text:
Q: Schema Based - Multitenant - Spring Boot I am trying to create minimalistic Schema Based - Multitenant - Spring Boot but I am getting following error. Application can be downloaded from GitHub https://github.com/ivoronline/spring_boot_db_multitenant
Error
Unable to instantiate specified multi-tenant connection provider [com.ivoronline.spring_boot_db_multitenant.config.TenantConnectionProvider]

application.properties
#spring.jpa.properties.hibernate.multiTenancy = SCHEMA
spring.jpa.properties.hibernate.multiTenancy                     = SCHEMA
spring.jpa.properties.hibernate.multi_tenant_connection_provider = com.ivoronline.spring_boot_db_multitenant.config.TenantConnectionProvider
spring.jpa.properties.hibernate.tenant_identifier_resolver       = com.ivoronline.spring_boot_db_multitenant.config.TenantIdentifierResolver

# JPA / HIBERNATE
spring.jpa.hibernate.ddl-auto = create

DataSourceConfig.java
@Configuration
public class DataSourceConfig {

      @Bean
      public DataSource dataSource()   {
        DataSourceBuilder dataSourceBuilder = DataSourceBuilder.create();
                          dataSourceBuilder.url("jdbc:postgresql://localhost:5432/multitenant");
                          dataSourceBuilder.username("postgres");
                          dataSourceBuilder.password("letmein");
                          dataSourceBuilder.driverClassName("org.postgresql.Driver");
        return            dataSourceBuilder.build();
      }

    }

TenantIdentifierResolver.java
@Component
public class TenantIdentifierResolver implements CurrentTenantIdentifierResolver {

  static final String DEFAULT_TENANT = "public";

  @Override
  public String resolveCurrentTenantIdentifier() {
    return "public";
  }

  @Override
  public boolean validateExistingCurrentSessions() {
    return true;
  }

}

TenantConnectionProvider.java
@Component
public class TenantConnectionProvider implements MultiTenantConnectionProvider {

  private DataSource datasource;

  public TenantConnectionProvider(DataSource dataSource) {
    this.datasource = dataSource;
  }

  @Override
  public Connection getAnyConnection() throws SQLException {
    return datasource.getConnection();
  }

  @Override
  public void releaseAnyConnection(Connection connection) throws SQLException {
    connection.close();
  }

  @Override
  public Connection getConnection(String tenantIdentifier) throws SQLException {
    final Connection connection = getAnyConnection();
    //connection.createStatement().execute(String.format("SET SCHEMA \"%s\";", tenantIdentifier));
    connection.createStatement().execute("SET Schema 'public'");
    return connection;
  }

  @Override
  public void releaseConnection(String tenantIdentifier, Connection connection) throws SQLException {
    //connection.createStatement().execute(String.format("SET SCHEMA \"%s\";", TenantIdentifierResolver.DEFAULT_TENANT));
    connection.createStatement().execute("SET Schema 'public'");
    releaseAnyConnection(connection);
  }

  @Override
  public boolean supportsAggressiveRelease() {
    return false;
  }

  @Override
  public boolean isUnwrappableAs(Class unwrapType) {
    return false;
  }

  @Override
  public <T> T unwrap(Class<T> unwrapType) {
    return null;
  }

}

A: Hibernate expects that property hibernate.multi_tenant_connection_provider defines either already initialized object or class name which Hibernate can instantiate. In your case TenantConnectionProvider class has no default constructor, thus Hibernate fails (moreover, you expect that TenantConnectionProvider is a spring component). There are typically two options to configure such Hibernate SPIs:

*

*Hibernate way - interact with spring context using ManagedBeanRegistry
public class TenantConnectionProvider implements MultiTenantConnectionProvider, ServiceRegistryAwareService {

    private ServiceRegistryImplementor serviceRegistry;

    // default constructor
    public TenantConnectionProvider() {
        super();
    }

    @Override
    public void injectServices(ServiceRegistryImplementor serviceRegistry) {
        this.serviceRegistry = serviceRegistry;
    }

    protected DataSource getDataSource() {
        return serviceRegistry.getService(ManagedBeanRegistry.class)
                .getBean(DataSource.class)
                .getBeanInstance();
    }

    ...

}

*spring-boot way - configure JPA properties in Java code:

@Bean
public HibernatePropertiesCustomizer tenantConnectionProviderCustomizer(TenantConnectionProvider tenantConnectionProvider) {
    return hibernateProperties -> {
        hibernateProperties.put(AvailableSettings.MULTI_TENANT_CONNECTION_PROVIDER, tenantConnectionProvider);
    };
}


text:
Sarah Cortes
WPersonal site
GGoogle Scholar
Escortes@ccs.neu.edu
MS, Boston University
AB, Harvard University
Sarah Cortes, MS, CISA, AAFS, is President of Inman Technology. She earned her undergraduate degree at Harvard University, and holds an MS from Boston University, in Computer Science, Information Security. She is in the Cybersecurity PhD program at Northeastern University's Khoury College of Computer Sciences and studied Forensic Science at Boston University Medical School. Her research focuses on the darknet, network security, criminal legal treaties (MLATs), and digital forensics.
Prior to undertaking her PhD, Sarah was a Senior Vice President for Security, IT Audit and Disaster Recovery at Putnam Investments, an investment management firm with over $400 billion in assets under management. She oversaw Putnam's recovery on 9/11 when then-parent company Marsh & McLennan's World Trade Center 99th floor data center was destroyed. She also supervised over 65 IT audits per year in that capacity. As a senior executive and later consultant for Putnam and other Fortune 500 firms, Sarah also had responsibility for major applications development, data center and other operations, staff and budgets. Before that, Sarah was a Sr. VP for Data Center and Security Operations with BNY Mellon Bank, a global investments company with $1.6 trillion in assets under management, previously a part of Shearson/Lehman/American Express.
Sarah has published articles on computer security, privacy, mutual criminal legal assistance treaties (MLATs), and the darknet, including MLAT.is World Treaty Cartel Internet Overlay for Digital Traffic Analytics, featured in the 2017 IEEE International Symposium on Technologies for Homeland Security (HST17). She regularly serves as a referee for Computers & Security Journal.
She has implemented numerous other computer applications. Together with Department Chair, Boston University School of Medicine, Department of Biomedical Forensic Sciences and former Cellmark lab director Dr. Robin Cotton et al., Sarah implemented the DNA Mixtures online tool, with a grant from the US Department of Justice. DNA Mixtures was highlighted in the Executive Office of the President, President's Council of Advisors on Science and Technology (PCAST), Report to the President: Forensic Science in Criminal Courts: Ensuring Scientific Validity of Feature-Comparison Methods in 2016.
A former analyst for the US Department of Energy, she led the National Institute for Science and Technology (NIST) Cybersecurity Working Group sub-team, as co-author of the 2014 NIST: Guidelines for Smart Grid Cyber Security: Vol. 2, Privacy and the Smart Grid, as well as the 2010 volume, that created the security and privacy laws section of the report. She served on the privacy use cases team for two years and the NIST cybersecurity working group (CSWG) on Smart Grid privacy for seven years. She has co-led Northeastern University Law School Legal Skills in Social Context (LSSC) clinics on surveillance law and online privacy tools and technology, as well as an MIT Co-Design Studio class at MIT Media Lab. She has helped draft data breach laws, and testified before the Massachusetts legislature and regulatory agencies.
In addition to her work on various industry standards bodies, Sarah serves on the IEEE (Institute of Electrical and Electronics Engineers) P1912 Privacy and Security Architecture for Consumer Wireless Devices Working Group. While completing her PhD, Sarah interns at the Alameda County Sheriff's Office Crime Lab in Digital and Multimedia Evidence. In her work to help end cyberstalking and abuse through technology, Sarah serves on the Boards of Emerge, the first Abuser Intervention Program (BIP), and Each One Teach One, dedicated to training for technology employment.
Hometown: Cambridge, Massachusetts
Field of Study: Information Assurance
PhD Advisor: Thomas H. Koenig
20,000 In League Under the Sea: Anonymous Communication, Trust, MLATs, and Undersea Cables
Aaron Jaggard, Aaron Johnson, Sarah Cortes, Paul Syverson, and Joan Feigenbaum, 20,000 in League Under the Sea, Anonymous Communication, Trust, MLATs, and Under-sea Cables, [pdf] Proceedings on Privacy Enhancing Technologies (PETS-15th Interna-tional Symposium). Volume 1, Issue 1, Pages 4–24, ISSN (Online) 2299-0984, DOI: 10.1515/popets-2015-0002, April 2015.
Motivated by the effectiveness of correlation attacks against Tor, the censorship arms race, and observations of malicious relays in Tor, we propose that Tor users capture their trust in network elements using probability distributions over the sets of elements observed by network adversaries. We present a modular system that allows users to efficiently and conveniently create such distributions and use them to improve their security. To illustrate this system, we present two novel types of adversaries. First, we study a powerful, pervasive adversary that can compromise an unknown number of Autonomous System organizations, Internet Exchange Point organizations, and Tor relay families. Second, we initiate the study of how an adversary might use Mutual Legal Assistance Treaties (MLATs) to enact surveillance. As part of this, we identify submarine cables as a potential subject of trust and incorporate data about these into our MLAT analysis by using them as a proxy for adversary power. Finally, we present preliminary experimental results that show the potential for our trust framework to be used by Tor clients and services to improve security.
MLAT Jiu-Jiutsu and Tor: Mutual Legal Assistance Treaties in Surveillance
Sarah Cortes, Legalizing Domestic Surveillance: The Role of Mutual Legal Assistance Treaties in Deanonymizing TorBrowser Technology, 22 Rich. J.L. & Tech. 2 (2015).
A corrupt Australian Law Enforcement Agency (LEA) wishes to track the communications of a journalist who has published leaked whistleblowing documents from a confidential source, revealing the Australian LEA's complicity in illegal narcotics activity. The target journalist lives in New York and is a U.S. citizen. She opens her laptop, goes online and fires up Tor Browser. She is communicating with her whistleblowing source in Australia, who faces death if his identity is uncovered. Her communication and network traffic passes through Tor relays in Canada, Finland, and Malaysia before arriving at her source in Australia.
MLAT World Treaty Cartel Internet Overlay for Digital Traffic Analytics
Cortes, Sarah. MLAT World Treaty Cartel Internet Overlay for Digital Traffic Analytics. MLAT.is, Proceedings of the 2017 IEEE International Symposium on Technologies for Homeland Security (HST17), 2017.
MLAT.is is a scalable service providing accurate predictions of treaty partner cooperating jurisdictions for internet routing and path selection algorithms. MLAT.is builds a structural model of all world jurisdictions. We have constructed an annotated map of world jurisdictions by treaty partners. We have related MLATs to the Internet and reviewed their impact. We have predicted risk impact by composing measured performance of clusters of known MLA treaty partners. This method allows us to accurately and efficiently predict the effects of MLAs on path selection risk between arbitrary Internet hosts. We have studied the feasibility and utility of the MLAT.is service by applying it to several representative overlay services in use today: undersea cables, anonymous network communications, and ASes. In each case, we observe that using MLAT.is's predictions leads to a significant improvement in end user performance.

redpajama_set_name: RedPajamaCommonCrawl


text:
< blurb about Jupyter Notebook extensions here and what we're doing >

### App Cell extension pattern
Detection
Initialization
Cell transformation

## 2. App Cell Widget as controller
Main controller
Finite State Machine

## 3. App Cell Tabs

### A. Configure Tab

### B. Job Status Tab

redpajama_set_name: RedPajamaGithub


text:
A chemical embrace from the perfect host
An industrial process that currently consumes vast amounts of energy in petrochemical plants around the globe could be replaced by an alternative process so efficient that it requires no heating or elevated pressure.
Niveen Khashab from KAUST's Advanced Membranes and Porous Materials Center and her colleagues have developed a new way to separate derivates of benzene, called xylenes.
"Discussions with industry to implement the technology are already underway," Khashab says.
Xylenes come in three different forms, known as isomers, which differ from each other only in the location of a single carbon atom. Xylenes are used in many large-scale applications, including in polymers, plastics and fibers, and as fuel additives, but many uses rely on just one of the three isomers. Because the isomers are so similar, their physical properties, such as boiling point, are very close. Thus, separating them requires a lot of energy.
"Every year, the global energy costs of separating these isomers using distillation is about 50 gigawatts, enough to power roughly 40 million homes," says Gengwu Zhang, a postdoc in Khashab's team and first author of the study. "We wanted to develop a method with high efficiency and low energy consumption to separate and purify these isomers for the petrochemical industry."


Separating your hands from your feet, or your upper-body from your lower-body is a skill that is often overlooked.
These programs are built in 8-week sessions that continue for a full year. Each player is put through a baselining process to determine exactly where they need to focus to improve. At the end of 8-weeks they are tested again and the process is re-tuned to help them achieve the most efficient gains. We accept a maximum of 20 athletes per session. Returning players (and Belleville Bearcats) players are given priority, both in entry to the program and on our waiting lists.
We are working on acquiring ice for a boys' program.


It's not amazing, and it's not surprising, but at the same time, it is. Something as harmless as an award for writing a children's book is such a threat to these people. It is a real threat. They're really irritated. They're really bothered by it. And they really think it's illegitimate.
The Associated Press even has a story. Snerdley found it. I don't read the AP. The AP is his responsibility. And he says, "Yeah, the AP, they've got this real long story," he said, "Rush, it doesn't matter. They spell your name right in it in every instance." Yeah, I know. But the AP didn't even know I had a book out. See, these people are the ones out of touch. They're the ones not aware of what's going on.
I've got two books in the current New York Times Top 10, the children's list. One's at number three, one's at number five. And they go back and forth. The second book, The First Patriots is at number three. Brave Pilgrims is at number five, and Pilgrims goes back and forth to four and five. But we've got two books and the first book has been on the list now for seven months, and it was number one for half of that time. They don't even know it. So I get the award and they're shocked. A children's book, Rush Limbaugh? And then they can't believe that it isn't political.
So AP has this long story today where they got hold of Robin Adelson, the Children's Book Council, and they just demand for her to admit that the vote was fraudulent. They just demand that she tell them that the vote was something they couldn't police and it really may not be legitimate. And she stands up for the vote. She explains how it all happens. She's really a gutsy woman because her friends are coming after her on this. She's holding firm, and she's trying to maintain the integrity and dignity of the organization she leads, that she's proud to lead.
The Children's Book Council is all about children's literacy. They've got a great objective and agenda. But the Drive-Bys are just obsessed with discrediting, 'cause they just can't accept, A, they didn't know it, B, they can't accept that people are buying it, C, they can't accept it would win an award. Now, I'm gonna tell you something, folks. I know that many of you are gonna be shouting back at your radio, "Why are you surprised? You're the one that's always telling us who these people are." I'm not surprised, but I do continue to learn.
America's conservatives, what they really believe. They really believe this three-eyed monster, all these stereotypes. And you can see the puzzlement on their face when you show up amongst 'em and you're not that.
They are really confused. It's not that they're mad. They're just genuinely confused. They really believe. Talk about the low-information crowd, this is it. They really believe what they've been told. They believe that over half of their fellow citizens are really subhuman, when you get right down to it, when you look at the things that they believe about conservatives.
So anything that upsets that applecart is difficult for them to process and comprehend. And so it can't be real. Therefore there has to be fraud involved or there has to be cheating involved. And of course that's just projection because that's in large part how they arrange things for themselves, stacking the deck, you name it. (interruption) Well, Dawn just said, "Wait 'til they see the stuffed Libertys on the shelves." There aren't any stuffed Libertys on the shelves yet. But this whole Rush Revere series is just in its infancy here.
They have no idea. And I could announce every day what we're gonna do and they would never know until it happened, unless, you know, some leftist media watchdog website happened to reprint what we said here. It's amazing how disconnected they are from the mainstream and the bloodstream and the heartbeat of this country. It is genuinely amazing how removed they are. I know I shouldn't be amazed, but I am.
Anyway, just a little sound bite to illustrate Drive-Bys all across the country reporting on Author of the Year. I mean, I knew it was gonna be sort of a big deal. I had no idea, folks. This just goes to show you, no matter how much you know, how much you learn, no matter how open you are to learning, as I am, the ability to be shocked and surprised never goes away.
And this award, children's book Author of the Year has just discombobulated these people. They're turning this into such a big story. We've got a little montage here of TV, a couple radio stations, just all across the country. This is a sample of, if you happen to be a Drive-By Media person or if you happen to be an average, ordinary American sampling media yesterday, you probably heard this.
NEAL BARTON: The winner of the Children's Choice Book Award for Author of the Year is Rush Limbaugh!
JULIA DUNN: Rush Limbaugh receives another award and this time it's thanks to fourth and fifth graders.
LARRY KANTER: Rush Limbaugh wins an award for his children's book.
MARIANNE MCCLARY: Conservative radio host Rush Limbaugh has won a children's book award. LimbaughÂ's book, titled, Rush Revere and the Brave Pilgrims, won the Children's Choice Book Award Author of the Year. The book has been a best seller.
RUSH: Can you imagine these leftists driving around hearing this, just in stunned shock? It's fun. Now, there were six or seven other winners. They had winners in categories by age, you know, books for 6- and 7-year-olds and then first and second graders. I forget all the categories. There's six or seven other winners. Have you heard about any of them? (interruption) You haven't? I mean, you saw 'em listed in your AP story? (interruption) You haven't? Yeah, you don't know who they are, right?
There's six or seven — well, it was funny because the one network that I've banned here and don't mention anymore devoted almost their whole day yesterday to the concept that voter fraud was involved here and that there is no way that I would ever win Book of the Year in a legitimate vote among kids. And it wasn't Book of the Year. It was Author of the Year. I didn't win the award for Book of the Year. The woman who wrote the book Divergent won that. She won Book of the Year. These idiots don't even know what they're talking about. They're so sent into orbit with all of this news.
So, anyway, life for me every day is an adult Christmas. I've been saying this for a long time. And this is another Christmas morning, winning this award, and the aftershock, it's like an earthquake. Everywhere there's a leftist. (interruption) Well, I know, wait 'til they find out teachers are letting it in the schools! Oh, wait 'til they find that out! And we're not in any danger of them finding it out because I say it here, 'cause they're not listening, folks, so don't worry about that.
Now, this next story is a classic example of something I have been talking about for… well, forever, but in an intense way in the recent past.
RUSH: Listen to this. You want to hear how funny this is, the AP story, this very, very long AP story on the potential illegitimate result that saw me win Author of the Year, Children's Book Council, the potentially illegitimate result. Listen to this from the AP story.
Quote, "An individual voter can vote multiple times and does not need to provide a verifiable e-mail address or proof of his or her age." You're kidding? The AP is outraged over no voter ID in the children's book awards? What, we have to have voter ID for the children's book awards but not for political office? Hmm. Yeah. You know, here's the thing. The left owns the awards industry, folks. This is the bottom line. They own it. They give themselves awards for things that people never see. This is famous for stuff that's on NPR and PBS.
Dan Rather got an award for his fake National Guard story. Tom Brokaw, Peter Jennings arranged a dinner to give Rather an award to try to save Rather and liberalism and the credibility of journalism after that hoax. And people like me are not supposed to win awards. That whole industry is for themselves. And something went wrong. And what went wrong is that actual citizens can vote in the award I happened to win, not just leftists.
"A book that landed high on the best-seller lists of Amazon.com and other outlets despite limited mainstream coverage." They're admitting they ignored it. They admit they don't review it, and yet it's there. And they're perplexed. Now, to you and me it's only common sense. You have the most popular, most listened to radio program in the country, to them it's not mainstream. It's so easy to tweak these people.
RUSH: Jennifer is in Floyd, Iowa. Hi, Jennifer. Great to have you here.
CALLER: Rush, congratulations on children's book Author of the Year. We are so excited to hear about that. We're just thrilled.
RUSH: Well, thank you. Thank you very much. I'll bet you were. My brother said, "You gotta understand, you winning is like everybody in your audience winning." It's a big deal. And when the word spread about having won the award, I was hearing from all kinds of people. I know that the written word is a very powerful thing. I've gotten more feedback on this book award than anything in a long time, and I was telling my brother, David, about it, said he said that's because everybody, they're excited for you that this has happened. And I guess he's got a point. So I thank you.
CALLER: I just had a comment to make, too. I just think that maybe the liberal media needs to talk to their own kids to find out what the popular books are out there.
RUSH: Yeah. I don't quite know how to express this. There are very few things, that I say it that way, as a professional communicator and as highly trained specialist and as one who's mastered brevity as the soul of wit. I generally don't have any problem saying what I want to say in as few words as possible. And I don't want to convey native, either, because I'm not. But despite all that, I still — and I shouldn't be. I mean, we should just be able to see what our Millennials believe to understand how easy it is to propagandize people. But I guess in my case, I'm here every day, 15 hours a week. How many hundreds of thousands of hours have I been doing this radio program? For 25 years.
You don't need a password to listen to this program. You don't need a secret decoder. All you have to do is find one of 600 radio stations or go to any number of websites and turn on the radio and listen to it. It's not a secret. It's not shortwave. It's not pirate radio. It's out there. And it's been the most listened to radio talk show in America for most of these 25 years, and yet, despite who I am every day on this program, the left has succeeded in turning me into a caricature and figure that I am nowhere near being, that millions of people really believe.
And it's not just about me. It's every conservative. And the things that they believe when you run into it, you see how shocked they are that you actually breathe air and don't walk into a room and start beating people up. I mean, it's a testament to see what these people have been convinced of, people on the left, what they have been made to believe. It's a stunning thing, each and every day.


text:
The Wild Hunt (https://wildhunt.org/2019/01/pagan-community-notes-reported-wiccan-accused-of-human-trafficking-comiss-network-and-more.html)
Pagan Community Notes: Reported "Wiccan" accused of human trafficking, COMISS Network, and more!
FREESTONE COUNTY, Texas – Last week, charges of human trafficking were filed against a woman that centered around a minor in her care in Mexia, Texas. The initial bond being set at $25,000, and one day later was increased to $250,000. There are reports that Amber Michelle Parker, allegedly had ties to a Witchcraft or Wicca groups. A Facebook account under the name Zhoe Singer displays a picture of Parker as well a number of memes and photos that contain "Witch" and "pentacle."
A report from news station KWTX contained a statement that Parker's husband had given to deputies investigating the case, "Mr. Parked explained that at some point during the year his wife had created an anonymous Facebook page to where she could secretly communicate with strange men associated with the Wicca organization," the document reads. "During the year his wife had left to go to Louisiana to meet with her healer and again to Waco to meet with someone in her group."
The news story goes on to say that members of the Wicca religion have come forward to dispel any connection to their beliefs and practices and the actions Parker is accused of, sex trafficking. The KWTX story did not list who contacted the station or reporter as representing the Wiccan or Pagan community. This is a developing story, TWH will continue to follow and report on any updates.
ARLINGTON, Virginia – The 2019 COMISS Network Forum, a national chaplaincy and specialized ministries conference is being held January 13 and 14 in Arlington, Virginia. Several Pagan leaders participated in the conference: representing Sacred Well Congregation–Rev. Ryan Adams, Officer-at-Large from Louisiana, representing Circle Sanctuary–Rev. Selena Fox, Senior Minister and Endorser from Wisconsin and Rev. Tim (Cern) Staker, Board Certified Hospital Chaplain from Indiana.
COMISS Network is a network of professional organizations, institutions, and faith communities engaged in theological and clinical education and competent practice of interfaith spiritual care through chaplaincy and spiritual counseling and research in specialized settings. Rev. Selena Fox also attended the Association of Religious Endorsing Bodies conference held January 11 and 12 at the same location.
[Courtesy Circle Sanctuary – Rev. Ryan Adams (left) Rev. Selena Fox (center) and Rev. Tim (Cern) Staker, (right)
Gregory Tillett, a native of Australia and a noted academic in Religious Studies, also holding a degree in Law in Australia, has died. He is best known for his research in Occult studies, particularly his work concerning C.W. Ledbetter and Theosophy. He was also a recognized authority on conflict resolution. He was ordained as a Priest in the Orthodox Church. When he retired from university work, and from an Australian federal appellate Tribunal, he became a hermit in the Orthodox tradition. What is remembered, lives.
The Pagan Heart of the West: Embodying Ancient Beliefs and Practices from Antiquity to the Present, Vol I. Deities and Kindred Beings by Randy P. Connor is the first of five volumes and due to be released next week by Mandrake of Oxford.
Waking the Witch exhibit to open on January 19 at 20-21 Visual Arts Centre in Scunthorpe in the UK. The display will highlight the British Isles' strong relationship to magic and the occult. "…it looks to the importance of craft, ritual and land on the practice of the ever shifting figure of the witch."
In the Heart of the Beast (HOBT) Puppet and Mask Theatre announced last week that this year would mark the final May Day parade in Minneapolis. This will be the 45th year for the event. Corrie Zoll, HOBT's executive director said it was possible that the festival might continue beyond this year but that HOBT could no longer financially afford to be sole sponsor of the event. An online petition has been created in attempts to save the festival.
Circle Sanctuary announced that the 2019 Pagan Spirit Gathering (PSG) has officially opened registration for the Summer Solstice Festival, occurring June 16 – 23 at Hannon's Camp America, near Oxford Ohio.
Tarot of the week by Star Bustamonte
Deck: Black Cat Tarot by Maria Kurara, published by Lo Scarabeo
Card: Five (5) Wands
Look for opportunities to gain greater understanding of one's own skills and deeper nature this week. There is emphasis on fairness in competition with an eye towards building the future.
The Wild Hunt
Circle Sanctuary
George Tillett
Selena Fox
The Wild Hunt is a daily, nonprofit news journal serving the collective Pagan, Heathen and Polytheist communities worldwide. Follow us each day to stay up to date with the latest news and commentary.
Unleash the Hounds: Archaeology Edition


text:
Cryptogenic fibrosing alveolitis, diffuse fibrosing alveolitis, usual interstitial pneumonitis[1]
Figure A shows the location of the lungs and airways in the body. The inset image shows a detailed view of the lung's airways and air sacs in cross-section.
Figure B shows fibrosis (scarring) in the lungs. The inset image shows a detailed view of the fibrosis and how it damages the airways and air sacs.[1]
Shortness of breath, dry cough[1]
Pulmonary hypertension, heart failure, pneumonia, pulmonary embolism[1]
Usual onset
Gradual[1]
Unknown[2]
Cigarette smoking, certain viral infections, family history[1]
Diagnostic method
CT scan, lung biopsy[3]
Sarcoidosis, other interstitial lung diseases, hypersensitivity pneumonitis[4]
Pulmonary rehabilitation, supplemental oxygen, lung transplantation[1]
Pirfenidone, nintedanib[2]
Life expectancy ~ 4 years[1]
12 per 100,000 people per year[4]
Idiopathic pulmonary fibrosis (IPF) is a type of chronic lung disease characterized by a progressive and irreversible decline in lung function.[3][4] Symptoms typically include gradual onset of shortness of breath and a dry cough.[1] Other changes may include feeling tired and abnormally large and dome shaped nails (nail clubbing).[1] Complications may include pulmonary hypertension, heart failure, pneumonia, or pulmonary embolism.[1]
The cause is unknown.[2] Risk factors include cigarette smoking, certain viral infections, and a family history of the condition.[1] The underlying mechanism involves scarring of the lungs.[1] Diagnosis requires ruling out other potential causes.[3] It may be supported by a CT scan or lung biopsy which show usual interstitial pneumonia (UIP).[3] It is a type of interstitial lung disease (ILD).[3]
People often benefit from pulmonary rehabilitation and supplemental oxygen.[1] Certain medications like pirfenidone or nintedanib may slow the progression of the disease.[2] Lung transplantation may also be an option.[1]
About 5 million people are affected globally.[5] The disease newly occurs in about 12 per 100,000 people per year.[4] Those in their 60s and 70s are most commonly affected.[4] Males are affected more often than females.[4] Average life expectancy following diagnosis is about four years.[1]
1 Signs and symptoms
4.1 Differential diagnosis
4.2 Classification
4.3 Radiology
4.4 Histology
4.5 Bronchoalveolar lavage
4.6 Pulmonary function tests
5.1 Oxygen therapy
5.2 Pulmonary rehabilitation
5.3 Medications
5.3.1 Pirfenidone
5.3.2 N-acetylcysteine and triple therapy
5.3.3 Nintedanib
5.4 Lung transplantation
5.5 Palliative care
5.6 Follow-up
5.7 Acute exacerbations
6 Prognosis
8 Other animals
Signs and symptoms[edit]
Clubbing of the fingers in idiopathic pulmonary fibrosis
Lung sound in IPF
velcro crackles on auscultation in a person with IPF
In many people, symptoms are present for a considerable time before diagnosis.[5] The most common clinical features of IPF include the following:[3][6][7]
Age over 50 years
Dry, non-productive cough on exertion
Progressive exertional dyspnea (shortness of breath with exercise)
Dry, inspiratory bibasilar "velcro-like" crackles on auscultation (a crackling sound in the lungs during inhalation similar to Velcro being torn apart slowly, heard with a stethoscope).[3][8][9]
Clubbing of the digits, a disfigurement of the finger tips or toes (see image)
Abnormal pulmonary function test results, with evidence of restriction and impaired gas exchange.
Some of these features are due to chronic hypoxemia (oxygen deficiency in the blood), are not specific for IPF, and can occur in other pulmonary disorders. IPF should be considered in all patients with unexplained chronic exertional dyspnea who present with cough, inspiratory bibasilar crackles, or finger clubbing.[3]
Assessment of "velcro" crackles on lung auscultation is a practical way to improve the earlier diagnosis of IPF. Fine crackles are easily recognized by clinicians and are characteristic of IPF.[10]
If bilateral fine crackles are present throughout the inspiratory time and are persisting after several deep breaths, and if remaining present on several occasions several weeks apart in a subject aged ≥60 years, this should raise the suspicion of IPF and lead to consideration of an HRCT scan of the chest which is more sensitive than a chest X-ray.[9] As crackles are not specific for IPF, they must prompt a thorough diagnostic process.[3]
The cause of IPF is unknown but certain environmental factors and exposures have been shown to increase the risk of getting IPF.[11] Cigarette smoking is the best recognized and most accepted risk factor for IPF, and increases the risk of IPF by about twofold.[11] Other environmental and occupation exposures such as exposure to metal dust, wood dust, coal dust, silica, stone dust, biologic dusts coming from hay dust or mold spores or other agricultural products, and occupations related to farming/livestock have also been shown to increase the risk for IPF.[11] There is some evidence that viral infections may be associated with idiopathic pulmonary fibrosis and other fibrotic lung diseases.[12]
Pathogenesis[edit]
Despite extensive investigation, the cause of IPF remains unknown.[3] The fibrosis in IPF has been linked to cigarette smoking, environmental factors (e.g. occupational exposure to gases, smoke, chemicals or dusts), other medical conditions including gastroesophageal reflux disease (GERD), or to genetic predisposition (familial IPF). However, none of these is present in all people with IPF and therefore do not provide a completely satisfactory explanation for the disease.[3][13]
IPF is believed to be the result of an aberrant wound healing process including/involving abnormal and excessive deposition of collagen (fibrosis) in the pulmonary interstitium with minimal associated inflammation.[14]
It is hypothesized that the initial or repetitive injury in IPF occurs to the lung cells, called alveolar epithelial cells (AECs, pneumocytes), which line the majority of the alveolar surface.[15] When type I AECs are damaged or lost, it is thought that type II AECs undergo proliferation to cover the exposed basement membranes. In normal repair, the hyperplastic type II AECs die and the remaining cells spread and undergo a differentiation process to become type I AECs. Under pathologic conditions and in the presence of transforming growth factor beta (TGF-β), fibroblasts accumulate in these areas of damage and differentiate into myofibroblasts that secrete collagen and other proteins.[15] In the past, it was thought that inflammation was the first event in initiating lung tissue scarring. Later findings showed that the development of fibroblastic foci precedes the accumulation of inflammatory cells and the consequent deposition of collagen.[16] This pathogenetic model is indirectly supported by the clinical features of IPF, including an insidious onset over several years, relatively infrequent acute exacerbations, and failure to respond to immunosuppressive therapy.[14][17] A number of therapies that target fibroblast activation or the synthesis of extracellular matrix are currently in early testing or are being considered for development.
Familial IPF accounts for less than 5% of the total of patients with IPF and is clinically and histologically indistinguishable from sporadic IPF.[3] Genetic associations include mutations in pulmonary surfactant proteins A1, A2, C (SFTPA1, SFTPA2B) and mucin (MUC5B).[18] A remarkable aspect of the MUC5B variant is its high frequency of detection, as it is found in approximately 20% of individuals with Northern and Western European ancestry and in 19% of the Framingham Heart Study population.[19] Mutations in human telomerase genes are also associated with familial pulmonary fibrosis and in some patients with sporadic IPF (e.g. the TERT, TERC genes).[18] Recently an X-linked mutation in a third telomerase-associated gene, dyskerin (DKC1), has been described in a family with IPF.[20][unreliable medical source?]
Diagnosis[edit]
An earlier diagnosis of IPF is a prerequisite for earlier treatment and, potentially, improvement of the long-term clinical outcome of this progressive and ultimately fatal disease.[3] If IPF is suspected, diagnosis can be challenging but a multidisciplinary approach involving a pulmonologist, radiologist and pathologist expert in interstitial lung disease has been shown to improve the accuracy of IPF diagnosis.[3][21][22]
A Multidisciplinary Consensus Statement on the Idiopathic Interstitial Pneumonias published by the American Thoracic Society (ATS) and the European Respiratory Society (ERS) in 2000 proposed specific major and minor criteria for establishing the diagnosis of IPF.[3] However, in 2011, new simplified and updated criteria for the diagnosis and management of IPF were published by the ATS, ERS, together with the Japanese Respiratory Society (JRS) and Latin American Thoracic Association (ALAT).[3] Currently, a diagnosis of IPF requires:
Exclusion of known causes of ILD, e.g., domestic and occupational environmental exposures, connective tissue disorders, or drug exposure/toxicity
The presence of a typical radiological pattern of usual interstitial pneumonia (UIP) on high-resolution computed tomography (HRCT).
In the right clinical setting, it is possible to make the diagnosis of IPF by HRCT alone, obviating the need for surgical lung biopsy.[3][6]
Differential diagnosis[edit]
Recognizing IPF in clinical practice can be challenging as symptoms often appear similar to those of more common diseases, such as asthma, chronic obstructive pulmonary disease (COPD) and congestive heart failure (www.diagnoseipf.com). The key issue facing clinicians is whether the presenting history, symptoms (or signs), radiology, and pulmonary function testing are collectively in keeping with the diagnosis of IPF or whether the findings are due to another process. It has long been recognized that patients with ILD related to asbestos exposure, drugs (such as chemotherapeutic agents or nitrofurantoin), rheumatoid arthritis and scleroderma/systemic sclerosis may be difficult to distinguish from IPF. Other differential diagnostic considerations include interstitial lung disease related to mixed connective tissue disease, advanced sarcoidosis, chronic hypersensitivity pneumonitis, pulmonary Langerhan's cell histiocytosis and radiation-induced lung injury.[3][6]
Classification[edit]
Classification of IIPs.[6]
Idiopathic pulmonary fibrosis (IPF) belongs to a large group of more than 200 lung diseases known as interstitial lung diseases (ILDs), which are characterized by the involvement of the lung interstitium,[6] the tissue between the air sacs of the lung. IPF is one specific presentation of idiopathic interstitial pneumonia (IIP), which is in turn a type of ILD, also known as diffuse parenchymal lung disease (DPLD).
The 2002 American Thoracic Society/European Respiratory Society (ATS/ERS) classification of IIPs was updated in 2013.[6] In this new classification there are three main categories of idiopathic interstitial pneumonias (IIPs): major IIPs, rare IIPs, and unclassifiable IIPs. The major IIPs are grouped into chronic fibrosing IPs (this includes IPF and non-specific interstitial pneumonia [NSIP]); smoking-related IPs (i.e. respiratory bronchiolitis–interstitial lung disease [RB-ILD] and desquamative interstitial pneumonia [DIP]); and acute/subacute IPs (i.e. cryptogenic organizing pneumonia [COP] and acute interstitial pneumonia [AIP]).[6]
The diagnosis of IIPs requires exclusion of known causes of ILD. Examples of ILD of known cause include hypersensitivity pneumonitis, pulmonary Langerhan's cell histiocytosis, asbestosis, and collagen vascular disease. However, these disorders frequently affect not only the interstitium, but also the airspaces, peripheral airways, and blood vessels.[6]
Radiology[edit]
Chest X-rays are useful in the follow up routine of IPF patients. Plain chest X-rays are unfortunately not diagnostic but may reveal decreased lung volumes, typically with prominent reticular interstitial markings near the lung bases.[3]
A chest radiograph of a patient with IPF. Note the small lung fields and peripheral pattern of reticulonodular opacification.
The radiological evaluation through HRCT is an essential point in the diagnostic pathway in IPF. HRCT is performed using a conventional computed axial tomographic scanner without injection of contrast agents. Evaluation slices are very thin, 1–2 mm.
Typical HRCT of the chest of IPF demonstrates fibrotic changes in both lungs, with a predilection for the bases and the periphery. According to the joint ATS/ERS/JRS/ALAT 2011 guidelines, HRCT is an essential component of the diagnostic pathway in IPF which can identify UIP by the presence of:[3]
Reticular opacities, often associated with traction bronchiectasis
Honeycombing manifested as cluster cystic airspaces, typically of comparable diameters (3–10 mm) but occasionally large. Usually sub-pleural and characterized by well-defined walls and disposed in at least two lines. Generally one line of cysts is not sufficient to define honeycombing
Ground-glass opacities are common but less extensive than the reticulation
Distribution characteristically basal and peripheral though often patchy.
High-resolution computed tomography scans of the chest of a patient with IPF. The main features are of a peripheral, predominantly basal pattern of coarse reticulation with honeycombing
Histology[edit]
According to the updated 2011 guidelines, in the absence of a typical UIP pattern on HRCT, a surgical lung biopsy is required for confident diagnosis.[3]
Histologic specimens for the diagnosis of IPF must be taken at least in three different places and be large enough that the pathologist can comment on the underlying lung architecture. Small biopsies, such as those obtained via transbronchial lung biopsy (performed during bronchoscopy) are usually not sufficient for this purpose. Hence, larger biopsies obtained surgically via a thoracotomy or thoracoscopy are usually necessary.[3][6]
Lung tissue from people with IPF usually show a characteristic histopathologic UIP pattern and is therefore the pathologic counterpart of IPF.[3] Although a pathologic diagnosis of UIP often corresponds to a clinical diagnosis of IPF, a UIP histologic pattern can be seen in other diseases as well, and fibrosis of known origin (rheumatic diseases for example).[1][3] There are four key features of UIP including interstitial fibrosis in a 'patchwork pattern', interstitial scarring, honeycomb changes and fibroblast foci.
Fibroblastic foci are dense collections of myofibroblasts and scar tissue and, together with honeycombing, are the main pathological findings that allow a diagnosis of UIP.
Photomicrograph of the histopathological appearances of usual interstitial pneumonia. High-power magnification (on the right) shows a focus of fibroblastic proliferation, close to an area of fibrosis within which a mild, non-specific, chronic inflammatory cell infiltrate can be observed. In the subpleural space, a typical honeycombing aspect can be recognized.
Bronchoalveolar lavage[edit]
Bronchoalveolar lavage (BAL) is a well-tolerated diagnostic procedure in ILD.[7] BAL cytology analyses (differential cell counts) should be considered in the evaluation of patients with IPF at the discretion of the treating physician based on availability and experience at their institution. BAL may reveal alternative specific diagnoses: malignancy, infections, eosinophilic pneumonia, histiocytosis X, or alveolar proteinosis. In the evaluation of patients with suspected IPF, the most important application of BAL is in the exclusion of other diagnoses. Prominent lymphocytosis (>30%) generally allows excluding a diagnosis of IPF.[23]
Pulmonary function tests[edit]
Spirometry classically reveals a reduction in the vital capacity (VC) with either a proportionate reduction in airflows, or increased airflows for the observed vital capacity. The latter finding reflects the increased lung stiffness (reduced lung compliance) associated with pulmonary fibrosis, which leads to increased lung elastic recoil.[24]
Measurement of static lung volumes using body plethysmography or other techniques typically reveals reduced lung volumes (restriction). This reflects the difficulty encountered in inflating the fibrotic lungs.
The diffusing capacity for carbon monoxide (DLCO) is invariably reduced in IPF and may be the only abnormality in mild or early disease. Its impairment underlies the propensity of patients with IPF to exhibit oxygen desaturation with exercise which can also be evaluated using the 6-minute walk test (6MWT).[3]
Terms such as 'mild', 'moderate', and 'severe' are sometimes used for staging disease and are commonly based on resting pulmonary function test measurements.[3] However, there is no clear consensus regarding the staging of IPF patients and what are the best criteria and values to use. Mild-to-moderate IPF has been characterized by the following functional criteria:[25][26][27][28]
Forced Vital Capacity (FVC) of ≥50%
DLCO of ≥30%
6MWT distance ≥150 meters.
Treatment[edit]
The goals of treatment in IPF are essentially to reduce the symptoms, stop disease progression, prevent acute exacerbations, and prolong survival. Preventive care (e.g. vaccinations) and symptom-based treatment should be started early in every patient.[29]
Oxygen therapy[edit]
In the 2011 IPF guidelines, oxygen therapy, or supplementary oxygen for home use, became a strong recommendation for use in those patients with significantly low oxygen levels at rest. Although oxygen therapy has not been shown to improve survival in IPF, some data indicate an improvement in exercise capacity.[3][30]
Pulmonary rehabilitation[edit]
Fatigue and loss of muscular mass are common and disabling problems for patients with IPF. Pulmonary rehabilitation may alleviate the overt symptoms of IPF and improve functional status by stabilizing and/or reversing the extrapulmonary features of the disease.[31][32] The number of published studies on the role of pulmonary rehabilitation in idiopathic pulmonary fibrosis is small, but most of these studies have found significant short-term improvements in functional exercise tolerance, quality of life, and dyspnea on exertion.[33] Typical programs of rehabilitation include exercise training, nutritional modulation, occupational therapy, education and psychosocial counseling. In the late phase of disease, IPF patients tend to discontinue physical activity due to increasing dyspnea. Whenever possible, this should be discouraged.
Medications[edit]
A number of treatments have been investigated in the past for IPF, including interferon gamma-1β,[34] bosentan,[35] ambrisentan,[36] and anticoagulants,[37] but these are no longer considered effective treatment options. Many of these earlier studies were based on the hypothesis that IPF is an inflammatory disorder.
Pirfenidone[edit]
A Cochrane review comparing pirfenidone with placebo, found a reduced risk of disease progression by 30%.[38] FVC or VC was also improved, even if a mild slowing in FVC decline could be demonstrated only in one of the two CAPACITY trials.[25] A third study, which was completed in 2014 found reduced decline in lung function and IPF disease progression.[27] The data from the ASCEND study were also pooled with data from the two CAPACITY studies in a pre-specified analysis which showed that pirfenidone reduced the risk of death by almost 50% over one year of treatment.[27]
N-acetylcysteine and triple therapy[edit]
N-Acetylcysteine (NAC) is a precursor to glutathione, an antioxidant. It has been hypothesized that treatment with high doses of NAC may repair an oxidant–antioxidant imbalance that occurs in the lung tissue of patients with IPF. In the first clinical trial of 180 patients (IFIGENIA), NAC was shown in previous study to reduce the decline in VC and DLCO over 12 months of follow-up when used in combination with prednisone and azathioprine (triple therapy).[39]
More recently, a large randomized, controlled trial (PANTHER-IPF) was undertaken by the National Institutes of Health (NIH) in the USA to evaluate triple therapy and NAC monotherapy in IPF patients. This study found that the combination of prednisone, azathioprine, and NAC increased the risk of death and hospitalizations[40] and the NIH announced in 2012 that the triple-therapy arm of the PANTHER-IPF study had been terminated early.[41]
This study also evaluated NAC alone and the results for this arm of the study were published in May 2014 in the New England Journal of Medicine, concluding that "as compared with placebo, acetylcysteine offered no significant benefit with respect to the preservation of FVC in patients with idiopathic pulmonary fibrosis with mild-to-moderate impairment in lung function".[42]
Nintedanib[edit]
Nintedanib is a triple angiokinase inhibitor that targets receptor tyrosine kinases involved in the regulation of angiogenesis: fibroblast growth factor receptor (FGFR), platelet-derived growth factor receptor (PDGFR), and vascular endothelial growth factor receptor (VEGFR),[43] which have also been implicated in the pathogenesis of fibrosis and IPF. In both phase III trials, nintedanib reduced the decline in lung function by approximately 50% over one year.[28] It was approved by the US FDA in October 2014[44] and authorised in Europe in January 2015.[45]
Lung transplantation[edit]
Lung transplantation may be suitable for those patients physically eligible to undergo a major transplant operation. In IPF patients, lung transplant has been shown to reduce the risk of death by 75% as compared with patients who remain on the waiting list.[46] Since the introduction of the lung allocation score (LAS), which prioritizes transplant candidates based on survival probability, IPF has become the most common indication for lung transplantation in the USA.[31]
Symptomatic patients with IPF younger than 65 years of age and with a body mass index (BMI) ≤26 kg/m2 should be referred for lung transplantation, but there are no clear data to guide the precise timing for LTx. Although controversial, the most recent data suggest that bilateral lung transplantation is superior to single lung transplantation in patients with IPF.[47] Five-year survival rates after lung transplantation in IPF are estimated at between 50 and 56%.[3][48][49]
Palliative care[edit]
Palliative care focuses on reducing symptoms and improving the comfort of patients rather than treating the disease. This may include treatment of worsening symptoms with the use of chronic opioids for severe dyspnea and cough. Further, oxygen therapy may be useful for palliation of dyspnea in hypoxemic patients.
Palliative care also includes relief of physical and emotional suffering and psychosocial support for patients and caregivers.[3] With disease progression, patients may experience fear, anxiety and depression and psychological counseling should therefore be considered. In a recent study of outpatients with ILDs, including IPF, depression score, functional status (as assessed by walk test), as well as pulmonary function, all contributed to the severity of dyspnea.[50]
In selected cases of particularly severe dyspnea morphine could be considered. It can reduce dyspnea, anxiety and cough without significant decrease in oxygen saturation.[51]
Follow-up[edit]
IPF is often misdiagnosed, at least until physiological and/or imaging data suggest the presence of an ILD leading to delay in accessing appropriate care.[31] Considering that IPF is a disease with a median survival of three years after diagnosis, early referral to a center with specific expertise should therefore be considered for any patient with suspected or known ILD. On the basis of the complex differential diagnostic, multidisciplinary discussion between pulmonologists, radiologists, and pathologists experienced in the diagnosis of ILD is of the utmost importance to an accurate diagnosis.[3]
After diagnosis of IPF, and the appropriate treatment choice according to symptoms and stage of disease, a close follow-up should be applied. Due to the high variable course of disease, the higher incidence of complications such as lung cancer (up to 25% of patients has been reported in IPF) a routine evaluation every 3 to 6 months, including spirometry (body plethysmography), diffusion capacity testing, chest X-rays, 6MWT, assessment of dyspnea, quality of life, oxygen requirement is mandatory.
In addition, the increasing awareness of complications and common concomitant conditions frequently associated with IPF requires a routinely evaluation of comorbidities, most of them simply reflecting concurrent diseases of aging, and medications with their interaction and side effects.
Acute exacerbations[edit]
Acute exacerbations of IPF (AE-IPF) are defined as an unexplained worsening or development of dyspnea within 30 days with new radiological infiltrates at HRCT abnormality often superimposed on a background consistent with UIP pattern. The yearly incidence of AE-IPF is between 10 and 15% of all patients. The prognosis of AE-IPF is poor, with mortality ranging from 78% to 96%.[52] Other causes of AE-IPF such as pulmonary embolism, congestive heart failure, pneumothorax, or infection need to be excluded. Pulmonary infection have to be ruled out by endotracheal aspirate or BAL.
Many patients experiencing acute deterioration require intensive care treatment, particularly when respiratory failure is associated with hemodynamic instability, significant comorbidities or severe hypoxemia.[53] However, mortality during hospitalization is high.[52] Mechanical ventilation should be introduced only after carefully weighing the patient's long-term prognosis and, whenever possible, the patient's wishes. However, current guidelines discourage the use of mechanical ventilation in patients with respiratory failure secondary to IPF.[3]
Prognosis[edit]
Comparison of the 5-year survival rate for IPF and common malignancies. Adapted from Bjoraker et al. 1998.[54]
The clinical course of IPF can be unpredictable.[3][54][55] IPF progression is associated with an estimated median survival time of 2 to 5 years following diagnosis.[1][3] The 5-year survival for IPF ranges between 20–40%,[55] a mortality rate higher than that of a number of malignancies, including colon cancer, multiple myeloma and bladder cancer.[54][55]
Recently a multidimensional index and staging system has been proposed to predict mortality in IPF.[56] The name of the index is GAP and is based on gender [G], age [A], and two lung physiology variables [P] (FVC and DLCO that are commonly measured in clinical practice to predict mortality in IPF. The highest stage of GAP (stage III) has been found to be associated with a 39% risk of mortality at 1 year.[56] This model has also been evaluated in IPF and other ILDs and shown good performance in predicting mortality in all main ILD subtypes. A modified ILD-GAP Index has been developed for application across ILD subtypes to provide disease-specific survival estimates.[57] In IPF patients, the overall mortality at 5 years rate is high but the annual rate of all-cause mortality in patients with mild to moderate lung impairment is relatively low. This is the reason why change in lung function (FVC) is usually measured in 1-year clinical trials of IPF treatments rather than survival.[58]
In addition to clinical and physiological parameters to predict how rapidly patients with IPF might progress, genetic and molecular features are also associated with IPF mortality. For example, it has been shown that IPF patients who have a specific genotype in the mucin MUC5B gene polymorphism (see above) experience slower decline in FVC and significantly improved survival.[59][60] Even if such data are interesting from a scientific point of view, the application in the clinical routine of a prognostic model based on specific genotypes is still not possible.
Epidemiology[edit]
Although rare, IPF is the most common form of IIP.[6] The prevalence of IPF has been estimated between 14.0 and 42.7 per 100,000 persons based on a USA analysis of healthcare claims data, with variation depending on the case definitions used in this analyses.[8][61] IPF is more common in men than in women and is usually diagnosed in people over 50 years of age.[3]
The incidence of IPF is difficult to determine as uniform diagnostic criteria have not been applied consistently.[3][8] A recent study from the USA estimated the incidence of IPF to be between 6.8 and 16.3 per 100,000 persons. In the 27 European Union countries, a range of sources estimate an incidence of 4.6–7.4 people per 100,000 of the population,[62][63] suggesting that approximately 30,000–35,000 new patients will be diagnosed with IPF each year.[61][64]
A recent single-centre, retrospective, observational cohort study including incident patients diagnosed with ILD at Aarhus University Hospital (Denmark) between 2003 and 2009 revealed an incidence of 4.1 per 100,000 inhabitants/year for ILD. IPF was the most common diagnosis (28%) followed by connective tissue disease-related ILD (14%), hypersensitivity pneumonitis (7%) and non-specific interstitial pneumonia (NSIP) (7%). IPF incidence was 1.3 per 100,000 inhabitants/year.[65]
Due to a heterogeneous distribution of the disease across European countries, epidemiological data needs to be updated through a Europe-wide registry for ILD and IPF.
Other animals[edit]
IPF has been recognized in several breeds of both dogs and cats,[66] and has been best characterized in West Highland White Terriers.[67] Veterinary patients with the condition share many of the same clinical signs as their human counterparts, including progressive exercise intolerance, increased respiratory rate, and eventual respiratory distress.[68] Prognosis is generally poor.
A number of agents are currently being investigated in Phase II clinical trials for IPF, including the monoclonal antibodies simtuzumab, tralokinumab, lebrikizumab and FG-3019, a lysophosphatidic acid receptor antagonist (BMS-986020). A Phase II study of STX-100 is also ongoing.[69] These molecules are directed against several growth factors and cytokines that are known to play a role in the proliferation, activation, differentiation or inappropriate survival of fibroblasts.
mir-29 microRNA precursor investigations in mice have produced reversal of induced IPF. MRG-201 is currently being tested as-of 2016, but not in IPF patients yet, and no human trials for IPF use have been scheduled as-of January, 2016.[70]
Stem cell therapies for IPF are an area of research.[71][72]
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ICD-10: J84.112
ICD-9-CM: 516.31
OMIM: 178500
MeSH: D011658
DiseasesDB: 4815
MedlinePlus: 000069
eMedicine: radio/873
Patient UK: Idiopathic pulmonary fibrosis
Wikimedia Commons has media related to Idiopathic pulmonary fibrosis.
Idiopathic pulmonary fibrosis at Curlie
Diseases of the respiratory system (J, 460–519)
Upper RT
(including URTIs,
common cold)
sinuses
Vasomotor rhinitis
Nasal polyp
Rhinorrhea
nasal septum
Nasal septum deviation
Nasal septum perforation
Nasal septal hematoma
Adenoid hypertrophy
Laryngopharyngeal reflux (LPR)
Laryngomalacia
Laryngeal cyst
Laryngospasm
vocal folds
Vocal fold nodule
Vocal fold paresis
Vocal cord dysfunction
Laryngotracheal stenosis
Lower RT/lung disease
(including LRTIs)
Bronchial/
Acute exacerbations of chronic bronchitis
Acute exacerbation of COPD
Emphysema)
Asthma (Status asthmaticus
Aspirin-induced
Exercise-induced
Diffuse panbronchiolitis
Interstitial/
restrictive
(fibrosis)
External agents/
Aluminosis
Baritosis
Bauxite fibrosis
Chalicosis
Coalworker's pneumoconiosis
Talcosis
Hypersensitivity pneumonitis
Bagassosis
Lycoperdonosis
Combined pulmonary fibrosis and emphysema
Löffler's syndrome/Eosinophilic pneumonia
Hamman-Rich syndrome
Obstructive or
Pneumonia/
pneumonitis
By pathogen
Pneumococcal
Klebsiella)
Atypical bacterial
Chlamydiae
Pneumocystis
noninfectious
Chemical/Mendelson's syndrome
Aspiration/Lipid
By vector/route
Community-acquired
Healthcare-associated
Hospital-acquired
By distribution
Broncho-
BOOP-COP
NSIP
Pleural cavity/
Pleuritis/pleurisy
Pneumothorax/Hemopneumothorax
Empyema/pyothorax
Fibrothorax
Mediastinal disease
Other/general
Idiopathic pulmonary haemosiderosis
Retrieved from "https://en.wikipedia.org/w/index.php?title=Idiopathic_pulmonary_fibrosis&oldid=904934357"
Respiratory diseases principally affecting the interstitium
Idiopathic diseases
Articles lacking reliable references from June 2019
Articles with Curlie links


A hand crafted Yixing teapot in a modern style Ban Piao shape by artist Wu Hong Cai. In the box: teapot, 2 cups, certificate from artist.
Fully crafted by hand in a Ban Piao shape which was originally created by Man Sheng Chen during the Qing dynasty.
The teapot is stamped with the name of the artist Wu Hong Cai.
The filter inside the spout has more than a hundred small holes to make sure it keeps the smallest leaves inside the pot, while pouring.
Baked in the oven at 1120 ºC.
In the box: teapot, 2 cups, certificate from artist.


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The North West Province provides a complete tourism package, with breath-taking scenic beauty, rolling fields of maize, golden sunflowers and vast plains of untamed African bushveld. The various towns and suburbs offer a range of Bed & Breakfasts, guest houses, holiday apartments & suites, holiday cottages & chalets, holiday homes & Villas to self -catering options and 5 star luxury resorts and lodges.
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Museum, which has exhibits relating to the Siege of Mafeking, the Barolong people and the Bushmen.
aha Ivory Tree Game Lodge is situated within the Pilanesberg Game Reserve, one of the largest volcanic complexes of its kind in the world.
aha Shepherd's Tree Game Lodge is a magnificent lodge concession awarded by the North West Parks and Tourism Board within the existing Pilanesberg Game Reserve.
aha Madikwe River Lodge is beautifully situated on the banks of the Groot Marico River in the heart of Madikwe Game Reserve, offering guests a place to relax and unwind.
Set within a riverine canopy surrounded by an impressive diversity of fauna and flora, aha Thakadu River Camp offers guests beautifully appointed, 5-star tented suites.


text:
Q: What does "using var_name = data_type;" in C++ means? I found a piece of code that uses the following statement:
using var_name = data_type;

This is the first time that I encountered it. What does it mean or do?

A: This is a type alias. Quite simply it is a way of identifying an existing data type with a new name. More like giving a synonym since it does not create a new data type.
using diameter = int;
diameter circle = 10;

using is used in C++. typedef which is a keyword in C can be used to do the same thing.
typedef unsigned int size;

typedef int* IntPtr ;
IntPtr x, y, z;

This could be used as an alternative to long/ complicated names of data types. And also in the 1st example if you later on want to change the diameter to float, you would just have to change the definition rather than all the places in the program.

redpajama_set_name: RedPajamaStackExchange


I have several Hoogendorn Holly bushes that were planted in front of my house last spring, 2013. One of them began to show brown sections early this season. Now there are a few others that have, all of a sudden started turning brown, even though, until now they have been growing and, seemingly, prospering. I am attaching pictures for you to evaluate. This first one is of the bush that started gradually showing brown spots this spring. I would appreciate your feedback. These bushes are in full sun and were planted after consultation with a landscaper, who evaluated the soil and the area before recommending that we plant them.
There could be several reasons for the browning of the hollies in your photo. Usually plants are not subject to many disease or insect problems within the first year of planting. Some issues to consider are winter damage, lack of establishment, poor drainage, etc.
You may want to replace at least two of the three shrubs. When you dig them up look at the root system. Make sure the roots look firm and whitish, not black and decayed. These hollies can be susceptible to a root rot. At this point, prune out any dead plant material on the shrubs you keep. Make sure the soil drains well and there are no drainage spouts nearby dumping water into the area.
See our website for instructions on planting shrubs and posts planting care. If container plants, make sure the root system is not encircled in the container. Tease the root system apart. Plant and water well up until the ground freezes.
Thank-you for your quick response.


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Magento is a big advantage when it comes to e-commerce if your website's retail business is struggling to control costs because Magento is an open-source solution used for e-commerce applications. Yes, the big retail websites do use this system which was formerly owned by the Varien firm but if you are a small player trying to compete against the big boys then every cent you save matters in the future. Because of this also major auction site ebay.com recognizes the usefulness of being related to Magento (eBay has already bought out 100% ownership of Magento). So maybe you should too as well.