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Maryam Rajavi: Terrorism and Warmongering Are the Strategic Means of Iranian Regime's Survival- Part I
Written by Yoosef Lesani on October 31, 2019 . Posted in NEWS
Mrs. Maryam Rajavi, President-elect of the National Council of Resistance of Iran (NCRI), delivers a speech at the French National Assembly on 29 October 2019
In a conference at the French National Assembly on 29 October, Mrs. Maryam Rajavi, the President-elect of the National Council of Resistance of Iran (NCRI), stressed that since Rouhani took office, four thousand death penalties were issued. She said that she hoped Europe and France would stand with the Iranian people and their legitimate demands and aspirations.
In her speech, Mrs. Rajavi first thanked the members of the National Assembly for their invaluable efforts against the mullahs' religious rule in Iran in support of the Iranian people and their resistance, stressing that these efforts will never be forgotten.
The President-elect of the NCRI first reviewed the human rights' record in the past four decades in Iran and said:
" The people of Iran have been struggling for more than 40 years against a regime which is the world's record holder of executions per capita. Since 2013, when Hassan Rouhani became president, some 4,000 people have been executed. And 120,000 political executions have been carried out under the mullahs' regime since 1981, including the massacre of 30,000 political prisoners in the summer of 1988."
#MaryamRajavi : #France must take the initiative to open the path to #democracy in #Iranhttps://t.co/NclubJe94c#MEK #NoImpunity4Mullahs @USAdarFarsi pic.twitter.com/4DRijE0tQs
— MEK Iran (Mujahedin-e Khalq) (@MEK_Iran) October 30, 2019
She then pointed to a new book containing part of the names of massacred MEK members. This book has recently been published by the Call-for-Justice movement.
Mentioning that the 1988 massacre in Iran was the worst state-sponsored massacre since World War II, Mrs. Rajavi said:
" Some of the key perpetrators of this massacre are presently holding positions such as the Head of the Judiciary and the Minister of Justice in Rouhani's government.
Can you imagine? What kind of justice this is?
This regime has institutionalized discrimination against women in its laws. The highest number of executions of women in the world and their most vicious tortures have been carried out by this regime. Presently, a large number of women are incarcerated in Iran for their peaceful activities or their faith."
Mrs. Rajavi then discussed the destructive role of the Iranian regime outside Iran and said:
" Outside Iran, the clerical regime is the main cause of instability and wars in the Middle East.
Over the past years, the world has heard a lot about the crimes of ISIS, or Daesh. Their crimes are similar to those committed by the clerical regime in Iran and in the region in the past four decades. They have the same anti-human ideology: dictatorship and savagery under the banner of religion, terrorism, and expansionism, and misogyny. When this ideology dominates a big country like Iran, it becomes a hundred times more dangerous than Daesh, which emerged as a result of the clerical regime's crimes in Iraq and Syria coupled with international silence."
Mrs. Rajavi stressed that if inaction vis-à-vis the regime's crimes in Iran and abroad persists, the clerics and their actions will reproduce groups like Daesh (ISIS). The regime is quite concerned over the latest setback to Daesh.
Regime and Daesh have the same anti-human ideology: in dictatorship and savagery under the banner of religion, in terrorism and expansionism, and in misogyny. #NoImpunity4Mullahs
— Maryam Rajavi (@Maryam_Rajavi) October 29, 2019
The regime's Revolutionary Guards (IRGC) and their militias slaughter people in Iraq, Syria, Lebanon, and Yemen.
Discussing the mullahs' terrorism and warmongering in Iran, the President-elect of the NCRI said:
" This medieval regime belongs to the past. Terrorism and warmongering are the strategic means of survival. For this reason, they undermined European efforts, including those by the French President to reduce tensions. They continued attacking tankers in international waters and oil installations in neighboring countries.
Why did the regime step up its terrorism and domestic suppression, and refuse the initiatives put forth by France? Because it cannot moderate itself, because the president carries out the whims of the Supreme Leader because the regime's leaders want to ensure their own survival instead of caring for the interests of the people, and, finally, because the regime lacks the minimum stability.
They are playing a duplicitous game by using these initiatives to buy time and continue their aggression in the region and expand their ballistic missile program. All the while, in their domestic propaganda, they insult France and Europe.
This is what we have experienced in the past 40 years. If this regime had the slightest capacity for reform, we would have not paid such a heavy price in this long and arduous struggle against it.
The Mojahedin quickly learned that the only means for the survival of this theocratic regime are domestic suppression, foreign wars, and crises-making.
The regime understands only the language of firmness. The ruling mullahs consider silence, leniency, and calls for negotiation as signs of weakness.
While they try to make it appear as though Europe needs mediation, they are the ones in need of it. They have been emboldened because of inaction towards their regime's outlaw behavior and belligerence."
An exhibition in this regard was on display all day close to the National Assembly.
Tags: 1988 Massacre, Human Rights, Iran human rights, Iran Terrorism, Maryam Rajavi, MEK, National Council of Resistance of Iran (NCRI), NCRI, People's Mojahedin organization of Iran, PMOI, Regime Change


Usher is not dead. One retweet from Twitter and suddenly there are rumors flying that Usher is dead.
The problem with that website, it's fake. It's a website where you can make up your own story about celebrities. They say on their home page to enter a celebrity name, browse a pre-formatted fake story, then prank your friends and spin a hoax.
They do allow celebrities to be removed from the list, "Believe it or not, we have never received a celebrity name removal request! If you are a celebrity or the business manager for celebrity and wish to have a name blocked from working on the site, please follow the instructions below." Which has a person go through steps of removal. They do warn not to submit a fake removal because some celebrities enjoy the hoax of a death for press reasons.
While the website might be fake and starting rumors like Usher dead, Twitter catches wind of it and suddenly it's believable.
Although, people on Twitter are starting to get the hang of the death hoax from this fake website.


In 1939, Bishop Paul Yu Pin of Nanking, China, came to Philadelphia wishing to visit the city's Chinese Catholics. Because he found very few, a local mission was soon formed.
What church was eventually founded as a result of this mission?
According to its website, the Holy Redeemer Chinese Catholic Church, located in Philadelphia's Chinatown at 915 Vine Street, was the "first church built for the Chinese in the western hemisphere." A few years prior to the church's opening, Bishop Paul Yu Pin, vicar of Nanking, China, visited Philadelphia in 1939 and wished to see the city's Chinese Catholic families. Unfortunately, he found very few Chinese Catholics. As a result, and with the help of Cardinal Dennis Dougherty, Father William A. Kavanagh, and others, a mission was formed in the Chinese community to develop Catholicism. After several months of work, over 50 Chinese people were prepared to become part of the Catholic Church. Successful fundraising efforts brought about the Holy Redeemer Chinese Catholic Church and School, a mission church of the parish of St. John the Evangelist. Holy Redeemer opened to the public in late 1941.
Image: Paul Yu Pin, HSP archives.
HSP has a small collection of ephemera and correspondence, as well as a collection of photographs, related to the Holy Redeemer Chinese Catholic Church. (#MSS030 and #PG120).


Even after the end of October and Halloween has been and gone, I always think November is a spooky time of year. This 4.5% volume Hoptical Illusion Dry Hop Lager from Sadler's Brewery, in the Midlands, has a spooky skull on the front of the bottle with hops for eyes. It's supposed to look like a regular lager, but have a strong hoppy aroma of zesty Mediterranean Lemons, as well as subtle sweet malts. So if it's supposed to look like a regular lager, I'm hoping it doesn't bloat me like some regular mass produced off the shelf lagers can do!
On opening this Hoptical Illusion there was a very understated fizz. I know I wasn't expecting a champagne pop, but I usually get more than that when opening a bottle of beer or carbonated cider. I worried slightly and checked the date on the label, no that was fine, so I had a sniff. If Mediterranean Lemons smell so understated I'll stick to some other ones! Not that I sniff lemons often, but usually they are pretty sour without getting too close.
On pouring this Hoptical Illusion the fizz did liven up a little and this golden beer does look like a regular lager. On taste I'd say that the smell transcends perfectly, I'd argue against a mega citrus blast of lemons though, as the herbal hops fought against and mostly overwhelmed any flavour of citrus hops. Having said that, there is certainly nothing wrong with the flavour. The herbal hops have a good bitterness to start with, which almost instantly complements the sweet malts, whilst the citrus hops reared their lemon flavour towards and into the aftertaste for a slightly complex journey through my tastebuds. It also didn't blow me up with wind, so I'd certainly have this Hoptical Illusion Dry Hop Lager again, but be a little more wary of what the label says.


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Geodiversity is essential for conservation of natural resources
To advance sustainable stewardship, we must document not only biodiversity but also geodiversity. This is the main message of an opinion article now published in the leading scientific magazine PNAS, written by an international group of geoscientific experts, including researchers of the UvA Institute for Biodiversity and Ecosystem Dynamics.
Mining is one example of human impact on geodiversity. Active mines cause a decrease in local biodiversity but in some cases they can provide an important habitat for specialised and rare species after the mine has been abandoned. Image credit: Shutterstock/1968
Geodiversity is a novel concept that describes the combined spatial variability of soils, geology and waterways within all landscapes, ranging from lowlands to high mountains. The opinion paper raises the issue that geodiversity is essential for human wellbeing, but that it is insufficiently managed and considered in a global policy context. As a result of poor global governance and missing international regulations, soils are degraded and natural resources such as minerals, rare earths and fresh water are becoming depleted.
Monitoring geodiversity
Harry Seijmonsbergen is one of the involved researchers and works at the UvA Institute for Biodiversity and Ecosystem Dynamics (IBED): 'In this paper, we argue that geodiversity needs to be considered as an essential good for humanity, and that we need to develop a system to monitor, regulate and manage natural resources including soils and fresh water needs. Various services of geodiversity can be directly linked to the UN Sustainable Development Goals. We lay out an action plan to identify key components of geodiversity that could aid monitoring, stewardship and support policy making.'
While it is widely recognized that climate and biodiversity require global protection and monitoring, it is surprising that no such recognition exists for protecting minerals and fresh water sources. Seijmonsbergen: 'We recommend collaborative development of comprehensive and interoperable databases of geodiversity globally, following common protocols, a standardised terminology (e.g. controlled vocabularies) and a consistent metadata reporting. This work will set a new agenda to establish a global (ideally UN regulated) commission to implement the conservation and sustainable management of geodiversity.'
Franziska Schrodt, Joseph J. Bailey, W. Daniel Kissling, Kenneth F. Rijsdijk, Arie C. Seijmonsbergen, Derk van Ree, Jan Hjort, Russell S. Lawley, Christopher N. Williams, Mark Anderson, Paul Beier, Pieter van Beukering, Doreen S. Boyd, José Brilha, Luis Carcavilla, Kyla M. Dahlin, Joel C. Gill, John E. Gordon, Murray Gray, Mike Grundy, Malcolm L. Hunter, Joshua J. Lawler, Manu Monge-Ganuzas, Katherine R. Royse, Iain Stewart, Sydne Record, Woody Turner, Phoebe L. Zarnetske, Richard Field: 'To advance sustainable stewardship, we must document not only biodiversity but geodiversity' in PNAS 116 (33) (14 August 2019):16155-16158. DOI: https://doi.org/10.1073/pnas.1911799116
Dr. A.C. (Harry) Seijmonsbergen
Assistant Professor – Geodiversity Expert
A.C.Seijmonsbergen@uva.nl 0205258137
BIOMAC lab
The involved UvA researchers are working at the Biogeography & Macroecology (BIOMAC) lab, which is part of the UvA Institute for Biodiversity and Ecosystem Dynamics (IBED) and has leaders in the quantification of geodiversity. We have field expertise in geodiversity as well as in designing workflows to develop geodiversity variables globally. This can support global policy making as well as scientific studies on how the geodiversity influences biodiversity across our planet. The central aim of the BIOMAC lab is to quantify how biodiversity and geodiversity vary across space and time, how they interact, and how responses of species and ecosystems to changing environmental conditions can be predicted.

redpajama_set_name: RedPajamaCommonCrawl


ING has completed the issuance of €1.1 billion in subordinated notes that will, in line with the completion of the intended IPO of NN Group, be exchanged into NN Group, its European insurance unit, shares.
The group said the transaction represents an important investment into NN Group ahead of the intended IPO of ING's European and Japanese insurance and investment management activities.
As announced on April 30, 2014, ING has secured investments totalling €1.3 billion into NN Group ahead of its intended IPO by agreeing to sell €150 million in NN Group shares at the IPO to RRJ Capital, Temasek, and SeaTown Holdings International, three Asia-based investors.
The investors will be issued with €1.1 billion subordinated notes that will over time be mandatorily exchanged into NN Group shares.


When the head of Germany's main Jewish organization said only one Bundestag party was not invited to Friday's commemoration of the Kristallnacht pogroms, few had any doubt: He meant the anti-immigrant Alternative for Germany, or AfD. And it was the only remark at the event that drew spontaneous applause.
Speaking at the soaring Rykestrasse Synagogue in Berlin, with German Chancellor Angela Merkel looking up at him from the front pew, Josef Schuster called on Germans to fight xenophobia, anti-Semitism and anti-Muslim sentiments, and in particular to oppose the unnamed "spiritual arsonists" who belittle the Holocaust and "mock its victims and survivors."
At a ceremony broadcast live nationwide, Schuster called the recent demonstrations against hate in Germany "encouraging." He cited hundreds of thousands of courageous people, dedicated to democracy, who "won't let Germany just drift off to the right."


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The Gift That Gives Back
A fixed payment for life and a gift to UPF.
What is a Charitable Gift Annuity?
A Charitable Gift Annuity (CGA) is a contractual agreement whereby a donor makes an irrevocable contribution of capital in exchange for guaranteed payments for life (or the life of another person) at a specified rate. This is a safe investment, payments are fixed for life and, depending on age, a major portion of the income may be tax free.
Benefits of a CGA:
Immediate Tax Deductions. Because the gift is an irrevocable gift you generally qualify for an immediate tax deduction for your contributions into your CGA. The assets used to fund the gift annuity are typically removed from your estate therefore avoiding estate tax.
Income payments. A CGA produces an income stream for life with rates generally higher than CDs. A portion of the income is tax-free.
Flexibility. CGAs are an extremely flexible way to make a gift. You can choose to name another person (typically your spouse, parent, sibling) to receive payments with you, instead of you, or following your lifetime. You can choose to receive your payments quarterly, semi-annually, or annually. CGA payouts can be immediate or deferred.
Christian Values. In establishing a charitable gift annuity through the UPF, you can rest assured that your gift will ultimately be directed to ministries and charities that operate in accordance with United Pentecostal values.
Impact. You can make a significant gift to the work of the Kingdom!
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The United Pentecostal Church is blessed to have a person like Brother Drury directing our Stewardship Department. It was through him that we learned of the Donor Advised Fund in the Foundation. This is a fund whereby one can make a cash contribution of a desired amount. That contribution is placed in an investment fund directed by the Foundation. The donor has the privilege of directing proceeds, and even principal if desired, from those funds for support to any UPCI ministry they wish. Examples are: a Bible school of choice, Home Missions, Foreign Missions, Urshan Graduate School of...
Albert & Gayle Skaggs - Read More
We have chosen to purchase a Charitable Gift Annuity with the United Pentecostal Foundation because it is a win/win proposition. You receive quarterly payments at a higher rate of return than the bank, with the payments partially tax-free. The tax deduction received when you purchase the Gift Annuity is a great blessing too. In the past we have purchased other Charitable Gift Annuities, but when the Foundation started offering them, there was no question—we would buy the next ones from the United Pentecostal Foundation. Why? Because at the end of our lives, the balance of each annuity...
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When I walked across the street to tell my nephew that I would provide the necessary funds to help complete their international adoption, I felt the Lord's presence walking with me. Twenty-one years later, their little baby girl is now a beautiful, Apostolic lady filled with the Holy Ghost and baptized in Jesus' name. When her grandfather (my younger brother) was diagnosed with terminal cancer, she moved 1,000 miles to help her "Grandpa and Grandma." Little did I realize the blessing God would return simply because I obeyed His voice. When I chose to give a sizable...
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Our desire to participate in the United Pentecostal Foundation stemmed from our awareness of God's blessings to our family and a desire to invest in something with a lasting impact. Being a middle-class family, we approached our lawyer about our wishes and soon realized the expense of establishing a Trust Fund was prohibitive for the amount of funds we had available. The United Pentecostal Foundation provided us an avenue of meeting our goal with no cost to us. We chose a Donor Advised Fund as we wanted our family to be involved in the designation of the funds. Our enthusiasm grew as...
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The Internal Revenue Service has provided some interesting data on the state of the supply, the average mortgage rate and the repayment installments from 2006 to 2016. One of the most important aspects for those who want to invest in a property, if it is their first or second home, is the interest rate that, up to now has been preferred in the fixed shape due to its very low value, but in the coming years it will excel on variable according to the latest forecasts of Euris and Euribor. In fact it is estimated that from 2021 the growth of the interest rates will be clear. 2017 still seems to be a suitable moment to buy home and benefit from competitive interest rates on mortgages, before the ascent will begin from 2018.


72 Inch White Bathroom Vanity Dream Buy Vanities Cabinets Online At Overstock Pertaining To 17 | Puacomic.com 72 inch bathroom vanity white. 32 inch white bathroom vanity. 72 inch white bathroom vanity without top.


Please complete all mandatory fields in the below form to claim your cash back. Online redemption closes July 31, 2019 after which no further claims will be accepted. Please read the FAQs and Terms & Conditions before entering this promotion.
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Noble Pen Meeting, March 4, 2010
February 27, 2010 Newsletterssryan
Noble Pen Meeting
Happy Chef, 1906 Blairs Ferry Rd NE, Cedar Rapids
Tragedy is when I cut my finger. Comedy is when you walk into an open sewer and die..
— Mel Brooks
I believe that the government that governs best is a government that governs least, and by these standards we have set up a fabulous government in Iraq.
— Stephen Colbert
George is working on a new project. He doesn't know what it is yet. He will supply us with full details as soon as he hears back from himself.
Christine is in the top 1000 contestants for the Amazon Breakthrough Novel Award. Currently, she is lamenting the exorbitant cost of 999 hitmen.
Ciuin has sent a completed Petty Theft to beta readers. I volunteered as a beta reader as I am already a beta male.
Dylan posted his commission piece to forums. Readers gushed over it. For those of you that don't attend regularly, that's an inside joke. Get it? Inside? Oh, never mind.
Don't read this. You will cry.
Rosemary Clement-Moore explains what writers can learn from the Winter Olympics.
It's not news, but here's Terry Pratchett telling a dirty joke.
Again we tried the new critique method. I have not seen overwhelming complaints as of yet, so I'm letting it ride. I slightly altered the instructions to make them more clear.
Author is coned
We go around the table and everyone gives up to three positives and up to three things that need work
At this point the author is un-coned and should ask for any clarification.
Group conversation including author
I did not include a formal rebuttal in the critique process, even though it is part of many critique groups. Personally, I feel this is counterproductive. However, I'm open to any thoughts on this position.
Thursday, March 4th. Happy Chef, 7pm Welcome and Victories, 7:30pm Critique
Nick – Something new and mysterious
Thursday, March 11th. Happy Chef, 7pm Welcome and Victories, 7:30pm Critique
Ciuin – young adult fantasy
Shannon – Kodiak, a short story.
Keep Writing, Penites.
Noble Pen Meeting, February 25, 2010
Pundits are always blaming TV for making people stupid, movies for desensitizing the world to violence, and rock music for making kids take drugs and kill themselves. These things should be the least of our worries. The main problem with mass media is that it makes it impossible to fall in love with any acumen of normalcy. There is no 'normal,' because everybody is being twisted by the same sources simultaneously.
— Chuck Klosterman, Sex, Drugs, and Cocoa Puffs: A Low Culture Manifesto
Dylan is submitting a short story to a cyberpunk romance collection, a genre in which the Blazing Saddles quote, "We'll make Rock Ridge think it's a chicken that got caught in a tractor's nuts" actually makes sense.
Nick wrote the ending of his current manuscript, which will cease to be a secret in two weeks. I hope it's a love story involving dolphins.
I sent out 2 queries, got one rejection, and followed up with and editor, to whom I may not have a current email address, or he just wont talk to me.
John joined the group and received a form rejection–the two events were deemed unrelated.
Lena read some of her stories to an audience and was well received. She received two tomatoes and three eggs.
The Intern tells you why editor's email responses suck.
The BBC has some information about the current state of Google Books.
We tried a new critique method this week, and it seemed to work pretty well. We're going to stick with it for the time being.
Here's the rundown:
Author has a chance to ask questions
A few people talked less than usual and a few talked more, but the consensus seemed to be a more streamlined and useful critique.
Thursday, February 25th. Happy Chef, 7pm Welcome and Victories, 7:30pm Critique
Ian – The Comet – email him for a copy
Lena- email her for a copy
THERE was death afoot in the darkness.
It crept furtively along a steel girder. Hundreds of feet below yawned glass-and-brick-walled cracks' New York streets. Down there, late workers scurried homeward. Most of them carried umbrellas, and did not glance upward.
Even had they looked, they probably would have noticed nothing. The night was black as a cave bat. Rain threshed down monotonously. The clammy sky was like an oppressive shroud wrapped around the tops of the tall buildings.
–Keneth Robeson, The Man of Bronze
Dylan got feedback on his commission piece. The commissioner only wanted a hairstyle changed. I think he's one of these guys.
Nick donned a poncho, lit a cigarillo, and loaded his colt revolver to go in search of his missing manuscript. He also got to speak with the publisher of The Writer magazine about it.
An Iowa man was sentenced to six months after pleading guilty to possessing 'obscene' comic books. Without the guilty plea, he would have faced a 15 year sentence. Neil Gaiman weighed in on this case last year.
The New York Times has an interesting article on William Faulkner's family history and its link to his novel, Go Down, Moses.
A big thank-you to George for his work on the new member guide.
Shannon – Solomon's Heist, Chapter 2. You know the drill, email or website.
Dylan – Flight of the Scions, Chapter 4. Email or website.
Ian – ?
Dylan – Flight of the Scions, Chapter 5? Email or website.
February 7, 2010 Newslettersbhart
In Sleep we lie all naked and alone, in Sleep we are united at the heart of night and darkness, and we are strange and beautiful asleep; for we are dying the darkness and we know no death.
– Thomas Wofle
Lena has a friend who is going to record her reading. She is planning to submit her reading to This American Life. (My all time favorite story from This American Life is the Squirrel Cop story from the First Day episode.)
Dylan finished working on his commission piece.
Nick finished two chapters of his mystery piece.
Dylan – Chapter 3 of his piece. Email author for a copy.
George – Untitled. Should be available Monday. Email for a copy.
George (Substituting for Shannon)


Pair's breach of 111.82 resistance indicates a recoil restoration from 109.76. Trading turned up on the upside to 100% projection of 109.76 to 111.82 from 110.37 at 112.43. Following pivot points include: (S1) 111.39; (P) 111.69; (R1) 112.24.
Breach will head towards a test of 113.17 maximum. Under the minor support of 111.10, the bullish sentiment will be clouded and trading will become neutral.


These stylish trousers employ intricate pattern cutting to create the side seam detail to intersect with the waist band. Choose smart black for these smart tailored trousers. Inside leg length is 73cm on size small.


May is National Physiotherapy month in Canada, and physiotherapists, physiotherapy aides, and physiotherapy students across our country celebrate our profession!
As many people know, or learn as they meet a physiotherapist .... you do NOT need a referral to seek our help! We are a primary health care service, where more and more individuals are self-referring to us, meaning they are getting the help they need sooner, which in turn leads to a faster path to recovery and life!
For more information and some interesting facts, check out the Canadian Physiotherapy Association's 'Self-Referral for Physiotherapy Services' article.
Proper posture is a key element to injury prevention and recovery from a wide variety of conditions. Learning how to sit and stand in the correct position can seem so incredibly simple, but have such large impacts of movement patterns, strength and reducing pain.


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Home » Travel » Airline will pay you £7,300 if you catch coronavirus after flying with them
2020-03-25 Comments Off on Airline will pay you £7,300 if you catch coronavirus after flying with them Travel
Airline will pay you £7,300 if you catch coronavirus after flying with them
Vietnamese airline Vietjet has announced that it's prepared to pay customers up to 200m VND (£7,344) if they catch coronavirus after flying with them.
The payout will be part of its new "SKY COVID CARE insurance" scheme, which will cover all domestic flights between 23 March and 30 June 2020.
It will be offered free of charge to all eligible customers, regardless of age and nationality.
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In a statement announcing the launch of the insurance, the airline said: "With the insurance, passengers are eligible for insurance coverage and benefits from Vietjet within 30 days starting at 00:01 of the flight date, regardless of how passengers are infected with the disease."
The airline said it has set aside "tens of billion dong" of its own money to cover the scheme, which is designed to "bring passengers assurance".
In order to qualify for the coverage, the airline said prospective customers must provide "all information in accordance with Vietjet's terms and conditions" when purchasing tickets.
This includes full name with relevant ID as proof, date of birth, contactable phone number and email address.
In addition, customers must "comply with all regulations on disease prevention and control of Vietjet, the Ministry of Health and authorities".
While the airline doesn't discriminate against customers of certain ages or nationalities, those who have already been confirmed positive for Covid-19 are ineligible, as are those who breach any safety regulations, such as isolation or travel bans, outlined by the Vietnamese Ministry of Health or other government authorities.
However, the airline has said it won't cover passengers with epilepsy, mental illness or suicidal behaviours under the policy either.
Customers hoping to make a claim can do so via the form on its website, and will need to provide proof that they've tested positive for Covid-19 as well as proof of treatment.
This is not the first time the airline has courted controversy.
In 2012, the airline was fined after it hosted a bikini show on one of its planes.
Vietnam's Civil Aviation Authority issued a 20m VND (£735) fine as it said the airline staged the show without receiving official approval.
Vietnam currently has 113 confirmed cases of coronavirus according to the latest World Health Organisation report, dated 23 March.
The Holiday Guru answers readers' Covid-related travel questions
Spain, Turkey, Portugal and Greece voted as best value holidays for Brits
Rocky Mountain National Park's Bear Lake reopens after East Troublesome fire
Turkey axes testing requirement for vaccinated Britons – what are the latest travel rules?
Queen Elizabeth: Royal always packs this 5p item in her luggage when she travels
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Q: How to combine 2 oracle queries with differrent where clauseses into 1 query I have below 2 oracle queries with different where conditions
(Some criteria in where condition is same). Is it possible to combine these 2 queries to 1 query?
queries are here
Different conditions: TX_TYPE, TX_STATUS
Common conditions: SUBSCRIBER_ID, MERCHANT_ID, IS_TAXABLE, TX_DATE
Query1:
select sum(t.AMOUNT) Amt1
  from RS_TRANSACTION_LOG t, RS_MERCHANT m
 where t.SUBSCRIBER_ID = 11338329
   and t.MERCHANT_ID = m.MERCHANT_ID
   and t.TX_TYPE = '1'
   and t.TX_STATUS in (5, 42)
   and m.IS_TAXABLE = 'Y'
   and TX_DATE between to_date('11/01/2015 00:00:00','MM/dd/YYYY HH24:MI:SS')
                   and to_date('11/30/2015 23:59:59','MM/dd/YYYY HH24:MI:SS');

Query2:
select sum(t.AMOUNT) Amt2
  from RS_TRANSACTION_LOG t, RS_MERCHANT m
 where t.SUBSCRIBER_ID = 11338329
   and t.MERCHANT_ID = m.MERCHANT_ID
   and t.TX_TYPE = '5'
   and t.TX_STATUS = 5
   and m.IS_TAXABLE = 'Y'
   and TX_DATE between to_date('11/01/2015 00:00:00','MM/dd/YYYY HH24:MI:SS')
                   and to_date('11/30/2015 23:59:59','MM/dd/YYYY HH24:MI:SS');

A: What about using an OR to combine the conditions and CASE to separate the amounts:
select sum(case when t.TX_TYPE = '1' and t.TX_STATUS in (5,42) then t.AMOUNT else 0 end) Amt1,
       sum(case when t.TX_TYPE = '5' and t.TX_STATUS = 5 then t.AMOUNT else 0 end) Amt2
from   RS_TRANSACTION_LOG t,
       RS_MERCHANT m
where  t.SUBSCRIBER_ID=11338329
and    t.MERCHANT_ID=m.MERCHANT_ID
and    ((t.TX_TYPE = '1' and t.TX_STATUS in (5,42)) or
        (t.TX_TYPE='5' and t.TX_STATUS = '5'))
and    m.IS_TAXABLE='Y'
and    TX_DATE between
       to_date('11/01/2015 00:00:00','MM/dd/YYYY HH24:MI:SS') and
       to_date('11/30/2015 23:59:59','MM/dd/YYYY HH24:MI:SS');

redpajama_set_name: RedPajamaStackExchange


text:
Q: how to interpolation this array from sevice I make a service to inerpolate data, and all is ok but imgs array, id, img and p interpolate fine, but I tried a lot with imgs but I did;nt find a solution, thanks in advance
this is in projects.service.ts
const projects = [

{
    'id': 'project1',
'img': 'assets/project.png',
'p': 'Lorem ipsum dolor sit amet, consectetur adipiscing elit, Aliquet
 risus feugiat in ante metus.',
'imgs': [{'photo': 'assets/project.png'}, {'photo':
'assets/project.png'}, {'photo': 'assets/project.png'} ]

 },

{
    'id': 'project2',
'img': 'assets/project.png',
'p': 'Lorem ipsum dolor sit amet, consectetur adipiscing elit, Aliquet
 risus feugiat in ante metus.',
'imgs': [{'photo': 'assets/project.png'}, {'photo':
 'assets/project.png'}, {'photo': 'assets/project.png'} ]

 },

{
    'id': 'project3',
'img': 'assets/project.png',
'p': 'Lorem ipsum dolor sit amet, consectetur adipiscing elit, Aliquet
 risus feugiat in ante metus.',
'imgs': [{'photo': 'assets/project.png'}, {'photo':
'assets/project.png'}, {'photo': 'assets/project.png'} ]

 }

];
and this in project.component.html :

{{project.id}}

{{project.p}}

A: Check WORKING STACKBLITZ
You just needed to iterate the imgs object *ngFor="let collection of project.imgs" like below

{{project.id}}

{{project.p}}

On a side note: Check your assets folder if you actually have an image named project.png at that path as it is in your response object projects like assets/project.png
Hopefully this helps !


text:
<?php

namespace LightSaml\Tests\Action\Profile\Outbound\Message;

use LightSaml\Action\Profile\Outbound\Message\SendMessageAction;
use LightSaml\Context\Profile\MessageContext;
use LightSaml\Model\Metadata\SingleSignOnService;
use LightSaml\SamlConstants;
use LightSaml\Tests\BaseTestCase;
use Symfony\Component\HttpFoundation\Response;

class SendMessageActionTest extends BaseTestCase
{
    public function test_constructs_with_logger_and_binding_factory()
    {
        new SendMessageAction($this->getLoggerMock(), $this->getBindingFactoryMock());
        $this->assertTrue(true);
    }

    public function test_calls_binding_factory_with_endpoint_type_and_calls_binding_and_sets_response_to_context()
    {
        $action = new SendMessageAction(
            $loggerMock = $this->getLoggerMock(),
            $bindingFactoryMock = $this->getBindingFactoryMock()
        );

        $context = $this->getProfileContext();
        $context->getEndpointContext()->setEndpoint(new SingleSignOnService(
            $location = 'http://example/com',
            $bindingType = SamlConstants::BINDING_SAML2_HTTP_POST
        ));

        $bindingFactoryMock->expects($this->once())
            ->method('create')
            ->with($bindingType)
            ->willReturn($bindingMock = $this->getBindingMock());

        $bindingMock->expects($this->once())
            ->method('send')
            ->with($this->isInstanceOf(MessageContext::class))
            ->willReturn($response = new Response());

        $loggerMock->expects($this->once())
            ->method('info')
            ->with('Sending message', $this->isType('array'));

        $action->execute($context);

        $this->assertSame($response, $context->getHttpResponseContext()->getResponse());
    }
}

redpajama_set_name: RedPajamaGithub


Geo was facing a jail term for killing a man in self-defence. So the last thing he expected was for Princess Celestia to save him from the slammer. All she wants in return is for him to share a conversation with her and her sister.
It is this conversation that makes Geo, and the Princesses, realise that love is there for everypony to enjoy - regardless of who they are.


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A Placerville woman who failed to appear for her May arraignment on drug trafficking charges is back in Douglas County custody.
Laura C. Thrash, 43, was picked up in California on two warrants issued out of district court.
She faces charges stemming from her August 2017 arrest for selling a dozen ounces of methamphetamine on three occasions.
She was scheduled to change her plea, but didn't turn up in court.
■ A man facing sentencing on a drug charge was arrested at Topaz Lake on Thursday morning after deputies responded to a disturbance.
Mark A. Redding, 57, has been out of jail since Aug. 6 when he was released after admitting to a methamphetamine charge.
Redding had two vehicles parked in front of the park's restrooms and was behaving oddly witnesses said.
He told deputies he was taking a shower. He was taken into custody on an alternative sentencing violation and the vehicles impounded.
During a search, deputies found what they believe is methamphetamine and items of paraphernalia.
Redding was previously arrested July 20 after deputies responded to a disturbance at a Gardnerville grocery store.
An Oct. 1 sentencing date was set in Redding's district court case.


text:
Clostridioides difficile (bacteria)
(Redirected from Clostridium difficile (bacteria))
This article is about the bacterium. For the disease, see Clostridioides difficile infection.
Clostridioides difficile
C. difficile colonies on a blood agar plate
Micrograph of Clostridioides difficile
Domain: Bacteria
Phylum: Firmicutes
Class: Clostridia
Order: Clostridiales
Family: Peptostreptococcaceae
Genus: Clostridioides
(Hall & O'Toole, 1935) Lawson & Rainey, 2016
Bacillus difficilis Hall & O'Toole, 1935[1]
Clostridium difficile (Hall & O'Toole, 1935) Prévot, 1938[2]
Clostridioides difficile (syn. Clostridium difficile), also known as Peptoclostridium difficile, C. difficile, or C. diff (/siː dɪf/), is Gram-positive species of spore-forming bacteria.[3]
Clostridioides spp. are anaerobic, motile bacteria, ubiquitous in nature, and especially prevalent in soil. Its vegetative cells are rod-shaped, pleomorphic, and occur in pairs or short chains. Under the microscope, they appear as long, irregular (often drumstick- or spindle-shaped) cells with a bulge at their terminal ends (forms subterminal spores). Under Gram staining, C. difficile cells are Gram-positive and show optimum growth on blood agar at human body temperatures in the absence of oxygen. C. difficile is catalase- and superoxide dismutase-negative, and produces two types of toxins: enterotoxin A and cytotoxin B, which disrupts cytoskeleton signal transductions in the host.[4] Under stress conditions, the bacteria produce spores that are able to tolerate extreme conditions that the active bacteria cannot tolerate.[5]
C. difficile may become established in the human colon; it is present in 2–5% of the adult population.[5] Sometimes antibiotic therapy for various infections has the adverse effect of disrupting the normal balance of the gut microbiota, in which case C. difficile may opportunistically dominate, causing C. difficile infection (CDI).
2 Human pathogen
4 Host range
5 Signs and symptoms
7 Strains
8 Genome
9 Epigenome
10 Bacteriophage
11 Etymology and pronunciation
Taxonomy[edit]
The species was transferred from the genus Clostridium to Clostridioides in 2016, thus giving it the binomial Clostridioides difficile.[6][7][8] This new name reflects the taxonomic differences between this species and other members of the genus Clostridium, while maintaining the common name as C. diff.[9] As of 2018[update], the only other species in this new genus Clostridioides mangenotii (formerly known as Clostridium mangenotii).[10] A July 2013 paper from Environmental Microbiology proposed to rename the species Peptoclostridium difficile.[11][12]
Human pathogen[edit]
Pathogenic C. difficile strains produce multiple toxins.[13] The best-characterized are enterotoxin (C. difficile toxin A) and cytotoxin (C. difficile toxin B), both of which may produce diarrhea and inflammation in infected patients (C. difficile colitis), although their relative contributions have been debated. The diarrhea may range from a few days of intestinal fluid loss to life-threatening pseudomembranous colitis, which is associated with intense inflammation of the colon and formation of pseudomembranes on the intestinal mucosal surface.[5] Toxins A and B are glucosyltransferases that target and inactivate the Rho family of GTPases. Toxin B (cytotoxin) induces actin depolymerization by a mechanism correlated with a decrease in the ADP-ribosylation of the low molecular mass GTP-binding Rho proteins.[14] There is also a binary toxin (AB toxin), but its role in disease is not fully understood.[15]
Additional virulence factors include an adhesin factor that mediates the binding to human colonic cells and a hyaluronidase.[16] The bacterium also produces the chemical para-cresol, which inhibits the growth of other microbes in its vicinity and allows it to outcompete normal human gut flora.[17]
Antibiotic treatment of C. diff infections may be difficult, due both to antibiotic resistance and physiological factors of the bacterium (spore formation, protective effects of the pseudomembrane).[5] The emergence of a new, highly toxic strain of C. difficile, resistant to fluoroquinolone antibiotics, such as ciprofloxacin and levofloxacin, said to be causing geographically dispersed outbreaks in North America, was reported in 2005.[18] The U.S. Centers for Disease Control in Atlanta warned of the emergence of an epidemic strain with increased virulence, antibiotic resistance, or both.[19] Resistance to other antibiotics such as metronidazole, the first choice of antimicrobial drug when treating CDI, has been observed in up to 12% of clinical isolates, so as treatment with various antibiotics continues, more diverse and stronger resistances will continue to evolve in C. difficile populations, further complicating attempts at effective treatment.[20]
Transmission[edit]
C. difficile is transmitted from person to person by the fecal-oral route, shed in faeces. Any surface, device, or material (e.g., toilets, bathing tubs, and electronic rectal thermometers) that becomes contaminated with faeces may serve as a reservoir for the C. difficile spores. C. difficile spores are transferred to patients mainly by the hands of healthcare personnel who have touched a contaminated surface or item. C. difficile can live for long periods of time on surfaces.[21] The organism forms heat-resistant spores that are not killed by alcohol-based hand cleansers or routine surface cleaning, thus, these spores survive in clinical environments for long periods. Because of this, the bacterium may be cultured from almost any surface. Once spores are ingested, their acid resistance allows them to pass through the stomach unscathed. They germinate and multiply into vegetative cells in the colon upon exposure to bile acids. Consequently, the World Health Organization advocates the use of soap in addition to alcohol solutions to limit the spread of the spores.[22] Sporulation was shown to be significantly reduced after inactivation of C. diffiicile's DNA methyltransferase CamA[23], raising the prospect of developing a drug that may inhibit this bacterium in a specific manner.
Host range[edit]
C. difficile infects pigs, calves, and humans, and inhabits a natural reservoir of soil, faeces of domestic animals and humans, sewage, the human intestinal tract, and retail meat.[24]
A 2015 CDC study estimated that C. diff afflicted almost half a million Americans and caused 29,000 deaths in 2011. The study estimated that 40% of cases began in nursing homes or community health-care settings, while 24% occurred in hospitals.[25]
C. difficile is common in the human digestive system. However, it is a poor competitor, and is often outcompeted for nutrients by other bacteria in the digestive system. As a result, C. difficile is kept to a manageable number. If the sudden introduction of antibiotic disrupts the microbiome, C. difficile may be able to grow as a result of many of its competitors being killed off. The incubation period is 5–10 days, with a range of 1 day to weeks following antibiotic treatment for antibiotic associated diarrhea. Additionally, carriage of C. difficile with high levels of toxins is common in young children, while disease is rare. The production of one or even both toxins is not always sufficient for producing symptoms.[26]
Signs and symptoms[edit]
Symptoms of C. difficile infection include: diarrhea (at least three loose bowel movements a day), dehydration, abdominal pain that can be severe, loss of appetite, and nausea.[27]
Patients being treated with antibiotics when symptoms begin should stop taking them, if possible. This break in antibiotic therapy can sometimes lead to spontaneous resolution of symptoms. Patients who do not respond to the cessation of broad-spectrum antibiotics will need to be treated with antibiotics capable of killing C. difficile spores. Primary infections are typically treated with vancomycin, with a usual dosage of 125 mg every 6 hours.[28] The vancomycin regimen has replaced the traditional use of metronidazole due to its greater efficacy, safety profile, and lower recurrence rates. In patients who cannot tolerate vancomycin, fidaxomicin is an acceptable option with similar efficacy and even lower recurrence rates than vancomycin.[29] In cases of fulminant CDI, adjuvant therapy with parenteral metronizadole plus oral vancomycin or fidaxomicin is suggested.[30]
About 20% of patients who successfully complete therapy of primary infection with metronidazole or vancomycin will experience a relapse. A fraction of those patients will experience continuous reoccurrences of the infection. The first relapse of C. difficile is usually treated with the same antibiotic used to treat the primary infection. Any subsequent infections should not be treated with metronidazole. Occasionally, a standard 10-day course of oral vancomycin will not work. In these cases, a vancomycin taper is the preferred treatment. Patients take decreasing doses of vancomycin over a period of up to 3 months, depending on the severity of the infection.[27]
Each subsequent relapse of C. difficile tends to be more severe than previous infections. Long-term treatment with a vancomycin taper supplemented with probiotics, especially Saccharomyces boulardii, is associated with a higher rate of success.[31]
After three relapses, patients may be treated with oral fidaxomicin, a narrow-spectrum antibiotic. The usual dosage is 200 mg twice a day orally for 10 days. Fidaxomicin is considered to be superior to vancomycin for severe CDI.[32] The major downside of treatment with fidaxomicin is the cost of medication. A 10-day course may cost up to US$3500.
Patients who do not respond to traditional antibiotic therapy may be eligible for a Fecal microbiota transplant (FMT). Healthcare providers can transfer stool from a healthy person to the colon of a patient with repeated CDI. This process is the most successful treatment for severe CDI with a cure rate around 93%. Recurrence rates of CDI in patients treated with a FMT are generally low, around 19%, which makes it very effective at treating chronic CDI cases. However, in some cases, flares of inflammatory bowel disease are a possible side effect of the treatment.[33] Long-term effects of FMT are unknown, as the procedure has only been FDA approved since 2011 and relatively few procedures have been performed. If transplantation is not an option, removal of the infected part of the colon can cure CDI.[32][27]
Strains[edit]
In 2005, molecular analysis led to the identification of the C. difficile strain type characterized as group BI by restriction endonuclease analysis, as North American pulse-field-type NAP1 by pulsed-field gel electrophoresis and as ribotype 027; the differing terminology reflects the predominant techniques used for epidemiological typing. This strain is referred to as C. difficile BI/NAP1/027.[34]
As of 2016, the NAP1 strain has been replaced by novel strains in some areas of British Columbia. These novel strains include NAP2 and NAP4, and some strains that do not have a NAP designation. The frequency of these novel strains increased from 2008 to 2013 in one studied region, displacing the originally more common and recognizable NAP1 bacteria.[35]
Two strains, ribotypes RT078 and RT027, can live on low concentrations of the sugar trehalose; both strains became more common after trehalose was introduced as a food additive in the early 2000s, thus increasing dietary trehalose intake.[36]
Genome[edit]
Genomic information
NCBI genome ID
Ploidy
Number of chromosomes
The first complete genome sequence of a C. difficile strain was first published in 2005 by Sanger Institute in the UK. This was of the strain 630, a virulent and multiple drug-resistant strain isolated in Switzerland in 1982. Scientists at Sanger Institute have sequenced genomes of about 30 C. difficile isolates using next-generation sequencing technologies from 454 Life Sciences and Illumina.[37]
Researchers at McGill University in Montreal sequenced the genome of the highly virulent Quebec strain of C. difficile in 2005 using ultra-high throughput sequencing technology. The tests involved doing 400,000 DNA parallel-sequencing reactions of the bacterium's genome, which had been fragmented for sequencing. These sequences were assembled computationally to form a complete genome sequence.[18][38]
In 2012, scientists at University of Oxford sequenced C. difficile genomes from 486 cases arising over four years in Oxfordshire using next-generation sequencing technologies from Illumina.[39]
Epigenome[edit]
C. difficile has a highly diverse epigenome, with 17 high-quality methylation motifs reported so far, the majority pertaining to the 6mA type. Methylation at one of these motifs - CAAAAA, was shown to impact sporulation, a key step in C. difficile disease transmission, as well as cell length, biofilm formation, and host colonization[23].
At least eight mainly temperate bacteriophages have been isolated from C. difficile, ranging in genome size from about 30 to about 60 kb.[40] Both environmentally and clinically derived C. difficile strains carry a diverse and prevalent set of prophages.[40]
Etymology and pronunciation[edit]
See Clostridioides difficile infection § Etymology and pronunciation.
^ Hall, Ivan C.; O'Toole, Elizabeth (1935). "Intestinal flora in new-born infants: with a description of a new pathogenic anaerobe, Bacillus difficilis". American Journal of Diseases of Children. 49 (2): 390–402. doi:10.1001/archpedi.1935.01970020105010.
^ Prévot, A.-R. (1938). "Études de systématique bactérienne. IV. Critique de la conception actuelle du genre Clostridium". Annales de l'Institut Pasteur. 61 (1): 84.
^ Moreno MA, Furtner F, Rivara FP (June 2013). "Clostridium difficile: A Cause of Diarrhea in Children". JAMA Pediatrics. 167 (6): 592. doi:10.1001/jamapediatrics.2013.2551. PMID 23733223.
^ di Masi, Alessandra; Ascenzi, Paolo; Siarakas, Steven; Petrosillo, Nicola; Di Bella, Stefano (2016). "Clostridium difficile Toxins A and B: Insights into Pathogenic Properties and Extraintestinal Effects". Toxins (Basel). 8 (5): 134. doi:10.3390/toxins8050134. PMC 4885049. PMID 27153087.
^ a b c d Ryan KJ, Ray CG, eds. (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. pp. 322–4. ISBN 978-0-8385-8529-0.
^ Oren, Aharon; Garrity, George M. (2017). "List of new names and new combinations previously effectively, but not validly, published". International Journal of Systematic and Evolutionary Microbiology. 67 (9): 3140–3143. doi:10.1099/ijsem.0.002278. PMC 5817221. PMID 28891789.
^ Lawson, Paul A.; Citron, Diane M.; Tyrrell, Kerin L.; Finegold, Sydney M. (August 2016). "Reclassification of Clostridium difficile as Clostridioides difficile (Hall and O'Toole 1935) Prévot 1938". Anaerobe. 40: 95–99. doi:10.1016/j.anaerobe.2016.06.008. ISSN 1095-8274. PMID 27370902.
^ Zhu, Duolong; Sorg, Joseph A.; Sun, Xingmin (2018). "Clostridioides difficile Biology: Sporulation, Germination, and Corresponding Therapies for C. difficile Infection". Frontiers in Cellular and Infection Microbiology. 8: 29. doi:10.3389/fcimb.2018.00029. ISSN 2235-2988. PMC 5809512. PMID 29473021.
^ Galperin, Michael Y.; Brover, Vyacheslav; Tolstoy, Igor; Yutin, Natalya (2016). "Phylogenomic analysis of the family Peptostreptococcaceae (Clostridium cluster XI) and proposal for reclassification of Clostridium litorale (Fendrich et al. 1991) and Eubacterium acidaminophilum (Zindel et al. 1989) as Peptoclostridium litorale gen. nov. comb. nov. and Peptoclostridium acidaminophilum comb. nov". International Journal of Systematic and Evolutionary Microbiology. 66 (12): 5506–5513. doi:10.1099/ijsem.0.001548. PMC 5244501. PMID 27902180.
^ Yutin N, Galperin MY (2013). "A genomic update on clostridial phylogeny: Gram-negative spore formers and other misplaced clostridia". Environ. Microbiol. 15 (10): 2631–41. doi:10.1111/1462-2920.12173. PMC 4056668. PMID 23834245.
^ Gerard J. Tortora; Berdell R. Funke; Christine L. Case (2015-01-13). Microbiology: An Introduction. Pearson Education. ISBN 978-0-13-392339-1.
^ Di Bella, Stefano; Ascenzi, Paolo; Siarakas, Steven; Petrosillo, Nicola; di Masi, Alessandra (2016-01-01). "Clostridium difficile Toxins A and B: Insights into Pathogenic Properties and Extraintestinal Effects". Toxins. 8 (5): 134. doi:10.3390/toxins8050134. ISSN 2072-6651. PMC 4885049. PMID 27153087.
^ Just I, Selzer J, von Eichel-Streiber C, Aktories K (1995). "The low molecular mass GTP-binding protein Rh is affected by toxin a from Clostridium difficile". The Journal of Clinical Investigation. 95 (3): 1026–31. doi:10.1172/JCI117747. PMC 441436. PMID 7883950.
^ Barth H, Aktories K, Popoff MR, Stiles BG (2004). "Binary Bacterial Toxins: Biochemistry, Biology, and Applications of Common Clostridium and Bacillus Proteins". Microbiology and Molecular Biology Reviews. 68 (3): 373–402, table of contents. doi:10.1128/MMBR.68.3.373-402.2004. PMC 515256. PMID 15353562.
^ [Medical Micriobiology, Fifth Edition, Patrick Murray, Elsevier Mosby, 2005, page 412]
^ "The chemical weapon that helps bacterium wreak havoc in the gut". Nature: International Journal of Science. 14 September 2018. Retrieved 8 October 2018.
^ a b Loo VG, Poirier L, Miller MA, Oughton M, Libman MD, Michaud S, Bourgault AM, Nguyen T, Frenette C, Kelly M, Vibien A, Brassard P, Fenn S, Dewar K, Hudson TJ, Horn R, René P, Monczak Y, Dascal A (December 2005). "A predominantly clonal multi-institutional outbreak of Clostridium difficile-associated diarrhea with high morbidity and mortality". The New England Journal of Medicine. 353 (23): 2442–9. doi:10.1056/NEJMoa051639. PMID 16322602.
^ McDonald LC (August 2005). "Clostridium difficile: responding to a new threat from an old enemy" (PDF). Infection Control and Hospital Epidemiology. 26 (8): 672–5. doi:10.1086/502600. PMID 16156321.
^ Saeed S. Banawas (21 February 2018). "Clostridium difficile Infections: A Global Overview of Drug Sensitivity and Resistance Mechanisms". Hindawi. BioMed Research International. Retrieved 4 November 2018.
^ "Clostridium difficile Infection Information for Patients | HAI | CDC". www.cdc.gov. Retrieved 22 May 2017.
^ "WHO Guidelines on Hand Hygiene in Health Care: a Summary" (PDF). World Health Organization. 2009. p. 31. Retrieved June 18, 2018.
^ a b Oliveira, Pedro H.; Ribis, John W.; Garrett, Elizabeth M.; Trzilova, Dominika; Kim, Alex; Sekulovic, Ognjen; Mead, Edward A.; Pak, Theodore; Zhu, Shijia; Deikus, Gintaras; Touchon, Marie (2019-11-25). "Epigenomic characterization of Clostridioides difficile finds a conserved DNA methyltransferase that mediates sporulation and pathogenesis". Nature Microbiology: 1–15. doi:10.1038/s41564-019-0613-4. ISSN 2058-5276. PMID 31768029.
^ Gould, L. Hannah; Limbago, Brandi (2010). "Clostridium difficile in Food and Domestic Animals: A New Foodborne Pathogen?". Clinical Infectious Diseases. 51 (5): 577–82. doi:10.1086/655692. PMID 20642351.
^ Belluck, Pam (February 25, 2015). "Death Toll From C. Difficile Is Raised". The New York Times. Retrieved 25 February 2015.
^ [Medical Microbiology, Fifth Edition, Patrick Murray, Elsevier Mosby, 2005, page 412]
^ a b c https://www.cdc.gov/hai/organisms/cdiff/cdiff-patient.html
^ McDonald, L. Clifford; Gerding, Dale N.; Johnson, Stuart; Bakken, Johan S.; Carroll, Karen C.; Coffin, Susan E.; Dubberke, Erik R.; Garey, Kevin W.; Gould, Carolyn V. (2018-03-19). "Clinical Practice Guidelines for Clostridium difficile Infection in Adults and Children: 2017 Update by the Infectious Diseases Society of America (IDSA) and Society for Healthcare Epidemiology of America (SHEA)". Clinical Infectious Diseases. 66 (7): e1–e48. doi:10.1093/cid/cix1085. ISSN 1537-6591. PMC 6018983. PMID 29462280.
^ Mullane, Kathleen M.; Miller, Mark A.; Weiss, Karl; Lentnek, Arnold; Golan, Yoav; Sears, Pamela S.; Shue, Youe-Kong; Louie, Thomas J.; Gorbach, Sherwood L. (September 2011). "Efficacy of fidaxomicin versus vancomycin as therapy for Clostridium difficile infection in individuals taking concomitant antibiotics for other concurrent infections". Clinical Infectious Diseases. 53 (5): 440–447. doi:10.1093/cid/cir404. ISSN 1537-6591. PMC 3156139. PMID 21844027.
^ Shane, Andi L.; Mody, Rajal K.; Crump, John A.; Tarr, Phillip I.; Steiner, Theodore S.; Kotloff, Karen; Langley, Joanne M.; Wanke, Christine; Warren, Cirle Alcantara (2017-11-29). "2017 Infectious Diseases Society of America Clinical Practice Guidelines for the Diagnosis and Management of Infectious Diarrhea". Clinical Infectious Diseases. 65 (12): e45–e80. doi:10.1093/cid/cix669. ISSN 1537-6591. PMC 5850553. PMID 29053792.
^ "Treatment of Recurrent Clostridium difficile Colitis with Vancomycin and Saccharomyces boulardii" (PDF). The American Journal of Gastroenterology.
^ a b Surawicz, Christina M; Brandt, Lawrence J; Binion, David G; Ananthakrishnan, Ashwin N; Curry, Scott R; Gilligan, Peter H; McFarland, Lynne V; Mellow, Mark; Zuckerbraun, Brian S (2013-02-26). "Guidelines for Diagnosis, Treatment and Prevention of Clostridium difficile Infections". The American Journal of Gastroenterology. 108 (4): 478–498. doi:10.1038/ajg.2013.4. ISSN 0002-9270. PMID 23439232.
^ Chen, Yu-Gen; Zheng, Xiao; Zhou, Jin-Yong; Wu, Jing; Jiang, Feng; Zhang, Dan; Zhou, Qun; Chen, Tuo (2018-05-25). "Effect of Faecal Microbiota Transplantation for Treatment of Clostridium difficile Infection in Patients With Inflammatory Bowel Disease: A Systematic Review and Meta-Analysis of Cohort Studies". Journal of Crohn's and Colitis. 12 (6): 710–717. doi:10.1093/ecco-jcc/jjy031. ISSN 1873-9946. PMID 29528385.
^ Rupnik M, Wilcox MH, Gerding DN (July 2009). "Clostridium difficile infection: New developments in epidemiology and pathogenesis". Nature Reviews. Microbiology. 7 (7): 526–36. doi:10.1038/nrmicro2164. PMID 19528959.
^ Jassem, Agatha; Prystajecky, Natalie; Marra, Fawziah; Kibsey, Pamela; Tan, Kennard; Umlandt, Patricia; Janz, Loretta; Champagne, Sylvie; Gamage, Bruce; Golding, George; Mulvey, Michael; Henry, Bonnie; Hoang, Linda (29 Mar 2016). "Characterization of Clostridium difficile Strains in British Columbia, Canada: A Shift from NAP1 Majority (2008) to Novel Strain Types (2013) in One Region". Canadian Journal of Infectious Diseases and Medical Microbiology. 2016: 8207418. doi:10.1155/2016/8207418. PMC 4904575. PMID 27366181.
^ Collins, J.; Robinson, C.; Danhof, H.; Knetsch, C. W.; van Leeuwen, H. C.; Lawley, T. D.; Auchtung, J. M.; Britton, R. A. (2018). "Dietary trehalose enhances virulence of epidemic Clostridium difficile". Nature. 553 (7688): 291–294. doi:10.1038/nature25178. ISSN 0028-0836. PMC 5984069. PMID 29310122.
^ He M, Sebaihia M, Lawley TD, Stabler RA, Dawson LF, Martin MJ, Holt KE, Seth-Smith HM, Quail MA, Rance R, Brooks K, Churcher C, Harris D, Bentley SD, Burrows C, Clark L, Corton C, Murray V, Rose G, Thurston S, van Tonder A, Walker D, Wren BW, Dougan G, Parkhill J (April 2010). "Evolutionary dynamics of Clostridium difficile over short and long time scales". Proceedings of the National Academy of Sciences of the United States of America. 107 (16): 7527–32. Bibcode:2010PNAS..107.7527H. doi:10.1073/pnas.0914322107. PMC 2867753. PMID 20368420.
^ Scientists map C. difficile strain – Institute of Public Affairs, Montreal
^ Didelot X, Eyre DW, Cule M, Ip CL, Ansari MA, Griffiths D, Vaughan A, O'Connor L, Golubchik T, Batty EM, Piazza P, Wilson DJ, Bowden R, Donnelly PJ, Dingle KE, Wilcox M, Walker AS, Crook DW, A Peto TE, Harding RM (December 2012). "Microevolutionary analysis of Clostridium difficile genomes to investigate transmission" (PDF). Genome Biology. 13 (12): R118. doi:10.1186/gb-2012-13-12-r118. PMC 4056369. PMID 23259504.
^ a b Hargreaves KR, Clokie MR (2014). "Clostridium difficile phages: Still difficult?". Frontiers in Microbiology. 5: 184. doi:10.3389/fmicb.2014.00184. PMC 4009436. PMID 24808893.
Pathogen Safety Data Sheets: Infectious Substances – Clostridium Difficile, Public Health Agency, Canada, 10 September 2014.
Type strain of Clostridium difficile, BacDive - the Bacterial Diversity Metadatabase.
Firmicutes (low-G+C) Infectious diseases
Bacterial diseases: G+
primarily A00–A79, 001–041, 080–109
Lactobacillales
(Cat-)
optochin susceptible
S. pneumoniae
Pneumococcal infection
optochin resistant
Viridans streptococci: S. mitis
S. mutans
S. oralis
S. sanguinis
S. sobrinus
S. anginosus group
bacitracin susceptible: S. pyogenes
Group A streptococcal infection
Streptococcal pharyngitis
Rheumatic fever
bacitracin resistant, CAMP test+: S. agalactiae
Group B streptococcal infection
Streptococcus iniae
Cutaneous Streptococcus iniae infection
BEA+: Streptococcus bovis
BEA+: Enterococcus faecalis
Enterococcus faecium
Bacillales
(Cat+)
Staphylococcal scalded skin syndrome
Cg-
novobiocin susceptible
S. epidermidis
novobiocin resistant
S. saprophyticus
Clostridium (spore-forming)
motile:
Clostridium tetani
nonmotile:
Clostridial necrotizing enteritis
Peptostreptococcus (non-spore forming)
Peptostreptococcus magnus
Mollicutes
Mycoplasmataceae
Ureaplasma infection
Mycoplasma genitalium
Mycoplasma pneumoniae
Mycoplasma pneumonia
Anaeroplasmatales
Erysipelothrix rhusiopathiae
Erysipeloid
Biology portal
Wikispecies: Clostridium difficile
LPSN: clostridium.html#difficile
NZOR: b212b1f2-123c-4ff3-8b3d-60313e54feab
Wikidata: Q56290719
BacDive: 2582
LPSN: clostridioides.html#difficile
Retrieved from "https://en.wikipedia.org/w/index.php?title=Clostridioides_difficile_(bacteria)&oldid=929354009"
Antibiotic-resistant bacteria
Clostridiaceae
Medically important anaerobes
Bacteria described in 1935
Taxonbars using multiple manual Wikidata items
This page was last edited on 5 December 2019, at 07:52 (UTC).


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Tyler Lange
Affiliate Assistant Professor
James Lin
Mark Metzler
Professor, Joint Appointment: Jackson School of International Studies, Giovanni and Amne Costigan Endowed Professor in History
New Course: The Holocaust and American Life (March 19, 2015)
"Self-Determination, Economic Development, and Native History," The Panorama: Expansive views from the Journal of the Early Republic, December 4, 2017 (http://thepanorama.shear.org/2017/12/04/self-determination-economic-development-and-native-history/). Learn more
Tyler Lange, Excommunication for Debt in Late Medieval France: The Business of Salvation (New York and Cambridge: Cambridge University Press, 2016) Learn more
Morrow, Alexander. Laboring for the Day: The Pacific Coast and the Economy of Contingent Labor, 1919-1933. Diss. University of Washington, 2015. Chair: James Gregory. Learn more
Myers, Polly. Capitalist Family Values: Gender, Work, and Corporate Culture at Boeing. Lincoln: University of Nebraska Press, 2015. Print. Learn more
Nam, Hwasook. Building Ships, Building a Nation: Korea's Democratic Unionism Under Park Chung Hee. Seattle: University of Washington Press, 2009. Print. Learn more
O'Mara, Margaret. Cities of Knowledge: Cold War Science and the Search for the Next Silicon Valley. Princeton, NJ: Princeton University Press, 2005. Print. Learn more
Yang, Anand. Bazaar India: Markets, Society, and the Colonial State in Bihar. California: University of California Press, 1999. Print. Learn more
Bergquist, Charles. Cafe Y Conflicto en Colombia. Bogota?: Ancora Editores, 1999. Print. Learn more
Jonas, Raymond. Industry and Politics in Rural France: Peasants of the Isère, 1870-1914. Ithaca: Cornell University Press, 1994. Learn more
Pyle, Kenneth. The Trade Crisis: How Will Japan Respond?. Seattle, WA, U.S.A.: Society for Japanese Studies, 1987. Print. Learn more
Bergquist, Charles. Coffee and Conflict in Colombia. Durham, NC: Duke University Press, 1978. Print. Learn more
Alden, Dauril. Essays Concerning the Socioeconomic History of Brazil and Portuguese India. Gainesville: The University Presses of Florida, 1977. Print. Learn more
Margaret O'Mara, The Code: Silicon Valley and the Remaking of America (New York: Penguin Press, 2019) Learn more
Mahoney, Eleanor. Beyond Wilderness: Parks, People, and Politics in the Age of Environmentalism. Diss. University of Washington, in progress. Chairs: James Gregory and Linda Nash. Learn more


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During the process of purchasing a home, there are many decisions to be made, documents to sign, and unfortunately many traps the inexperienced and even experienced home buyers can fall into if not careful. Puchasing a home is a substantial financial investment. Working with an experienced Realtor to guide you through makes the process much easier.
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Bacteria and Humans Have Been Swapping DNA for Millennia
Bacteria inhabit most tissues in the human body, and genes from some of these microbes have made their way to the human genome. Could this genetic transfer contribute to diseases such as cancer?
Kelly Robinson and Julie Dunning Hotopp
© TIM VERNON/SCIENCE SOURCE
Before we understood that DNA was the genetic code, scientists knew that bacteria transferred it between cells. In 1928, 25 years before the structure of DNA was solved, British bacteriologist Frederick Griffith demonstrated that live, nonvirulent bacteria could transform into virulent microbes after being incubated with a heat-killed virulent strain. Fifteen years later, a trio of researchers at the Rockefeller Institute for Medical Research (now Rockefeller University), Oswald Avery, Colin MacLeod, and Maclyn McCarty, demonstrated that this transformation was mediated by DNA. Even dead bacteria, it seemed, could share their genes.
Almost all bacterial genomes show evidence of past LGT events, and the phenomenon is known to have profound effects on microbial biology.
This DNA-sharing process, known as horizontal or lateral gene transfer (LGT), is now understood to occur by the direct movement of DNA between two organisms. Almost all bacterial genomes show evidence of past LGT events, and the phenomenon is known to have profound effects on microbial biology, from spreading antibiotic resistance genes to creating new pathways for degrading chemicals. But LGT is not limited to bacteria. Scientists now recognize that microbes transfer DNA to the plants, fungi, and animals they infect or reside in, and conversely, human long interspersed elements (LINEs) have been found in bacterial genomes. Moreover, researchers have documented LGT from fungi to insects and from algae to sea slugs. There is reason to believe that any two major groups of organisms—including humans—can share their genetic codes.
People have long been intrigued by the prospect of foreign DNA within our own genomes. Human genomes harbor evidence of beneficial LGTs from bacteria in the recent past, and there is evidence that transfers may occur regularly between resident bacteria and somatic cells of the body. How commonly bacteria-animal LGT occurs is unclear, as are the mechanisms of these transfers. But if LGTs induce harmful mutations, they may be an unrecognized cause of disease.
Gene swap
GENE SWAP: Horizontal or lateral gene transfer (LGT) is a regular event among bacteria, and research over the past decade has shown that microbes can also transfer their DNA to multicellular hosts. One of the most well studied examples of LGT between microbe and animal is the transfer of DNA from an intracellular Wolbachia endo-symbiont to its Drosophila host.
See full infographic: WEB | PDF© EVAN OTO/SCIENCE SOURCEBacteria are a genomically promiscuous bunch. They do not reproduce sexually but are among the most genetically varied species because they are constantly exchanging bits of their genetic code via LGT. Their diversity has allowed them to adapt to every ecological niche on the planet, from deep-sea hydrothermal vents to the frozen lakes of Antarctica, from rock crevices to our own intestines. LGT between bacteria has been categorized as transformation by free DNA (genetic material is released into the environment by bacteria and taken up by living microbes, as in Griffith's experiment), transduction by viruses, and direct cell-cell transfer through conjugation.
The mechanisms of transfer from bacteria to other organisms are less clear, but are likely similar. Bacteria's type IV secretion system is a syringe-like protein known to inject molecules from bacteria into their host cell though cell-cell contact. It is an important mediator of LGT between Agrobacterium and plants in the wild, as well as in the lab, where it can be used to create genetically modified crops and can even mediate transfer between Agrobacterium and human cells. Using whole genome sequencing, researchers have found that the genomes of numerous insects and nematode worms sometimes contain DNA from microbes inhabiting or infecting their bodies. Some species contain vast arrays of Wolbachia endosymbiont DNA, for example—up to many complete copies of the bacterial genome. (See illustration.)
These large LGTs can be nearly identical in sequence to the endosymbiont genome, suggesting that they happened quite recently. Some insect species carry remnants of much older gene transfers that were beneficial to the recipient species and have been selected for over time. The coffee berry borer, for example, coopted a bacterial mannanase gene that allows it to eat coffee berries.1 Coopted bacterial mannanase genes may also underlie crop destruction caused by the invasive brown marmorated stink bug.2 And aphids synthesize their own carotenoids using genes transferred from fungi to produce a colorful appearance important to defense.3 As more examples of LGT among diverse organisms crop up in the literature, it's only natural to focus on the human angle. Does it occur in us, and if so, how often, and what are the consequences?
LGT in humans
The extent and importance of LGT in vertebrate animals is less clear, in part because fewer of their genomes have been sequenced, and/or analyzed with suitable methods, compared with those of invertebrates. One vertebrate species whose genome has been extensively studied—humans—has yielded solid evidence of ancient LGT events.
In 2001, the first draft sequence of the human genome was suggested to have 223 LGT-derived regions that were not present in other species' genomes that had been sequenced at that time.4 Some researchers quickly disputed this number as an overestimate, even suggesting that all of the proposed LGTs were more likely explained through alternative mechanisms such as gene loss or convergent evolution.5 A new analysis published last year by Alastair Crisp of the University of Cambridge and colleagues found more than 130 traces of possible LGT events in the human genome—including the presence of fungal hyaluronan synthases, a fat mass and obesity associated gene (FTO), and the gene responsible for blood types (ABO). But most, if not all, of the identified events predate the human and primate lineages and were identified because the researchers chose to no longer limit the results to LGTs that exist only in humans and not in other animal species.6
In order for a nonhuman gene to appear in the genomes of many people, however, the LGT needs to occur in the germline so that it can be passed to future generations; and it has to confer some benefit to the host. Such LGTs may be rare, because humans may not experience strong selection for new functions in our genome, and because our germ cells are thought to be protected from other organisms and their DNA. However, LGT might be possible in the somatic human genome; such insertional mutations would be very difficult to detect, though, without sequencing large numbers of human cells.
Studies suggest that LGT events can and do occur in human tissues, perhaps with devastating consequences.
Once they are present in the human somatic genome, it's not hard to imagine how LGT insertions could cause disease. In fact, while definitive evidence of recent LGT in humans is still lacking, there are other types of DNA transfer that are well known to negatively impact humans. For example, human papillomavirus (HPV) is the cause of 80 percent to 100 percent of cervical cancers. The virus can integrate into the chromosomes of cervical cells, and if the integration is incomplete, certain HPV proteins can become unregulated, leading to disruption of apoptosis, an increase in cell proliferation, and ultimately cancer. Likewise, hepatitis B virus (HBV) causes hepatocellular cancer and has been found to insert its DNA into infected hepatocytes as the cells regenerate. HBV recurrently integrates its viral enhancer gene and its core gene into cancer-related genes, causing increased cell growth and survival, two hallmarks of cancer.7
Given the known risk of such integrations, we have focused on identifying LGT of bacterial DNA in the human genome. We knew that we needed to look at data from a large number of individuals, so we relied on publicly available human sequence data from the original public and private human genome projects and the 1000 Genomes Project. We quickly realized that if an LGT happened in a terminally differentiated cell that no longer replicates its DNA, it would exist in only one copy, and we would never be able to distinguish it from noise during sequencing. So we turned to tumors. We figured that, should an insertion occur in a progenitor cell of the tumor, it should be propagated in the tumor and be detected multiple times.
We analyzed genome sequence data from nine different tumor types from Cancer Genome Atlas projects and used bioinformatics tools to identify potential DNA integrations. In results published in 2013, we found sequences from Acinetobacter species in acute myeloid leukemia (AML) samples and from Pseudomonas species in stomach adenocarcinoma (STAD) samples. There were recurrent insertions in cancer-related genes in the STAD samples.8
In both the AML and STAD cancer samples, we only identified evidence of bacterial 16S and 23S rRNA fragments integrating into the human genome. Karsten Sieber, then a graduate student in the Dunning Hotopp lab, created models of the STAD integrations in cancer-related genes and observed that these pieces of the rRNA genes contain secondary structures that form numerous stem-loops, or hairpin loops. These integrations occur in the 5'-untranslated region (5'-UTR) of the cancer-related genes, meaning that they are transcribed but not translated. The stem-loops predicted in the inserted rRNA gene fragments could alter the secondary structures of the transcripts, thereby disrupting transcription and/or translation. We also noticed that the putative STAD integrations occur in G-rich regions of the cancer-related genes, which can also be important for gene regulation.9
LGT-CAUSED CARCINOGENESIS? If DNA is transferred from resident bacteria to human somatic cells, the integration risks transforming normal cells into cancerous ones.© EVAN OTO/SCIENCE SOURCE
Ying Xu at the University of Georgia has also identified LGT events in human tumors. His team looked for evidence of genetic material from Helicobacter pylori bacteria and the Epstein-Barr virus, both of which have been associated with gastric cancer. The researchers identified H. pylori integrations in 36 genes in the gastric samples, with more integrations present in the tumors relative to controls.10 Chronic infection with H. pylori can cause double-strand DNA breaks, and human cells may "heal" these double-strand breaks by inserting pieces of stray DNA. Often this is nuclear or mitochondrial DNA, but if bacterial DNA is present, including H. pylori DNA, it could become integrated. These integrations could therefore be a side effect, rather than a cause, of cancer.
It's unclear how bacterial DNA evades the human immune system, which recognizes most forms of nucleic acids. But these studies suggest that LGT events can and do occur in human tissues, perhaps with devastating consequences. So far, these are the only reported cases of bacterial DNA integrations in human cancers. Whether such events cause cancer, and if so, how commonly, remains to be seen.
A steep road ahead
A number of challenges face researchers hoping to assess the presence and impact of bacterial DNA integrations in the genomes of human cells. A thorough study of this sort is still expensive, and after the samples have been sequenced it takes significant resources to develop, implement, and run a computational tool to identify LGT.
Contamination also remains a barrier. This was an issue in an analysis of the human genome in 2001, and it continues to be a problem today. DNA extraction kits have been shown to contain bacterial nucleic acids. Contaminants can also be introduced via sample handling, from reagents, and during sequencing. During the process of creating the DNA library to be sequenced, chimeras that look like bacterial DNA integrations might form. Sure enough, earlier this year, researchers found that the extent of LGT in the tardigrade genome was initially overestimated; some proposed LGTs likely arose from the genomes of bacterial contaminants and not from the tardigrade genome itself.11
Despite skepticism from some corners of the scientific community and the difficulties of studying bacterial DNA integrations, we believe that LGTs are an important form of insertional mutagenesis. Perhaps now that putative bacterial DNA integrations have been identified in cancer, more researchers will look for these mutations in other diseases. A bacterial DNA integration that occurs in a human cell and leads to the expression of a bacterial compound recognized by the human immune system has the potential to trigger autoimmune disease, for example. Further research on the occurrence and consequences of LGT in human cells will likely reveal the phenomenon to be much more common and important than currently appreciated.
Kelly Robinson is a PhD candidate in the Molecular Medicine program at the University of Maryland, Baltimore. Julie Dunning Hotopp is an associate professor at the Institute for Genome Sciences at the University of Maryland School of Medicine.
R. Acuña et al., "Adaptive horizontal transfer of a bacterial gene to an invasive insect pest of coffee," PNAS, 109:4197-202, 2012.
P. Ioannidis et al., "Rapid transcriptome sequencing of an invasive pest, the brown marmorated stink bug Halyomorpha halys," BMC Genomics, 15:738, 2014.
N.A. Moran, T. Jarvik, "Lateral transfer of genes from fungi underlies carotenoid production in aphids," Science, 328:624-27, 2010.
E.S. Lander et al., "Initial sequencing and analysis of the human genome," Nature, 409:860-921, 2001.
S.L. Salzberg et al., "Microbial genes in the human genome: Lateral transfer or gene loss?" Science, 292:1903-06, 2001.
A. Crisp et al., "Expression of multiple horizontally acquired genes is a hallmark of both vertebrate and invertebrate genomes," Genome Biol, 16:50, 2015.
K.M. Robinson, J.C. Dunning Hotopp, "Mobile elements and viral integrations prompt considerations for bacterial DNA integration as a novel carcinogen," Cancer Lett, 352:137-44, 2014.
D.R. Riley et al., "Bacteria-human somatic cell lateral gene transfer is enriched in cancer samples," PLOS Comput Biol, 9:e1003107, 2013.
K.B. Sieber et al., "Modeling the integration of bacterial rRNA fragments into the human cancer genome," BMC Bioinformatics, 17:134, 2016.
J. Cui et al., "Comprehensive characterization of the genomic alterations in human gastric cancer," Int J Cancer, 137:86-95, 2015.
G. Koutsovoulos et al., "No evidence for extensive horizontal gene transfer in the genome of the tardigrade Hypsibius dujardini," PNAS, 113:5053-58, 2016.
horizontal gene transfer
lateral gene transfer
Wolbachia
The Human Brain: Blessing and Curse
What A Long, Strange Decade It's Been
Homo sapiens Might Not Be Responsible for Neanderthal Demise


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AMD Ryzen 7 1800X reviewed: Zen is an amazing workstation chip with a 1080p gaming Achilles heel
By Joel Hruska on March 2, 2017 at 9:00 am
After years of waiting, AMD's Ryzen has finally arrived. The company has spent years in the proverbial desert, struggling with Bulldozer improvements while simultaneously designing its new Zen architecture. It's no exaggeration to say AMD's future as a PC company literally depends on Ryzen's success.
AMD has positioned Ryzen aggressively with price points that match extremely favorably with Intel's Core i7 family and HEDT desktop parts, but there have always been questions about how well Ryzen would perform. It's been years since AMD fielded a high performance CPU design and the company doesn't have the same market share it once commanded. If the company is serious about pushing Ryzen into workstations, consumer PCs, and servers, it's got a very high bar to clear.
Today's review will focus on the Ryzen 7 1800X's performance, rather than rehashing Ryzen's design or architecture. Anyone with questions is invited to peruse those articles or ask in comments below. Before discussing Ryzen's performance, however, we need to talk about its launch. Normally, a manufacturer gives us 7-10 days at minimum; the more significant the product, the longer the review window. AMD bucked this trend by launching Ryzen less than a week after we received our hardware kits. Because I'd previously committed to attend Nvidia's GTX 1080 Ti launch at GDC, I only had 60 hours to test the Ryzen 7 1800X.
AMD plans to hit Intel where it hurts — its wallet.
As short as our review window was, I may have gotten lucky. In at least a few cases, reviewers didn't receive their kits until 24-48 hours before the launch. I've run enough benchmarks on the Ryzen 7 1800X to feel comfortable characterizing this article as a review, but it's also something of a hot mess. I suspect you'll see wide variation in reported benchmarks and experiences; don't be surprised if different people have different results.
The limited testing time was exacerbated by the motherboard AMD shipped us for testing. Asus has a well-deserved reputation for quality, but my Crosshair VI Hero threw so many errors, AMD ultimately concluded I might have a bad board, not just a wonky BIOS. To be clear: I was scarcely the only reporter to experience problems or see odd performance, but our board seems to have been at the low end of the bell curve. Both Asus and AMD helped troubleshoot our problems, but the hours we devoted to this cut deeply into test time and required us to repeatedly benchmark certain tests rather than moving on to other hardware. After switching to a Gigabyte Aorus X370 motherboard I retested our game benchmarks, beginning around 12 AM this morning. While the Gigabyte motherboard did improve the situation slightly and was markedly more stable, it didn't resolve the gaming Achilles heel I referred to in the title (we'll be exploring that issue in greater detail below).
As a result, our tests are not as thorough as we would have liked. We redesigned our CPU benchmark suite in preparation for Ryzen, but didn't have time to run every CPU through every new test. Because we needed to test in parallel, not every CPU could be benchmarked with the same cooler or the same SSD. We chose the tests we did partly to ensure that these differences would not meaningfully impact our results, and our future deep dives into the chip will standardize on common hardware once again.
With those caveats in mind, let's check the numbers.
Test setup:
We've expanded our CPU test suite since the Core i7-7700K launched. Our Intel Core i7-6700K, 7700K, 6900K, and 6950X all used 32GB of G-Skill DDR4-3200 (F4-3200C14Q-32GTZ) clocked at that frequency. Neither of the Ryzen testbeds we tested, however, was capable of running four DIMMs at these clocks. Since we'd already tested the Intel systems, we had to make a choice: 16GB of DDR4-3200 or 32GB of DDR4-2133. Since none of our benchmarks require >16GB of RAM and AMD isn't using quad-channel memory for Ryzen, we opted for 16GB.
All of our GPU and 3D benchmarks were run using a GeForce GTX 1070. All of our game benchmarks are run at 1920×1080. While this isn't considered an enthusiast resolution anymore, the point of these tests is to stress the CPU, not the GPU. All of our testbeds ran Windows 10 with the latest patches and updates installed. All of our GPU benchmarks were performed with Nvidia's ForceWare 376.88.
We're going to split our benchmark results between workstation and application tests and 3D benchmarks with workstation and content creation tests up first. Our test results and analysis are in the slideshow below. As always, you can click on any slide to expand it in a new window.
In workstation and computation tests, Ryzen is a beast to be reckoned with. Even when it doesn't match Intel in raw performance, its performance-per-dollar gives it a huge advantage over its much larger, more expensive, rival. That said, there's a narrow case to be made for chips like the Core i7-7700K, particularly in lightly threaded workloads. If you're still dealing with single-thread or dual-threaded applications, the Core i7-7700K can still deliver the best performance per dollar. In most cases, however, the Ryzen 7 1800X is in a class of its own. That's also true for gaming — but in very different contexts.
Results like these are guaranteed to raise questions, and we've spoken to AMD extensively over the past few days to explore the issue. According to AMD, there are three issues collectively contributing to these problems. First, Ryzen's SenseMi technology and Precision Boost are extremely fine-grained controls that offer significantly finer granularity than any previous AMD solution, which means BIOS implementations of these features are new and not necessarily working at 100% efficiency yet. Second, AMD has been out of the high-performance market for so long, virtually no software is written explicitly for or optimized to perform well on AMD CPUs. Ryzen puts AMD on a far better footing, but software patches don't arrive overnight. Third, there are some games that are far more sensitive to the differences between AMD and Intel CPUs than others. We happened to pick a test suite that had more of these slowdowns in it than others, and even we don't see it every test (Vulkan, for example, runs quite well).
The other reason AMD missed it is because they chose 1440p for a minimum resolution, figuring that no one with a $500 CPU would still be gaming in 1080p. I can understand that argument even if I don't normally find it persuasive (I prefer to keep a lower resolution to allow CPU performance to shine through). According to AMD, the difference in performance between itself and Intel is much reduced at 1440p and completely eliminated in 4K. I haven't had the opportunity to verify those figures yet, but it does make sense — as resolution rises, the bottleneck in the system moves from the CPU to the GPU. If you game at 1440p or above, these results may not have much bearing on your experience.
I had a number of conversations with AMD on the game performance question as well as discussions of board stability in general. Having tested a second motherboard, I think many of my stability and performance concerns were driven, at least in part, by faulty hardware. That said, Ryzen's relative weakness in gaming while being such a vast improvement over the FX-9590 and offering extremely strong application/workstation performance is a bit odd. It's possible that AMD's heavy reliance on multi-threading, while effective in non-gaming tests, made it take a whack in game tests. This last, however, is merely speculation on my part.
Last but not least, here's a touch of icing for the proverbial cake.
There is one caveat to be aware of. Remember, all of our Intel rigs used 32GB of DDR4-3200, while the AMD systems could only use 16GB of the same RAM. While this is undoubtedly having an impact on the results, it's not going to tilt them in some crazy direction; 16GB of RAM doesn't consume 42W of power, and that's how much it would have to draw to bring the 1800X and 6900K into line with one another. Even with this caveat in mind, when was the last time you saw AMD hitting lower power consumption figures than Intel?
We still have plenty of questions about Ryzen and its performance, and we'll be revisiting these topics in days to come. How strong Ryzen is, in an absolute sense, depends on where your interests lie. Evaluated strictly as a gaming chip, Ryzen is a good (but not great) option, due to its significant deficits against Intel. Evaluated as a workstation processor or 3D rendering solution, it's extraordinary. The formal list price on the Core i7-6900K is $1089 – $1109. List price on the Ryzen R7 1800X is $500 bucks. I still think AMD should've held off launching until its partners had a bit more time to improve their boards, but that's not my decision.
If you're unhappy about Ryzen's gaming weaknesses relative to Intel, I'd suggest taking a walk down memory lane. When AMD began to gain ground on Intel in the late 1990s, it didn't leap from budget chip manufacturing to the Athlon 64 X2 in a single bound. The K6 and K6-2 were adequate chips for budget-conscious gamers and Windows desktop software, but they weren't going head-to-head with Intel's Pentium II's and winning the competition. It took years, and multiple product iterations, before the Athlon 64 was ready to tackle Intel in the server room. Given how far AMD's market share has fallen, it's going to take the company at least a year to build up any serious market share.
I've said for years that Ryzen didn't need to beat Intel in every particular, it simply needed to offer a viable alternative at a good price. Ryzen more than does that. It may not be the best chip at everything, but it's more than good enough to help AMD win back some badly-needed market share. Even more importantly, this is a CPU core that AMD can scale up and out as the need arises. It's great to have competition back in the CPU market.
K6-2
R7 1800X
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So, if you are planning to give yourself some extra pampering this 'love month', visit HAIR X REMOVAL and check out what services you can avail of, with no downtime!
HAIRX REMOVAL is a local concept inspired by Musee, Japan's No.1 Hair Removal salon.
HairX caters to men and women from 14-40 years old. Visit HairX Hair Removal at the 2nd Level, Conrad S Maison, Marina Way, Mall of Asia Complex, 1300 Pasay City T: (02) 772-4587 M: 0915-774-3139 Operations: Mon-Sun (10:00AM - 10:00PM). HairX Hair Removal BGC branch is located at 2F Eight Forbes Town Road, Forbes Town Center, Fort Bonifacio, Taguig T: (02) 403-6346 M: 0977-855-5793; Operations: Mon-Sun (11:00AM - 8:00PM). Facebook: Hairxph / Instagram:hairxhairremoval.