REDMOND, Wash. Microsoft unwittingly let an online security certificate expire Friday, triggering a worldwide outage in an online service that stores data for a wide range of business customers.
The sloppy housekeeping represents an embarrassing lapse for Microsoft Corp. as the software maker tries to bring in more revenue from the storage service, which is called Azure.
The expired certificate is needed to properly run online services such as Azure which use an "https" protocol to block unauthorized users from accessing information.
Microsoft's failure to renew the security certificate apparently caused the Azure service to go down shortly before 4 p.m. EST Friday. The breakdown prevented Azure customers from accessing files kept in Microsoft's data centers.
The service still hadn't been fully restored more than four hours later, according to a post on Microsoft's website.
"We apologize for any inconvenience this causes our customers," Microsoft said.
Azure's failure illuminates the pitfalls of storing important information in remote data centers. Online storage, often called "cloud computing," is growing in appeal because it allows workers to pull up data, wherever they are, to an Internet-connected device.
Cloud computing's convenience can turn into a major aggravation when a problem crops up like the one that tripped up Microsoft Friday.
Mobile World Congress will be upon us next week and?LG has announced they will debut the Optimus F5 and Optimus F7 Android-powered LTE phones at the global venue. Both will have Android 4.1.2 (Jelly Bean) and be 4G LTE capable. Though the Optimus F5 will have a?1.2 GHz dual-core processor,?4.3-inch IPS screen (256 ppi resolution), 5-megapixel rear-facing camera plus 1.3-megapixel front-facing camera, with 8 GB internal storage plus supports up to 32 GB SD card storage. The?Optimus F7 will have a?1.5 GHz dual-core processor,?4.7-inch True IPS screen (312 ppi resolution- comparable to Apple?s Retina Display), 8-megapixel rear-facing camera plus 1.3-megapixel front-facing camera, with 8 GB internal storage plus supports up to 32 GB SD card storage.
We should have more info on the phones next week so try back. Check out the specs in the meantime?
NCAA and Olympic Wrestling Legend Danny Gable weighed in on the decree that came out last week that wrestling will no longer be in the Olympics starting in 2020. ?I cried right away,? Gable said. ?I am a guy where wrestling was my best sport.? I?ve influenced a lot of people over the world and I?ve been able to help a lot of people over the world.? And because of that, the opportunity needs to be out there,?he explained.
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Hopkins scientists create method to personalize chemotherapy drug selectionPublic release date: 14-Feb-2013 [ | E-mail | Share ]
Contact: Vanessa Wasta wasta@jhmi.edu 410-614-2916 Johns Hopkins Medicine
Patient-specific cancer cell lines designed to predict chemotherapy sensitivity
In laboratory studies, scientists at the Johns Hopkins Kimmel Cancer Center have developed a way to personalize chemotherapy drug selection for cancer patients by using cell lines created from their own tumors.
If the technique is successful in further studies, it could replace current laboratory tests to optimize drug selection that have proven technically challenging, of limited use, and slow, the researchers say.
Oncologists typically choose anticancer drugs based on the affected organs' location and/or the appearance and activity of cancer cells when viewed under a microscope. Some companies offer commercial tests on surgically removed tumors using a small number of anticancer drugs. But Anirban Maitra, MBBS, professor of pathology and oncology at the Johns Hopkins University School of Medicine, says the tissue samples used in such tests may have been injured by anesthetic drugs or shipping to a lab, compromising test results.
By contrast, he says "our cell lines better and more accurately represent the tumors, and can be tested against any drug library in the world to see if the cancer is responsive."
The Johns Hopkins scientists developed their test-worthy cell lines by injecting human pancreatic and ovarian tumor cells into mice genetically engineered to favor tumor growth. Once tumors grew to one centimeter in diameter in the mice, the scientists transferred the tumors to culture flasks for additional studies and tests with anticancer drugs.
In one experiment, they successfully pinpointed the two anticancer drugs from among more than 3,000 that were the most effective in killing cells in one of the pancreatic cancer cell lines. A report on the success was published online Jan. 22 in the journal Clinical Cancer Research.
The new method was designed to overcome one of the central problems of growing human tumor cell lines in a laboratory dish -- namely the tendency of noncancerous cells in a tumor to overgrow cancerous ones, says James Eshleman, M.D., Ph.D., professor of pathology and oncology and associate director of the Molecular Diagnostics Laboratory at Johns Hopkins. As a consequence, it has not been possible to conventionally grow cell lines for some cancers. Still other cell lines, Eshleman says, don't reflect the full spectrum of disease.
To solve the problem of overcrowding by noncancerous cells, Maitra and Eshleman bred genetically engineered mice that replace the noncancerous cells with mouse cells that can be destroyed by chemicals, leaving pure human tumor cells for study.
"Our technique allows us to produce cell lines where they don't now exist, where more lines are needed, or where there is a particularly rare or biologically distinctive patient we want to study," says Eshleman.
In its proof of concept research, the Johns Hopkins team created three pancreatic ductal adenocarcinoma cell lines and one ovarian cancer cell line. They then tested one of the pancreatic cancer cell lines (called Panc502) against the Johns Hopkins Drug Library of 3,131 drugs, identifying tumor cells most responsive to the anticancer drugs digitoxin and nogalamycin.
For 30 days, they watched the effects in living mice of the two drugs and a control medicine on tumors grown from implanted cells derived from Panc502 and an additional pancreatic cell line, Panc410. They measured the size of tumors twice a week. Both drugs demonstrated more activity in reducing the tumor appearance and size in Panc502 than in Panc410, supporting the notion that the cell line technology may better predict sensitivity to the two drugs.
The investigators have given one type of their genetically engineered mice to The Jackson Laboratory in Bar Harbor, ME, a mouse genetics research facility, for breeding and distribution to other laboratories and are looking to partner with a company to distribute two other types.
###
Study co-authors were Hirohiko Kamiyama, Sherri Rauenzahn, Joong Sup Shim, Collins A. Karikari, Georg Feldmann, Li Hua, Mihoko Kamiyama, F. William Schuler, Ming-Tseh Lin, Robert M. Beaty, Balasubramanyam Karanam, Hong Liang, Michael E. Mullendore, Guanglan Mo, Manuel Hidalgo, Elizabeth Jaffee, Ralph H. Hruban, Richard B. S. Roden, Antonio Jimeno, and Jun O. Liu, of Hopkins; and H. A. Jinnah of Emory University School of Medicine in Atlanta.
The work was supported by the National Institutes of Health, National Cancer Institute (CA130938, CA62924 and CA122581), the Sol Goldman Pancreatic Cancer Research Center, the Stewart Trust Fund, the Lustgarten Foundation, the Mary Lou Wootton Pancreatic Pancreatic Cancer Research Fund, the Michael Rolfe Pancreatic Cancer Foundation and the HERA Foundation.
Rauenzahn, Maitra and Eshleman may receive royalty payments if the mice are licensed, and Eshleman is an advisory board member for Roche Molecular Diagnostics. These relationships have been disclosed and are under the management of the Johns Hopkins University School of Medicine Conflict of Interest Committee.
On the Web:
www.hopkinskimmelcancercenter.org
Photo of cell lines available upon request.
Johns Hopkins Kimmel Cancer Center
Office of Public Affairs Media Contacts:
Vanessa Wasta
410-614-2916; wasta@jhmi.edu
Amy Mone
410-614-2915, amone@jhmi.edu
February 14, 2013
[ | 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.
Hopkins scientists create method to personalize chemotherapy drug selectionPublic release date: 14-Feb-2013 [ | E-mail | Share ]
Contact: Vanessa Wasta wasta@jhmi.edu 410-614-2916 Johns Hopkins Medicine
Patient-specific cancer cell lines designed to predict chemotherapy sensitivity
In laboratory studies, scientists at the Johns Hopkins Kimmel Cancer Center have developed a way to personalize chemotherapy drug selection for cancer patients by using cell lines created from their own tumors.
If the technique is successful in further studies, it could replace current laboratory tests to optimize drug selection that have proven technically challenging, of limited use, and slow, the researchers say.
Oncologists typically choose anticancer drugs based on the affected organs' location and/or the appearance and activity of cancer cells when viewed under a microscope. Some companies offer commercial tests on surgically removed tumors using a small number of anticancer drugs. But Anirban Maitra, MBBS, professor of pathology and oncology at the Johns Hopkins University School of Medicine, says the tissue samples used in such tests may have been injured by anesthetic drugs or shipping to a lab, compromising test results.
By contrast, he says "our cell lines better and more accurately represent the tumors, and can be tested against any drug library in the world to see if the cancer is responsive."
The Johns Hopkins scientists developed their test-worthy cell lines by injecting human pancreatic and ovarian tumor cells into mice genetically engineered to favor tumor growth. Once tumors grew to one centimeter in diameter in the mice, the scientists transferred the tumors to culture flasks for additional studies and tests with anticancer drugs.
In one experiment, they successfully pinpointed the two anticancer drugs from among more than 3,000 that were the most effective in killing cells in one of the pancreatic cancer cell lines. A report on the success was published online Jan. 22 in the journal Clinical Cancer Research.
The new method was designed to overcome one of the central problems of growing human tumor cell lines in a laboratory dish -- namely the tendency of noncancerous cells in a tumor to overgrow cancerous ones, says James Eshleman, M.D., Ph.D., professor of pathology and oncology and associate director of the Molecular Diagnostics Laboratory at Johns Hopkins. As a consequence, it has not been possible to conventionally grow cell lines for some cancers. Still other cell lines, Eshleman says, don't reflect the full spectrum of disease.
To solve the problem of overcrowding by noncancerous cells, Maitra and Eshleman bred genetically engineered mice that replace the noncancerous cells with mouse cells that can be destroyed by chemicals, leaving pure human tumor cells for study.
"Our technique allows us to produce cell lines where they don't now exist, where more lines are needed, or where there is a particularly rare or biologically distinctive patient we want to study," says Eshleman.
In its proof of concept research, the Johns Hopkins team created three pancreatic ductal adenocarcinoma cell lines and one ovarian cancer cell line. They then tested one of the pancreatic cancer cell lines (called Panc502) against the Johns Hopkins Drug Library of 3,131 drugs, identifying tumor cells most responsive to the anticancer drugs digitoxin and nogalamycin.
For 30 days, they watched the effects in living mice of the two drugs and a control medicine on tumors grown from implanted cells derived from Panc502 and an additional pancreatic cell line, Panc410. They measured the size of tumors twice a week. Both drugs demonstrated more activity in reducing the tumor appearance and size in Panc502 than in Panc410, supporting the notion that the cell line technology may better predict sensitivity to the two drugs.
The investigators have given one type of their genetically engineered mice to The Jackson Laboratory in Bar Harbor, ME, a mouse genetics research facility, for breeding and distribution to other laboratories and are looking to partner with a company to distribute two other types.
###
Study co-authors were Hirohiko Kamiyama, Sherri Rauenzahn, Joong Sup Shim, Collins A. Karikari, Georg Feldmann, Li Hua, Mihoko Kamiyama, F. William Schuler, Ming-Tseh Lin, Robert M. Beaty, Balasubramanyam Karanam, Hong Liang, Michael E. Mullendore, Guanglan Mo, Manuel Hidalgo, Elizabeth Jaffee, Ralph H. Hruban, Richard B. S. Roden, Antonio Jimeno, and Jun O. Liu, of Hopkins; and H. A. Jinnah of Emory University School of Medicine in Atlanta.
The work was supported by the National Institutes of Health, National Cancer Institute (CA130938, CA62924 and CA122581), the Sol Goldman Pancreatic Cancer Research Center, the Stewart Trust Fund, the Lustgarten Foundation, the Mary Lou Wootton Pancreatic Pancreatic Cancer Research Fund, the Michael Rolfe Pancreatic Cancer Foundation and the HERA Foundation.
Rauenzahn, Maitra and Eshleman may receive royalty payments if the mice are licensed, and Eshleman is an advisory board member for Roche Molecular Diagnostics. These relationships have been disclosed and are under the management of the Johns Hopkins University School of Medicine Conflict of Interest Committee.
On the Web:
www.hopkinskimmelcancercenter.org
Photo of cell lines available upon request.
Johns Hopkins Kimmel Cancer Center
Office of Public Affairs Media Contacts:
Vanessa Wasta
410-614-2916; wasta@jhmi.edu
Amy Mone
410-614-2915, amone@jhmi.edu
February 14, 2013
[ | 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.
Feb. 8, 2013 ? Genes that have roles in the same biological pathways change their rate of evolution in parallel, a finding that could be used to discover their functions, said a researcher at the University of Pittsburgh School of Medicine in the February issue of Genetics.
Humans have nearly 21,000 genes that make as many proteins, but the functions of most of those genes have not been fully determined, said lead investigator Nathan Clark, Ph.D., assistant professor of computational and systems biology at the Pitt School of Medicine. Knowing what a particular gene does could help unravel the workings of the body, foster understanding of disease processes and identify targets for new drugs.
"For our study, we took a close look at the way genes evolved between species and we found an interesting signature," he said. "Genes that perform biological functions together have similar evolutionary histories in that the rates at which they change parallel each other. This could allow us to identify partner genes that we might never have suspected to work together in biochemical pathways."
The researchers studied the evolving genomes of 18 yeast species and 22 mammalian species, looking particularly at genes that are involved in meiosis, a cell division process, and in DNA repair. They found parallel changes, such as acceleration or deceleration, in evolutionary rates among not only genes encoding proteins that physically interact with each other, but also among those that had no direct contact but still participated in meiosis or DNA repair pathways.
All genes mutate over time, which can be beneficial, harmful or meaningless. Some yeast species evolved a different method of reproduction and meiosis stopped as it was no longer essential for survival, Dr. Clark said. Through subsequent generations, the rate of change in the genes involved in making meiosis proteins accelerated, leading to deterioration of the unnecessary DNA sequences.
"A key question is: How important is that gene at that time?" he said. "If a species encounters a new challenge in its environment, the genes associated with it might have to evolve through subsequent generations in order to adapt that important pathway and ensure species survival."
By tracking those complementary rate changes, it could be possible to identify which genes participate in the same important pathways, providing clues to their function.
"In the future, a researcher studying a particular disease process might be able to plug in a couple of known genes in a database of evolutionary rate changes to find others that have a parallel history," Dr. Clark said. "That could provide new insight into the workings of the biological pathway of interest."
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The above story is reprinted from materials provided by University of Pittsburgh Schools of the Health Sciences.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
N. L. Clark, E. Alani, C. F. Aquadro. Evolutionary Rate Covariation in Meiotic Proteins Results from Fluctuating Evolutionary Pressure in Yeasts and Mammals. Genetics, 2012; 193 (2): 529 DOI: 10.1534/genetics.112.145979
Note: If no author is given, the source is cited instead.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.
In this Tuesday, Aug. 21, 2012, photo, the sun is reflected in the exterior of Dell Inc.'s offices in Santa Clara, Calif. Slumping personal computer maker Dell announced Tuesday, Feb. 5, 2013, it is bowing out of the stock market in a $24.4 billion buyout that represents the largest deal of its kind since the Great Recession dried up the financing for such risky maneuvers. (AP Photo/Paul Sakuma)
Tech ? Founder-led deal comes as PC giant tries to stay relevant in mobile world.
San Francisco ? In the biggest leveraged buyout since the financial crisis, personal computer maker Dell Inc. is being taken private in a deal valued at $24.4 billion after struggling for years to remake itself.
Under the terms of the agreement, the company will be acquired by Dell founder and CEO Michael Dell and global technology investment firm Silver Lake Partners.
Microsoft Corp. will invest $2 billion, a move the software giant said it was undertaking to help support "the long-term success of the entire PC ecosystem."
The complex agreement announced Tuesday allows slumping Dell to bow out of the stock market as it attempts yet another turnaround away from the glare and financial pressures of Wall Street.
Dell stockholders will be paid $13.65 per share to leave the company on its own. That?s 25 percent more than the $10.88 the stock was going for before word of the buyout talks trickled out last month. But it?s a steep markdown from the shares? price of $26 less than five years ago, when Michael Dell returned for a second go-round as CEO.
Dell shares rose 15 cents, to $13.42 per share in trading, indicating that investors don?t believe a better offer is likely. The company will solicit competing offers for 45 days.
Dell?s decision to go private is a reflection of the tough times facing the personal computer industry as more technology spending flows toward smartphones and tablet computers. PC sales fell 3.5 percent last year, according to the research group Gartner Inc., the first annual decline in more than a decade. Tablet computers are expected to outsell laptops this year.
The shift has weakened long-time stalwarts such as Dell, fellow PC maker Hewlett-Packard Co., chip maker Intel Corp. and Microsoft.
Once Dell?s sale is finalized, its stock will stop trading on the Nasdaq Stock Market nearly 25 years after the company raised $30 million in an initial public offering of stock. The IPO and Dell?s rapid growth through the 1990s turned its founder into one of the world?s richest people. His fortune today is estimated at $16 billion. Michael Dell, who owns nearly 16 percent stake in the company, will remain the CEO after the sale closes and will contribute his existing stake in Dell to the new company.
Dell?s sale is the second highest-priced leveraged buyout of a technology company, trailing the $27 billion paid for First Data Corp. in 2007.
story continues below
The deal is the largest leveraged buyout of any type since November 2007, when Alltel Corp. sold for $25 billion to TPG Capital and a Goldman Sachs subsidiary. Within a few months, the U.S. economy had collapsed into the worst recession since World War II.
Leveraged buyouts refer to deals that saddle the acquired company with the debt taken on to finance the purchase.
Like other PC makers, Dell has seen revenue shriveling and its stock sinking amid worries that the company might not be able to regain its technological edge.
Both Dell and its larger rival HP are trying to revive their fortunes by expanding into business software and technology consulting, two niches that are more profitable than making PCs.
The PC downturn has hurt Microsoft by reducing sales of its Windows operating system. As the world?s third largest PC maker, Dell is one of Microsoft?s biggest customers.
By becoming a major Dell backer, Microsoft could gain more influence in the design of the devices running on a radically redesigned version of Windows that was released in late October. The closer ties with Dell, though, could poison Microsoft?s relationship with HP, the largest PC maker, and other manufacturers that buy Windows and other software.
In a statement, Michael Dell said that while the company has made progress, turning it around will be easier under private ownership.
"We recognize that it will still take more time, investment and patience, and I believe our efforts will be better supported by partnering with Silver Lake in our shared vision," he said.
As a private company, Dell won?t have to pander to the stock market?s fixation on whether the company?s earnings are growing from one quarter to the next.
Taking the company private is a major risk, however. It will leave Dell without publicly traded shares to entice and reward talented workers or to help buy other companies.
As part of its shift toward business software and technology services, Dell already has spent $9 billion on acquisitions in the past three years.
Leveraged buyouts also require companies to earmark some of their incoming cash to reduce the debt taken on as part of the process of going private. The obligations mean Dell will have less money to invest in innovation and expansion of its business.
The buyout will mark a new era in another technology company that began humbly and matured into a juggernaut.
With just $1,000, Michael Dell, then a freshman at the University of Texas at Austin, started his company as "PCs Limited" in his dorm room. He would go on to revolutionize the PC industry by taking orders for custom-made machines at a reasonable price ? first on the phone, then on the Internet.
Initially valued at $85 million in its 1988, Dell went on a growth tear that turned the company into a stock market star. At the height of the dot-com boom in 2000, Dell was the world?s largest PC maker, with a market value of more than $100 billion.
But Dell began to falter as other PC makers were able to lower their costs. At the same time, HP and other rivals forged relationships with stores that gave them the advantage of being able to showcase their machines. By 2006, HP had supplanted Dell as the world?s largest PC maker.
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