You know the frustration of driving down the road and not being able to make a U-turn: the islands in the middle of the roadway prevent it. Or do they? If you?re an aggressive driver you might decide to take on the island in order to reduce the distance you have to drive to get to your destination. But if you decide to drive over the island, also known as the safety zone, you?ll not only be breaking the law, but you may also be putting yourself at great risk.
ARS 28-734 prohibits drivers from driving in a safety zone, even if it is to facilitate a U-turn. Drivers may also be at significant risk for causing or becoming involved in a car crash, overturning their own vehicle or damaging their vehicle.
How to Avoid an Arizona Traffic Collision
Avoiding an Arizona traffic collision requires your utmost attention, not only to the road but also to the law. The best ways that you can protect yourself and your passengers from unnecessary harm include:
Never take unnecessary risks. Although it may be quicker to cross over the safety zone to make a U-turn than to go down to a light where it is allowed, this will endanger you.
Provide yourself plenty of time to get where you are going. Most drivers take unnecessary risks because they are pressed for time. Always allow yourself plenty of time to reach your destination.
Follow the law. Safety zones are an impediment placed in the road to protect you and all other motorists. Trust the law and the placement of these islands and do not cross them or drive on them.
What to Do If You Are Harmed in an Arizona Traffic Collision
If you are injured by a driver who ignored the safety zones in an Arizona traffic collision you should contact an experienced personal injury attorney at the Breyer Law Offices, P.C. Our team will assist you in getting fair compensation for your medical bills and injuries, emotional suffering, and other expenses related to your accident and injuries. For a free consultation and assistance with your case, reach out to the Husband and Wife Law Team.
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A cautionary tale on genome-sequencing diagnostics for rare diseasesPublic release date: 10-May-2013 [ | E-mail | Share ]
Contact: Patrick Bartosch pbartosch@sanfordburnham.org 407-745-2097 Sanford-Burnham Medical Research Institute
Sanford-Burnham researchers discover that several children born with rare diseases called Congenital Disorders of Glycosylation don't contain the mutation in every cell type—raising new questions about inheritance, genomic sequencing, and diagnostic
LA JOLLA, Calif., May 10, 2013 Children born with rare, inherited conditions known as Congenital Disorders of Glycosylation, or CDG, have mutations in one of the many enzymes the body uses to decorate its proteins and cells with sugars. Properly diagnosing a child with CDG and pinpointing the exact sugar gene that's mutated can be a huge relief for parentsthey better understand what they're dealing with and doctors can sometimes use that information to develop a therapeutic approach. Whole-exome sequencing, an abbreviated form of whole-genome sequencing, is increasingly used as a diagnostic for CDG.
But researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) recently discovered three children with CDG who are mosaicsonly some cells in some tissues have the mutation. For that reason, standard exome sequencing initially missed their mutations, highlighting the technique's diagnostic limitations in some rare cases. These findings were published April 4 in the American Journal of Human Genetics.
"This study was one surprise after another," said Hudson Freeze, Ph.D., director of Sanford-Burnham's Genetic Disease Program and senior author of the study. "What we learned is that you have to be carefulyou can't simply trust that you'll get all the answers from gene sequencing alone."
Searching for a rare disease mutation
Complicated arrangements of sugar molecules decorate almost every protein and cell in the body. These sugars are crucial for cellular growth, communication, and many other processes. As a result of a mutation in an enzyme that assembles these sugars, children with CDG experience a wide variety of symptoms, including intellectual disability, digestive problems, seizures, and low blood sugar.
To diagnose CDG, researchers will test the sugar arrangements on a common protein called transferrin. Increasingly, they'll also look for known CDG-related mutations by whole-exome sequencing, a technique that sequences only the small portion of the genome that encodes proteins. The patients are typically three to five years old.
A cautionary tale for genomic diagnostics
In this study, the researchers observed different proportions and representations of sugar arrangements depending on which tissues were examined. In other words, these children have the first demonstrated cases of CDG "mosaicism"their mutations only appear in some cell types throughout the body, not all. As a result, the usual diagnostic tests, like whole-exome sequencing, missed the mutations. It was only when Freeze's team took a closer look, examining proteins by hand using biochemical methods, did they identify the CDG mutations in these three children.
The team then went back to the three original children and examined their transferrin again. Surprisingly, these readings, which had previously shown abnormalities, had become normal. Freeze and his team believe this is because mutated cells in the children's livers died and were replaced by normal cells over time.
"If the transferrin test hadn't been performed early on for these children, we never would've picked up these cases of CDG. We got lucky in this case, but it just shows that we can't rely on any one test by itself in isolation," Freeze said.
###
This research was funded by The Rocket Fund at Sanford-Burnham and the U.S. National Institutes of Health National Institute of Diabetes and Digestive and Kidney Diseases grant R01DK55615 and National Human Genome Research Institute grant 1U54HG006493.
The study was co-authored by Bobby G. Ng, Sanford-Burnham; Kati J. Buckingham, University of Washington; Kimiyo Raymond, Mayo Clinic; Martin Kircher, University of Washington; Emily H. Turner, University of Washington; Miao He, Emory University School of Medicine; Joshua D. Smith, University of Washington; Alexey Eroshkin, Sanford-Burnham; Marta Szybowska, McMaster University; Marie Estelle Losfeld, Sanford-Burnham; Jessica X. Chong, University of Washington; Mariya Kozenko, McMaster University; Chumei Li, McMaster University; Marc C. Patterson, Mayo Clinic; Rodney D. Gilbert, Southampton Children's Hospital; Deborah A. Nickerson, University of Washington; Jay Shendure, University of Washington; Michael J. Bamshad, University of Washington; University of Washington Center for Mendelian Genomics; Hudson H. Freeze, Sanford-Burnham.
About Sanford-Burnham Medical Research Institute
Sanford-Burnham Medical Research Institute is dedicated to discovering the fundamental molecular causes of disease and devising the innovative therapies of tomorrow. Sanford-Burnham takes a collaborative approach to medical research with major programs in cancer, neurodegeneration, diabetes, and infectious, inflammatory, and childhood diseases. The Institute is recognized for its National Cancer Institute-designated Cancer Center and expertise in drug discovery technologies. Sanford-Burnham is a nonprofit, independent institute that employs 1,200 scientists and staff in San Diego (La Jolla), California, and Orlando (Lake Nona), Florida. For more information, visit us at sanfordburnham.org.
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A cautionary tale on genome-sequencing diagnostics for rare diseasesPublic release date: 10-May-2013 [ | E-mail | Share ]
Contact: Patrick Bartosch pbartosch@sanfordburnham.org 407-745-2097 Sanford-Burnham Medical Research Institute
Sanford-Burnham researchers discover that several children born with rare diseases called Congenital Disorders of Glycosylation don't contain the mutation in every cell type—raising new questions about inheritance, genomic sequencing, and diagnostic
LA JOLLA, Calif., May 10, 2013 Children born with rare, inherited conditions known as Congenital Disorders of Glycosylation, or CDG, have mutations in one of the many enzymes the body uses to decorate its proteins and cells with sugars. Properly diagnosing a child with CDG and pinpointing the exact sugar gene that's mutated can be a huge relief for parentsthey better understand what they're dealing with and doctors can sometimes use that information to develop a therapeutic approach. Whole-exome sequencing, an abbreviated form of whole-genome sequencing, is increasingly used as a diagnostic for CDG.
But researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) recently discovered three children with CDG who are mosaicsonly some cells in some tissues have the mutation. For that reason, standard exome sequencing initially missed their mutations, highlighting the technique's diagnostic limitations in some rare cases. These findings were published April 4 in the American Journal of Human Genetics.
"This study was one surprise after another," said Hudson Freeze, Ph.D., director of Sanford-Burnham's Genetic Disease Program and senior author of the study. "What we learned is that you have to be carefulyou can't simply trust that you'll get all the answers from gene sequencing alone."
Searching for a rare disease mutation
Complicated arrangements of sugar molecules decorate almost every protein and cell in the body. These sugars are crucial for cellular growth, communication, and many other processes. As a result of a mutation in an enzyme that assembles these sugars, children with CDG experience a wide variety of symptoms, including intellectual disability, digestive problems, seizures, and low blood sugar.
To diagnose CDG, researchers will test the sugar arrangements on a common protein called transferrin. Increasingly, they'll also look for known CDG-related mutations by whole-exome sequencing, a technique that sequences only the small portion of the genome that encodes proteins. The patients are typically three to five years old.
A cautionary tale for genomic diagnostics
In this study, the researchers observed different proportions and representations of sugar arrangements depending on which tissues were examined. In other words, these children have the first demonstrated cases of CDG "mosaicism"their mutations only appear in some cell types throughout the body, not all. As a result, the usual diagnostic tests, like whole-exome sequencing, missed the mutations. It was only when Freeze's team took a closer look, examining proteins by hand using biochemical methods, did they identify the CDG mutations in these three children.
The team then went back to the three original children and examined their transferrin again. Surprisingly, these readings, which had previously shown abnormalities, had become normal. Freeze and his team believe this is because mutated cells in the children's livers died and were replaced by normal cells over time.
"If the transferrin test hadn't been performed early on for these children, we never would've picked up these cases of CDG. We got lucky in this case, but it just shows that we can't rely on any one test by itself in isolation," Freeze said.
###
This research was funded by The Rocket Fund at Sanford-Burnham and the U.S. National Institutes of Health National Institute of Diabetes and Digestive and Kidney Diseases grant R01DK55615 and National Human Genome Research Institute grant 1U54HG006493.
The study was co-authored by Bobby G. Ng, Sanford-Burnham; Kati J. Buckingham, University of Washington; Kimiyo Raymond, Mayo Clinic; Martin Kircher, University of Washington; Emily H. Turner, University of Washington; Miao He, Emory University School of Medicine; Joshua D. Smith, University of Washington; Alexey Eroshkin, Sanford-Burnham; Marta Szybowska, McMaster University; Marie Estelle Losfeld, Sanford-Burnham; Jessica X. Chong, University of Washington; Mariya Kozenko, McMaster University; Chumei Li, McMaster University; Marc C. Patterson, Mayo Clinic; Rodney D. Gilbert, Southampton Children's Hospital; Deborah A. Nickerson, University of Washington; Jay Shendure, University of Washington; Michael J. Bamshad, University of Washington; University of Washington Center for Mendelian Genomics; Hudson H. Freeze, Sanford-Burnham.
About Sanford-Burnham Medical Research Institute
Sanford-Burnham Medical Research Institute is dedicated to discovering the fundamental molecular causes of disease and devising the innovative therapies of tomorrow. Sanford-Burnham takes a collaborative approach to medical research with major programs in cancer, neurodegeneration, diabetes, and infectious, inflammatory, and childhood diseases. The Institute is recognized for its National Cancer Institute-designated Cancer Center and expertise in drug discovery technologies. Sanford-Burnham is a nonprofit, independent institute that employs 1,200 scientists and staff in San Diego (La Jolla), California, and Orlando (Lake Nona), Florida. For more information, visit us at sanfordburnham.org.
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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.
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Walks, an error and a bases-clearing double resulted in a six-run third inning for Class 4A No. 1 Floyd Central on Wednesday, and the undefeated Highlanders advanced to Friday?s Hoosier Hills Conference Tournament championship game with an 8-1 win against Seymour.
Seymour?s lone run in the seventh came when two batters were hit by a pitch, Logan Richey singled and Jeremiah Tracey walked. Both teams had five hits, but Seymour had two errors to none for Floyd Central.
Billy Rayburn pitched the first three innings and took the loss, striking out three, walking six and giving up four hits and eight runs. On Friday, the Owls (11-9) will play for third place at Madison, which lost to Jeffersonville 1-0 in eight innings in the other semifinal.
This story appears in the print edition of The Tribune. Subscribers can read the entire story online by signing in here or in our e-Edition by clicking here.
Apple violates German data protection law by asking for users? broad, overall consent in its privacy policy, the Regional Court of Berlin ruled.
Apple?s terms for sharing personal information with the company are too broadly formulated, the court ruled on April 30, according to?a verdict?published by the Federation of German Consumer Organisations (VZBV)?on Tuesday.
The VZBV demanded in 2011 that Apple Sales International should stop using unfair contractual clauses in its?privacy policy?as posted on its German website, said Helke Heidemann-Peuser, a lawyer and head of the VZBV?s legal enforcement section. After this warning, Apple committed to change five of those clauses, but this was not enough, which is why the VZBV decided to sue Apple in February 2012, she said.
After Apple was sued, the company committed to change two more clauses, after which the lawsuit continued over the eight remaining disputed clauses, said Heidemann-Peuser. The court found that Apple violates the law with all those clauses, she added.
In its German privacy policy, which is similar?to the one used in the U.S., Apple states for instance that when someone contacts Apple and its affiliates, they may share information about that person with each other. Apple also states that this information may be combined with other information to provide and improve products, services, content and advertising.
This clause violates the law because customers are unaware which data is used and to what extend, the court ruled,?according to?the VZBV.
Another problematic clause gives Apple the right to collect the information someone provides about friends and family such as name, mailing address, email address and phone number when someone sends a gift certificate or products or invites others to join a user on an Apple forum, Heidemann-Peuser said. This is illegal because Apple would need consent from the third party to process this data, she said.
Apple also states that it may collect, use and share precise location data, including the real-time geographic location of a users? Apple computer or device, in order to provide location based services like advertising on Apple products. The data, as collected, is anonymous, according to Apple?s policy. However, when location-based services are used, the data can always be traced back to an individual, according to the court, so this clause was also prohibited.
Apple now needs to change these clauses, said Heidemann-Peuser. ?They need to be very specific,? she said, adding that Apple needs to ask for users? explicit consent instead of letting them agree to an overly broad privacy policy.
However, the company does not need to do so immediately because Apple can appeal the verdict, which the VZBV expects the company to do.
LONDON (AP) ? Japanese stocks outperformed all others Tuesday as traders in the country returned from a public holiday in buoyant mood, sending the Nikkei index above 14,000 for the first time in nearly five years.
The Nikkei surged 3.6 percent to 14,180.24 on its first day of trading following the Golden Week holiday ? that's the first time the Nikkei has breached the 14,000 mark since June 2008.
Japanese stocks have been marked up heavily this year after the Bank of Japan announced a new aggressive monetary policy to get the country out of its near two-decade stagnation. One repercussion of the plan to pump huge amounts of yen into the Japanese economy has been to sharply weaken the currency. A lower yen potentially boosts economic growth by making the country's exports cheaper in international markets.
Elsewhere, investors remained largely positive amid a dearth of scheduled economic and corporate news, as they continued to draw encouragement from Friday's better than anticipated U.S. payrolls figures. The data often set the market tone for a week or two after their release.
In Europe, the FTSE 100 index of leading British shares as up 0.3 percent at 6,540 while Germany's DAX rose 0.6 percent to 8,164. The CAC-40 in France was 0.4 percent higher at 3,921.
Wall Street was poised for a steady opening, with both Dow futures and the broader S&P 500 futures up 0.1 percent. Both indexes have touched record highs in recent days.
"Wall Street may be eyeing a relatively unchanged start to Tuesday, but there's no denying the current levels remain bullish and the fact the S&P is holding above 1,600 is certainly worthy of note," said Fawad Razaqzada, market strategist at GFT Markets.
The dollar was also fairly steady after gaining in the wake of the payrolls data. The euro was flat at $1.3075 while the dollar was 0.2 percent lower at 99.19 yen.
Earlier in Asia, Hong Kong's Hang Seng rose 0.6 percent to 23,047.09, while South Korea's Kospi fell 0.4 percent to 1,954.49 . Mainland Chinese shares were higher. The Shanghai Composite Index gained 0.2 percent to 2,235.58 and the smaller Shenzhen Composite Index added 0.1 percent to 955.33.
Australia was in focus after the Reserve Bank of Australia lowered its official interest rate by a quarter percentage point to 2.75 percent amid some signs the economy is coming off the boil as the Australian dollar rises. Following the reduction, the Aussie dollar fell 0.9 percent to $1.0169. However, the S&P/ASX 200 stock index fell 0.2 percent to 5,143.70.
Oil prices drifted lower after a strong run, with the benchmark New York rate down 63 cents at $95.53 a barrel.
ASCII?aka the American Standard Code for Information Interchange, aka the numeric codes that represent those little shapes on your keyboard?turns fifty this year. And while it?s since been surpassed by UTF-8, it still holds a special place in our hearts (and computers).
Yesterday we got a deep dive into the history of ASCII art thanks to Rhizome?s Tom McCormack, who leads us from the text art ephemera of the 1910s to the sexy ladies of anonymous late 1980s ASCII artists. When it was first published in 1963, ASCII was a coding standard, cut and dry. But later, in the era of Usenet, users began illustrating their posts with characters and animals. Before long, ASCII had evolved into a graffiti-like language for staking claims and making jokes amongst the Internet's earliest users. According to McCormack, art made with text articulated the optimism and excitement of the early web:
ASCII art was an aesthetic foreshadowing of what would become the culture?s social vision for the Web: the Internet would be the paradisaical city of our dreams; the ultimate melting pot; the high-tech global village we?d been promised. Home to a natural, nearly-inevitable democratic virtue, it would be a place where your identity could merge with the crowd, and even be shed entirely; and a super-speed air-tram could transport you from uptown to down in the amount of time it takes to register for a gonzo pornography subscription service.
Obviously, that vision of the web didn?t exactly turn out as planned (we get our gonzo pornography for free, thank you very much!). The web browser came along, and with it the image file. ASCII art was relegated to the fringe, where it flourished through the 1990s. But not all was lost: ASCII art gave birth to another very current part of our digital vernacular?emoji. More on that in the next chapter of McCormack?s saga. [Rhizome]
The first emotion-esque characters, hailing from the early 1980s.
"Horny Giant Girl spying at the wall," another hit from the mid-80s.
An early 2000s specimen from the artist Roy was done in "newskool" style, which usually incorporated actual words.
An ASCII chain email from the early 2000s.
Peter Nitsch's ASCII Street View turns Google Street View into text, a project Gizmodo covered in 2012.
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Public release date: 10-May-2013
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Apple violates German data protection law by asking for users? broad, overall consent in its privacy policy, the Regional Court of Berlin ruled.
