ROME ? The cruise captain who grounded the Costa Concordia off the Tuscan coast with 4,200 people on board did not relay correct information either to the company or crew after the ship hit rocks, the cruise ship owner's CEO said Friday as the search resumed for 21 missing passengers.
CEO Pierluigi Foschi told Italian state TV that the company spoke to the captain at 10:05 p.m. (2105 GMT; 4:05 p.m. EST), some 20 minutes after the ship ran aground on Jan. 13, but could not offer proper assistance because the captain's description "did not correspond to the truth."
Capt. Francesco Schettino said only that he had "problems" on board but did not mention hitting a reef.
Likewise, Foschi said crew members were not informed of the gravity of the situation.
Passenger video shown on Italian TV indicates crew members telling passengers to go to their cabins as late as 10:25 p.m. (2125 GMT; 4:25 p.m. EST). The abandon ship alarm sounded just before 11:00 p.m. (2200 GMT; 5:00 p.m. EST).
"That's because they also did not receive correct information on the gravity of the situation," Foschi said.
The $450 million Costa Concordia was carrying more than 4,200 passengers and crew when it slammed into well-charted rocks off the island of Giglio a week ago. Eleven people have been confirmed dead.
The Concordia shifted again on its rocky perch Friday, forcing the suspension of diving search operations for the 21 people still missing and raising concerns about the stability of the ship's resting place. But the search in areas above the waterline resumed in the evening after the ship was deemed stable.
The remarks by Costa CEO Foschi are the latest to indicate a lack of proper communication with authorities on land as the emergency unfolded.
An audiotape of the Concordia's first contact with maritime authorities has a Concordia office repeatedly replying that the ship had experienced a blackout, even though it had hit the reef more than half an hour earlier.
Italian media reported the officer on the call was Schettino, but that could not be independently confirmed.
Costa Crociere SpA, which offered support to the captain in the hours after the emergency, has now turned its back on the man who is under investigation for manslaughter, causing a shipwreck and abandoning his ship. Schettino, who was jailed after he left the ship, is under house arrest near Naples.
Costa in recent days has suspended Schettino, announced it is no longer paying his legal fees and has signed on as a civil party in the prosecution, a move that positions it as an injured party and would allow it to seek damages in the case of a guilty verdict.
Coast Guard spokesman Cmdr. Cosimo Nicastro said crews will evaluate the ship's stability Saturday morning to see if the diving operation can resume, focusing on an area where passengers would have sought lifeboats, Nicastro said.
It was not clear if the slight movements registered by sensors placed on board the Costa Concordia were just vibrations as the ship settles on the rocks off the Tuscan island of Giglio or if the massive ocean liner is slowly slipping off the reef. Salvage experts suggest it could be because of pockets of air gradually escaping.
The sensors detected that the ship's bow was moving about 15 millimeters (half an inch) an hour and the stern about 7 millimeters (one-quarter inch) an hour, said Nicola Casagli of the University of Florence, who was called in by Italian authorities to monitor the ship's stability.
The Concordia's movements are being watched since any significant shift could be dangerous for divers trying to locate those missing since the Concordia ran aground Jan. 13. An additional fear is that movement could damage tanks holding a 500,000 gallons of fuel oil and lead to leaks.
The sea floor drops off sharply a few meters (yards) from where the ship is resting, and Italy's environment minister has warned it risks sinking.
On Friday, relatives of some of the 21 missing were at Giglio's port getting briefings from rescue teams.
Casagli told Sky TG24 that some movement in the Concordia was only natural given the immense weight of the steel-hulled ship, which is being held in place by two huge rocks at bow and stern.
But the latest movements indicate it isn't stable, he said. "These are small, regular movements that are being monitored because they're going in the same direction," he told Sky.
Late Thursday, Carnival Corp., the U.S.-based company that owns Costa, announced it was conducting a comprehensive audit of all 10 of its cruise lines to review safety and emergency response procedures in the wake of the Costa disaster. The evacuation was chaotic and the alarm to abandon the ship was sounded after the Concordia had capsized too much to get many life boats down.
___
Colleen Barry reported from Milan. Andrea Foa contributed from Giglio, Italy.
The winner of this week's Android Central photo contest is Travis Detweiler with his picture of sunrise over Tampa Bay. Taken with his HTC EVO 3D while heading out into the gulf to catch a few Amberjack and Grouper. Travis says he didn't use any particular camera app or effects, just the camera as-is on his 3VO. He captured the theme and framed the perfect shot. Congrats, Travis!
We had well over a thousand entries, and while it took a while to look through them all it was quite enjoyable -- you guys and gals can take some awesome pictures. We've collected the 10 runners-up for you to enjoy as well, hit the break to see them. Don't forget, we're starting up a new round tomorrow, so keep an eye out.
LONDON (Reuters) ? Oil giant BP will likely agree to pay the U.S. Department of Justice $20-$25 billion next month to settle all civil and criminal charges around the Deepwater Horizon rig blast and Gulf of Mexico oil spill, a leading industry analyst predicted on Thursday.
Martijn Rats, head of European oil research at Morgan Stanley said in a research note that he saw a 70-80 percent chance that the two sides would agree a deal sometime between BP's full year results on February 7, and the scheduled start of legal hearings in New Orleans on February 27.
BP sources have told Reuters that talks are ongoing with the Department of Justice about a possible settlement and that the London-based company's board has shifted to weekly meetings to discuss progress.
Chief Executive Bob Dudley has previously said BP would like to settle, although not at any price. When asked about the matter by reporters on Wednesday, he declined to make any comment, saying it was a sensitive time to be discussing it.
When contacted by Reuters, BP had no comment to make over the likelihood or size of a settlement.
BP senses the U.S. administration would like to settle the matter, not least because it is a U.S. presidential election year, the sources said but any outcome is still seen as uncertain.
The estimated level of settlement in the Morgan Stanley note - the most detailed analysis Reuters has seen on the potential cost of the spill - is much higher than other analysts have predicted, and around double the amount BP has taken a provision for.
Senior company sources last year told Reuters that the company was prepared for a massive payout. One source predicted BP would offer "the mother of all settlements."
Another said the settlement would likely be the second-largest in U.S. legal history, putting it between the $206 billion the tobacco industry agreed to pay U.S. states for treating smoking-related illnesses and the $7.2 billion banks agreed to pay to settle litigation related to Enron's collapse.
SHARES LAG
BP has the money to pay a $20-25 billion settlement - it is sitting on cash pile of more than $20 billion and has billions of dollars worth of assets on the block as part of its restructuring.
Nonetheless, Morgan Stanley predicts the larger-than- expected size of the payout will weigh on BP's shares. It rates the shares "underweight" and has a target price of 435 pence, against a Wednesday close of 481 pence.
The shares traded down 0.6 percent at 0905 GMT, against a flat STOXX Europe 600 Oil and Gas index.
BP investors are expecting the company to announce a dividend hike at its full year results, after Dudley said late last year that it had reached a turning point after the oil spill and was now returning to growth mode.
A big settlement would limit BP's ability to lift the shareholder payout.
Morgan Stanley believes the DoJ deal will cover all criminal and civil proceedings being pursued by the government against BP under the Clean Water Act, Alternative Fines Act, other laws and BP's obligation to make good any natural resources damages.
(Reporting by Tom Bergin; Editing by Hans-Juergen Peters and Mike Nesbit)
SAN JUAN, Puerto Rico (AP) ? U.S. banking regulators have filed suit against the director of a Puerto Rican bank, alleging that reckless lending and improper management led to the April 2010 collapse that cost the deposit insurance fund nearly $1.5 billion.
Officers and directors of R-G Premier Bank failed to adequately supervise the huge increase in commercial lending during the housing boom and bust in the U.S. island territory, the Federal Deposit Insurance Corp. said in the lawsuit filed Wednesday in federal court in San Juan.
The suit seeks at least $257 million in damages and names 19 bank officials, including founder and CEO Victor Galan Alvarez. The suit also names the spouses of 17 of the directors and officers so that it can go after their assets to recover losses from the failure.
U.S. regulators have filed dozens of similar lawsuits over the past two years to recover losses from bank failures that regulators say resulted from negligence and misconduct. FDIC attorneys have been in settlement talks with many of the executives.
The FDIC says that directors of R-G Premier Bank didn't adequately supervise the chief loan officer, ignored warnings that should have led them to tighten control of their operations and made dozens of loans to developers who were already heavily in debt and were poor credit risks.
"Between November 2004 and December 2008 alone, the bank extended over $350 million in loans that any prudent banker should have known would probably never be repaid," the suit says. "The directors and officers also exacerbated and accelerated these losses by robotically approving virtually any loan request that crossed their desks, even though such loan requests had been processed through the obviously deficient lending structure they had created at the bank."
A lawyer for Galan, Mary Gill of Atlanta, Georgia, had no immediate comment but said the CEO may issue a statement later.
Are you ready to destroy the Dragons of Skyrim with your trusty orcish arrows and shortsword? Do you wish to hop on your trusty horse and ride endlessly up steep slopes and through wooded glens? Do you have a TI-84 graphing calculator? Well you're kind of in luck.
Contact: Bill Schaller william_schaller@dfci.harvard.edu 617-632-5357 Dana-Farber Cancer Institute
BOSTON--They are the Robinson Crusoes of the intracellular world -- lone chromosomes, whole and hardy, stranded outside the nucleus where their fellow chromosomes reside. Such castaways, each confined to its own "micronucleus," are often found in cancer cells, but scientists haven't known what role, if any, they play in the cancer process.
In a paper published online on Jan. 18 by the journal Nature, Dana-Farber Cancer Institute researchers have mapped out a mechanism by which micronuclei could potentially disrupt the chromosomes within them and produce cancer-causing gene mutations. The findings may point to a vulnerability in cancer cells that could be attacked by new therapies.
"The most common genetic change in cancer is the presence of an incorrect number of intact chromosomes within cancer cells -- a condition known as aneuploidy," says Dana-Farber's David Pellman, MD, the study's senior author. "The significance of aneuploidy has been hard to pin down, however, because little is known about how it might trigger tumors. In contrast, the mechanism by which DNA damage and broken chromosomes cause cancer is well established -- by altering cancer genes in a way that spurs runaway cell division.
"The new study demonstrates one possible chain of events by which aneuploidy and specifically 'exiled' chromosomes could lead to cancer-causing mutations, with potential implications for cancer prevention and treatment," says Pellman, who is a Howard Hughes Medical Institute investigator and the Margaret M. Dyson Professor of Pediatric Oncology at Dana-Farber, Children's Hospital Boston and Harvard Medical School.
Whole chromosomes can end up outside the nucleus as a result of a glitch in cell division. In normal division, a cell duplicates its chromosomes and dispatches them to the newly forming daughter cells: the original set to one daughter, the twin set to the other. For a variety of reasons, the chromosomes sometimes aren't allocated evenly -- one daughter receives an extra one, the other is short one. Unlike the rest of the chromosomes, these stragglers sometimes don't make it to the nucleus. Instead, they're marooned elsewhere within the cell and become wrapped in their own membrane, forming a micronucleus.
"In some respects, micronuclei are similar to primary nuclei," Pellman remarks, "but much about their function and composition is unknown. Previous studies differ on whether micronuclei replicate or repair their chromosomes as normal nuclei do. The ultimate fate of these chromosomes is unclear as well: Are they passed on to daughter cells during cell division or are they somehow eliminated as division proceeds?"
One clue that odd-man-out chromosomes themselves may be subject to damage -- and therefore be involved in cancer -- emerged from Pellman's previous research into aneuploidy. "We found that cancer cells generated from cells with micronuclei also have a great deal of chromosome breakage," Pellman explains. But researchers didn't know if this was a sign of connection or of coincidence.
Another clue came from a recently discovered phenomenon called "chromothripsis," in which one chromosome of a cancer cell shows massive amounts of breakage and rearrangement, while the remainder of the genome is largely intact. "That finding leapt off the page of these studies -- that such extensive damage could be limited to a single chromosome or single arm of a chromosome," Pellman says. "We wondered if the physical isolation of chromosomes in micronuclei could explain this kind of highly localized chromosome damage."
To find out, Karen Crasta, PhD, of Pellman's lab and the study's lead author, used a confocal microscope to observe dividing cells with micronuclei. She found that while micronuclei do form duplicate copies of their chromosomes, the process is bungled in two respects. First, it is inefficient: part of the chromosome is replicated and part isn't, leading to chromosome damage. Second, it is out of sync: the micronucleus keeps trying to replicate its chromosomes long after replication of the other chromosomes was completed. For cell division to be successful, every step of the process must occur in the proper order, at the proper time. In fact, when study co-author Regina Dagher directly analyzed the structure of the late-replicating chromosomes, she found them to be smashed to bits -- exactly what was predicted as the first step in chromothripsis.
The final piece of the puzzle came when Pellman's colleague Neil Ganem, PhD, examined what happens to these pulverized fragments, using an imaging trick that marked the chromosome in the micronucleus with its own color.
"It has been theorized that micronuclei are garbage disposals for chromosomes that the cell doesn't need anymore," Pellman comments. "If that were true, the smashed pieces would be discarded or digested, but we found that, a third of the time, they're donated to one of the daughter cells and therefore cold be incorporated into that cell's genome.
Pellman says that the findings suggest that, unexpectedly, whole chromosome aneuploidy might promote cancer in a very similar way to other kinds of genomic alterations. The key event may be mutations in oncogenes and tumor suppressors. This mechanism may also explain how cancer cells acquire more than one such mutation at a time.
"Although chromothripsis occurs in only a few percent of human cancers, our findings suggest that it might be an extreme instance of a kind of chromosome damage that could be much more common," says Pellman, who adds that accelerating this process in cancer cells, thus generating so many mutations that the cells die, may represent a possible strategy for new therapies against certain tumors.
###
The research was supported by the National Institutes of Health, the Howard Hughes Medical Institute, and the Leukemia and Lymphoma Society.
Dana-Farber Cancer Institute (www.dana-farber.org) is a principal teaching affiliate of the Harvard Medical School and is among the leading cancer research and care centers in the United States. It is a founding member of the Dana-Farber/Harvard Cancer Center (DF/HCC), designated a comprehensive cancer center by the National Cancer Institute. It provides adult cancer care with Brigham and Women's Hospital as Dana-Farber/Brigham and Women's Cancer Center and it provides pediatric care with Children's Hospital Boston as Dana-Farber/Children's Hospital Cancer Center. Dana-Farber is the top ranked cancer center in New England, according to U.S. News & World Report, and one of the largest recipients among independent hospitals of National Cancer Institute and National Institutes of Health grant funding. Follow Dana-Farber on Twitter: @danafarber and Facebook: www.facebook.com/danafarbercancerinstitute
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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Contact: Bill Schaller william_schaller@dfci.harvard.edu 617-632-5357 Dana-Farber Cancer Institute
BOSTON--They are the Robinson Crusoes of the intracellular world -- lone chromosomes, whole and hardy, stranded outside the nucleus where their fellow chromosomes reside. Such castaways, each confined to its own "micronucleus," are often found in cancer cells, but scientists haven't known what role, if any, they play in the cancer process.
In a paper published online on Jan. 18 by the journal Nature, Dana-Farber Cancer Institute researchers have mapped out a mechanism by which micronuclei could potentially disrupt the chromosomes within them and produce cancer-causing gene mutations. The findings may point to a vulnerability in cancer cells that could be attacked by new therapies.
"The most common genetic change in cancer is the presence of an incorrect number of intact chromosomes within cancer cells -- a condition known as aneuploidy," says Dana-Farber's David Pellman, MD, the study's senior author. "The significance of aneuploidy has been hard to pin down, however, because little is known about how it might trigger tumors. In contrast, the mechanism by which DNA damage and broken chromosomes cause cancer is well established -- by altering cancer genes in a way that spurs runaway cell division.
"The new study demonstrates one possible chain of events by which aneuploidy and specifically 'exiled' chromosomes could lead to cancer-causing mutations, with potential implications for cancer prevention and treatment," says Pellman, who is a Howard Hughes Medical Institute investigator and the Margaret M. Dyson Professor of Pediatric Oncology at Dana-Farber, Children's Hospital Boston and Harvard Medical School.
Whole chromosomes can end up outside the nucleus as a result of a glitch in cell division. In normal division, a cell duplicates its chromosomes and dispatches them to the newly forming daughter cells: the original set to one daughter, the twin set to the other. For a variety of reasons, the chromosomes sometimes aren't allocated evenly -- one daughter receives an extra one, the other is short one. Unlike the rest of the chromosomes, these stragglers sometimes don't make it to the nucleus. Instead, they're marooned elsewhere within the cell and become wrapped in their own membrane, forming a micronucleus.
"In some respects, micronuclei are similar to primary nuclei," Pellman remarks, "but much about their function and composition is unknown. Previous studies differ on whether micronuclei replicate or repair their chromosomes as normal nuclei do. The ultimate fate of these chromosomes is unclear as well: Are they passed on to daughter cells during cell division or are they somehow eliminated as division proceeds?"
One clue that odd-man-out chromosomes themselves may be subject to damage -- and therefore be involved in cancer -- emerged from Pellman's previous research into aneuploidy. "We found that cancer cells generated from cells with micronuclei also have a great deal of chromosome breakage," Pellman explains. But researchers didn't know if this was a sign of connection or of coincidence.
Another clue came from a recently discovered phenomenon called "chromothripsis," in which one chromosome of a cancer cell shows massive amounts of breakage and rearrangement, while the remainder of the genome is largely intact. "That finding leapt off the page of these studies -- that such extensive damage could be limited to a single chromosome or single arm of a chromosome," Pellman says. "We wondered if the physical isolation of chromosomes in micronuclei could explain this kind of highly localized chromosome damage."
To find out, Karen Crasta, PhD, of Pellman's lab and the study's lead author, used a confocal microscope to observe dividing cells with micronuclei. She found that while micronuclei do form duplicate copies of their chromosomes, the process is bungled in two respects. First, it is inefficient: part of the chromosome is replicated and part isn't, leading to chromosome damage. Second, it is out of sync: the micronucleus keeps trying to replicate its chromosomes long after replication of the other chromosomes was completed. For cell division to be successful, every step of the process must occur in the proper order, at the proper time. In fact, when study co-author Regina Dagher directly analyzed the structure of the late-replicating chromosomes, she found them to be smashed to bits -- exactly what was predicted as the first step in chromothripsis.
The final piece of the puzzle came when Pellman's colleague Neil Ganem, PhD, examined what happens to these pulverized fragments, using an imaging trick that marked the chromosome in the micronucleus with its own color.
"It has been theorized that micronuclei are garbage disposals for chromosomes that the cell doesn't need anymore," Pellman comments. "If that were true, the smashed pieces would be discarded or digested, but we found that, a third of the time, they're donated to one of the daughter cells and therefore cold be incorporated into that cell's genome.
Pellman says that the findings suggest that, unexpectedly, whole chromosome aneuploidy might promote cancer in a very similar way to other kinds of genomic alterations. The key event may be mutations in oncogenes and tumor suppressors. This mechanism may also explain how cancer cells acquire more than one such mutation at a time.
"Although chromothripsis occurs in only a few percent of human cancers, our findings suggest that it might be an extreme instance of a kind of chromosome damage that could be much more common," says Pellman, who adds that accelerating this process in cancer cells, thus generating so many mutations that the cells die, may represent a possible strategy for new therapies against certain tumors.
###
The research was supported by the National Institutes of Health, the Howard Hughes Medical Institute, and the Leukemia and Lymphoma Society.
Dana-Farber Cancer Institute (www.dana-farber.org) is a principal teaching affiliate of the Harvard Medical School and is among the leading cancer research and care centers in the United States. It is a founding member of the Dana-Farber/Harvard Cancer Center (DF/HCC), designated a comprehensive cancer center by the National Cancer Institute. It provides adult cancer care with Brigham and Women's Hospital as Dana-Farber/Brigham and Women's Cancer Center and it provides pediatric care with Children's Hospital Boston as Dana-Farber/Children's Hospital Cancer Center. Dana-Farber is the top ranked cancer center in New England, according to U.S. News & World Report, and one of the largest recipients among independent hospitals of National Cancer Institute and National Institutes of Health grant funding. Follow Dana-Farber on Twitter: @danafarber and Facebook: www.facebook.com/danafarbercancerinstitute
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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
It's always helpful when tech start-ups scheme new ways for you to burn through that bank account. Like YBUY, the membership-only site that charges a monthly fee in exchange for trying out the latest and greatest in gadgetry, like an iPad 2 or Xbox 360, sans shipping fees. The fresh-out-of-beta portal offers approved users the ability to return or purchase the pre-selected goods after a 30 day trial period, with that recurring charge going towards the full retail price if you choose to opt-in. Its co-founders claim to curate the ever-changing roster of high-end kit, taking into account the best product reviews (ahem) and even featuring certified refurbs. So, what's the catch? Well, there doesn't really appear to be any. It's simply up to you to curb that tech enthusiasm and keep your credit card balance resting peacefully at zero.
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Public release date: 19-Jan-2012
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