukin eight. Fas can also advertise neurite outgrowth and regeneration. Therefore, it can be conceivable that TIMP 3 might play an extra purpose in inflammation and regeneration in the nervous technique.
In conclusion, expression of TIMP 3 was improved in cultured cortical neurons undergoing apoptosis as well as in neurons undergoing degeneration while in the lumbar ventral horn of G93A transgenic mice of ALS. TIMP three appears to stabilize and activate Fas by inhibiting MMP 3, which triggers activation on the Fas pathways to mediate SDIA and in neurodegenerative ailments which include ALS and AD.
The remaining sufferers who met the main endpoint represented histologies that consisted of the two large and lower grade serous tumours and mucinous form tumours demonstrating that ENMD natural product libraries activity just isn't certain to one subtype of ovarian cancer or to reduced or higher grade tumours. Unexplored areas with the kinase, namely anyplace however the ATP cleft, hold the potential to reveal novel web sites for inhibitor development. Owing to your intricate regulation of protein kinases and their conformational versatility, this kind of allosteric sites may possibly potentially exist. A short while ago quite a few allosteric kinase inhibitors are already recognized via novel screening techniques. One example is, the inclusion of regulatory domains as well as use of differential screening with various ATP concentration have identified various allosteric ligands of AKT isoforms. Nevertheless, approaches for identifying allosteric ligands that target the kinase domain directly are already additional elusive.
A current technique Cellular differentiation combining HTS employing MS and NMR has identified MAPK inhibitors with eleven?sixteen lM Kd values for the unactive kinase and prevent activation. In an additional instance, differential cytotoxicity screening towards BCR ABL positive cells was utilized and after discarding hits resembling recognized ATP aggressive compounds, a fresh class of inhibitors containing a 4, 6 pyrimidine core have been identified. These new inhibitors were shown to operate in an allosteric fashion by focusing on a distal myristoyl binding pocket of c ABL. Betzi and co staff in a different illustration of allosteric inhibitor screening mixed fluorescent probes and protein crystallography in which the probe, eight anilino one naphthalene sulfonate, bound an allosteric pocket near the ATP internet site in CDK2 with an obvious Kd of 37 lM.
As a consequence of the reduced affinity of most original allosteric hits, that are typically better than 10 lM, numerous allosteric ligands may perhaps be possibly missed during common HTS campaigns. On the other hand, the probable for selectivity for these new classes of allosteric ligands delivers the impetus for redesigning JZL184 concentration latest methodologies to learn this kind of inhibitors. Unlike most little molecule inhibitors, peptides are possibly amenable to targeting the peptide binding web site or kinase surface as opposed to binding the ATP cleft, and therefore possess the potential benefit of probing significantly less conserved areas. An exciting application of those surface targeting ligands has been within the generation of selective bivalent inhibitors, which covalently combine surface binding peptide moieties with tiny molecules which might be regarded to target the ATP binding web page.
This combined targeting is efficiently employed towards protein kinases to produce inhibitors of enhanced potency and selectivity in comparison with their starting fragments.
data suggest that subtiligase may recognize N leader acetylation of numerous proteins that's dependent on NatA appearance. To examine this question, we tested whether knock-down of ATP citrate lyase or acetyl CoA synthetase to generate acetyl CoA, results in reduced levels of N leader acetylated Evacetrapib caspase 2. Indeed, we observed increased biotin labeling of caspase 2 in knock-down cells in comparison to control cells following subtiligase analysis. This implies that caspase 2-is hypoacetylated when acetyl CoA technology is reduced and for that reason, protein N alpha acetylation is susceptible to metabolic regulation. We reasoned that regulation of protein N alpha acetylation of certain apoptotic regulators may provide a system to regulate apoptotic awareness, because decreased quantities of protein N alpha acetylation results in apoptotic lack. Bcl xL, an antiapoptotic Bcl 2 family member, is famous with an influence on metabolism. We asked whether protein N leader acetylation levels are sensitive to Bcl xL term using subtiligase assay. A rise Lymph node in biotin labeling of caspase 3, and Bax was noticed by Bcl xL expression in 293T, HeLa, and Jurkat cells compared to that of control. However, a decline in biotin labeling was apparent in bcl x mouse embryonic fibroblasts in comparison to that of bcl x MEFs. Because Bcl xL is known for maintaining mitochondrial reliability by blocking oligomerization of Bax/Bak, we measured the quantities of protein N leader acetylation in Bax/Bak deficient cells. Remarkably, the levels of protein N leader acetylation were related in bax, bak, or bax/bak MEFs in comparison to that of WT MEFs by subtiligase assay. This implies that Bcl xL mediated regulation of protein N alpha acetylation is in-dependent of Bax/Bak. Recent studies show that histone lysine acetylation is dependent o-n acetyl CoA generation in yeast and mammalian cells. Nevertheless, we found that lysine acetylation of histone H3 and H4 were untouched in Bcl xL cells in comparison with control. This means that histone lysine acetylation is not sensitive purchase Everolimus towards the changes in acetyl CoA levels related to Bcl xL expression. We next examined whether protein N leader acetylation levels in Bcl xL cells are affected by changes in acetyl CoA k-calorie burning. Addition of acetate or citrate stimulates cytosolic acetyl CoA manufacturing by acetyl CoA synthetase or ATP citrate lyase, respectively. We confirmed these metabolites increase acetyl CoA amounts in mammalian cells. Under metabolite therapy, protein N alpha acetylation levels were restored in Bcl xL expressing cells to that of control levels. Thus, a decrease in acetylCoA generation in Bcl xL cells could be accountable for the observed hypoacetylation. The expression of Bcl xL is often elevated in tumors.
Aurora B has recently received significant attention as a possible target for anti cancer drugs. HTERT RPE1, HeLa, and NRK cells were cultured in DMEM supplemented with 1% Penicillin/Steptomycin and 10 % fetal calf serum, and grown o-n natural compound library LabTek chambered coverslips for live microscopy. All live imaging experiments applying HeLa or hTERT RPE1 cells were performed with monoclonal cell lines stably expressing combinations of the fluorescent markers as indicated throughout the manuscript. Confocal live imaging was on the tailored Zeiss LSM 510 Axiovert microscope using a 633, 1. 4 N. A. Gas Plan Apochromat or 403, 1. 3-n. A. Oil EC Plan Neofluar purpose, or over a Zeiss Axiovert designed with a VisiTech Spinning computer and Hamamatsu ORCA ER camera and a 1003, 1. 4 D. A. Gas Program Apochromat goal. Both microscopes were equipped with piezo emphasis drives, custom designed EMBL incubation chambers, and filters, providing a humidified atmosphere at 3-7 C with five minutes CO2. Long haul shows for Figures 1B 1E were received on the Molecular Devices ImageXpressMicro microscope, designed with a 103 and incubation step, 0. 5 N. A. S Fluor target. Sample illumination was generally kept to the absolute minimum Papillary thyroid cancer and had no adverse influence on cell division and proliferation. Image evaluation was by Zeiss LSM510 and ImageJ pc software. Linear contrast modifications were applied with constant settings for different experimental conditions. For quantification of antibody stainings, 3D image loads were predicted by mean fluorescence intensity. History deduced power was then tested in an area of constant size centered across the peak fluorescence signal at midbodies, or chromosome bridges. For studies shown in Figures 2C and 2-d, S-2 and 5E, PAGFP was triggered by radiating an outlined area with 30 mW 405 nm diode laser at one hundred thousand indication. Service of PAGFP on the PALM microscope was by UV epifluorescence light through the closed area aperture for about 1 s. FRAP findings used 5-0 iterations of photobleaching at 100% transmission of 488 nm laser at parts just like the one indicated in Figure 6E. Restoration kinetics E3 ligase inhibitor of mean fluorescence intensity were measured in a spot of constant size at the place of the Aurora B ring, and after back ground subtraction were normalized to first and pre postbleach figure. Fluorescence loss in photobleaching findings used 20 iterations of photobleaching at 100% sign of 488 nm laser at places just like the one indicated in Figure 6G before acquisition of each time point. Suggest fluorescence was measured in elements of constant size as indicated in Figure 6G, and after background subtraction normalized to the prebleach framework. Intracellular Microsurgery was performed on the PALM MicroLaser System equipped with a pulsed 355 nm UV A laser utilizing a 10-0 3 1. 3NA Gas DICIII EC Strategy NeoFluar goal.
it implies that the stomodeum is specified but doesn't separate properly in embryos treated with ClO start at 24 hpf. In many of these embryos, the archenteron extended over the blastocoel and bent toward the ectoderm of the presumptive oral area, showing that the tip of the archenteron identified this area of ectoderm as oral. However, the archenteron tip did not blend with the overlying oral ectoderm where presumptive stomodeal cells expressed bra. Hence the mouth formation problem doesn't seem to be because of failure of dental structure specification. Furthermore, though OA polarity was repaired, mouth development was not often recovered by addition of SO4 to ClO Fostamatinib 1025687-58-4 treated embryos. Thus, ClO therapy prevents stomodeal invagination and the common tissue fusion function but undersulfation mightn't be direct the cause of the observed mouth creation trouble. Take-n together, our experiments give evidence that sulfation is important for the proper func-tion of GAGs and proteoglycans in institution and/or notion of the TGF beta signals released by ectodermal cells leading on track OA patterning in the developing urchin embryo. Our results show that right nodal expression and Nodal signaling depends on continuous sulfation, probably through an aftereffect of sulfated GAGs on the diffusion of the TGF beta ligand. We suggest that discussion of Nodal with sulfated GAGs must maintain an organizing center of Nodal signaling in the oral field at a sufficient local concentration to definitely Infectious causes of cancer autoregulate an unique expression and increase the specification and differentiation of oral tissue and proper patterning of aboral ectoderm. Furthermore, sulfation may possibly play important roles in convergent extension, tissue blend and/or cell adhesion events involved in gastrulation. Adult S. purpuratus sea urchins from Vancouver Island, British Columbia, were induced to lose gametes by electrostimulation. CHK1 inhibitor Embryos were cultured in SW at 1-2 C. Devel-oping embryos were treated with 30 mM NaClO at different times post fertilization. Embryos were also treated with 3 mM Na2SeO, 20 mM Na2SO4, 1mM 4 nitrophenyl beta D xylopyranoside, or 0. 5 and 5. 0 lM SB 431542. Synthetic SW was organized in accordance with Kester et al.. Low sulfate SW, containing just 10mM sulfate, was prepared by replacing the main Na2SO4 with NaCl. DNA fragments of a minimum of 500 bp of coding sequence were PCR amplified and cloned in the pBluescript II KS+ plasmid. RNA probes were synthesized with T7 or T3 RNA polymerase, 2 lg linear template DNA and the DIG RNA labeling mix based on manufacturer instructions. Design DNA was degraded applying RNAse free DNAse I. Probes were passed through a Micro Bio spin 30 Column before use.


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Using special federal and local housing funds, the City of Lakewood is offering grants of up to $3,000 and interest-free, deferred-payment loans up to $18,000 for low-income residents to repair and rehabilitate their homes.
Hundreds of Lakewood residents have successfully used the city-run program to make needed repairs they otherwise would not have been able to afford. Often times it is a senior living alone on a low, fixed income. Other times it is a family struggling economically.
The smaller $3,000 grants never need to be paid back. The larger loans only need to be paid back when the house is sold or refinanced or the title is transferred.
The smaller grants can help with exterior painting and minor repairs to windows, doors and stucco.
The home must be a single-family, owner-occupied dwelling in Lakewood. Other restrictions apply. The program is designed to help low-income residents make needed repairs to their homes and to maintain and improve the look of Lakewood neighborhoods.
For more information, call Lakewood City Hall at 562-866-9771, extension 2320 or go to www.lakewoodcity.org/HomeRehabProgram.


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Home Biography Jillian Shea Spaeder
Jillian Shea Spaeder Biography
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Talents are meant to be discovered. And, if it hadn't been for Susie Mains, the world wouldn't have been able to be entertained and enjoy the young child artist, Jillian Shea Spaeder.
Jillian Shea Spaeder; An Artist At Heart
It was in the recommendation of talent agent Susie Mains that the uprising actress and singer, Jillian Shea Spaeder's parents decided to leave hometown Philadelphia and move to Los Angeles to flourish their little daughter's career.
Jillian Spaeder rocks a colorful dress at an event. SOURCE: Pinterest
Amazingly, not long after making the move in just two months, Disney liked Jillian's audition for Walk The Prank and offered the role of Bailey. And, likewise, the rest is history.
Life As The Teenager
Despite the stardom with an increasing half a million followers on Instagram, the Barely Changed prefers to live an ordinary life. Also, Shea, who is currently seventeen years old, and grew up with an elder brother and a sister is like any teenager in the US.
Walk The Prank Star Jillian Shea pictured with her best friends. SOURCE: Jillian Shea Instagram
Jillian's Instagram feed that consists of casual hangouts with her friends and travel diaries can be evidence for that. Other than that, Jullian is also single in the meantime as she highly prioritizes her career.
Net Worth & Career Of Jillian Shea Spaeder
Spaeder grew passionate about acting and music since her early days and would participate in school plays and theatres concerts. And, it was during the summer when she was in her sixth grade, fate united Jillian with her manager at a Hollywood art seminar.
Jillian Shea is best known for Walk The Prank. SOURCE: Pinterest
Impressed with her talents, Mains did what she had to do. Jillian's success is also the result of her hard work though. Matter of fact, more than nine hours of her day is spent working and attending acting classes. And, the determination and hard work did pay off as her role in Walk The Prank was highly appreciated.
The Something Better singer is also known for her work in OMG!. And, at the age of only seventeen years, Shea already added a career earning of no less than $100,000.
Some Quick Facts Of Jilian Shea Spaeder
Inspired by The Beatles and music from the 70s and 80s.
Describes herself as a fun-loving, musical and fearless person.
Favorite show includes Grey's Anatomy.
Enjoys listening to James TW, Meghan Trainer, and Shawn Mendes.
Wishes to play the lead girl in the A Tale Dark and Grimm.
Visited Ecuador with her parents for Children International where the Sheas sponsor.
View more Biographies and Gossips on Marriedwiki.com.
#american actress
#walk the prank


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