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Wray on Digital Surveillance: 'The Good Guys Are Constrained by the Rule of Law'
'The good guys are constrained by the rule of law and international norms, bad guys aren't'
WRAY: "The good guys are constrained by the rule of law and international norms. Bad guys aren't, which you could argue in a sense that gives them a competitive advantage. The competitive advantage the good guys have is that for all the reasons Matthew said when we're all working together, then there are no match."
LICHFIELD: "Yes."
WRAY: "Because the bad guys relationships with each other are purely transactional. And they'll turn on each other in a heartbeat if -- if it suits them. But because they're not constrained by the rule of law, because they're not constrained by international norms, we have to be mindful of the advance that gives them and work together in partnership."


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How to rename a file in Linux (batch file)
By using the batch file utility you can rename files in Linux in batch files.
Batch files are used to organize files in folders and to transfer files between computers.
In Linux, the batch files are located in /var/folders and can be accessed by using the cp command.
The batch file format has many advantages: they are easy to write, write fast, have the ability to copy files and folders, and they are a powerful alternative to the more traditional copying utilities such as cp or ucp.
In this article, we will learn how to rename files and rename folders in Linux.
The instructions are based on the Debian GNU/Linux distribution.
There are many other distributions that support the batch format, so we will not cover them here.
This article uses the batch utility in Ubuntu 14.04.4.
For Ubuntu 13.10 and older, use the following command: sudo apt-get install batch_file sudo bash -c "batch_file –version" This command will show you the version number of the batch tool, and it will also display the version of your computer.
For example, the version in this example is 13.0.2-8ubuntu1.
The version numbers are a useful indication for what version of the tool you are using, as Ubuntu 14 is not compatible with previous versions of the program.
You can see the version numbers for the batchfile utility in the Ubuntu Software Center: https://software.ubuntu.com/download/main/desktop/gtk/gtksource/ubuntu/source/bin/batchfile/13.0/version.
If you are interested in the version, you can download the latest version here: http://download.ubuntu-gtk.org/~ubuntu/main/?version=13.10.3.
Note that the versions shown in the table above are the latest versions available in the Software Center, but it is possible to upgrade from a previous version of batchfile.
For this guide, we are using the latest (version 13.11.0) for this tutorial.
To run the command, you will need to have a copy of the Ubuntu 13 LTS distribution installed on your computer, as described in the section How to install the latest release of Ubuntu (see section How do I upgrade from Ubuntu 13 to Ubuntu 13)?
Once the program is running, it will start by searching for files in the following locations: /var /foldings/:/usr/local/bin:/usr /bin: /usr/share/bin /usr :/usr:/usr:

redpajama_set_name: RedPajamaCommonCrawl


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Global Investigative Journalism Network (https://gijn.org/2018/08/06/a-new-collaboration-sets-a-higher-bar-for-working-with-whistleblowers/)
A New Collaboration Sets a Higher Bar for Working with Whistleblowers
By Rowan Philp | August 6, 2018
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The Whistleblower: Edward Snowden
Holger Stark and his colleagues have broken global, policy-changing stories, thanks to the proactive courage of whistleblowers like Edward Snowden and Chelsea Manning.
But these journalists had to wait, passively, for those mass surveillance disclosures. And Stark, the investigations director at Die Zeit, recalls at least three occasions where potential whistleblowers have withdrawn and his own major stories have collapsed because he and his colleagues lacked the knowledge and resources to guarantee the legal, physical, reputational or psychological cover his sources needed to release their bombshells.
In response, a new investigative journalism model has launched as an organized effort to separate the responsibility for the welfare of at-risk sources from the responsibility for the content they provide, so that reporters can focus wholly on their own areas of expertise.
Protecting Whistleblowers
Set up by The Signals Network – a San Francisco-based nonprofit formed in 2017 to support whistleblowers — the model involves a collaboration between the investigative teams at The Telegraph, Die Zeit, The Intercept, Mediapart and WikiTribune.
In the model's pilot project – launched in late June – the five media groups have called for whistleblowers to use the project's secure communications system to report on the misuse of big data, a notably broad subject that they chose in a vote at a meeting organized by Signals in March.
According to Delphine Halgand, executive director at The Signals Network, the parties made formal agreements about a co-embargo, a rotational system to monitor a shared encryption information system and the use of Signals' resources which, they say, offer six levels of whistleblower protection.
Halgand, however, conceded that not all invited media signed on to the project.
And interviews with two of the media parties revealed the two central unknowns of the project: which of the myriad big data sectors might be tackled and, in general, how the five media groups will actually work together in verifying and reporting the incoming claims.
Here is how the overall architecture is supposed to work:
For the pre-reporting phase, the five media groups make themed calls inviting whistleblowers to make disclosures on encrypted channels; the groups take turns monitoring the incoming messages; and they can refer sources, on request, to a list of pro bono lawyers provided by Signals. For the reporting phase, Signals remains strictly uninvolved, while the five news organizations – having received the disclosures simultaneously – choose stories and reporting strategies collaboratively. In the post-publication phase, the 30 journalists within the collaboration step away, and the Signals Network steps in to actively support the whistleblowers with their legal, emotional, logistical and PR needs.
"In the past, (investigative teams) were like a one-stop shop – where the journalists were also the guys who had to handle or at least try to pass on all the legal problems, personal problems and logistical challenges facing these potential sources," said Stark. "For example, I worked with the Chelsea Manning documents in 2010, when I coordinated Der Spiegel's coverage of the diplomatic cables on Iraq and Afghanistan and, in 2013, I worked with the Snowden documents. In those cases, we had to deal with whistleblowers facing astonishingly complex pressures, and as journalists we found it overwhelming. In this case that Signals has established, we have separated those two fields. It's a really remarkable idea."
Collaborating for Impact
In an impact incentive for whistleblowers, the model offers a potential combined audience of 46 million readers and users between the five groups, although Halgand said individual partners could elect not to publish.
Doug Haddix, executive director of Investigative Reporters and Editors (IRE), said the project "offers a promising approach to tackle a complex story."
"When I came forward in 2013, sources had to try and patch together this kind of reporting infrastructure journalist by journalist, in total secrecy with crude tools…The Signals Network is sending a message that this time, the newsroom is ready." — Ed Snowden
Stories run by each media partner will likely be different, with agreed-upon pieces then contextualized to their local markets; the groups currently hold a weekly call.
Dedicated to creating "a proactive dynamic toward whistleblowers," The Signals Network is registered as a 501(c)(3) nonprofit in the US — and is currently seeking equivalent status in France – and was founded on the belief that "we need more whistleblowers to build a more transparent society … (and that) those who risk their lives and livelihoods to bring us the truth deserve our support."
Its founder, entrepreneur Gilles Raymond, provided seed funding of around $300,000 for the group after his second media venture, News Republic, was acquired for $57 million.
The nonprofit claims to offer whistleblowers six levels of protection post-publication, including legal help, PR, safe housing, advocacy and counseling. And it has provided the five media partners, and potential whistleblowers, with two channels of secure communication: an encrypted app and an email system featuring PGP encryption. All five media partners have included the app on their home pages, where they have also broadcast the call for sources.
Jimmy Wales – founder of WikiTribune and co-founder of Wikipedia – said he was confident in the security of the twin systems: "Nothing is perfect, or impenetrable, (but) strong encryption is one of the most important tools that we have … and they are using the right tools."
Halgand said the foundation has set up a network of pro bono lawyers with expertise in public interest disclosure, including Ben Wizner, Snowden's lead attorney, and William Bourdon, who has acted for several high-profile European sources. She said that – to their surprise – whistleblowers consulted on the project indicated that psychological and emotional support represented key unaddressed needs.
Having previously served as US director for Reporters Without Borders, Halgand was involved in the release of Washington Post correspondent Jason Rezaian in Iran and worked closely with the family of imprisoned CIA whistleblower Jeffrey Sterling. Referring to her motivation for joining The Signals Network, Halgand recalled her frustration in highlighting the injustice and lack of help suffered by Sterling with this emotional summation: "And nobody cared."
Investigative journalists used to be one-stop shops – not only reporting leaks but also dealing with the welfare of at-risk sources.
Snowden has also voiced support for the project in a statement which, Halgand said, he insisted include concerns about the existing ad hoc infrastructure facing whistleblowers: "When I came forward in 2013, sources had to try and patch together this kind of reporting infrastructure journalist by journalist, in total secrecy, and with crude tools … The Signals Network is sending a message to whistleblowers that this time, the newsroom is ready."
However, the architecture of the model involves some fascinating legal wrinkles.
According to Halgand, while the five media partners will initially refer whistleblowers to a list of local pro bono lawyers provided by Signals, the nonprofit is to actively engage with whistleblowers only after publication in order to protect identities.
"This preserves the privileged relationship for the source with the journalist and lawyer; we don't want to be a potential weakness in any legal case, in terms of protecting identities," she said. "Post-publication — and especially once their identity is known — it is much easier for us to provide psychological support, legal support, PR management and so on."
Starting with Big Data
Meanwhile, Stark revealed that the exact wording of the "Big Data Call" – the message now broadcast by all five media – was the subject of intense legal wrangling, due to statute differences between the countries that are home to the media partners. Language that might have been fine in Europe, he said, needed to be pared back out of concern that US prosecutors might deem that language an incitement to commit a crime, or illegally breach a contract. And so all five media now simply "welcome(s) information from whistleblowers within the technology industry," and there is no mention in the joint call for "confidential documents," for instance.
Halgand said a "second call" on a new subject – and possibly involving new media partners – could take place this fall.
She revealed that the finalized pilot project was born at a late winter meeting in France, in which representatives of more than half a dozen news outlets were invited to submit three subject areas that they felt would most benefit from a source-protection media collaboration that featured an active call to whistleblowers. Halgand said abuses in the pharmaceuticals industry and government corruption featured on many lists, but that the misuse of big data was the area common to all.
"We need whistleblowers to build a more transparent society. Those who risk their lives and livelihoods to bring us the truth deserve support."
Of course, leaks on the abuse of big data – including illegal surveillance and invasions of consumer privacy – have already characterized some of the most dramatic recent media investigations.
Indeed, Halgand said, "It is notable that this choice was made just two weeks before the Cambridge Analytica scandal exploded."
And the Signals Network's pilot project call is remarkably open-ended, "whether the data in question is being used for social media, marketing, healthcare, law enforcement, machine learning/AI … or, for example, why companies have chosen specific product updates and their effect on consumers."
"Our interest is not just with the big tech firms like Google and Microsoft," said Stark. "For instance, the big car companies and the automotive insurance companies are collecting a huge amount of data about people; way beyond traditional business models. There is the sensitive data that health insurers possess. And personal voice assistants monitor almost everything. We've spoken to prosecutors who speak of this like it's a new gold era for investigation. So the project has no limits here."
Rowan Philp is a multiple award-winning journalist who has worked in more than two dozen countries. Currently based in Boston, Philp was the chief reporter and London bureau chief for South Africa's Sunday Times for 15 years.
Investigative Reporters & Editors
GIJN Bookshelf: A Dozen Books for Muckrakers in 2021
At GIJN we're fortunate to come across various books and reports on the state of the news media and great investigative reporting. Here are 12 of the more interesting recent volumes we've found that investigative journalists might want to pick up in 2021, as well as a novel written by an investigative reporter for a little light relief.
The Rise of Digital Whistleblowing Platforms — and How They Work
Digital technologies have changed whistleblowing, with a growth in new tactics and strategies based on the use of encryption-based communication tools. Philip Di Salvo writes for GIJN about his research into new platforms.
What We're Reading: Pegasus and The New York Times Journalist
This week's Friday 5 surfaced some of our must reads from around the English-language web, including research from Citizen Lab on Pegasus targeting a New York Times reporter, the Media Impact Fund's insight for nonprofit media donors, and the out-of-beta Google Dataset Search.


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RIAA Trims More Staff, But Bonuses Already Well Paid Execs
LOS ANGELES (Hypebot) – The RIAA represents over 1,600 U.S. record labels that collectively create and distribute about 90% of recorded music sold in the United States. It's largest and most influential of the members are the "Big Three" – Universal, Sony and Warner Music.
Continuing a multi-year trend of staff cuts, The Recording Industry Association Of America (RIAA) has cut staff while still rewarding its top executives.
In the fiscal year ending March 31st, the headcount at the RIAA dropped from 58 in the year before to 55. That continues a downward trend from a peak of 117 staffers just 5 years ago, according to new fiscal filings.
At the same time, the trade group has continued to reward its top executives handsomely. CEO Cary Sherman earned $1.6 million last year, including a half million in bonuses and other compensation. Senior EVP Mitch Glazier, General Council Steve Marks and EVP of International Neil Turkewitz earned $776,616, $728,959 and $657,952 respectively, including more than $250,000 in bonuses. The RIAA's top execs account for 25% of total payroll.


"Co-dependency" is so named because it's especially clear in the dynamics between an addict and a significant other. In this situation, the "co-dependent" is tightly engaged with the addict's disease, trying desperately to change the other's life. Trying to understand. Trying to please. Screaming. Crying. Begging. All in the service of "getting" the addict to be "good."
The "co-dependent" often appears to be the more functional partner, getting work done, making money, taking care of the family, keeping things under wraps. But make no mistake, she suffers every bit as much as the active addict.
I say "she" because girls, especially, are brought up to be pleasing, so it's not surprising that a large percentage of "co-dependents" are female. Girls are trained to be more aware of an Other — usually a dysfunctional parent, sometimes a mentally ill sibling — than of themselves. It's a survival mechanism, rooted in the need to be always on guard against danger. A co-dependent grows up highly competent, and almost always a little on edge. And very focused on being pleasing. Maybe if we're "good," Mommy will smile, or Daddy will promise a bicycle. How much we NEED that smile!
It gets so that they'll do pretty much anything in the hopes of getting a sign of affection from the person they care most about. She — or he — will soothe, placate, offer themselves up, just to keep peace at home. And that's how their own lives go to waste.
There are those who don't have what Alanon calls a "qualifier" — who are not actively in relationship with an addict — who nevertheless are crippled with the attitudes of the co-dependent. Some have grown up in "alcoholic" families without the presence of alcohol — but with all the dynamics of addiction. Black-and-white thinking. Perfectionism. Possibly the worst: the belief that emotions can be controlled.
"Co-dependency" is best treated as a "process addiction" — that is, an emotional dependence on something a person must have to survive . In this case, it's an emotional dependence on a particular relationship.
Treatment and recovery in co-dependency involves first, an understanding that what is often considered "good" (putting another first) is, in fact, crippling. And second, learning to create emotional separation from the Other. To create a life of one's own.


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Core Infrastructure Initiative Adds New Members to Fund and Support Critical Open Source Projects
By The Linux Foundation8月 20, 20148月 22nd, 2017Press Release
The Linux Foundation's CII adds Hitachi and NEC to roster of companies working to identify and fund open source projects in need of assistance
Chicago, Ill. LINUXCON & CLOUDOPEN, August 20, 2014 – The Core Infrastructure Initiative (CII), a project hosted by The Linux Foundation that enables technology companies, industry stakeholders and esteemed developers to collaboratively identify and fund open source projects that are in need of assistance, today announced new backers. Hitachi and NEC will work with existing CII members to collaboratively identify and support the critical infrastructure projects most in need of support.
These newest backers join other members of CII who include Adobe, Amazon Web Services, Bloomberg, Cisco, Dell, Facebook, Fujitsu, Google, HP, Huawei, IBM, Intel, Microsoft, NetApp, Rackspace, salesforce.com and VMware. Comments from the newest members are included below.
"Hitachi and NEC are prioritizing support for some of the world's most important open source projects and will help the industry move from crisis-driven responses to a measured, proactive approach to funding projects that are most in need," said Jim Zemlin, executive director at The Linux Foundation. "Open source projects are the foundation for most of today's global infrastructure and need be supported by the companies and users who rely on them."
CII provides funding for fellowships for key developers to work full-time on open source projects, security audits, computing and test infrastructure, travel, face-to-face meeting coordination and other support. The Steering Committee, comprised of members of the Initiative, and the Advisory Board of industry stakeholders and esteemed developers, are tasked with identifying underfunded open source projects that support critical infrastructure and administering the funds through The Linux Foundation.
Projects currently receiving funding include Network Time Protocol, Open Crypto Audit Project (OCAP), OpenSSH and OpenSSL. Other projects are under consideration and will be funded as assessments are completed and budget allows.
The Advisory Board includes Linux kernel developer Alan Cox; security and cryptography researcher Matthew Green; Radio Free Asia's Open Technology Fund Director Dan Meredith; professor of law and legal history at Columbia University and founder of Software Freedom Law Center Eben Moglen; Fellow at the Berckman Center for Internet & Society at Harvard Law School Bruce Schneier; Program Officer for Human Rights for MacArthur Foundation; Eric Spears; and Linux kernel developer Ted Ts'o.
The computing industry has increasingly come to rely upon shared source code to foster innovation. But as this shared code has become ever more critical to society and more complex to build and maintain, there are certain projects that have not received the level of support commensurate with their importance. CII changes funding requests from the reactive post-crisis asks of today to proactive reviews identifying the needs of the most important projects. By raising funds at a neutral organization like The Linux Foundation, the industry can effectively give these projects the support they need while ensuring that open source projects retain their independence and community-based dynamism.
"The Core Infrastructure Initiative is going to address the needs in today's software industry – a neutral, collaborative project that allows companies to support the work of today's most critical open source projects," said Susumu Okuhara, General Manager of Service Development Operation, IT Platform R&D Management Division, Hitachi. "We're proud to be a part of this group and look forward to the impact it can have on the long-term health of our global infrastructure."
"NEC has long valued Linux and open source software and supported their development," said Naoki Hashitani, vice president, NEC. "CII gives us the opportunity to extend the support to open source projects and developers who might not be funded or supported if there were not initiatives like CII."
Anyone can donate to the Core Infrastructure Initiative fund. To join or donate or find out more information about the Core Infrastructure please visit https://www.linuxfoundation.org/programs/core-infrastructure-initiative
News Release: Amazon Web Services, Cisco, Dell, Facebook, Fujitsu, Google, IBM, Intel, Microsoft, NetApp, Rackspace, VMware and The Linux Foundation Form New Initiative to Support Critical Open Source Projects
News Release: The Linux Foundation's Core Infrastructure Initiative Announces New Backers, First Projects to Receive Support and Advisory Board Members
About The Linux Foundation
The Linux Foundation is a nonprofit consortium dedicated to fostering the growth of Linux and collaborative software development. Founded in 2000, the organization sponsors the work of Linux creator Linus Torvalds and promotes, protects and advances the Linux operating system and collaborative software development by marshaling the resources of its members and the open source community. The Linux Foundation provides a neutral forum for collaboration and education by hosting Collaborative Projects, Linux conferences, including LinuxCon and generating original research and content that advances the understanding of Linux and collaborative software development. More information can be found at http://www.linuxfoundation.org.
The Linux Foundation, Linux Standard Base, MeeGo, Tizen and Yocto Project are trademarks of The Linux Foundation. OpenBEL is a trademark of OpenBEL Consortium. OpenDaylight is a trademark of the OpenDaylight Project, Linux is a trademark of Linus Torvalds


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Archive for the 'Virology' Category
Nanotechnology against malaria parasites
After maturation, malaria parasites (yellow) are leaving an infected red blood cell and are efficiently blocked by nanomimics (blue). (Fig: Modified with permission from ACS)
Malaria parasites invade human red blood cells, they then disrupt them and infect others. Researchers at the University of Basel and the Swiss Tropical and Public Health Institute have now developed so-called nanomimics of host cell membranes that trick the parasites. This could lead to novel treatment and vaccination strategies in the fight against malaria and other infectious diseases. Their research results have been published in the scientific journal ACS Nano.
For many infectious diseases no vaccine currently exists. In addition, resistance against currently used drugs is spreading rapidly. To fight these diseases, innovative strategies using new mechanisms of action are needed. The malaria parasite Plasmodium falciparum that is transmitted by the Anopheles mosquito is such an example. Malaria is still responsible for more than 600,000 deaths annually, especially affecting children in Africa (WHO, 2012).
Artificial bubbles with receptors
Malaria parasites normally invade human red blood cells in which they hide and reproduce. They then make the host cell burst and infect new cells. Using nanomimics, this cycle can now be effectively disrupted: The egressing parasites now bind to the nanomimics instead of the red blood cells.
Researchers of groups led by Prof. Wolfgang Meier, Prof. Cornelia Palivan (both at the University of Basel) and Prof. Hans-Peter Beck (Swiss TPH) have successfully designed and tested host cell nanomimics. For this, they developed a simple procedure to produce polymer vesicles – small artificial bubbles – with host cell receptors on the surface. The preparation of such polymer vesicles with water-soluble host receptors was done by using a mixture of two different block copolymers. In aqueous solution, the nanomimics spontaneously form by self-assembly.
Blocking parasites efficiently
Usually, the malaria parasites destroy their host cells after 48 hours and then infect new red blood cells. At this stage, they have to bind specific host cell receptors. Nanomimics are now able to bind the egressing parasites, thus blocking the invasion of new cells. The parasites are no longer able to invade host cells, however, they are fully accessible to the immune system.
The researchers examined the interaction of nanomimics with malaria parasites in detail by using fluorescence and electron microscopy. A large number of nanomimics were able to bind to the parasites and the reduction of infection through the nanomimics was 100-fold higher when compared to a soluble form of the host cell receptors. In other words: In order to block all parasites, a 100 times higher concentration of soluble host cell receptors is needed, than when the receptors are presented on the surface of nanomimics.
"Our results could lead to new alternative treatment and vaccines strategies in the future", says Adrian Najer first-author of the study. Since many other pathogens use the same host cell receptor for invasion, the nanomimics might also be used against other infectious diseases. The research project was funded by the Swiss National Science Foundation and the NCCR "Molecular Systems Engineering".
More information: Adrian Najer, Dalin Wu, Andrej Bieri, Françoise Brand, Cornelia G. Palivan, Hans-Peter Beck, and Wolfgang Meier. "Nanomimics of Host Cell Membranes Block Invasion and Expose Invasive Malaria Parasites." ACS Nano, Publication Date (Web): November 29, 2014 | DOI: 10.1021/nn5054206
Journal reference: ACS Nano
Provided by University of Basel
Categories: Infectious Diseases, Medicine, Virology Tags: Health, host cell nanomimics, infection, Infectious disease, malaria, malaria treatment, malaria vaccination, medicine, nanotechnology, parasite, science
A Flu Virus That Killed Millions In 1918 Has Now Been Recreated
Scientists have recreated a nearly exact replicate of the deadly flu virus that killed an estimated 50 million in the 1918 Spanish flu pandemic.
But don't worry, they say it's totally safe.
Researchers at the University of Wisconsin-Madison reverse engineered an influenza virus from a similar one found in birds, combining several strains to create one that is nearly identical to the one that caused the 1918 outbreak. They then mutated the genes to make it airborne, and to study how it spreads between animals.
"Our research indicates the risks inherent in circulating avian influenza viruses," Yoshihiro Kawaoka, the scientist who led the research team, told VICE News. "Continued surveillance of avian influenza viruses — and not only viruses that we know pose risks for humans, such as H5N1 and H7N9 influenza viruses, and attention to pandemic preparedness measures is important."
According to the statement summarizing the project published this week, the "analyses revealed the global prevalence of avian influenza virus genes whose proteins differ only a few amino acids from the 1918 pandemic influenza virus, suggesting that 1918-like pandemic viruses may emerge in the future."
In other words, a common avian flu virus that has been circulating in wild ducks is pretty much the exact same one that infected humans a century ago. And now is in a lab.
The research was funded by the National Institute of Health as a way to find out more about similar virus' and their transmissibility from animals to humans. It was done in a lab that complied with full safety and security regulations, said Carole Heilman, director of the Division of Microbiology and Infectious Diseases, at National Institute of Allergy and Infectious Diseases (NIAD), a division of NIH.
"It was an question of risk versus benefit," Heilman told VICE News. "We determined that the risk benefit ratio was adequate if we had this type of safety regulations."
But many scientists disagree and have condemned research that recreates virus' such this, stating that if released accidentally, a virus could spread to humans and cause a pandemic. Marc Lipsitch, an epidemiologist at Harvard, has criticized research such as Kawaoka's as unnecessarily risky.
"There is a quantifiable possibility that these novel pathogens could be accidentally or deliberately released. Exacerbating the immunological vulnerability of human populations to PPPs is the potential for rapid global dissemination via ever-increasing human mobility," Lipsitch said in a paper about experiments with transmissible virus'. "The dangers are not just hypothetical."
Lipsitch points out that many of the H1N1 flu outbreaks that have occurred between 1977 and 2009 were a result of a lab accident.
Kawaoka disagrees, saying, "We maintain that it is better to know as much as possible about the risk posed by these viruses so we may be able to identify the risk when viruses with pandemic potential emerge, and have effective countermeasures on-hand or ready for development."
This article originally appeared at VICE News. Check them out on YouTube, Facebook, and Instagram. Copyright 2014. Follow VICE News on Twitter.
Categories: Infectious Diseases, Virology Tags: 1918, avian influenza, birds, ducks, flu, genes, H1N1, H5N1, h7n9, Health, influenza, medicine, science, spanish flu, virus
Pithovirus: 30,000-year-old giant virus 'comes back to life'
A new virus called Pithovirus sibericum has been isolated from 30,000 year old Siberian permafrost. It is the oldest DNA virus of eukaryotes ever isolated, showing that viruses can retain infectivity in nature for very long periods of time.
Pithovirus was isolated by inoculating cultures of the amoeba Acanthamoeba castellani with samples taken in the year 2000 from 30 meters below the surface of a late Pleistocene sediment in the Kolyma lowland region. This amoeba had been previously used to propagate other giant viruses, such as Mimivirus and Pandoravirus. Light microscopy of the cultures revealed the presence of ovoid particles which were subsequently shown by electron microscopy to resemble those of Pandoravirus. Pithovirus particles are flask-shaped and slightly larger than Pandoravirus – 1.5 microns long, 500 nm in diameter, encased by a 60 nm thick membrane. One end of the virus particle appears to be sealed with what the authors call a cork (photo). This feature, along with the shape of the virus particle, inspired the authors to name the new isolate Pithovirus, from the Greek word pithos which refers to the amphora given to Pandora. The name therefore refers both to the morphology of the virus particle and its similarity to Pandoravirus.
Although the Pithovirus particle is larger than Pandoravirus, the viral genome – which is a double-stranded molecule of DNA – is smaller, a 'mere 610,033 base pairs', to use the authors' words (the Pandoravirus genome is 2.8 million base pairs in length). There are other viruses with genomes of this size packed into much smaller particles – so why is the Pithovirus particle so large? Might it have recently lost a good deal of its genome and the particle size has not yet caught up? One theory of the origin of viruses is that they originated from cells and then lost genes on their way to becoming parasitic.
We now know of viruses from two different families that have similar morphology: an amphora-like shape, an apex, and a thick electron-dense tegument covered by a lipid membrane enclosing an internal compartment. This finding should not be surprising: similar viral architectures are known to span families. The icosahedral architecture for building a particle, for example, can be found in highly diverse viral families. The question is how many viruses are built with the pithovirus/pandoravirus structure. Prof. Racaniello's guess would be many, and they could contain either DNA genomes. We just need to look for them, a process, as the authors say that 'will remain a challenging and serendipitous process'.
Despite the physical similarity with Pandoravirus, the Pithovirus genome sequence reveals that it is barely related to that virus, but more closely resembles members of the Marseillviridae, Megaviridae, and Iridoviridae. These families all contain large icosahedral viruses with DNA genomes. Only 32% of the 467 predicted Pithovirus proteins have homologs in protein databases (this number was 61% for Mimivirus and 16% for Pandoravirus). In contrast to other giant DNA viruses, the genome of Pithovirus does not encode any component of the protein synthesis machinery. However the viral genome does encode the complete machinery needed to produce mRNAs. These proteins are present in the purified Pithovirus particle. Pithovirus therefore undergoes its entire replication cycle in the cytoplasm, much like other large DNA viruses such as poxviruses.
Pithovirus is an amazing virus that hints about the yet undiscovered viral diversity that awaits discovery. Its preservation in a permafrost layer suggests that these regions might harbor a vast array of infectious organisms that could be released as these regions thaw or are subjected to exploration for mineral and oil recovery. A detailed analysis of the microbes present in these regions is clearly needed, both by the culture technique used in this paper and by metagenomic analysis, to assess whether any constitute a threat to animals.
The above story is reprinted from materials provided by Virology blog: About Viruses and Viral Disease.
Categories: Medicine, Virology Tags: amoeba, DNA, dsDNA, eukaryotes, Health, marseillevirus, medicine, Megaviridae, Mimivirus, Pandoravirus, permafrost, Pithovirus, science, Siberia, sibericum, viral, virology, virus
Source 3: Protein Essential for Ebola Virus Infection Is a Promising Antiviral Target
September 30, 2012 Luka Ahčin	Leave a comment
In separate papers published online in Nature, two research teams report identifying a critical protein that Ebola virus exploits to cause deadly infections. The protein target is an essential element through which the virus enters living cells to cause disease.
The first study was led by four senior scientists: Sean Whelan, associate professor of microbiology and immunobiology at Harvard Medical School; Kartik Chandran, assistant professor at Albert Einstein College of Medicine; John Dye at the U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID) and Thijn Brummelkamp, originally at the Whitehead Institute for Biomedical Research and now at the Netherlands Cancer Institute. The second study was led by James Cunningham, a Harvard Medical School associate professor of medicine at Brigham and Women's Hospital, and also co-authored by Chandran.
"This research identifies a critical cellular protein that the Ebola virus needs to cause infection and disease," explained Whelan, who is also co-director of the HMS Program in Virology. "The discovery also improves chances that drugs can be developed that directly combat Ebola infections."
Both papers are published in the August 24 online issue of Nature.
The African Ebola virus — and its cousin, Marburg virus — are known as the filoviruses. Widely considered one of the most dangerous infections known, Ebola was first identified in 1976 in Africa near the Ebola River, an area in Sudan and the Democratic Republic of the Congo. Infections cause severe hemorrhage, multiple organ failure and death. No one quite knows how the virus is spread, and there are no available vaccines or anti-viral drugs that can fight the infections.
Through conducting a genome-wide genetic screen in human cells aimed at identifying molecules essential for Ebola's virulence, Whelan and his colleagues homed in on Niemann-Pick C1 (NPC1).
NPC1 has been well known in the biomedical literature. Primarily associated with cholesterol metabolism, this protein, when mutated, causes a rare genetic disorder in children, Niemann-Pick disease.
Using cells derived from these patients, the group found that this mutant form of NPC1 also completely blocks infection by the Ebola virus. They also demonstrated that mice carrying a mutation in the NPC1 gene resisted Ebola infection. Similar resistance was found in cultured cells in which the normal molecular structure of the Niemann-Pick protein has been altered.
In other words, targeting NPC1 has real therapeutic potential. While such a treatment may also block the cholesterol transport pathway, short-term treatment would likely be tolerated.
Indeed in the accompanying paper, Cunningham's group describes such a potential inhibitor.
Cunningham and his group at Brigham and Women's Hospital investigated Ebola by using a robotic method developed by their colleagues at the National Small Molecule Screening Laboratory at Harvard Medical School to screen tens of thousands of compounds. The team identified a novel small molecule that inhibits Ebola virus entry into cells by more than 99 percent.
The team then used the inhibitor as a probe to investigate the Ebola infection pathway and found that the inhibitor targeted NPC1.
For Cunningham and Chandran, this finding builds on a 2005 paper of theirs for which Whelan was also a collaborator. In that study, he and his group discovered how Ebola exploits a protein called cathepsin B. This new study completes the puzzle. It now seems that cathepsin B interacts with Ebola in a way that preps it to subsequently bind with NPC1.
"It is interesting that NPC1 is critical for the uptake of cholesterol into cells, which is an indication of how the virus exploits normal cell processes to grow and spread," said Cunningham. "Small molecules that target NPC1 and inhibit Ebola virus infection have the potential to be developed into anti-viral drugs."
The paper coauthored by Whelan was funded by the U.S. National Institute of Allergy and Infectious Diseases and the National Human Genome Research Institute, the U.S. Army, and the Burroughs Wellcome Foundation. Cunningham's work was funded by the New England Regional Center of Excellence for Biodefense and Emerging Infectious Diseases at Harvard Medical School.
The above story is reprinted from materials provided by Harvard Medical School, via ScienceDaily. The original article was written by Robert Cooke and Lori Shanks.
Journal References:
Jan E. Carette, Matthijs Raaben, Anthony C. Wong, Andrew S. Herbert, Gregor Obernosterer, Nirupama Mulherkar, Ana I. Kuehne, Philip J. Kranzusch, April M. Griffin, Gordon Ruthel, Paola Dal Cin, John M. Dye, Sean P. Whelan, Kartik Chandran, Thijn R. Brummelkamp. Ebola virus entry requires the cholesterol transporter Niemann–Pick C1. Nature, 2011; DOI: 10.1038/nature10348
Marceline Côté, John Misasi, Tao Ren, Anna Bruchez, Kyungae Lee, Claire Marie Filone, Lisa Hensley, Qi Li, Daniel Ory, Kartik Chandran, James Cunningham. Small molecule inhibitors reveal Niemann–Pick C1 is essential for Ebola virus infection. Nature, 2011; DOI: 10.1038/nature10380
Categories: Infectious Diseases, Virology Tags: ebola, Ebolavirus, filovirus, Health, hemorrhagic fever, infection, Marburg, medicine, Niemann-Pick, NPC1, NPC1 inhibitor, protein, science, virus
Source 2: Scientists Identify Point of Entry for Deadly Ebola Virus
Ebola virus, the cause of Ebola hemorrhagic fever (EHF), is one of the deadliest known viruses affecting humans. Like anthrax and smallpox virus, Ebola virus is classified by the U.S. Centers for Disease Control and Prevention (CDC) as a category A bioterrorism agent. Currently, there is no vaccine to prevent EHF, and patients are treated only for their symptoms.Although outbreaks are rare, Ebola virus, the cause of Ebola hemorrhagic fever (EHF), is one of the deadliest known viruses affecting humans. According to the World Health Organization (WHO), approximately 1,850 EHF cases with more than 1,200 deaths have been documented since the virus was identified in 1976.
This negatively-stained transmission electron micrograph (TEM) revealed some of the ultrastructural curvilinear morphologic features displayed by the Ebola virus discovered from the Ivory Coast of Africa. (Credit: Charles Humphrey). (up)
EHF's clinical presentation can be devastating: fever, intense weakness, and joint and muscle aches progress to diarrhea, vomiting, and in some cases, internal and external bleeding caused by disintegrating blood vessels. Currently, there is no approved vaccine and patients are treated only for their symptoms. Like anthrax and smallpox virus, Ebola virus is classified as a category A bioterrorism agent by the U.S. Centers for Disease Control and Prevention (CDC).
Until now, however, researchers had only a limited understanding of how Ebola virus gains entry to a host cell.
Using an unusual human cell line, Whitehead Institute scientists and collaborators from Harvard Medical School, Albert Einstein College of Medicine and U.S. Army Medical Research Institute of Infectious Diseases, have identified the Niemann-Pick C1 (NPC1) protein as crucial for Ebola virus to enter cells and begin replicating. The discovery may offer a new and better approach for the development of antiviral therapeutics, as it would target a structure in the host cell rather than a viral component.
The findings are reported online in Nature this week.
Where all of us inherit one copy of each chromosome from each of our two parents, cell lines exist with only a single set, and thus with a single copy of each individual gene, instead of the usual two. Using an unusual human cell line of this type, Whitehead Institute researchers and their collaborators performed a genetic screen and identified a protein used by Ebola virus to gain entry into cells and begin replicating. The discovery may offer a new approach for the development of antiviral therapeutics.
"Right now, people make therapeutics to inactivate the pathogen itself. But the problem is that pathogens can quickly change and escape detection and elimination by the immune system," says former Whitehead Fellow Thijn Brummelkamp, now a group leader at the Netherlands Cancer Institute (NKI). "Here we get a good idea of the host genes that are needed for the pathogen to enter the cell for replication. Perhaps by generating therapeutics against those host factors, we would have a more stable target for antiviral drugs."
The method developed by the Brummelkamp lab to identify host factors relies on gene disruption — knocking out gene function in the host cells, one gene at a time — and documenting which cells survive due to mutations that afford protection from viral entry.
But human cells are diploid with two copies of each chromosome and its genes. Researchers can reliably target and knock out one copy of a gene, but doing so for both copies is far more difficult and time-consuming. If only a single copy is silenced, the other continues to function normally and masks any effect of the knockout.
To sidestep this obstacle, Jan Carette, a first co-author on the Nature paper and a former postdoctoral researcher in the Brummelkamp lab, employed a technique he had previously applied to study the cytolethal distending toxin (CDT) family that is secreted by multiple pathogenic bacteria, including Escherichia coli, Shigella dysenteriae, and Haemophilus ducreyi. Each bacterial species has developed its own twists on the CDT structure, which may link to the target tissues of the toxin's bacterium.
In his CDT work published in Nature Biotechnology, Carette together with co-lead authors of Whitehead Member Hidde Ploegh's lab, used a line of haploid cells isolated from a chronic myeloid leukemia (CML) patient. Because these cells, called KBM7 cells, have only one copy of each chromosome except chromosome 8, the researchers could disrupt the expression of each gene and screen for mutants with the desired properties, in this case survival of a lethal dose of toxin.
After knocking out individual genes by disrupting the normal structure of the gene, the resulting mutant KBM7 cells were exposed to various CDTs. In the cells that survived, Carette and coauthors knew that genes that had been disrupted were somehow crucial to CDT intoxication. By analyzing the surviving cell's genomes, Carette and coauthors identified ten human proteins that are used by CDTs during intoxication, and those host factors seem to be tailored to each CDT's targeted cell.
"I found it surprising that there is quite some specificity in the entry routes for each toxin," says Carette. "If you take CDTs that are very similar to each other in structure, you could still see significant differences in the host factors they require to do their job. So it seems that every pathogen evolved a specific and unique way of its toxin entering the cells."
To study Ebola virus, Carette and co-lead authors from Harvard Medical School and the Albert Einstein College of Medicine made use of an otherwise harmless virus cloaked in the Ebola virus glycoprotein coat. Using this virus and by altering the haploid cells somewhat, Carette and coauthors were able to pinpoint the cellular genes that Ebola virus relies on to enter the cell.
Carette and coauthors identified as necessary for Ebola virus entry several genes involved in organelles that transport and recycle proteins. One gene in particular stood out, NPC1, which codes for a cholesterol transport protein, and is necessary for the virus to enter the cell's cytoplasm for replication. Mutations in this gene cause a form of Niemann-Pick disease, an ultimately fatal neurological disorder diagnosed mainly in children.
Collaborators at the U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID) tested the effects of active Ebola virus on mice that had one copy of the NPC1 gene knocked out. Control mice, with two functioning copies of the NPC1 gene, quickly succumbed to infection, while the NPC1 knockout mice were largely protected from the virus.
"This is pretty unexpected," says Carette, who is currently an Acting Assistant Professor in Microbiology & Immunology at Stanford School of Medicine. "This might imply that genetic mutations in the NPC1 gene in humans could make some people resistant to this very deadly virus. And now that we know that NPC1 is an Ebola virus host factor, it provides a strong platform from which to start developing new antivirals."
This research was supported by the National Institutes of Health (NIH), the U.S. Army, Boehringer Ingelheim Fonds and a Burroughs Wellcome Award.
The above story is reprinted from materials provided by Whitehead Institute for Biomedical Research, via ScienceDaily. The original article was written by Nicole Giese.
Jan E Carette, Carla P Guimaraes, Irene Wuethrich, Vincent A Blomen, Malini Varadarajan, Chong Sun, George Bell, Bingbing Yuan, Markus K Muellner, Sebastian M Nijman, Hidde L Ploegh, Thijn R Brummelkamp. Global gene disruption in human cells to assign genes to phenotypes by deep sequencing. Nature Biotechnology, 2011; 29 (6): 542 DOI: 10.1038/nbt.1857
Categories: Infectious Diseases, Virology Tags: CDC, ebola, Ebola virus, Ebola virus disease, EHF, entry, Health, hemorrhagic fever, medicine, Niemann-Pick, NPC1, science, vaccine, virus, World Health Organization
Source 1: Researchers Find 'Key' Used by Ebola Virus to Unlock Cells and Spread Deadly Infection
Researchers at Albert Einstein College of Medicine of Yeshiva University have helped identify a cellular protein that is critical for infection by the deadly Ebola virus. The findings, published in the August 24 online edition of Nature, suggest a possible strategy for blocking infection due to Ebola virus, one of the world's most lethal viruses and a potential bioterrorism agent.
The study was a collaborative effort involving scientists from Einstein, the Whitehead Institute for Biomedical Research, Harvard Medical School, and the U.S. Army Medical Research Institute of Infectious Diseases
Ebola virus is notorious for killing up to 90 percent of the people it infects. Ebola hemorrhagic fever — the severe, usually fatal disease that Ebola virus causes in humans and in nonhuman primates — first emerged in 1976 in villages along the Ebola River in the Sudan and the Democratic Republic of the Congo, Africa. Since then, about two dozen outbreaks have occurred.
This drawing illustrates the sequence of events from the time the Ebola virus first enters the host cell (top) until the virus gains its release into the cytoplasm, where it can multiply (bottom). Researchers have shown that Ebola exists in the lysosome and enters the cytoplasm by interacting with NPC1 protein molecules (orange) embedded in the lysosomal membrane. (Credit: Image courtesy of Albert Einstein College of Medicine) (right)
Though Ebola and Marburg hemorrhagic fevers are fortunately rare diseases, "even small outbreaks of Ebola or Marburg virus can cause fear and panic," said co-senior author Kartik Chandran, Ph.D., assistant professor of microbiology & immunology at Einstein "And then there's the worry that these viruses could be used for bioterrorism."
Ebola virus's ability to enter cells is reminiscent of the Trojan Horse used by the ancient Greeks to defeat their archenemies. Ebola virus binds to the host cell's outer membrane, and a portion of host cell membrane then surrounds the virus and pinches off, creating an endosome — a membrane-bound bubble inside the cell (see image). Endosomes carry their viral stowaways deep within the cell and eventually mature into lysosomes — tiny enzyme-filled structures that digest and recycle cellular debris.
The viruses captive in the lysosome manage to escape destruction by exploiting components of the cell to gain entry to the cytoplasm, the substance between the cell membrane and the nucleus where the virus can replicate. But the identities of many of these components have remained unknown.
In seeking the answer, Einstein researchers and colleagues searched for proteins that Ebola virus might exploit to enter the cell's cytoplasm. One such cellular protein, known as Niemann-Pick C1 (NPC1), stood out.
"We found that if your cells don't make this protein, they cannot be infected by Ebola virus," said Dr. Chandran. "Obviously it's very early days, but we think our discovery has created a real therapeutic opportunity." At present, there are no drugs available to treat people who have been infected with Ebola virus or approved vaccines to prevent illness."
The NPC1 protein is embedded within cell membranes, where it helps transport cholesterol within the cell. However, the absence of NPC1 due to gene mutations causes a rare degenerative disorder called Niemann-Pick disease, in which cells become clogged up with cholesterol and eventually die.
To confirm their finding that NPC1 is crucial for Ebola virus infection, the researchers challenged mice carrying a mutation in NPC1 with Ebola virus. Remarkably, most of these mutant mice survived the challenge with this normally deadly virus. Similarly, fibroblast cells (found in connective tissue) from people with Niemann-Pick disease were resistant to Ebola virus infection, as were human cells from other organs that were manipulated to reduce the amount of NPC1 they contained.
The researchers also tested whether other major viruses need NPC1 to infect human cells. Only Ebola virus and its close relative, Marburg virus, were found to require the presence of NPC1 protein for infection. Like Ebola virus, Marburg virus also needs NPC1 to kill mice.
"Our work suggests that these viruses need NPC1, which is embedded in the lysosomal membrane, to escape from the lysosome into the cytoplasm," said Dr. Chandran. "We are now testing that hypothesis in the laboratory."
The discovery of NPC1's crucial role in Ebola infection raises the possibility that Ebola and Marburg virus outbreaks could be thwarted by a drug that blocks the action of NPC1. "Even though such a treatment would also block the cholesterol transport pathway, we think it would be tolerable," said Dr. Chandran. "Most outbreaks are short-lived, so treatment would be needed for only a short time." Einstein, in conjunction with the Whitehead Institute of Biomedical Research and Harvard Medical School, has filed a patent application related to this research that is available for licensing to partners interested in further developing and commercializing this technology.
Remarkably, an anti-Ebola virus inhibitor Dr. Chandran found as a postdoctoral fellow at the Brigham and Women's Hospital in Boston, MA turns out to be just such an NPC1 blocker, as described in a separate manuscript by Côté and co-workers to be published in the same issue of Nature.
The above story is reprinted from materials provided by Albert Einstein College of Medicine, via ScienceDaily.
Categories: Infectious Diseases, Virology Tags: Africa, ebola, Ebola virus, Ebola virus disease, Health, hemorrhagic fever, infection, Marburg, Marburg virus, medicine, Niemann-Pick, NPC1, science, virology, virus
How Deadly Marburg Virus Silences Immune System: Breakthrough Findings Point to Targets for Drugs and Vaccines
Scientists at The Scripps Research Institute have determined the structure of a critical protein from the Marburg virus, a close cousin of Ebola virus. These viruses cause similar diseases and are some of the deadliest pathogens on the planet, each killing up to 90 percent of those infected.
The Marburg virus VP35 protein (beige) surrounds the virus's double-stranded RNA (blue), masking it from immune system detection. (Credit: Image by Christina Corbaci, The Scripps Research Institute) (up)
Described in the Sept. 13, 2012 publication of the journal PLoS Pathogens, the new research reveals how a key protein component of the Marburg virus, called VP35, blocks the human immune system, allowing the virus to grow unchecked. The structure provides a major step forward in understanding how the deadly virus works, and may be useful in the development of potential treatments for those infected.
"The immune system is designed to recognize certain hallmarks of virus infection," said Erica Ollmann Saphire, the Scripps Research scientist who led the effort. "When these are sensed, an immediate antiviral defense is launched. However, the Marburg and Ebola viruses mask the evidence of their own infection. By doing so, the viruses are able to replicate rapidly and overwhelm the patient's ability to launch an effective defense."
Ebola virus outbreaks have occurred in the last month in both Uganda and the Democratic Republic of the Congo, while Marburg virus broke out in Angola in 2005 to 2006 and again in Uganda in 2007. The Angolan Marburg virus outbreak began in a pediatric ward and killed 88 percent of those it infected. The virus has since been imported into the United States (Colorado) and the Netherlands by tourists who had visited Africa.
There is currently no cure for Marburg hemorrhagic fever. The virus is spread when people come into contact with the bodily fluids of a person or animal who is already infected. The best treatment consists of administering fluids and taking protective measures to ensure containment, like isolating the patient and washing sheets with bleach.
Most people, however, die within two weeks of exposure from a combination of dehydration, massive bleeding, and shock. A smaller number of people have stronger and immediate immune responses against the virus and survive.
A New Roadmap for Defense
The breakthrough described in the PLoS Pathogens article explains a key reason why the viruses are so deadly and provides the necessary templates to develop drugs to treat the infection.
The study's lead author, Research Associate Shridhar Bale, explains that a key signature of Marburg virus infection is the double-stranded RNA that results from its replication inside cells. When human immune system proteins detect this virus-specific RNA, they sound an alarm to signal the rest of the immune system to respond. The new research describes how the VP35 protein of the Marburg virus binds to the viral double-stranded RNA and hides it to prevent the alarm from being sounded.
The new research also revealed a surprise. Images from the Marburg virus reveal the VP35 protein spirals around the double-stranded RNA, enveloping it completely. This is in contrast to previous images of the similar VP35 protein from Ebola virus that showed it only capping the ends of the RNA, leaving the center of the RNA helix exposed for possible recognition.
In addition to Ollmann Saphire and Bale, the article, "Marburg virus VP35 can both fully coat the backbone and cap the ends of dsRNA for interferon antagonism," was authored by Jean-Philippe Julien, Zachary A. Bornholdt, Michelle A. Zandonatti, Gerard J.A. Kroon, Christopher R. Kimberlin, Ian J. MacRae, and Ian A. Wilson of The Scripps Research Institute, and Peter Halfmann, John Kunert, and Yoshihiro Kawaoka of the University of Wisconsin.
Support for the research was provided by grants from the Burroughs Wellcome Fund and The Skaggs Institute for Chemical Biology at Scripps Research.
The above story is reprinted from materials provided by Scripps Research Institute, via ScienceDaily
Bale S, Julien J-P, Bornholdt ZA, Kimberlin CR, Halfmann P, et al. Marburg Virus VP35 Can Both Fully Coat the Backbone and Cap the Ends of dsRNA for Interferon Antagonism. PLoS Pathog. PLoS Pathogens, 2012; 8(9): e1002916 DOI: 10.1371/journal.ppat.1002916
Categories: Infectious Diseases, Virology Tags: disease, ebola, Health, hemorrhagic fever, Immune system, infection, interferon, Marburg, medicine, science, virology, virus, VP35


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What Is MI
MI Capital is Strong
Private MI vs FHA MI
PMI By the Numbers
MI is Reliable
MI Helps Lenders
MI Helps Borrowers
MI is Cancelable
MI Protects Taxpayers
Setting and Using GSE Fees
Extending and Preserving Tax Deductibility of MI
Strengthening State Regulation of MI
Capacity for Risk Sharing with MI
Reducing Taxpayer Risk with MI
Current Expected Credit Loss Accounting Model
It's Time to Reform the Housing Finance System
MI in Your State
Reliability Factsheet
Risk Sharing Factsheet
PMIERs Factsheet
Polling Results
Low Down Payment Facts
Expanding Homeownership
MI Consumer Options
Announcements & Statements
USMI Statement on March 2017 FHFA Credit Risk Transfer Progress Report and RFI
The following statement can be attributed to Lindsey Johnson, USMI president and executive director:
"Private mortgage insurance is a 60-year old bedrock of the housing system that for decades has helped low down payment borrowers qualify for mortgage financing—more than 25 million borrowers to date—and has provided critical credit risk protection to the government and taxpayers through numerous housing cycles. MI works and is a reliable form of credit risk protection, as evidenced by the more than $50 billion in claims that mortgage insurers paid to the GSEs through the downturn. As FHFA states in its progress report, private mortgage insurance remains the primary form of credit enhancement used on mortgages sold to the GSEs with loan-to-value ratios over 80 percent, and in the first quarter of 2017 MI covered $48 billion of mortgages the agencies purchased.
"In the absence of comprehensive GSE reform, FHFA is rightfully exploring options in the credit risk share market through various pilots, and USMI encourages greater balance, transparency, and comparable standards among these options. The cost of credit enhancement has more than doubled for many of the back-end CRT tranches sold, which indicates price volatility continues to be present for these transactions. Our industry remains confident that greater potential benefits can be realized through front-end risk sharing, specifically as outlined in our proposal last year to explore deeper MI coverage, where even more risk is transferred away from the government before it ever touches the GSEs' balance sheets. The vast majority (more than 97 percent based on risk in force) of CRT transactions to date have been done on the back-end, with the GSEs warehousing credit risk before transferring to the private sector. The GSEs need not carry this level of risk considering there is ample opportunity to increase or at a minimum balance the level of front-end transactions.
"We also encourage equivalent counterparty standards for other CRT transactions, similar to the stringent requirements of mortgage insurers. Doing this will ensure taxpayers are better protected. In the last two years, MIs have materially increased their claims paying ability in both good and bad economic times due to new higher capital standards under the Private Mortgage Insurance Eligibility Requirements (PMIERs). All MIs have met or exceeded PMIERs requirements as of December 31, 2015."
U.S. Mortgage Insurers (USMI) is dedicated to a housing finance system backed by private capital that enables access to housing finance for borrowers while protecting taxpayers. Mortgage insurance offers an effective way to make mortgage credit available to more people. USMI is ready to help build the future of homeownership. Learn more at www.usmi.org.
Nine Trade Associations Send Joint Letter to CFPB in response to its Rulemaking on QM Definition
January 21, 2020 The Honorable Kathleen L. Kraninger Director Consumer Financial Protection Bureau 1700 G Street NW Washington, DC 20552 Dear Director Kraninger: The undersigned...
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WASHINGTON — U.S. Mortgage Insurers (USMI) President Lindsey Johnson issued the following statement on the decision made by the U.S. Congress to extend the tax...
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Some hailed the Department of Housing and Urban Development's annual report on the Federal Housing Administration's financial status as evidence that the government mortgage insurance program should...
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5 2021 Poetry Collections by AAPI Poets
May is Asian American and Pacific Islander Heritage Month, a time for recognizing the contributions Asian Americans and Pacific Islander Americans have made to U.S. history and culture. Poets with AAPI heritage have enriched the American literary landscape for over a century, but only began to gain mainstream recognition in the 1970s.
The work of AAPI poets has continued to shape contemporary literature. In her 2004 introduction to Asian American Poetry: The Next Generation, Victoria Chang writes, "new Asian American poets have captured the power of the past but have ventured into new territories and discovered, created, and revealed new voices and styles." To celebrate this, we've highlighted five outstanding poetry collections by AAPI poets released in 2021.
The Sunflower Cast A Spell To Save Us From The Void by Jackie Wang
Author Jackie Wang is both a poet and an Assistant Professor of Culture and Media Studies at The New School. Her highly anticipated and acclaimed collection The Sunflower Cast A Spell To Save Us From The Void taps into the subconscious to reveal deeper truths about ourselves. Informed by her own dream journal, this collection analyzes how social processes and traumas show up in our dreams—from interpersonal conflict to generational trauma. Released Feb. 2, 2021.
Divine Fire by David Woo
Award-winning poet David Woo draws on themes of childhood, personal space, and privacy to analyze race and class inequality through an intimate lens. His latest poetry collection, Divine Fire, links these personal experiences to ever-vaster scales of meaning, like the global issue of climate change and finding spirituality in a time of crisis. Released March 1, 2021.
Dēmos: An American Multitude by Benjamín Naka-Hasebe Kingsley
Poet Benjamín Naka-Hasebe Kingsley places multiculturalism at center stage in his newest collection. Drawing on his Onondaga, Japanese, Cuban, and Appalachian cultures, the poet merges the personal and political to discuss themes of anger, violence, and oppression. Released March 9, 2021.
Peach State by Adrienne Su
Chinese-American poet Adrienne Su brings the literary and culinary together in this inventive poetry collection. Through the settings of restaurants, home kitchens, and grocery stores, Su reveals the Chinese-American influence on her hometown's food and culture. Toying with sonnets, villanelles, palindromes, and more, Peach State reveals the immigrant and Southern experience in Atlanta, Georgia. Released March 23, 2021.
Cleave by Tiana Nobile
In her debut poetry collection, Cleave, poet Tiana Nobile brings a compassionate and lucid voice to the story of transnational adoption. Extrapolating the personal to the broader, collective experience, Nobile untangles the complexities of adoptee childhood and offers insight on the America we currently live in. Released April 6, 2021.
Audio, Poetry


Research at the University of California-Irvine demonstrated that patients in Network Care reported significant improvement in Physical Health and symptoms, Emotional/Mental Health and symptoms, Stress, and Life Enjoyment. A unique Wellness Index was developed to assess these categories for overall quality of life. Seventy Six percent of the over 2,800 patients improved in every category. Although physical symptoms changed most often within the first couple of months, patients reported their overall life enjoyment and quality of life continuing to improve year after year. During Network Spinal Analysis™ (NSA) care two "healing waves" develop which are unique to Network. One is a breathing wave that releases tension throughout the spine and body and relaxes a person. The other is called a somatopsychic (or body-mind) wave, which is associated with a dolphin type undulation or movement of the spine. These waves are related to a significant increase in wellness and quality of life.
Once people experience these Network "healing" waves, they tend to make healthier choices. Suddenly the exercise, diet, supplements, meditation or prayer that may have been resulting in minimal wellness benefits increased in effectiveness. Saying it differently, people in Network care, who experience these waves, often double their perceived wellness. As these "healing waves" progress along a person's spine, it revitalizes, energizes, and helps the body to self-correct distortions of alignment and posture. They move "stuck energy" and are a resource of new energy and vitality. Vertebra of the spine spontaneously realign as one of the by products.
NSA helps the person "inside" who is experiencing disease, and must deal with a prognosis, treatment, and symptoms. With care they are better able to develop innate strategies to find tension in their bodies and spontaneously move and breathe to dissipate it. NSA helps the person to use the energy within their spinal tension (and unresolved past and current stressful or traumatic experiences) to fuel the healing process. Network Care helps the internal cues to become so available that people more often act, think, feel, and respond in a more productive and healthier fashion. The internal communication systems become clearer to coordinate the body more effectively even during periods of stress and trauma. People have been shown to make healthier choices and enjoy life more. Also, a wide range of physical complaints such as headaches, stiffness, pain, eczema, menstrual cramps, dizziness, and many others have been reported by the Network patients to improve or resolve.
Why is it that we lose our wellness and health?
It seems associated with the way we experience our world. When an event occurs that our brain determines is not safe for us to fully experience, the energy and information of the event is translated into vibration and tension, which is then stored in the body. It is not unlike the after-image of a flashbulb. Our body then walls off the offending energy and tension over time with muscular spasm, spinal distortion, reduced breathing into the area, and reduced movement. Much of what many disciplines seek to correct through manipulation, massage, and therapy is often a symptom of this process.
Through gentle contacts along the neck and lower spine (where the spinal cord attaches inside the vertebral column), called Network adjustments or entrainments, greater body awareness is achieved. The body moves away from defense and towards growth. The brain becomes aware of the spine, which is a main conduit of consciousness, the coordinator of body function, and a proposed location of the subconscious mind. Our posture, spinal alignment, and tension patterns all reflect our emotional reactions to our perceived world.
Most of us remain in defense throughout our lives, and the higher more evolved brain does not have the opportunity to develop its unique properties and evolve new strategies for experiencing and responding to life. When at peace, the internal growth "programs" can be switched on because the body does not need to protect itself from injury. It can then assess if our reactions, adaptations, and symptoms are appropriate or not. We can feel more profoundly and use subtle information within to make healthier choices. We can be more compassionate to others, and to ourselves. We can activate "internal" software for experiencing life, changing our course, and for healing. Our brain can pay attention to the body's tension patterns, its spinal alignment, its posture, and its current state.
In order to fix something we must first be able to find it. As our brain is better able to inventory the body, it can better orchestrate healing. This naturally occurs as NSA care progresses, and the individual not only becomes aware of spinal tension patterns, vertebral motion and respiration, but also even the energetic motion through the body. Natural outcomes of Network care include this awareness, and even the self-regulation of spinal tension and alignment.
For those people who have had the greatest wounds, or stresses and traumas in life, they may tap stored tension or blocked energy through NSA care, to develop the statistically greatest positive changes in wellness. This is part of the "stress busting" effect demonstrated in Network Care. I interpret this to suggest that the greater the wound, the greater the potential gift–that is, if new strategies can be developed to access the internal storehouse of energy for healing. This is what appears to happen in NSA care.
The NSA practitioner seeks to promote new strategies for your spine and nervous system so that you can be more effective at being well. The spinal assessments the doctor makes are matched with your personal health and wellness inventory. Allow the practitioner's expertise, and your ability to heal, to join in celebrating the wellness that is available to you . . . even in the presence of disease.
Network Spinal Analysis™, originally developed as a subluxation classification analysis as well as a low force adjustment application. This has evolved into a system of enhancing spinal and neural integrity though development of biologically entrained responses purported to advance emerging properties of the spine and nervous system. Evidence exists to support the benefits of NSA care in relationship to enhanced health, quality of life, healthier lifestyles, and life choices. It is currently being represented and taught as a unique discipline, which has very specific benefits to a wide range of disciplines and is well adapted for the scope of vertebral subluxation based chiropractic.
Network Spinal Analysis™ involves a clinical assessment of individuals that also incorporates a patient centered education process. Through specific contacts with the tissues overlying the spine, it utilizes a low force protocol employing concepts derived from a variety of health professions and theoretical sciences.
A. Promote practice member self-awareness of the spinal structures, including gross and subtle movement of spinal structures, spinal and somatic tension patterns, associated participation with the respiratory system, and responses to stress.
F. To evaluate the efficacy of the above by relating the application of NSA to practice member self-ratings regarding their wellness and quality of life, and to conduct research investigating the hypothesis advanced relative to the above objectives of NSA.
Results of a study performed at the University of California, Medical School at Irvine.


several days as a full report has to be written and translated before the outcome can be made public.
soccer's world governing body to open disciplinary proceedings against him.
that he would receive his bronze.
FIFA decides on any suspension.


Dantis Amore by Dante Gabriel Rossetti, ca. 1860.
Saturday is Oldies day, and A Night to Remember dates back to 1958. Unlike later versions of the movie, this one uses the old British melody that was actually played when the great ship went down. A very touching scene.
Who can tell what a day might bring? Therefore, gracious God, cause me to live every day as if it were to be my last, for I cannot know not that it is not. Help me to live this day as I shall wish I had done when I come to die.
"When they persecute you in one town, flee to the next, for truly, I say to you, you will not have gone through all the towns of Israel before the Son of Man comes.
The first phrase reiterates what Christ told the apostles earlier in verse 14: "And if anyone will not receive you or listen to your words, shake off the dust from your feet when you leave that house or town." The apostles were not looking for trouble. The advice is to spread the Gospel where people are interested in it, but not to argue and not to seek martyrdom — for there will be trouble and persecution enough.
Christ gives yet another reason for it here, though. He doesn't want them to waste time on hopeless causes, but to make reasonable haste. His death, resurrection and ascension are closer at hand than the apostles know, and they will be converting people in Israel long after Jesus is gone.
The teaching "a disciple is not above his master" seems to say something that it does not. Perhaps it came across more clearly in Aramaic, when Christ said it, but the plain meaning of the sentence in English simply is not what Christ meant. It sounds as if Christ has changed to a new topic of great importance; but this is misleading.
And so with discipleship. The servant is not above the master, and we know that the master will suffer an agonizing crucifixion. Who are the disciples, to expect better treatment than the very Son of God?
The illustration ("if they have called the master of the house Beelzebul") references one of the many accusations made in Chapter 9, that Jesus was able to cast out demons because he was in league with their boss, Satan. So all that the important-sounding "disciple is not above his teacher" is that the apostles should expect exactly the same problems, hostility, and accusations as Jesus himself had encountered. But, they should avoid persecution any greater than that of Christ.
They did manage to follow his advice; the first martyr, Stephen, was not stoned until after the crucifixion.


If you are one of those bloggers who check their stats every now and then (and still wonder where the heck are your visitors?), you have a friend in minekey.
Minekey is a recommendation service that aims to deliver highly personalized content recommendations to readers of blogs and websites based on what they are looking at or have read in the past.
And the obvious qn – why another recommender service?
Most companies in the recommendations space use collaborative filtering, which looks at aggregated data and "wisdom of crowds" rather than specific interests. Minekey's service integrates behavioral targeting, contextual matching, personalization affinity and the collective wisdom of the experts to ensure that users get content specifically relevant to their individual needs.
Once you have registered, you need to enter the feed id of sites that deliver the same sort of content (as yours). If you are wondering that this can potentially take your site visitor to competitor's page, don't worry. In that case, you can simply enter your own feed id and MineKey will deliver the content from your blog/site only. Once you are done with entering feed data, select the widget colors/type and you will get a custom code which you can install in your blog.
MineKey's USP is that it goes beyond using the meta keywords and post metadata; and infact uses behavioral data too to display the related posts. The business case for Minekey is very simple – too many bloggers writing too many posts, and as the guy who is reading a post, I get all related posts in one place. Contextually served. Period.
Though the current avatar has all the jazziness to attract bloggers to use the product, there are a few jaggy edges. For e.g. one cannot fully customize the widgets as one would like to (and that's why I had to remove the widget from this site, because I couldn't change the widget's header colors).
While I write this post, Minekey is presenting at AlwaysOn Stanford summit (they were the chosen company@ Proto too) and am sure they will gain good traction in the coming days.
If you are a serious blogger, I strongly suggest you to give Minekey a spin and share your comments,.


The extremely intricate process of rendering 3D heart models requires a coordinated effort across the highly specialized disciplines of radiology, congenital cardiology and engineering. Even within these fields the expertise required to generate a digital copy of a heart from medical images remains very limited, as such we are unable to meet all requests for model creation.
However, the primary goal of this library is to share and facilitate the growth of this amazing technology throughout the field of congenital cardiology. In an effort to efficiently manage these requests, it is necessary that all requests come through a physician member of the treating team. As mentioned above, this process requires a coordinated effort and details regarding patient privacy, image quality, pathology specific background, and intended purpose of the model creation (surgical planning, diagnostic, or educational) all play a critical role in the selection of cases where these limited resources can be applied.
We encourage families interested in this technology to discuss their thoughts with their cardiologist or surgeon. Members of the treatment team can contact Jump Simulation with information about the case. We will evaluate these requests efficiently. We relish the opportunity to discuss our work and encourage submission of cases as it is through direct patient impact that the greatest value of this technology will be fully realized.


text:
SPA contest from 1969
on October 23, 2019 in Features
John MacFadyen.
We received a query from a reader asking about the 1969 Scottish Pipers' Association (SPA) competition. The contest that year was notable as a new system of judging was tried out, one that saw five judges – Pipe Majors Donald MacLeod, Peter Bain and Hector MacLean, Lieut. John MacLellan and Mr Alfred Morrison – sit at separate tables and at the end of each performance rate the performance by holding up a mark.
The top and bottom marks were to be ignored and the other three averaged to arrive at a result.
The man behind the idea was the late John MacFadyen who was SPA President at the time. He was quoted in the Oban Times: "Although the system has not previously been tried in piping, a similar method of adjudication has been employed successfully in other aesthetic spheres familiar to most of us after the recent Olympic Games. So there seems no reason to suppose that it should not work for us.
"By trying out this system of judging we are merely attempting to get an order of merit in as unbiased a way as possible.
"We hope the competing pipers will support the experiment and that many non-competitors will be sufficiently interested to come along and see it in action."
The front cover of the programme. Click to enlarge.
The competition took place in the Woodside Halls, Glasgow on February 1 that year.
We checked our archives and found that the competition was reported (including the scores) in the following month's 1969 Piping Times. In his editorial comment, Seumas MacNeill declared the idea to be an "outstanding success" and one that was welcomed by what he termed the "most important and hitherto neglected section at a competition", the audience. There were less complaints about the results, probably due to the fact that now the audience knew in considerable detail just how the final result was arrived at.
Seumas wrote:
"The size of the audience reflected the value of this experiment. It would appear that large numbers can be attracted to listen to piping when they are no longer treated as children who can't be told the facts of piping life.
"A big round of congratulations is in order to the SPA for having the courage to break away from tradition, and a special thanks should be expressed to the competitors who risked all to make the experiment possible. Many well-known players did not take part, but it is to be hoped that they will come forward in large numbers next time.
"The biggest thanks however are due to the five judges, who had the bravery literally to stand up and be counted. Without men displaying such courage this milestone in the history of piping competitions could never have been reached."
Although considered a success, the format was never repeated.
The relevant pages from the March 1969 Piping Times pages which included John MacFadyen's report and the judges' scores are reproduced below. Click on them to enlarge.
The SPA is now in its centenary year and in the midst of its latest Knockout series for the Piping Times Trophy. The semi-finals for this event will take place on 8th February and 7th March, with the Final taking place on the 2nd May 2020. All SPA events are held at The National Piping Centre Otago Street.


The hills behind Malibu are a pretty magical place, and the perfect setting for Matt and Caitlin's summer wedding. The couple are old high school friends of mine (and high school sweethearts of each other's) and shooting their day was the perfect way to catch back up. While the guys went for a surf, Caitlin and her girls got ready at a local hotel and then we headed over to Saddlerock Ranch, a beautiful winery and venue. The grounds were gorgeous and the old oak and willow trees made for the perfect backdrops to shoot under.
Vows were said in an open field set against the local rolling hills. Matt's older brother married the couple in a very heartfelt and personal ceremony. After the big kiss I stole the couple away for a little photo tour of the property. This venue is truly built to shoot weddings, with incredible architecture and fun backdrops, like giant picture frames and doors to nowhere, placed throughout. There was more to shoot than we could ever imagine, but the sun was dipping low and it was time to get the couple back to their party.
As the last rays of light lit the sky, Matt and Caitlin had their first dance in a big open field backed by old oaks. It was beautiful and the perfect start to a night of dancing under the stars.


This online course describes patient barriers to care, innovations in healthcare, and education for those in refugee camps as well as for resettled refugees. This course also discusses refugee camp economies, local social entrepreneurship, and cross-cultural understanding. The contents of this course are relevant and essential to anyone interested in or planning to participate in a refugee camp.
This course is freely and publicly available. It is also part of the Certificate in Refugee Health. Enroll in the Refugee Health Certificate Program Through Global Health University.


Florence is the capital of Tuscany. Like every cities in Italy, it inherited an unbelievable richness in terms of culture and art. There is no better way to see Florence than driving a Maserati rented in Florence. Go directly to the Palazzo Vecchio where the masterpieces of Michelangelo, da Vinci and Bronzino are awaiting your visit. You cannot help gaping in admiration when facing them.
Then cross over the oldest bridge in Florence, the Ponte Vecchio, and admire the diamond cutters and goldsmiths that have replaced the tanneries and butcheries which used to decorate the bridge in the past. Exploring the city of Florence and discovering its attractive places will be much easier if you choose to rent a Maserati in Florence at GP Luxury car hire.
Renting a Maserati in Florence will enable you to travel all over the city and pay a visit to every attractive spots in the towns surrounding this city. Experience the thrill of driving a luxury car and head to Lucca. Apart from the original defensive walls which surround the city, take the time to visit the Palazzo Ducale, ancient residence of Maria Luisa of Borbone and Elisa Bonaparte.
The charming villas in Lucca are also worth to be visited. Then drive back to the city center and taste the delicious Tuscan food such as the bistecca alla Fiorentina or the minestra di fagioli at the restaurants. Since you are in Florence, you may as well have a try to a glass of Chianti and appreciate the gelato, the legendary ice cream that made this region so popular throughout the world.