Dinner In The Park: Union Station Homeless Services
Wednesday, November 23, 2011, 10am-6pm Adult Center, 412 South Raymond Ave., Pasadena, CA
Thursday, November 24, 2011, 8am-3pm Central Park, 219 South Fair Oaks Ave., Pasadena (near the Del Mar Station, Metro Gold Line)
Friday, November 25, 2011, 8am-noon Adult Center, 412 South Raymond Ave., Pasadena, CA
Every year, Union Station Homeless Services provides Thanksgiving meals to the homeless in Pasadena's Central Park and Adult Center. Online volunteer registration is currently open for the three events above.
Founded in 1973, Union Station is the San Gabriel Valley's largest and most comprehensive social service agency assisting homeless and very low-income people.
Shoppers look for bargains at Toys "R" Us last year. The big-box chain is opening at 9 p.m. on Thanksgiving this year.
By Marisa Taylor
Call it Black Friday fatigue.
With stores racing to open ever earlier on Thanksgiving (Wal-Mart?s doors will open at 10 p.m.!), a backlash is growing, with some retailers and analysts questioning the madness.
?The lunacy of opening at 12 midnight or even earlier on Thanksgiving evening shows that this whole Black Friday thing has run out of legs,? said IDC Retail Insights program director Greg Girard. ?Black Friday is a race to the bottom, and it?s just become another ad avenue.?
Other analysts think this year's extended hours are meant to distract shoppers from a lack of exciting inventory.
?If you build it, they will come,? said NPD Group chief industry analyst Marshal Cohen, ?but they won?t come in the dead of night. To me, you?re not going to sell more product just because you?re open more hours. It?s more of a smoke screen than it is a solution to the issue.?
This year, some stores are choosing not to take extreme measures to lure in bargain-hungry customers as they kick off a season that is expected to bring in about $465.6 billion in sales, a modest 2.8 percent increase over last year.
Sears, for one, has decided to pass on the trend for midnight openings set by big-box retailers including Best Buy, Kohls and Target. Toys 'R' Us is opening at 9 p.m. Thanksgiving night, an hour ahead of Wal-Mart.
Last year, Sears chose to keep its doors open on Thanksgiving from 7 a.m. until noon, with the idea that shoppers would come in early to rack up a few deals and then head home to their families for a midday meal.
But while the company did have good numbers that day, ?The customer feedback was very clear,? said Sears spokesman Tom Aiello. ?The customers liked the deals, but they didn?t like the idea of Thanksgiving shorted as a holiday.?
So the chain will revert to its original plan to open at 4 a.m. on Friday. ?I think there?s a group of customers that don?t aspire to get up in the middle of the night,? Aiello said.
Retail chain JC Penneyalso decided to stick with a 4 a.m. opening time this year so employees can spend Thanksgiving with friends and family, according to a company spokesman.
Employees at Target and Best Buy have launched petition drives on the website change.org protesting the early openings. ?A midnight opening robs the hourly and in-store salary workers of time off with their families on Thanksgiving Day,? wrote petition creator Anthony Hardwick, who identifies himself as a Target employee.
Some local retailers are still undecided on their Black Friday hours and will make last-minute decisions, according to Cohen.
Others are resisting the bonanza that is Black Friday altogether?or at least, they engage in more subtlety. Seattle-based retail chain Nordstrom has avoided opening its doors on Thanksgiving throughout the company?s history and in recent years has posted signs in its stores that read, ?One holiday at a time.?
Nordstrom waits until the morning of Black Friday to unveil its Christmas decorations, though it will open doors early that morning in some locations.
?It?s not as in your face,? said Forrester vice president and senior analyst Sucharita Mulpuru, ?but there?s a reason that Thanksgiving weekend that people work longer hours and [the stores] pull out all the stops as far as offering sales and promotions?because that?s the nature of that weekend.?
Analyst Greg Girard of IDC said?Black Friday is virtually absent from the websites of brand-oriented stores like Gap, Nordstrom and Lord & Taylor.
"And they?re doing something much more surgical in that they?re moving towards direct communications, like text messaging to consumers," he said. "They?re getting to consumers with whom they have a longer lifetime relationship."
Nordstrom, like many higher-end stores, doesn?t rely as heavily on Black Friday to make or break its sales year. Black Friday ?is among our most high volume days. But it isn?t our largest sales day of the year, unlike many retailers,? said Nordstrom spokesman Colin Johnson.
Do you plan to shop Black Friday?
With some major chains opening the doors on Thanksgiving for "Black Friday" sales, retail employees are beginning to publicly complain about sales creeping into their Thanksgiving holiday. KNSD's Bob Hansen reports.
BALI, Indonesia ? After a nine-day trip through Asia in which he showed command on the world stage, President Barack Obama is headed back to debt-deadlocked Washington, where he'll confront fresh reminders of the limits of his power at home.
Obama departed from Bali's international airport Saturday afternoon for a 21-hour flight that, factoring in time-zone changes, was to return him to the White House before dawn Sunday. He'll be arriving days ahead of a deadline for a congressional supercommittee to produce recommendations to attack the country's yawning deficit.
But even though the president spoke to the supercommittee leaders from Air Force One as he headed out of town and urged them to get a deal, the panel is no further along than when Obama left Washington: frozen stuck along partisan lines.
If no agreement is reached, steep cuts would be enacted across the federal government that both sides say they want to avoid, particularly to the defense budget. But no end game was in sight as Obama made his way back home from the other side of the globe.
Also awaiting him are presidential politics heading into the 2012 election year, something Obama largely avoided while traveling in Hawaii, Australia and Indonesia. And with his opponents on the attack over his stewardship of the listless economy, Obama will renew his largely futile efforts to get Congress to pass his jobs bill as he aims to cast Republicans as the ones to blame.
For Obama, it may amount to something of a harsh homecoming after playing proud host in his native Hawaii to a summit of Pacific Rim nations, and traveling on to two countries where he remains highly popular and received warm welcomes.
Obama set out in his Asia-Pacific tour to deepen U.S. engagement in a fast-growing region that the White House views as increasingly critical to America's security and economic prosperity. He achieved some successes, including progress on a regional free-trade deal that could pay off with U.S. jobs, and a new military agreement with Australia that will boost the U.S. defense posture in the region by deploying more marines and U.S. aircraft to Australia.
Obama also announced he was dispatching his secretary of state to Myanmar in a significant step to prod forward reforms in that country, and throughout the trip the complexities of the U.S. relationship with China were on display.
But domestic issues were on Obama's mind as he wrapped up his trip. Obama focused his Saturday morning radio and Internet address on the trade deals he presided over and the jobs they were likely to create back home, including a multi-billion-dollar Boeing sale of commercial planes to Indonesia and a deal to export General Electric engines.
He portrayed his trip around the Pacific Rim as a hunt for new markets.
"As the fastest-growing region in the world, no market is more important to our economic future than the Asia Pacific ? a region where our exports already support five million American jobs," he said.
In a further reminder of what awaits Obama in Washington, Saturday's Republican address focused on the work of the supercommittee. Sen. Patrick Toomey of Pennsylvania, a member of the panel and architect of one of the central GOP proposals, said that despite the fast-approaching deadline he remained hopeful lawmakers could still accomplish some deficit reduction.
"We have what is truly a once-in-a-lifetime opportunity to pass legislation that will generate millions of jobs, create a simpler, fairer tax system with lower rates for everyone, and put our government on a path toward fiscal sanity," he said.
On China, throughout his trip Obama sent both public and private signals to the rising giant, cementing American power in a manner seen to counter China, and scolding Chinese leaders about the need to play by the rules economically.
On the final day of his trip, Saturday in Indonesia, Obama held a surprise meeting with Chinese Premier Wen Jiabao on the sidelines of an East Asia summit, focusing on the economic matters that have prompted disputes between the two major world powers.
White House National Security Advisor Tom Donilon told reporters that Obama stressed the importance of China adjusting the value of its currency, which the United States contends is deeply undervalued, and he said Obama and Wen also briefly discussed territorial disputes in the South China Sea.
China's state broadcaster, CCTV, reported that Wen told Obama the grim global economic picture made it practical and necessary for the U.S. and China to strengthen their economic and trade relationship.
He said more trade and investment would help ease the Sino-U.S. trade imbalance. Wen also restated Beijing's call for the U.S. to relax restrictions on high-tech exports to China, CCTV reported.
China, Wen said, had made strides in reforming its currency exchange and would continue to do so, the broadcaster said.
Later, Obama and leaders at an East Asia summit retreat raised the issue of maritime security, prompting Wen to respond. A senior U.S. administration official told reporters aboard Air Force One that Wen's remarks signaled a gradual evolution toward resolving quarrels with Asian neighbors over the major shipping route. He said U.S. officials were encouraged by Wen's response.
Donilon downplayed tensions and rejected suggestions that the nine-day mission in the Asia-Pacific was designed to thwart a rising China. The U.S. policy, Donilon said, was about rebalancing U.S. interests and focusing once more on the Asia-pacific region.
"This has nothing to do with isolating or containing anybody," he said.
Protection from severe malaria explained Public release date: 18-Nov-2011 [ | E-mail | Share ]
Contact: Prof. Michael Lanzer, Ph. D. michael.lanzer@med.uni-heidelberg.de 49-622-156-7845 University Hospital Heidelberg
Defective hemoglobin prevents the establishment of an important transport system of the malaria parasite in infected blood cells- Heidelberg researchers' results published in Science
Why do people with a hereditary mutation of the red blood pigment hemoglobin (as is the case with sickle-cell anemia prevalent in Africa) not contract severe malaria? Scientists in the group headed by Prof. Michael Lanzer of the Department of Infectious Diseases at Heidelberg University Hospital have now solved this mystery. A degradation product of the altered hemoglobin provides protection from severe malaria. Within the red blood cells infected by the malaria parasite, it blocks the establishment of a trafficking system used by the parasite's special adhesive proteins adhesins to access the exterior of the blood cells. As a result, the infected blood cells do not adhere to the vessel walls, as is usually the case for this type of malaria. This means that no dangerous circulatory disorders or neurological complications occur. The research study has been published in the journal Science, appearing initially online.
In the 1940s, researchers already discovered that sickle-cell anemia with its characteristic blood mutation was particularly prevalent in certain population groups in Africa. They also survived malaria tropica, whose course is usually especially virulent. With malaria tropica, the malaria parasites (Plasmodia) enter the person after a bite of an infected Anopheles mosquito. The mosquito first multiplies in the person's liver cells and then infects the red blood cells (erythrocytes). Once inside the erythrocytes, they divide again and ultimately destroy them. The nearly simultaneous bursting of all infected blood cells causes the characteristic symptoms, which include bouts of fever and anemia.
Adhesins on red blood cells cause circulatory disorders
In patients with malaria tropica, neurological complications such as paralysis, seizures, coma and severe brain damage also frequently occur. This is caused by an anomaly of the parasite Plasmodium falciparum. It forms special adhesins that reach the cell surface of the infected blood cell. Once there, it causes the erythrocytes to adhere to the vessel walls, preventing them from being recognized in the spleen as damaged and removed from circulation. The parasite's protective mechanism results in smaller vessels closing, becoming inflamed and for example, prevents parts of the nervous system from being adequately supplied with oxygen.
In humans with mutated hemoglobin, these complications occur in a weakened form or not at all. "At the cell surface of infected erythrocytes with mutated hemoglobin, there are significantly fewer adhesins of the parasite than in normal red blood cells," explained Prof. Lanzer, Director of the Dept. of Infectious Diseases, Parasitology. "For this reason, we had a closer look at the trafficking system within the host cell." To this end, the team compared the blood cells with normal hemoglobin and two hemoglobin variants (hemoglobin S and hemoglobin C), which occur in around one-fifth of the African population in malaria-infected areas.
Trafficking system of the malaria parasite visualized for the first time
In so doing, the scientists used high-resolution microscopy techniques such as cryoelectron tomography to discover a new transport mechanism. The parasite uses a certain protein (actin) from the cytoskeleton (cellular skeleton) of the erythrocytes for its own trafficking network. "It forms a completely new structure that has nothing in common with the rest of the cytoskeleton," explained Dr. Marek Cyrklaff, group leader at the Dept. of Infectious Diseases, Parasitology and first author of the article. "The vesicles with the adhesins reach the cell surface of the red blood cells directly via these actin filaments."
In contrast to erythrocytes with the two hemoglobin variants, here only short pieces of actin filaments are found. Targeted transport to the surface is not possible. "The entire transport system of the malaria parasite is degenerated in these blood cells," Cyrklaff added. Laboratory tests showed that the hemoglobins themselves were not responsible for this, but rather a degradation product, ferryl hemoglobin. This is an irreversibly damaged, chemically altered hemoglobin that is no longer able to bind oxygen. The hemoglobins S and C are considerably more unstable than normal hemoglobin. As a result, blood cells with these variants contain ten times more ferryl hemoglobin than other erythrocytes. This high concentration destabilizes the binding of the actin structure and it disintegrates.
"With these results, we have now described a molecular mechanism for the first time that explains this hemoglobin variant's protective effect against malaria," Lanzer said.
###
Literature:
Hemoglobins S and C interfere with Actin Remodeling in Plasmodium falciparum-Infected Erythrocytes: Marek Cyrklaff, Cecilia P. Sanchez, Nicole Kilian, Cyrille Bisseye, Jacques Simpore, Friedrich Frischknecht and Michael Lanzer. Science DOI: 10.1126/science.1213775
Heidelberg University Hospital and Medical Faculty:
Internationally recognized patient care, research, and teaching
Heidelberg University Hospital is one of the largest and most prestigious medical centers in Germany. The Medical Faculty of Heidelberg University belongs to the internationally most renowned biomedical research institutions in Europe. Both institutions have the common goal of developing new therapies and implementing them rapidly for patients. With about 10,000 employees, training and qualification is an important issue. Every year, around 550,000 patients are treated on an inpatient or outpatient basis in more than 50 clinics and departments with 2,000 beds. Currently, about 3,600 future physicians are studying in Heidelberg; the reform Heidelberg Curriculum Medicinale (HeiCuMed) is one of the top medical training programs in Germany.
Requests by journalists:
Prof. Michael Lanzer, Ph. D.
University Hospital of Heidelberg
Dept. of Infectious Diseases, Parasitology
Im Neuenheimer Feld 324
D-69120 Heidelberg
Germany
phone: 49-6221-567845
fax: 49-6221-564643
e-mail: michael.lanzer@med.uni-heidelberg.de
Dr. Annette Tuffs
Head of Public Relations and Press Department
University Hospital of Heidelberg and
Medical Faculty of Heidelberg
Im Neuenheimer Feld 672
D-69120 Heidelberg
Germany
phone: 49-6221-56-45-36
fax: 49-6221-56-45-44
e-mail: annette.tuffs@med.uni-heidelberg.de
Selected english press releases online:
http://www.klinikum.uni-heidelberg.de/presse
[ | E-mail | Share ]
?
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.
Protection from severe malaria explained Public release date: 18-Nov-2011 [ | E-mail | Share ]
Contact: Prof. Michael Lanzer, Ph. D. michael.lanzer@med.uni-heidelberg.de 49-622-156-7845 University Hospital Heidelberg
Defective hemoglobin prevents the establishment of an important transport system of the malaria parasite in infected blood cells- Heidelberg researchers' results published in Science
Why do people with a hereditary mutation of the red blood pigment hemoglobin (as is the case with sickle-cell anemia prevalent in Africa) not contract severe malaria? Scientists in the group headed by Prof. Michael Lanzer of the Department of Infectious Diseases at Heidelberg University Hospital have now solved this mystery. A degradation product of the altered hemoglobin provides protection from severe malaria. Within the red blood cells infected by the malaria parasite, it blocks the establishment of a trafficking system used by the parasite's special adhesive proteins adhesins to access the exterior of the blood cells. As a result, the infected blood cells do not adhere to the vessel walls, as is usually the case for this type of malaria. This means that no dangerous circulatory disorders or neurological complications occur. The research study has been published in the journal Science, appearing initially online.
In the 1940s, researchers already discovered that sickle-cell anemia with its characteristic blood mutation was particularly prevalent in certain population groups in Africa. They also survived malaria tropica, whose course is usually especially virulent. With malaria tropica, the malaria parasites (Plasmodia) enter the person after a bite of an infected Anopheles mosquito. The mosquito first multiplies in the person's liver cells and then infects the red blood cells (erythrocytes). Once inside the erythrocytes, they divide again and ultimately destroy them. The nearly simultaneous bursting of all infected blood cells causes the characteristic symptoms, which include bouts of fever and anemia.
Adhesins on red blood cells cause circulatory disorders
In patients with malaria tropica, neurological complications such as paralysis, seizures, coma and severe brain damage also frequently occur. This is caused by an anomaly of the parasite Plasmodium falciparum. It forms special adhesins that reach the cell surface of the infected blood cell. Once there, it causes the erythrocytes to adhere to the vessel walls, preventing them from being recognized in the spleen as damaged and removed from circulation. The parasite's protective mechanism results in smaller vessels closing, becoming inflamed and for example, prevents parts of the nervous system from being adequately supplied with oxygen.
In humans with mutated hemoglobin, these complications occur in a weakened form or not at all. "At the cell surface of infected erythrocytes with mutated hemoglobin, there are significantly fewer adhesins of the parasite than in normal red blood cells," explained Prof. Lanzer, Director of the Dept. of Infectious Diseases, Parasitology. "For this reason, we had a closer look at the trafficking system within the host cell." To this end, the team compared the blood cells with normal hemoglobin and two hemoglobin variants (hemoglobin S and hemoglobin C), which occur in around one-fifth of the African population in malaria-infected areas.
Trafficking system of the malaria parasite visualized for the first time
In so doing, the scientists used high-resolution microscopy techniques such as cryoelectron tomography to discover a new transport mechanism. The parasite uses a certain protein (actin) from the cytoskeleton (cellular skeleton) of the erythrocytes for its own trafficking network. "It forms a completely new structure that has nothing in common with the rest of the cytoskeleton," explained Dr. Marek Cyrklaff, group leader at the Dept. of Infectious Diseases, Parasitology and first author of the article. "The vesicles with the adhesins reach the cell surface of the red blood cells directly via these actin filaments."
In contrast to erythrocytes with the two hemoglobin variants, here only short pieces of actin filaments are found. Targeted transport to the surface is not possible. "The entire transport system of the malaria parasite is degenerated in these blood cells," Cyrklaff added. Laboratory tests showed that the hemoglobins themselves were not responsible for this, but rather a degradation product, ferryl hemoglobin. This is an irreversibly damaged, chemically altered hemoglobin that is no longer able to bind oxygen. The hemoglobins S and C are considerably more unstable than normal hemoglobin. As a result, blood cells with these variants contain ten times more ferryl hemoglobin than other erythrocytes. This high concentration destabilizes the binding of the actin structure and it disintegrates.
"With these results, we have now described a molecular mechanism for the first time that explains this hemoglobin variant's protective effect against malaria," Lanzer said.
###
Literature:
Hemoglobins S and C interfere with Actin Remodeling in Plasmodium falciparum-Infected Erythrocytes: Marek Cyrklaff, Cecilia P. Sanchez, Nicole Kilian, Cyrille Bisseye, Jacques Simpore, Friedrich Frischknecht and Michael Lanzer. Science DOI: 10.1126/science.1213775
Heidelberg University Hospital and Medical Faculty:
Internationally recognized patient care, research, and teaching
Heidelberg University Hospital is one of the largest and most prestigious medical centers in Germany. The Medical Faculty of Heidelberg University belongs to the internationally most renowned biomedical research institutions in Europe. Both institutions have the common goal of developing new therapies and implementing them rapidly for patients. With about 10,000 employees, training and qualification is an important issue. Every year, around 550,000 patients are treated on an inpatient or outpatient basis in more than 50 clinics and departments with 2,000 beds. Currently, about 3,600 future physicians are studying in Heidelberg; the reform Heidelberg Curriculum Medicinale (HeiCuMed) is one of the top medical training programs in Germany.
Requests by journalists:
Prof. Michael Lanzer, Ph. D.
University Hospital of Heidelberg
Dept. of Infectious Diseases, Parasitology
Im Neuenheimer Feld 324
D-69120 Heidelberg
Germany
phone: 49-6221-567845
fax: 49-6221-564643
e-mail: michael.lanzer@med.uni-heidelberg.de
Dr. Annette Tuffs
Head of Public Relations and Press Department
University Hospital of Heidelberg and
Medical Faculty of Heidelberg
Im Neuenheimer Feld 672
D-69120 Heidelberg
Germany
phone: 49-6221-56-45-36
fax: 49-6221-56-45-44
e-mail: annette.tuffs@med.uni-heidelberg.de
Selected english press releases online:
http://www.klinikum.uni-heidelberg.de/presse
[ | E-mail | Share ]
?
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.
CHEYENNE, Wyo. ? A fiery, head-on crash that killed five people in central Wyoming last week was a murder-suicide by a distraught teen who veered his SUV into a family in a minivan at nearly 100 mph on a dark highway, authorities said Thursday.
The crash happened just after midnight Nov. 10 four miles south of Lander, a town of about 7,400 at the foot of the Wind River Range. Seventeen-year-old Matthew Denton deliberately turned the 2002 Chevrolet Suburban he was driving into oncoming traffic, Fremont County Coroner Ed McAuslan said.
The Suburban was going 97 mph when it crashed head-on into a 2005 Dodge Caravan, instantly killing all four people in the minivan. Denton, who was alone in the Suburban, died at a Casper hospital shortly after the wreck.
The van was going between 50 and 55 mph. There was no evidence Denton was targeting anyone inside the van, officials said.
"I don't think he had a clue who he was running into. It was dark. He picked the next vehicle that was coming down the road, is what it looked like to us," Wyoming Highway Patrol Lt. Tom Adams said.
Killed in the minivan were 41-year-old Corina Surrell-Norman; her ex-husband, Arvin Surrell; their 25-year-old son, Ethan Surrell, who was driving the minivan; and his 20-year-old girlfriend, Melinda Escamilla. All lived within about 30 miles of the crash: Denton was from Lander, the Surrells lived in Fort Washakie, and Escamilla was from Riverton.
The Surrells and Escamilla were headed to Salt Lake City for a doctor's appointment, Adams said.
Authorities determined the crash was intentional after inspecting a vehicle data recording device in the Suburban. The "black box" device showed how fast the Suburban was going and that Denton didn't attempt to brake.
Denton was "well into the throttle, almost to floor" when the crash happened, Adams said.
He said text messages on Denton's phone from the hour before the crash revealed he was having "personal problems." Denton was not texting at the moment of impact.
Adams declined to release the texts or say more about Denton's personal issues.
McAuslan's official finding, reported by KOVE-KDLY Radio ( http://bit.ly/rCrftN), was that Denton's death was a suicide and the deaths of the four others were homicides. McAuslan called it a murder-suicide.
"He did an intentional act that took the lives of four people," McAuslan said.
A toxicology report wasn't back yet.
The crash happened on a stretch of Wyoming Highway 789 that had two southbound lanes and a northbound lane. Denton was headed north when he crossed into both southbound lanes, according to a patrol release Monday.
The collision occurred in the inner southbound lane. The van tumbled off the highway and caught fire. Two people were ejected from the van and the other two burned inside, but McAuslan said the collision killed all four instantly.
Denton was a senior at Lander Valley High School, a well-liked, top-notch student who played the alto saxophone, said the school's band director, Tyler Surrell.
Surrell, who said he is not related to any of the crash victims who share his last name, suggested Denton may not have deliberately caused the wreck.
"He could have been upset, could have been crying," Surrell said. "And by the time he looked up, it could have been too late."
The four killed in the van were American Indians: The Surrell family members were Eastern Shoshone, and Escamilla was Northern Arapaho, said Ivan Posey of the Eastern Shoshone Business Council.
"As a community, we're still absorbing the losses and supporting the families," Posey said.
The two tribes share the nearby Wind River Indian Reservation.
Lisa Hafer, principal at Lander Valley High School where Denton was a student, declined to comment Thursday.
___
Associated Press writers Ben Neary and Bob Moen contributed to this report.
Fanny Wang lets you design the loudest and wackiest pair of headphones you can think up
If most cans you see for sale are too tame for your tastes, you'll enjoy Fanny Wang's customizable headphones service that you can use to create the wackiest pair you can dream up.?Fanny Wang explicitly states that it won't "stop anyone from making the ugliest pair possible," so go to town!
You can choose from three models by the company: an on-ear style for $220, an over-ear pair for $300, or pay $50 more for over-ear cans that pack?noise canceling technology. An additional $50 with any pair will net you customization privileges, so you can create any color scheme you want by changing the colors of seven different parts of the headphones.
If you're planning to buy a pair as a gift for the holidays, better do so now ? each order takes three weeks to arrive from the time you place it. Seeing as you can't change anything once you get through the checkout process, it's up to you to create a pair the recipient of your gift won't be ashamed of wearing in public.
[via Engadget]
This article was written by Mariella Moon and originally appeared on Tecca
Google's open marketplace means a greater threat of insidious apps
Google's Android platform sees new devices join its ranks on a regular basis. This widespread adoption of the operating system has allowed it to claim a huge share of the smartphone market, but it also makes it a big target for malware developers looking to cash in on stolen data. This year has been particularly gruesome for the OS, and security firm Juniper Networks has determined that the number of Android malware attacks has seen a 472% increase since July 2011.
Android's vulnerability to various types of malicious programs stems from Google's app publishing process, which is lax when compared with Apple's. When you submit an app for the iPhone or iPad, various code signing, verification, and approval steps are required before the application is allowed onto the store. These steps usually kill all malware-ridden programs before they make it to consumers' devices.
Android, on the other hand, requires just a $25 developer fee, after which you can publish any type of app you see fit. The programs aren't reviewed before hitting the virtual storefront, so it's much easier for seedy individuals to trick unsuspecting customers into installing malicious applications. The Android marketplace can and does remove applications that have been reported, but oftentimes the damage has already been done.
In order to ensure you don't fall victim to one of these insidious ploys, it's important to always thoroughly research an application before installing it on your device. You can often find the developer's website in the app description, so be sure to fully vet each program ahead of time. If you can't verify the developer as legitimate, or find enough positive reviews of the app to ensure the app works as intended, it's always better to skip it and err on the side of caution.
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Public release date: 18-Nov-2011
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