text:
Q: Dynamically resize iframe Situation:
I'm working on a responsive design that involves the typical HTML/CSS combo. Everything is working nicely except in one case where there is an iframe inside of a div. The iframe should adjust automatically to the size of the parent div. A purely css solution has not presented itself so I'm going with a JQuery approach. It works nicely except in one scenario, when resizing from a smaller width to a larger width screen.
HTML:

CSS:
.container {
    width: 100%;
    height: 250px;
}
.iframe-class {
    width: 100%;
    height: 100%;
    border: 1px solid red;
    overflow: auto;
}

Javascript:
$(function () {
    setIFrameSize();
    $(window).resize(function () {
        setIFrameSize();
    });
});

function setIFrameSize() {
    var ogWidth = 700;
    var ogHeight = 600;
    var ogRatio = ogWidth / ogHeight;

    var windowWidth = $(window).width();
    if (windowWidth < 480) {
        var parentDivWidth = $(".iframe-class").parent().width();
        var newHeight = (parentDivWidth / ogRatio);
        $(".iframe-class").addClass("iframe-class-resize");
        $(".iframe-class-resize").css("width", parentDivWidth);
        $(".iframe-class-resize").css("height", newHeight);
    } else {
        // $(".iframe-class-resize").removeAttr("width");
        // $(".iframe-class-resize").removeAttr("height");
        $(".iframe-class").removeClass("iframe-class-resize");
    }
}

http://jsfiddle.net/TBJ83/
Problem:
As the window is resized smaller, it continually checks the window width and once it hits < 480 px, the code adds a class called iframe-class-resize and sets the width and height to that class. As the window is resized larger, it removes the class once the size hits 480 px. The problem is that setting the width and height attributes adds them directly to the element and not the class itself. Therefore, removing the class does not remove the new width and heights. I tried to force removing the attributes using removeAttr() (commented out above) but that didn't work.
Anyone see where the code above went wrong? Or any suggestions on how to accomplish having a responsive iframe more effectively? The main things that are required are that the iframe has to be inside the

 and the div may not necessarily have a width or height defined. Ideally, the parent div should have the width and height explicitly defined but the way this site is currently setup, that won't always be possible.
Additional:
In case the above wasn't clear enough, try the following to reproduce the issue:

*

*Open up a browser on a desktop machine. I'm using Chrome on a Windows machine. Don't maximize the browser.

*Open up the jsfiddle above (http://jsfiddle.net/TBJ83/). You'll notice that the iframe content spans the entire width of the Preview panel.

*Manually resize the width down until the entire window is < 480px. At this point, the iframe content will be pretty tiny.

*Manually resize the width back up until the entire window is >> 480px. The goal is to have that iframe content to regain the entire width of the Preview panel. Instead, the content is retaining the resized width and height since the .css() function applies css changes directly to elements rather than to the classes.

Thanks in advance!

A: You can do this in about 30 characters. Change:
$(".iframe-class").removeClass("iframe-class-resize")

to:
$(".iframe-class").removeClass("iframe-class-resize").css({ width : '', height : '' })

This will reset the width/height you applied to the element. When you use .css() you add whatever you pass-in to the style attribute of the element. When you pass a blank value, jQuery removes that property from the style attribute of the element.
Here is an updated fiddle: http://jsfiddle.net/TBJ83/3/
EDIT
OK, here's something tweaked for performance (and just some other ways to do things):
$(function () {

    //setup these vars only once since they are static
    var $myIFRAME   = $(".iframe-class"),//unless this collection of elements changes over time, you only need to select them once
        ogWidth     = 700,
        ogHeight    = 600,
        ogRatio     = ogWidth / ogHeight,
        windowWidth = 0,//store windowWidth here, this is just a different way to store this data
        resizeTimer = null;

    function setIFrameSize() {
        if (windowWidth < 480) {

            var parentDivWidth = $myIFRAME.parent().width(),//be aware this will still only get the height of the first element in this set of elements, you'll have to loop over them if you want to support more than one iframe on a page
                newHeight      = (parentDivWidth / ogRatio);

            $myIFRAME.addClass("iframe-class-resize").css({ height : newHeight, width : parentDivWidth });
        } else {
            $myIFRAME.removeClass("iframe-class-resize").css({ width : '', height : '' });
        }
    }

    $(window).resize(function () {

        //only run this once per resize event, if a user drags the window to a different size, this will wait until they finish, then run the resize function
        //this way you don't blow up someone's browser with your resize function running hundreds of times a second
        clearTimeout(resizeTimer);
        resizeTimer = setTimeout(function () {
            //make sure to update windowWidth before calling resize function
            windowWidth = $(window).width();

            setIFrameSize();

        }, 75);

    }).trigger("click");//run this once initially, just a different way to initialize
});

A: This can be done using pure CSS as below:
iframe {
  height: 300px;
  width: 300px;
  resize: both;
  overflow: auto;
}

Set the height and width to the minimum size you want, it only seems to grow, not shrink.

A: This is how I would do it, code is much shorter: http://jsfiddle.net/TBJ83/2/

I did it that way for read-ability, but you could make it even shorter and faster...
function setIFrameSize() {
    f = $("#myframe");
    f[0].setAttribute("width", f.parent().width());
    f[0].setAttribute("height", f.parent().height());
}

One selector, so you only look through the DOM once instead of multiple times.

A: For those using Prestashop, this is how I used the code.
In the cms.tpl file I added the below code:
{if $cms->id==2}

{/if}

Then created a new js file: formj.js and added the below code:
$(function () {

    //setup these vars only once since they are static
    var $myIFRAME   = $(".iframe-class"),//unless this collection of elements changes over time, you only need to select them once
        ogWidth     = 970,
        ogHeight    = 800,
        ogRatio     = ogWidth / ogHeight,
        windowWidth = 0,//store windowWidth here, this is just a different way to store this data
        resizeTimer = null;

    function setIFrameSize() {
        if (windowWidth < 480) {

            var parentDivWidth = $myIFRAME.parent().width(),//be aware this will still only get the height of the first element in this set of elements, you'll have to loop over them if you want to support more than one iframe on a page
                newHeight      = (parentDivWidth / ogRatio);

            $myIFRAME.addClass("iframe-class-resize").css({ height : newHeight, width : parentDivWidth });
        } else {
            $myIFRAME.removeClass("iframe-class-resize").css({ width : '', height : '' });
        }
    }

    $(window).resize(function () {

        //only run this once per resize event, if a user drags the window to a different size, this will wait until they finish, then run the resize function
        //this way you don't blow up someone's browser with your resize function running hundreds of times a second
        clearTimeout(resizeTimer);
        resizeTimer = setTimeout(function () {
            //make sure to update windowWidth before calling resize function
            windowWidth = $(window).width();

            setIFrameSize();

        }, 75);

    }).trigger("click");//run this once initially, just a different way to initialize
});


The 9 Best Places to Pick Pumpkins Around Philly!
Before it's time to pick out Halloween costumes you must first set the fall atmosphere. What says fall is here than pumpkins and jack-0-lanterns for decoration. Whether it be for your kids or the big kid in yourself, going out and picking your own pumpkins is a classic American tradition that everyone can enjoy. So in a city full of parking lots and sparse green spaces where can you find a place to pick a pumpkin? Well it looks like you will have to travel outside of the city. To make things easier for you (as always) we put together a list of the best places to pick pumpkins around Philly. Happy hunting!
Your Guide to the 2019 Philadelphia Science Festival!
The Philadelphia Zoo is Hosting Boo at the Zoo, an Overnight Halloween Experience for Kids!
Piazza's Opening The New Pod Park Next With Over a Dozen Food Vendors and Roof Deck!
The Daily Meal Names Ishkabibble's One of America's Best Hole-in-the-Wall Restaurants!


Here for the Wrong Reasons | Weekly commentary on all things Bachelor.
Weekly commentary on all things Bachelor.
Take our poll: Who's here for the wrong reasons?
Take our poll and let your voice be heard, Bachelor Nation! Results will be forwarded directly to Chris Harrison.
You dolphinately don't want to miss our Bachelor recap podcast!
Y'all. We have a blog.
Welcome back, rose ceremony lovers. The newest season is upon us.
All of last year, as we podcasted our way through Ben's and Jojo's seasons, and then Bachelor In Paradise (ugh…I'm still recovering from that. PS– word on the street is that Jamanda (Amandosh?) has split. That's a shocker. Will she ever be able to wash the sweat out of her sheets?), we kept saying that we needed a blog to post links to articles, offer further commentary on each episode (because really– how is an hour long podcast ever enough?), and even bring in some exciting listener polls, charts, and graphs.
And so, here we are. We have a blog. Our microphone is ready for another season of podcasting. And Nick Viall is the Bachelor.
We'll talk about this more on the podcast (obviously), but we actually only know Nick from Bachelor in Paradise (relatively speaking). I (Anna) watched him on both Andi's and Kaitlyn's seasons, but I bowed out of those early. The Bachelorette isn't always my fave, as I've admitted on the podcast– the boys are so boring compared to the ladies on the Bachelor– and so, in my pre-podcast years, I'd often start a season but stop watching about halfway through.
So, long story short, having only really seen Nick on Bachelor in Paradise– we're excited. He's witty and smart, with a sarcastic sense of humor that I don't think we've seen in a bachelor since…gosh, Matt Grant maybe?! For a long time (particularly after the disaster that was Juan Pablo), it seemed like the producers were steering the show choices in the direction of a Ken Doll-esque Bachelor– attractive, sure, but also bland, basic, and in some cases, almost incoherent (Chris Soules, I love you, but you know I'm looking at you buddy).
I kind of think of Nick as the male Kaitlyn– sassier, more sexual, and definitely more sarcastic than the show's typical choice of suitor. I'm *hoping* that this means we're in for an interesting season.
Welcome back, rose lovers. It's going to be a wild ride.


Some E-coli bacteria can take the heat, according to researchers from the University of Alberta.
Here's a great reason to turn up the heat on your grill.
A group of researchers from the University of Alberta and China's Huazhong Agricultural University found that cooking ground beef at the 160-degree F (71 degrees C) temperature recommended by government officials in the U.S. and Canada may not be hot enough to kill all the strains of Escherichia coli (E. coli), according to a research article.
E. coli, a bacteria that's found in the gut of both animals and humans, is not always harmful. However, some strains, such as O157, can cause kidney failure or even death, according to a news release from the University of Alberta.
According to the research article, the scientists discovered 16 genes in fresh meat that are extremely heat-resistant. These genes make up about 2% of the entire E. coli strains.
Lynn McMullen and Michael Gänzle, food microbiologists at the University of Alberta, along with several graduate students, led the E. coli research. According to the statement from the University, they first became aware of the inconsistent behavior of E. coli eight years ago.
In 2008, McMullen and Gänzle asked a student to look at the differences amongst organisms in a batch of E. coli from ground beef. Elena Dlusskaya, the student who conducted the experiment, found that one organism survived in the beef despite being in 140 degree F heat. The results were odd, considering most E.coli is killed in a matter of seconds after a certain temperature is applied. McMullen and her colleagues decided to investigate.
Now, the team is researching how problematic the occasional survival is across strains of E. coli. The findings call the temperature recommendation of cooking ground beef to a minimum of 160 degrees F (71 degrees C) into question as well as suggesting heat resistance could be the reason for sporadic cases of E. coli.


text:
Documentary shows worldwide struggle to educate girls
By Merle Exit Posted on April 8, 2016
By Merle Exit
While many American students spend their days dreaming of summer vacation and not going to school, plenty of young people around the world, particularly girls, struggle to receive an education.
Late last month, the Briarwood Action Network sponsored a screening of "Girl Rising," a documentary depicting young women who had to overcome challenges to go to school, in honor of Women's History Month.
In the film, nine of these girls' stories — each one written by a well-known woman author from her country — are narrated by Hollywood A-listers, including Meryl Streep, Anne Hathaway and Liam Neeson.
"Girl Rising" was released in 2013 and documents the sad state of educational opportunities for young women around the globe. According to the film, there are 33 million fewer girls than boys in primary school.
One of those girls is Wadley, from Haiti, who in the aftermath of her country's devastating earthquake in 2010, is determined to attend classes despite the fact that her family cannot afford to pay the tuition.
During the film, Wadley expresses her wish that some of the essays she was required to memorize and recite in front of the class had been written by women.
It is a scene that resonated with social studies teacher Melissa Aguirre, who works at JHS 217 in Briarwood.
"At our school we have novels where the protagonists are strong women who are not only leading their families, but seeking education rights," Aguirre said.
Other stories told include Senna's, a Peruvian girl who writes poetry in tribute to her father, who made her attend school. In Nepal, Suma was able to free herself from a life of forced labor by learning to read and write.
Amina, from Afghanistan, does not show her face for fear of her own safety. When she was 11, Amina's father sold her to a relative to be married. He used the money to purchase a car for his son. Despite pregnancy at the age of 12, Amina wants to learn and stops at nothing to get her education.
Mala Panday, is the principal of the Young Women's Leadership School of Queens, part of a network of all-girls public secondary schools that aims to empower girls to fulfill their learning and leadership potential.
"We are in the process of showing this movie to these young women at our school," Panday said. "These themes, clips and movies are not a shock. We have heard speakers from all over the world talk about genital female mutilation and the effect it has on women across the world as well as the government's control over our bodies."
Panday stressed the importance of girls having a mentor.
Both Aguirre and Panday commented that because a number of public schools have children of immigrants, educators are finding that there is a lack of communication at home as these children need to understand the language of their parents in order to teach English to them.
Author Talk with Sergey Kadinsky at the BHS Castle in Fort Totten
Bayside Historical Society
Stillness Concert by Sputter Box
Art House Astoria

redpajama_set_name: RedPajamaCommonCrawl


text:
Neither left nor right, but international environmentalism: Australia reflections part 8
I'm reblogging this compelling post by Jeff Ollerton, Professor of Biodiversity at the University of Northampton. I share Jeff's immense frustration at the relentless demonisation of "The Other" that not only characterises so much of our political discourse but has come to define how we communicate with each other in general. Not everyone with whom we disagree politically is, as some would have it, a sociopath or a simpleton. It is refreshing to see that Jeff — whose politics, like my own, are very firmly left of centre — foregoes the usual "Boris is a buffoon" sloganeering to remind us that some members of Johnson's family have strong environmentalist credentials.
As Jeff puts it so well,
"…there are plenty of historical and current examples of rapacious right-wing and left-wing governments, and also examples of such governments being highly pro-active at reducing their country's environmental impact. The one thing that seems to me to be environmentally damaging is a rigid ideology that is followed through regardless of where it is positioned."
Jeff Ollerton's Biodiversity Blog
The NASA Earth Observatory reported this week that "explosive fire activity" has caused smoke from the Australian bushfires to enter the stratosphere and be carried half way around the world. That smoke is currently creating hazy skies and colourful sunrises and sunsets across South America. In the coming months the smoke will complete a full circuit and arrive back in Australia, and then continue onwards … for who knows how long?
Nothing I've read this week sums up better the fact that the world's environmental challenges, including climate change, are global in scale and scope. They therefore require global initiatives to solve. But as I'll argue below, equating "green" politics with the left and "anti-environmental" policies with the right is an unhelpful characterisation.
Despite the need for global action, the world's political landscape seems to be going in the opposite direction. Inward-looking, right-wing populism is on the rise, and governments…
Author Philip MoriartyPosted on January 15, 2020 January 15, 2020 Categories climate change, PoliticsTags Jeff Ollerton1 Comment on Neither left nor right, but international environmentalism: Australia reflections part 8
Neil Peart (1952 – 2020)
Suddenly you were gone
From all the lives you left your mark upon…
From Afterimage, Track 2 of Grace Under Pressure.
This one hurts. RIP Neil Peart. pic.twitter.com/e1KjUmBhFY
— Reverb (@reverb) January 10, 2020
Yes, this one hurts.
Author Philip MoriartyPosted on January 11, 2020 January 11, 2020 Categories Lost for words, Neil Peart, Rush1 Comment on Neil Peart (1952 – 2020)
Random Acts Of Selfless Kindness
The piece below features in this week's Times Higher Education as part of an article entitled "Is these still a place for kindness in today's harsh academic environment?". My original title was that above, which is a play on Jack Womack's almost criminally overlooked "Random Acts of Senseless Violence", a cyberpunk-esque tale of a crumbling society. Given the lack of impact of Womack's meisterwerk, the THE sub-editors were absolutely right to re-title my contribution to the article as "Kicking Against The Me, Me, Me". And, as ever, the piece was improved immensely by Paul Jump's edits. I'm posting my contribution to the article here for those who don't have a subscription to the THE.
It's exactly one month to Christmas Day as I write this. Academics and students alike should be drafting their letters to Santa and looking forward to the festive season after toiling all term in lecture theatres, seminar rooms, workshops and – very occasionally – libraries.
Except that today is also the first day of the latest round of strike action by members of the UK's University and College Union. This time, the issue isn't just pensions: the strike is also in protest at pay, equality, casualisation and workloads. But universities' reactions are familiar from the previous strike in 2018, with reports of draconian measures being taken against not only striking staff but also, unforgivably, students who support them.
It is clear that senior management and rank-and-file staff are unlikely to be on each other's Christmas card lists this year. Nonetheless, in these days of ever-increasing and ever-more-infuriating corporatisation and depersonalisation of universities, it's important not to lose sight of the collegiality that still exists, and the sense of community that is fostered when students and staff (of all stripes – from the cleaners to the professoriate) look out for each other.
This has certainly been the case during my 25 years in the University of Nottingham's School of Physics and Astronomy. Indeed, the often-clueless, metrics-driven management style foisted upon us from on high results in an "us versus them" mentality that only serves to bring us even closer together. I hesitate to use the hoary old Dunkirk spirit cliché, especially in these days of Brexit-inspired Little-Englander fervour, but it certainly captures that sense of fighting back from the chalkface. In solidarity.
It's the little things that matter most: those seemingly small acts that cultivate a culture of kindness, kicking against the me, me, me of metrics and the tediously relentless pseudostatistics of league tables. I've lost count of the number of times that students and staff have gone the extra mile to brighten up someone else's day, week, month or year. Examples range from the tea-room coordinators who put aside particular fruit, biscuits and cakes because they remember just what each member of staff likes with their beverage of choice for "elevenses" (Anna, we salute you!) to the tutees who turn up with gifts, cards and messages of thanks for their tutor; the anonymous faces in the lecture theatre who take the time to nominate members of staff for various teaching awards; and the graduates who email unexpectedly, years after they finished their degrees, to describe how fondly and gratefully they look back on their time at university.
Sometimes these random acts of kindness make you smile. And other times, I've been moved to tears. A couple of years ago, I was in the middle of a phone call when a knock on the door interrupted the conversation.
"Just one second!" I called out, and finished the call as quickly as I could. When I opened the door, there was no one there. But at my feet there was a big box of chocolates and a card containing the simple message: "Thanks for everything". It was from a student who was severely autistic, with whom I had communicated almost exclusively via email over the years of their degree.
Forget my latest publication, or research grant, or citation count. That simple message meant so much more.
Author Philip MoriartyPosted on December 22, 2019 December 22, 2019 Categories academia, Christmas cheer, Education, UCU, universitiesTags Paul Jump, Times Higher Education2 Comments on Random Acts Of Selfless Kindness
Bowled Over in Pakistan — a guest post from Oli Gordon
In these days of "Rule Britannia" populism, "Get Brexit Done", and rampant Little Englander fervour, it's great to have a guest post that highlights just how science transcends small-minded nationalism and crosses borders. Oli Gordon, a second year PhD in the Nanoscience Group here at Nottingham, recently visited Pakistan for the 2nd International Conference on Nanoscience and Nanotechnology (ICONN-2019), along with eight other British Council-sponsored PhD researchers from across the UK. Over to you, Oli…
Sitting at my desk on an otherwise normal day, I received a rather curious email. It asked if, fully funded by the British Council in Pakistan, I wished to give a talk at a nanoscience conference at LUMS University Lahore, sight-see, meet students and researchers, and travel with eight (or more?) other PhDs from different UK institutions with distance ranging from UCL to Glasgow and Strathclyde. There would of course be 5* hotels, top tier flights, amazing food, and armed police escorts, all while being a UK dignitary and taken round by the same people that hosted the Duke and Duchess of Cambridge a couple of weeks prior to the visit.
"Ahhh… hmmm… yes?"
One quick day trip to Gerry's Visas in Birmingham later, I arrived at Manchester Airport not quite knowing what I had got myself in for. After a short layover in Qatar (plus a few hours to sleep off the jet lag!) I found myself in Lahore in the company of the other researchers and our front-facing representatives from the British Council; Mubbashir, Hajira and Namra.
Hosted at LUMS, the ICONN nanoscience and nanotechnology conference contained an absolutely packed two days of talks, and was attended by several hundred people, including a pleasingly large number of university students. I was invited to give a 12 minute talk on the PhD I do with the nanoscience group here in Nottingham, applying the latest in machine learning technologies to automatically run the millions of pounds of probes we use for our research. (Going back through this blog, you may find a post I wrote on this topic during a summer internship during my undergraduate here).
My expectations of the conference were for it to be like a nanoscience conference in the UK –far-out future technologies and new-found properties of surfaces, using eye-wateringly expensive equipment. Instead, local research was specific, and highly focused on practical solutions to the immediate issues facing Pakistan: pollution, healthcare, clean drinking water and reliable battery storage. LUMS even offers space and expertise to start-up companies working towards this end.
The whole experience gave us a real taste of Pakistani science and was a real joy. In particular, the conference, visits to other universities, and allowing us to judge the conference posters during the cultural night at LUMS gave us plenty of chances to speak to loads of students, PhDs and researchers from up and down the country. This in particular was quite eye-opening to me – some of them explained that low funding meant that they often have to travel and pay out of pocket to use equipment and do analysis that we could routinely do in the first year undergraduate lab in Nottingham. Science is held in incredibly high regard in Pakistan, and I can only admire people doing work for the immediate benefit of their nation, even when it comes at their own expense. I must also mention how touching it was to see how enthusiastic and just proud the students were to be involved with science in general.
This conference only made up two days of the week we had, though. Besides the university visits, we also had time to do some sightseeing. Lahore fort and the old walled city was a real gem, as well as having dinner by the largest Mosque in the country – capable of holding 100,000 worshippers. We also squeezed in a visit to the British Council HQ, where they support people taking UK educational qualifications. Their library is wonderful (and open to international e-members) – it is a bustling, cross-cultural community hub with a real international spirit, and the British Council should be proud of what they have created there.
I will, however, confess that the real highlight of the trip for me was playing cricket at COMSAT University Lahore. The first thing we saw at COMSAT was their cricket green and pavilion – the faculty and cricket team were more than happy to arrange a five-over game with us over lunch. Unfortunately, I (captaining) found myself run out trying to steal a quick single…
But after some long goodbyes and games of ping-pong in our hotel, I found myself back in Manchester and welcomed by the UK's torrential rain. It had to end at some point!
I need to say an absolutely massive thank you to Walther Schwarzacher at the University of Bristol for arranging the trip (plus his great talk on clouds), as well as to Mubbashir, Hajira, Namra, and the rest of the British Council team for their incredible hospitality. This trip really left me feeling genuinely quite inspired about just how much of a privilege and pleasure research is, and looking forward to getting to my lab to do more.
"A memorable two days international conference on nanoscience and nanotechnology (ICONN-2019) at LUMS in collaboration with the British Council and NUST… Wonderful opportunity to present and awarded by Prof Walther."#photooftheday #OSALUMS pic.twitter.com/Cmer5fTxse
— Office of Student Affairs LUMS (@osalums) December 3, 2019
The moral of the story? Check your emails!
…and here's a clip of Oli posted by The British Council shortly after the ICONN 2019 conference.
We caught up with Oliver Gardon @UniofNottingham after ICONN 2019. Oliver was part of the student researches from the UK visiting Pakistan.#pakukeducationgateway pic.twitter.com/yeJtWBTzsH
— British Council (@pkBritish) November 5, 2019
Author Philip MoriartyPosted on December 14, 2019 December 14, 2019 Categories Communicating Science, nanoscienceTags British Council, ICONN-2019, LUMS, Oliver Gordon, Walter SchwarzacherLeave a comment on Bowled Over in Pakistan — a guest post from Oli Gordon
Let's pick(et) our battles wisely
VROOMFONDEL: We demand that machine not be allowed to think about this problem!
DEEP THOUGHT: If I might make an observation…
MAJIKTHISE: We'll go on strike!
VROOMFONDEL: That's right. You'll have a national philosophers' strike on your hands.
DEEP THOUGHT: Who will that inconvenience?
MAJIKTHISE: Never you mind who it'll inconvenience you box of black legging binary bits! It'll hurt, buster! It'll hurt!
From Fit The Fourth of The Hitch-Hiker's Guide To The Galaxy, Douglas Adams. Broadcast on BBC Radio 4, March 29 1978.
I suspect that this is going to be a contentious post.
Having spent my time on the picket lines over the last eight (non-)working days…
Come on @UoN_Physics. We need as many of you as poss, out here fighting for our pensions, pay and casualisation. The more we have the stronger our fight and quicker this is sorted!!! The humanities are showing us up with their solidarity. #uss @ucu @UoNUCU pic.twitter.com/nSBO1jtTys
— Tony Padilla 🌹 #VoteLabour 🌹 (@DrTonyPadilla) November 28, 2019
…and last year,
UUK may have sent in the rain but we're still down the picket. Make it worthwhile people: don't cross picket today and join the strike @UoNUCU @UniofNottingham @UoN_Physics pic.twitter.com/YvNm9jjT72
— Tony Padilla 🌹 #VoteLabour 🌹 (@DrTonyPadilla) March 12, 2018
… I am acutely aware of, and deeply sympathetic to, the issues underpinning the strike. The speeches at yesterday's closing rally — including that from the ever-impressive Lilian Greenwood, Labour MP for Nottingham South (and someone for whom I will again be voting in a week's time) — brought home the exceptionally precarious and deeply unfair working conditions that so many university employees endure under zero hours contracts. Even Spiked! magazine — whose coverage of universities usually fixates on hysterical fantasies about the infestation of evil, leftist, free-speech-suppressing, no-platforming Cultural Marxists indoctrinating our children — saw fit to publish a rousing article supporting the strikes.
There has similarly been a series of compelling and affecting pieces over the last few weeks that drive home the damage that the ever-accelerating corporatisation and marketisation of our universities is doing to education. One of the more comprehensive analyses I've seen is The Seven Deadly Sins of Marketisation in British Higher Education by Lee Jones, Reader in International Politics at Queen Mary University of London. Thoroughly recommended.
But what have these eight days on strike actually achieved?
Yes, I know that we've demonstrated a great deal of solidarity and that the time on the picket lines has been morale-boosting (and at least it wasn't as sodding cold as last year). But still, pragmatically, what did we achieve?
Here at Nottingham, at least, the response from the "powers that be" has been a deafening silence. (And Nottingham's hardly alone in this.) For many departments, including my own, it's been business as usual; the car park has been full, lectures and lab sessions went ahead with nary a disturbance, and coursework was dutifully marked and returned to students. This is not to downplay in any way, I hasten to add, the heartening efforts of my UCU colleagues and our incredibly supportive students, including, in particular, those who occupied UoN's iconic Trent Building…
#UoN Trent Building #occupation treach-ins #UCUstrike #UCUStrikesBack @ucu @UoNUCU pic.twitter.com/cMNZVyotRl
— Mark Jago is on strike (@Mark_Jago) December 4, 2019
And I've also got to highlight the incredible energy, charisma, and tenacity of Matt Green, the President of Nottingham's UCU Committee, who has been as outstanding as ever.
But the upshot of our eight day strike is that …drum roll… the UCU is going to call for yet more strikes in January. The argument is that we've got to keep the pressure up. But who, exactly, are we pressuring? Or, as Deep Thought puts it in that salient quote that opens this post, who, exactly, are we inconveniencing? We've hardly brought senior university management to their knees, have we?
For those who, like me, were on the picket lines — and, indeed, for those who weren't — ask yourself this: which of the options below hurts the university more? Which is more likely to cause some sleepless nights for the senior executive?
A. An empty seminar room or lecture theatre,
B. A five- or ten-strong picket line chanting at a university entrance,
C. A low score in the National Student Survey/ low league table ranking/ damaging media coverage for their university?
Not only did we have PVCs and other senior staff crossing picket lines with wild abandon, but quite a few union members — and, indeed, some erstwhile union reps — didn't strike, let alone picket. University management will be well aware of this lack of engagement with the strike either now or when the figures for non-pay in January are returned. They save on the salary bill and they can rest easy that the impact on students' progression is minimal, at best, and negligible, at worst.
Because what most matters to universities is their brand. If we want to have greater influence and bargaining power I would argue that we have to be a little more canny in our tactics and exploit exactly the corporatisation and marketisation culture we criticise and that underpins the behaviour of the 21st century university. (I've written before about the frustrating tendency of the left to not always be entirely cognisant of the value of "optics" and PR.)
Sceptical? Here are a few examples of brand management that might help to make my case…
Along with a number of APM colleagues, I spent six months chasing up a (very modest) honorarium payment for an invited speaker. Six months. The speaker eventually reached the point where, exasperated, she tweeted about the University's lack of payment to her tens of thousands of followers (tagging in @UniOfNottingham). Within minutes she had a response from UoN, and within days the money was in her account.
Down the road, at Nottingham-Trent University (Guardian University Of The Year 2019), Liz Morrish was subject to disciplinary proceedings when a post hit 10,000 views on Liz's own blog and trended at the Times Higher website, as described in the article linked in the tweet below.
Why the audit culture made me quit my job in a UK university. https://t.co/n2Y71KJJj2 via @timeshighered
— Dr Liz Morrish (@lizmorrish) May 7, 2017
And Warwick hardly covered itself in glory in this appalling case because they placed their brand management well ahead of students' safety. That's how engrained the importance of protecting the university brand can be.
"The top six universities are like the most beautiful cities in the world, reputable even if they have failing sewers, arrogant mayors and dodgy no-go areas…A folklore builds up around them, as do money and fans."
(From Beyond the super-brands, universities are strengthening their positions, Times Higher Education)
So let's stop trying to repeatedly use the same seventies strategies to attack a 21st century problem. Let's think a little bit more about what really matters to university managers.
It's not the students*.
It's not the staff.
It's the brand.
* …although it's certainly the student numbers.
Author Philip MoriartyPosted on December 5, 2019 December 5, 2019 Categories academia, Brands, early career researchers, Education, UCU, universities4 Comments on Let's pick(et) our battles wisely
Radio, Someone Still Loves You…
I'd sit alone and watch your light
My only friend through teenage nights
And everything I had to know
I heard it on my radio
From "Radio Ga Ga", Track 1, Side 1 of Queen's "The Works" (EMI Capitol 1984).
Written by Roger Taylor.
I've been delighted by the response to the "Joy Of Radio", and accompanying "Resonant Frequency" [1], video that Brady uploaded to Sixty Symbols a couple of weeks ago. In addition to the very many kind, supportive, and heart-warming messages left under the video — which have done a lot to almost restore my faith in the humanity of YT's comment sections — I've received a number of affecting e-mails telling me how much the video brought back happy memories.
One of these came from Rocco Cuffaro, a third year Mathematical Physics student here at Nottingham. Rocco saw the video, immediately thought of his crystal-radio-loving granddad (who is eighty years young), and emailed him a link to the video. Rocco's granddad's wonderfully engaging response is below. Thank you both for sharing this with me (and for giving me permission to post it here). Over to you, Rocco's granddad…
After you and I built the Meccano type of Rocket steam engine it was my intention for you and I to build a crystal set exactly as the simple circuit in Prof Moriarty's book. For the coil we would have used the cardboard centre of a toilet roll as a former. For the crystal I would have used a crystal from a ex war time radar if I still had some or more likely buy a silicon diode from Maplins. I have or did have plenty of variable vane capacitors that we could have used. The box of capacitors that Prof Moriarty showed us included some wide vane capacitors that were probably I guess ex transmitter components.
I very much like his approach with the experiment set up live and using a corroded penny with a wire whisker very much as it was with crystals in the early days before my time. Just a hook up of components rather than a workshop prepared demonstration.The early sets used a crystal and a wire whisker and just as he said there were many swear words so it was when people tried to find the right spot on the crystal and were then afraid to jog the thing.
I attended an exhibition at the IET's home in Savoy place in London( I am still a member but thinking of cancelling as I am in information overload with so many and varied things to read) which I believe marked the anniversary of the broadcast station 2LO which was the forerunner of the BBC. Many crystal sets from way back were on display and included some with more complex circuits that I was not aware of until then.
Before we became the affluent society in the 1960s I knew the elderly lady that occupied the old observatory tower in Falmouth. There was not much money around in those days so I built her a crystal set in an old cigar box and used an ex service radar diode for the crystal. The aerial was one to envy in that situation. A vertical wire 50 feet down the side of the building. The lady came from London and was thrilled to hear Big Ben for the first time in years. That happened not very long after the war.
When Nan and I lived in Ware we had a reel to reel tape recorder. I do not recall how it came about but I discovered that if I put a wire in the microphone socket the recorder thought it was a radio and picket up a strong radio signal of one programme only from obviously Brookmans Park not a million miles away. This can easily happen if all the real and stray capacitances and inductances etc allow this to happen with some non-linearity in a component giving that rectifier action that Prof Moriarty was demonstrating. I was able to record a complete set of the Gilbert and Sullivan operettas in this way.
The converse of this phenomena is modulation and also cross modulation. At Lands End Radio the receiving aerials were close to the building housing the receivers. The transmit aerials were not very far away by a couple of fields. A problem arose when unwanted radio stations were splashing across the entire spectrum of the receivers (around and either side of 2182khz) [Editor's note — see footnote #2 below]. I traced this to a dustbin (!) in the grounds of the station. The lid was placed lightly over the bin. On removing and replacing the lid the problem cleared. This was in my view caused by rust around the edge acting like the penny and whisker in Prof Moriarty's experiment in reverse. The bin would have been receiving a very strong signal from the transmitting aerials of course plus a multitude of other radio signals from all over the place. The bin was transmitting a cross modulation of the lot and dumping it on the receiver aerial system.
I will wind up there except to mention that there were a number of interesting cases of interference including a grandfather clock with no electrical connection interfering with television and the static from a lady combing her hair interfering with television through a party wall.(not mine but a colleagues) The frequencies in use then were much more susceptible to interference than now.
[1] I only realised this after reading the comments, but, remarkably, when I hit the desk to "kick start" the crystal radio at the start of the Resonant Frequency video, the song that blasts out is…Queen's Radio Ga Ga. I was entirely oblivious to this while making the video. (This is a good thing. I'm already as overly enthusiastic as a litter of labrador puppies in that video. (Those five coffees before Brady arrived probably didn't help.) If I had realised at the time that we'd picked up a broadcast of Radio Ga Ga I may well have melted down with excitement…)
[2] I deliberately set up the simulation of the crystal radio described in this post to mimic this "bleeding" of signals across the frequency spectrum.
Author Philip MoriartyPosted on December 3, 2019 December 3, 2019 Categories Radio, Sixty SymbolsTags Brady Haran, Crystal radio, Modulation, Queen, Radio GaGa, Rocco CuffaroLeave a comment on Radio, Someone Still Loves You…


Microsoft creative director Adam Orth, who angered the Twitterverse last week with a rant about always-on technology, is no longer working for Redmond.
Microsoft creative director Adam Orth, who angered the Twitterverse last week with a rant about always-on technology, is no longer working for Redmond, Game Informer reported.
Citing anonymous sources, Game Informer said Orth left Microsoft after the micro-blogging debacle, but the site was unable to confirm whether the resignation was voluntary or forced.
Microsoft declined to comment on the issue; Orth did not immediately respond a request for comment.
Last month, leaked screen shots of a new Xbox console tipped an always-on, always-connected approach, though Microsoft has not confirmed any details about its next-gen console. In the wake of the disastrous SimCity launch, which also embraced always on, the blogosphere and Twitter were abuzz with commentary from those who were not pleased by the prospect of an "always on" Xbox.
Orth addressed those critics on Twitter. "I want every device to be 'always on,'" he wrote in an April 4 message. That garnered a response from user @TheonlyAlexW, who argued for those gamers without Internet access. "They would be screwed," he wrote to Orth.
"Those people should definitely get with the times and get the internet," Orth said. "It's awesome."
Orth's tweets are private, but Game Informer posted a screenshot of his exchanges, including one with user @manveerheir, who also defended players who don't have reliable Web access.
"Sorry, I don't get the drama around having an 'always on' console. Every device now is 'always on'. That's the world we live in," Orth wrote last week, capping the tweet with the #dealwithit hashtag.
When another user brought up SimCity and similar troubles surrounding Diablo III, Orth countered by saying that electricity goes out, too. The conversation took an offensive turn, though, when the Twitter user pointed out that Orth has lived in Los Angeles, San Francisco, and Seattle — "very connected places" — while plenty of Xbox users are playing games in Janesville, Wis., or Blacksburg, Va., where broadband access can be spotty.
"Why on earth would I live there?" Orth retorted.
"We apologize for the inappropriate comments made by an employee on Twitter yesterday. This person is not a spokesperson for Microsoft, and his personal views do not reflect the customers centric approach we take to our products or how we would communicate directly with our loyal consumers. We are very sorry if this offended anyone, however we have not made any announcements about our product roadmap, and have no further comment on this matter."
Orth's comments may have cost him his job, but it's the closest Xbox fans have gotten to confirmation of new console features. Earlier today, The Verge reported that the new Xbox may include television integration. Users may be able to connect a cable box to the Xbox via HDMI, allowing Microsoft's machine to overlay a user interface on top of an existing TV channel, much like Google TV, the blog said.
Editor's Note: This story was updated at 2:10 p.m. Eastern.


text:
package com.amazonaws.services.sns.model.transform;

import java.util.Map;
import javax.annotation.Generated;

import com.amazonaws.SdkClientException;
import com.amazonaws.Request;
import com.amazonaws.DefaultRequest;
import com.amazonaws.http.HttpMethodName;
import com.amazonaws.services.sns.model.*;
import com.amazonaws.transform.Marshaller;
import com.amazonaws.util.StringUtils;

/**
 * SubscribeRequest Marshaller
 */

@Generated("com.amazonaws:aws-java-sdk-code-generator")
public class SubscribeRequestMarshaller implements Marshaller<Request<SubscribeRequest>, SubscribeRequest> {

    public Request<SubscribeRequest> marshall(SubscribeRequest subscribeRequest) {

        if (subscribeRequest == null) {
            throw new SdkClientException("Invalid argument passed to marshall(...)");
        }

        Request<SubscribeRequest> request = new DefaultRequest<SubscribeRequest>(subscribeRequest, "AmazonSNS");
        request.addParameter("Action", "Subscribe");
        request.addParameter("Version", "2010-03-31");
        request.setHttpMethod(HttpMethodName.POST);

        if (subscribeRequest.getTopicArn() != null) {
            request.addParameter("TopicArn", StringUtils.fromString(subscribeRequest.getTopicArn()));
        }

        if (subscribeRequest.getProtocol() != null) {
            request.addParameter("Protocol", StringUtils.fromString(subscribeRequest.getProtocol()));
        }

        if (subscribeRequest.getEndpoint() != null) {
            request.addParameter("Endpoint", StringUtils.fromString(subscribeRequest.getEndpoint()));
        }

        java.util.Map<String, String> attributes = subscribeRequest.getAttributes();
        int attributesListIndex = 1;
        for (Map.Entry<String, String> entry : attributes.entrySet()) {
            if (entry.getKey() != null) {
                request.addParameter("Attributes.entry." + attributesListIndex + ".key", StringUtils.fromString(entry.getKey()));
            }
            if (entry.getValue() != null) {
                request.addParameter("Attributes.entry." + attributesListIndex + ".value", StringUtils.fromString(entry.getValue()));
            }
            attributesListIndex++;
        }

        if (subscribeRequest.getReturnSubscriptionArn() != null) {
            request.addParameter("ReturnSubscriptionArn", StringUtils.fromBoolean(subscribeRequest.getReturnSubscriptionArn()));
        }

        return request;
    }

}

redpajama_set_name: RedPajamaGithub


Graphics Designing is one of the most prominent new age career segment in India and abroad. Since 2012, graphic designers have held almost 259,500 jobs in America. This sector is also growing leaps and bounds in India from small towns to smart cities requirement of good graphic designers are always there in get me know state.
Chennai is one of the faster growing cities in southern India and there are many good institutes provide graphics designing courses in chennai ranging from degree to short term certificate courses in Graphics Designing. If you see the local results of Google for this keyword 'Best Graphics designing courses in chennai" you easily get names of many institutes in results. To name a few Web D School in Vadapalani (Opp Bus Terminus), Chennai , VFX India Arumbakkam, DreamZone in annanagar, kolathur , mylapour,Poonamallee etc are there. Apart from these if you are looking for best Graphics Designing courses in chennai and want to have an experience of national wide media and design training institute you can even look for 'Image Institutes' as they run their training programme from various locations like Adyar, Alwarpet, Anna Nagar, Perambur, T.Nagar, Vadapalani and Velachery. According to a popular education search portal Shiksha.com FIDA the Design school at Kilpauk, Reliance Education at Anna Nagar, ICAT in mylapour and Arena Animation T. Nagar can also be checked before selecting the best Graphics Designing Courses in Chennai.
The industry has a high level of fragmentation, as it is comprised of many small, independently operated graphic designers and freelance graphic designers. According to industry statistics , only 23% of B.C. graphic design service establishments have formal employees. Hence if you want to do graphics designers course in Chennai be prepared to have your career as Freelancer too.
But while choosing the best among st all I am making my opinions very clear that best institute is not compulsory the one who is coming top in search results. For ticking on the best amongst all, use the 5 level parameters testing of judging the overall quality of institute.
Well, if you still have any doubts feel free to email me on principal@veda-edu.com. I normally reply the career related questions in 2 to 3 working days. Be assured I shall quickly try to solve your doubts.
Like to help thousands of students worldwide who want to make their good career in AVGC industry.
Next PostNext Which are the best ways to learn the Pay Per Click ads?


text:
Anthony Athanas (July 28, 1911 – May 20, 2005) was a multi-millionaire Albanian American restaurateur and philanthropist. His restaurants included Anthony's Pier 4, known throughout United States. In 1976 the National Restaurant Association named him Restaurateur of the Year.

Life
Born in Korçë, southern Albania, then part of the Manastir Vilayet of the Ottoman Empire, on July 28, 1911, Athanas and his mother Evangeline traveled on a donkey to a port and emigrated to Bedford, New York in 1915–16, where his father, who was a mason, and siblings had settled. At the age of thirteen Athanas left school and worked in several restaurants until 1938, when he bought his first restaurant: Anthony's Hawthorne Café in Lynn, Massachusetts, which by the early 1950s had become the highest-grossing restaurant in Massachusetts, with profits of more than $1 million annually. The Lynn restaurant closed in 2008. In 1963, he opened Anthony's Pier 4, which by the early 1980s was grossing about $12 million annually and was the highest-grossing restaurant in the United States, though it closed in August 2013. His other restaurants included the Hawthorne by-the-sea Tavern and The General Glover House in Swampscott, Massachusetts (The General Glover House closed in the late 1990s), and Anthony's Cummaquid Inn in Yarmouth Port. Cummaquid Inn closed in 2016.  Hawthorne-By-The-Sea Tavern in Swampscott, MA is the only remaining of his restaurants.

Athanas had also served as president of Massachusetts's Restaurant Association, a member of the board of the National Restaurant Association, while in 1976 he was named "Restaurateur of the Year". In 1999 during the Kosovo War, he became a member of the congressional delegation of the United States, Albania, Kosovo, and Macedonia. Although Athanas had no formal education he was a popular lecturer at Harvard Business School, the University of New Hampshire and Cornell University, and was awarded the "Horatio Alger Award" by the Horatio Alger Association of Distinguished Americans in 1978. He died at his Swampscott home on May 20, 2005, of Alzheimer's disease at the age of 93. The funeral was held at St. George Albanian Orthodox Cathedral in South Boston.

References

1911 births
2005 deaths
People from Korçë
People from Manastir vilayet
Albanian emigrants to the United States
People from Swampscott, Massachusetts
American restaurateurs
Deaths from Alzheimer's disease
Neurological disease deaths in Massachusetts
American people of Albanian descent

redpajama_set_name: RedPajamaWikipedia


text:
Symposium and Mini-Symposium
Dysregulation of Mammalian Target of Rapamycin Signaling in Mouse Models of Autism
Kimberly M. Huber, Eric Klann, Mauro Costa-Mattioli and R. Suzanne Zukin
Journal of Neuroscience 14 October 2015, 35 (41) 13836-13842; DOI: https://doi.org/10.1523/JNEUROSCI.2656-15.2015
Kimberly M. Huber
1Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, Texas 75390,
Eric Klann
2Center for Neural Science, New York University, New York, New York 10003,
Mauro Costa-Mattioli
3Department of Neuroscience, Baylor College of Medicine, Houston, Texas 77030, and
R. Suzanne Zukin
4Dominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, New York, New York 10461
The mammalian target of rapamycin (mTOR) is a central regulator of a diverse array of cellular processes, including cell growth, proliferation, autophagy, translation, and actin polymerization. Components of the mTOR cascade are present at synapses and influence synaptic plasticity and spine morphogenesis. A prevailing view is that the study of mTOR and its role in autism spectrum disorders (ASDs) will elucidate the molecular mechanisms by which mTOR regulates neuronal function under physiological and pathological conditions. Although many ASDs arise as a result of mutations in genes with multiple molecular functions, they appear to converge on common biological pathways that give rise to autism-relevant behaviors. Dysregulation of mTOR signaling has been identified as a phenotypic feature common to fragile X syndrome, tuberous sclerosis complex 1 and 2, neurofibromatosis 1, phosphatase and tensin homolog, and potentially Rett syndrome. Below are a summary of topics covered in a symposium that presents dysregulation of mTOR as a unifying theme in a subset of ASDs.
mTOR signaling
Fragile X syndromes
protein synthesis pathway
mouse models of autism
Autism is a widespread disorder characterized by deficits in social interactions, impairments in communication, and repetitive and stereotypic behaviors. Identification of genetic markers has proved difficult, because of the highly complex and variable nature of the disease. Although autism spectrum disorders (ASDs) arise as a consequence of mutations in genes with multiple molecular functions, they appear to converge on common biological pathways to give rise to autism-relevant behaviors (Abrahams and Geschwind, 2008). One such pathway is the phosphatidylinositol 3-kinase (PI3K)–mammalian target of rapamycin (mTOR) signaling cascade. The mTOR pathway is a central regulator of a diverse array of cellular processes, including growth, proliferation, survival, and protein translation that requires a modified guanosine, termed a cap, at the 5′ end of the RNA. In the brain, components of the mTOR pathway are present at synapses, in which they regulate dendritic spine morphology and are essential for synaptogenesis. Growing evidence indicates that dysregulation of mTOR is involved in human diseases, including cancer, diabetes, and autism. Mutations in tuberous sclerosis complex 1 (TSC1), TSC2, neurofibromatosis 1 (NF1), and phosphatase and tensin homolog (PTEN) lead to an overactivated PI3K–mTOR pathway, autism-relevant behaviors, and tuberous sclerosis, neurofibromatosis, or macrocephaly (Kwon et al., 2006). Recent findings that PI3K–mTOR signaling is overactivated at synapses of fragile X syndrome (FXS) mice (Sharma et al., 2010) and in humans with FXS (Hoeffer et al., 2012) provide the first evidence that genetic mutation not only of components within the mTOR signaling cascade, but also distant regulatory proteins, can lead to autism-related phenotypes. mTOR signaling and protein synthesis are also impaired in a mouse model of Rett syndrome (Ricciardi et al., 2011; Jiang et al., 2013). In this symposium, we focus on four signaling mechanisms upstream and downstream of mTOR, including the following: (1) the translation initiation machinery; (2) metabotropic glutamate receptor 5 (mGluR5)–Homer scaffolds; (3) mTOR-dependent synaptic plasticity; and (4) actin polymerization. These four components of the mTOR signaling pathway, although separate and distinct under physiological conditions, lead to a common pathological phenotype that is most closely associated with ASDs and ASD-associated syndromes.
Exaggerated cap-dependent translation causes synaptic and behavioral aberrations associated with ASDs
Excessive translation is posited to be a common molecular anomaly that contributes to aberrant synaptic plasticity and behaviors associated with a number of neurodevelopmental disorders (Kelleher and Bear, 2008; Hoeffer and Klann, 2010; Auerbach et al., 2011). This idea was based primarily on the observation that FXS, the most commonly inherited form of mental retardation, has a high incidence of autism and is caused by lack of fragile X mental retardation protein (FMRP), usually a translational repressor (Darnell and Klann, 2013). FXS model mice exhibit excessive protein synthesis, exaggerated mGluR-dependent synaptic plasticity, and multiple autism-related behaviors. In addition, it has been shown that FXS mice exhibit upregulated mTOR complex 1 (mTORC1) signaling at hippocampal synapses (Sharma et al., 2010; Ronesi et al., 2012), which result in enhanced assembly of the cap-dependent translation initiation complex as measured by interactions of the eukaryotic initiation factor 4 (eIF4E; the cap-binding translation factor) with eIF4G (Sharma et al., 2010; Ronesi et al., 2012) and enhanced activation of p70 S6 kinase 1 (S6K1) (Bhattacharya et al., 2012). Moreover, direct evidence that upregulation of mTORC1 signaling plays a role in FXS pathophysiology was provided in studies in which Fmr1 knock-out (KO) mice were crossed with mice that lack both copies of the gene that encodes S6K1 (Bhattacharya et al., 2012). The genetic reduction of S6K1 prevented molecular, morphological, synaptic, and behavioral phenotypes displayed by Fmr1 KO mice (Bhattacharya et al., 2012). Notably, S6K1 has a wide range of substrates, many of which are not translational control molecules (Magnuson et al., 2012). Thus, direct evidence that excessive protein synthesis via S6K1 is a causative factor for exaggerated plasticity and ASD-like behaviors is still lacking in FXS mice (Darnell and Klann, 2013).
A direct genetic link between ASD and the cap-binding translation factor eIF4E was reported in 2009. It was shown that a boy with classic autism had a de novo chromosome translocation between 4q and 5q, and the breakpoint site was mapped to an alternative transcript of EIF4E (Neves-Pereira et al., 2009). Mutation screening identified two additional unrelated autism families that harbored the same single nucleotide insertion in the EIF4E promoter. In vitro studies demonstrated that this mutation enhances the binding of a nuclear factor and EIF4E promoter activity, suggesting that overexpression of eIF4E may be causative for ASD. Moreover, because eIF4E–eIF4G interactions are elevated in FXS model mice (Sharma et al., 2010), a similar aberrant translational control mechanism may be involved in behavioral abnormalities in FXS (Darnell and Klann, 2013).
The first direct evidence demonstrating that excessive cap-dependent translation can result in ASD-like behaviors was provided by studies of transgenic mice that overexpress eIF4E (Santini et al., 2013). It was observed that eIF4E transgenic mice exhibit a 25–50% increase in eIF4E expression throughout the brain (Santini et al., 2013). Increased expression of eIF4E resulted in increased eIF4E–eIF4G interactions in the striatum and hippocampus, which were blocked with intracerebroventricular injections of 4EGI-1 (Santini et al., 2013), which blocks eIF4E–eIF4G interactions (Moerke et al., 2007; Hoeffer et al., 2011). The increase in eIF4E–eIF4G interactions resulted in exaggerated protein synthesis, which also was blocked by 4EGI-1 (Santini et al., 2013). Behavioral analysis demonstrated that the eIF4E transgenic mice display enhanced repetitive behaviors as measured by self-grooming and marble burying. In addition, the eIF4E transgenic mice exhibited impaired arm choice reversal in the water-based Y maze. These behavioral abnormalities were correlated with exaggerated long-term depression (LTD) in both corticostriatal and hippocampal slices from the eIF4E transgenic mice. The behavioral and synaptic plasticity abnormalities displayed by the eIF4E transgenic mice could be reversed with 4EGI-1 treatments (Santini et al., 2013). Consistent with these findings, it was shown that mice that lack 4E-binding protein 2 (4EBP2), a repressor of eIF4E, exhibit synaptic plasticity and behavioral phenotypes similar to those displayed by the eIF4E transgenic mice (Banko et al., 2005; Gkogkas et al., 2013), which are reversed by 4EGI-1 (Gkogkas et al., 2013). In addition, it has been shown that altered eIF4E-dependent translation plays a role in FXS. Either genetic reduction or pharmacological inhibition of eIF4E phosphorylation prevented molecular, morphological, synaptic, and behavioral phenotypes exhibited by Fmr1 KO mice (Gkogkas et al., 2014). Notably, excessive translation of matrix metalloproteinase-9, which plays an important role in FXS pathophysiology (Sidhu et al., 2014), was normalized in FXS mice with reduced eIF4E phosphorylation (Gkogkas et al., 2014). Finally, crossing eIF4E transgenic mice with Fmr1 KO mice causes cognitive dysfunction in hippocampus-dependent memory tasks in the double mutant mice that are not exhibited by either the eIF4E transgenic mice or the Fmr1 KO mice (Huynh et al., 2015). Together, these findings indicate that increased eIF4E-dependent translation can cause synaptic dysfunction and behavioral aberrations associated with intellectual disabilities and ASD.
mGluR5–Homer scaffolds regulate signaling to PI3K and mTOR: implications for FXS and ASDs
Activation of the PI3K–mTORC1 pathway and signaling to translation control is necessary for rapid translation of new proteins and induction of translation-dependent long-term synaptic plasticity in response to Gq-coupled neurotransmitter receptors, including the mGluR5 and M1 muscarinic acetylcholine receptors (Hou and Klann, 2004; Volk et al., 2007). Furthermore, alterations in mGluR5 signaling to mTORC1 and translation-dependent synaptic plasticity occur in many mouse models of autism, such as FXS (Hou et al., 2006; Nosyreva and Huber, 2006; Sharma et al., 2010), tuberous sclerosis (Auerbach et al., 2011), Angelman syndrome, 16p11.2 microdeletion (Tian et al., 2015), and may contribute to disease-relevant behaviors. Recent work has provided a better understanding of the molecular mechanisms that couple mGluR5 signaling to mTORC1 and translational activation in both healthy and diseased neurons.
Pharmacological activation of acute hippocampal slices from wild-type mice with the group 1 mGluR agonist, (RS)-3,5-dihydroxyphenylglycine, results in a rapid activation of the PI3K–mTORC1 pathway as measured with phospho-specific antibodies to downstream effectors, such as p70 ribosomal S6K and 4EBP, which promotes mRNA translation initiation (Hou and Klann, 2004; Ronesi and Huber, 2008). Importantly, activation of PI3K–mTORC1 is necessary for mGluR5-stimulated LTD and synapse elimination, both of which rely on translation of dendritic mRNAs (Hou and Klann, 2004; Wilkerson et al., 2014). In Fmr1 KO mice, a mouse model of FXS, mGluR5-induced activation of PI3K and mTORC1 is deficient (Ronesi and Huber, 2008), but basal levels of PI3K and mTORC1 activity, as well as protein translation rates, are elevated in Fmr1 KO cortical regions. Basal or constitutive activity of mGluR5 may drive these changes, because enhanced PI3K activity and translation rates in Fmr1 KO tissues are sensitive to the mGluR5 antagonist MPEP (Gross et al., 2010; Osterweil et al., 2010; Sharma et al., 2010; Ronesi et al., 2012). These results suggest that there is constitutive signaling of mGluR5 to the PI3K–mTORC1 pathway in FXS that may reduce or occlude agonist-induced activation of the pathway.
Recent work by Huber and colleagues suggests that dissociation of mGluR5 with its postsynaptic scaffolding protein Homer mediates the abnormal mGluR5 signaling to PI3K–mTORC1 in the Fmr1 KO mouse (Giuffrida et al., 2005; Ronesi et al., 2012). The Homer family of proteins binds to the intracellular C-terminal tail of group 1 mGluRs and function to scaffold mGluRs to signaling complexes within the postsynaptic density through other Homer binding proteins (Shiraishi-Yamaguchi and Furuichi, 2007). Homers (Homer 1–Homer 3) share a common EVH1 domain at the N terminus, which binds to mGluR1α, mGluR5, and other scaffolding proteins (e.g., SHANK), ion channels (e.g., TrpC, CaV1.2), and signaling pathways [e.g., PI3K enhancer (PIKE), IP3 receptor]. Homers multimerize through their coiled-coil domains to form large signaling complexes at the postsynaptic density (Shiraishi-Yamaguchi and Furuichi, 2007). An activity-dependent short variant of Homer (Homer1a) lacks a coiled-coil domain and disrupts Homer scaffolds by competing with long Homers for mGluR5 and other Homer interacting proteins (Xiao et al., 1998).
A group 1 mGluR agonist stimulates association of Homer with PIKE, a GTPase that enhances PI3K activity by binding to the p85 subunit of PI3K. Homer and PIKE are both necessary for mGluR5 to stimulate PI3K activity in neurons (Rong et al., 2003). Consistent with this finding, acute disruption of mGluR5–Homer interactions in hippocampal slices, using a peptide that mimics the proline-rich Homer binding motif in the C terminus of mGluR5, blocks agonist-induced activation of PI3K–mTOR, mGluR–LTD, and the rapid translation of proteins required for LTD, such as Arc (Ronesi and Huber, 2008; Ronesi et al., 2012). In Fmr1 KO forebrain, mGluR5 is less associated with long Homer isoforms and more associated with Homer1a, suggesting that the disrupted mGluR5–Homer mediates the deficit in mGluR5 signaling to PI3K–mTOR and translation machinery in Fmr1 KO neurons (Giuffrida et al., 2005; Ronesi et al., 2012). In support of this idea, genetic deletion of Homer1a restores mGluR5–Homer scaffolds and mGluR5-induced activation of mTORC1 pathway, as well as mGluR5-induced activation of translation initiation (Ronesi et al., 2012). Homer is not necessary for all mGluR5 signaling because peptide disruption of mGluR5–Homer or Fmr1 KO has no effect on agonist-induced ERK activation in hippocampal slices (Ronesi and Huber, 2008; Ronesi et al., 2012), suggesting a specific role for Homer in coupling mGluR5 to PI3K–mTORC1 via PIKE.
Homer1a binding results in constitutive, agonist-independent activity of mGluR5 (Ango et al., 2001), suggesting that the Homer1a-bound mGluR5 in Fmr1 KO neurons may constitutively signal and contribute to the enhanced, mGluR5-dependent PI3K, mTORC1, translation initiation complex formation, and basal translation rates. In support of this idea, acute peptide-mediated disruption of mGluR5–Homer results in elevated protein synthesis rates in wild-type slices but not those from the Fmr1 KO slices. Homer1a deletion in the Fmr1 KO rescues elevated protein synthesis rates and enhanced translation initiation complex formation (Ronesi et al., 2012). The role of Homer or constitutive mGluR5 activation in driving elevated mTORC1 in Fmr1 KO is currently unknown. There may also be some regional differences in the contribution of PI3K–mTORC1 to enhanced basal translation rates in Fmr1 KOs. However, in both regions, protein synthesis rates are sensitive to mGluR5 antagonism, suggesting the constitutive mGluR5 signaling, as a result of Homer1a interactions, is driving signaling to enhance protein synthesis rates. What is unclear at this time is whether the enhanced constitutive signaling of mGluR5 saturates the PI3K–mTORC1 pathway, which prevents subsequent agonist-induced activation of the pathway, or whether Homer coupling is selectively required for agonist-induced, but not constitutive, activation of PI3K–mTORC1.
The blockade of agonist-induced activation of PI3K–mTORC1 by disruption of Homer interactions may have additional consequences on mGluR5-dependent translational activation (Fig. 1). mGluRs stimulate phosphorylation of elongation factor 2 (EF2) through activation of EF2 kinase (EF2K). Although P-EF2 inhibits elongation rate, EF2K and moderate inhibition of elongation are necessary for mGluR-induced synthesis of Arc, as well as mGluR–LTD (Park et al., 2008). Subthreshold inhibition of global elongation is thought to promote rate-limiting translation factors, which translate mRNAs that are poorly initiated and cannot compete effectively for these factors (Scheetz et al., 2000). EF2K is a Homer binding protein and also binds directly to mGluR5 (Park et al., 2008). Homer appears not to be required to couple mGluR5 activation to EF2K. On the contrary, peptide-mediated disruption of Homer–mGluR5 enhances agonist-induced activation of P-EF2, suggesting that Homer inhibits activation of EF2K (Ronesi et al., 2012). Consistent with this idea, agonist-induced activation of P-EF2 is enhanced in hippocampus of Fmr1 KO mice and rescued by deletion of Homer1a (Ronesi et al., 2012). Although as yet untested, the bidirectional effects of Homer on mGluR5 stimulation of mTORC1 and EF2K may be explained by the known inhibitory effects of S6K phosphorylation of EF2K. Homer disruption, via peptide or in Fmr1 KOs, prevents mGluR5 activation of mTORC1–S6K, which would also be expected to block the S6K phosphorylation and inhibition of EF2K, thus resulting in an overall increase in mGluR stimulation of P-EF2. Thus, the Homer–mGluR5 scaffold functions to balance mGluR5 signaling pathways for optimal translational activation. Homer is necessary for stimulation of translation initiation through activation of the PI3K–mTOR pathway (Ronesi and Huber, 2008) and limiting activation of EF2K and subsequent inhibition of elongation, which is necessary for rapid translation of new proteins required for synaptic plasticity.
Working model of Homer scaffolds in agonist-stimulated mGluR5 signaling to translation machinery in wild-type (A) and FXS model (B) cortical neurons.
Abnormal mGluR5–Homer scaffolds may be a common deficiency across different genetic causes of autism. Recent work indicates that mGluR5–Homer interactions are enhanced in the Angelman syndrome mouse model (Ube3A maternal deletion), which may contribute to impairments in mGluR-induced LTD (Pignatelli et al., 2014). More work is needed to know whether and how the enhanced mGluR5–Homer interactions regulate Angelman syndrome pathophysiology.
Dysregulation of mTOR signaling is critical to impaired synaptic plasticity and aberrant spine morphology in a mouse model of FXS
FXS is the most common heritable form of intellectual disabilities and a leading genetic cause of autism. Whereas other syndromic ASDs arise from mutations in components of the PI3K–mTOR pathway, FXS arises from silencing of the gene encoding FMRP (Fmr1). FMRP is an RNA-binding protein that represses translation of a large array of RNAs, including PIKE. PIKE, an upstream activator of mTOR and identified target of FMRP (Darnell et al., 2011), is elevated at the synapses of Fmr1 KO mice (Gross et al., 2010; Sharma et al., 2010), humans (Hoeffer et al., 2012), and flies (McBride et al., 2005), providing a functional link between loss of FMRP and overactivated mTOR signaling (Fig. 2).
Scheme showing the link between deficits in FMRP and overactivated mTOR signaling in the dendritic spine. Our findings support a model whereby FMRP represses PIKE, thereby inhibiting mTOR signaling, in wild-type mice. Under basal conditions, mTOR regulates LIM kinase and cofilin through Rac1, a member of the Rho family of GTPases. In FXS mice, we propose that dysregulation of mTORC2 leads to impaired actin polymerization and spine structure. DHPG, (RS)-3,5-dihydroxyphenylglycine.
Recent work from Sharma et al. (2010) has demonstrated that, in hippocampal neurons of Fmr1-deficient mice, upregulation of the PI3K-enhancer PIKE results in overactivation of PI3K/Akt and mTOR signaling in the hippocampus, as assessed by several functional readouts, including mTOR phosphorylation, binding to the regulatory protein Raptor, and formation of the eIF4F translation initiation complex. Moreover, synaptic plasticity in the form of mGluR–LTD is exaggerated and insensitive to the mTOR inhibitor rapamycin at hippocampal CA3–CA1 synapses of Fmr1-deficient mice (Sharma et al., 2010). These findings are consistent with a model in which, in the FXS mouse, the protein(s) required for mGluR-dependent AMPA receptor internalization and mGluR–LTD are already accumulated at CA1 synapses under basal conditions (Bear et al., 2004). These observations provide an important functional link between overactivated mGluR signaling, aberrant protein synthesis, and exaggerated mGluR–LTD in Fmr1-deficient mice (Sawicka and Zukin, 2012).
A hallmark feature of FXS that is also observed in Fmr1-deficient mice is synaptic spine abnormalities (Bagni and Greenough, 2005). Spines on hippocampal and cortical neurons of Fmr1 KO mice exhibit enhanced density and are thinner and longer than those of age-matched wild-type mice, resembling an immature morphology. These observations indicate that FMRP might normally repress local translation of proteins that inhibit synapse maturation, stabilization, and elimination (Bagni and Greenough, 2005). Cofilin is an actin depolymerizing factor and central regulator of apoptosis, activity-dependent synaptic plasticity, and spine morphology. Emerging evidence indicates that cofilin signaling is downstream of the mTORC2 pathway, an mTOR signaling complex insensitive to rapamycin and a critical regulator of embryonic development, actin cytoskeleton dynamics, synaptic efficacy, and the consolidation of long-term memory. Dysregulation of cofilin signaling has been linked to aberrant spine morphology in Tsc1+/− and Tsc2+/− mice (Tavazoie et al., 2005). Because mTOR is overactivated in FXS and is an upstream regulator of the postulated cofilin signaling pathway, an intriguing possibility currently under exploration is that aberrant cofilin signaling may be causally related to the spine abnormalities that are a neuroanatomical hallmark of FXS (Pyronneau et al., 2015) reminiscent of the morphological abnormalities and synaptic deficits observed in PTEN mutant mice (Kwon et al., 2006; Takeuchi et al., 2013).
mTORC2 and its role in ASDs
The evolutionarily conserved mTOR forms two functionally distinct complexes. mTORC1, which consists of mTOR, Raptor, and mLST8 (GβL), is sensitive to rapamycin and is thought to regulate mRNA translation rates. mTORC2 is mostly insensitive to rapamycin and contains the core components mTOR, mSIN1, mLST8, and Rictor. Rictor is highly expressed in the brain, in which it associates with membranes and regulates the actin cytoskeleton. Dysregulation of mTORC1 and mTORC2 signaling appears to have a crucial role in memory disorders, such as the cognitive deficits associated with ASDs. Notably, the activity of mTORC2 is altered in the brain of ASD patients harboring mutations in PTEN and/or TSC1 and TSC2 (two upstream negative regulators of mTORC1; Costa-Mattioli and Monteggia, 2013; Buffington et al., 2014). These findings raise the intriguing possibility that the neurological dysfunction in ASD is caused by dysregulation of mTORC2 rather than by mTORC1 signaling. Indeed, mTORC2 activity is altered in several cognitive disorders, including Huntington's disease, parkinsonism, Alzheimer-type dementia, and ASDs. Recent work from Huang et al. (2013) found that mTORC2 is an essential component of memory consolidation via its regulation of actin polymerization. Conditional deletion of Rictor in the postnatal murine forebrain greatly reduces mTORC2 activity and selectively impaired both long-term memory and the late phase of hippocampal long-term potentiation (L-LTP). A comparable impairment of long-term memory is also discovered in dTORC2-deficient Drosophila, highlighting the evolutionary conservation of long-term memory in the mTORC2 signaling pathway. Basal levels of actin polymerization are reduced in the hippocampus of mTORC2-deficient mice, and treatment with jasplakinolide restores actin polymerization to wild-type levels and rescues both L-LTP and long-term memory. Moreover, a small-molecule activator of mTORC2 activity converts early LTP into L-LTP and enhanced long-term memory. These results identify both the molecular and synaptic events occurring upstream and downstream of mTORC2 in the brain and suggest that mTORC2 could be a therapeutic target for the treatment of cognitive dysfunction.
The topics highlighted in this symposium support the central hypothesis that dysregulation of mTOR-dependent signaling, both upstream and downstream of its kinase activity, contributes to the pathophysiology associated with multiple ASDs. Mutations in components of the mTOR signaling cascade, including TSC1, TSC2, NF1, and PTEN, as well as the more distant regulatory proteins FMRP and MeCP2, present similar phenotypes in both mice and humans. Although these ASD-associated syndromes have their own distinct clinical features, the unifying theme of mTOR dysregulation underscores the significance of synaptic deficits and its relevance to autism-relevant behaviors, such as social deficits and cognitive impairment. On the basis of observations that mTOR signaling, synaptic plasticity, and protein translation are overactivated in many of these disorders, compounds that can potentially inhibit the mTOR pathway represent promising therapeutic candidates for their treatment. Indeed, the mTORC1 inhibitor rapamycin has shown promising results in PTEN KO mice (Zhou et al., 2009) and TSC2+/− mice (Ehninger et al., 2008). Thus, interventions that target mTOR signaling should be at the leading edge of future translational research in the autism field.
Correspondence should be addressed to Dr. R. Suzanne Zukin, Dominick P. Purpura Department of Neuroscience, Rose F. Kennedy Center, Room 610, Albert Einstein College of Medicine, 1300 Morris Park Avenue, New York, NY 10461. suzanne.zukin{at}einstein.yu.edu
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Journal of Neuroscience
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Mechanisms of Neuronal Alternative Splicing and Strategies for Therapeutic Interventions
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As many of you are aware, we successfully launched the Callisto (CLO) main net on April 15th, 2018.
We would like to thank our community for the outstanding support shown to us during the launch, and in the months leading up to our launch.
The team is working hard in the background to bring Callisto to even more exchanges and to improve the Callisto Network.
Our team operates in complete transparency on all financial matters involving Callisto. For more information on our payments policy, click here.


We are needing a 3D model of a mascot character created for our business Partychaser.com. The mascot we have chosen is a Panther (Black). He would be wearing a Letterman Jacket with our company logos on it but he would also need to be created in a way in which his outfit can change for different occasions. This character will mostly be used for snapchat lenses and video. Attached is a mockup and our company logos.
Hello, i'm working on this project, can you add extra time, 1 day?
actually I found my winner but thanks.
you want exact image in 3d (mockup)or we can do some tweaks and make new ones ?
We are working. Wait for us please.


Macka Diamond had to clapback at a social media user who accused her of stealing another woman's husband.
The "Dye Dye" singer uploaded a photo online with her new boyfriend Spotlight Kunta last week when a fan made the damning statement.
"Donkey Face Macka Diamond carry back Andrea husband, yuh a walk and mash up de ppl dem life it nuh look good yuh a big woman," the user wrote.


In this post, you will read the process to change taskbar, Start Menu and background color in Windows 10. You can also choose to switch off the transparency of the Start Menu through the Personalization category of the Settings.
Not caring for the way you install the latest version, you can get yourself explored too many new things. Till this version, any changes to the background and color were done from the Personalization window only. Now you can change the color of background along with the taskbar and Start Menu and make taskbar transparent or pellucid through the Personalization category of the Settings.
Launch the Settings from the Start Menu.
Make a click on Personalization.
The left column exhibits you the subcategories of the Personalization.
The right side of the Background displays the Preview of the background. You observe three options to place something for the background. You need to single out either of a Picture, Solid Color or Slide show.
You can now see many solid colors and you can choose anyone. Pick up your desired solid color and set it as the background color.
Here, also you need to navigate to the Personalization category of the Settings.
Be into the Colors subsection.
On the right pane of the Colors, you can see the Preview.
There you can check or uncheck the setting labeled Automatically pick a color from my background.
Just above it, you see a list of Accent color from where you can choose your preferred and set it as your taskbar and Start Menu color.
One more option is to Show color on Start, taskbar and action center. If you turn this Off, the taskbar and Start Menu will turn to the default black color.
The next option is Make Start, taskbar and action center transparent. If you are not happy with the transparency of the Start Menu, you can turn it Off.


For purposes of developing a detailed fertilizing plan, we synthesized the soil analysis results with the researched and observed needs of the plants on the property. For a detailed analysis, go to the following link: Hamilton – Gardens – Fertilizing Plan. A capsule summary of the plan is below.


text:
// This file is automatically generated.

package adila.db;

/*
 * HTC Desire P
 *
 * DEVICE: magniu
 * MODEL: HTC Desire P
 */
final class magniu {
    public static final String DATA = "HTC|Desire P|";
}