Britain’s Queen Elizabeth goes 3D for Olympics tribute






LONDON (Reuters) – Britain‘s Queen Elizabeth will use her traditional Christmas Day message, filmed in 3D for the first time, to pay tribute to the world’s athletes for delivering a “splendid summer of sport” at the London Olympics.


In her personal address to the nation, the monarch will pay tribute to the competitors’ “skill, dedication, training and teamwork”, her office said on Monday.






The 86-year-old head of state provided an Olympic highlight when she made a surprise comic turn with James Bond actor Daniel Craig in a short film for the opening ceremony.


“In pursuing their own sporting goals, they gave the rest of us the opportunity to share something of the excitement and drama,” she will say, according to advance extracts.


Queen Elizabeth missed a church service at her country retreat on Sunday due to a cold, Buckingham Palace said. Her message was pre-recorded and will go out as expected.


It comes at the end of a landmark year for the royal family.


Queen Elizabeth marked 60 years on the throne with the Diamond Jubilee celebrations and her grandson Prince William and his wife Kate are expecting their first baby.


Prime Minister David Cameron issued his own Christmas message in which he talked of Britain’s “extraordinary year”.


“We cheered our queen to the rafters with the Jubilee, showed the world what we’re made of by staging the most spectacular Olympic and Paralympic Games ever and – let’s not forget – punched way above our weight in the medals table,” he said.


The first Christmas broadcast was given by Queen Elizabeth’s grandfather George V in 1932. It has become a Christmas Day tradition for many families to watch it together after lunch.


(Reporting by Peter Griffiths; Editing by Stephen Powell)


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News Analysis: Scientists to Seek Clues to Violence in Genome of Gunman in Newtown, Conn.





In a move likely to renew a longstanding ethical controversy, geneticists are quietly making plans to study the DNA of Adam Lanza, 20, who killed 20 children and seven adults in Newtown, Conn. Their work will be an effort to discover biological clues to extreme violence.




The researchers, at the University of Connecticut, confirmed their plans through a spokeswoman but declined to provide details. But other experts speculated that the geneticists might look for mutations that might be associated with mental illnesses and ones that might also increase the risk for violence.


They could look at all of Mr. Lanza’s genes, searching for something unusual like gene duplications or deletions or unexpected mutations, or they might determine the sequence of his entire genome, the genes and the vast regions of DNA that are not genes, in an extended search for aberrations that could determine which genes are active and how active they are.


But whatever they do, this apparently is the first time researchers will attempt a detailed study of the DNA of a mass killer.


Some researchers, like Dr. Arthur Beaudet, a professor at the Baylor College of Medicine and the chairman of its department of molecular and human genetics, applaud the effort. He believes that the acts committed by men like Mr. Lanza and the gunmen in other rampages in recent years — at Columbine High School and in Aurora, Colo., in Norway, in Tucson and at Virginia Tech — are so far off the charts of normal behavior that there must be genetic changes driving them.


“We can’t afford not to do this research,” Dr. Beaudet said.


Other scientists are not so sure. They worry that this research could eventually stigmatize people who have never committed a crime but who turn out to have a genetic aberration also found in a mass murder.


Everything known about mental illness, these skeptics say, argues that there are likely to be hundreds of genes involved in extreme violent behavior, not to mention a variety of environmental influences, and that all of these factors can interact in complex and unpredictable ways.


“It is almost inconceivable that there is a common genetic factor” to be found in mass murders, said Dr. Robert C. Green, a geneticist and neurologist at Harvard Medical School. “I think it says more about us that we wish there was something like this. We wish there was an explanation.”


Scientists are well aware of the fraught history behind the questions of biology and violence.


In the early 20th century, claims that criminal behavior was inherited arose during the eugenics movement and led to sterilizations of mental patients and felons.


On Christmas Day in 1965, two researchers published a paper saying men with an extra Y chromosome, the chromosome that confers maleness, were “super males” and born criminals. The hypothesis was helped along by the fact that these men “fit the classic Hollywood criminal — big, awkward, thuglike and with low I.Q.’s,” said Dr. Philip Reilly, a lawyer and clinical geneticist who has studied this history.


The idea persisted for about 15 years, Dr. Reilly said, but eventually the epidemiological evidence convinced scientists that these men were no more violent than men without an extra Y chromosome.


In 1993, in a paper published in the journal Science, researchers reported that a mutation leading to a lack of the enzyme monoamine oxidase caused violence in a Dutch family. Every family member who inherited the mutation was a violent criminal; those without it had no criminal behaviors.


“It was a stunning piece of work,” said James Blair, the chief of the unit on affective cognitive neuroscience at the National Institute of Mental Health. But, he added, it turned out not to be generalizable. For the most part, “it was just this family,” he said.


The National Institutes of Health was embroiled in controversy about 20 years ago simply for proposing to study the biological underpinnings of violence. Critics accused researchers of racism and singling out minorities, especially black men.


Shortly after, the N.I.H. took back financing for a conference at the University of Maryland to examine genetics and criminal behavior. The conference was canceled.


But genetics has come of age in recent years with new and powerful methods to determine DNA sequences and analyze the results. Studies of people at the far end of a bell curve can be especially informative, because the genetic roots of their conditions can be stark and easy to spot, noted J. H. Pate Skene, a Duke University neurobiologist.


“I think doing research on outliers, people at an end of a spectrum on something of concern like violent behavior, is certainly a good idea,” he said, but he advised tempering expectations.


“I would call it a caution, not about whether to do this research but about what to expect,” he added.


Perhaps it will be fruitless to search for one or a few major gene mutations that always lead to extreme violence, Dr. Beaudet said. But what if a significant fraction of the shootings were linked to gene variants? What if scientists were to discover genes that were risk factors, increasing a person’s chance of violent behavior but not foreordaining it?


“If we know someone has a 2 percent chance or a 10 percent chance or a 20 percent chance of violent behavior, what would you do with that person?” Dr. Skene said. “They have not been convicted of anything — have not done anything wrong.”


But a genetic profile might play a role if someone were convicted of violent offenses, Dr. Beaudet countered. Criminals are routinely denied parole based solely on psychiatric evaluations. Perhaps a genetic test could add to the certainty of the decision, he said.


Ultimately, understanding the genetics of violence might enable researchers to find ways to intervene before a person commits a horrific crime. But that goal would be difficult to achieve, and the pursuit of it risks jeopardizing personal liberties. Some scientists shudder at the thought of labeling people potential violent criminals.


“The idea of screening with a view of preventing those kinds of incidents is basically unthinkable,” said Dr. Steven E. Hyman, director of the Stanley Center for Psychiatric Research at the Broad Institute of Harvard and M.I.T. “You would fail. You would stigmatize.”


Some day, he added, it might be important to know the phenotypes — the characteristics — of violent killers and have their DNA, but not for the reasons many think.


“I am always happy to store DNA and phenotype information and freeze cells, thinking that one day we would have usable clues,” Dr. Hyman added. “But that would be biology, not prevention.”


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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











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South Africa’s Mandela responding to treatment in hospital






JOHANNESBURG (Reuters) – Former South African president and anti-apartheid hero Nelson Mandela, who is 94, continues to respond to treatment two weeks after being taken to hospital, the government said on Saturday.


The Nobel Peace laureate, who has been treated for a lung infection and gallstones after being hospitalized on December 8, was visited by South African President Jacob Zuma, presidency spokesman Mac Maharaj said in a statement.






“Madiba has been in hospital since the 8th of December and continues to respond to treatment,” Maharaj said, referring to Mandela by his clan name.


President Zuma assured him of the love and support of all South Africans, young and old, and the whole world.”


The country’s first black president was admitted to hospital in Pretoria earlier this month after being flown from his home village of Qunu in a remote part of the Eastern Cape province.


It seems likely that Mandela, admired at home and abroad as a global icon against injustice for his lifetime of struggle against minority white rule, will end up spending Christmas in the hospital.


On Thursday, following his re-election as leader of the ruling African National Congress (ANC), Zuma reported Mandela had “steadily improved”.


Zuma said then the former president was receiving “the best care possible” but recalled that Mandela was “at an age where medical challenges require extraordinary care”.


He praised Mandela as an “unparalleled fighter”.


In an interview broadcast on Saturday but recorded a day earlier, the ANC’s newly elected Deputy President Cyril Ramaphosa said he believed Mandela was “on the mend”.


Mandela spent 27 years in apartheid prisons, including 18 years on the windswept Robben Island off Cape Town. He was released in 1990 and went on to use his prestige to push for reconciliation between whites and blacks as the bedrock of the post-apartheid “Rainbow Nation”.


He stepped down in 1999 after one term in office and has been largely removed from public life for the last decade.


Mandela spent time in a Johannesburg hospital in 2011 with a respiratory condition, and again in February this year because of abdominal pains. He was released the following day after a keyhole examination showed there was nothing serious.


He has since spent most of his time in Qunu.


His fragile health prevents him from making any public appearances in South Africa, although he has continued to receive high-profile domestic and international visitors, including former U.S. president Bill Clinton in July.


(Reporting by David Dolan; Editing by Pascal Fletcher)


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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.





CITY BEAT: Life in the Southland


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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Alan Ball’s ‘Banshee’ Screeches Onto Cinemax in January






LOS ANGELES (TheWrap.com) – “True Blood” creator Alan Ball‘s new television series “Banshee” will premiere January 11 at 10 p.m. on Cinemax, the network said Thursday.


The drama, which is executive-produced by Ball and “House M.D.” executive producer Greg Yaitanes, centers on ex-con and master thief Lucas Hood (played by “Rush” star Anthony Starr), who assumes the identity of the sheriff of Banshee, Pa., where he continues his criminal ways while being hunted by a team of gangsters from his past. Ivana Milicevic (“Charlie’s Angels”) and Ulrich Thomsen (“The Celebration”) also star.






Series writers Jonathan Tropper and David Schickler also executive-produce, along with Peter Macdissi.


The pilot episode will re-air at 11:05 p.m. and 12:10 a.m., with additional re-airings on January 12, 13, 14, 15, 16 and 30.


TV 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.




The Neediest CasesFor 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.








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.


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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