Raging fire guts Kabul market

KABUL, Afghanistan -- Firefighters battled through the night to contain a raging fire that swept through a market in the Afghan capital.

No injuries were reported, but the blaze destroyed hundreds of stores and millions of dollars worth of merchandise, Afghan police and firefighters said at the scene. 

Dealers at the neighboring currency exchange, the city’s largest, said they evacuated cash, computer equipment and records from their shops as the flames approached during the night. But in the morning, the market was jammed with people haggling over thick stacks of notes as smoke billowed overhead.

Col. Mohammed Qasem, general director of the Kabul fire department, said he suspected an electrical short was to blame for the fire. 

Gas canisters used to heat the stores propelled the flames, along with the cloth and clothing sold by many of the vendors, Qasem said. “It made it very big in a short time.”

Firefighters from the Afghan defense department and NATO forces were sent to assist. But the city’s notorious traffic and the market’s narrow lanes made it difficult for responders to maneuver their vehicles, Qasem said.

Abdulrahman, who like many Afghans has only one name, squatted near a fire truck with his head in his hands  as responders aimed a hose at the blackened ruins of a building still smoldering at noon Sunday, more than 12 hours after the fire broke out.

He said the building had contained three shops that he owned and a warehouse full of glassware, crockery and kitchen utensils. 

“I lost everything,” he said.

Shirali Khan complained that police hadn't allowed him to remove the goods from his four clothing stores.

“They thought we were all robbers,” he said.  “There’s only ashes left.”

ALSO:

Pope pardons former butler convicted of theft

Bombing kills local official, 7 other people in Pakistan

Tensions high as vote on proposed Egyptian constitution continues

Special correspondent Hashmat Baktash contributed to this report.

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Wired Science Space Photo of the Day: Hourglass Nebula

This Hubble telescope snapshot of MyCn18, a young planetary nebula, reveals that the object has an hourglass shape with an intricate pattern of "etchings" in its walls. A planetary nebula is the glowing relic of a dying, Sun-like star.

The results are of great interest because they shed new light on the poorly understood ejection of stellar matter that accompanies the slow death of Sun-like stars. According to one theory on the formation of planetary nebulae, the hourglass shape is produced by the expansion of a fast stellar wind within a slowly expanding cloud, which is denser near its equator than near its poles.

Image: Raghvendra Sahai and John Trauger (JPL), the WFPC2 science team, and NASA [high-resolution]

Caption: Hubble Heritage site

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Disney Sets August 9 Release for ‘Cars’ Spin-off ‘Planes’

NEW YORK (TheWrap.com) – Disney will release “Planes,” a spin-off of Pixar‘s “Cars” franchise, August 9, 2013, in the United States. DisneyToon Studios is behind the film with Pixar/Disney Animation chief creative officer John Lasseter producing.

The film follows a fleet of planes, in particular Dusty. “Two and a Half Men” star Jon Cryer was to voice Dusty, but he has dropped out and the studio is now casting the part.

Disney initially intended to release “Planes” direct to video, but it will now send it into theaters domestically and overseas.

“Planes” will compete against a pair of films that summer weekend, both of which should have more adult followings. The big-ticket item will be Sony’s “Elysium,” Neill Blomkamp‘s follow-up to “District 9.” Also opening that weekend is “We’re the Millers,” a New Line drug-smuggling comedy starring Jason Sudeikis and Jennifer Aniston.

Next summer’s biggest animated movies should all be sequels save “Epic,” Fox’s story of a teenage girl caught in a forested battle. Beyonce Knowles‘ leads the voice cast. The other big openers are Despicable Me 2,” “Monsters University” and “Smurfs 2.”

Movies News Headlines – Yahoo! News

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Genetic Gamble : Drugs Aim to Make Several Types of Cancer Self-Destruct

C.J. Gunther for The New York Times

Dr. Donald Bergstrom is a cancer specialist at Sanofi, one of three companies working on a drug to restore a tendency of damaged cells to self-destruct.

For the first time ever, three pharmaceutical companies are poised to test whether new drugs can work against a wide range of cancers independently of where they originated — breast, prostate, liver, lung. The drugs go after an aberration involving a cancer gene fundamental to tumor growth. Many scientists see this as the beginning of a new genetic age in cancer research.

Great uncertainties remain, but such drugs could mean new treatments for rare, neglected cancers, as well as common ones. Merck, Roche and Sanofi are racing to develop their own versions of a drug they hope will restore a mechanism that normally makes badly damaged cells self-destruct and could potentially be used against half of all cancers.

No pharmaceutical company has ever conducted a major clinical trial of a drug in patients who have many different kinds of cancer, researchers and federal regulators say. “This is a taste of the future in cancer drug development,” said Dr. Otis Webb Brawley, the chief medical and scientific officer of the American Cancer Society. “I expect the organ from which the cancer came from will be less important in the future and the molecular target more important,” he added.

And this has major implications for cancer philanthropy, experts say. Advocacy groups should shift from fund-raising for particular cancers to pushing for research aimed at many kinds of cancer at once, Dr. Brawley said. John Walter, the chief executive officer of the Leukemia and Lymphoma Society, concurred, saying that by pooling forces “our strength can be leveraged.”

At the heart of this search for new cancer drugs are patients like Joe Bellino, who was a post office clerk until his cancer made him too sick to work. Seven years ago, he went into the hospital for hernia surgery, only to learn he had liposarcoma, a rare cancer of fat cells. A large tumor was wrapped around a cord that connects the testicle to the abdomen. “I was shocked,” he said in an interview this summer.

Companies have long ignored liposarcoma, seeing no market for drugs to treat a cancer that strikes so few. But it is ideal for testing Sanofi’s drug because the tumors nearly always have the exact genetic problem the drug was meant to attack — a fusion of two large proteins. If the drug works, it should bring these raging cancers to a halt. Then Sanofi would test the drug on a broad range of cancers with a similar genetic alteration. But if the drug fails against liposarcoma, Sanofi will reluctantly admit defeat.

“For us, this is a go/no-go situation,” said Laurent Debussche, a Sanofi scientist who leads the company’s research on the drug.

The genetic alteration the drug targets has tantalized researchers for decades. Normal healthy cells have a mechanism that tells them to die if their DNA is too badly damaged to repair. Cancer cells have grotesquely damaged DNA, so ordinarily they would self-destruct. A protein known as p53 that Dr. Gary Gilliland of Merck calls the cell’s angel of death normally sets things in motion. But cancer cells disable p53, either directly, with a mutation, or indirectly, by attaching the p53 protein to another cellular protein that blocks it. The dream of cancer researchers has long been to reanimate p53 in cancer cells so they will die on their own.

The p53 story began in earnest about 20 years ago. Excitement ran so high that, in 1993, Science magazine anointed it Molecule of the Year and put it on the cover. An editorial held out the possibility of “a cure of a terrible killer in the not too distant future.”

Companies began chasing a drug to restore p53 in cells where it was disabled by mutations. But while scientists know how to block genes, they have not figured out how to add or restore them. Researchers tried gene therapy, adding good copies of the p53 gene to cancer cells. That did not work.

Then, instead of going after mutated p53 genes, they went after half of cancers that used the alternative route to disable p53, blocking it by attaching it to a protein known as MDM2. When the two proteins stick together, the p53 protein no longer functions. Maybe, researchers thought, they could find a molecule to wedge itself between the two proteins and pry them apart.

The problem was that both proteins are huge and cling tightly to each other. Drug molecules are typically tiny. How could they find one that could separate these two bruisers, like a referee at a boxing match?

In 1996, researchers at Roche noticed a small pocket between the behemoths where a tiny molecule might slip in and pry them apart. It took six years, but Roche found such a molecule and named it Nutlin because the lab was in Nutley, N.J.

But Nutlins did not work as drugs because they were not absorbed into the body.

Roche, Merck and Sanofi persevered, testing thousands of molecules.

At Sanofi, the stubborn scientist leading the way, Dr. Debussche, maintained an obsession with p53 for two decades. Finally, in 2009, his team, together with Shaomeng Wang at the University of Michigan and a biotech company, Ascenta Therapeutics, found a promising compound.

The company tested the drug by pumping it each day into the stomachs of mice with sarcoma.

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Genetic Gamble : Drugs Aim to Make Several Types of Cancer Self-Destruct

C.J. Gunther for The New York Times

Dr. Donald Bergstrom is a cancer specialist at Sanofi, one of three companies working on a drug to restore a tendency of damaged cells to self-destruct.

For the first time ever, three pharmaceutical companies are poised to test whether new drugs can work against a wide range of cancers independently of where they originated — breast, prostate, liver, lung. The drugs go after an aberration involving a cancer gene fundamental to tumor growth. Many scientists see this as the beginning of a new genetic age in cancer research.

Great uncertainties remain, but such drugs could mean new treatments for rare, neglected cancers, as well as common ones. Merck, Roche and Sanofi are racing to develop their own versions of a drug they hope will restore a mechanism that normally makes badly damaged cells self-destruct and could potentially be used against half of all cancers.

No pharmaceutical company has ever conducted a major clinical trial of a drug in patients who have many different kinds of cancer, researchers and federal regulators say. “This is a taste of the future in cancer drug development,” said Dr. Otis Webb Brawley, the chief medical and scientific officer of the American Cancer Society. “I expect the organ from which the cancer came from will be less important in the future and the molecular target more important,” he added.

And this has major implications for cancer philanthropy, experts say. Advocacy groups should shift from fund-raising for particular cancers to pushing for research aimed at many kinds of cancer at once, Dr. Brawley said. John Walter, the chief executive officer of the Leukemia and Lymphoma Society, concurred, saying that by pooling forces “our strength can be leveraged.”

At the heart of this search for new cancer drugs are patients like Joe Bellino, who was a post office clerk until his cancer made him too sick to work. Seven years ago, he went into the hospital for hernia surgery, only to learn he had liposarcoma, a rare cancer of fat cells. A large tumor was wrapped around a cord that connects the testicle to the abdomen. “I was shocked,” he said in an interview this summer.

Companies have long ignored liposarcoma, seeing no market for drugs to treat a cancer that strikes so few. But it is ideal for testing Sanofi’s drug because the tumors nearly always have the exact genetic problem the drug was meant to attack — a fusion of two large proteins. If the drug works, it should bring these raging cancers to a halt. Then Sanofi would test the drug on a broad range of cancers with a similar genetic alteration. But if the drug fails against liposarcoma, Sanofi will reluctantly admit defeat.

“For us, this is a go/no-go situation,” said Laurent Debussche, a Sanofi scientist who leads the company’s research on the drug.

The genetic alteration the drug targets has tantalized researchers for decades. Normal healthy cells have a mechanism that tells them to die if their DNA is too badly damaged to repair. Cancer cells have grotesquely damaged DNA, so ordinarily they would self-destruct. A protein known as p53 that Dr. Gary Gilliland of Merck calls the cell’s angel of death normally sets things in motion. But cancer cells disable p53, either directly, with a mutation, or indirectly, by attaching the p53 protein to another cellular protein that blocks it. The dream of cancer researchers has long been to reanimate p53 in cancer cells so they will die on their own.

The p53 story began in earnest about 20 years ago. Excitement ran so high that, in 1993, Science magazine anointed it Molecule of the Year and put it on the cover. An editorial held out the possibility of “a cure of a terrible killer in the not too distant future.”

Companies began chasing a drug to restore p53 in cells where it was disabled by mutations. But while scientists know how to block genes, they have not figured out how to add or restore them. Researchers tried gene therapy, adding good copies of the p53 gene to cancer cells. That did not work.

Then, instead of going after mutated p53 genes, they went after half of cancers that used the alternative route to disable p53, blocking it by attaching it to a protein known as MDM2. When the two proteins stick together, the p53 protein no longer functions. Maybe, researchers thought, they could find a molecule to wedge itself between the two proteins and pry them apart.

The problem was that both proteins are huge and cling tightly to each other. Drug molecules are typically tiny. How could they find one that could separate these two bruisers, like a referee at a boxing match?

In 1996, researchers at Roche noticed a small pocket between the behemoths where a tiny molecule might slip in and pry them apart. It took six years, but Roche found such a molecule and named it Nutlin because the lab was in Nutley, N.J.

But Nutlins did not work as drugs because they were not absorbed into the body.

Roche, Merck and Sanofi persevered, testing thousands of molecules.

At Sanofi, the stubborn scientist leading the way, Dr. Debussche, maintained an obsession with p53 for two decades. Finally, in 2009, his team, together with Shaomeng Wang at the University of Michigan and a biotech company, Ascenta Therapeutics, found a promising compound.

The company tested the drug by pumping it each day into the stomachs of mice with sarcoma.

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This bus' next stop: doing good

Maybe you want to help others. Maybe you long to lend a hand. But you're not sure where and you're not sure how and you don't know who to call.

You could ask around. Or you could book a seat on the Do Good Bus.

You will pay $25. You will get a box lunch. You will put yourself in the hands of a stranger.

When the bus takes off, you will not know where you are going — only that when you get there, you will be put to work.

You find yourself on this weekday afternoon one of an eclectic group, gathered a little shyly on an East Hollywood curb.

There's a Yelp marketer, a grad student, an actor, a novelist, a Manhattan Beach mother with her son and daughter, who just got home from prep school and college.

You see a school bus pull up. You step on board. It feels nostalgic, like day camp or a field trip.

Rebecca Pontius welcomes you, wearing jeans and sneakers and a black fleece vest. She looks like the kind of person who would plunge her hands deep into dirt, who wouldn't be afraid of the worms, who could lead you boldly.

The bus takes off, and Pontius stands toward the front, sure-footed. She founded the Do Good Bus, she tells you, to 1) build awareness, 2) build community, 3) encourage continued engagement.

Oh, she says, and to 3a) have fun. Hence the element of mystery, the faux holly branches that decorate some of the rows of seats, the white felt reindeer antlers she's wearing on her head.

She smiles a wide, toothy smile that makes you automatically reciprocate.

So you go along when she asks you to play get-to-know-you games. Even though you're embarrassed, you don't object when she assigns you one of the 12 days of Christmas to sing and act out when it's your turn.

Everyone's singing and laughing as the bus fits-and-starts down the freeway.

Maids-a-milking, geese-a-laying, bus-a-exiting somewhere in South Los Angeles.

It stops outside a boxy blue building — the Challengers Boys and Girls Club — where, finally, Pontius tells you you'll be helping children in foster care build the bicycles that will be their Christmas gifts.

She did it last year, she says. It was great. And she's brought along some powder that turns into fake snow, which the kids will like.

You step inside a large gym, where nothing proceeds quite as expected.

It's the holiday season, so way too many volunteers have shown up. The singer Ne-Yo is coming to lead a toy giveaway. There's a whole roomful of presents the children can choose from, including pre-assembled bikes — which means no bikes will need to be built.

You stand and you sit and you wait. Then the kids come. You try to help where you can — making sure they get in the right lines, handing out raffle tickets.

You see their joy at getting gifts, which is nice. You're in a place you might not ordinarily be, which is interesting. And as the children head out, you offer them snow. You put the powder in their cupped hands. You add water. The white stuff grows and begins to look real. It's even cold.

It makes them go wide-eyed. It makes them laugh. And you feel such moments of simple happiness are something.

It's chilly as you wait to get back on the bus. You get in a group hug with your fellow bus riders, who seem like old friends.

On the trip back in the dark, Pontius plays Christmas music. She serves you eggnog in Mason jars.

And she says she's sorry your help wasn't more needed today.

She promises the January ride will be more hands-on.

Come or don't, she tells you. But whatever you do, find a way to do something.

nita.lelyveld@latimes.com

Follow City Beat @latimescitybeat on Twitter or at Los Angeles Times City Beat on Facebook.

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Maker Mom Builds Cookie-Cutter Empire With 3-D Printers

Athey Moravetz is doing some tasty work with her 3-D printers.

The video game designer has worked on PlayStation games like Resistance Retribution and Uncharted Golden Abyss. She's also a self-described "jack-of-all-trades," skilled with 3-D modeling tools like Maya, and knows how to design compelling characters with them.

After having two children she decided to work from home, and in addition to keeping active in the computer graphics industry, she also created a wildly successful Etsy shop, where she sells 3-D printed cookie cutters based on nerd culture favorites Pokemon, Dr. Who and Super Mario Brothers.

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Hundreds pay tribute to legendary Indian sitarist Ravi Shankar

ENCINITAS, California (Reuters) – Ravi Shankar‘s daughters, Norah Jones and Anoushka Shankar, along with the wife of late Beatle George Harrison said their final goodbyes to the Indian sitar virtuoso on Thursday at a public memorial service in Encinitas, California.

The legendary musician and composer, who helped introduce the sitar to the Western world through his collaboration with The Beatles, died on December 11 in Southern California. He was 92.

About 700 people joined Shankar’s wife, Sukanya, and family at the service held at a spiritual center in the coastal town about 25 miles north of San Diego.

Olivia Harrison, the widow of Beatles guitarist George Harrison, told Reuters the three-time Grammy winner who formed a musical and spiritual bond with The Beatle “expressed music at its deepest level.”

“As a person he was just sweet and seemed to know everything,” she added. “He was a true citizen of the world.”

Shankar is credited with popularizing Indian music through his work with violinist Yehudi Menuhin and The Beatles beginning in the mid-1960s, inspiring George Harrison to learn the sitar and the British band to record songs like “Norwegian Wood” (1965) and “Within You, Without You” (1967).

“He completely transformed (George’s) musical sensibilities,” a tearful Harrison told the crowd. “They exchanged ideas and melodies until their hearts and minds were intertwined like a double helix.”

‘LITTLE CRUMB’

His friendship with Harrison led him to appearances at the Monterey and Woodstock pop festivals in the late 1960s and the 1972 Concert for Bangladesh. He became one of the first Indian musicians to become a household name in the West.

His influence in classical music, including on composer Philip Glass, was just as large. His work with Menuhin on their “West Meets East” albums in the 1960s and 1970s earned them a Grammy, and he wrote concertos for sitar and orchestra for both the London Symphony Orchestra and the New York Philharmonic.

“I always felt like a little crumb in his presence,” Zubin Mehta, a former music director of the New York Philharmonic and collaborator with Shankar, said at the service.

Jazz pianist Herbie Hancock also attended the service along with “Anna Karenina” director Joe Wright, the husband of Shankar’s daughter Anoushka.

Shankar, who had lived in Encinitas for the past 20 years, had suffered from upper respiratory and heart issues over the past year and underwent heart-valve replacement surgery last week at a hospital in San Diego.

The surgery was successful but he was unable to recover.

Shankar’s final concert was on November 4 in Long Beach, California, with his Grammy-winning sitarist daughter Anoushka, who spoke giving thanks to those who came. Jones, the third Grammy-winner in the family, did not speak at the service.

(Writing by Eric Kelsey; editing by Philip Barbara)

Music News Headlines – Yahoo! News

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The Neediest Cases: The Daughter of a Sick Woman Falls Prey to a Craigslist Scam

Sitting side by side on their living room sofa, Patricia Morales and her daughter, Katherine, could be any mother-daughter duo. Both have dark hair, dark eyes and welcoming, infectious smiles.

Librado Romero/The New York Times

Patricia Morales, 62, at home in the Bronx. Her treatment for ailments like rheumatoid arthritis and hepatitis C led to depression.

2012-13 Campaign

Previously recorded:

$3,375,394

Recorded Wednesday:

182,251

*Total:

$3,557,645

Last year to date:

$3,320,812

*Includes $709,856 contributed to the Hurricane Sandy relief efforts.

For the past 100 years, The New York Times Neediest Cases Fund has provided direct assistance to children, families and the elderly in New York. To celebrate the 101st campaign, an article will appear daily through Jan. 25. Each profile will illustrate the difference that even a modest amount of money can make in easing the struggles of the poor.

Last year donors contributed $7,003,854, which was distributed to those in need through seven New York charities.

The Youngest Donors

If your child or family is using creative techniques to raise money for this year’s campaign, we want to hear from you. Drop us a line on Facebook or talk to us on Twitter.

But the ties that bind them go beyond their genes, beyond the bodies they were born with.

“It’s called a neck ring. It’s a silver curved barbell, one inch,” Katherine, 20, said as she swept aside her shoulder-length black hair to show the piercing in the back of her neck, a show of solidarity with her mother. She had it done when she was 16. “I wanted to know what it felt like for my mom.”

Her mother then turned around and outlined with her finger two lengthy scars that run down her back.

“I’ve had a lot of physical problems,” Ms. Morales, 62, said. Shaking her head at her daughter’s piercing, she added, “I’ve had rods put in my upper and lower spine, but I could never do that.”

The rods were surgically planted to treat herniated discs, the result of having a cruel combination of osteoporosis, hepatitis C, fibromyalgia and rheumatoid arthritis. Ms. Morales contracted hepatitis C from a blood transfusion she received in 1972 after the birth of her only son, she said.

“I didn’t even know about it until 10 years ago,” she said. “My liver blood count was a little high.”

Since the diagnosis, Ms. Morales, a former schoolteacher, has ridden the arduous highs and lows common to patients with hepatitis C. Her treatments for the disease, which debilitates the liver over time, have included pills and injections that can cause depression. Ms. Morales, a single parent, found an unforgiving salve in alcohol.

“I was depressed; I was totally drunk,” she said. “I didn’t want to live anymore.”

Then, about a year ago, she reached a turning point when visiting her hepatitis C specialist.

“I was 210 pounds,” she said. “The doctor said: ‘You have to stop drinking. You have to lose weight.’ ”

To help combat the depression, her doctor referred her to Jewish Association Serving the Aging, a beneficiary agency of UJA-Federation of New York, one of the organizations supported by The New York Times Neediest Cases Fund. She began weekly counseling sessions with a social worker and started taking an antidepressant medication. The federation drew about $600 from the fund in May so that Ms. Morales could buy a mattress.

“I had a horrible bed,” she said. “I felt like I was sleeping on rocks, and with rods in my back, I was waking up every hour.”

After several months of therapy and starting a diet, Ms. Morales was on her way to losing 60 pounds. Today, she weighs 148.

Light was starting to show itself again when the family took an unexpected financial hit this summer. While taking time off from attending Hostos Community College, Katherine Morales looked for work on Craigslist.

“I saw my mom, and I realized I needed to get a job,” Katherine said shyly. “This guy asked me to be his personal assistant, and he asked me to wire money.”

Offering $400 a week, the man requested help transferring almost $2,000 from what he said was his wife’s account. He transferred the money to Katherine’s account, asking her to wire it to a bank account in Malaysia.

Shortly after she wired the money, the bank froze the account, which Katherine and her mother shared. It was then that Katherine realized she had been the victim of a scam. The money transferred into her account turned out to have been stolen, and she was responsible for repaying it.

Katherine went to detectives immediately with more than 20 pages of evidentiary e-mails, but found that she was unable to file a complaint.

“They told me it wasn’t enough,” she said. “These things happen all the time.”

They lost almost $2,000.

Ms. Morales lives on a fixed income. She receives just over $700 a month from Social Security and $200 month in food stamps. The rent for the apartment she shares with her daughter in the Throgs Neck neighborhood of the Bronx is $230, and Ms. Morales has a monthly combined phone and cable bill of $140. Ms. Morales has a son, but he is unable to help the family.

Falling behind on her bills, Ms. Morales turned once again to JASA for help paying a combined phone and cable bill of nearly $200, a grant the agency drew from the Neediest Cases Fund.

“It was terrible, because my intention was to help my mom,” said Katherine, who has since found a part-time job at a vitamin shop.

Ms. Morales has been feeling much better, but she is nervous about an appointment with her hepatitis C specialist in January.

“I’m taking things one day at a time, but I’m looking forward to someone taking care of me,” she said. “I want to live a little bit longer, but not that long.”

“Why are you putting a time limit on it?” Katherine said, jokingly. “Seventy’s the new 20!” she added, nudging her mother in the side. “Remember, the doctor said you wouldn’t live past your late 50s, but you did.”

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As Shoppers Hop From Tablet to PC to Phone, Retailers Try to Adapt

Jim Wilson/The New York Times

Shoppers often visit ModCloth, a Web site that sells women’s clothes, on their phones but return on a different kind of device to buy something, said Sarah Rose, a vice president at ModCloth.

Ryan O’Neil, a Connecticut government employee, was in the market to buy a digital weather station this month. His wife researched options on their iPad, but even though she found the lowest-price option there, Mr. O’Neil made the purchase on his laptop.

“I do use the iPad to browse sites,” Mr. O’Neil said, but when it comes time to close the deal, he finds it easier to do on a computer.

Many online retailers had visions of holiday shoppers lounging beneath the Christmas tree with their mobile devices in hand, making purchases. The size of the average order on tablets, particularly iPads, tends to be bigger than on PCs. So retailers poured money and marketing into mobile Web sites and apps with rich images and, they thought, easy checkout.

But while visits to e-commerce sites and apps on tablets and phones have nearly doubled since last year, consumers like Mr. O’Neil are more frequently using multiple devices to shop. In many cases, they are more comfortable making the final purchase on a computer, with its bigger screen and keyboard. So retailers are trying to figure out how to appeal to a shopper who may use a cellphone to research products, a tablet to browse the options and a computer to buy.

“I’ve been yelling at customers for two years, saying, ‘Mobile, mobile, mobile,’ ” said Jason Spero, director of mobile sales and strategy at Google. “But the funny thing is, now we’re going to say: ‘Don’t put mobile in a silo. It’s also about the desktop.’ ”

The challenges are daunting, though. It is technically difficult to track consumers as they hop from phone to computer to tablet and back again. This means customers who, say, fill shopping carts on their tablets have to do all the work again on their PCs or other devices. The biggest obstacle, retailers say, is that the tools used to track shoppers on computers — cookies, or bundles of data stored in Web browsers — don’t transfer across devices.

Instead, retailers are figuring out how to sync the experience in other ways, like prompting shoppers to log in on each device. And being able to track people across devices gives retailers more insight into how they shop.

The retailers’ efforts are backed by research. While one-quarter of the visits to e-commerce sites occur on mobile devices, only around 15 percent of purchases do, according to data from I.B.M. According to Google, 85 percent of online shoppers start searching on one device — most often a mobile phone — and make a purchase on another.

At eBags, customers are shopping on their tablets in the evening and returning on their work computers the next day. But eBags has not yet synced the shoppers across devices, so customers must build their shopping carts from scratch if they switch devices.

“That is a blind spot with a lot of sites,” said Peter Cobb, co-founder of eBags. “It is a requirement moving forward.”

At eBay, one-third of the purchases involve mobile devices at some point, even if the final purchase is made on a computer.

At eBay, once shoppers log in on a device, they do not need to log in again. Their information, like shipping and credit card details and saved items, syncs across all their devices. If an eBay shopper is interested in a certain handbag, and saves that search on a computer, eBay will send alerts to her cellphone when a new handbag arrives or an auction is about to end.

“They might discover an item on a phone or tablet, do a saved-search push alert later on some other screen and eventually close on the Web site,” said Steve Yankovich, who runs eBay Mobile. “People are buying and shopping and consuming potentially every waking moment of the day.”

ModCloth, an e-commerce site for women’s clothes, said that while a quarter of its visits come from mobile devices, people are not yet buying there in the same proportion, though they are becoming more comfortable with checking out on those devices.

“She’s visiting us more on the phone, but she’s actually transacting somewhere else,” said Sarah Rose, vice president of product at ModCloth.

For example, a shopper will skim through new arrivals on her phone while on the bus and add items to her wish list, then visit that evening on her tablet to make a purchase, Ms. Rose said.

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