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Our Sentence is Up: Seeing Grant Morrison's The Invisibles, a non-fiction look at the landmark series, is in this month's Previews catalog (order code SEP091084). The book, authored by Patrick Meaney, is published by Sequart Research & Literacy Organization.
Our Sentence is Up offers an accessible look at Grant Morrison's complicated and ambitious comics masterpiece, paying attention to its themes, philosophy, and how it changes with each reading.
The Invisibles has been hailed as a seminal comic, called the key to Morrison's overall body of work, and seen as the inspiration for The Matrix and its successors. But it's also frequently written off as incomprehensible or just too out there.
Written in a conversational, personal style, Our Sentence is Up opens up The Invisibles through an in-depth, issue-by-issue analysis of the series, making sense of its complex ideas, fractured chronology, and delirious blend of fiction and reality. The book also explores the real-world relevance of the comic, particularly how its fictional conspiracy theories became reality in the 2000s.
The book also features a wide-ranging interview with Grant Morrison, covering how his formative childhood experiences found their way into The Invisibles and how his life and the comic became intertwined in the '90s. Morrison also explores the series in retrospect, how it holds up to the War on Terror and the Obama presidency, and what he currently thinks will happen in 2012.
The book sports an afterword by Morrison expert Timothy Callahan (CBR), author of Sequart's Grant Morrison: The Early Years. The book also sports an original cover by award-winning artist Kevin Colden (Fishtown, I Rule the Night).
Our Sentence is Up (softcover, 6"x9", 372 pages, B&W, $26.95 MSRP) is available exclusively through comic book stores. See the books section of the September 2009 Previews catalog (bottom of page 315), where the book is a spotlighted item. Please be sure to ask your store to order a copy (order code SEP091084), as you cannot be assured your store will order any copies.
About the Publisher: Sequart Research & Literacy Organization is a non-profit devoted to the study and promotion of comic books as a legitimate art. It publishes a line of books aimed at making comics scholarship accessible. For more information and to check out the revamped website, click here.
Legal Disclaimer: the Invisibles and related characters are © and TM Grant Morrison. This book is not endorsed by DC Comics or Vertigo.
We're still waiting on Amazon to post up the third chapter of Tumor, but, in the meantime, I wanted to direct you to a brand new short story by yours truly for Kindle and the iPhone/iPod Touch Kindle App. It's called Belly Button Reset, and I'm very proud of it. It's sort of a Vonnegut-y sci-fi romance drama thing, and it's only a buck, so, why not? You can purchase it here: http://tinyurl.com/ltxpmm
But, what's that? You don't have a Kindle or iPhone? Well, you're in luck. You can check out a non-Kindle version over here at http://feedbooks.com/userbook/7446
But, I do ask that if you download it over on Feedbooks, PLEASE, post a brief review over on the site or over on Amazon. Reviews get people to try books out, especially with low price points, so it'd be a huge help.
Thanks for reading, and I hope you enjoy the story!
www.thefialkov.com
FILMS BY TEN FINALISTS POSTED FOR ONLINE VOTING IN
'HALLOWEEN HORROR NIGHTS-CHILLER SCARY GOOD FILM COMPETITION'
AS CHILLER AND UNIVERSAL STUDIOS HOLLYWOOD
SEARCH FOR THE BEST NEW 'SHORT SCARE'
Universal City, CA-—Ten films, selected by industry judges from well over a hundred eligible entries, have been posted for online public voting in the "Halloween Horror Nights-Chiller Scary Good Film Competition," offering filmmakers an opportunity to have their scariest short film rewarded with a broadcast on Chiller of their work, a $1,000 cash prize and a trip for two to the October 2 opening night of Halloween Horror Nights at Universal Studios Hollywood.
Voting is open to all members of the public at www.HalloweenHorrorNights.com/Chiller. Only one vote per person may be cast.
Prospective filmmakers were invited to submit short films of 90 seconds to three minutes in length. Selected films were first judged by a panel of horror industry professionals with storytelling skill, originality and the degree of the "good scare" used as criteria. Finalists were selected by three industry judges: "Saw VI" Director Kevin Greutert, Syfy's Executive Vice President of Programming and Original Movies, Thomas P. Vitale and Universal Studios Hollywood Halloween Horror Nights Creative Director John Murdy. Entries were received from every part of the United States and the ten finalists represent five states, contrasting styles and varying degrees of experience and technical skill.
The winning "Scary Good" film will be announced on September 25. In addition to the prize and the Chiller broadcast of the film, the winning filmmaker will be honored in front of celebrities, studio executives and media at the October 2 Chiller-Eyegore Awards ceremony, which will kick off this year's all-new Halloween Horror Nights event at Universal Studios Hollywood.
Finalists in the "Halloween Horror Nights-Chiller Scary Good Film Competition" are: "Appetence" (Director, Brian H. Robbins), "Bedfellows" (Director, Drew Daywalt), "Chinese Chiller" (Director, Christopher Baker), "Do No Harm" (Director, John Gehrke), "Lamaze of the Dead" (Whitney Baltz), "Mockingbird" (Director, Marichelle Daywalt), "The Nightmare" (Director, Jeff M. Breyer), "Samaritan" (Director, Charles C. Wills), "Shadow Puppets" (Director, David Schneider), and "Stranger Danger" (Director, Luke Nelson).
This year's all-new Halloween Horror Nights" at Universal Studios Hollywood will feature new maze experiences including "Saw: Game Over," "Halloween: The Life and Crimes of Michael Myers," "My Bloody Valentine: Be Mine 4 Ever," and "Chucky's Funhouse." Six new "scare zones," and "The Rocky Horror Picture Show: A Tribute." The re-imagined "Halloween Horror Nights" for 2009 will be the most intense and terrifying "live" horror event ever to be presented in a theme park environment. "Halloween Horror Nights" will continue on consecutive weekends and selected weekday nights beginning on Friday, October 2 through Halloween, Saturday, October 31. Event dates are: October 2-3, 9-11, 15-18, 23-25, 28-31. The event will begin nightly at 7:00 p.m.; closing hours vary by night throughout the event. Tickets are now on sale at http://www.universalstudioshollywood.com/hhn including limited-time advance purchase discounts.
Chiller, the recently-launched channel from NBC Universal, is the only network devoted to delivering viewers round-the-clock scares. Chiller's eclectic slate of adrenaline-fueled, soul-stirring entertainment includes classic drama and anthology series (Tales from the Darkside, Twin Peaks, Nightmare Cafe), international programming (Spine Chillers, Strange) and a broad offering of films, including feature-length premieres on the first Friday of each month. Chiller is currently available in nearly 34 million homes. To learn more, visit: www.chillertv.com. To learn more, visit: www.chillertv.com.
Universal Studios Hollywood is a unit of Universal Parks & Resorts, a division of NBC Universal.
NBC Universal is one of the world's leading media and entertainment companies in the development, production, marketing of entertainment, news, and information to a global audience. Formed in May of 2004 through the combining of NBC and Vivendi Universal Entertainment, NBC Universal owns and operates a valuable portfolio of news and entertainment networks, a premier motion picture company, significant television production operations, a leading television stations group, and world-renowned theme parks. NBC Universal is 80% owned by General Electric, with 20% controlled by Vivendi.
ROCK 'N' ROLL COMICS GETS AN ENCORE AS GRAPHIC NOVELS THROUGH BLUEWATER PRODUCTIONS
Throughout the 90's, "Rock 'N' Roll Comics", was a popular staple on the newsstands. Now the title will be receiving an encore as newly-packaged graphic novels through Bluewater Productions in partnership with the original creators Revolutionary Comics.
More than seventy biographies of notable bands and rock legends will be published in ten bi-monthly volumes starting in December 2009. They include The Beatles, Elvis Presley, Led Zeppelin, The Rolling Stones, The Who and dozens of others.
"Great ideas, like the marriage of rock 'n' roll and comics, have the half-life of uranium and will always be popular," says Jay Allen Sanford of Revolutionary Comics. "The folks at Bluewater clearly have their fingers on the same pop culture pulse that enabled the original Rock 'N' Roll Comics to become one of the top-selling indie comics of the '90s. Truth is often stranger than fiction...and certainly much more interesting!"
According to Bluewater the issues will be packaged into ten graphic novels ranging from 150 to 300 pages. Each graphic novel, which covers a particular band, era, or style, will sport new covers. Bluewater who is known best for their biographical comics, such as Female Force and Political Power, will create forewords and epilogues written by music journalists, and industry insiders.
"In some cases we will add an epilogue for groups that experienced notable milestones after the issues original publishing," Bluewater president Darren Davis said. "Like Pink Floyd's reunion concert at Live8, or the passing of the Who's John Entwistle or even the release of the long delayed Guns N' Roses album 'Chinese Democracy.'"
Volume 1: Hard Rock Heroes
Guns N' Roses; Metallica; AC/DC; Black Sabbath/Ozzy Osbourne; Motley Crue; Poison; Van Halen; Black Crowes; Motorhead; Pantera; Megadeth; Sammy Hagar; Anthrax; Joan Jett/Lita Ford; Skid Row (unpublished RnR Comics #8)
Volume 2: The Beatles (8 issues)
Volume 3: The Spirit of the '60s
Doors; Grateful Dead; Bob Dylan; Jimi Hendrix; Spirit; Janis Joplin; 60s San Francisco Scene (Bill Graham, Jefferson Airplane, etc); British Invasion (Herman's Hermits, the Animals, Yardbirds, Zombies, Small Faces, etc.)
Volume 4: Led Zeppelin Experience (5 issues)
Volume 5: A Rock Pantheon
Eric Clapton; Rolling Stones; Elton John; Bruce Springsteen; Aerosmith, Alice Cooper; ZZ Top; The Jackson 5; Rod Stewart; Def Leppard
Volume 6: Pink Floyd Experience (5 issues)
Volume 7: The Art of Rock
The Who; Queen; Rush; Genesis; David Bowie, Frank Zappa; Kate Bush; ELO; The Cure
Volume 8: The King: Elvis Presley (7 issues)
Volume 9: SMASH! A Punk/Alternative Retrospective
Sex Pistols; REM; Jane's Addiction; Nirvana; Red Hot Chili Peppers; Soundgarden; Alice in Chains; Pearl Jam; Dead Kennedys; Ramones; The Runaways; Iggy Pop/Stooges; MC5; New York Dolls; U2
Volume 10: Hip-Hop and Funk Heroes
Public Enemy, 2 Live Crew, NWA. Ice Cube, Ice-T, George Clinton and Parliament Funkadelic, MC Hammer, Janet Jackson
The original series published by Revolutionary Comics ran from 1989 to 1994. At it's height in the early 1990's sources report that Revolutionary Comics was the largest independent comic publisher in the industry. Circulation for each issue regularly surpassed 50,000. During its run, the company won several high profile First Amendment cases securing the right to publish the unauthorized biographies as "illustrated articles."
The suggested retail price (SRP) for each upcoming graphic novel release is $17.99.
Terry O'Quinn Is
THE STEPFATHER
AVAILABLE FOR FIRST TIME ON DVD
FEATURING NEW HIGH-DEFINITION MASTER AND
ALL-NEW BONUS FEATURES
REMAKE STARRING DYLAN WALSH (NIP/TUCK) IN THEATERS OCT. 16
DVD Available On Shout! Factory October 13
He wanted a perfect family in a perfect town. But they couldn't measure up —
Neither could the others . . .
Los Angeles, CA - 80's cult classic horror flick The Stepfather is set for DVD release for the first time ever, remastered and featuring all-new bonus features. Available on Shout! Factory on October 13, the film stars Terry O'Quinn (Lost),in a role that won him a nomination for Best Actor at the 1988 Independent Spirit Awards and the Saturn Awards. The Stepfather was selected as one of the year's Top 10 movies by Vanity Fair, Village Voice and LA Weekly and featured on Bravo's 100 Scariest Movie Moments special. A remake of the film starring Dylan Walsh (Nip/Tuck) will be in theaters October 16.
Jerry Blake (Terry O'Quinn) is a man obsessed with having the perfect "American Dream" life — including the house with the white picket fence in the suburbs, an adoring wife and loving children. He believes he's found it when he marries Susan Maine (Shelley Hack) and becomes the stepfather to Susan's 16-year-old daughter, Stephanie (Jill Schoelen). But Stephanie gets an uneasy feeling when she is around Jerry with his "Father Knows Best" attitude — she can see that there is a darker side behind his cheerful exterior. Could he be the same man who brutally murdered his family just one year earlier?
Inspired in part by a gruesome true story and written by Donald E. Westlake (The Grifters, The Hunter, later made as Point Blank), and Brian Garfield (Death Wish, Hopscotch, Death Sentence) the script was picked up by ITC Entertainment, and Joseph Ruben (Sleeping With The Enemy, The Good Son, The Forgotten) was chosen to direct the film.
Special features include an audio commentary with director Joseph Ruben, and The Stepfather Chronicles – an all-new retrospective featuring interviews with director Joseph Ruben, producer Jay Benson, actress Jill Schoelen, author Brian Garfield and others on the making of the film and its enduring legacy.
" . . . The Stepfather is one of the great horror movies of the '80s." —Michael J. Weldon,
The Psychotronic Video Guide
"For a horror fan who's missed this brilliant independent production, it's required viewing."
—Mike Mayo, Videohound's Horror Show
"Engrossing thriller . . . Thoughtful screenplay by Donald E. Westlake and taut direction by Joseph Ruben highlight this sleeper." —Leonard Maltin's 2007 Movie Guide
- Audio commentary with director Joseph Ruben
- The Stepfather Chronicles – An all-new retrospective featuring interviews with director Joseph Ruben, producer Jay Benson, actress Jill Schoelen, author Brian Garfield and others on the making of the film and its enduring legacy.
ABC's HIT TV SHOW "LOST"-THE AUCTION
AT DISNEY'S D23 IN ANAHEIM SEPTEMBER 10-13, 2009
Come See Original Props And Costumes From The Show And Meet Cast Members
Who Will Be Signing Autographs
Calabasas, CA, September 8, 2009- If you are a fan of all things LOST, then Disney's D23, taking place September 10-13, 2009 at the Anaheim Convention Center, is definitely the place to be. Profiles in History, the world's largest Hollywood memorabilia auctioneer, will offer fans of the hit ABC television series, LOST a special preview of their Summer, 2010 auction, with a display of authentic props, costumes and set pieces including Kate's toy plane, Hurley's winning lottery ticket, Locke's hunting knife, Sawyer's letter and many other surprises! This four-day sneak preview will be at booth 1930 and runs from 9:00am-5:00pm each day.
ABC is pleased to announce the "LOST" Auction will take place after the series finale in May 2010. "In celebration of our fans around the world, Profiles in History has been selected to auction a selection of original props, set pieces, costumes and collectors' artifacts from the entire series in order to give our fans a chance to own a piece of one of the greatest, most iconic shows in history.
Profiles in History President, Joseph Maddalena: "Profiles in History is thrilled to be holding the LOST Auction. LOST is one of the most iconic TV shows ever created, and we are working in conjunction with ABC to offer fans from around the world an opportunity to own a memento of this amazing show. This is a once in a lifetime auction event that will celebrate one of the most beloved shows in television history."
For more information about Profiles in History and to download complete catalogs from previous auctions, please visit HYPERLINK "http://www.profilesinhistory.com/" \o "http://www.profilesinhistory.com/\"www.profilesinhistory.com.
About Profiles in History:
Founded in 1985 by Joseph Maddalena, Profiles in History is the world's leading auctioneer of Hollywood memorabilia. Profiles in History has held some of the most prestigious and successful auctions of Hollywood memorabilia. Their auctions include costumes, props and set pieces from both vintage and contemporary film, television, and rock 'n roll. Profiles in History's location in Calabasas Hills, CA- virtually a stone's throw away from every major Hollywood studio - ensures a constant flow of fantastic and rare artifacts. With an extensive network of dealers, collectors, and public & private institutions, they are proud to play an important role in the preservation of motion picture history.
Prior Profiles in History Hollywood auctions highlights include the "Cowardly Lion" costume from The Wizard of Oz ($805,000); a full-scale model T-800 Endoskeleton from Terminator 2: Judgment Day ($488,750); a T.I.E. Fighter filming miniature from Star Wars ($402,500); a King Kong six-sheet movie poster ($345,000); the Command Chair from the "U.S.S. Enterprise" ($304,750); Harrison Ford's hero blaster from Blade Runner ($258,750); the original "Robot" from Lost in Space ($264,500); Luke Skywalker's lightsaber ($240,000); a Frankenstein one-sheet movie poster ($212,400); the Black Beauty car from The Green Hornet ($192,000); George Reeves' Superman costume from The Adventures of Superman ($126,500); the H.R. Giger designed Alien creature suit from Alien ($126,500); a full-scale T-Rex head from Jurassic Park ($126,500), the Leaping Alien Warrior figure from Aliens ($126,500), Christopher Reeve's 'Superman' costume from Superman: The Movie ($115,000), C-3PO's helmet ($120,000), The Wizard of Oz 'Winkie' Guard Costume ($115,000); a "Ming the Merciless" cape from Flash Gordon ($115,000) and the Hydraulic screen-used Velociraptor from The Lost World: Jurassic Park II. ($115,000).
HARPE:
AMERICA'S FIRST SERIAL KILLERS
SHOOTS UP STORE SHELVES THIS NOVEMBER!
Advanced Reviews are in: HARPE is the book to get in November
Gritty Western Realism for fans of JONAH HEX and DEAD IRONS
Nashville, TN – Sept 8th, 2009 - A gutted corpse! That was the calling card of Wiley and Micajah Harpe, America's First Serial Killers! Shipping this November to a local comic shop near you, HARPE: AMERICA'S FIRST SERIAL KILLERS reveals the little known true story as seen through the eyes of Wiley himself and will leave you scarred for life!
At the true beginning of the Old West, the brothers Harpe began a murderous spree that could only end badly. A blood-curdling true-crime tale for fans of DEAD IRONS and JONAH HEX!
An original graphic novel written by award-winning writer Chad Kinkle and illustrated by Adam Shaw (Image's BLOOD STREAM), HARPE is sure to grab readers by the throat and not let go!
Advance praise is in, making HARPE: AMERICA'S FIRST SERIAL KILLERS the book to read this November:
"...for those that like gritty Western movies..." - Fangoria
"...entertaining... well worth the read." - Comics Bulletin
Published by Cave in Rock, HARPE: AMERICA'S FIRST SERIAL KILLERS is an original graphic novel written by Chad Kinkle, illustrated in black and white by Adam Shaw and is 96 pages in length. HARPE: AMERICA'S FIRST SERIAL KILLERS carries a Diamond Code of SEP090728 and ships this November.
More information can be found at the website : www.harpegraphicnovel.com
Reserve Your Hotel Room Now!
Contract Deadline is TODAY, September 9th.
My name is Brad Tree and I am one of the people that help to organize and run the Baltimore Comic-Con. Thank you for your past and future support of the Baltimore Comic-Con.
Today is Wednesday, September 9th, and it is deadline day for reserving a room within a Baltimore Comic-Con block, and your likely deadline for getting those great rates. We have contracted special convention rates at key city hotels, all located near and around the Baltimore Convention Center, and all at rates below those listed on common Internet sites. The hotels may be willing to extend the deadline, but there is no guarantee, and they have no obligation. Help us show the power of the Baltimore Comic-Con by making a reservation TODAY!
We are celebrating 10 years, and this will be our best show ever. We will have more guests, more publishers, more retailers, more artist alley tables, and more exhibitors than ever. You can help us to grow the show and increase our standing with the city of Baltimore by reserving your hotel room for the show through our website and the City of Baltimore. You can reach this directly from http://www.baltimorecomiccon.com/hotels.htm.
If you would prefer to register for your room over the phone, please contact our reservations center at 410-837-466 or 1-800-282-6632.
By reserving these hotel rooms, using the links provided here and on the show site, you will help to reinforce the reputation of the Baltimore Comic-Con as a thriving contributor to the community, which will enhance our position and reputation with the city of Baltimore. This will allow us to grow the show in future years!
If you have reserved a room through this link already, THANK YOU!
If you have a room reserved already, please check our rates (and hotel quality) against what you have.
If you have not reserved a room already, please do so NOW!
We are in October this year, so we do not have to compete with the Orioles, but the Ravens will be in town. Reserve now, and beat the opposing NFL fans to those key downtown hotel rooms.
If you have questions, please let me know. If you have worked with me in the past to gain a hotel room, please feel free to contact me again. I look forward to seeing all of you in Baltimore October 10-11, 2009.
About The Baltimore Comic-Con
The Baltimore Comic-Con is celebrating its 10th year of bringing the comic book industry to the Baltimore and Washington D.C. area. With a guest list unequaled in the industry, the Baltimore Comic-Con will be held October 10-11, 2009. For more information, please visit www.baltimorecomiccon.com.
PRESS RELEASE - ELEPHANTMEN OVERSHIPS ITS ULTIMATE JUMPING ON POINT THIS THURSDAY!
ELEPHANTMEN #21 comes to participating retailers this week with a very special overship!
8 September 2009 (Berkeley, CA) - This Thursday, the acclaimed sci-fi series, ELEPHANTMEN, will give readers a chance to jump on board as participating stores receive a special 25% overship.
"I'm so glad we're overshipping this particular issue, because I want it to get into as many people's hands as possible," Starkings said. "We've sold out of EVERY issue since #16 – the Marian Churchland issues were a huge hit – and our numbers have been holding very steady since we returned to our regular monthly schedule with our series of standalone stories, DANGEROUS LIAISONS. I envision ten hefty ELEPHANTMEN collections by the time we're done, so readers have a lot to look forward to."
ELEPHANTMEN #21 is an action-packed, pulls-no-punches story with Totally Kick Ass artwork by regular cover artist Boo Cook, and acts as a direct sequel to the series' first issue as it picks up on the stories of Elephantman Ebony Hide and his human friend, Savannah. This issue also sows the seeds for the next big storyline, QUESTIONABLE THINGS. Image's overship will ensure participating stores have the chance to bring new readers onboard along with the fans of the collections looking for an entry point to the ongoing series!
Starkings added, "In addition, original series artist Moritat returns with issue #23 as Hip Flask and Ebony are forced to deal with a MAPPO sleeper cell which seeks to reactivate the Elephantmen as the weapons of mass destruction they intended them to be! We also have knockout covers by J Scott Campbell and Steve Skroce, and a couple other big surprises in the months to come. Watch this space!"
ELEPHANTMEN #21 (JUL090393), a 32-page full color comic book for $3.50, will be in-stores September 10th, 2009. For more information, please see http://www.hipflask.com/issues/elephantmen21/.
Image Comics is a comics and graphic novels publisher formed in 1992 by a collective of best-selling artists. Since that time, Image has gone on to become one of the largest comics publishers in the United States. There are currently five partners in Image Comics (Robert Kirkman, Erik Larsen, Todd McFarlane, Marc Silvestri, and Jim Valentino), and Image is currently divided into four major houses (Todd McFarlane Productions, Top Cow Productions, Shadowline, and Image Central). Image comics and graphic novels cover nearly every genre, sub-genre, and style imaginable, offering science fiction, romance, horror, crime fiction, historical fiction, humor, and more by the finest artists and writers working in the medium today. Visit www.imagecomics.com.
Our Sentence is Up: Seeing Grant Morrison's The I...
Hey gang, We're still waiting on Amazon to post up...
FILMS BY TEN FINALISTS POSTED FOR ONLINE VOTING IN...
ROCK 'N' ROLL COMICS GETS AN ENCORE AS GRAPHIC NOV...
Terry O'Quinn Is THE STEPFATHER AVAILABL...
ABC's HIT TV SHOW "LOST"-THE AUCTION AT DISNEY'S D...
HARPE: AMERICA'S FIRST SERIAL KILLERS SHOOTS UP S...
Reserve Your Hotel Room Now! Contract Deadline is ...
PRESS RELEASE - ELEPHANTMEN OVERSHIPS ITS ULTIMATE...


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Prices of Next-Gen iPhones Could Be Similar To That Of The iPhone 12 Pro According To iPhone 13 Leaks
Every year, Apple unveils a new generation of iPhones in September. iPhone 13 leaks and rumors have already begun to circulate in the tech sector as the American tech giants prepare to release their latest iPhone.
Apple 13 could be introduced at the same price as the current generation of Apple iPhone 12 according to a recent study from a well-known market research agency, TrendForce.
As a result, the tech community is interested in knowing the iPhone 13's price. Everything you need to know about the impending iPhone 13 that you can find on the internet.
The iPhone 13's price has been leaked.
A new report from TrendForce reveals that the iPhone 13's price will start at Rs 1,22,900 and will be subject to changes.
Because the current edition of Apple iPhone 12 Pro costs roughly Rs 1,19,900, this does not appear to be a significant increase.
A new report from TrendForce says that Apple is actively working on expanding the battery capacity of the iPhone 13's smartphone.
Compared to the iPhone 12 series, the phone's display is said to have a high refresh rate and stronger 5G connectivity.
After witnessing new innovations like Samsung's first under-display camera, Apple could potentially start working on minimizing the size of their notch.
High-end models are said to include LTPO displays with a 120Hz refresh rate. Also equipped with LTPO displays, but with a 60Hz refresh rate.
Must read: Reasons to Buy Apple iPhone 12 instead of iPhone 12 Mini
What's New with the iPhone 13?
Analyst Ming-Chi Kuo has confirmed that Apple Inc will introduce a total of four flagship phones in September.
Among them are the iPhone 13, the iPhone 13 small, and both versions of the iPhone 13 Pro and the iPhone 13 Pro max.
In addition to the MagSafe magnets, the wireless charging coils will be larger, according to other sources from Weinbach.
The new Apple iPhone 13 reverse charging capability can be enabled by adding these to the phone.
It's unclear what else will be included with the next iPhone 13. Keep an eye on Apple's official social media handles for any changes.
Best Virtual Reality Headsets in India for PC, iPhone, & Android [+Buyer Guide]
Best Free Horoscope Apps for Android and iPhone
Categories News Tags smartphonePost navigation
There will be four 50MP cameras on the back of the Redmi 10 & a 90hz screen refresh rate
Important Grooming Tips For Indian Men

redpajama_set_name: RedPajamaCommonCrawl


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4 PM Update: A severe thunderstorm watch will be cancelled
Posted: Sep 25, 2018 3:32 AM CST | Updated: Sep 25, 2018 11:48 AM CST
Thankfully the greatest instability has remained south across northern Illinois this afternoon. That area is experiencing strong to severe storms. Closer to home we are watching a line of rain and a few embedded storms; however, it's not showing severe characteristics.
The NWS will cancel the watch as the rain moves through. Expect rain through the next couple of hours. Severe weather is not expected.
Heat and humidity will combine to produce strong to severe thunderstorms this afternoon and evening. A new severe thunderstorm watch has been issued for the majority of the area until 10 pm.
Damaging winds and hail are the primary threats. The main line of storms will arrive between 4 pm and 8 pm.
A surface cold front will swing into the area today and bring in cooler air the rest of the week. However, ahead of the front we are anticipating warm and muggy air. Highs could track into the upper 70s to around 80 today with dew points in the mid-60s. With those conditions and a front, this could lead to a chance for severe weather.
Take a look at the temperature contrast late this morning
It's a tale of two sides with warming across our area and cooler temps behind the front. That dividing line of temperatures will be the focus for storm development later today. In fact, storms are already firing across portions of Iowa. We are seeing a strengthening trend with the intense rain in red along with lightning. That line is still set to arrive around the commute and through our mid evening.
At this point the storms look to hit the lake front by 7pm. Wind remains the primary threat in these storms today.
The Storm Prediction Center is forecasting a slight risk of severe weather for a chunk of southeastern Wisconsin. This setup could bring a line of thunderstorms into the area by this afternoon and evening. The biggest threats will be large hail and damaging winds with any storms that fire. There could be heavy downpours embedded in this line, which could lead to minor flooding and ponding of the roads. The storms will be out by 10 pm this evening.
Behind the front expect fall-like air with highs in the 60s the rest of the week. Another cold front late this week could drive in even cooler air with daytime temps in the 50s by early this weekend.
Contributions to this story also made by: Rebecca Schuld


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Home News SUB. NEWS: TOMMY & THE HIGH PILOTS ANNOUNCE NATIONAL SUMMER...
SUB. NEWS: TOMMY & THE HIGH PILOTS ANNOUNCE NATIONAL SUMMER TOUR
Nici Arsenault
Santa Barbara quartet Tommy & The High Pilots is pleased to announce Summer tour dates with The Dangerous Summer and Rare Monk kicking off in Scottsdale, Arizona at The Pub Rock Live on July 30th. The tour takes the band through major markets to the east coast and back concluding in Houston, TX on September 6th. Full dates below with tickets on sale starting June 13th HERE.
Tommy & The High Pilots made an appearance on Last Call with Carson Daly for an interview that included live footage from previous performances and also shared their new video, "Outta My Head" from the the new full-length album Only Human. The album was released on May 28th through Redbird Records and features a 10-song set united by frontman Tommy Cantillon's bold vocal range and themes of perseverance, redemption and humanity. Now available through iTunes and Amazon.
MTV Buzzworthy exclusively premiered Tommy & The High Pilots' music video for the first single off of Only Human, "Outta My Head" which showcases the band's colorful dance party moves. The video can always be viewed on the band's YouTube Channel.
Tommy & The High Pilots are Tommy Cantillon (vocals/guitar), Michael Cantillon (keys), Steve Libby (bass), and Matt Palermo (drums). Only Human was helmed by a trio of prolific producers – Matt Wallace (Maroon 5, Train) Jason McEntire (Son Volt, Ha Ha Tonka) and Marc McClusky (Weezer, Ludo).
Tommy & The High Pilots Tour Dates
*Tickets go on Sale June 13th HERE.
7/30 Scottsdale, AZ – Pub Rock Live
7/31 Anaheim, CA – Chain Reaction
8/01 San Francisco, CA – Cafe Du Nord
8/02 Seattle, WA – El Corazon
8/03 Portland, OR – Backspace Cafe
8/04 Boise, ID – The Venue
8/07 Denver, CO – The Marquis Theatre
8/09 Des Moines, IA – The Vaudeville Mews
8/10 Minneapolis, MN – First Avenue
8/11 Chicago, IL – Reggie's Rock Club
8/13 St. Louis, MO – Firebird
8/14 Indianapolis, IN – Irving Theatre
8/15 Detroit, MI – Magic Stick
8/17 Toronto, ON – Hard Luck Bar
8/18 Montreal, QC – Cabaret Underworld
8/22 Philadelphia, PA – The Barbary
8/23 Baltimore, MD – The Ottobar
8/24 West Springfield, VA – Empire
8/25 Greensboro, NC – Greene Street Club
8/27 West Columbia, SC – New Brookland Tavern
8/28 Orlando, FL – Backbooth
8/29 Jacksonville, FL – Jack Rabbits
9/04 Oklahoma City, OK – The Conservatory
9/05 Dallas, TX – The Prophet Bar
9/06 Houston, TX – Mango's Cafe
*additional summer tour dates to be announced
Only Human Tracklisting:
1. Get Up
2. Outta My Head
3. Devil To Pay
4. Broken Down
5. Only Human
6. Here In My Hands
7. Young & Hungry
8. Somebody Make A Move
9. Innocent
10. Painted Cave
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Dorian – How have your friendships changed?
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Some have, some haven't. Most of them haven't. Sometimes people don't know what to say, so they just back off. Some people don't understand that it's okay to ask questions. It's okay to say,... Show More
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Psalm 49, Verse 6-7
6 Why should I FEAR in evil days, with the iniquity of my assailants surrounding me, 7 of those who trust in their wealth and boast of their abundant riches?
Trust in Christ our savior and live the virtues of our Lady: humility, generosity, chastity, patience, temperance and love of fellow man. Do not put your faith in coin for the bankruptcy of our cultural heart is that we allow the innocent to be killed in this nation. God cries over the sacrifices of future unborn children for the dreams of the mother. No amount of future happiness or gain in independence is worth the life of an innocent. Know that life is greater than liberty and liberty is greater than wealth.
Beloved: Teach and urge these things. Whoever teaches something different and does not agree with the sound words of our Lord Jesus Christ and the religious teaching is conceited, understanding nothing, and has a morbid disposition for arguments and verbal disputes. From these come envy, rivalry, insults, evil suspicions, and mutual friction among people with corrupted minds, who are deprived of the truth, supposing religion to be a means of gain. Indeed, religion with contentment is a great gain. For we brought nothing into the world, just as we shall not be able to take anything out of it. If we have food and clothing, we shall be content with that. Those who want to be rich are falling into temptation and into a trap and into many foolish and harmful desires, which plunge them into ruin and destruction. For the love of money is the root of all evils, and some people in their desire for it have strayed from the faith and have pierced themselves with many pains. But you, man of God, avoid all this. Instead, pursue righteousness, devotion, faith, love, patience, and gentleness. Compete well for the faith. Lay hold of eternal life, to which you were called when you made the noble confession in the presence of many witnesses. (Tm. 6:2-12)
If we truly wish to build back better; we ourselves must grow in holiness and then in turn our families will build holy communities and holy communities will build a Holy Nation.
NOVENA TO THE HOLY FACE
DAILY PREPARATORY PRAYER
O Most Holy and Blessed Trinity, through the intercession of Holy Mary, whose soul was pierced through by a sword of sorrow at the sight of the passion of her Divine Son, we ask your help in making a perfect Novena of reparation with Jesus, united with all His sorrows, love and total abandonment.
We now implore all the Angels and Saints to intercede for us as we pray this Holy Novena to the Most Holy Face of Jesus and for the glory of the most Holy Trinity, Father, Son and Holy Spirit. Amen.
Fourth Day
Psalm 51, 8-9.
Indeed, you love truth in the heart; then in the secret of my heart teach me Wisdom. O purify me, then I shall be clean; O wash me, I shall be whiter than snow.
O Lord Jesus, who has said, learn of me for I am meek and gentle of heart, and who did manifest upon Thy Holy Face the sentiments of Thy divine heart, grant that we may love to come frequently and meditate upon Thy divine features. We may read there Thy gentleness and Thy humility and learn how to form our hearts in the practice of these two virtues which Thou desires to see shine in Thy servants. Mary our Mother and Saint Joseph help us.
Through the merits of Thy precious blood and your Holy Face, O Jesus, grant us our petition, Pardon and Mercy.
Prayer in Honor of the Dolors of the Blessed Virgin
O Most Holy and afflicted Virgin, Queen of Martyrs! Who stood beneath the cross, witnessing the agony of your dying Son, look down with a mother's tenderness and pity on us as we kneel before you to venerate your Dolors, and place our requests, with filial confidence, in the sanctuary of your wounded heart. Present them on our behalf to Jesus, through the merits of His most sacred Passion and Death, together with your sufferings at the foot of the cross, and through the united efficacy of both, obtain the favor which we humbly ask. To whom shall we go in our wants and miseries if not to you. O Mother of Mercy, who having so deeply drunk of the chalice of your Son, graciously alleviate the sufferings of those who still sigh in this land of exile. Amen.
Prayer to the Souls in Purgatory
My Jesus, by the sorrows you suffered in your agony in the garden, in your scourging and crowning with thorns, in the way to Calvary, in your crucifixion and death, have mercy on the souls in Purgatory, and especially on those that are most forsaken. Deliver them from the dire torments they endure. Call them and admit them to your most sweet embrace in Paradise. Amen.
Pray one (1) Our Father, (3) Hail Mary's, (1) Glory Be.
O Bleeding Face, O Face Divine, be every adoration Thine. (Three times)
Lent begins next Wednesday[1]
During Lent, we are asked to devote ourselves to seeking the Lord in prayer and reading Scripture, to service by giving alms, and to sacrifice self-control through fasting. Many know of the tradition of abstaining from meat on Fridays during Lent, but we are also called to practice self-discipline and fast in other ways throughout the season. Contemplate the meaning and origins of the Lenten fasting tradition in this reflection. In addition, the giving of alms is one way to share God's gifts—not only through the distribution of money, but through the sharing of our time and talents. As St. John Chrysostom reminds us: "Not to enable the poor to share in our goods is to steal from them and deprive them of life. The goods we possess are not ours, but theirs." (Catechism of the Catholic Church, no. 2446).
Lent is a favorable season for opening the doors to all those in need and recognizing in them the face of Christ."-- Pope Francis
In Lent, the baptized are called to renew their baptismal commitment as others prepare to be baptized through the Rite of Christian Initiation of Adults, a period of learning and discernment for individuals who have declared their desire to become Catholics.
The key to fruitful observance of these practices is to recognize their link to baptismal renewal. We are called not just to abstain from sin during Lent, but to true conversion of our hearts and minds as followers of Christ. We recall those waters in which we were baptized into Christ's death, died to sin and evil, and began new life in Christ.
Preparing for Battle[2] Know Your Armor
Prayer and fasting, worship and adoration, Scripture and sacraments and sacramentals all provide the weapons of our spiritual warfare. With them we go on the offensive against the Evil One. But the virtues provide our defensive armor. St. Paul sums it up: "Put on, therefore, as God's chosen ones, holy and beloved, a heart of mercy, kindness, humility, meekness, patience. Bear with one another, if anyone has a grievance against any other; even as the Lord has forgiven you, so also you must forgive. But above all these things have charity, which is the bond of perfection" (Col 3: 12– 14). Only with such armor will we be fully covered and protected from the Evil One's attacks.
· The Shield of Faith. St. Paul reminds us that faith must be firmly grasped and held up as a barrier between ourselves and the Enemy.
· The Helmet of Hope. It is essential for protecting the mind. If we have no hope of winning why fight? We must never take off the helmet of hope or we will be overcome before we start.
· The Breastplate of Love. The breastplate protects our heart-keeping it for God alone. Love Him with all your heart, soul, and mind; and be rightly related to others is to love them as we love ourselves (see Mt 22: 36– 40).
· Cincture of Truth. Being truthful with God, yourself, and others is a spiritual form of ballistic groin protection. Nothing can hurt like the truth. We must not let the intimate parts of our inner selves be led astray by blinding passion, and the Devil's enticement. We must seek the truth and live the truth. We must not seek to gratify the desires of the flesh, but instead we must "put on the Lord Jesus Christ," imitating the virtues displayed in His character.
· Feet shod in Peace. Wherever we go, we must be prepared to bring the good news of salvation, of peace with God, to all we may encounter. The Devil will try to turn us back. He'll scatter across our path, like so many rocks and thorns, a wagonload of doubts, accusations of our inadequacy, and fear of conflict and rejection. But if we've put on the "boots" of readiness— if we've prepared ourselves, through faithful study and prayer, to share the gospel— then we'll walk safely over these obstacles, crushing them as we go.
· The Mantle of Humility. Humility is the essential virtue that provides the soil in which all the other virtues grow. Humility keeps us from dangerous "high places" where the Enemy could tempt us to pride and vainglory.
The Italian culture has always had a close association with St. Joseph perhaps you could make Wednesdays centered around Jesus's Papa. Plan an Italian dinner of pizza or spaghetti after attending Mass as most parishes have a Wednesday evening Mass. You could even do carry out to help restaurants. If you are adventurous, you could do the Universal Man Plan: St. Joseph style. Make the evening a family night perhaps it could be a game night. Whatever you do make the day special.
II. Transmit the faith: catechesis
5 "Catechesis is an education in the faith of children, youth and adults, which especially includes a teaching of Christian doctrine, generally given in an organic and systematic way with a view to initiating them in the fullness of Christian life" ( CT 18).
· Unite in the work of the Porters of St. Joseph by joining them in fasting: Today's Fast: An end to the use of contraceptives.
· Pray Day 4 of the Novena for our Pope and Bishops
· 54 Day Rosary for Priest's and Religious Day 4
· Total Consecration to St. Joseph Day 8
[1]http://www.usccb.org/prayer-and-worship/liturgical-year/lent/index.cfm


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African American Literature and Culture Society
ALA Symposium CFP: Come Present with the AALCS in Washington, DC!
ALA CFP: Come present with the AALCS in San Diego!
2019 AALCS AWARDS RECIPIENTS
Call for Papers: 30th American Literature Association Conference, Boston, May 23-26, 2019.
Get to know the AALCS! Introducing the Monthly Member Spotlight: First up, President Grégory Pierrot
The African American Literature and Culture Society is proud to announce the recipients of the Stephen E. Henderson Award for Outstanding Achievement in Prose, and the Darwin T. Turner Award for Excellence in Scholarship in African American Culture and Literature for the year 2019.
John Edgar Wideman, our Henderson Award recipient, needs no introduction. From his first novel A Glance Away to his most recent collection American Histories, Wideman's writing career spans five decades during which he has asserted himself as one of the most singular voices in American literature. Wideman's works have been widely celebrated: he has notably won the International PEN/Faulkner Award twice for Sent for You Yesterday (1984) and for Philadelphia Fire (1990), which also won the American Book Award. His novel The Cattle Killing won the James Fenimore Cooper prize for best historical fiction in 1997. In 1993, he was the recipient of a Macarthur Genius Grant, and most recently in 2016 was elected to the American Academy of the Arts and Letters. Wideman founded and chaired the African American Studies department at the University of Pennsylvania. He has also taught at the University of Wyoming, the University of Massachusetts and Brown University.
Keith Byerman, our Turner Award recipient, is Professor in the Department of English at Indiana State University and current president of the John Edgar Wideman Society. He is the author of eight books from Fingering the Jagged Grain: Tradition and Form in Recent Black Fiction (1986) to The Life and Works of John Edgar Wideman (2013). He has been Associate Editor for the African American Review and has notably published in College Literature, ALH, CLA Journal, MELUS. Keith is a founding member of the African American Literature and Culture Society and has been Treasurer of the Society for many years.
Award recipients will be recognized and honored during the AALCS Reception and Reading held at the American Literature Association 30th Annual Conference (Westin Copley Place, Boston, MA) on Friday, May 24, 2019. The reception will feature readings from John Edgar Wideman's work.
March 31, 2019 Gregory Pierrot


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Home > Authors Index > Browse all available works of Richard King > Text of I Wonder If . . .
An essay by Richard King
I Wonder If . . .
Title: I Wonder If . . .
Author: Richard King [More Titles by King]
But I sometimes wonder if this indifference towards the facts which are "big" to so many people and ought, perhaps, to be "big" to everybody, be a sign of national weakness or of national strength. Personally, I longed, metaphorically speaking, to tear that female limb from limb and send that young man to a village under bombardment, there to make him stay a week in the very hottest portion of Hell's Corner. But had I done so, I realised that I should not have accomplished the very slightest good. The moment that you take a crank seriously, from that very moment he imagines that his "crankiness" is divinely inspired. Far better laugh at him and let him alone. Laughter is the one unanswerable contradiction, and ridicule is a far more deadly thing to fight against than fury, no matter if fury wields a hatchet. Perhaps this utter indifference to the firebrand is our national strength--even though it comes from a too-sluggish imagination, a too great imperviousness to new dangers. English people possess too great a sense of humour ever to become Bolshevik. They may not be witty and vivacious and effervescingly bright, but they possess an innate sense of the ridiculous which is their national safeguard against any very bloody form of revolution. So we suffer infuriated cranks--if not gladly, at least, in the same manner as we suffer baboons in the Zoo--interesting, and even amusing in their proper place, but to be shot at sight should they venture to play the "baboon" amid those hideous red-brick villas which have been termed an Englishman's castle and his home. After all, every new system has its ridiculous side, and strangely enough, it is this ridiculous side which is most apparent at the outset. Only after you have delved below the "comic froth" do you begin to realise that there is a very vital truth hidden beneath. Well, a sense of humour blows away that froth in time, and then--as for example after the Suffragette antics--the real argument behind the capers and the words becomes known. Thus in England all revolutions are gradual, and in their very slowness lies their incalculable strength of purpose.
[The end]
Richard King's essay: I Wonder If . . .


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Precision Medicine and Therapeutic Resistance
Journal Press Releases
Germline Mutations in the CDKN2B Tumor Suppressor Gene Predispose to Renal Cell Carcinoma
Mariam Jafri, Naomi C. Wake, David B. Ascher, Douglas E.V. Pires, Dean Gentle, Mark R. Morris, Eleanor Rattenberry, Michael A. Simpson, Richard C. Trembath, Astrid Weber, Emma R. Woodward, Alan Donaldson, Tom L. Blundell, Farida Latif and Eamonn R. Maher
Mariam Jafri
1Medical and Molecular Genetics, School of Clinical and Experimental Medicine, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.
2Department of Oncology, University Hospital Birmingham Foundation Trust, Birmingham, United Kingdom.
Naomi C. Wake
David B. Ascher
3Department of Biochemistry, University of Cambridge, Cambridge, United Kingdom.
Douglas E.V. Pires
Dean Gentle
Mark R. Morris
4School of Applied Sciences, University of Wolverhampton, Wolverhampton, United Kingdom.
Eleanor Rattenberry
5West Midlands Region Genetics Service, Birmingham Women's Hospital, Birmingham, United Kingdom.
Michael A. Simpson
6Division of Genetics and Molecular Medicine, King's College London School of Medicine, Guy's Hospital, London, United Kingdom.
Richard C. Trembath
7Queen Mary University of London, Barts and The London School of Medicine and Dentistry, London, United Kingdom.
Astrid Weber
8Royal Liverpool Children's Hospital, Liverpool, United Kingdom.
Emma R. Woodward
Alan Donaldson
9Department of Clinical Genetics, University Hospital Bristol NHS Trust, St. Michael's Hospital, Bristol, United Kingdom.
Tom L. Blundell
Farida Latif
Eamonn R. Maher
10Department of Medical Genetics, University of Cambridge and NIHR Cambridge Biomedical Research Centre, Cambridge, United Kingdom.
For correspondence: erm1000@medschl.cam.ac.uk
DOI: 10.1158/2159-8290.CD-14-1096 Published July 2015
Familial renal cell carcinoma (RCC) is genetically heterogeneous and may be caused by mutations in multiple genes, including VHL, MET, SDHB, FH, FLCN, PTEN, and BAP1. However, most individuals with inherited RCC do not have a detectable germline mutation. To identify novel inherited RCC genes, we undertook exome resequencing studies in a familial RCC kindred and identified a CDKN2B nonsense mutation that segregated with familial RCC status. Targeted resequencing of CDKN2B in individuals (n = 82) with features of inherited RCC then revealed three candidate CDKN2B missense mutations (p.Pro40Thr, p.Ala23Glu, and p.Asp86Asn). In silico analysis of the three-dimensional structures indicated that each missense substitution was likely pathogenic through reduced stability of the mutant or reduced affinity for cyclin-dependent kinases 4 and 6, and in vitro studies demonstrated that each of the mutations impaired CDKN2B-induced suppression of proliferation in an RCC cell line. These findings identify germline CDKN2B mutations as a novel cause of familial RCC.
Significance: Germline loss-of-function CDKN2B mutations were identified in a subset of patients with features of inherited RCC. Detection of germline CDKN2B mutations will have an impact on familial cancer screening and might prove to influence the management of disseminated disease. Cancer Discov; 5(7); 723–9. ©2015 AACR.
This article is highlighted in the In This Issue feature, p. 681
The identification of the genetic basis for familial cancer syndromes can provide important insights into the molecular mechanisms of familial and sporadic tumorigenesis. Furthermore, improved understanding of the molecular factors involved in tumorigenesis has provided a basis for the rational development of targeted therapies. This is exemplified in inherited renal cell carcinoma (RCC; MIM#144700) in which the identification of mutations in the VHL tumor suppressor gene (TSG) as the cause of von Hippel–Lindau (VHL) disease (MIM#193300) led to the recognition that the VHL TSG is somatically inactivated in the majority of sporadic clear-cell RCC. Subsequently, elucidation of the role of the VHL gene product in the regulation of hypoxia response pathways enabled the development of novel targeted treatments that have revolutionized the clinical management of RCC (1).
About 3% of all cases of RCC occur in individuals with familial RCC (2). A number of genetic mechanisms have been implicated in RCC predisposition. Thus, genome-wide association studies have identified several common genetic variants that predispose to RCC, and at least two loci are linked to pVHL-regulated hypoxic gene response pathways [at 2p21 (rs11894252) and 11q13.3 (rs7105934) close to EPAS1 (HIF2A) and CCND1 (Cyclin D1), respectively; ref. 3]. In familial RCC, in addition to VHL, germline mutations in MET, FLCN, FH, SDHB, PTEN, and BAP1 have all been associated with inherited RCC [2 (and references within), 4–6]. Constitutional translocations, particularly involving chromosome 3, can also cause inherited RCC (7). However, overall less than 20% of patients with features of nonsyndromic inherited RCC have a detectable mutation in a known familial RCC gene (2, 4–6, 8, 9). To identify novel inherited RCC genes, we undertook exome sequencing and targeted resequencing studies in individuals with features of inherited RCC and no detectable mutation in known RCC predisposition genes.
Identification of CDKN2B Mutations in Inherited RCC
Analysis of exome resequencing in a male proband diagnosed with familial clear-cell RCC (see Fig. 1A) at age 57 years revealed no candidate mutations in RCC predisposition genes (VHL, SDHB, FLCN, FH, PTEN, or BAP1). Further bioinformatic analysis was undertaken for the presence of pathogenic mutations in genes linked to cancer. A candidate nonsense mutation in CDKN2B was highlighted for further investigation, and the CDKN2B c.103G>T (p.Glu35Stop) mutation was confirmed by Sanger sequencing (see Fig. 1B). Two of his eight siblings had been diagnosed with clear-cell RCC (two brothers diagnosed at ages 56 and 60 years, respectively), and his mother had been diagnosed with RCC at age 60 years. DNA was available from four living relatives, and family genotyping studies demonstrated the c.103G>T CDKN2B nonsense mutation was present in the only living sibling affected by RCC, but not in three unaffected siblings (Fig. 1A). The c.103G>T CDKN2B nonsense mutation was not previously reported in publicly available large exome/genome sequencing sets comprising >13,000 CDKN2B alleles (0/1,092 sample chromosomes in 1,000 genomes; ref. 10; and 0 of >6,000 samples in the NHLBI Exome Variant Server; ref. 11). In addition, no other CDKN2B truncating mutations were reported in the latter set of >12,000 CDKN2B alleles.
A, family pedigree for familial RCC kindred in which exome sequencing was performed. B, electropherogram showing heterozygous nonsense mutation (c.103G>T). C, electropherogram showing heterozygous missense mutation c.68C>A p.Ala23Glu (A23E) and evolutionary conservation of residue; D, electropherogram showing heterozygous missense mutation c. 118C>A p.Pro40Thr (P40T) and evolutionary conservation of residue; E, electropherogram showing heterozygous missense mutation. c.256G>A p.Asp86Asn (D86N) and evolutionary conservation of residue.
To further investigate the potential role of CDKN2B mutations in inherited renal cancer, mutation screening was performed in 50 individuals with features of nonsyndromic inherited RCC [either familial RCC (n = 37) or multiple RCC aged <50 years (n = 13)], and three candidate missense mutations were detected (Fig. 1C–E). A rare sequence variant (c.256G>A) predicted to cause a pathogenic missense substitution, p.Asp86Asn, was detected in a proband who was diagnosed with clear-cell RCC at age 35 years. No other family members (her mother had died from RCC) were available for testing. In addition, a novel candidate mutation [c.118C>A (p.Pro40Thr)] was identified in an individual who developed bilateral RCC at age 42 years. No other family members were available for testing. Mutation analysis of CDKN2B in a cohort of 34 individuals with features of possible inherited RCC (familial RCC, multicentric RCC, or young onset RCC) revealed candidate heterozygous missense substitutions [c. 68C>A (p.Ala23Glu)] in one case. Two of the three candidate CDKN2B missense mutations (p.Ala23Glu and p.Pro40Thr) were absent from publicly available large exome/genome sequencing sets comprising >12,000 CDKN2B alleles, and the p.Asp86Asn variant occurred with a frequency of <1 in 200 individuals (11). All three substitutions occurred at evolutionarily conserved residues (see Fig. 1C–E) and were predicted to be pathogenic by Polyphen and SIFT algorithms (12, 13).
Structural Predictions
To understand the potential impact of the mutations on CDKN2B, the mutations were analyzed in the context of the apo (unbound) structure, and in complex with cyclin-dependent kinases (CDK) 4 or 6. The overall structure of CDKN2B is very similar to CDKN2D and is expected to bind through its concave face to the cleft between the N- and C-terminal domains of CDK4 and CDK6. Binding of CDKN2B prevents productive binding of ATP to the CDKs, and potentially inhibiting movement of the PLSTIRE helix to its active conformation (14).
The three variants identified were spread across the protein (Fig. 2A), with p.Ala23 and p.Asp86 located close to the surface, and along the interface with CDK4 and CDK6, whereas p.Pro40 is a buried residue distal to the interaction interface. CDKN2B p.Pro40 is located on a hydrogen-bonded turn leading into the sheet of the first ankyrin repeat and forming interactions with helices in the first and second ankyrin repeats (Fig. 2B). The first two ankyrin repeats mediate the majority of the interactions with the CDKs (14). Mutation to threonine relaxes this loop, altering the packing of the helices and the overall stability of CDKN2B, as predicted by mCSM and DUET (Table 1).
Structural analysis of the interaction network of variant residues in CDKN2B (for the wild-type CDKN2B–CDK6). Ionic interactions and hydrogen bonds are depicted as yellow dashes, hydrophobic interactions are presented in green, and weak polar interactions are presented in orange. A, overview: atoms from CDKN2B and CDK6 are shown in light green and dark gray, respectively; (B) p.Pro40, (C) p.Ala23, and (D) p.Asp86. CDK, cyclin-dependent kinase.
Predicted effects of mutations upon CDKN2B stability and protein interactions
CDKN2B p.Ala23 is located on an α-helix at the periphery of the interface among CDKN2B and CDK4 and CDK6, where it makes a series of inter- and intramolecular weak hydrophobic interactions (Fig. 2C). This space is not sufficient to accommodate the larger, charged glutamate residue in the mutant, leading to a reduced affinity for the CDKs as predicted by mCSM-PPI (Table 1). CDKN2B p.Asp86 is also located on an α-helix and makes strong intermolecular ionic/hydrogen bonds with CDK4 and CDK6 (Fig. 2D). In the variant, the asparagine side chain is unable to make these interactions, leading to a significant reduction in affinity as predicted by mCSM-PPI (Table 1).
Functional Effects of Germline CDKN2B Variants
To evaluate the pathogenicity of the candidate germline mutations detected in inherited RCC cases, we undertook in vitro studies of growth suppressor activity. Thus, the effects on growth of the two RCC cell lines were compared for (i) wild-type CDKN2B, (ii) vector only [empty vector (EV)], and (iii) the three candidate missense substitutions: p.Pro40Thr, p.Ala23Glu, and p.Asp86Asn. Initially, the effects of transfecting a vector expressing wild-type CDKN2B and an EV into the SKRC47 (wild-type VHL) and KTCL26 (VHL-null) RCC cell lines were compared with the colony formation assay. For both cell lines, there were significantly fewer colonies after transfection with wild-type CDKN2B than with the EV control. The effects of the three candidate missense mutations (p.Pro40Thr, p.Ala23Glu, and p.Asp86Asn) were then studied, and each missense mutation impaired in vitro growth suppressor activity of CDKN2B (Fig. 3).
Functional evaluation of CDKN2B mutations using colony formation assays. A, comparison of EV and wild-type (WT) CDKN2B expression in KTCL26 and SKRC47 RCC cell lines. Transfection with wild-type CDKN2B significantly reduced the number of colonies formed (t = 3.936, degree of freedom = 6, P = 0.007 and t = 18.2, P = 0.0002, respectively). **, P= 0.007; ***, P = 0.0002. B, comparison of growth suppression (by colony formation assay) of EV, wild-type CDKN2B, and three candidate missense mutations [p.Pro40Thr (P40T), p.Ala23Glu (A23E), and p.Asp86Asn (D86N)] in KTCL26 RCC (VHL-null) and SKRC47 (VHL-positive) cell lines. There were no statistically significant differences (P > 0.4 for KTCL26 and P > 0.1 for SKRC47) between the number of colonies in cell lines transfected with EV compared with those transfected with missense mutants containing variants. C and D, representative colony formation assay plates stained using crystal violet from colonies derived from KTCL26 (VHL-null) and SKRC47 (VHL-positive) cell lines transfected with either wild-type CDKN2B, EV, or vector containing the following variants: p.Pro40Thr (P40T), p.Ala23Glu (A23E), and p.Asp86Asn (D86N). E, representative CDKN2B expression levels for the colony formation assays. Expression levels for the three missense mutations were comparable to that for wild-type protein expression [data represents the mean (of 3 experiments) with error bars representing the SE].
We identified germline-inactivating CDKN2B mutations in approximately 5% (95% confidence interval, 0.21%–9.43%) of patients with features of nonsyndromic inherited RCC analyzed. Thus, the frequency of germline CDKN2B mutations is approximately similar to that which can be attributed to germline FLCN and SDHB mutations (8, 9) but larger than that accounted for by germline BAP1 mutations (5, 6). These mutations lead to the deregulation of CDK4 and CDK6 by CDKN2B, by altering the binding interfaces or overall stability of CDKN2B. The identification of CDKN2B as an inherited RCC gene will facilitate the diagnosis and management of this disorder. In addition to a nonsense mutation that segregated with RCC in familial RCC kindred, we identified three rare missense mutations in individuals with features of inherited RCC. Two of these missense mutations were novel, but one (NM_004936 c.256G>A p.Asp86Asn) had previously been reported in a patient with parathyroid adenoma and in a patient with a metastatic pancreatic endocrine tumor (15, 16). The p.Asp86Asn substitution occurs at a highly conserved residue and has an allele frequency of approximately 0.2% in Single Nucleotide Polymorphism database (dbSNP) build 137 (17), and, consistent with the in silico structural predictions reported here, Costa-Guda and colleagues (15) demonstrated that the p.Asp86Asn substitution inhibited binding of CDKN2B/p15 to CDK6.
CDKN2B encodes the p15INK4B protein, which binds to and inhibits CDK4 and CDK6 (18). In the absence of CDKN2B, CDK4- and CDK6-dependent phosphorylation of pRb inhibits the interaction between pRb and E2F and promotes cell growth. Overexpression of p15INK4B causes cell-cycle arrest in G1 phase and redistribution of CDK4 from cyclin D–CDK4 complexes to CDK4–p15INK4B complexes, leading to degradation of unbound cyclin D by the ubiquitin-dependent proteasome degradation pathway (18). Interestingly, cyclin D1 is a downstream target of pVHL, inactivation of the VHL TSG is associated with HIF2-dependent upregulation of cyclin D1 (19), and genome-wide association studies identified genetic variation linked to CCND1 expression with RCC susceptibility (3). The CDKN2B gene maps close to the CDKN2A locus that encodes two tumor suppressor proteins (p16INK4a and p14ARF), and many deletions found in human cancer encompass both CDKN2B and CDKN2A. However, experiments in mice demonstrated that Cdkn2b also possesses critical tumor suppressor activity (20). Though somatic CDKN2B mutations are uncommon in human neoplasia, somatic inactivation of CDKN2B by allele loss and/or promoter hypermethylation has been reported in a variety of human cancers, most notably hematologic neoplasms, including leukemia, lymphoma, and myelodysplastic syndrome (21). Cytogenetic studies have identified chromosome 9p deletions in approximately 15% of clear-cell RCC, array-based studies of copy-number abnormalities have confirmed that the 9p critical region contains the CDKN2A/CDKN2B loci, and Girgis and colleagues (22) found that a subset of RCC exhibited hypermethylation of CDKN2A and CDKN2B (13% and 21%, respectively).
Previously, CDKN2B mutations have been linked to predisposition to endocrine tumors (15, 16, 23). Thus, in addition to p.Asp86Asn mutation that was reported in individuals with a parathyroid adenoma (wild-type allele loss was detected in the tumor tissue) and metastatic pancreatic endocrine tumor (15, 16), two further missense mutations (p.Asn41Asp and p.Leu64Arg) were reported in patients with suspected multiple endocrine neoplasia: one with primary hyperparathyroidism (3 parathyroid tumors), skin schwannoma, meningioma, and liver hemangioma, and one with primary hyperparathyroidism (3 parathyroid tumors), Zollinger–Ellison syndrome, adrenal mass, and prostate cancer. Both p.Asn41Asp and p.Leu64Arg substitutions impaired binding to CDK6 (23). The finding of multiple phenotypes with mutations in a single gene is not uncommon and may reflect variable modes of ascertainment and/or genotype–phenotype correlations. Thus, germline BAP1 mutations were initially described in association with uveal melanoma, mesothelioma, and other tumors before being recognized as a cause of familial RCC (5, 6), and, recently, mutations in FH were detected in individuals with pheochromocytoma/paraganglioma without features of hereditary leiomyomatosis–RCC (Reed syndrome; refs. 24, 25). In our study, none of the confirmed CDKN2B mutation carriers were known to have a nonrenal neoplasm, but further studies will define the full range of tumor types associated with CDKN2B mutations. It is interesting to note that germline mutations in CDC73 (cell division cycle 73) predispose to both parathyroid and renal tumors (26), and the CDC73 gene product (parafibromin) has been reported to repress cyclin D1 expression and induce cell-cycle arrest (27).
As the inventory of genetic and epigenetic changes described in RCC enlarges, the challenge of differentiating "driver" and "passenger" events increases. Identification of the genetic basis of inherited cancer provides a powerful strategy for highlighting key pathways in oncogenesis. Thus, though the VHL TSG is frequently somatically inactivated in sporadic RCC, other inherited RCC genes, such as FH, FLCN, and SDHB, are infrequently implicated in RCC but, like pVHL, have been linked to regulation of hypoxic gene response pathways. The finding that germline CDKN2B mutations predispose to RCC is consistent with the observation that VHL inactivation is associated with disordered cell-cycle regulation and provides a basis for investigating the role of cell-cycle inhibitors (e.g., palbociclib) for the treatment of advanced RCC—particularly in patients with germline CDKN2B mutations. Thus, inclusion of CDKN2B mutation analysis in the routine investigation of individuals could facilitate the management of both affected individuals and their at-risk relatives.
Whole-exome sequencing was undertaken in the proband from a kindred with familial RCC (see Fig. 1A). Following the identification of a candidate germline CDKN2B mutation in the proband, mutation analysis of CDKN2B was performed in other family members and in a further 50 unrelated probands with (i) a diagnosis of RCC and a family history of one or more close relatives with a history of RCC (n = 37, 19 males and 18 females; mean age, 52.9 years; range, 29–71 years) or (ii) two or more primary RCC before age 50 years (n = 13, 7 males and 6 females; mean age, 41 years; range, 17–49 years). In addition, a further 32 DNA samples were tested from an anonymized cohort of individuals with evidence of possible inherited predisposition to RCC [i.e., a diagnosis of RCC plus one of (i) positive family history or (ii) multiple primary RCC or (iii) early onset RCC (<40 years)]. All subjects gave consent for genetic studies; the investigations were approved by the South Birmingham Research Ethics committee and were conducted in accordance with the Declaration of Helsinki.
Molecular Genetic Analysis
Exome resequencing was performed at the Biomedical Research Centre at King's College London as described previously (28). Briefly, after extraction of DNA from peripheral blood lymphocytes using standard techniques, exon capture was performed using the Agilent Sure Select All Exon 50 Mb Target Enrichment System. The Illumina Analyser IIA with 76 base paired ends and reads was used for sequencing, and the depth of sequence coverage was calculated using the BedTools software package (29). Sequence alignment, identification of SNPs, and small deletions were identified by the SAMTools software package (30). The ANNOVAR software package (31) was used to filter data for variants identified in dbSNP and common SNPs in the 1,000 genomes data. Furthermore, data were compared with 250 control exomes sequenced by the same method.
Sanger Sequencing
Sanger sequencing was performed using standard techniques. The following primer pairs were used:
CDKN2B exon 1: 5′-AAGAGTGTCGTTAAGTTTACG-3′ and 5′-ACATCGGCGATCTAGGTTCCA-3′,
CDKN2B exon 2: 5′-TGAGTATAACCTGAAGGTGG-3′ and 5′-GGGTGGGAAATTGGGTAAG-3′.
The following conditions were used: (i) 95°C for 5 minutes, (ii) 95°C for 45 seconds, (iii) 58°C for 45 seconds, decreasing by 1°C per cycle, (iv) repeat steps (i) to (iii) for 4 cycles, (v) 95°C for 45 seconds, (vi) 54°C for 45 seconds, (vii) 72°C for 45 seconds, (viii) repeat (v) to (vii) 30 times, (viii) incubate at 72°C for 5 minutes.
Colony Formation Assays
The CDKN2B clone was obtained from Cambridge Bioscience (True ORF Gold RC204895). The sequence of the clone was confirmed by direct sequencing. Site-directed mutagenesis was performed on the CDKN2B clone using the Quik Change II Site Directed Mutagenesis Kit (Stratagene; obtained from Agilent Technologies; primer details available on request). Mutant plasmids were sequenced in order to confirm the presence of the variant. Silver competent cells (Bioline) were transformed with mutant plasmid, and the plasmid was amplified to a stock concentration of 1 μg/μL using the Endotoxin-Free Maxi Spin Kit (Qiagen). The VHL-null cell line KTCL26 and the VHL–wild-type cell line SKRC47 were plated at a density of 6 × 104/mL in 6-well plates on day 1. Transfection was carried out on day 2 using 2 μg plasmid diluted in 200 μL of OptiMem (Gibco) and 6 μL of Fugene HD (Promega) per well. A serial dilution was performed in KTCL26 cells treated with EV and wild-type using the following dilutions: undiluted, 1:5, 1:10, 1:20. Dilutions (1:5) were used for subsequent experiments. The KTCL26 and SKRC47 cell lines were obtained from a collaborator prior to 2006, and no authentication was performed apart from confirming a VHL mutation [(c.370 C>T) p.Gln124Stop] in KTCL26 and the absence of a VHL mutation in SKRC47 (32).
Molecular Modeling
Models of CDKN2B in complex with CDK4 or CDK6 were based on the X-ray crystal structure of CDK6 in complex with CDKN2D (PDB code: 1BLX; ref. 14) and generated using Modeller (33) and MacroModel (Schrodinger). The models were then minimized using the MMF94s forcefield in Sybyl-X 2.1.1 (Certara L.P.). The resulting models were then aligned to the nuclear magnetic resonance (NMR) structure of CDKN2B (PDB code 1D9S; ref. 34) and showed minimal variation in the overall structure [root mean square difference (r.m.s.d) over Cαs of 1.6 Å]. The difference is mainly due to a small long-range bending of the molecule. The model of CDK4 was also compared with the CDK4 apo structure (PDB code: 3G33. r.m.s.d over Cαs of 1.1 Å). The effects of the mutations on the stability of CDKN2B were analyzed by mCSM (35) and DUET (36) using both the models and the apo NMR structure (PDB code: 1D9S). The effects of the mutations on the affinity of CDKN2B for CDK4 and CDK6 were analyzed by mCSM-PPI (35) using the models of the complexes. DUET and mCSM are novel machine-learning algorithms that use the three-dimensional structure in order to quantitatively predict the effects of point mutations on protein stability and protein–protein and protein–nucleic acid affinities.
T tests were performed using SPSS Statistics 21 (IBM software). To allow for multiple comparisons in Fig. 3 (wild-type and four mutants), a P value of <0.01 was taken to be statistically significant.
T.L. Blundell is a deputy chair trustee at the Institute of Cancer Research; President and Chair of the Science Council; and a consultant/advisory board member for Astex Therapeutics and BBSRC; has received a commercial research grant from UCB Celltech; and has provided expert testimony for Isogenica, Pfizer, and Syntaxin. No potential conflicts of interest were disclosed by the other authors.
Conception and design: M. Jafri, E.R. Woodward, F. Latif, E.R. Maher
Development of methodology: M. Jafri, N.C. Wake, M.R. Morris, M.A. Simpson, R.C. Trembath, T.L. Blundell
Acquisition of data (provided animals, acquired and managed patients, provided facilities, etc.): M. Jafri, E. Rattenberry, M.A. Simpson, R.C. Trembath, A. Weber, E.R. Woodward, A. Donaldson, E.R. Maher
Analysis and interpretation of data (e.g., statistical analysis, biostatistics, computational analysis): M. Jafri, N.C. Wake, D.B. Ascher, D.E.V. Pires, M.R. Morris, E. Rattenberry, M.A. Simpson, T.L. Blundell
Writing, review, and/or revision of the manuscript: M. Jafri, D.B. Ascher, D.E.V. Pires, M.R. Morris, E.R. Woodward, F. Latif, E.R. Maher
Administrative, technical, or material support (i.e., reporting or organizing data, constructing databases): M. Jafri, D. Gentle
Study supervision: E.R. Maher
M. Jafri is in receipt of a Medical Research Council Clinical Research Fellowship. D.B. Ascher is supported by a National Health and Medical Research Council CJ Martin Fellowship. D.E.V. Pires is supported by the Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)—Brazil. M.A. Simpson thanks the National Institutes for Health Research (NIHR) Biomedical Research Centre based at Guy's and St. Thomas' NHS Foundation Trust and King's College London for financial support. E.R. Maher thanks the Association for International Cancer Research (AICR; now Worldwide Cancer Research), The Eveson Charitable Trust, and the NIHR Biomedical Research Centre based at Cambridge for financial support.
The authors thank the patients, families, and referring clinicians for their assistance.
Received September 18, 2014.
Revision received April 1, 2015.
Accepted April 9, 2015.
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The boats continue arriving to the European coasts through the Mediterranean. All the travel risks, the waves or the low temperatures are insufficient to stop all the refugees that every day trying to arrive to Europe.
The refugees arrive to European coasts exhausted, wet and frozen. They are exposed to the death but it doesn't matter, they prefer suffer this situation before that continue living with the concern that one day a bomb may hit in their home or that a bomb may explodes near them when they are in the street.
Despite the difficulties, there is no evidence that this situation will change. From the beginning of the year, 31.500 refugees have arrived to Greece. Last year in the same period, this data was 1.700 refugees.
Unfortunately, when refugees arrive to Europe, their situation doesn't improve. European countries don't know how to manage the flow of refugees neither humanistic or logistically. For example, only 322 refugees of 160.000 (that the European countries had promised) have been relocated in the whole European territory. In addition, some countries have started to monitor the number of persons who cross the borders.
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Together we have to avoid that this situation becomes "something normal" for us. Syrian refugees still need protection and humanitarian aids.
At the end of September 2015, 193 UN's Member States met to endorse the 2030 Agenda for Sustainable Development. The 2030 Agenda includes 17 Sustainable Development Goals (SDG) and 169 targets in order to reach 3 extraordinary purposes over the next 15 years: ending extreme poverty, fight against inequalities and injustice and combat climate change.
The reason to create these 17 goals is the following, at the end of 2000 the Millennium Development Goals (MDGs) were launched with a deadline of 2015 but then a new Agenda had to be created. For that reason in 2002, the countries agreed to set up an open-ended working group to develop a set of sustainable development goals. It was agreed that the summit of the new Agenda adoption would have taken place from 25 to 27 September 2015 in New York.
The 17 Sustainable Development Goals looking forward to complete what the Millennium Development Goals could not accomplish. These goals are broad and ambitious in scope as the interconnected elements of sustainable development will be addressed: the economic growth, social inclusion and the environment protection. Unlike the Millennium Development Goals, the Sustainable Development Goals address the needs of people in both developed and developing countries, emphasising that no one should be left behind.
With the 2016 arrival, the 2030 Agenda for Sustainable Development has started. Since the beginning of 2016 until December 31, 2030, different economies, companies and citizens of the world will have to follow the itinerary marked by the 2030 Agenda for Sustainable Development in order to build a more just, equitable and sustainable world.
UNEP has created an interactive page where you can find out more about different points that make up each goal. Furthermore, you will be able to use an interactive resource where you may discover the different pathways to achieve the Sustainable Development Goals.


"Organic hotel, organic restaurant - you have really made a career out of your passion, haven't you?", the guest asked Domenico who had joined the man for a glass of wine. "I can only be good at something I am deeply convinced of," the innkeeper replied. The guest raised his glass. "To the good life here in Oberpfaffenhofen. By the way, I'm planning a party at the moment. Can I enjoy your great food at home, as well?" - "Of course you can. All meals of our organic restaurant can be delivered to your home. We will prepare something according to your wishes, something that suits the occasion and the season. Organic catering with regional ingredients is one of our most popular specialties." Suddenly, the door to the secondary room opened with a head peeking out. "Domenico, do you have a minute...?"


Kwashiorkor is a form of severe protein–energy malnutrition characterized by edema, irritability, ulcerating dermatoses, and an enlarged liver with fatty infiltrates. Sufficient calorie intake, but with insufficient protein consumption, distinguishes it from marasmus. Kwashiorkor cases occur in areas of famine or poor food supply. Cases in the developed world are rare. Jamaican pediatrician Cicely Williams introduced the name into the medical community in a 1935 Lancet article, two years after she published the disease's first formal description in the Western medical literature. The name is derived from the Ga language of coastal Ghana, translated as "the sickness the baby gets when the new baby comes" or "the disease of the deposed child", and reflecting the development of the condition in an older child who has been weaned from the breast when a younger sibling comes.Breast milk contains proteins and amino acids vital to a child's growth. In at-risk populations, kwashiorkor may develop after a mother weans her child from breast milk, replacing it with a diet high in carbohydrates, especially sugar. Signs and symptoms The defining sign of kwashiorkor in a malnourished child is pitting edema (swelling of the ankles and feet). Other signs include a distended abdomen, an enlarged liver with fatty infiltrates, thinning hair, loss of teeth, skin depigmentation and dermatitis. Children with kwashiorkor often develop irritability and anorexia. Generally, the disease can be treated by adding protein to the diet; however, it can have a long-term impact on a child's physical and mental development, and in severe cases may lead to death. In dry climates, marasmus is the more frequent disease associated with malnutrition. Another malnutrition syndrome includes cachexia, although it is often caused by underlying illnesses. These are important considerations in the treatment of the patients. Causes Kwashiorkor is a severe form of malnutrition, caused by a deficiency in dietary protein. The extreme lack of protein causes an osmotic imbalance in the gastro-intestinal system causing swelling of the gut diagnosed as an edema or retention of water.
Extreme fluid retention observed in individuals suffering from kwashiorkor is a direct result of irregularities in the lymphatic system and an indication of capillary exchange. The lymphatic system serves three major purposes: fluid recovery, immunity, and lipid absorption. Victims of kwashiorkor commonly exhibit reduced ability to recover fluids, immune system failure, and low lipid absorption, all of which result from a state of severe undernourishment. Fluid recovery in the lymphatic system is accomplished by re-absorption of water and proteins which are then returned to the blood. Compromised fluid recovery results in the characteristic belly distension observed in highly malnourished children. Capillary exchange between the lymphatic system and the bloodstream is stunted due to the inability of the body to effectively overcome the hydrostatic pressure gradient. Proteins, mainly albumin, are responsible for creating the colloid osmotic pressure (COP) observed in the blood and tissue fluids. The difference in the COP of the blood and tissue is called the oncotic pressure. The oncotic pressure is in direct opposition with the hydrostatic pressure and tends to draw water back into the capillary by osmosis. However, due to the lack of proteins, no substantial pressure gradient can be established to draw fluids from the tissue back into the blood stream. This results in the pooling of fluids, causing the swelling and distention of the abdomen. The low protein intake leads to some specific signs: edema of the hands and feet, irritability, anorexia, a desquamative rash, hair discolouration, and a large fatty liver. The typical swollen abdomen is due to two causes: ascites because of hypoalbuminemia (low oncotic pressure), and enlarged fatty liver. Ignorance of nutrition can be a cause. Latham, director of the Program in International Nutrition at Cornell University, along with Keith Rosenberg cited a case where parents who fed their child cassava failed to recognize malnutrition because of the edema caused by the syndrome and insisted the child was well-nourished despite the lack of dietary protein. Protein should be supplied only for anabolic purposes. The catabolic needs should be satisfied with carbohydrate and fat. Protein catabolism involves the urea cycle, which is located in the liver and can easily overwhelm the capacity of an already damaged organ. The resulting liver failure can be fatal. This means in patients suffering from kwashiorkor, protein must be introduced back into the diet gradually. Clinical solutions include weaning the affected with milk products and increasing the intake of proteinaceous material to daily recommended amounts.


Shoe wood brush. Polisher mini. Plastic shoes women. Wholesale leather liquid. Cotton paper. Elegance shoes. Boots. Shoe polish dauber. Non-folding rack. Wholesale shoes clean. Hair washing portable. Blister.
Leather polishing cleaning brush. Make up brush. Hand brush and dustpan. Detail1: Dustpan material: Wire height: Colourful. Cleaning supplies cartoon. Model number: 5 pieces. Cleaning brush size (l x w x h): 3-5cm. Package included: Cleaner carpet. Carpet cleaner brush. Shaft material: Item height: Polish boot. Ae012305.


For the 2018-19 school year, there are 7 top public schools in North Bend, Oregon, serving 4,270 students.
North Bend, OR public schools have a diversity score of 0.39, which is higher than the Oregon average of 0.37.
The most diverse school in North Bend is North Bend Middle School. Read more about public school diversity statistics in Oregon or national school diversity statistics.
Minority enrollment is 23% (majority Hispanic) and the student:teacher ratio is 25:1.


The plumbing division is responsible for the administration and enforcement of the Michigan Plumbing Code (Part 7 rules incorporating the International Plumbing Code), related laws, ordinances and standards.
The plumbing division inspector and plan reviewer John Dobberteen is an independent contractor and duly registered with the State of Michigan to perform inspections of plumbing work and plan reviews.
Call our office (269-651-4567) on application questions and you can download an application for a plumbing permit here or on our forms page.
Follow the permit requirements and contact John Dobberteen's office (plumbing inspections only) when the work (portion to be inspected) is ready for inspection. Inspections must be scheduled on the phone with at least 24 hours notice. Call 269-651-4567 and have permit number, location, type of inspection, site access information available.
Approvals (green sticker) and disapprovals (red sticker) of work by inspectors will be noted and communicated to the permit holder. Green sticker (approval) means you may proceed and conceal the approved work. Red sticker (disapproval) means deficiencies/code violations have been identified and you may not proceed to conceal work until the deficiencies/code violations have been corrected and the work has been re-inspected and approved (green sticker) by the inspector.
Once the final inspections and approvals have been obtained you will be issued a certificate of use and occupancy for the building/structure or portion of the work therein. You may not use or occupy areas of construction under permit until the certificate of use and occupancy has been issued by Niles Charter Township.