Jury sought child abuse charges against Ramseys

BOULDER, Colo. (AP) — A grand jury that reviewed evidence in the death of 6-year-old JonBenet Ramsey believed her parents were involved in the crime but that another unknown person killed the young beauty queen, according to documents released Friday, 14 years after the grand jury made its recommendation.

At the time, the panel recommended that both her parents be charged with child abuse resulting in death and being an accessory to a crime, including murder.

However, the documents allege that both parents intended to delay or prevent the arrest of the person who killed their daughter.

The proposed charges were disclosed for the first time in the documents. However, no new light was shed on who committed the killing.

Prosecutors at the time declined to actually file charges against John and Patsy Ramsey, who have since been treated as victims in the case.

The district attorney at the time, Alex Hunter, who presented the evidence to the grand jury, said in 1999: "I and my prosecutorial team believe we do not have sufficient evidence to warrant the filing of charges against anyone who has been investigated at this time."

John Ramsey's attorney, Hal Haddon, issued a letter earlier this week opposing release of the indictments, pointing out that Hunter's successor, former district attorney Mary Lacy, cleared the Ramseys based on new DNA testing in 2008.

He also cited Lacy's apology in a letter to John Ramsey at the time, in which she said "no innocent person should have to endure such an extensive trial in the court of public opinion, especially when public officials have not had sufficient evidence to initiate a trial in a court of law."

Haddon said Friday he would have no further comment on the release of the indictments.

Patsy Ramsey died in 2006.

Lurid details of the crime and striking videos of the child in adult makeup and costumes performing in pageants propelled the case into one of the highest profile mysteries in the U.S. in the mid-1990s.

The grand jury met three years after JonBenet's body was found bludgeoned and strangled in the family home in Boulder on Dec. 26, 1996.

The Ramseys maintained their innocence, offering a $100,000 reward for information about the killer and mounting a newspaper campaign seeking evidence.

Boulder Police Chief Mark Beckner said the case remains open but is not an active investigation. He predicted the indictment's release wouldn't change anything.

"Given the publicity that's been out there, many people have formed their opinions one way or another," he said.

Former prosecutor and law professor Karen Steinhauser said grand juries sometimes hear evidence that won't be admitted during trial that can form the basis of indictments.

But she added that prosecutors must have a good faith belief that they could prove a case beyond a reasonable doubt before pursuing charges.

"I'm not sure that the release of this indictment is going to change the fact that there has not been able to be a prosecution and probably won't be able to be a prosecution," she said.

David Lane, a defense attorney who was not involved in the case, said the indictments could have been an attempt to force the parents to turn against each other, which he said was unlikely because both were protected by laws that limit testimony of one spouse against another.

"Somebody killed JonBenet Ramsey," Lane said. "It sounds like they were accused of aiding and abetting each other, with the hope someone would crack and break. That didn't happen, and prosecutors may have decided not to go forward."

The Daily Camera reported earlier this year that the grand jury had issued the indictment. The actual documents were released Friday in response to a lawsuit by the Daily Camera and the Reporters Committee for Freedom of the Press.

Boulder County District Attorney Stan Garnett determined the release would not violate grand jury secrecy rules, and transferred the documents to Robert Lowenbach, a retired Weld County judge, for review.

Lowenbach said Wednesday that only pages signed by the grand jury foreman would be releasable as official actions of the jury. His order mentioned 18 pages in all — nine relating to each of JonBenet's parents. Four pages — two each relating to the parents — were released Friday.

John Ramsey didn't immediately return a call seeking comment.

Patsy Ramsey died of cancer in 2006, the same year a globe-hopping school teacher was arrested in Thailand after falsely claiming to have killed JonBenet. Former District Attorney Mary Lacy cleared the Ramseys in 2008 based on new DNA testing that suggested the killer was a stranger, not a family member.

Lacy did not return a phone call on Friday.

Over the years, some experts have suggested that investigators botched the case so thoroughly that it might never be solved.

Earlier this week, John Ramsey asked officials to release the entire grand jury record if the unprosecuted indictment was made public.

However, Lowenbach said transcripts of grand jury proceedings and evidence presented to it are not considered official action under the law governing criminal court records. He also said releasing such information could hurt other grand juries, whose work is secret.

An attorney representing John Ramsey, L. Lin Wood, has said he's confident that no evidence in the grand jury case implicated the Ramsey family and the public should be able to see that for themselves.

_____

Associated Press writers Steven K. Paulson and Dan Elliott contributed to this report.

• Society & Culture
• Crime & Justice
• JonBenet Ramsey
• Patsy Ramsey

Source: http://news.yahoo.com/jury-sought-child-abuse-charges-against-ramseys-165942442.html
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Netgear Nighthawk AC1900 Smart WiFi Router (R7000)

The Nighthawk, is Netgear's latest router in the company's premium dual-band 802.11ac router line-up. The router looks as cool as its name suggests, with a trapezoid design and flared sides. The shape is reminiscent of the famed fighter jet of the same name. Yet the Nighthawk (model R7000) is not just dressed to impress: Excellent speeds on the 5GHz band when paired with Netgear's latest mini 11ac A6100 USB adapter and enhanced Quality-of-Service (QoS) that really shortens the time to buffer and stream video make the Nighthawk one of the top 802.11ac routers currently on the market for heavy-duty throughput tasks.

It's not a perfect device, with just okay throughput at 2.4GHz—at least testing in a heavy RF signal environment. It also takes quite some time to apply settings changes. However, with 802.11ac, the speed factor is most important at 5GHz, and the Nighthawk delivers the goods not just in data rate but in range, too. Bonus for router geeks: Nighthawk can be flashed with open-source firmware.

Specs and Design
The R7000 is a large router. It measures 1.97" x 11.22" x 7.26" (HWD) and weighs a little over 1.6 pounds. Netgear revamped the design from its last release of dual-band routers including the Centria and the R6300, both of which have an upright design with the devices meant to operate vertically in attached bases.

The Nighthawk operates horizontally (although it can be wall-mounted). The design represents Netgear's slickest router look yet. The wide base of the R7000 makes it very sturdy, even with cables connected to every port. With its wide base and rubber feet, this big router won't slip and slide all over a surface.

A beefy router certainly deserves beefy specs. Inside the Nighthawk is a dual-core 1GHz processor—powerful, for a consumer router. The R7000 supports 600Mbps at 2.4GHz and up to 1300Mbps at the 5GHz band. Three external antennas ship with the router and attach to the back panel. The R7000 also has 128MB flash memory and 256MB RAM.
There are two USB ports; one on the front of the router and the second on the rear. The front port is USB 3.0 and the back port is USB 2.0. The USB 3.0 port was deliberately placed on the front, away from the 2.4GHz radio, to reduce Wi-Fi signal interference. Both ports support USB storage and printers.

On the back panel are Gigabit WAN and four Gigabit LAN ports, a reset button, and a power button. LEDs on the top of the router indicate wireless, Internet, USB device connection, and other network activity status.

I wasn't surprised that with its hardware specs, the R7000 runs a tad warm. Not hot, just a little warmer than room temperature. I would place it in a location with good air circulation.

One other design aspect to note: The brick on the power cord is huge. It is thin, though, so you shouldn't have a problem placing it alongside other power adapters in a strip plug.

Setup
As is the case with most of the newer routers, the R7000 is easy to set up. An installation guide is in the package and outlines the few steps needed to set the device up. The instructions are clear, concise, and easy to follow.

The last step instructs users to launch a Web browser to finish configuration. When I did, a page displayed that the router was successfully connected to the Internet and the pre-configured wireless SSID and passphrase. I had the option to print this page or click a button "Take me to the internet." Clicking this button redirected the page to Netgear's external website where I could download management apps for the router, including the Genie desktop or mobile app, the ReadyVault app (for using the router as part of a backup solution), or access a link for help and support.

I have reviewed the two aforementioned apps, and they have not changed significantly since those reviews. You can read the provided link to the reviews for more details. The R7000's setup process is streamlined, well done, and should not present a problem for most users.

Source: http://feedproxy.google.com/~r/ziffdavis/pcmag/~3/jbNvJlYgRDQ/0,2817,2426296,00.asp
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Targeting cancer's sweet tooth

PUBLIC RELEASE DATE:

21-Oct-2013

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Contact: Rachel Steinhardt
rsteinhardt@licr.org
212-450-1582
Ludwig Institute for Cancer Research

A study of how cancer cells get energy and raw materials for growth from glucose opens doors to new therapies

October 21, 2013, New York, NY Ludwig researchers have elucidated a key mechanism by which cancer cells change how they metabolize glucose to generate the energy and raw materials required to sustain runaway growth.

Published online in Cell Metabolism, the Ludwig Cancer Research study also reveals how the aggressive brain cancer glioblastoma harnesses the mechanism to resist targeted therapies that should disrupt this capabilityknown as the Warburg effectand suggests how such resistance might be overcome. In detailing the molecular circuitry of the phenomenon, the researchers uncover several possible targets for new drugs that might disrupt cancer cell metabolism to destroy tumors.

"Cancer and other fast-growing cells extract energy from glucose using a process that ordinarily kicks in only when oxygen is in short supply," explains Ludwig scientist Paul Mischel, MD, who is based at the University of California, San Diego School of Medicine. "This allows them to thread the needle: they get the energy they need from glucose but also retain the carbon-based building blocks for molecules like lipids, proteins and DNA, which dividing cells need in large quantities."

Until recently, relatively little was known about the biochemical circuits that induce this vital metabolic shift in cancer cells. Earlier this year, however, Mischel and his colleagues published a study describing how an aberrant growth signal found in many glioblastomas is channeled to induce the Warburg effect. That signaling cascade, which involves the key proteins PI3 kinase (PI3K), Akt and mTORC1, culminates in the activation of a transcription factora controller of gene expressionnamed c-Myc. "In many cancer cells," says Mischel, "c-Myc seems to be a lever that links growth signaling pathways with the machinery that controls the uptake and use of nutrients."

In the current study, Mischel, who did the research in collaboration with Ludwig researchers Kenta Masui, MD, PhD and Web Cavenee, PhD, both also at UC San Diego, identifies a second interacting biochemical cascade that is independent of the PI3K-Akt-mTORC1 signal and uses distinct biochemical circuits and an unusual mechanism to turn on c-Myc. This pathway, Mischel and his colleagues report, depends on signals from a protein complex named mTORC2. The researchers show that when mTORC2 is switched on, it silences two other transcription factors, FoxO1 and FoxO3, which would otherwise suppress the activation of c-Myc in the nucleus of the cell. Further, they learned that the silencing of the FoxOs occurs through a chemical modificationknown as acetylationa process that has not been well understood.

The study has significant implications for cancer therapy. "Many drugs have recently been devised to block PI3K-Akt-mTORC1 signaling," explains Mischel. "What we show is that when you use those drugs, you will probably drive the acetylation of the FoxOs through mTORC2, and inadvertently fuel the Warburg effect. In other words, this new pathway is likely to be responsible for resistance to those drugs. Our data suggest that to disrupt the Warburg effect and kill cancer cells, you have to develop therapies that target both signaling pathways. That's the main clinical ramification of this finding."

Mischel and his colleagues find that glioblastomas that rely predominantly on the mTORC2-mediated pathway tend to have the worse prognosis. Further, their studies suggest that lung cancer cells, too, use this pathway to induce the Warburg effect.

"Increasingly," says Mischel, "we're using glioblastoma as a system to understand a variety of other cancers and, in fact, this finding has broader relevance because the signaling pathways identified here are conserved across cancer types." Different cancers, he explains, are fueled by different types of mutations to growth factor receptors, but the signals these mutated receptors transmit tend to converge on a subset of signaling proteins.

"Our identification of the key moleculesand novel signaling mechanismsinvolved in this pathway, has opened up a landscape rich in possible targets for novel cancer drugs," says Mischel. His laboratory, he says, is now working with other Ludwig researchers to identify small drug-like molecules that might disrupt key steps of the mTORC2-mediated pathway.

###

About Ludwig Cancer Research

Ludwig Cancer Research is an international collaborative network of acclaimed scientists with a 40-year legacy of pioneering cancer discoveries. Ludwig combines basic research with the ability to translate its discoveries and conduct clinical trials to accelerate the development of new cancer diagnostics and therapies. Since 1971, Ludwig has invested more than $1.6 billion in life-changing cancer research through the not-for-profit Ludwig Institute for Cancer Research and the six U.S.-based Ludwig Centers. http://www.ludwigcancerresearch.org

Paul Mischel is a member of the Ludwig Institute for Cancer Research and is based at the University of California, San Diego. Lead author Kenta Masui is a post-doctoral fellow in the Mischel lab. Web Cavenee is the director of Ludwig San Diego.

For further information please contact Rachel Steinhardt, rsteinhardt@licr.org or +1-212-450-1582.

---

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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

PUBLIC RELEASE DATE:

21-Oct-2013

[


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]

Contact: Rachel Steinhardt
rsteinhardt@licr.org
212-450-1582
Ludwig Institute for Cancer Research

A study of how cancer cells get energy and raw materials for growth from glucose opens doors to new therapies

October 21, 2013, New York, NY Ludwig researchers have elucidated a key mechanism by which cancer cells change how they metabolize glucose to generate the energy and raw materials required to sustain runaway growth.

Published online in Cell Metabolism, the Ludwig Cancer Research study also reveals how the aggressive brain cancer glioblastoma harnesses the mechanism to resist targeted therapies that should disrupt this capabilityknown as the Warburg effectand suggests how such resistance might be overcome. In detailing the molecular circuitry of the phenomenon, the researchers uncover several possible targets for new drugs that might disrupt cancer cell metabolism to destroy tumors.

"Cancer and other fast-growing cells extract energy from glucose using a process that ordinarily kicks in only when oxygen is in short supply," explains Ludwig scientist Paul Mischel, MD, who is based at the University of California, San Diego School of Medicine. "This allows them to thread the needle: they get the energy they need from glucose but also retain the carbon-based building blocks for molecules like lipids, proteins and DNA, which dividing cells need in large quantities."

Until recently, relatively little was known about the biochemical circuits that induce this vital metabolic shift in cancer cells. Earlier this year, however, Mischel and his colleagues published a study describing how an aberrant growth signal found in many glioblastomas is channeled to induce the Warburg effect. That signaling cascade, which involves the key proteins PI3 kinase (PI3K), Akt and mTORC1, culminates in the activation of a transcription factora controller of gene expressionnamed c-Myc. "In many cancer cells," says Mischel, "c-Myc seems to be a lever that links growth signaling pathways with the machinery that controls the uptake and use of nutrients."

In the current study, Mischel, who did the research in collaboration with Ludwig researchers Kenta Masui, MD, PhD and Web Cavenee, PhD, both also at UC San Diego, identifies a second interacting biochemical cascade that is independent of the PI3K-Akt-mTORC1 signal and uses distinct biochemical circuits and an unusual mechanism to turn on c-Myc. This pathway, Mischel and his colleagues report, depends on signals from a protein complex named mTORC2. The researchers show that when mTORC2 is switched on, it silences two other transcription factors, FoxO1 and FoxO3, which would otherwise suppress the activation of c-Myc in the nucleus of the cell. Further, they learned that the silencing of the FoxOs occurs through a chemical modificationknown as acetylationa process that has not been well understood.

The study has significant implications for cancer therapy. "Many drugs have recently been devised to block PI3K-Akt-mTORC1 signaling," explains Mischel. "What we show is that when you use those drugs, you will probably drive the acetylation of the FoxOs through mTORC2, and inadvertently fuel the Warburg effect. In other words, this new pathway is likely to be responsible for resistance to those drugs. Our data suggest that to disrupt the Warburg effect and kill cancer cells, you have to develop therapies that target both signaling pathways. That's the main clinical ramification of this finding."

Mischel and his colleagues find that glioblastomas that rely predominantly on the mTORC2-mediated pathway tend to have the worse prognosis. Further, their studies suggest that lung cancer cells, too, use this pathway to induce the Warburg effect.

"Increasingly," says Mischel, "we're using glioblastoma as a system to understand a variety of other cancers and, in fact, this finding has broader relevance because the signaling pathways identified here are conserved across cancer types." Different cancers, he explains, are fueled by different types of mutations to growth factor receptors, but the signals these mutated receptors transmit tend to converge on a subset of signaling proteins.

"Our identification of the key moleculesand novel signaling mechanismsinvolved in this pathway, has opened up a landscape rich in possible targets for novel cancer drugs," says Mischel. His laboratory, he says, is now working with other Ludwig researchers to identify small drug-like molecules that might disrupt key steps of the mTORC2-mediated pathway.

###

About Ludwig Cancer Research

Ludwig Cancer Research is an international collaborative network of acclaimed scientists with a 40-year legacy of pioneering cancer discoveries. Ludwig combines basic research with the ability to translate its discoveries and conduct clinical trials to accelerate the development of new cancer diagnostics and therapies. Since 1971, Ludwig has invested more than $1.6 billion in life-changing cancer research through the not-for-profit Ludwig Institute for Cancer Research and the six U.S.-based Ludwig Centers. http://www.ludwigcancerresearch.org

Paul Mischel is a member of the Ludwig Institute for Cancer Research and is based at the University of California, San Diego. Lead author Kenta Masui is a post-doctoral fellow in the Mischel lab. Web Cavenee is the director of Ludwig San Diego.

For further information please contact Rachel Steinhardt, rsteinhardt@licr.org or +1-212-450-1582.

---

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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

Source: http://www.eurekalert.org/pub_releases/2013-10/lifc-tcs101913.php
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Brett Favre dismisses possibility of joining Rams

FILE - In this July 30, 2012, file photo, Former NFL quarterback Brett Favre, left, now an assistant football coach at Oak Grove High School explains a pass route to receiver Shane McClendon in Hattiesburg, Miss. Favre dismissed the possibility of returning to the NFL with St. Louis Rams. (AP Photo/Rogelio V. Solis, File)

FILE - In this July 30, 2012, file photo, Former NFL quarterback Brett Favre, left, now an assistant football coach at Oak Grove High School explains a pass route to receiver Shane McClendon in Hattiesburg, Miss. Favre dismissed the possibility of returning to the NFL with St. Louis Rams. (AP Photo/Rogelio V. Solis, File)

ST. LOUIS (AP) — Brett Favre dismissed the possibility of returning to the NFL with St. Louis, and Rams coach Jeff Fisher declined to address reports he tried to lure the quarterback out of retirement to replace the injured Sam Bradford.

Favre told Washington sports station WSPZ-AM he doesn't feel physically able to compete and expressed fear that he has been affected by concussions.

"It's flattering, but you know there's no way I'm going to do that," Favre said.

Fisher changed the subject after practice, then said "Nice try" when asked whether the 44-year-old Favre could be ready to play. Bradford is out for the season with a knee injury.

"I don't remember my daughter playing soccer, playing youth soccer, one summer," Favre told WSPZ. "I don't remember that. I got a pretty good memory, and I have a tendency like we all do to say, 'Where are my glasses?' and they're on your head. This was pretty shocking to me that I couldn't remember my daughter playing youth soccer, just one summer, I think. I remember her playing basketball, I remember her playing volleyball, so I kind of think maybe she only played a game or two. I think she played eight. So that's a little bit scary to me. For the first time in 44 years, that put a little fear in me. ...

"I think after 20 years, God only knows the toll."

Rams defensive end Robert Quinn didn't think there was anything to the reports.

"Brett Favre is staying retired," Quinn said. "Brett hasn't played since 2010 and he's comfortable down there in Mississippi on a boat or something. Have fun with it, Brett."

Kellen Clemens, the backup the past two seasons, will make his 13th career start Monday night against the Seattle Seahawks. The Rams also signed Brady Quinn and Austin Davis.

Fisher said he wouldn't discuss players contacted after Bradford tore his left ACL on Sunday at Carolina, although he confirmed Tyler Thigpen also worked out.

"I don't feel any need to disclose information after the process," Fisher said. "That's how we are. I'll be happy to talk about Thigpen, and the two that we signed."

___

AP NFL website: www.pro32.ap.org

Associated PressSource: http://hosted2.ap.org/APDEFAULT/347875155d53465d95cec892aeb06419/Article_2013-10-24-Rams-Favre/id-bb9fcf2ae6ac470caecccf6d46c0ea93
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5 things to know after Panthers rout Bucs 31-13

TAMPA, Fla. (AP) — From an 0-2 start to back over .500 for the first time in five years. Cam Newton and the surging Carolina Panthers are gaining confidence with each victory.

"At no point did I ever doubt this group of guys," coach Ron Rivera said Thursday night. "Maybe because I'm an optimist, but I really did believe that it was just a matter of time."

Newton continued a dazzling string of performances by throwing for two touchdowns and running for a third in a 31-13 rout of the winless Tampa Bay Buccaneers.

The victory was the third straight for the Panthers (4-3), who've won four of five after dropping their first two of the season. An efficient Newton has thrown for 667 yards, six TDs and no interceptions, while also rushing for two TDs during the winning streak.

"I just feel as if my production is off a lot of other people's production," Newton said. "If you want to solely say I'm playing great, it also means that a lot of other guys are playing great behind the scenes. This is not a one-man show. I understand that, and I will not have that type of attitude."

Newton tossed a 1-yard TD pass to Greg Olsen in the first quarter and added a 3-yarder to Mike Tolbert on the first play of the fourth quarter for a 28-6 lead. Newton had his way against the Bucs in between those scores, too, setting up a nifty 12-yard TD run by DeAngelo Williams and getting into the end zone himself with a 6-yard run midway through the third quarter.

"You're going to win a lot of football games with your quarterback playing like that," Olsen said. "We didn't turn the ball over, our running game was consistent. With a defense like ours, those are ingredients that make you very hard to beat."

The Bucs (0-7), one of two NFL teams yet to win, have dropped the first seven games in a season for the seventh time in franchise history. They've lost 12 of 13 dating to last year, and some fans showed up at Raymond James Stadium carrying signs and wearing paper bags over their heads urging that second-year coach Greg Schiano be fired.

"We got licked," Schiano said, adding that calls for his dismissal haven't become a distraction for him or his players.

"It doesn't affect me. 'People are certainly entitled to their opinion. ... You sit there and cry about it, but that's not going to help."

Newton was 23 of 32 for 221 yards passing. He also rushed for a team-high 50 yards on 11 attempts. Just as important, he hasn't turned the ball over in the past three weeks.

"He's just got to continue to work hard at it," Rivera said. "He did a great job protecting the football, doing the things that he needed to, making good decisions. The guys around him are making plays."

Here are five reasons the Panthers are over .500 for the first time since 2008 and the Bucs — like the Jacksonville Jaguars — remain winless:

HEAVY BURDEN: Rookie Mike Glennon threw for 275 yards, one touchdown and no interceptions in his fourth start for Tampa Bay. But he threw the ball 51 times after attempting 43, 43 and 44 in his previous three outings. That's 181 times, a NFL record for a player in the first four games of a career. Not the way you win with a first-year quarterback.

WE RUN IT, TOO: Newton has been outstanding throwing the ball in wins over Minnesota, St. Louis and Tampa Bay, but Carolina also has been able to run the ball. With Newton leading the way with 50 yards on 11 attempts (he lost 5 while kneeling down on the last two plays of the game), the Panthers finished with 129 yards on the ground.

WE CAN'T RUN IT: With leading rusher Doug Martin sidelined with a shoulder injury, rookie Mike James made his first pro start and gained 39 yards on 10 carries. Playing from behind all night, only two other players had rushing attempts. Brian Leonard had one carry for 7 yards and Glennon gained 2 on three attempts.

NOT-SO-HOME-SWEET-HOME: The Bucs are 3-9 at home under Schiano and have lost seven straight at Raymond James Stadium dating to last season. That's their longest home skid since 1977, when as a second-year expansion team they won their season finale against St. Louis to stop a 13-game streak.

CAROLINA 'D': The Panthers began the night with the league's No. 3 defense. They limited the Bucs to 48 yards rushing and 297 yards overall. They allowed points in the first quarter for the first time when Tampa Bay's Rian Lindell kicked a 47-yard field goal, but the unit kept the Bucs out of the end zone until Glennon threw a 10-yard pass to Tim Wright with just under three minutes left.

___

AP NFL website: www.pro32.ap.org

• Sports & Recreation
• American Football
• Carolina Panthers
• Cam Newton
• Tampa Bay Buccaneers
• the Panthers

Source: http://news.yahoo.com/5-things-know-panthers-rout-bucs-31-13-072331856--spt.html
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Kendall Jenner, Kylie Jenner Deny Underage Partying: "We're Smarter Than That"

Kendall and Kylie Jenner have had enough. Earlier this week, TMZ reported that Kendall, almost 18, and Kylie, 16, used fake IDs to enter a 21-and-over Wax Rabbit event at Vignette Lounge in West Hollywood on Oct. 15. The teenage Keeping Up With the Kardashians stars, however, took to Twitter on Wednesday, Oct. 23 to blast new reports that they were partying underage.

PHOTOS: Biggest celebrity feuds ever

"I am so done with everyone making my little sister and I out to be something that we are not. Shut up with these stupid rumors and stories," Kendall tweeted. "No one has fake ID's and no one's partying. We know that's what all you slimy media people want to see but that is not going to happen. We're smarter than that, we have goals and personally I think it's sad that some people sit at their desk making things up . . . about girls that are trying to have a career just like everybody else. Get over it. No story here."

PHOTOS: Kendall Jenner's bikini body

Kylie expressed similar sentiments on her own Twitter account that same day. "Bout to be straight up because I'm sick & tired of the rumors this past week," she tweeted. "I'm sorry to disappoint, but Kendall & I will not grow up to be let downs. I know that's what some people would unfortunately like to see . . . but I'm not going to sit around and let grown adults create untrue stories about me underage drinking & partying every night with a fake I.D." 

"And F.Y.I. regarding the 'club nights,' I was with my father & family supporting my brother and sister-in-law," Kylie added. "We can stop with all the stories now."

PHOTOS: Kardashian family album

But Kendall didn't seem to hold a grudge for too long. Immediately following her Twitter rant she wrote, "On another note, I got a new Great Dane puppy and she's awesome." Indeed, the young model stepped out with her adorable new puppy in L.A. on Oct. 23. Kendall celebrates her 18th birthday on Nov. 3, and older brother Rob Kardashian gave her the dog as an early birthday present.

Source: http://www.usmagazine.com/celebrity-news/news/kendall-jenner-kylie-jenner-deny-underage-partying-were-smarter-than-that-20132410
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Vine now lets you edit and work on multiple posts over time

Vine may have caught on in a fairly big way, but it's been a decidedly limited app even beyond the six-second constraint on videos. It's become a bit more capable today, though, with two new features giving users more room to work with. The first of those, called Sessions, will let you save and work ...

Source: http://feeds.engadget.com/~r/weblogsinc/engadget/~3/FZo4DgTAT4A/
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