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Chicago Weather: Light Snow Throughout The WeekendCBS 2 Meteorologist Robb Ellis has the 10 p.m. forecast for Friday, Jan. 15, 2021.
Lightfoot Asks Judge Not To Sanction Anjanette Young's Attorney Over Raid VideoChicago Mayor Lori Lightfoot asked a judge Friday not to sanction the attorney for Anjanette Young, the victim of a botched police raid first exposed by the CBS 2 Investigators.
Restaurants Continue Dine-In As Governor Says Indoor Dining Ban Will ContinueChicago Mayor Lori Lightfoot says she is open to indoor dining, but Gov. JB Pritzker says not yet. While we wait and see, some restaurants say they have no choice but to break the rules.
Illinois Renewing Car Registrations Even Without A Required Emissions Test--Until March 1Illinois drivers can still get their vehicle registrations renewed online, even without a required emissions test.
Markham Mayor Roger Agpawa Could Be Booted From Ballot Due To Felony ConvictionA new lawsuit means the mayor of Markham could get booted from the ballot in April due to a felony conviction.
Former Chicago Firefighter Fights To Clear Name After Being Falsely Blamed For Death Of Capitol Police OfficerA retired Chicago firefighter has received all sorts of threats this week after he was wrongly identified online and accused of throwing a fire extinguisher at police during the assault on the United States Capitol.
Chicago School Closings
Flight Delays O'Hare
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White Sox Sign Top International Prospect, Cuban OF Yoelqui CéspedesCéspedes is rated the No. 1 international prospect by MLB Pipeline, and was a two-time Cuban Serie Nacional champion with Granma.
White Sox Sign Closer Liam Hendriks To 4-Year, $54 Million ContractWith the signing of Hendriks, the White Sox now have four pitchers who finished in the top 10 in the AL Cy Young Award voting in 2020.
Naperville North Teacher Has His Students Build Race Car With Help From A NASCAR TeamWith most high school sports on pause, one Naperville North teacher who has a background in racing found a great way to keep kids busy.
Blackhawks Place Captain Jonathan Toews On Long-Term Injured ReserveThe 32-year-old Toews announced prior to the start of training camp last month he was experiencing symptoms that left him feeling "drained and lethargic."
Former Cubs President Theo Epstein Hired As MLB Consultant To Evaluate Rules Changes"As the game evolves, we all have an interest in ensuring the changes we see on the field make the game as entertaining and action-packed as possible for the fans, while preserving all that makes baseball so special," Epstein said in a statement.
PAWS Pet Of The Week: FrancaFranca is a great companion and will make a fantastic addition to a dedicated family who will provide her with lots of love and attention.
PAWS Pet Of The Week: MariaMaria loves going for walks and she is very obedient.
PAWS Pet Of The Week: JensenHe also has a few goals for the year including finding an adult family, going on adventures with his new humans and finding a place for a comfy nap.
Chicago Author Gabriel Bump Named 2020 Winner Of The Ernest Gaines Award"To do this impractical thing, you have to really love it Writing is a total part of me."
PAWS Pet Of The Week: RoscoeBecause he loves his humans so much, he would prefer finding a home where people are home often and where Roscoe is the only pet.
PAWS Pet Of The Week: PippaShe would like a family where she can get lots of love and attention, and of course, lots of cookies.
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Top 3 Eco-Friendly Vacation SpotsCheck out the three best spots for an eco-friendly vacation!
Final Four Guide: Top 10 Most Instagram-Worthy Spots In Downtown MinneapolisWith thousands of Final Four fans heading to downtown Minneapolis in the coming days, you better believe the Instagram filters will be flying.
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School Board President: 'We Want Our Kids Back In School'
Filed Under:CBS 2 Morning News, Chicago School Board, Chicago Teachers' Strike, David Vitale, Karen Lewis, Teachers' Strike
Chicago School Board President David Vitale. (Credit: CBS)
CHICAGO (CBS) — Chicago School Board President David Vitale says the board has issued more than 20 proposals in an effort to end the teachers' strike, and he wants to see children back in school by Wednesday.
Speaking on the CBS 2 Morning News Tuesday, Vitale said the disagreement between the Chicago Public Schools and the Chicago Teachers Union is down to two issues – one dealing with teacher evaluations, and the other with recalling teachers for work if they are laid off through a school closure.
"There are a number of other issues that we are really not very far apart on, and they worked late into the night to close a lot of those last night, so we continue to say that we have, in fact, been responsive," he said. "We've been working hard. We've made over 20 proposals over the last few days to close the gap, and we think the process is moving ahead, and we see no reason why we won't solve this, and we have an urgency to get this solved, because we think our kids ought to be in school."
Vitale reiterated Mayor Rahm Emanuel's statement Sunday that the teachers' strike is a "strike of choice." He also disputed Teachers Union President Karen Lewis' remark that the board has made "no movement."
"We wouldn't have the same point of view," Vitale said. "As I've pointed out, since last Thursday, we've made over 20 proposals for change and improvement to meet their needs, and so we've not been obstinate."
A major issue for teachers is a proposal to evaluate their performance based on student test scores – a plan they say fails to take into account other factors that such as poverty. Vitale said the evaluation proposal is required to comply with state law.
"We have to implement the law, and the law requires that. And we've, in fact, worked with them almost for the better part of a year to design something that meets the law, and even in that regard, we have agreed to compromise in a variety of different ways, including saying that the first year, implementation of that would not be what's called high stakes – in other words, the information that's gathered from that would be used to help both principals and teachers understand the system better, and we've agreed to a committee that would analyze that work, and if there need to be changes, we've agreed to make the changes," Vitale said.
Vitale said he thought the two sides were close on Monday morning, and he hopes all issues will be settled Tuesday.
"When we left last night, we said we could probably get there today – or at least we could get everybody comfortable enough that we could get our kids back in school, and we believe we can do that, and we can get our kids back in school tomorrow," he said.
He added that the Children First programs that have been set up to accommodate children at some schools has gone well so far.
"I would say that us and the Chicago community have made every effort to help parents and students in that regard, and yesterday went reasonably well in providing that support, and so we want our kids back in school. We want them back in school tomorrow."
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Markham Woman Furious After She Pays Home Depot Contractor To Build Fence, Gets Caught Up In Red Tape
'I Don't Want You In The Store, I Don't Want You Near Me:' Elmhurst Cigar House Owner Puts Up Sign Reading, 'Biden Voters Keep Out'
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Opcional: Parte 1: Cómo NO hacer una prueba, Entrevista al Dr. Richard Felder y a la Dra. Rebecca Brent
Aprendiendo a aprender: Poderosas herramientas mentales con las que podrás dominar temas difíciles (Learning How to Learn)
맥마스터대학교
Este curso te brinda acceso a invaluables técnicas de aprendizaje utilizadas por expertos en arte, música, literatura, matemáticas, ciencia, deportes y muchas otras disciplinas. Aprenderemos cómo el cerebro utiliza dos modos de aprendizaje muy distintos y cómo encapsula ("fragmenta") la información. También hablaremos sobre ilusiones de aprendizaje, técnicas de memoria, cómo ocuparse de la procrastinación y las mejores prácticas, según lo demuestra la investigación, para ayudarte a dominar los temas más complicados. Con estos enfoques, más allá de tus niveles de destreza en los temas que quieras dominar, puedes cambiar tu pensamiento y tu vida. Si ya eres un experto, este vistazo de la maquinaria cerebral te dará ideas para disparar un nuevo aprendizaje poderoso, con consejos contraintuitivos para presentar exámenes y perspectivas que te ayudarán a aprovechar al máximo el tiempo que dedicas a las tareas y a la resolución de problemas. Si estás teniendo dificultades, descubrirás un cofre del tesoro estructurado con técnicas prácticas que te orientan acerca de lo que debes hacer para mejorar. Si alguna vez deseaste ser mejor en algún ámbito del aprendizaje, este curso te servirá como guía. Este curso también está disponible otros idiomas: Para unirte a la versión en inglés, visita: https://www.coursera.org/learn/learning-how-to-learn Para unirte a la versión en portugués, visita: https://www.coursera.org/learn/aprender Para unirte a la versión en chino, visita: https://www.coursera.org/learn/ruhe-xuexi
Learning To Learn, Organizing (Management), Pomodoro Technique, Meta Learning
es un curso muy completo, con cada vídeo aprendes muchas cosas sobre el funcionamiento cerebral al memento de aprender. no solo en lo académico, si no en cada cosa que uno realiza a lo largo del día.
Descubrí que en mi están todas las herramientas para aprender día a día de una forma menos estresante, aceptando mis debilidades para trabajar en ella y desarrollando nuevas competencias importantes
Renacimiento del aprendizaje y cómo liberar tu potencial
En este módulo vamos a hablar más sobre ideas y técnicas importantes que mejorarán tu capacidad de aprender. También descubrirás cómo interactuar mejor con otros estudiantes, cómo reconocer tus propias fortalezas y cómo evitar el "síndrome del impostor". Los pilotos de combate y los cirujanos usan listas de comprobación para ayudarles con su tareas fundamentales... tú puedes usar una lista similar para prepararte para las evaluaciones. En definitiva, aprenderás más acerca del placer de vivir aprendiendo.
Opcional: Parte 1: Cómo NO hacer una prueba, Entrevista al Dr. Richard Felder y a la Dra. Rebecca Brent11:03
Opcional: Parte 2: Aprender algo nuevo, Entrevista al Dr. Richard Felder y a la Dra. Rebecca Brent9:05
Opcional: Parte 3: El síndrome del impostor y ocuparse de la procrastinación, Entrevista al Dr. Richard Felder y a la Dra. Rebecca Brent9:55
Opcional: El escritor John Maguire (readablewriting.com) habla sobre la importancia de colocar objetos en la escritura20:16
Entrevista opcional a William Craig Rice sobre aprendizaje en humanidades40:48
Dr. Barbara Oakley
Ramón y Cajal Distinguished Scholar of Global Digital Learning, McMaster University
Dr. Terrence Sejnowski
Francis Crick Professor at the Salk Institute for Biological Studies
M.S. Orlando Trejo
언어 선택하기그리스어네덜란드어독일어러시아어루마니아어몽골어버마어베트남어벵골어세르비아어스페인어아랍어에스토니아어영어우크라이나어이탈리아어중국어 (간체자)체코어크로아티아어타밀어페르시아어포르투갈어 (브라질)포르투갈어 (유럽)폴란드어프랑스어헝가리어히브리어
In this video, I'm very pleased to introduce you to Dr. Richard Felder and Dr. Rebecca Brent, two educators who have had an enormous impact on the landscape of education. I first met Rich and Rebecca at the very beginning of my teaching career. I was lucky enough to attend a workshop they taught on student-centered learning, that workshop changed the whole focus of my teaching and allowed me to understand learning in a whole new deeper way. I think you'll find that your own understanding of learning will change as you listen to this interview. Rich Felder has written the best selling book on Introductory Chemical Engineering in the country and possibly in the world. He's also won the Lifetime Achievement Award from the American Society of Engineering Education for his enormously influential work, but don't make the mistake of thinking that Dr. Felder's work is only useful for engineers. A big reason he's so influential is that the approaches he uses are applicable to virtually any field of study. It is actually Dr. Felder's enormously gifted wife, Dr. Rebecca Brent, the President of the education consulting firm, Education Designs, and longtime director of the NSF Sponsored Succeed Coalition Faculty Development Program, who has helped spearhead the broad multidisciplinary impact of the couples work on education. I think you'll find Dr. Felder and Dr. Brent's work to have as powerful an influence on you as it's had on me. So, you've written some extraordinarily helpful advice for students about how to prepare for tests. If you could sum that advice up in a nutshell, what would you say? Let me first say something about how not to prepare for tests, which is probably what 90 plus percent of my students do to prepare for tests. One, generally they ignore the book but they may read the book like a novel, just going flipping through it, maybe they underline, which as far as I can tell is a singularly useless strategy for doing anything. Then when they've done that, maybe they look through the old homework solutions and read through them, again like a novel, and then imagine that they've studied, and that provides them with no help at all in preparing for the test. First of all, the test is not going to be just the homework again. It's going to be new problems that they have to solve. So, if that's how not to do it, how do you do it? The only way that I've ever found that works to prepare for tests is, and I'm talking about problem-solving tests, not the kind that I give in engineering, is to work problems, to set problems up, not to work through them in detail. So, I tell the students, you can start with the homework problems that you solve and then solve it again. Set up the solution without looking back at the worked-out solution that was graded and see how far you get. If you can set it up, so the only thing that's left to do is algebra or simple math, then you're done, then go on to another problem. Don't waste your time doing algebra and arithmetic, you're not learning anything from that. Then maybe go to your book and pick out another couple of problems and try to set those up. The more of that you do, the better you're going to be at solving problems, the more likely you are to be able to solve the problems that show up on the test. The other thing that I strongly advise is work with other people. Get into a study group, make it a serious study group, and try to make sure that at least somebody in the study group is smarter than you are and really knows how to solve the problem so that if you get stuck on something, this person is likely to be able to figure it out and all of you go marching along together. Leave the beer and the snacks in the refrigerator. Just spend your time working through problems, setting them up, making sure you know how to solve it, going on doing more problems. Then, when you're either exhausted or you've covered as much as you need to cover, you can then hit the refrigerator. This is so much like what we've talked about throughout this course as far as simply, reading a book is not putting it necessarily in your brain, and to have to actively grasp the material, and working with others sometimes is a very good way to help reinforce what you're learning, and also filling gaps in what you're trying to learn about. So, I think that's a fabulous advice and I have to say thank you for that wonderful checklist. You're welcome. I think there's also some things you can do when you get in the test because sometimes it's a high pressure situation, you may feel a lot of anxiety. So, taking a moment when you get the test, looking through the whole thing, just to get a sense of where you're going. Pick out the easy questions and start there. Then if you get stuck somewhere, go on to something else that you feel confident you can handle. Keep moving, don't stop. Sometimes when we're anxious, we just freeze. Keep moving, keep working even if you can't get everything, though for partial credit. Right. Get some of it, put something down and that'll help you be more successful in the test. Also, I've had students who really felt rising anxiety if they got to a question that they couldn't answer right away. If you find yourself really getting upset, just stop, take a deep breath, pause for a moment, and then look back at it. Just calming down a little bit can go a long way. Oh, it can. Well, that's one of the things we've also talked about in the course, is breathing from the belly to help draw in and really do deep breathing, that's a very effective technique to neurophysiologically allow yourself to calm down. Another interesting thing, and I think for our viewers, this shows a bit of the difference in approach of different top quality educators. One thing we've talked about is, just touch, at the very beginning when you're starting to look through a test, touch on and start working some of the more difficult problems just until you get stuck. So, it takes willpower, you have to pull yourself off quickly as soon as you can detect that you're getting stuck. But that actually gets your focused attention on it, then pulls that attention away and when you're working another easier problem, it allows you to in the background, your diffuse mode is working away. Then when you revisit that more difficult problem, you've got a little bit more going on intellectually because you've had time to think about. If you wait for the hardest problems later in the tests, sometimes that can create problems. So, there's different approaches and I think different folks, if they're aware of the different kinds of approaches, it gives them more tools that they can use for their intellectual toolkits. Exactly. I think that's always important to look at all the advice, look at all the suggestions, try things, give them enough of the try that you see how well they work. S, I think that's important for your students. Always be doing. I would extend that actually. The advice you just gave, I think is life advice not just for taking tests. There's this magical phenomenon that I've experienced many times in my life. If I'm working on something, a problem when I was a student that might be a problem on a homework assignment, it could have been a problem on a test, it could be a problem in my doctoral research, or something I'm working on. When I went into research as a faculty member but I'm struggling with something, I can't make any headway on it, my natural tendency is just to keep grinding on it, keep banging my head against that concrete wall and it doesn't the damage to the wall at all. It's not too good for my head. What I found is when at of desperation ,or just because I needed a break or whatever, I stopped grinding on it and I went off and I did something else. I took a walk, I took a nap, I went to work on something else I was working on. Then when I came around later, got back to work on the problem, the solution was magically there. I tend to believe what I've read in cognitive science about all of the stuff going on underneath the conscious part that I'm aware of. Somewhere in that part of my brain is somebody or something that's a lot smarter than whatever I think of as me. Once I've gotten started on the problem, exactly as you've just described, and then I get away from it, and it's like I'm turning it over to that part of my brain which is smarter, and it somehow solves the problem. When I come back, there's the solution like magic. Yes, that's the idea. It's basically when you purposefully pull your attention off, or allow your attention to drift off, that actually opens access to the neural resting states that you need to be able to solve the problem. Just alluding to some of these same life issues, sometimes my husband and I, we'll be thinking about a problem that we have to solve, for example, how do we schedule interviews, how do we, and we'll say, you know we don't have to solve this tonight. Sure enough, within another day or two, the answers will come to us. MY mother you used to call there gave their subconscious an assignment. I often think about that. Your mother was very, very smart.

redpajama_set_name: RedPajamaCommonCrawl


Fast is fun and fun is fast!
I am a midwest kid that started biking when I was very young. I remember bombing down water ditches with my friends just to see who could ride it the fastest.
It wasn't till college that I got my first true hardtail bike. It was only then that everything started to make sense - I fell in love with mountain biking and dumped a stage 5 clinger. When college ended, I decided to move to Colorado for the epic mountain biking. But, I told my parents it was for a job, I teach kids how to mountain bike. I still don't think they bought it for a minute. Now I am ready to start racing some xc/enduro.
From Genesee down Enchanted Forest and Apex = a great local epic.
I ride as light as possible. Give me my helmet, shoes, and gloves.
My two front teeth aren't real.


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January 7, 2014 January 8, 2014 Jana J. Monji
It's time for the Edwardian Ball!
After the holiday season, are you still looking for a party? Want to dress up in something out of the ordinary and even a bit extraordinary? Need an out-of-town trip or want to trip into another century or alternative universe. Even if you're comfy on your couch, you might see you couch differently if you get Edwardian.
You have a choice then: San Francisco or Los Angeles. Paradox Media and Vau de Vire present the 14th annual award-winning Edwardian Ball and World's Faire on Friday and Saturday, January 17th and 18th, 2014 at the stunning historic San Francisco venue, The Regency Ballroom.
The historic Regency Center was built in 1909, and is considered the finest example of Scottish Rite architecture in the country, featuring neoclassic and Beaux-Arts styles. The stunning Regency Ballroom is a treasure with 35-foot ceilings, a wraparound balcony, 22 turn-of-the-century teardrop chandeliers, blonde hardwood floors, and ornate décor. The newly renovated stage provides top-notch, state-of-the-art sound, lighting and video production for concerts and performances.
Then less than a month later, Paradox Media and Vau de Vire will be in Los Angeles for the Edwardian Ball on Saturday, February 8th, 2014 at The Fonda Theatre in Los Angeles. The Fonda Theatre is a historic 1920's venue originally built as Carter De Haven's Music Box and is formerly known as The Henry Fonda Theatre and The Music Box.
Edwardian Ball founders Rosin Coven and co-hosts Vau de Vire Society bring a featured Edward Gorey story to life on stage with original music, theatrical choreography and narration……this year presenting 'The Curious Sofa' which the co-producer Justin Katz describes it as "the ultimate in pornographic joy, combining naughtiness to the limit of the imagination and laughter to the point of breathlessness." It's where literary fans are as welcome as Goth clubgoers and where the high-flying trapeze and steam-powered machines create the backdrop for elegantly dressed ballgoers waltzing their way from absinthe to the dance floor.
Founded in 1997 by husband and wife team Shannon and Mike Gaines, the San Francisco-based entertainment company Vau de Vire Society has been titillating crowds around the world with its unique brand of interactive and thematic art, dance and circus events. This avant-cabaret community consists of classically-trained dancers, some of the nation's most acclaimed acrobats, aerial artists, sideshow acts, fire-performers, thespians and beautiful circus freaks. The group has been cross-pollinating genres by collaborating with an eclectic variety of world-renowned musicians and DJs in their creation of original stage shows.
For over 16 years Paradox Media, owned and operated by Justin Katz, has been producing an eclectic variety of art and music events in the San Francisco Bay Area. These have included festivals such as ArtCar Fest, How Berkeley Can You Be!?, Oakland World Music & Jazz Festival, ArtFest's Spectra Ball, Mission Bazaar, and Burning Man's annual SF Decompression; independent theater with Everyday Theatre's "The Bright River" and nonprofit community events with Epic Arts. Paradox Media is the exclusive presenter of Rosin Coven, Founders of The Edwardian Ball in 1999. Katz is the bassist for Rosin Coven and a founding member of this unique ensemble. Katz also works for Goldenvoice / AEG Live, producing hundreds of concerts and special events in the San Francisco region at the Warfield Theatre, The Regency Ballroom, festivals, and arena concerts.
Since 1999, The Edwardian Ball has steadily grown from a Bay Area underground club phenomenon into a full-fledged festival of arts and culture, focusing on the esteemed works of the late, great author/illustrator Edward Gorey…bringing his tales to life on stage. Now with the blessing of The Edward Gorey Charitable Trust, the truly prodigious and original artist, Edward St. John Gorey (1925-2000), will be honored for his body of over 100 works.
Step into a uniquely immersive world, where turn-of-the-century meets world-to-be in a fantastic blend of performance and audience, of sights, sounds, and magic. One can expect an irreverently elegant blend of theatre, circus, live music, DJs, ballroom dancing, parlour games, steam machinery, aerial performances, obscure props, period technology, games, fashion shows and a Vendor Bazaar & Piano Saloon. All in attendance are invited to return to a time of well-dressed gentility by creating characters and costumes for the occasion – instilling a madhouse slapdashery of costumery by nearly every single attendee.
San Francisco on Friday night is The Edwardian World's Faire – a little more rambunctious than the Saturday night Ball, The Faire presents an authentic tea parlor and an interactive night of Barbary-themed Midway Games, bicycle-powered carnival rides by Cyclecide, an exposition of steam-powered machinery by Kinetic Steam Works, circus sideshows, burlesque, and longtime Edwardian disc jockey Delachaux and Vau de Vire Society.
San Francisco and Los Angeles on Saturday night is The Edwardian Ball – Friday's rides and games are cleared away, making way for Ballroom Dancing followed by performances by Dark Garden Corsetry, "Belle of the Ball" Jill Tracy, DJs Miz Margo and Delachaux. Capture a moment of history in the antique portrait studio, sip an absinthe cocktail, and dance the night away. Later in the night, Rosin Coven and Vau de Vire Society will perform the 'not-to-miss' theatrical interpretation of an Edward Gorey story.
Both nights in San Francisco attendees can visit the widely acclaimed "Museum of Wonders – an Edwardian Odditorium" located in the opulent Regency Lodge. Be transported in a nostalgic turn-of-the-century elevator with costumed operator and enter an entire floor dedicated to natural wonders, unusual and peculiar artifacts, a living human statue garden, fortune tellers and sideshows, along with haunted mysteries and curiosities. These are all to be discovered through self-guided tours from 8-11pm, while being serenaded by a haunting soundtrack from an authentic 1900's pipe organ. Guests can also enjoy a special cocktail concoction from the St. George Spirits Absinth Bar.
In San Francisco at the extensive Vendor Bazaar located on the lower level each night ($5 on Saturday from noon to 5 p.m.) attendees can browse and/or purchase authentic fashion, costumes, accessories, jewelry and plenty of relevant, rare oddities. The Vendor Bazaar will also feature fashion shows, strolling performers and a hosted Edwardian Gaming Parlour.
The Edwardian Ball Los Angeles – February 8, 2014: It's returning to Hollywood's beautiful Fonda Theatre
for a night of music, dance, theatrics, circus arts, ballroom dancing, midway gaming, mischief, and, of course, the art and stories of Edward Gorey! The Edwardian Ball Creators & Co-Hosts, Rosin Coven & Vau de Vire Society will perform an original presentation of Edward Gorey's "The Curious Sofa." Plus Delachaux, Shakti Bliss, The John Bros. Piano Company, The Klown, Gentlemen Callers, BellHop, Malvoye The Mentalist, Shovelman, Portrait Booth, and Rooftop Vendor Bazaar and Midway Gaming. Dark Garden Corsetry will be presenting their famous fashion show featuring a new collection in vibrant jewel tones, suitable for cocktail parties or the boudoir. Also, attendees can enjoy absinthe cocktails, full food menu and ample parking.
San Francisco Events:
What: The 14th Annual Edwardian Ball & World's Faire
When: Friday & Saturday, January 17 & 18, 2014 –
Doors and Show at 8:00pm
Where: The Regency Ballroom
1300 Van Ness
San Francisco, CA 94109.
Phone (415) 673-5716 or visit http://www.theregencyballroom.com.
Fri: $40 GA, $80 VIP – Purchase: http://www.ticketfly.com/purchase/event/406851
Sat: $50 GA, $95 VIP – Purchase: http://www.ticketfly.com/purchase/event/405947
All prices increase $5 at the door
2-day discount GA: $80, advance only – Purchase: http://www.ticketfly.com/purchase/event/372355
Check the website www.edwardianball.com for Ticket Outlets.
Vendor Bazaar: $5 Saturday, January 19th from noon to 5pm. Free both nights with admission.
Purchase: http://www.ticketfly.com/purchase/event/406925
Los Angeles Event:
What:The Edwardian Ball presents Edward Gorey's "The Curious Sofa"
When: Saturday, February 8, 2014 – Doors and Show at 8:00pm – All Ages Welcome
The Fonda Theatre
(323) 464-0808 or visit http://www.fondatheatre.com/.
Tickets: Purchase: http://www.ticketfly.com/purchase/event/372385
GA Tickets: $45. Includes main floor and rooftop Carnival, limited seating on a first-come, first-served basis.
VIP Tickets: $75. Includes all GA access plus admission to seated balcony with cocktail service and prime view of stage.
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Breast tissue is among the most sensitive tissues to the carcinogenic actions of ionizing radiation and epidemiological studies have linked radiation exposure to breast cancer. Currently, molecular understanding of radiation carcinogenesis in mammary gland is hindered due to the scarcity of in vivo long-term follow up data. We undertook this study to delineate radiation-induced persistent alterations in gene expression in mouse mammary glands 2-month after radiation exposure.
Six to eight week old female C57BL/6J mice were exposed to 2 Gy of whole body γ radiation and mammary glands were surgically removed 2-month after radiation. RNA was isolated and microarray hybridization performed for gene expression analysis. Ingenuity Pathway Analysis (IPA) was used for biological interpretation of microarray data. Real time quantitative PCR was performed on selected genes to confirm the microarray data.
Compared to untreated controls, the mRNA levels of a total of 737 genes were significantly (p<0.05) perturbed above 2-fold of control. More genes (493 genes; 67%) were upregulated than the number of downregulated genes (244 genes; 33%). Functional analysis of the upregulated genes mapped to cell proliferation and cancer related canonical pathways such as 'ERK/MAPK signaling', 'CDK5 signaling', and '14-3-3-mediated signaling'. We also observed upregulation of breast cancer related canonical pathways such as 'breast cancer regulation by Stathmin1', and 'HER-2 signaling in breast cancer' in IPA. Interestingly, the downregulated genes mapped to fewer canonical pathways involved in cell proliferation. We also observed that a number of genes with tumor suppressor function (GPRC5A, ELF1, NAB2, Sema4D, ACPP, MAP2, RUNX1) persistently remained downregulated in response to radiation exposure. Results from qRT-PCR on five selected differentially expressed genes confirmed microarray data. The PCR data on PPP4c, ELF1, MAPK12, PLCG1, and E2F6 showed similar trend in up and downregulation as has been observed with the microarray.
Exposure to a clinically relevant radiation dose led to long-term activation of mammary gland genes involved in proliferative and metabolic pathways, which are known to have roles in carcinogenesis. When considered along with downregulation of a number of tumor suppressor genes, our study has implications for breast cancer initiation and progression after therapeutic radiation exposure.
We know from epidemiological studies that exposure to ionizing radiation (IR) is one of the major risk factors for breast cancer especially if exposure occurs at a young age[1, 2]. Exposure to radiation, which is increasingly used in diagnostic and therapeutic interventions, is unavoidable and is predicted to pose carcinogenic risk[3, 4]. Radiation induces a myriad of damage to biomolecules including DNA and the carcinogenic potential of radiation has been attributed to alterations in the expression of genes, which could induce proliferation and provide survival advantage to cells. Changes in gene expression in response to radiation have been reported to vary depending on the dose and the tissue exposed; and, there are significant differences in acute and delayed responses to IR exposure. Delayed effects of IR on gene expression are not only associated with cancer initiation and promotion in normal cells but are also known to play a critical role in the development of resistance to therapy in cancer cells. Therefore, radiation treatment of breast cancer has on the one hand the potential for cancer recurrence and on the other the risk for developing new cancer in the contralateral breast. Despite the fact that radiation exposure causes persistent changes in gene expression, data on radiation-induced long-term alterations in gene expression in mammary tissues are of limited availability. Furthermore, there are no reports in the literature of long-term microarray-based studies of changes in mouse mammary gland gene expression after exposure to radiation doses relevant to therapeutic procedures. Considering the carcinogenic potential of radiation exposure to mammary glands, it is important to understand how radiation modulates long-term gene expression changes and how these changes relate to oncogenic signaling pathways known to be involved in breast cancer initiation and progression. Therefore, the goals of this study were to characterize persistent transcriptomic alterations and explore how these alterations relate to biological functions in whole body exposed 6 to 8 week old female C57BL6/J mouse mammary glands 2 months after exposure to 2 Gy γ radiation.
Mice (C57BL/6J, female, 6-8 week old) were purchased from Jackson Laboratories (Bar Harbor, ME, USA) and were housed at the Georgetown University's (GU) animal facility. All the animal procedures were performed as per protocol approved by GU Animal Care and Use Committee (GUACUC). Mice were placed in a circular pie shaped, well-ventilated plastic mouse holder, the mouse holder with mice was positioned on a rotating turntable inside the irradiator, and mice were exposed to γ radiation using a 137Cs source. Radiation dose was delivered at a rate of 1 Gy/min and a total dose of 2 Gy was delivered to the whole body and the control groups were sham irradiated. After irradiation mice were returned to their home cage, and monitored regularly.
Mice were euthanized by asphyxiation using CO2 as per GUACUC approved protocol and mammary glands were surgically removed 2 month after radiation exposure for RNA extraction. For RNA extraction, we used no. 4 mammary gland from the left side of each mouse and four such mice were used in each experimental group. Total RNA was isolated with Trizol reagent (Invitrogen, Carlsbad, CA) from fresh or flash frozen mammary glands followed by purification over an RNeasy column according to the manufacturer's instructions (Qiagen, Germantown, MD) and stored at -80°C for further use. RNA quality was determined using a Bioanalyzer (Agilent Technologies, Palo Alto, CA).
Cy3-labeled cRNA was generated from 300 ng total RNA using Agilent's Low RNA Input Linear Amplification PLUS kit. Cy3-labeled cRNA (1.65 μg) was hybridized to Agilent's Mouse Whole Genome arrays (G4122F) with Agilent's GEx Hybridization HI-RPM Buffer. The samples were hybridized for 16 hours in a rotisserie hybridization oven (G2545A, Agilent Technologies, Santa Clara, CA, USA), then washed with Agilent's gene expression wash buffers and scanned with an Agilent DNA Microarray Scanner 2505A in an ozone hood. Subsequent image analysis, data extraction, and background corrections were performed with Agilent's Feature Extraction Software 9.1. Extracted data were then analyzed using GeneSpring GX 10.0 (Agilent Technologies) to identify genes that had significantly changed expression between control and the irradiated group. Although small sample size (3 to 5 biological replicates) conventionally used in microarray experiments has its limitations, the large data sets used in comparative analysis provide enough statistical power to derive biologically meaningful inferences from the results (discussed in Prolla, 2002). Genes considered significantly (p<0.05, t-test with Benjamini-Hochberg correction) and differentially (fold change ≥2.0) regulated were listed separately.
Significantly perturbed gene lists generated from microarray analysis were uploaded onto Ingenuity Pathway Analysis (IPA, Ingenuity Systems Inc., Redwood City, CA, USA) for assignment of biological function as well as for identifying perturbed signal transduction networks. IPA combines the uploaded data and the Ingenuity Pathways Knowledge Base (IPKB), created with information from available literature, to identify biological networks that are significantly over-represented in the gene expression data. Right-tailed Fisher's exact test is applied to determine the level of significance for each network and the p-value is displayed as score, which is the negative log of that p-value. A score of 8 indicates that there is a 1 in 108 chance that the focus genes are together in a network due to random chance alone. Furthermore, IPA uses a built-in library to identify association between the uploaded genes with the canonical pathways present in the knowledge base. In addition to providing a significance score, IPA also calculates the number of genes within a dataset that are present in each significantly perturbed pathway.
For confirmation of microarray data by qRT-PCR, cDNA was generated from 1.5 μg RNA using the RT2 First Strand Kit as per recommendation (SA Biosciences, Frederick, MD, USA). Primers for PPP4c (protein phosphatase 4, catalytic subunit; Cat# PPM28940A), MAPK12 (mitogen-activated protein kinase 12; Cat#PPM04541C), PLCG1 (phospholipase C, gamma 1; Cat#PPM004022B), and β-actin (Cat# PPM02945A) were obtained from SA Biosciences. Primers for E2F6 (Forward primer: 5'-GATGGCATCGAACTGGTGGAA-3'; reverse primer: 5'-CCCCAAAGTTGTTCAGGTCAG-3'), and ELF1 (Forward primer: 5'-TGTCCAACAGAACGACCTAGT-3'; reverse primer: 5' CACACAAGCTAGACCAGCATAA-3') were obtained from Eurofins MWG Operon (Huntsville, AL, USA). Primer for NFkβ, which is the nodal molecule of the top scoring molecular pathway network identified from the microarray data set by IPA, was also obtained from Eurofins MWG Operon (Forward primer: 5'-AGCACATAGATGAACTCCG-3'; reverse primer: 5'- CTGTAAAGCTGAGTTTGCG-3'). Using the RT2 SYBR Green/Fluorescein qPCR Master mix (SA Biosciences) qRT-PCR was performed on an ABI 7900HT (Applied Biosystems, Carlsbad, CA, USA) platform with temperature settings: 95°C (denaturation) for 10 min and then 40 cycles of 95°C for 15 sec, annealing/extension at 60°C for 1 min. The fold change was calculated using β-actin as an endogenous control following the comparative Ct (ΔΔCt) method as described previously. Results were expressed relative to control samples, and three biological replicates were used in each experimental group. The error bar represents standard error of mean (SEM).
Global analysis of microarray data indicated that compared to control the mRNA level of a total of 737 genes remained perturbed 2-month after exposure to 2 Gy of γ radiation. While 67% (493 genes) of the genes were upregulated, we observed that only 33% (244 genes) of the genes were downregulated (Figure 1A). When we assessed the scale of variation in the significantly perturbed genes' list (relative to control p<0.05 and above 2-fold), the majority of the upregulated fold changes were between 1 and 3 fold and the majority of the downregulated fold changes were between 1 and 2 fold (Figure 1B).
Exposure to ionizing radiation results in persistent perturbations of mammary gland gene expression. A) Total number of transcripts perturbed 2-month after exposure to 2 Gy of whole body γ radiation. About 67% of the transcriptomes were upregulated and 33% remained downregulated. B) Transcripts significantly modulated relative to control (p<0.05 and more than 2-fold change) were plotted showing fold change distribution. Most of the upregulated genes were between 1 and 3 fold and the downregulated genes were clustered mostly between -1 and -2 fold.
We performed qRT-PCR on five selected differentially expressed genes to confirm microarray data. The PCR data on PPP4c, ELF1, MAPK12, PLCG1, and E2F6 exhibited a trend similar to our microarray measurements (Figure 2). Compared to control, PPP4c (fold change -3.14 ± 0.41 standard error of mean (SEM); p<0.001; microarray fold change -1.54) and ELF1 (fold change -2.49±0.55; p<0.003; microarray fold change -1.78) was downregulated and were consistent with microarray results. Also, in agreement with our microarray data, we observed upregulation of MAPK12 (2.47±0.47; p<0.02; microarray fold change 1.85), PLCG1 (3.28±0.76; p<0.02; microarray fold change 1.96), and E2F6 (1.69±0.28; p<0.04; microarray fold change 1.7) expression. We also performed qRT-PCR of NFkβ, which is the nodal molecule of the highest scoring molecular network obtained from IPA (fold change 1.65 ± 0.12; p<0.03 in γ irradiated samples compared to control; Figure 2).
Confirmation of microarray data by PCR analysis. Results of PCR analysis of 2 downregulated (PPP4C, and ELF1) and 3 upregulated (MAPK12, PLCG1, and E2F6) genes showed a trend similar to the microarray fold change. NFkβ is the nodal molecule of the top upregulated network.
To identify which pathways were perturbed 2 months after radiation exposure, we subjected the up and downregulated gene sets to IPA. The results of the analysis associating altered genes to specific canonical pathways are presented in Table 1 (Upregulated) and 2 (Downregulated), and also in Figure 3A (Upregulated) and B (Downregulated). While the upregulated gene sets were significantly associated with 37 canonical pathways (35 presented in Table 1) with a p value cutoff of 0.05 (corresponds to -log p value of 1.3), the downregulated genes were mapped to 7 pathways with similar level of significance (Table 2). Most of the upregulated pathways were involved in cellular growth and proliferation including 'ERK/MAPK signaling', '14-3-3-mediated signaling', 'endothelin-1 Signaling', 'protein kinase A signaling', 'AMPK signaling', and 'corticotropin releasing hormone signaling'. At least two pathways related to breast cancer – 'breast cancer regulation by Stathmin1' and 'HER-2 signaling in breast cancer' – were also found to be upregulated. Metabolism was, also, a common theme among the upregulated pathways with the highest scoring pathways being 'oxidative phosphorylation' and 'mitochondrial dysfunction'. Additionally, 'glycolysis/gluconeogenesis', 'inositol metabolism', and 'ubiquinone biosynthesis' were in the top 10 upregulated pathways. The downregulated gene sets were mapped to fewer canonical pathways none of which are associated with cellular metabolism or proliferation except for the 'G-protein coupled receptor signaling'. All the up and downregulated canonical pathways obtained from the IPA are presented in Additional files1 (Upregulated) and2 (Downregulated) for reference.
Radiation-induced alterations in canonical pathways identified by Ingenuity Pathway Analysis. A) A total of 37 canonical pathways were significantly upregulated (p<0.05 indicated by threshold line). B) A total of 7 canonical pathways were downregulated (p<0.05).
When we used IPA to map the sets of perturbed genes to gene interaction networks in the Ingenuity Pathways Knowledge Base (IPKB), the upregulated genes were mapped to a total of 23 networks, whereas the downregulated genes were associated with 13 signaling networks. Networks with score ≥8 for the up and downregulated genes are presented in Tables 3 (12 upregulated networks had a score of ≥8) and4 (4 downregulated networks had a score of ≥8), respectively, and genes from the microarray dataset are identified in bold. Graphical presentation of the up and downregulated networks with a score of ≥8 demonstrates long-term signaling pathway alterations after radiation exposure (Figures 4,5,6,7,8,9,10 and11). The functions related to upregulated networks ranges from cell death, cell cycle, cell growth and development to carbohydrate and lipid metabolism. Among the upregulated genes, the network with highest score has NFkβ as the nodal molecule (Figure 4A) and, as shown above, qRT-PCR analysis illustrated a 1.65-fold increase in expression of NFkβ in irradiated samples relative to control samples (Figure 2). The network with second highest score has the IL5 (interleukin 5) and HTT (huntingtin) as the nodal molecules and are presented in Figure 4B. The third highest scoring network is involved in the regulation of reproductive system development and function with LH (luteinizing hormone) and FSH (follicle stimulating hormone) as the nodal molecule (Figure 5A) and the fourth is involved in cellular metabolism with KCNJ11 (potassium inwardly-rectifying channel, subfamily J, member 11) as the nodal molecule (Figure 5B). The fifth pathway is involved in cell cycle and cell death and has TP53 as the nodal molecule (Figure 6A). Importantly, the sixth, seventh, and the eighth pathway networks have IL1β (Figure 6B), tumor necrosis factor (TNF; Figure 7A), and IL4/IFNγ (Figure 7B) respectively as the nodal molecules. We also observed that angiotensin receptor type 1 (AGTR1; Figure 8A) and ERBB2 (Figure 8B) are the nodal molecules in ninth and tenth IPA network and has relevance to breast cancer. The eleventh network with PI3K complex (Figure 9A) as its nodal molecule and the twelfth pathway with p38 MAPK (Figure 9B) as its nodal molecule are also known to play important roles in breast cancer initiation and progression. Among the downregulated networks 4 had scores ≥8 and the networks with score in descending order have TGFβ (Figure 10A), PRKCβ (Figure 10B), IFNγ (Figure 11A), and TNF (Figure 11B) as the nodal molecules respectively and are involved in a variety of cellular functions from cell growth and proliferation to lipid metabolism and small molecule biochemistry. Genes, which were significantly associated with the pathway networks in IPA were searched in the literature for their roles in breast cancer and are compiled along with relevant references in Table 5 for upregulated genes and in Table 6 for downregulated genes. A total of 27 upregulated (ACHE, HSPA1L, NES, P2RY2, PLCG1, PPARGC1A, PRKCQ, SNTA1, ALDOA, GNAO1, SLC16A3, TPI1, ELL2, CCNG1, E2F6, ESRRG, MAPK12, HSD17B7, TACC2, DDX1, MYH1, UCP1, PACSIN3, PGM1, TLN2, ADIPOR1, PITX1) and 8 downregulated genes (CELSR2, PRKCB, KIT, MAP2, TDGF1, ELF1, RUNX1, TYMS) showed association with breast cancer. Furthermore, the data files with the complete list of the upregulated and downregulated networks are presented in Additional files3 and4, respectively, for further reference.
Highlighted genes are from the microarray dataset.
IPA identified two top signaling networks with genes involved in carcinogenesis. A) The first network is cellular growth and development network with NFkB as the nodal molecule. At least 12 (ACHE, HSPA1L, MYOD1, NES, NOL3, P2RY2, PGK1, PLCG1, PPARGC1A, PRKCQ, S100B, and SNTA1) genes from this upregulated network are associated with initiation and progression of human cancer. B) The second network is genetic disorder, neurological disease, skeletal and muscular disorders and at least 4 upregulated genes (ALDOA, GNAO1, SLC16A3, and TPI1) are known to be involved in cancer.
Upregulation of cellular proliferation and metabolic pathways involved in neoplasia. A) The third upregulated network involves reproductive system development and function, cellular development, cellular growth and proliferation and upregulation of at least one gene (LBX1) has been associated with cellular transformation. B) The fourth upregulated network involves molecular transport, genetic disorder, carbohydrate metabolism and at least 5 (ALDOA, LDHB, SLC16A3, TPI1, VDAC1) genes are related to carcinogenesis.
Cell cycle and cell death related pathways were upregulated . A) The fifth upregulated network is involved in cell cycle, cell death, hematological system development as well as estrogen signaling such as CCNG1, E2F6, and ESRRG. B) The molecules in the sixth network are know to regulate cell death, neurological disease, and tissue morphology.
Two networks were associated with energy production and cell proliferation. A) Major functions associated with this network are energy production, lipid metabolism, and small molecule biochemistry, and has a score of 16. B) The eighth network had a score of 14 and major functions associated with this network are cellular growth and proliferation, hematological system development and function, and tissue development.
Cell-to-cell signaling and molecular transport related to carcinogenesis were upregulated. A) With a score of 14 this pathway network is associated with cellular function and maintenance, molecular transport, cellular assembly and organization. B) Eleven genes from the microarray data set were associated with this pathway and identified cell death, cell-to-cell signaling and interaction, nervous system development and function as major functions.
Cancer and cell death related pathways were upregulated. A) Genes in this pathway are involved in cancer, tissue development, and embryonic development. B) The twelfth network had a score of 8 and 9 genes from the data set are associated with the network which is involved in cellular movement, cell death, and immune cell trafficking.
The downregulated networks may accelerate cellular transformation. A) The top downregulated network has TGFβ as the nodal molecule and downregulation of at least 8 genes (ARHGAP17, BAMBI, BCL9, BRCC3, CELSR2, NAB2, PRKCB, SEMA4D) in the network facilitates carcinogenesis. B) The second downregulated network has 6 genes (ACPP, GPRC5A, KIT, LYN, MAP2, and TDGF1) which may paly a role in cellular transformation.
Balancing promotion and inhibition of cell proliferation in the downregulated networks. A) Although 1 gene (GHRH) involved in cell proliferation is downregulated in the third network, we observed downregulation of at least 4 key genes (ELF1, MTA3, RUNX1, and TYMS) related to tumor suppressor function. B) The fourth downregulated network with a significant score of 18 has TNF as the nodal molecule and downregulation of at least 2 genes (APOBEC3B, CHSY3) are known to promote carcinogenesis.
"Tumor size was significantly higher when the ACHE gene was amplified in breast cancer.".
"….HSPA1L and HSPA2 could represent potential biomarkers to follow up the effectiveness of 17AAG in breast cancer".
"Among the breast cancer subtypes, nestin is highly expressed in basal breast cancer subtype".
"P2Y2 receptor-mediated modulation of estrogen-induced proliferation of breast cancer cells".
"Phospholipase Cgamma1 is required for metastasis development and progression".
"Associations of genetic variants in the estrogen receptor coactivators PPARGC1A, PPARGC1B and EP300 with familial breast cancer".
"PKCtheta promotes c-Rel-driven mammary tumorigenesis in mice".
"….significant increase in expression of SNTA1 protein compared with the normal tissue was observed in breast carcinoma samples".
"…hypoxia-responsive; prognostic significance in breast cancer".
"GNAO1 (Gαo) gene was identified in breast carcinomas and shown to promote oncogenic transformation when introduced into cells".
"Expression of SLC16A3 gene is higher in breast cancer distant metastasis….".
"Glycolytic cancer associated fibroblasts promote breast cancer tumor growth, without a measurable increase in angiogenesis: evidence for stromal-epithelial metabolic coupling".
ELL2 is a Breast Cancer Antioestrogen Resistance (BCAR) 1 gene which control anti-oestrogen-resistant cell growth resistance (BCAR).
"We have identified cyclin G as being overexpressed in breast and prostate cancer cells".
"E2F6 represses transcription of the brca1, ctip, art27, hp1 α, and the rbap48 genes….".
"Estrogen-related receptor γ modulates cell proliferation and estrogen signaling in breast cancer & ERRγ mRNA was up-regulated dose-dependently by estrogen….".
"…elevated expression of p38γ is associated with lower overall survival of patients with breast cancer".
The stimulation of HSD17B7 expression by estradiol provides a powerful feed-forward mechanism for estradiol biosynthesis in breast cancer cells.
"This suggests that increased TACC2 may mediate an oncogenic effect on breast cancer cells and indicates that TACC2 may be a potential therapeutic target".
"Here, we identify DDX1 RNA overexpression as an independent prognostic marker for early recurrence in primary breast cancer……".
Recently, MYH1 encoding skeletal muscle myosin heavy polypeptide 1 and MYH9 encoding non-muscle myosin heavy chain type A, were identified as candidate breast cancer genes in systematic analyses of the breast cancer genome.
We conclude that UCP1 is up-regulated in breast cancer cell lines and primary breast as well as other tumors.
"New targets for breast cancer treatment were identified such as ZONAB, PACSIN3, MRP8 and SUMO1, which have human homologues".
"This gene has been identified as one of the ER status markers in the diagnosis and prognosis of breast cancer patients….".
"Serum estradiol levels associated with specific gene expression patterns in normal breast tissue and in breast carcinomas……".
"Variants of the Adiponectin and Adiponectin Receptor 1 Genes and Breast Cancer Risk…".
"The estrogen-regulated transcription factor PITX1 coordinates gene-specific regulation by estrogen receptor-alpha in breast cancer cells…".
"Celsr2 was down-regulated in one cell line and in 7% of breast cancers".
PRKCB has been observed to be downregulated in estrogen receptor negative breast cancer.
Loss of c-kit expression has been reported in 80-90% of breast cancer specimens, suggesting a possible role in the development of tumors.
"Elevation of MAP2 in breast cancer cell lines led to increased paclitaxel sensitivity" .
"Overexpression of human Cripto-1 in transgenic mice delays mammary gland development and differentiation and induces mammary tumorigenesis".
"All of the mouse and most human mammary tumors also displayed decreased expression of genes known to inhibit cell proliferation, including NFKBIA (IKBalpha), GADD45B, and CDKN1A (p21); transcription-related genes such as CEBP, JUN, JUNB, and ELF1;….".
"Furthermore, we found that RUNX1 expression was reduced in high-grade primary breast tumors compared to low/mid-grade tumors".
"Gene polymorphisms in TYMS, MTHFR, p53 and MDR1 as risk factors for breast cancer: a case–control study".
A number of genes identified with the downregulated networks are associated with breast cancer.
Mammary gland is sensitive to the carcinogenic actions of radiation and epidemiological data strongly correlates radiation exposure and breast cancer[1, 2]. Here we demonstrate that exposure of 6 to 8 week old female mice to 2 Gy of γ radiation, a dose relevant to fractionated radiotherapy, induced long-term gene expression changes in the mammary glands. These changes are associated with molecular pathways that have the potential to enhance the chance of malignant transformation. We show that even after two months, a significant number of genes remain perturbed and that the majority of them are upregulated. Broadly, these genes are categorized into two major interdependent cellular functions – proliferation and metabolism. Upregulation of proliferative functions supported by induction of adaptive energy producing pathways is also observed in cancer cells. Cancer, described as a chronic and multifactorial disease, was not observed in these mice within the study duration of 2 month. However, we did observe alterations in signaling pathways that may be considered potential carcinogenic precursors events.
The top network with a score of 44 associated 28 genes from the data set and literature indicates that at least 12 (ACHE, HSPA1L, MYOD1, NES, NOL3, P2RY2, PGK1, PLCG1, PPARGC1A, PRKCQ, S100B, and SNTA1) of them are involved in human cancer (genes relevant to breast cancer are presented with relevant references in Tables 5 and6). Indeed, dysregulation of ACHE, HSPA1L, NES, P2RY2, PLCG1, PPARGC1A, PRKCQ, S100B, and SNTA1 genes have been implicated in breast cancer progression and metastasis due to higher proliferation and increase cell migration (Tables 5 and6). Cellular metabolism and transportation related genes (ALDOA, SLC16A3, TPI1, LDHB, KCNQ5, and PGM1), which are implicated in human cancer, also remained upregulated even 2-month after radiation exposure. Importantly, induction of glycolytic enzymes like aldolase A (ALDOA), lactate dehydrogenase (LDH), triosephosphate isomerase 1 (TPI1), and phosphoglucomutase 1 (PGM1), we believe, is supporting cellular growth and development resulting from upregulated proliferative signaling pathways. It has been proposed that in a 'Reverse Warburg Effect' the glycolytic pathway is upregulated in stromal cells generating pyruvate/lactate, which can then be utilized by adjacent epithelial cells for oxidative phosphorylation in mitochondria. Indeed, upregulation of 'oxidative phosphorylation' and 'mitochondrial dysfunction' are the two top canonical pathways observed in the IPA and are reported to be associated with breast cancer. While stromal cell niche is known to play important roles in mammary gland carcinogenesis, we are yet to determine whether there are differential alterations of gene expression in stromal vs. epithelial cells and would require separate microarray analysis of stromal and epithelial compartment in mammary glands. However, considered along with the fact that in a whole boy irradiated mice all the tissue compartments are exposed to radiation, our results led us to speculate that differential alterations of gene expression in stromal vs. epithelial cells could occur in mammary gland to promote radiation carcinogenesis and is supportive of what has been reported in the literature[48, 49]. Interestingly, both ALDOA and SLC16A3 are also suggested to be hypoxia responsive and is upregulated in hypoxic breast cancer with poor outcome. SLC16A3 is known to allow efflux of lactate, which we believe is produced in excess due to radiation-induced upregulation of glycolytic enzymes. Increased glycolysis may have served as a trigger for increased mitochondrial oxidative metabolism observed in our results, and could lead to oxidative stress as has been indicated by upregulation of canonical pathways involved in 'mitochondrial dysfunction' and 'production of nitric oxide and reactive oxygen species in macrophages'. Interestingly, we also observed upregulation of UCP1 (uncoupling protein 1), a member of the UCP protein family known to uncouple respiratory chain events from ATP production. UPC1 is known to limit reactive oxygen species (ROS) production, which could result in oxidative stress below apoptotic threshold, and enhance cellular survival in the presence of irreversible injury to respiration[32, 50]. The presence of radiation-induced mitochondrial dysfunction and consequent oxidative injury to cells are further exemplified by the upregulation of ENDOG, which has been shown to be involved in cell death in the absence of caspases.
Previously, we reported that exposure to 2 Gy radiation led to persistent increase in estrogen levels in serum and estrogen receptors in mammary glands at 2- and 12-month after radiation exposure and was associated with activation of PI3K-Akt proliferative pathways. Microarray data showing upregulation of 17β hydroxysteroid dehydrogenase 7 (HSD17B7), an enzyme involved in conversion of weakly estrogenic estrone to biologically active estradiol in mammary glands, is reported to be induced by high serum estradiol and is in agreement with our earlier observations of increased serum estradiol after radiation. While systemic estradiol mediates its effects in mammary gland via ERα, higher expression of HSD17B7 could provide a 'positive feed-forward' mechanism for enhanced tissue estradiol level and could explain activation of cellular proliferative signals observed by us. Upregulation of estrogen-related receptor γ (ESRRG), which is induced by estrogen to enhance cell proliferation, provides further evidence of agreement between microarray data and our previous results. Importantly, even 2-month after exposure to 2 Gy radiation a high number of transcripts involved in cellular growth and development including strongly mitogenic MAPK12 remain significantly upregulated and are presented in Table 5.
Along with upregulation of genes involved in cellular growth and development, we also observed that a number of genes with tumor suppressor function (GPRC5A, ELF1, NAB2, Sema4D, ACPP, MAP2, RUNX1) persistently remained downregulated in response to radiation exposure further tilting the balance in favor of transformation (Table 6)[43, 53–58]. In contrast, a few genes (TDGF1, GHRH, and BCL9) reported to be involved in promoting cell proliferation are downregulated which highlights the fact that cellular transformation is a multistage process with a sustained tug of war between tumor suppressor and tumor promoter. An important observation of our study was the downregulation of BRCC3 (BRCA1/BRCA2-containing complex, subunit 3), a protein known to play key a role in the repair of DNA damage through its E3 ubiquitin ligase activity on the repair factors and may predispose the mammary gland cells to misrepair and genomic instability. A number of other downregulated genes positively affecting cellular growth and proliferation have been observed in our study and are listed in Table 6.
Molecular pathway networks identified by IPA allowed us to understand how genes in our data sets spatially relate to oncogenic precursor events relevant to breast cancer. The top-scoring pathway has NFkβ and Akt (Figure 4A) as the central molecules and both are known to be involved in breast carcinogenesis[60, 61]. Another high scoring upregulated network identified ERBB2, an important membrane bound receptor tyrosine kinase, as the nodal molecule (Figure 8B) and is known to crosstalk with NFkβ and PI3K-Akt to promote breast cancer. One of the important observations in our study was the recognition of inflammation related factors in the IPA network and a number of pathway showed IL-5 (Figure 4B), IL-1β (Figure 6B), TNF (Figure 7A), IL-4, and INFγ (Figure 7B) as the central molecules highlighting an already existing relationship between inflammation and breast cancer[63, 64]. Reproductive hormones LH and FSH are the central molecules in an upregulated pathway network (Figure 5A) and are known to regulate estrogen, which is strongly associated with risk of developing breast cancer. Indeed, in an earlier study, we have shown that exposure to a radiation dose (2 Gy) used in the current study significantly increased serum estrogen level, urinary oncogenic estrogen metabolite level, mammary gland estrogen receptor α (ERα) level, and cellular proliferation in mice. Estrogen has also been reported to influence TGFβ activity negatively, and interestingly our downregulated data sets mapped to a pathway, which has TGFβ as the nodal molecule (Figure 10A). In our earlier study, we focused on exploring one pathway, the PI3K-Akt pathway, in relation to increased estrogen and ERα and showed that radiation not only upregulated PI3K and Akt activity but also induced their downstream effectors leading to increased mammary gland cell proliferation determined by phospho-histone H3 staining. Current microarray based complete gene expression study after radiation exposure not only showed upregulation of additional pathways already discussed but also showed increased expression of genes associated with pathways having TP53 (Figure 6A), AGTR1 (Figure 8A), P38-MAPK and PLCG1 (Figure 9B), PI3K complex and MAPK3 (Figure 9A) as central molecule. The molecular pathways, which IPA identified to be significantly associated with the genes from the microarray data sets have been implicated in human cancer including breast cancer (Tables 5 and6) and provide evidence towards carcinogenic potential of therapeutic radiation exposure.
Exposure to diagnostic and therapeutic radiation has increased considerably over time[3, 68, 69] and knowledge of the molecular pathways that remain perturbed long-term after radiation exposure could inform us to devise strategies to tackle the carcinogenic potential of radiation. Taken together the microarray data presented here not only correlate with our earlier observations on long-term effects of radiation exposure on mammary gland pathophysiology, but they also further expand on the persistently perturbed molecular networks with potential for transformation after exposure to a clinically relevant radiation dose.
This study supported in part by NASA Grant# NNX07AH70G. DRH was supported, in part, by Grant Number T32 CA009078 from the NCI.
KD: planned and executed experiments, analyzed results, and prepared the manuscript; DH: executed experiments and analyzed results; SS: executed experiments and analyzed results; MJ: participated in preparing the manuscript; AF: participated in preparing the manuscript. All authors read and approved the final manuscript.


DSSSB Warder Admit Card 2018 Grade-II (DASS) Exam Date – Candidates who are looking for DSSSB Warder Exam Dates and also looking to download DSSSB Warder Admit Card 2018, get latest news updates related to release date of DSSSB Warder Admit Card and also the exam date on this the tests are scheduled to be commenced. We have provided all information related to Tier-I examinations for notifications 86/17 85/17 84/17 83/17 82/17 81/17.
Once there is any official confirmation about exam dates and DSSSB Warder Admit Card 2018 is made available 81/17 82/17 83/17 84/17 85/17 86/17 examinations. The same information and news update will be communicated through this page. Below we have listed DSSSB Warder Admit Card 2018 for Grade-II, Pharmacists, Legal Assistant, Warder, Matron, and Assistant Superintendent exam dates admit card release date and official links to download all these DSSSB Warder Admit Card 2018.
DSSSB Warder Admit Card 2018 Grade-II (DASS) Latest News About Exam Dates – Recently Delhi Subordinate Services Selection Board has released a notification for a total of 825 posts which included vacancies for Grade-II, Pharmacists, Legal Assistant, Warder, Matron, and Assistant Superintendent and many more posts. The application was invited from eligible candidates which received a very response from the hopefuls across the state.
Candidates submitted their Grade-II, Pharmacists, Legal Assistant, Warder, Matron, and Assistant Superintendent against notification numbers 81/17 82/17 83/17 84/17 85/17 86/17 are now waiting eagerly for the release of DSSSB Warder Admit Card 2018, so that they may appear in the examinations. Also, there has been no announcement about the exact date of DSSSB Warder examinations for the above-mentioned posts. As soon as Delhi Subordinate Services Selection Board announces the DSSSB Warder exam date and official links to download DSSSB Warder Admit Card 2018, we will communicate the same information to all respected candidates who are going to take on these examinations.
DSSSB or Delhi Subordinate Service Selection Board came into existence in the year of 50th anniversary of Independence Day of India. Managed by the Government of National Capital Territory of Delhi, the board was started with the objective of recruiting the most suitable and well-deserved employees who are skilled and competent in nature to tackle all the assigned tasks. DSSSB Selects most suitable candidates for every particular post by conducting examinations on the state level. Then is pick the most talented personnel and recruitment them on the vacant posts.
These selection procedures consist of techniques conforming to global standards of selection. Ultimately, this multilevel selecting procedure ensures that the most suitable candidates are shortlisted. To sort out the capable candidate's numbers of tests are conducted ranging from written exams to professional tests as well as personal interviews. All of these exams have the appropriate difficulty level to check the caliber of applicants. Not only these tests make the best out of available applicants get recruited for the job, but they also maintain the quality of workforce inflow in the organization.
In one of the same events, Delhi Subordinate Selection Board had released notifications and now all set to conduct the examinations for the same. There is no other way to appear in any of these examinations but by downloading DSSSB Warder Admit Card for Grade-II (DASS), Pharmacists, Legal Assistant, Warder, Matron, and Assistant Superintendent examinations scheduled to be conducted soon. The details about exam date, venue and all other details have been provided on this page along with DSSSB Warder Admit Card for notification numbers 86/17 85/17 84/17 83/17 82/17 81/17.
However, the individual details are available on the call letter for all eligible candidates for whom the DSSSB Hall Ticket has been issued. The confirmed examination date has also been updated adjacent to the examinations in the table below. Go ahead and find out all important details and release date of admit cards and official news information regarding new dates for the postponed DSSSB Warder examinations. Select the post for which you have submitted your application and download DSSSB Warder Admit Card 2018 and check Grade-II (DASS) New Exam Date online.
Download DSSSB Warder Admit Card 2017-18 – Candidates are advised to download the DSSSB Hall Tickets online from the official portal. The direct URL's have been provided below. Keep in mind that traditionally the call letters were being sent to your address by post. Gone are the days and now you must ensure that you download DSSSB Warder Admit Card 2108 online days before the exam date. If you fail to do so, your admission into the examination premises will be denied. Below we have tabulated all information regarding DSSSB Grade-II, Pharmacists, Legal Assistant, Warder, Matron, and Assistant Superintendent Admit Card 2017-2018. Go ahead and download the correct call letter by entering your personal information correctly which was provided at the time of the registration.
The examination will carry a total of 200 marks and it will be MCQ Question Paper (Multiple Choice Questions) also called objective examinations. After the commencement of the examinations, Answer keys will be available on our website, providing correct answers to all questions. The examination will be conducted for a duration of 2 Hours in which candidates must finish their exams and no additional time will be provided at any circumstances. Last but the most important thing, these examinations will carry negative marking which means, for every incorrect answer 0.25 (1/4) marks will be deducted from the correct answers you gave. So be very careful and attempt only when you are pretty sure about the answer.
How to Download DSSSB Warder Admit Card 2018?
Navigate to the official DSSSB website @ delhi.gov.in.
Now go to Delhi DSSSB Admit Card Section.
Select the desired admit card, direct links are available on this page as well.
Enter required personal details furnished at the time of application.
Submit the form and DSSSB Admit Card will be downloaded.


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Richard Blanco - London
NLA Representative
Richard.Blanco@landlords.org.uk
The National Landlord Association is the UK's largest membership organisation for private residential landlords, supporting and representing over 30,000 members. We help landlords navigate challenges and proudly offer some of the most comprehensive learning resources and market-leading intelligence available in the sector.
Richard buys and refurbishes properties, and manages his own portfolio across six London boroughs. Originally from a dance and theatre background and an HR and diversity specialist, Richard has been a landlord for 15 years. He has a keen interest in financing and development; landlord and tenant relations, and general housing policy. Richard has a strong commitment to improving the private rented sector; organises and speaks at events across London, and supports NLA media campaigns. He writes regularly for Property Investor News; produces and presents the NLA Podcast 'Inside Property', and presents London and Madrid editions of USA property show 'House Hunters International.'
Vision, Values & Objectives
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Within minutes of arriving in Marrakech, renowned author Jaspar Wills is kidnapped. Living with a loss far greater than his own death, Jaspar is a destroyed man…until an act of revenge leads to stunning revelations that will change everything. The truth will set you free. Can lies do the same?


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Q: Relationship between associated graded module and a quotient Let $R$ be a ring, $J \subset I$ ideals. Let $\mathfrak{I} = R\supset I \supset I^2 \supset \cdots$ be the $I$-adic filtration of $R$. I want to compare the associated graded module $\operatorname{gr}_\mathfrak{I}(R)$ to the associated graded module $\operatorname{gr}_\mathfrak{I}(R/J)$ where $R/J$ is viewed as an $R$-module.
According to an exercise in Eisenbud, we have $\operatorname{gr}_\mathfrak{I}(R/J) \simeq \operatorname{gr}_\mathfrak{I}(R)/\operatorname{in}(J)$ where $\operatorname{in}(J) = \left\langle \operatorname{in}(f) \,\mid\, f \in J\right\rangle$. I think I'm close, but I'm not quite there yet. Here's my reasoning so far.
Suppose that $J \subset I^n \,\forall n \in \mathbb{N}$. Then it is not difficult to show that $\operatorname{in}(J) = 0$, since by definition, $f \in I^n \,\forall n \in \mathbb{N}$, we have $\operatorname{in}(f) = 0$ so $\operatorname{in}(J) = 0$. So then we have for each index $k$, that $I^{k-1}(R/J)/(I^k(R/J)) = I^{k-1}/I^k$ and thus $\operatorname{gr}_\mathfrak{I}(R/J) = \operatorname{gr}_\mathfrak{I}(R)$.
Otherwise, for some $n \in\mathbb{N}$ we have $J \subset I^n$ but $J\not\subset I^{n+k}$ for all $k \ge 1$. So then the $n+k$ graded piece of $\operatorname{gr}_\mathfrak{I}(R/J)$ is $I^{n+k}(R/J) / I^{n+k+1}(R/J) = (I^{n+k} \cap J)/(I^{n+k+1}\cap J)$ and in the special case of $k=0$, we have $I^n/(I^{n+1}\cap J)$. I can't exactly see how to relate this to the quotient by the initial form of $J$.
For instance, for $f \in \operatorname{gr}_\mathfrak{I}(R)/\operatorname{in}(J)$, we have $f = \sum_{i=1}^k f_i + I^{n_i+1}$ where $f_i \in I^{n_i}$ but $f_i \not \in I^{n_i+1}$. I want to be able to consider this as something in the intersection with $J$ to relate it with the remarks in the previous paragraph, but I can't really see how to do it.
Can anyone provide a hint as to continue?

redpajama_set_name: RedPajamaStackExchange


On behalf of Sivin & Miller, LLP Attorneys at Law posted in blog on Monday, July 17, 2017.
American citizens are guaranteed certain rights within the United States Constitution. One of those rights is in the 4th Amendment, which protects citizens against unlawful searches and seizures.
Police officers may not always stay on the right side of the law, either intentionally or unintentionally. Therefore, it is up to New York citizens to educate themselves about their rights. All people should understand what protections the 4th Amendment provides, and understanding it more thoroughly may help one day.
A police officer cannot search a person's home without a warrant. There are some exceptions to this. For example, if a piece of evidence were to be in plain view, such as drug paraphernalia being visible from a window, then an officer could come into a home due to probable cause. Additionally, officers can search a home if the occupants invite them inside.
The police can only pull over a vehicle if it they suspect the driver committed a traffic violation. This means they cannot pull over people without any kind of explanation. The officer has to tell the driver the reason for the stop. A search of the vehicle cannot take place unless probable cause is present. For instance, if a drug dog is there and reacts a certain way, then the police could search the car.
When walking down the street, a police officer cannot randomly stop people. In New York, there have been controversies over the years about the stop-and-frisk policy, although there have been efforts to curb those tactics. The 4th Amendment generally states that a person must be suspected of involvement in a criminal activity, and an officer can only ask questions to gather more information about said activity.
An educated population is a safe population. All people should understand the Constitution because it may one day prove to be a great asset.


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India: The land of Dreams and Romance
Lata Mangeshkar: A Life in Music
Eternally Ethnic: Folk Paintings of India
The Vinayaka Mahatmya
Encyclopaedia of Upanisadic Philosophy (In 3 Volumes)
Kashmir Shaivism: A Philosophy of Being and Becoming
Jadunama: Javed Akhtar's Journey
Maan Sagari: An Ancient Astrological Treatise (In 2 Volumes)
Unani Medicines for Women
Buddhism in North-East India
Coins of the Delhi Sultanates
8.00 $ 8.89 $
Santali: A Linguistic Study
Conquering Quill: Studies in Commonwealth Literature
Baniya Legacy Of Old Delhi
Satyajit Ray Miscellany: On Life, Cinema, People and Much More
Silent Sentinels of Ranthambhore
The Coins of India: The Mughal Emperors, Part VIII (M8)
Indian Embroidery
Yoga-Nidra: Yogic Trance Theory, Practice and Applications
David Frawley (Vamadeva Shastri) is one of the few Westerners recognized in India as a Vedacharya or teacher of the ancient Vedic wisdom. He is the author of numerous books and articles on Vedic topics including Ayurveda, Vedic Astrology, Vedanta, Hinduism, Yoga and Tantra, as well as translations and interpretations from the Vedas. Dr. Frawley has been given many awards for his work in India including the Veda Vyasa award by the International Institute of Indian Studies. He is a Jyotish Kovid through the Indian Council of Astrological Sciences, and is also the President of the American Council of Vedic Astrology, the American offshoot of the Indian Council. He has a Doctor's degree in Chinese Medicine and has also been certified as an expert through the University of Poona for his knowledge of Yoga and Ayurveda. He is presently Director of the American Institute of Vedic Studies.
Monika Zin
Monika Zin taught Indian art history at the Ludwig-Maximilans-Universitat in Munich and the Freie Universität Berlin from 1994 to 2016. Among her research contributions are monographs such as Ajanta: Handbook of the Paintings. Devotional and Ornamental Paintings, Harrassowitz 2003 (English edition currently pending publication at the IGNCA); Compassion and Miracles: Difficult Conversions and Their Iconography in Indian Buddhism (in German, Harrassowitz 2006); Samsaracakra: The Wheel of Rebirth in the Indian Tradition (together with Dieter Schlingloff, in German, EKŌ House of Japanese Culture, 2007) and numerous articles on the identification of narrative art and Indian drama. Since 2016, Prof. Zin has led the research team of the Centre 'Buddhist Murals of Kucha on the Northern Silk Road' at the Saxon Academy of Sciences in Leipzig/Leipzig University.
Aryan Books International
Chowkhamba Sanskrit Series Office
D K Printworld
Indus Publishing Company
Motilal Banarsidass Publishers
Roli Books
CBH Publications
Lonavla Yoga Institute
Amar Chitra Katha
Niyogi Books


The art of Rian Gonzalez – Over the Rianbow !
Like a taste of sweet candy!
Colorful, shimmering and I would even dare to say sweet, are the words that the works of this Filipino artist inspire me. Rian Gonzalez is a freelance artist who appropriates characters from pop culture (mostly from comics or manga) by infusing them with her magic recipe based saturated colors so well chosen that one has almost the impression of them to taste.
You'll quickly recognize some of Marvel's famous characters, as well as those from stories published by Archie Comics (that you may know trough the Riverdale series) or Sailor Moon to name a few. I warmly invite you to go on her website, her twitter account and her instagram if you want to be amazed. You can even discover some videos of her working on her Facebook page. Yummy ! There's even sparkles !
Gorgeous The Two Towers Prints by Juan Esteban Rodriguez for the Bottleneck Gallery !


We build a virtual model. You enjoy the real-world benefits.
Q's Building Information Modelling (BIM) software is a wonderful thing, and we're implementing this innovative technology to save our clients time and money.
BIM is integral to our concept-to-completion process, making it easy to design, visualise and fine-tune every detail of your building – virtually – before a single bolt has been ordered, delivering real-world cost and time savings.
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No last-minute, costly site modifications. Just seamless construction.
BIM takes risk out of the equation, and replaces it with certainty. We're able to minimise or even eliminate the misunderstandings and miscommunications that lead to costly mistakes, which translates into a faster, more seamless and cost-effective building experience.


Today, Causal Bit Games released a new trailer for its Ghosts 'n Goblins inspired game Battle Princess Madelyn, which will be released soon for Xbox One, PlayStation 4, PlayStation Vita, Nintendo Switch, Nintendo Wii U, and PC. The video shows that Maldita Castilla's Don Ramiro will guest star to join Madelyn on her quest to save her family. Check out our interview with the CEO of Causal Bit Games, check out the video above, and stay tuned for more news here on Gaming Trend.


With the advent of spring CuCo Creative has gone to print with the latest DL for Athelhampton House & Gardens, one of Dorset's top attractions.
The information-packed flyer not only encourages day visitors to the historic manor but also promotes allied attractions such as the Athelhampton film club and the characterful Martyrs Inn in nearby Tolpuddle.
The DL – which will be widely available across the South and West of England – also includes a promo for Athelhampton House's wedding and reception facilities, showcased fully by CuCo in a lavish 16-page brochure published earlier this year.


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erik@erikwaterkotte.com
ERIK WATERKOTTE
operating an individual occult
Erik Waterkotte is an Associate Professor of Print Media in the Department of Art & Art History at the University of North Carolina-Charlotte. His creative research utilizes graphic and mixed media to create layered exhibits exploring representations of belief and ideology.
Erik Waterkotte has exhibited his artwork both nationally and internationally with recent exhibitions at the University of Alberta, Canada, the Appleton Museum of Art, Ocala, Florida, and the Landmarks Art Gallery of Texas Tech University. His work is part of several collections including the Weisman Art Museum, at the University of Minnesota and the Purdue University Galleries. Waterkotte has been the recipient of several awards and residencies including an Affiliate Artist Residency at the McColl Center for Art & Innovation. Waterkotte has been a visiting artist at universities throughout the United States. He received his M.F.A. from the University of Alberta and his B.F.A. from Illinois State University.
©2021 by Erik Waterkotte. Proudly created with Wix.com


Maybe it's best to elucidate; GPHG we're not. What we're is a consumer-focused commerce title that seeks to discern, perceive, and anticipate the burning questions and wishes of anybody who loves watches. To that finish, the classes and the novelties which were nominated or chosen as eventual winners are reflective of how a watch shopper may store or embark on a decision-making course of. That stated, the chosen watches are usually not curated in a vacuum; a panel of two editorial employees and two collectors had been chosen to choose from the novelties of 2018.
A hoop is historically used to suggest to a woman. Nonetheless, WOW is open to the concept of proposing with a watch! The "YES" Watch ought to be moderately embellished. Bonus factors if the nominated timepiece has a counterpart for the male social gathering to put on.
When one proposes to "have and to carry for so long as you each shall dwell", it's with a certainty that your partner possesses the world's first key to your coronary heart and soul. High fashion meets haute horlogerie within the new Roger Dubuis Velvet Caviar in a world's first of a distinct form. Due to artisanal abilities, the head-turning strap shimmers with black or white crystal beads combined with molten polymer, accentuating the distinctive case form of the Velvet. From case to strap, this timepiece is beautiful. Topped with a mother-of-pearl dial and studded with brilliant-cut diamonds alongside the bezel and lugs, the multi-facetted gleam of the Velvet Caviar is a suggestion that only a few would refuse.
WOW Awards consist a complete of 11 classes. The remainder of the winners will we introduced over the following three days.


Weddingz.in has 10 wedding decorators in Ludhiana listed on its platform. These wedding decorators offer range of services. Popular wedding decorators in Ludhiana are Indo Western Wedding Planner , Adarsh Decorator, Elegant Decor.
Package prices range quite a bit from Rs 1000/- to Rs 150000/- Budget wedding decorators in Ludhiana being Welcome Decorator, vicky-flower-decorator, Indo Western Wedding Planner . And on the high side being Banzer Blossoms and Greens, Elegant Decor, Kohli Wedding Planners and Caterers.


A typical Toastmasters meeting is divided into three parts: Warm-Up, Prepared Speeches and Evaluations. While the exact structure of the meeting varies from club to club, there are multiple elements common to every Toastmasters meeting worldwide. We have several roles taken by participants at Toastmaster meetings that help fulfill specific tasks. This article explains the structure of the meetings at Mannheim International Toastmaster Club.
Our meetings are usually scheduled for 2 hours, starting at 19:30. The meeting is started by the Sergeant at Arms who calls the meeting to order and hands over to the Presiding Officer. The links will explain these roles in more detail. After greeting the attendants and asking guests to introduce themselves, the Presiding Officer will start the meeting with a quick round-table talk. A question is asked and each participant in the meeting should answer in about 30 seconds. This helps us to get started talking and also to get to know each other a bit better. The Presiding Officer then hands over to the Toastmaster of the Evening.
The warm-up continues with the Word of the Day. This is a useful word for us to know that we do not usually have in our vocabulary (at least as non-native speakers of English). The participants of the meeting can then try to use this word which will be positively acknowledged.
Afterwards a Joke of the Evening is given to make us laugh and warm up more. Another smaller role that follows is the Thought of the Day that can give us something to think about after the meeting.
The meeting continues with Table-Topics, a section that is "feared by some and loved by others". Table-Topics is about giving impromptu, spontaneous speeches. The Table-Topic Master has prepared multiple questions – sometimes arranged around a specific theme – which they will ask the audience. Then they will pick someone to answer this question in 1 to 2 minutes time. Please note that as a guest you do not have to participate, but you can if you like (and if you are asked to). Also, you should try to answer the question, but you do not need to – you could digress from the topic and talk about something entirely different. Here you can find more tips on Table-Topics. We usually have 4-6 participants called up to speak. Afterwards, the timer will report on whether the speakers stayed in time and then we vote for the best Table-Topics speaker. The Toastmaster of the Evening will then announce a break.
The meeting proceeds with its second part: Prepared speeches. Speeches are prepared according to different Communication Manuals. These manuals are distributed by Toastmasters International and contain several speech projects. New Toastmasters always start out with the Competent Communication Manual that comprises 10 speech projects. Most of these speeches have a time of 5 to 7 minutes. We usually have 3 to 4 prepared speakers. As an example, the first speech project of a new member is called "The Ice Breaker". In this project, the speaker should introduce himself or herself to the audience and structure the speech into a beginning, a body, and an end. After each speech there is time for feedback. Every member can write down some positive remarks and suggestions for improvements on a sheet which will give additional feedback to the speaker. After all the speeches have been given, the timer will report once again and we will vote for the best speaker. Now the Toastmaster of the Evening will hand over control to the General Evaluator for the third part of the meeting: Evaluations.
Each prepared speaker has an Evaluator assigned who will give the speaker a written evaluation of the project in his manual, but also a verbal evaluation. For this evaluation speech the evaluator has a timeframe of 2 to 3 minutes. The evaluator will highlight the strengths of the speaker and the things that were done well and give few suggestions to make the next speech even better. After all evaluations were given, the timer will report for the last time and we will vote for the best evaluator.
Now the Ah-Counter and the Grammarian will give their respective feedback to the participants. Afterwards the General Evaluator will give feedback to the roles who have not yet received any dedicated feedback. The General Evaluator will also give suggestions to improve the meeting in general. At the end, they will hand back to the Presiding Officer.
The Presiding Officer will handle the Club Business section which includes announcements and decisions to be made. Awards are handed out for the best Table-Topics speaker, best prepared speaker and best evaluator. After the meeting we usually meet at a pub close-by and have a drink together.
Now if you read all of this, why don't you take a look at the agenda of our next meeting?