prompt_front: Now, answer the following question based on the text below, only give me the answer and do not output any other words.

Question: What were the vaccines trialed against?

Read the following text and answer briefly.

Context 1: A special tribute to Del Bigtree (pictured) and his team at ICAN for his stunning 88 page letter to the HHS regarding vaccine safety  As Del reported - in the latest edition of Highwire - the letter, in response to an earlier reply from the then acting Director National Vaccine Program Office, Melinda Wharton, took virtually a year to compile, and is a meticulous piece of research  Most sensationally they researched the HHS claim through US government archives that at least some pediatric vaccines had been trialed against genuine placebo, and came to a negative conclusion  Not only that, they established that none of the vaccines those vaccines had been trialed against had ever been trialed against genuine placebo either  At the end of the line the toxic products were only being compared with other toxic products, rather than against saline 
Leave aside the sceptics, for any believer in the vaccine program as a necessary intervention in public health, this should be a devastating finding  Fundamentally, the research into the safety of any of the products before marketing was simply not there  The manufacturers apparently had no faith that their proto-products could withstand this scrutiny, and for the rest they just did not care: under the alleged imperative of protecting the population it seems anything went  So even before all the sham monitoring procedures and reviews which Del and his team dismantle in forensic detail we are left with the proposition that none of the present products being given to US children – and frequently other children across most of the developed world – have any meaningful pre-marketing safety data all  If you are believer in the program you have been let down: if you wanted a program with any pretensions to safety - supposing such a thing to be possible - it looks like you would have to start from scratch  The manufacturers did this: the governments, the politicians and the regulators (internationally) let it happen 
This damning document is published simultaneously with a demand in the UK from the Royal Society for Public Health (which I had never heard of) to shut down comment about vaccines on the web  It echoes calls from Seth Berkley of GAVI, Heidi Larson of the Vaccine Confidence Project and the European Parliament  The pamphlet airily dismisses concerns that vaccines have side effects or that you could possibly have too many  It is pure public relations, and if the RSPH claims to be "independent" it also admits that the publication was paid for by Merck, a detail which was reported by British Medical Journal and the Guardian, but not true to form by the BBC  We have, in truth, been building to this moment for two decades: as the evidence piles up that every single aspect of the program lacks integrity or is simply rotten to the core all the perpetrators can do is call for the silencing of their critics, and maintain the products are safe because they say so 
Please help give the ICAN letter the widest possible distribution, particularly to politicians 
"The outcome of disease always depends both on the virulence of the pathogen and the health of the individual immune system "
Nope  This makes no sense  Lots of people who seemed vibrant will get a very severe case of the same illness that a vulnerable baby overcomes in a day 
And under the germ theory it doesn't matter how strong your immune system *was*  Once it's been overcome by the pathogen it is every bit as weak as anybody else's with that pathogen 
What you say makes no sense  There's no reason for me to reply to you again 
"Why do you think that within a few years (not many) of the introduction of the vaccines for them, pertussis, measles, mumps, rubella, tetanus, diphtheria, Hib disease, and chickenpox (and others) almost entirely disappeared?"
Why do you keep asking this question when I've already provided the answer hundreds of times? Why are you so desperate to believe the people who you already recognize are harming our children?
Why would Walter Reed be any more trustworthy than Paul Offit or Senator Pan? Why would Jenner or Pasteur?
And you went no way to explaining my arguments against germ theory  If we are attacked by billions of viruses every day then if even a tiny fraction of them are pathogenic then we couldn't possibly survive  And even if we could, we would already be immune rendering every vaccine pointless  Once we had survived our first few days on earth, then we could never get sick again 
If that's wrong then we must conclude that precisely 0% of germs are pathogenic 
Plus your comment about the immune system completely misunderstood my point  The immune system does not allow us to overcome our math problem  In fact, it makes it worse 
You did provide one solitary example of a patient with what are presumably yellow fever symptoms but you didn't say whether they had been given any toxic medical treatments 
And like I said before, the whole "incubation period" is more than a little suspicious  Clearly they never found what they thought they would and just rigged the results to tell them what they want to hear 
Like every other germ theorist/vaccine promoter in history 
Many kinds of bacteria are constantly evolving and changing, like flu viruses  Others are more stable over time, like the yellow fever virus  Those that change develop new ways of infiltrating the cells of the organism being attacked (from our point of view, from its unconscious point of view, it's just carrying out its need to replicate, which it can only do inside the cells of its host)  The changes which allow it to better infiltrate are more successful and result in more viruses with those traits 
Our immune system is designed to detect and destroy potentially dangerous invading pathogens  Many bacteria are usually harmless and absolutely necessary  The minority are dangerous, and most people's immune systems do a good job of analyzing them and killing them, often with no signs of disease  Others experience a clinical infection, and the immune system usually mounts a successful attack on them 
The outcome of disease always depends both on the virulence of the pathogen and the health of the individual immune system  Vaccines are usually effective in giving immunity to the targeted diseases  They also have many dangers which everyone should be aware of, and vaccines should be avoided whenever possible  But in the case of the most dangerous diseases, everyone should learn about them and think about what he wants to do to protect himself and his children from them, considering all the factors involved  And no one can have 100% certainty that he has made the right decision, but that's life  But if you live in the Congo and many people around you are currently dying of yellow fever, then that means that you yourself are at risk of being bitten by a loaded mosquito and getting, often dying, of yellow fever  The yellow fever vaccine is very effective at preventing yellow fever  From there, each person must make a choice 
At the end of this stage there is a remission of two or three days  About 80% of those with clinical disease recover at this point, with permanent immunity  The other 20% enter the toxic stage, with a return of the fever, black vomit (coffee-ground emesis), diarrhea, a slowing of the pulse (Faget's sign), jaundice, yellow eyes, yellow skin, and failure of the kidneys, liver, and heart  The patient gets a strange hiccup (like with Ebola, a related disease), falls into a coma, and dies  About half of those patients who enter the toxic stage dies, even now, even with the best of hospital care  The Faget's sign can also occur at the end of the first stage 
You asked specifically about the symptoms of the Americans on Dr  Reed's team who got yellow fever in Cuba in 1900  I'll give the passage from The American Plague (162-5), which describes the course of Jesse Lazear's illness  "In his logbook, Lazear wrote an unusual entry on September 13  In all cases before those, page after page of records, Lazear had used the soldier's name and simply the date he was bitten, with no other attention to the mosquito  A one-line entry with a name and a date  On that day, however, in his elegant hand, Lazear did not write the soldier's name, but instead wrote 'Guinea Pig No  1 ' He went on to write that this guinea pig had been bitten by a mosquito that developed from an egg laid by a mosquito that developed from an egg laid by a mosquito that fed on a number of yellow fever cases: Suarez, Hernández, De Long, Ferández  It was a precise, detailed history that proved beyond doubt that the mosquito was loaded with the virus when it bit a healthy soldier   (If he had entered his name, then his death would have been considered medical suicide by the insurance company, and his wife and two children would not have gotten any payment ) For the next few days, Lazear's life continued much as it had over the last few months in Cuba  He fed and cared for the mosquitoes in the lab    Then he began to lose his appetite  He skipped a few meals in the mess hall  He didn't mention it to anyone, nor did he ask to see one of the yellow fever doctors; instead, he worked hard in the lab trying to ignore the oncoming headache 
"On September 18, he complained of feeling 'out of sorts,' and stayed in his officer's quarters  His head pounded and L  decided to write a letter    (he wrote to his mother, and referred to his one-year old son Houston and the baby his wife Mabel was about to have: they were staying with his mother in the US)    That night, L  started to feel chilled as the fever came on  He never went to sleep but worked at his desk all through the night, trying to get all the information about the mosquitoes organized  By morning, he showed all the signs of a severe attack of yellow fever  The camp doctors made the diagnosis, and L  agreed to go to the yellow fever ward    L  was carried by litter out of the two-room, white pine board house in which he had lived since he and Mabel first arrived in Cuba    (In the yellow fever ward, in a separate one-room building), Lena Warner (the immune nurse who had survived the yellow fever in 1878, when she was nine, and was found in her boarded-up house by a former slave who first thought she was dead, and carried her to safety) nursed J L , recording his vitals  (I put up a link to his case record and vital signs last week  The surgeon general required that this record be made for every yellow fever patient )    (On September 25,) Lena Warner braced L's arms with all of her weight, shouting for help  Still he bolted from the bed, darting around the small frame-wood room as wildly as a trapped insect beating against glass  Two soldiers ran into the ward, pinning L to his bed, tying restraints around his wrists and elbows    Warner sponged his body with iced whiskey and water  She recorded his temperature, which had held at 104 degrees for days, on the chart beside his bed    (Warner watched him sleep ) But the quiet did not last  L's body began to lurch, and black vomit rolled from his mouth; through the bar hanging above his hospital cot  He writhed in the bed, and his skin grew deep yellow  His 104 temperature slowly fell, leveling out 99 degrees, and JL died at 8:45 p m  at the age of thirty-four "
As is obvious, there are many problems with vaccines  But, that being said, most of them usually work for a period of time to prevent the targeted diseases  The basic science behind vaccines is correct  Why do you think that within a few years (not many) of the introduction of the vaccines for them, pertussis, measles, mumps, rubella, tetanus, diphtheria, Hib disease, and chickenpox (and others) almost entirely disappeared? In the case of the routine childhood diseases, this was a bad thing, but it is a true thing 
Vaccines usually don't cause any obvious reactions  While they usually prevent the diseases, and that's why people continue to get them  With the increasing vaccination schedule, more and more are severely and permanently damaged, and it is immoral to mandate any vaccine for anyone for this reason  But it would also be immoral to prohibit vaccines for those who want them enough to take the risk 
Your article said as though it had any probative value that 90% of those who get pertussis had been vaxxed  The old DPT vaccine was MUCH more effective at preventing pertussis, but it was so dangerous (again, not to most, but to many), that developed countries replaced it with the acellular version, DTaP  From the beginning about twenty years ago, it was clear that it was not very effective and that huge numbers of vaxxed people got pertussis anyway, including my daughter who got pertussis at eight month old after having gotten three DTaPs  The pertussis vaccine continues to be very dangerous, and I do not recommend that anyone get it  It used to be a killer disease, but evolved to become much milder, to the extent that the disease is very rarely dangerous (usually only to newborns under three months old), while the vaccine is very dangerous  And they're trying to see how they can go back to the old DPT  This does not show that vaccine science has collapsed, but rather that the vaccine they developed to replace the DPT turned out to be much less effective than they first thought, while continuing to be much more dangerous than they first thought 
Your article extrapolated from that that modern medical science in general has collapsed, but that, again, is going too far  A older woman in Mexico City who is like my mother to me had a pacemaker inserted about two months ago to aid her failing heart, and it has restored her to optimism and energy, when she was despondent, weak, and close to death  I took my daughter to the dentist yesterday, who said she has three wisdom teeth coming in and that she said that the lower right one was sore  So, although I am cautious about X-rays, I made an appointment for a panoramic X-ray in a month to assess the wisdom teeth, and, if it seems appropriate, I'll take her to an oral surgeon to have one or more extracted under IV sedation, in his office, if possible (the dentist thought that it would be)  And I am confident that there will be no serious problems, but this is thanks to technology and training in modern medicine that haven't been available for that long 
I think that everyone should inform himself on all medical procedures before agreeing to anything, but I also think that he should have access to any medical procedure which is reasonable (and opinions can differ as to that) 
One problem is that you have not said how you think people should protect themselves against tetanus, bacterial meningitis, and yellow fever in the relevant cases, for example  These are diseases which healthy, well-nourished people used to die from very readily 
If most people stopped vaxxing and the mortality from these diseases rose to something like pre-vaccine levels, do you think they should just accept dying from them?
I put that in a separate paragraph because it is the crucial issue 
balinaheuchter Air Traffic Control You Tube - Colin Campbell example of - How to "Fudge a Nudge" -"Deal" or "No Deal" "Not in a month of Sundays" "No exceptions/no compromise?" -make a trade off -do an exception- everyone get's a good deal /good outcome!
Hans, you are right that we are looking at one of the biggest crimes in all history  When I read the story of that poor girl who was so healthy and is now confined to a wheelchair after getting her third Gardasil shot I could not believe that Merck could produce such a toxic vaccine and give it out to girls like it was something they absolutely had to have only to be mislead and made into cripples  Merck should be prosecuted for the damage they have done to so many girls who got the Gardasil vaccine and were physically debilitated for life  There is a place for the people who perpetrated this crime on young girls and women and it is called hell  They have destroyed people's lives and gotten away with it  My heart goes out to those who have suffered this damage for no damn good reason except to help make huge profits for Merck!
Here is the reason that the germ theory is nonsense 
1) Everyday we are bombarded with billions of germs  Presumably at least some of them are of the kind that germ theorists believe are dangerous (otherwise we would have to conclude that none of them are dangerous)  So how do we survive?
2) Let's just say that we ignore 1 and imagine that, by way of magic, none of the billions of viruses we get bombarded with are pathogenic but all those that are are tucked away somewhere  Ok  But presumably they reside in sick people right? So where are there lots of sick people? Doctor offices and hospitals! So everybody must be dying the moment they enter these places right?
3) I love this one because I have never seen anybody else ever raise it  Under the germ theory there are no negative feedbacks  This makes a stable biological system by definition impossible  The immune system is *not* a negative feedback it is the opposite  It actually reinforces our math problem because the immune system will weaken as the number of pathogens increase 
There is no way of resolving this problem without a discontinuity  A Deus ex Machina as The Almighty Pill so beautifully put it  So the germ theory is quite literally, mathematically impossible 
There is as much chance of it being true as 2+2 = 5 
There are plenty of other massive problems with germ theory such as why did things like SARS and bird flu magically disappear? Why do we have the symptoms that we do? Is our body controlling the symptoms to help fight the germs and if so, why would suppressing the symptoms with antibiotics or Tamiflu be considered a good idea? If the virus is causing the symptoms then why would it cause these kinds of things?
Context 2: Filip Fremo Minge – Ekofisk
Author: Filip Fremo Minge
Posted on 1  October 2019 12  October 2019
— Sunset over Ekofisk  Photo: Husmo Foto/Norwegian Petroleum Museum
The three are operated by ConocoPhillips on behalf of the Ekofisk licensees  The area also embraces former producers Albuskjell, Cod, Edda, Tor, West Ekofisk and Tommeliten G 
These fields all lie within production licence 018 apart from Tommeliten G, which was operated by Statoil from 1976 to 2003 
In all, 31 installations have been positioned in the Greater Ekofisk Area 
First Norwegian offshore field
Ekofisk began production on 15 June 1971, following its discovery in the autumn of 1969  Development of the field has occurred in several phases 
Its central facilities were installed during the early 1970s, with oil initially being buoy-loaded into tankers  From 1975, it has been piped to Teesside in the UK  The gas has been landed by pipeline at Emden in Germany from 1977 
ekofisk i et nøtteskall, engelsk
Jacked up six metres
The water depth in the Greater Ekofisk Area is 70-75 metres  However, declining pressure in the Ekofisk reservoir over the years has caused the seabed to subside 
Efforts began as early as 1985 to safeguard the installations against the effects of this development, and the steel platforms in the Ekofisk Complex were jacked up by six metres in 1987 
In addition, a protective breakwater was installed around the Ekofisk tank in 1989  The rate of seabed subsidence has declined sharply in recent years 
Waterflooding improves recovery
The Ekofisk 2/4 K water injection platform became operational in December 1987 as part of efforts to improve Ekofisk’s recovery factor – the share of petroleum in place actually produced 
Waterflooding capacity on the field to help maintain reservoir pressure was later expanded several times, and had reached just over 500 000 barrels per day by 2019 
Measured in barrels of oil equivalent, the recovery factor on Ekofisk has risen from an original estimate of 17 per cent to over 50 per cent 
Ekofisk I and II plus licence extension
The first phase of development and production on Ekofisk began with initial oil output from the converted Gulftide jack-up rig in 1971 and ended with the start-up of Ekofisk II in 1998 
Large parts of the Greater Ekofisk Area were restructured in the latter year, leading to plans for removing 15 installations – 14 steel platforms and the process facilities on the Ekofisk tank 
plattformer, historie, 2004, driftsenter åpnet,
Embla 2/7 D  Photo: ConocoPhillips/Norwegian Petroleum Museum
Designated Ekofisk I, these redundant structures include Ekofisk 2/4 A, 2/4 B, 2/4 FTP, 2/4 Q, 2/4 H, 2/4 R, 2/4 P and 2/4 T 
In addition come the Edda 2/7 C, Albuskjell 1/6 A, Albuskjell 2/4 F, Cod 7/11 A, West Ekofisk 2/4 D, Norpipe 36/22 A and Norpipe 37/4 A installations 
The concrete part of the tank – Ekofisk 2/4 T – will remain  Gulftide was removed as far back as 1974  Two platforms owned by other companies – Ekofisk 2/4 G and 2/4 S – have also gone 
A new plan for development and operation (PDO) of the field (Ekofisk II) was approved in 1994, at the same time as the Ekofisk licence was extended to 2028 
This creates a new Ekofisk Complex with two structures – the Ekofisk 2/4 X wellhead unit installed in the autumn of 1996 and the Ekofisk 2/4 J processing and transport platform in 1997 
Ekofisk II became operational in August 1998 and is intended to produce until 2028  Ekofisk, Eldfisk and Embla are tied back to the new complex, as was Tor until it shut down in December 2015 
Ekofisk West
historie, forsidebilde, 2003, ekofisk vekst godkjent i statsråd
Ekofisk Growth  Illustration: Ståle Ådland
In December 2002, soon after the Conoco-Phillips merger had been announced, the Ekofisk West project was presented to improve oil and gas recovery  Process capacity and reliability on Ekofisk were also to be enhanced 
This development primarily involved the construction and installation of a new platform, Ekofisk 2/4 M, with processing facilities and 24 new wells drilled over five years 
The latter could contribute to improved recovery both because there were more wells and because they would tap new locations in the reservoir  On stream in 2005, 2/4 M was linked to the Ekofisk Complex with a bridge 
Process capacity for produced water was also to be increased through upgrading on Ekofisk 2/4 J and Eldfisk 2/7 E  A third measure concerned laying a power cable from the Ekofisk Complex to 2/4 K in order to make electricity supplies more efficient 
New developments: Eldfisk II and Ekofisk South
Eldfisk 2/7 S løft
The deck of Eldfisk 2/7 S being mated with the steel jacket  Foto: Øyvind Sætre/ConocoPhillips
The plan for development and operation (PDO) of Eldfisk II, approved by the Storting (parliament) on 9 June 2011, includes a new wellhead, process and accommodation platform – Eldfisk 2/7 S 
In addition come 42 new wells as well as upgrades to existing platforms which extend their commercial life 
The PDO for Ekofisk South involves the construction of a new wellhead platform – Ekofisk 2/4 Z – as well as a new subsea water injection facility and 44 additional wells 
ConocoPhillips Norge, 2004 
Ministry of Petroleum and Energy, press release, “Vekstprosjekt på Ekofisk godkjent”, 6 June 2003 
https://www stortinget no/no/Saker-og-publikasjoner/Saker/Sak/?p=50343
https://www stortinget no/globalassets/pdf/innstillinger/stortinget/2010-2011/inns-201011-398 pdf
https://www regjeringen no/no/aktuelt/klart-for-40-nye-ar-pa-ekofisk-feltet/id642376/)
Published 1  October 2019 • Updated 12  October 2019
— Gassterminalen i Emden  Foto: Husmo Foto/Norsk Oljemuseum
Oil terminal in Teesside
Olje- og gassterminalene, engelsk,
Teesside terminal  Brian Henderson Thynne takes samples of refrigerated propane  Photo: Husmo Foto/Norwegian Petroleum Museum
The terminal at Teesside in north-east England receives oil and natural gas liquids (NGL) by pipeline from the Ekofisk field  It comprises stabilisation, NGL fractionation, storage tanks for crude oil and an export port 
After arriving through the Norpipe Oil line, crude and NGL are separated and the oil goes through a stabilisation process before reaching the 10 storage tanks, which each hold 750 000 barrels 
The NGLs go to the fractionation facility, with a daily capacity of 64 000 barrels, for separation into methane, ethane, propane, and normal and iso butane 
While the methane (natural gas) is used to fuel the plant, the other products (now known as liquefied petroleum gases – LPG) are made liquid by cooling and stored for export by sea 
One reason for the choice of Teesside as the landfall for the Ekofisk pipeline was the opportunity it offered to install deepwater quays 
The terminal has four of these, with those for crude oil able to handle tankers up to 150 000 deadweight tonnes  The LPG quays can accept carriers loading as much as 60 000 cubic metres 
Two of the crude oil quays lie on the main channel of the River Tees, while the others have been installed in dredged docks 
Gas terminal in Emden
Gas arriving at the Emden terminal from the Ekofisk Complex enters nine parallel treatment trains for cleaning, metering and onward distribution to the buyers 
The North Sea gas is very clean, and needs only limited treatment to remove small amounts of sulphur compounds using an absorption process  Impure molecules from the gas accumulate on the surface of small particles, which act as filter spheres 
Each of the nine trains comprises four process columns and a process oven  The gas enters the top of a column and leaves through the base after passing through the filter spheres 
That leaves the gas ready for sale, and it is piped to the fiscal metering station before entering the buyer receiving pipelines and distribution network 
Three separate commercial pipeline systems connect to the terminal, operated by Ruhrgas, BEB and Gastransport Services (previously Gasunie) respectively  They pipe the gas away on behalf of the gas buyers 
The Norsea Gas Terminal in Emden was officially opened in September 1977 by Norwegian industry minister Bjartmar Gjerde and Phillips executive Gordon Goerin 
Ranking as the first gas sales deal for the Norwegian continental shelf, the Ekofisk agreement paved the way for later contracts covering other fields off Norway 
Regularity at the Emden terminal has been very high, with its own equipment never causing shutdowns  Maintenance takes place when other parts of the system are off line 
The terminal has a daily capacity of about 2 1 million cubic feet of gas per day 
Gas transport restructured
Norpipe AS owned the gas pipeline from Ekofisk to Emden until the transport system for the Norwegian offshore sector was restructured at 1 January 2003 
Norsea Gas A/S furthermore served as the formal owner of the Emden facility, with Phillips Petroleum and then ConocoPhillips as operator for both pipeline and terminal 
olje- og gassterminalene,
Teesside gas terminal  Photo: Husmo Foto/Norwegian Petroleum Museum
Since 2007, Norway’s state-owned Gassco company has been responsible for technical operation of the facilities on behalf of their owners 
That included operator responsibility for the H7 and B11 booster platforms along the gas pipeline, which were shut down in 2007 and 2013 respectively and have since been removed 
The Gassled partnership is a project collaboration embracing 10 companies which collective own large parts of the gas infrastructure on the Norwegian continental shelf (NCS) 
A substantial proportion of Norway’s gas deliveries to Germany continues to arrive at the Emden terminal, including the volumes piped from Ekofisk 
Preliminary planning for a new terminal in the German port began in 2011, with Gassled taking the investment decision for this development in the autumn of 2012 
Construction work began in the following year, with the new facility being built on an unused part of the existing terminal site 
The new terminal has not expanded export capacity  But its functionality is well adapted to future processing needs for fields in the Greater Ekofisk Area and other parts of the NCS sending gas through the Norpipe system 
It was officially opened on 24 May 2016 by Elisabeth Aspaker, the Norwegian government minister for the EU and the European Economic Area  That closed a chapter in Ekofisk’s history 
Source: ConocoPhillips Norge
— Gas pipes at Ekofisk  Photo: Husmo Foto/Norwegian Petroleum Museum
In addition to ConocoPhillips’ own production from Ekofisk, these pipelines carry gas and oil from the company’s fields in the UK sector and from other fields on the Norwegian and British continental shelves 
The three fields in the Greater Ekofisk Area are also tied together by pipelines 
Oil pipeline to Teesside
rørledningene, engelsk,
Pipes and oil tanks at the Teesside plant  Photo: ConocoPhillips/Norwegian Petroleum Museum
The pipeline linking Ekofisk with the terminal for oil and natural gas liquids (NGL) at Teesside on the north-east English coast became operational in October 1975 
Pumps raise the pressure of the oil and NGL before they start their journey to land  Two pumping stations – 37/4 A and 36/22 A ­– originally stood along the pipeline to maintain this pressure, but have now been disconnected and removed 
The pipeline was installed with the ability to carry a million barrels per day  However, that much capacity has never been required 
In the UK sector, a 24-inch pipeline has been tied in with a Y connection to receive input from several British fields – including the J block developments operated by ConocoPhillips 
Output from the Greater Ekofisk Area is supplemented by crude from Valhall, Hod, Ula and Gyda heading for Teesside, optimising pipeline utilisation and thereby boosting value creation 
The pipeline is owned by Norpipe Oil AS and operated by ConocoPhillips 
Gas pipeline to Emden
Sandbags and gravel were used to cover Norpipe to Emden  Photo: Unknown/Norwegian Petroleum Museum
This pipeline became operational in September 1977  The starting pressure of around 132 bar is provided by compressors on the Ekofisk Complex 
The 443-kilometre distance to Emden was split into three equal sections, with platforms B11 and H7 located at the intermediate points to provide boosting if required 
However, additional compression was seldom needed on the final stage to Emden  H7 was shut down in 2007 and B11 in 2013, and both have since been removed 
These two booster platforms were located in the German sector of the North Sea, while the pipeline also crosses the Danish sector 
The pipeline has been trenched or covered with sand  Its final section passes the island of Juist before making landfall on the coast of East Friesland to the north of Emden 
Its daily capacity is roughly 59 4 million standard cubic metres (2 1 billion cubic feet)  In addition to gas from the Greater Ekofisk Area, it carries output from Valhall, Hod, Ula, Gyda and the Statpipe system (primarily Statfjord and Gullfaks) 
Posted on 24  June 2017 25  October 2019
Embla 2/7 D
This unmanned wellhead facility is remotely controlled from Eldfisk 2/7 S located 5 2 kilometres to the north, where oil and gas output from the platform is also processed 
Unmanned and remotely operated wellhead platform
On stream 12 May 1993
— Embla 2/7 D  Photo: ConocoPhillips
sokkelkart, illustrasjon, blokker, lisens, forsidebilde, engelsk,
Hand-colored map of the licenses of the first licensing round on the Norwegian continental shelf  Norwegian Continental Shelf Map, 1965 
The Phillips group was awarded block 2/7 as early as 1965, and the Embla reservoir lies in the southern part of this acreage  Drilling began there in 1974 to depths of 4 500-5 000 metres, but pressure and temperature in the wells were too high for testing with the available equipment 
The first production well was not drilled and tested until 1988, followed by a second in 1990  Both yielded very promising results, and the field came on stream in May 1993 
Embla comprises a sandstone reservoir at least 250 million years old  The other fields in the Greater Ekofisk Area comprise fine-grained carbonate rocks deposited about 70 million years ago 
The Embla reservoir has a temperature of 160°C compared with the 125°C normally found in the chalk formations 1 000 metres higher up, and its pressure is almost twice as high 
Fabricated by Heerema in the Netherlands, the Embla 2/7 D jacket (support structure) was installed by the M 7000 crane vessel  It stands 84 metres high and weighs 2 300 tonnes 
A 5 2-kilometre subsea umbilical from Eldfisk comprises three power cables for electricity supply and eight fibreoptic lines handling data transmission and telecommunication 
Eldfisk 2/7 S, embla,
Eldfisk 2/7 S  Photo: ConocoPhillips
The platform has six production wells and an average daily output of roughly 7 000 barrels of oil  All processing and metering took place on Eldfisk 2/7 FTP until 2015, and has now been switched to Eldfisk 2/7 S 
A 14-inch flowline linked 2/7 D with 2/7 FTP and runs today to 2/7 S  Produced at Wick in Scotland, this line was floated out to the field in one piece 
Topside equipment includes the wellhead area, helideck (built by Vindholmen Services in Arendal), crane, control room, workshop, test separator and glycol pump 
Normally unmanned, the platform is maintained as and when required and therefore incorporates a simplified accommodation module with lounge, mess, coffee room, galley, changing room, WC and 12 emergency beds 
More about platforms
Ekofisk 2/4 Z
This installation is a wellhead platform in the Ekofisk Complex 
Gulftide
This four-leg jack-up drilling rig was built in Glasgow during 1967 for Ocean Drilling & Exploration Co 
Posted on 1  September 2019 8  October 2019
— Gulftide with Ekofisk 2/4 A in the background  Photo: Aker Mek  Verksted/Norwegian Petroleum Museum
Gulftide was converted to cope with conditions on Ekofisk in the Åmøy Fjord near Stavanger  This jack-up drilling rig was equipped with process equipment and its derrick, helideck, hangar and legs were reinforced 
To win time, it was decided that the discovery well and three appraisals drilled on Ekofisk by Ocean Viking would be completed for production 
Principles for producing from Gulftide were relatively simple  Output flowed from the subsea wellheads to the platform, where it went through two-stage separation to remove gas and water 
With pressure also reduced, the gas was flared off and the oil sent on by flowlines to two loading buoys where shuttle tankers moored to take on cargo 
utbyggingen,
Tankskipet Donovania laster olje fra lastebøyen på Ekofisk  I bakgrunnen skimtes så vidt Gulftide  Foto: ConocoPhillips/Norsk Oljemuseum
Production could only continue while ships were loading  As soon as one tanker had been filled, the oil stream was diverted to the vessel waiting at the other loading buoy 
The problem with this approach was manifested when weather conditions ­– strong winds and/or high waves – forced the tankers to leave the buoys 
If that happened, production from the wellheads had to be suspended immediately  Given the prevailing weather on Ekofisk, that happened regularly  Output was halted for 20 per cent of the time during the first year 
https://ekofisk industriminne no/wp-content/uploads/sites/2/2019/09/Building-Ekofisk mp4
Gulftide was replaced as the temporary production installation in 1974 by the permanent Ekofisk 2/4 A (Alpha) and 2/4 B (Bravo) platforms for production, drilling and quarters 
In addition came the Ekofisk 2/4 C (Charlie) production, drilling and compression facility, the Ekofisk 2/4 FTP (field terminal platform) for production and risers, and Ekofisk 2/4 Q for accommodation 
Oil and gas were produced by 2/4 A, B and C through their own wells for processing in their separation plants and piping on the 2/4 FTP for a three-stage separation process 
At the same time, the tanker loading buoys were moved further from the platforms and the Ekofisk 2/4 T oil storage tank became operational 
This facility was extremely advantageous, because it allowed production to continue virtually regardless of whether bad weather prevented tankers from connecting to the buoys 
Ekofisktanken ble satt i drift i 1974  Foto: ConocoPhillips/Norsk Oljemuseum
The 2/4 FTP platform, where oil and gas from the three producing facilities was processed, had been planned to handle the level of output estimated for the main field 
Clear restrictions had been imposed by the Norwegian government on the amount of gas Phillips was allowed to flare  That also set a ceiling for oil production, since gas accompanies it up from the reservoir 
The solution was to install two powerful compression packages on 2/4 C in order to inject the gas under pressure back into the producing formation 
Accommodation facilities had to be provided on the two first platforms, 2/4 A and B  Where 2/4 C and FTP were concerned, however, they were tied together with bridges and to 2/4 Q 
Published 1  September 2019 • Updated 8  October 2019
Posted on 9  April 2019 25  October 2019
Jack-up drilling rig
Built 1967 in Glasgow for Ocean Drilling & Exploration Co 
Began test production on Ekofisk 15 June 1971
Produced on Ekofisk until 1974
— Gulftide at theEkofisk field  Photo: Terje Tveit/Norwegian Petroleum Museum
gulftide,
Gulftide  Photo: Unknown/Norwegian Petroleum Museum
A mere 17 months after the Ekofisk discovery was announced in December 1969, Gulftide was ready to come on stream as a temporary production platform 
Its official inauguration took place on 9 June, with initial test output commencing on 15 June  Full production began on 8 July 
The rig was chosen because it was available on the market  Established equipment for processing oil and gas was tailored to the limited space on board  Separate flowlines carried wellstreams from four subsea wells  Oil, gas and water were separated on board, with the gas flared and the oil piped to two buoys for loading into shuttle tankers 
Work on the process equipment was relatively simple



ground_truth: Other toxic products.

prompt_front: Now, answer the following question based on the text below, only give me the answer and do not output any other words.

Question: What is the water depth in the Greater Ekofisk Area?

Read the following text and answer briefly.

Context 2:  The problem was to tailor it to the rig  The subsea wellheads had to be reinforced to meet the demands posed by the North Sea, and a buoy loading system needed to be developed for waters where this technology had never been used before 
To gain time, it was decided that the three appraisal wells drilled by Ocean Viking to map the extent of the field – in addition to the discovery well – would be completed for production 
Første testflamme tent på Ekofisk  På Gulftide
1973, Teddy Broadhurst, gulftide,
arbeidsliv, hjelpearbeider
Gulftide, separator – på bildet kan man se at det er fire brønner 
arbeidsliv, gulftide, pionerkultur, arbeid, dekk, Norges første havbunnsbrønner, historie, 1971,
The producers would be topped with hydraulically controlled wellheads  Such equipment had been tried out on the seabed earlier, but on a limited scale and not in the deep and rough waters found on Ekofisk  This challenge was overcome by having the wellheads manufactured and then reinforced at the Phillips base in Dusavik outside Stavanger  Flowlines and control cables would also be laid from each well to Gulftide, with production comingled in a single riser to the topsides 
Weather conditions also represented a major problem when designing the loading buoys  Phillips itself had experience with such facilities, but the concept had only been used before in harbour-like conditions and waters no deeper than 27 metres  They were now to stand in 70 metres in the middle of the North Sea 
Gulftide was converted in the Åmøy Fjord outside Stavanger to cope with conditions on Ekofisk  The processing facilities were installed and reinforcements made to the derrick, helideck, hangar and leg structures 
Gulftide, Ekofisk 2/4 A, boretårn, flare, 1971, utbygging,
Gulftide with Ekofisk 2/4 A in the background  Photo: Aker Mek  Verksted/Norwegian Petroleum Museum
Planning began in late 1970, when Phillips received approval to begin laying the flowlines between wellheads and rig  Brown & Root won this contract, with the first oil pipelines on the Norwegian continental shelf laid by the Hugh W Gordon laybarge 
The production principle on Gulftide was relatively simple  Output flowed from the subsea wellheads to the rig, where it passed through two separation levels to be split into oil and gas while the huge pressure was reduced 
Gas was flared off and the oil was piped to one of the loading buoys where a shuttle tanker was moored  Production could only take place when a ship was present 
Offisiell åpning av norsk oljeproduksjon,
The Greek tanker, Theogennitor, unloads crude oil from loading buoys on the Ekofisk field  Gulftide in the background  Photo: ConocoPhillips/Norwegian Petroleum Museum
As soon as one tanker had become fully laden, the oil flow was switched to the other buoy where another ship was waiting to take on cargo 
The problem with this approach arose when weather conditions meant the tankers had to cast off from the buoys because of strong winds or high waves  The rig then had to shut down production from the wellheads immediately 
Given the weather conditions found on Ekofisk, output regularly had to cease  Production was suspended for 20 per cent of the first year for this reason 
Output began cautiously on 8 July 1971 from a single well  The second producer came on stream that September, the third was ready the following month and all four were producing by February 1972  They each flowed 10 000 barrels of oil per day 
Source: Kvendseth, Stig, Giant discovery, 1988 
Published 9  April 2019 • Updated 25  October 2019
Norpipe H-7
This platform served as a pumping/compressor station to maintain pressure in the 443-kilometre Norpipe gas pipeline from Ekofisk to Emden in Germany, which became operational in September 1977 
Kjappe fakta::
Compressor platform on Ekofisk-Emden gas pipeline
Installed 1976
Operational 1977
Shut down 29 October 2007
Removed 2013
— Norpipe GNSC-H7  Photo: Husmo Foto/Norwegian Petroleum Museum
Gas received initial compression to 132 bar at the Ekofisk Complex  The pipeline was divided into three equal lengths, with Norpipe GNSC B11 positioned at the end of the first third to maintain pressure as and when required 
From there, the gas then travelled the next third of the distance to the second and virtually identical compressor platform, H7 
This was also responsible for maintaining pressure, but additional compression was seldom required on this final leg of the journey to Emden 
Both platforms stood on the German continental shelf, but 48 kilometres of the pipeline also ran across the Danish North Sea sector 
The pipeline is trenched or covered with sand  On its final approach to the coast of East Friesland, it passes beneath the island of Juist before making landfall north of Emden 
Capacity in Norpipe is about 60 million standard cubic metres (scm) or 2 1 billion cubic feet per day  In addition to output from the Ekofisk-area fields, it carries gas from Valhall, Ula and the Statpipe system – primarily Statfjord and Gullfaks  Gas was also transported for a time from Hod and Gyda, but that has ceased 
fritid, Norpipe GNSC-H7,
Magnus Refsland and Werner Hein have pulled the crab trap (full of starfish) on the Norpipe H-7 platform  Photo: Husmo Foto/Norwegian Petroleum Museum
Built in 1976, the B11 platform had six decks  Its permanent staffing totalled 14 people, but various service personnel were also often on board  The regular crew included three in catering 
The 11 Phillips employees comprised the offshore installation manager, the nurse/radio operator, eight operators and a roustabout 
In addition to their direct function, the operators covered various other trades which meant the crew was self-sufficient in most circumstances 
Both platforms obtained a satellite antenna in 1986 which allowed them to received Norwegian TV, while the 24-bed accommodation were redecorated in 1981 and upgraded in the summer of 1990 
Work on the upgrading largely comprised converting all cabins to doubles with shower and WC  The galley and changing rooms were renewed and changing facilities for women provided 
A new module with a lounge for non-smokers, a smoking room, gym and pool room was also installed  During this work, the West Gamma accommodation rig was positioned alongside 
Upgrading equipment on the platform was also initiated in 1990  While the pipeline’s original daily capacity had been estimated at 2 100 million standard cubic feet, this was found to have declined after a number of years to 1 975 million 
To return to the original capacity, the compressors needed to be upgraded and power supply from the turbines increased  This was done both on the Ekofisk tank and on the H7 and B11 platforms  Gas coolers on the tank were replaced as well 
Norpipe GNSC-H7, yrker, radiooperatør,
Radio operator Torleif Førland on the platform Norpipe H-7, with his amateur radio  Photo: Husmo Foto/Norwegian Petroleum Museum
The control systems were also upgraded in parallel  Control panels on turbines and compressors were replaced and metering instruments installed to conduct measurements in this equipment 
While the nearest neighbour to B11 was a Danish oil field, H7 stood in the middle of the shipping channel  M/S Hero broke down 15 nautical miles west of the latter platform at around 13 00 on 12 November 1977 
By 21 00, the ship was still adrift and heading directly for H7, and all 14 crew on the platform made ready to evacuate by helicopter – the waves were too high for the lifeboats  The wreck passed at 21 40 with a clearance of 400 metres 
German cargo carrier Reint collided with H7 on 30 September 1995, despite efforts by the standby ship to avert the threat  Production was halted as a safety measure, but the platform luckily suffered only minor damage  The collision was caused by inadequate watchkeeping on the ship’s bridge 
Operator responsibility for B11 and H7 was transferred at the beginning of 2003 to Norway’s state-owned Gassco company, which runs the Norwegian gas transport network 
This change had little significance for operation of the platforms, since the actual work was still carried out by ConocoPhillips as a technical service provider to Gassco 
H7 was shut down in 2007, and removal had been completed in 2013  In connection with preparations to remove the structure, operator responsibility was transferred to Statoil as the company in charge of the project on Gassco’s behalf 
Published 24  August 2016 • Updated 22  October 2019
Phillips inundates Sola with oil revenues
person by Kristin Øye Gjerde
Stavanger and neighbouring Sola were the first Norwegian local authorities to experience fantastic oil-related growth after the award of the first exploration licences in 1965 
— Phillips er i ferd med å etablere seg på Norscobasen nederst til høyre Ca 1972 Foto: Norsk fly og flyfoto/Norsk Oljemuseum
The Shell refinery at Risavika in Sola was completed two years later, while the Norsco base in Tananger became operational as early as 1966 
But things really took off once the Ekofisk field had been discovered in the autumn of 1969 and started trial production on 14 July 1971 
Operator Phillips Petroleum Company moved its offices from the Dusavik base outside Stavanger to Tananger in Sola, and Shell could finally start refining Norwegian rather than imported crude 
Sola’s population now rose steadily from 8 400 in 1965 to 15 000 two decades later, and jobs grew even faster – from about 2 000 in 1970 to almost 8 000 in 1985  That averages 10 per cent annually 
Phillips and Shell became cornerstone companies  A large part of their workforce, particularly in Phillips, worked offshore  In addition came newly established oil supply firms 
More jobs were also created in retail, public administration, education, health and social care, personal services and so forth 
Although traditional agriculture remained important for the local authority, the number of farmers gradually declined as a result of mechanisation [REMOVE]Fotnote: This article is based on the chapter “Elverket i Oljealderen” in I det regionale spenningsfelt  Sola Energi 1913-1999, Kristin Øye Gjerde 
Boreskipet Drillship ligger ved kai på Norscobasen i Tananger (1968)  Foto: NOM/Norsk Fly og Flyfoto
Boreskipet Drillship ligger ved kai på Norscobasen i Tananger (1968)  Foto: Norsk Fly og Flyfoto/Norsk Oljemuseum
The “agio tax”
The sharp rise in Sola’s revenues was attributable entirely to the oil industry, and it found itself in an enviable position during this period  Tax revenues rose even faster than population and jobs 
To give an indication, the local authority’s overall income from wealth and income taxes rose from NOK 9 3 million in 1966 to NOK 198 million in 1990  The biggest growth came in 1978-82, when it averaged 39 per cent a year [REMOVE]Fotnote: Sola local authority, plans 
The secret behind this sharp increase was the tax paid by the oil companies – primarily Phillips – on agio, or the percentage fee charged when exchanging one currency for another 
Under Norwegian law at the time, the companies paid tax on their interest income to the local authority where they had their head office  In making this rule, however, the government had failed to take account of the considerable sums involved 
As operator of the Greater Ekofisk Area, Phillips had placed capital to be used for new investment in banks around the world – particularly the UK 
These deposits yielded substantial interest payments, and tax was payable on converting this income into Norwegian kroner [REMOVE]Fotnote: Toralv Torstenbø, former chief executive officer in Sola local authority, interviewed by Kristin Øye Gjerde, 22 February 2001 
Sola council is said to have almost gone into shock the first time Phillips paid this agio tax  It suddenly had more money than it could spend 
During the 1970s and early 1980s, Sola’s municipal income always exceeded the budgeted amount  Large sums could be transferred every year to a capital fund 
Since the local authority was in a growth phase, additional funding was needed for the big developments it faced  While the rest of Norway experienced a slump in the late 1970s, Sola continued in top gear without a sign of unemployment 
Net income tax revenues came to NOK 55 5 million in 1978, while net spending was NOK 31 9 million  And these fantastic results went on improving 
By 1982, wealth and income taxes yielded NOK 203 4 million – compared with a budget of NOK 146 million, which was upgraded to NOK 190 million during the year 
According to Toralv Torstensbø, the financial controller, agio tax accounted for almost half this amount – in other words, as much as the tax paid by all other enterprises, private individuals and industry in Sola 
Its chief executive officer became a little overweening  In his comments on the 1982 budget, he declared that it would be “natural for Sola local authority to feel a strong regional responsibility and not to be too strict about the traditional division of costs between state, county and local authority ”
In line with this open-handed policy, Sola paid for both road projects and an upper secondary modern school which the county council was supposed to fund [REMOVE]Fotnote: Chief executive officer’s budget proposal for Sola local authority covering 1974-85 
Tightening up petroleum tax
This unexpected prosperity undoubtedly created some jealously in the neighbouring local authorities, and the media began to show an interest in the issue 
Local daily Stavanger Aftenblad interviewed Sola’s chief executive and controller in 1981, when its photographer took a shot which illustrated the boundless wealth – Torstensbø stood showering hundred-krone notes over his colleague 
This story was not only read by the paper’s regular subscribers  The following day, 150 copies were distributed to members of the Storting (parliament) 
That in turn prompted Centre Party representative Lars Velsand to make a passionate speech in which he described the position as a misuse of tax revenues 
He called on the government to intervene so that individual local authorities were unable to benefit in this way  Nor was he alone in finding it unreasonable that a small community like Sola should get so much money 
The result was an amendment to the Petroleum Tax Act on 11 June 1982, which specified that the proceeds from the agio tax should be transferred in future to central government 
Løfteskipet Uglen i aksjon ved Norscobasen i juli 1980  Foto: NOM/Norsk Fly og Flyfoto
Løfteskipet Uglen i aksjon ved Norscobasen i juli 1980  Foto: Norsk Fly og Flyfoto/Norsk Oljemuseum
Unfortunately, however, Sola had got used to consuming these revenues  It is easy to learn expensive habits, but not so straightforward to shrug them off again 
Matters had become a little unusual when the council’s executive board adopted the style of the oil company chiefs and took a helicopter outing during an ordinary budget meeting [REMOVE]Fotnote: Oskar Goa, former chief technical officer in Sola local authority, interviewed by Kristin Øye Gjerde, 23 October 2000 
However, most of the tax money benefitted the general public  Paying for Sola upper secondary school and new national and county highways is an example of this 
The council also invested on local authority school buildings and community facilities such as the big sports complex at Åsen, with an outdoor athletics ground and two modern indoor arenas  Dysjaland and Tananger also acquired new sports arenas 
A new cultural centre built in central Sola has a distinctive architecture in brick and glass, with a grassed roof to blend with the surrounding Jæren landscape  With two stages and a public library, this became the community’s main venue for events and so forth 
The local authority thereby built up a very good infrastructure  Power cables were laid in the same trenches as water and sewage pipes, a network of cycle lanes was built and street lighting installed 
On the downside, virtually all these investments boosted operating expenses  The council’s running costs rose by an annual average of 30 per cent in 1978-84, with the biggest growth in the last three years of the period 
So the calls by Storting representatives to transfer agio tax receipts from councils to central government represented a real threat to local politicians 
Sola joined forces with other local authorities in the same position, including Stavanger, Oslo and Bærum as well as Rogaland county council 
A delegation met the Storting’s standing committee on finance to present their case, and secured a commitment to accept a phased reduction in revenues over four years 
The local authorities would receive 80 per cent of agio tax receipts during the first year, then 60 per cent, 40 per cent and finally 20 per cent [REMOVE]Fotnote: Amendment to the Petroleum Tax Act adopted on 14 May 1982 
In reality, however, the run-down percentages were adjusted to extend over five years in annual steps of 80, 60, 20, 20 and 20 per cent  The total amount going to the local authorities was the same 
The arrangement was controversial to the last, and also uncertain because it had to be approved in each annual government budget 
Living within its means
After the tax change, Sola’s chief executive officer saw the writing on the wall  It seemed “to be unquestionable that [Sola] has seen its best days in purely financial terms and must return to setting tougher priorities for various assignments,” he asserted in connection with the budget process for 1983 [REMOVE]Fotnote: Chief executive officer’s budget proposal for Sola local authority, 1983 
It took the politicians a little longer to accept this reality, but they were forced to reduce investment and operating expenditures in the years which followed 
Cutting back on the new sports arenas and cultural centre was not very desirable  Nor was it pleasant to have to slow down  But savings had to be made, and long-terms spending plans were removed from the budget for possible reintroduction later 
A raft of measures were stripped from the budget in 1985, such as extensions to and modernisation of schools, sports arenas and swimming pools, a new somatic nursing home, housing for the intellectually disabled and sheltered housing  Grants for national and county roads were reduced [REMOVE]Fotnote: Chief executive officer’s budget proposal for Sola local authority, 1985 
Once the government’s compensation scheme had ended, Torstensbø – now chief executive officer – told Stavanger Aftenblad that he did not want to paint too gloomy a picture 
“But it’s clear that we must set much more moderate financial priorities than we’ve been used to  To sum up the position, we were previously flush with cash and poor in facilities  We’re now flush with facilities and poor in cash ”[REMOVE]Fotnote: Stavanger Aftenblad, ”Alt blir dyrere i det rike Sola”, 19 May 1987 
Sola kulturhus fotografert vinteren 2004
Rogaland county council also raised the question of whether it would be possible to establish a permanent arrangement which allowed local authorities and counties to benefit from some of the tax revenues paid by local oil companies 
The council pointed out that it was otherwise normal practice for Norwegian companies to pay taxes to the local communities they were based in 
This request was turned by Labour finance minister Gunnar Berge because the councils concerned still benefitted from bigger tax payments by oil company employees and on property [REMOVE]Fotnote: Stavanger Aftenblad, “Rogaland reiser skattekrav på ny”, 16 January 1988 
According to Torstensbø, this was only partly true  The big oil companies were not so significant for Sola’s income once the agio tax was excluded 
About NOK 2 million was received annually from Phillips, primarily in property tax  The most important taxpayers in the local authority were the roughly 90 companies at Aker Base  These were service providers such as Halliburton, Schlumberger and Baker Hughes 
At the same time, Sola acquired a steadily growing number of affluent residents and a growing share of its revenue came from income tax  Despite the cut-backs, it remained prosperous 
Published 29  July 2019 • Updated 29  July 2019
More about economy
Participants in Ekofisk
The question of who “owns” Ekofisk is not straightforward  In simple terms, however, the field and the rest of Norway’s continental shelf (NCS) belongs to the Norwegian state  This was determined on 14 June 1963, when the Storting (parliament) passed the Act Relating to Exploration for and Exploitation of Submarine Natural Resources  This permits licences to be awarded on certain terms 
Riding out the oil crisis
The greatest-ever oil bonanza, with oil prices hitting USD 130 per barrel, came to an abrupt end in 2014, when the cost of a barrel of crude slumped to less than USD 50 from June to December  And the bottom had still not been reached – this was only the start of a new oil crisis which lasted several years  What effect did this have on ConocoPhillips’ financial position off Norway?
Context 3: Thalassaemia minor | definition of Thalassaemia minor by Medical dictionary
Thalassaemia minor | definition of Thalassaemia minor by Medical dictionary
https://medical-dictionary thefreedictionary com/Thalassaemia+minor
(redirected from Thalassaemia minor)
Related to Thalassaemia minor: thalassaemia major
Thalassemia describes a group of inherited disorders characterized by reduced or absent amounts of hemoglobin, the oxygen-carrying protein inside the red blood cells  There are two basic groups of thalassemia disorders: alpha thalassemia and beta thalassemia  These conditions cause varying degrees of anemia, which can range from insignificant to life threatening 
All types of thalassemias are considered quantitative diseases of hemoglobin, because the quantity of hemoglobin produced is reduced or absent  Usual adult hemoglobin is made up of three components: alpha globin, beta globin, and heme  Thalassemias are classified according to the globin that is affected, hence the names alpha and beta thalassemia  Although both classes of thalassemia affect the same protein, the alpha and beta thalassemias are distinct diseases that affect the body in different ways 
Beta thalassemia may be the most best-known type of thalassemia and is also called Cooley's anemia  It is caused by a change in the gene for the beta globin component of hemoglobin  Beta thalassemia causes variable anemia that can range from moderate to severe, depending in part on the exact genetic change underlying the disease  Beta thalassemia can be classified based on clinical symptoms  Beta thalassemia major usually causes severe anemia that can occur within months after birth  If left untreated, severe anemia can result in insufficient growth and development, as well as other common physical complications that can lead to a dramatically decreased life-expectancy  Fortunately, in developed countries beta thalassemia is usually identified by screening in the newborn period, before symptoms have developed  Children who are identified early can be started on ongoing blood transfusion therapy as needed  Although transfusion therapy prevents many of the complications of severe anemia, the body is unable to eliminate the excess iron contained in the transfused blood  Over time, the excess iron deposits in tissues and organs, resulting in damage and organ failure  Another medication must be administered to help the body eliminate the excess iron and prevent iron-over-load complications  Beta thalassemia intermedia describes the disease in individuals who have moderate anemia that only requires blood transfusions intermittently, if at all 
Alpha thalassemia is the result of changes in the genes for the alpha globin component of hemoglobin  There are two main types of alpha thalassemia disease: hemoglobin H disease and alpha thalassemia major  The two diseases are quite different from beta thalassemia as well as from one another  Individuals with hemoglobin H disease can experience events of hemolytic anemia—anemia caused by the rapid breakdown of the red blood cells  These events are thought to be triggered by various environmental causes, such as infection and/or exposure to certain chemicals  Hemoglobin H disease is in most cases milder than beta thalassemia  It does not generally require transfusion therapy  Alpha thalassemia major is a very serious disease that results in severe anemia that begins even before birth  Most affected babies do not survive to be born or die shortly after birth 
The thalassemias are among the most common genetic diseases worldwide  Both alpha and beta thalassemia have been described in individuals of almost every ancestry, but the conditions are more common among certain ethnic groups  Unaffected carriers of all types of thalassemia traits do not experience health problems  In fact, the thalassemia trait is protective against malaria, a disease caused by blood-borne parasites transmitted through mosquito bites  According to a widely accepted theory, most genetic changes—mutations—that cause thalassemia occurred multiple generations ago  Coincidentally, these mutations increased the likelihood that carriers would survive malaria infection  Survivors passed the mutation onto their offspring, and the trait became established throughout areas where malaria is common  As populations migrated, so did the thalassemia traits 
Beta thalassemia trait is seen most commonly in people with the following ancestry: Mediterranean (including North African, and particularly Italian and Greek), Middle Eastern, Indian, African, Chinese, and Southeast Asian (including Vietnamese, Laotian, Thai, Singaporean, Filipino, Cambodian, Malaysian, Burmese, and Indonesian)  Alpha-thalassemia trait is seen with increased frequency in the same ethnic groups  However, there are different types of alpha thalassemia traits within these populations  The frequency of hemoglobin H disease and alpha thalassemia major depends on the type of alpha thalassemia trait  The populations in which alpha thalassemia diseases are most common include Southeast Asians and Chinese (particularly Southern Chinese) 
It is difficult to obtain accurate prevalence figures for various types of thalassemia within different populations  This difficulty arises due to testing limitations in determining exact genetic diagnoses, as well as the fact that many studies have focused on small, biased hospital populations 
Two studies reflect prevalence figures that can be helpful counseling families and determining who to screen for beta thalassemia  Between the years of 1990 and 1996, the State of California screened more than 3 1 million infants born in the state for beta thalassemia  Approximately 1 in 114,000 infants had beta thalassemia major, with prevalence rates being highest among Asian Indians (about one in 4,000), Southeast Asians (about one in 10,000), and Middle Easterners (about one in 7,000)  Another type of beta thalassemia disease, E/beta thalassemia, was represented in approximately one in 110,000 births, all of which occurred in families of Southeast Asian ancestry  Among Southeast Asians, the prevalence of E/beta thalassemia was approximately one in 2,600 births  This is in keeping with the observation that hemoglobin E trait carrier rates are relatively high within the Southeast Asian population: 16% in a study of 768 immigrants to California, and up to 25% in some specific Southeast Asian populations such as Cambodians  While these California studies address some of the limitations of earlier population studies, the pattern observed in California is expected to be different in other areas of the United States and the world  For example, Italians are underrepresented in this population when compared to the population of the East Coast of the United States 
Determining prevalence figures for alpha thalassemia is even more difficult due to increased limitations in diagnostic testing  All types of alpha thalassemia disease are most common among people of Southeast Asian and Chinese descent, for reasons that become clearer with an understanding of the underlying genetics of alpha thalassemia  One study of 500 pregnant women in Northern Thailand estimated a frequency of one in 500 pregnancies affected by alpha thalassemia major, for example  Prevalence of alpha thalassemia disease is significantly lower in the United States primarily because of immigration patterns; although at least one state, California, has observed growing hemoglobin H disease incidence rates that are high enough to justify universal newborn screening for the condition 
Humans normally make several types of the oxygen-carrying protein hemoglobin  An individual's stage in development determines whether he or she makes primarily embryonic, fetal, or adult hemoglobins  All types of hemoglobin are made of three components: heme, alpha (or alpha-like) globin, and beta (or beta-like) globin  All types of thalassemia are caused by changes in either the alpha- or beta-globin gene  These changes cause little or no globin to be produced  The thalassemias are, therefore, considered quantitative hemoglobin diseases  All types of thalassemias are recessively inherited, meaning that a genetic change must be inherited from both the mother and the father  The severity of the disease is influenced by the exact thalassemia mutations inherited, as well as other genetic and environmental factors  There are rare exceptions, notably with beta thalassemia, where globin gene mutations exhibit a dominant pattern of inheritance in which only one gene needs to be altered in order to see disease expression  Scientists continue to study the causes  For instance, a new mutation for alpha-thalassemia was discovered for the first time among Iranian patients in 2004 
BETA-THALASSEMIA  Most individuals have two normal copies of the beta globin gene, which is located on chromosome 11 and makes the beta globin component of normal adult hemoglobin, hemoglobin A  There are approximately 100 genetic mutations that have been described that cause beta thalassemia, designated as either beta0 or beta + mutations  No beta globin is produced with a beta0 mutation, and only a small fraction of the normal amount of beta globin is produced with a beta + mutation 
When an individual has one normal beta globin gene and one with a beta thalassemia mutation, he or she is said to carry the beta thalassemia trait  Beta thalassemia trait, like other hemoglobin traits, is protective against malaria infection  Trait status is generally thought not to cause health problems, although some women with beta thalassemia trait may have an increased tendency toward anemia during pregnancy 
When two members of a couple carry the beta thalassemia trait, there is a 25% chance that each of their children will inherit beta thalassemia disease by inheriting two beta thalassemia mutations, one from each parent  The clinical severity of the beta thalassemia disease—whether an individual has beta thalassemia intermedia or beta thalassemia major—will depend largely on whether the mutations inherited are beta0 thalassemia or beta + thalassemia mutations  Two beta0 mutations generally lead to beta thalassemia major, and two beta+ thalassemia mutations generally lead to beta thalassemia intermedia  Inheritance of one beta0 and one beta + thalassemia mutation tends to be less predictable 
Although relatively uncommon, there are other thalassemia-like mutations that can affect the beta globin gene  Hemoglobin E is the result of a substitution of a single nucleotide  This change results in a structurally altered hemoglobin that is produced in decreased amounts  Therefore, hemoglobin E is unique in that it is both a quantitative (i e  thalassemia-like) and qualitative trait  When co-inherited with a beta thalassemia trait, it causes a disease that is almost indistinguishable from beta thalassemia disease  Large deletions around and including the beta globin gene can lead to delta/beta thalassemia or hereditary persistence of fetal hemoglobin (HPFH)  Interestingly, delta/beta thalassemia trait behaves very similarly to beta thalassemia trait in its clinical manifestations  However, HPFH trait does not tend to cause hemoglobin disease when co-inherited with a second thalassemia or other beta globin mutation 
ALPHA-THALASSEMIA  Most individuals have four normal copies of the alpha globin gene, two copies on each chromosome 16  These genes make the alpha globin component of normal adult hemoglobin, which is called hemoglobin A  Alpha globin is also a component of fetal hemoglobin and the other major adult hemoglobin called hemoglobin A2  Mutations of the alpha globin genes are usually deletions of the gene, resulting in absent production of alpha globin  Since there are four genes (instead of the usual two) to consider when looking at alpha globin gene inheritance, there are several alpha globin types that are possible 
Absence of one alpha globin gene leads to a condition known as silent alpha thalassemia trait  This condition causes no health problems and can be detected only by special genetic testing  Alpha thalassemia trait occurs when two alpha globin genes are missing  This can occur in two ways  The genes may be deleted from the same chromosome, causing the 'cis' type of alpha thalassemia trait  Alternately, they may be deleted from different chromosomes, causing the 'trans' type of alpha thalassemia trait  In both instances, there are no associated health problems, although the trait status may be detected by more routine blood screening 
Hemoglobin H disease results from the deletion of three alpha globin genes, such that there is only one functioning gene  Typically, this can occur when one parent carries the silent alpha thalassemia trait, and the other parent carries the 'cis' type of the alpha thalassemia trait  In this situation, there is a 25% chance for hemoglobin H disease in each of such a couple's children 
Hemoglobin H disease-like symptoms can also be a part of a unique condition called alpha thalassemia mental retardation syndrome  Alpha thalassemia mental retardation syndrome can be caused by a deletion of a significant amount of chromosome 16, affecting the alpha globin genes  This is usually not inherited, but rather occurs sporadically in the affected individual  Affected individuals have mild hemoglobin H disease, mild-to-moderate mental retardation, and characteristic facial features  This syndrome can also occur as a sex-linked form in which a mutation is inherited in a particular gene on the X-chromosome  This gene influences alpha globin production, as well as various other developmental processes  Individuals affected with this form of the syndrome tend to have more severe mental retardation, delayed development, nearly absent speech, characteristic facial features, and genital-urinary abnormalities  The remaining discussion will focus only on aspects of hemoglobin H disease 
Alpha thalassemia major results from the deletion of all four alpha globin genes, such that there are no functioning alpha globin genes  This can occur when both parents carry the 'cis' type of the alpha thalassemia trait  In this situation, there is a 25% chance for alpha thalassemia major in each of such a couple's children 
Beta thalassemia major is characterized by severe anemia that can begin months after birth  In the United States and other developed countries beta thalassemia is identified and treated early and effectively  Therefore, the following discussion of symptoms applies primarily to affected individuals in the past and unfortunately in some underdeveloped countries now  If untreated, beta thalassemia major can lead to severe lethargy, paleness, and delays in growth and development  The body attempts to compensate by producing more blood, which is made inside the bones in the marrow  However, this is ineffective without the needed genetic instructions to make enough functioning hemoglobin  Instead, obvious bone expansion and changes occur that cause characteristic facial and other changes in appearance, as well as increased risk of fractures  Severe anemia taxes other organs in the body—such as the heart, spleen, and liver—which must work harder than usual  This can lead to heart failure, as well as enlargement and other problems of the liver and spleen  When untreated, beta thalassemia major generally results in childhood death, usually due to heart failure  In 2004, the first known heart attack associated with beta thalassemia major was reported  Fortunately, in developed countries diagnosis is usually made early, often before symptoms have begun  This allows for treatment with blood transfusion therapy, which can prevent most of the complications of the severe anemia caused by beta thalassemia major  Individuals with beta thalassemia intermedia have a more moderate anemia that may only require treatment with transfusion intermittently, such as when infections occur and stress the body  As a person with beta thalassemia intermedia gets older, however, the need for blood transfusions may increase to the point that they are required on a regular basis  When this occurs their disease becomes more similar to beta thalassemia major  Other genetic and environmental factors can influence the course of the disease as well  For example, co-inheritance of one or two alpha thalassemia mutations can tend to ameliorate some of the symptoms of beta thalassemia disease, which result in part from an imbalance in the amount of alpha- and beta-globin present in the red blood cells 
Hemoglobin h disease
Absence of three alpha globin genes causes an imbalance of alpha and beta globin proteins in the red blood cells  The excess beta globin proteins tend to come together to form hemoglobin H, which is unable to release oxygen to the tissues  In addition, hemoglobin H tends to precipitate out in the cells, causing damage to the red blood cell membrane  When affected individuals are exposed to certain drugs and chemicals known to make the membrane more fragile, the cells are thought to become vulnerable to breakdown in large numbers, a complication called hemolytic anemia  Fever and infection are also considered to be triggers of hemolytic anemia in hemoglobin H disease  This can result in fatigue, paleness, and a yellow discoloration of the skin and whites of eyes called jaundice  Usually, the anemia is mild enough not to require treatment  Severe anemia events may require blood transfusion, however, and are usually accompanied by such other symptoms as dark feces or urine and abdominal or back pain  These events are uncommon in hemoglobin H disease, although they occur more frequently in a more serious type of hemoglobin H disease called hemoglobin H/Constant Spring disease  Individuals effected with this type of hemoglobin H disease are also more likely to have enlargement of and other problems with the spleen 
Alpha thalassemia major
Because alpha globin is a necessary component of all major hemoglobins and some minor hemoglobins, absence of all functioning alpha globin genes leads to serious medical consequences that begin even before birth  Affected fetuses develop severe anemia as early as the first trimester of pregnancy  The placenta, heart, liver, spleen, and adrenal glands may all become enlarged  Fluid can begin collecting throughout the body as early as the start of the second trimester, causing damage to developing tissues and organs  Growth retardation is also common  Affected fetuses usually miscarry or die shortly after birth  In addition, women carrying affected fetuses are at increased risk of developing complications of pregnancy and delivery  Up to 80% of such women develop toxemia, a disturbance of metabolism that can potentially lead to convulsions and coma  Other maternal complications include premature delivery and increased rates of delivery by cesarean section, as well as hemorrhage after delivery 
Thalassemia may be suspected if an individual shows signs that are suggestive of the disease  In all cases, however, laboratory diagnosis is essential to confirm the exact diagnosis and to allow for the provision of accurate genetic counseling about recurrence risks and testing options for parents and affected individuals  Screening is likewise recommended to determine trait status for individuals of high-risk ethnic groups 
The following tests are used to screen for thalassemia disease and/or trait:
hemoglobin electrophoresis with quantitative hemoglobin A2 and hemoglobin F
free erythrocyte-protoporphyrin (or ferritin or other studies of serum iron levels)
A complete blood count will identify low levels of hemoglobin, small red blood cells, and other red blood cell abnormalities that are characteristic of a thalassemia diagnosis  Since thalassemia trait can sometimes be difficult to distinguish from iron deficiency, tests to evaluate iron levels are important  A hemoglobin electrophoresis is a test that can help identify the types and quantities of hemoglobin made by an individual  This test uses an electric field applied across a slab of gel-like material  Hemoglobins migrate through this gel at various rates and to specific locations, depending on their size, shape, and electrical charge  Isoelectric focusing and high-performance liquid chromatography (HPLC) use similar principles to separate hemoglobins and can be used instead of or in various combinations with hemoglobin electrophoresis to determine the types and quantities of hemoglobin present  Hemoglobin electrophoresis results are usually within the normal range for all types of alpha thalassemia  However, hemoglobin A2 levels and sometimes hemoglobin F levels are elevated when beta thalassemia disease or trait is present  Hemoglobin electrophoresis can also detect structurally abnormal hemoglobins that may be co-inherited with a thalassemia trait to cause thalassemia disease (i e , hemoglobin E) or other types of hemoglobin disease (i e , sickle hemoglobin)  Sometimes DNA testing is needed in addition to the above screening tests  This can be performed to help confirm the diagnosis and establish the exact genetic type of thalassemia 
Diagnosis of thalassemia can occur under various circumstances and at various ages  Several states offer thalassemia screening as part of the usual battery of blood tests done for newborns  This allows for early identification and treatment  Thalassemia can be identified before birth through the use of prenatal diagnosis  Chorionic villus sampling (CVS) can be offered as early as 10 weeks of pregnancy and involves removing a sample of the placenta made by the baby and testing the cells  CVS carries a risk of causing a miscarriage that is between 0 5%-1%  Amniocentesis is generally offered between 15 and 22 weeks of pregnancy, but can sometimes be offered earlier  Two to three tablespoons of the fluid surrounding the baby is removed  This fluid contains fetal cells that can be tested  The risk of miscarriage associated with amniocentesis ranges from 0 33-0 5%  Pregnant woman and couples may choose prenatal testing in order to prepare for the birth of a baby that may have thalassemia  Alternately, knowing the diagnosis during pregnancy allows for the option of pregnancy termination  Preimplantation genetic diagnosis (PGD) is a relatively new technique that involves in-vitro fertilization followed by genetic testing of one cell from each developing embryo  Only the embryos unaffected by sickle cell disease are transferred back into the uterus  PGD is currently available on a research basis only and is relatively expensive 
Individuals with beta thalassemia major receive regular blood transfusions, usually on a monthly basis  This helps prevent severe anemia and allows for more normal growth and development  Transfusion therapy does have limitations, however  Individuals can develop reactions to certain proteins in the blood—called a transfusion reaction  This can make locating appropriately matched donor blood more difficult  Although blood supplies in the United States are very safe, particularly relative to the past and to other areas of the world, there remains an increased risk of exposure to such blood-borne infections as hepatitis  Additionally, the body is not able to get rid of the excess iron that accompanies each transfusion  An additional medication called desferoxamine is administered, usually five nights per week over a period of several hours, using an automatic pump that can be used during sleep or taken anywhere the person goes  This medication is able to bind to the excess iron, which can then be eliminated through urine  If desferoxamine is not used regularly or is unavailable, iron overload can develop and cause tissue damage and organ damage and failure  The heart, liver, and endocrine organs are particularly vulnerable  Desferoxamine itself may rarely produce allergic or toxic side effects, including hearing damage  Signs of desferoxamine toxicity are screened for and generally develop in individuals who overuse the medication when body iron levels are sufficiently low  Overall, however, transfusion and desferoxamine therapy have increased the life expectancy of individuals with the most severe types of beta thalassemia major to the 4th or 5th decade  This can be expected to improve with time and increased developments in treatment, as well as for those with more mild forms of the disease 
New treatments offer additional options for some individuals with beta thalassemia major  There are various medications that target the production of red blood cells (i e  erythropoeitin) or fetal hemoglobin (i e  hydroxyurea and butyrate)  Their effectiveness in ameliorating the severity of beta thalassemia is currently being investigated  Another promising new treatment is bone marrow transplantation, in which the bone marrow of an affected individual is replaced with the bone marrow of an unaffected donor  If successful, this treatment can provide a cure  However, there is an approximately 10-15% chance the procedure could be unsuccessful (i e  the thalassemia returns); result in complications (i e  graft-versus-host disease); or result in death  The risk for specific individuals depends on current health status, age, and other factors  Because of the risks involved and the fact that beta thalassemia is a treatable condition, transplant physicians require a brother or sister donor who has an identically matched tissue type, called HLA type  HLA type refers to the unique set of proteins present on each individual's cells, which allows the immune system to recognize "self" from "foreign " HLA type is genetically determined, so there is a 25% chance for two siblings to be a match  Transplant physicians and researchers are also investigating ways to improve the safety and effectiveness of bone marrow transplantation  Using newborn sibling umbilical cord blood—the blood from the placenta that is otherwise discarded after birth but contains cells that can go on to make bone marrow—seems to provide a safer and perhaps more effective source of donor cells  Donors and recipients may not have to be perfect HLA matches for a successful transplant using cord blood cells  Trials are also underway to determine the effectiveness of "partial transplants," in which a safer transplant procedure is used to replace only a percentage of the affected individual's bone marrow  Other possible treatments on the horizon may include gene therapy techniques aimed at increasing the amount of normal hemoglobin the body is able to make 
Hemoglobin H disease is a relatively mild form of thalassemia that may go unrecognized  It is not generally considered a condition that will reduce one's life expectancy  Education is an important part of managing the health of an individual with hemoglobin H disease  It is important to be able to recognize the signs of severe anemia that require medical attention  It is also important to be aware of the medications, chemicals, and other exposures to avoid due to the theoretical risk they pose of causing a severe anemia event  When severe anemia occurs, it is treated with blood transfusion therapy  For individuals with hemoglobin H disease, this is rarely required  For those with the hemoglobin H/Constant Spring form of the disease, the need for transfusions may be intermittent or ongoing, perhaps on a monthly basis and requiring desferoxamine treatment  Individuals with this more severe form of the disease may also have an increased chance of requiring removal of an enlarged and/or overactive spleen 
Anemia — A blood condition in which the level of hemoglobin or the number of red blood cells falls below normal values  Common symptoms include paleness, fatigue, and shortness of breath 
Bilirubin — A yellow pigment that is the end result of hemoglobin breakdown  This pigment is metabolized in the liver and excreted from the body through the bile  Bloodstream levels are normally low; however, extensive red cell destruction leads to excessive bilirubin formation and jaundice 
Bone marrow — A spongy tissue located in the hollow centers of certain bones, such as the skull and hip bones  Bone marrow is the site of blood cell generation 
Bone marrow transplantation — A medical procedure used to treat some diseases that arise from defective blood cell formation in the bone marrow  Healthy bone marrow is extracted from a donor to replace the marrow in an ailing individual  Proteins on the surface of bone marrow cells must be identical or very closely matched between a donor and the recipient 
Desferoxamine — The primary drug used in iron chelation therapy  It aids in counteracting the life-threatening buildup of iron in the body associated with long-term blood transfusions 
Globin — One of the component protein molecules found in hemoglobin  Normal adult hemoglobin has a pair each of alpha-globin and beta-globin molecules 
Heme — The iron-containing molecule in hemoglobin that serves as the site for oxygen binding 
Hemoglobin — Protein-iron compound in the blood that carries oxygen to the cells and carries carbon dioxide away from the cells 
Hemoglobin A — Normal adult hemoglobin that contains a heme molecule, two alpha-globin molecules, and two beta-globin molecules 
Hemoglobin electrophoresis — A laboratory test that separates molecules based on their size, shape, or electrical charge 
Hepatomegaly — An abnormally large liver 
HLA type — Refers to the unique set of proteins called human leukocyte antigens  These proteins are present on each individual's cell and allow the immune system to recognize 'self' from 'foreign'  HLA type is particularly important in organ and tissue transplantation 
Hydroxyurea — A drug that has been shown to induce production of fetal hemoglobin  Fetal hemoglobin has a pair of gamma-globin molecules in place of the typical beta-globins of adult hemoglobin  Higher-than-normal levels of fetal hemoglobin can ameliorate some of the symptoms of thalassemia 
Iron overload — A side effect of frequent blood transfusions in which the body accumulates abnormally high levels of iron  Iron deposits can form in organs, particularly the heart, and cause life-threatening damage 
Jaundice — Yellowing of the skin or eyes due to excess of bilirubin in the blood 
Mutation — A permanent change in the genetic material that may alter a trait or characteristic of an individual, or manifest as disease, and can be transmitted to offspring 
Placenta — The organ responsible for oxygen and nutrition exchange between a pregnant mother and her developing baby 
Red blood cell — Hemoglobin-containing blood cells that transport oxygen from the lungs to tissues  In the tissues, the red blood cells exchange their oxygen for carbon dioxide, which is brought back to the lungs to be exhaled 
Screening — Process through which carriers of a trait may be identified within a population 
Splenomegaly — Enlargement of the spleen 
Because alpha thalassemia major is most often a condition that is fatal in the prenatal or newborn period, treatment has previously been focused on identifying affected pregnancies in order to provide appropriate management to reduce potential maternal complications  Pregnancy termination provides one form of management  Increased prenatal surveillance and early treatment of maternal complications is an approach that is appropriate for mothers who wish to continue their pregnancy with the knowledge that the baby will most likely not survive  In recent years, there have been a handful of infants with this condition who have survived long-term  Most of these infants received experimental treatment including transfusions before birth, early delivery, and even bone marrow transplantation before birth, although the latter procedure has not yet been successful  For those infants that survive to delivery, there seems to be an increased risk of developmental problems and physical effects, particularly heart and genital malformations  Otherwise, their medical outlook is similar to a child with beta thalassemia major, with the important exception that ongoing, life-long blood transfusions begin right at birth 
As discussed above, the prognosis for individuals with the most serious types of thalassemia has improved drastically in the last several years following recent medical advances in transfusion, chemo-, and transplantation therapy  Advances continue and promise to improve the life expectancy and quality of life further for affected individuals 
"First Known Heart Attack Associated With Beta-thalassemia Major Reported " Heart Disease Weekly February 22, 2004: 10 
"Novel Alpha-thalassemia Mutations Identified " Hematology Week January 26, 2004: 19 
Children's Blood Foundation  333 East 38th St , Room 830, New York, NY 10016-2745  (212) 297-4336  cfg@nyh med cornell edu 
Cooley's Anemia Foundation, Inc  129-09 26th Ave  #203, Flushing, NY 11354  (800) 522-7222 or (718) 321-2873  http://www thalassemia org 
March of Dimes Birth Defects Foundation  1275 Mamaroneck Ave , White Plains, NY 10605  (888) 663-4637  resourcecenter@modimes org  http://www modimes org 
National Heart, Lung, and Blood Institute  PO Box 30105, Bethseda, MD 20824-0105  (301) 592-8573  nhlbiinfo@rover nhlbi nih gov  http://www nhlbi nih gov 
National Organization for Rare Disorders (NORD)  PO Box 8923, New Fairfield, CT 06812-8923  (203) 746-6518 or (800) 999-6673  Fax: (203) 746-6481  http://www rarediseases org 
Bojanowski J  "Alpha Thalassemia Major: The Possibility of Long-Term Survival " Pamphlet from the Northern California Comprehensive Thalassemia Center  (1999) 
Children's Hospital Oakland, Northern California Comprehensive Thalassemia Center website  http://www thalassemia com 
Cooley's Anemia Foundation, Inc  website  http://www thalassemia org/gohome html 
Joint Center for Sickle Cell and Thalassemic Disorders website  http://cancer mgh harvard edu/medOnc/sickle htm 
[thal″ah-se´me-ah]
a heterogeneous group of hereditary hemolytic anemias marked by a decreased rate of synthesis of one or more hemoglobin polypeptide chains, classified according to the chain involved (α, β, δ); the two major categories are α- and β-thalassemia 
α-thalassemia (alpha-thalassemia) that caused by diminished synthesis of alpha chains of hemoglobin  The homozygous form is incompatible with life, the stillborn infant displaying severe hydrops fetalis  The heterozygous form may be asymptomatic or marked by mild anemia 
β-thalassemia (beta-thalassemia) that caused by diminished synthesis of beta chains of hemoglobin  The homozygous form is called t  major and the heterozygous form is called t  minor 
thalassemia ma´jor the homozygous form of β-thalassemia, in which hemoglobin A is completely absent; it appears in the newborn period and is marked by hemolytic, hypochromic, microcytic anemia; hepatosplenomegaly; skeletal deformation; mongoloid facies; and cardiac enlargement 
thalassemia mi´nor the heterozygous form of β-thalassemia; it is usually asymptomatic, but there may be mild anemia 
sickle cell–thalassemia a hereditary anemia involving simultaneous heterozygosity for hemoglobin S and thalassemia 
thal·as·se·mi·a
, thalassanemia (thal'ă-sē'mē-ă, thă-las-ă-nē'mē-ă),
Any of a group of inherited disorders of hemoglobin metabolism in which there is impaired synthesis of one or more of the polypeptide chains of globin; several genetic types exist, and the corresponding clinical picture may vary from barely detectable hematologic abnormality to severe and fatal anemia 
[G  thalassa, the sea, + haima, blood]
/thal·as·se·mia/ (thal″ah-se´me-ah) a heterogeneous group of hereditary hemolytic anemias marked by a decreased rate of synthesis of one or more hemoglobin polypeptide chains, classified according to the chain involved (α, β, δ); the two major categories are α- and β-thalassemia 
α-thalassemia that caused by diminished synthesis of alpha chains of hemoglobin  The homozygous form is incompatible with life, the stillborn infant displaying severe hydrops fetalis  The heterozygous form may be asymptomatic or marked by mild anemia 
β-thalassemia that caused by diminished synthesis of beta chains of hemoglobin  The homozygous form is called t  major and the heterozygous form is called t  minor 
thalassemia ma´jor the homozygous form of &#x03B2;, in which hemoglobin A is completely absent; it appears in the newborn period and is marked by hemolytic, hypochromic, microcytic anemia, hepatosplenomegaly, skeletal deformation, mongoloid facies, and cardiac enlargement 
thalassemia mi´nor the heterozygous form of &#x03B2;, usually asymptomatic, although there is sometimes mild anemia 
(thăl′ə-sē′mē-ə)
An inherited form of anemia occurring chiefly among people of Mediterranean descent, caused by faulty synthesis of part of the hemoglobin molecule  Also called Mediterranean anemia 
thal′as·se′mic adj 
[thal′əsē′mē·ə]
Etymology: Gk, thalassa, sea, a + haima, without blood
production and hemolytic anemia characterized by microcytic, hypochromic red blood cells  Thalassemia is caused by inherited deficiency of alpha- or beta-globin synthesis  See also hemochromatosis, hemosiderosis 
Beta thalassemia, clinical thalassemia, Cooley's anemia, Mediterranean anemia, thalassemia major Hematology A group of genetic diseases by underproduction of hemoglobin due to mutations in the beta globin gene, which is more common in Mediterraneans Heredity Parents are carriers–heterozygotes; one in 4 children is homozygous for the mutation and thus has full-blown disease Clinical See Anemia  Cf Sickle cell anemia 
α-thalassemia
Hemoglobin Barts Hematology An inherited condition caused by a defect in the synthesis of the Hb α chain; Hb Barts hemoglobinopathy is characterized by the presence of 4 gamma chains; it is more common in southeast Asians; the most severe form of alpha thalassemia causes stillbirth due to hydrops fetalis Heredity Parents are carriers–heterozygotes; one in 4 children is homozygous for the mutation and thus has full-blown disease Clinical Pallor, fatiguability, FTT, fever, infections, diarrhea Management Transfusions
Thalassemia major Hematology A hemoglobinopathy caused by a defect in the synthesis of Hb β chain Clinical Pallor, fatigability, FTT, fever due to infections, diarrhea, bone deformities, hepatosplenomegaly Management Transfusions, but iron overload can damage the heart, liver, and endocrine systems, ergo iron chelation–early use of deferiprone, deferoxamine ↓ transfusion-related iron overload and may protect against DM, cardiac disease, early death
δ-thalassemia
Hematology A condition characterized by a defect of Hb A2–α2δ2; because Hb A2 comprises only 3% of the circulating Hb, even its complete absence; δ-thalassemia has little clinical or hematologic impact
γ-thalassemia
Hematology A condition characterized by a defect of gamma–γ Hb chains found in Hb F–α2γ2; because Hb F is present primarily in the fetus and newborns, it is rarely seen outside of the neonatal period, but may cause transient neonatal hemolytic anemia 
, thalassanemia (thal'ă-sē'mē-ă, -ă-să-nē'mē-ă)
Any of a group of inherited disorders of hemoglobin metabolism in which there is impaired synthesis of one or more of the polypeptide chains of globin; several genetic types exist, and the corresponding clinical picture may vary from barely detectable hematologic abnormality to severe and fatal anemia  People of Mediterranean, extraction are more often affected than others by this type of anemia 
Synonym(s): thalassaemia, thalassanaemia 
Any of a group of inherited disorders of hemoglobin metabolism with impaired synthesis of one or more polypeptide chains of globin; several genetic types exist 
<a href="https://medical-dictionary thefreedictionary com/Thalassaemia+minor">thalassemia</a>
Barts hemoglobin
beta hemoglobinopathy
beta-delta thalassemia
beta-thalassaemia
Bite Cell
black gallstone
I know of a couple, totally unrelated and unbeknownst to them, who are silent carriers of Thalassaemia minor 
Pakistan: Genetic factor: All in the genes
But, unfortunately, when one person with thalassaemia minor carrier happens to marry another with the same diagnosis, there is a strong possibility that their child would be thalassaemia major, as happened in the case of Taneja 
' My life depends upon a monthly blood transfusion '
0] thalassaemia demonstrates variable severity, ranging from a condition similar to [beta] thalassaemia minor to something approaching thalassaemia major 
A retrospective review of homozygous haemoglobin E patients
Thal, Alan P 
thalame
thalamencephalic
thalamencephalon
thalamic
thalamic fasciculus
thalamic nucleus
thalamic pain syndrome
thalamic peduncle
thalamic radiation
thalamo-
thalamocoele
thalamocortical
thalamocortical fibers
thalamogeniculate artery
thalamolenticular
thalamoperforating artery
thalamostriate radiation
thalamotuberal artery
Thalassaemia minor
thalassaemiaor Cooley's disease
thalassemic facies
thalasso-
Thalassobacter
Thalassobacter utilis
thalassoplankton
thalassoposia
thalidomide neuropathy
Thalidomider
thallium poisoning
Thalarctos
THALAS
Thalasaemia
Thalassaemia Association of Malaysia
thalassaemia major
Thalassaemias
thalassaemic
thalassanaemia
Thalassemia Action Group
Thalassemia Clinical Research Network
thalassemia syndrome



ground_truth: The water depth in the Greater Ekofisk Area is 70-75 meters.

prompt_front: Now, answer the following question based on the text below, only give me the answer and do not output any other words.

Question: How are thalassemias classified?

Read the following text and answer briefly.

Context 4:  The process is repeated for all the couplings obtaining then a fully connected adjacency matrix  The results here presented are obtained with $\lambda = 0 01$ 
   For the minimization we have used the MATLAB routine \emph{minFunc\_2012}\cite{min_func}  
      
      \begin{figure}[t!]
    	\centering
    	\includegraphics[width=1\linewidth]{Jor11_2D_l2_JR_soJR_TPJR}
    	\caption{Top panels: instances of single site coupling reconstruction for the case of $N=64$ XY spins on a 2D lattice with ordered $J$ (left column) and bimodal distributed $J$ (right column)  
    	
    	Bottom panels: sorted couplings }
    	\label{PL-Jor1}
    \end{figure}

   
To produce the data by means of numerical Monte Carlo simulations a system with $N=64$  spin variables  is considered on a deterministic 2D lattice with periodic boundary conditions  
Each spin has then connectivity $4$, i e , we expect to infer an adjacency matrix with $N c = 256$ couplings different from zero  
The dynamics of the simulated model is based on the Metropolis algorithm and parallel tempering\cite{earl05} is used to speed up the thermalization of the system 
The thermalization is tested looking at the average energy over logarithmic time windows and
the acquisition of independent configurations
starts only after the system is well thermalized 

   For the values of the couplings we considered two cases: an ordered case, indicated in the figure as  $J$ ordered (e g , left column of Fig  \ref{PL-Jor1}) where the couplings can take values $J_{ij}=0,J$, with $J=1$, 
   and a quenched disordered case, indicated in the figures as  $J$ disordered (e g , right column of Fig  \ref{PL-Jor1})
   where the couplings can take also  negative values, i e , 
    $J_{ij}=0,J,-J$, with a certain probability   The results here presented were obtained with bimodal distributed $J$s: 
   
    $P(J_{ij}=J)=P(J_{ij}=-J)=1/2$   The performances of the PLM have shown not to depend on $P(J)$  
   
    We recall that in Sec  \ref{sec:plm} we used the temperature-rescaled notation, i e , $J_{ij}$ stands for $J_{ij}/T$  
   
    To analyze the performances of the PLM, in Fig  \ref{PL-Jor1} the inferred couplings, $\mathbb{J}^R_{\rm inf}$, are shown on top of the original couplings,  $\mathbb{J}^R_{\rm true}$ 
     The first figure (from top) in the left column shows  the $\mathbb{J}^R_{\rm inf}$ (black) and the $\mathbb{J}^R_{\rm tru}$ (green) for a given spin
     at temperature $T/J=0 7$ and number of samples  $M=1024$  PLM appears to reconstruct the correct couplings, though zero couplings are always given a small inferred non-zero value  
     In the left column of Fig   \ref{PL-Jor1},  both the $\mathbb{J}^R_{\rm{inf}}$ and the $\mathbb{J}^R_{\rm{tru}}$ are sorted in decreasing order and plotted on top of each other  
     We can clearly see that $\mathbb{J}^R_{\rm inf}$ reproduces the expected step function  Even though the jump is smeared, the difference between inferred couplings corresponding to the set of non-zero couplings 
     and to the set of zero couplings can be clearly appreciated 
     Similarly, the plots in the right column of Fig  \ref{PL-Jor1} show the results obtained for the case with  bimodal disordered couplings, for the same working temperature and number of samples  
     In particular, note that the algorithm infers half positive and half negative couplings, as expected 
     
     
\begin{figure}
\centering
\includegraphics[width=1\linewidth]{Jor11_2D_l2_errJ_varT_varM}
\caption{Reconstruction error $\mbox{err}_J$, cf  Eq  (\ref{eq:errj}), plotted as a function of temperature (left) for three values of the number of samples $M$ and  as a function $M$ (right) for three values of temperature in the ordered system, i e , $J_{ij}=0,1$  
The system size is $N=64$ }
\label{PL-err-Jor1}
\end{figure}

In order to analyze the effects of the number of samples and of the temperature regimes, we plot in Fig  \ref{PL-err-Jor1} the reconstruction error, Eq  (\ref{err}), as a function of temperature for three different sample sizes $M=64,128$ and $512$  
The error is seen to sharply rise al low temperature, incidentally, in the ordered case, for  $T<T_c \sim 0 893$, which is the Kosterlitz-Thouless transition temperature of the 2XY model\cite{Olsson92}  
 However, we can see that if only $M=64$ samples are considered, $\mbox{err}_J$ remains high independently on the working temperature  
 In the right plot of Fig  \ref{PL-err-Jor1},  $\mbox{err}_J$ is plotted as a function of $M$ for three different working temperatures $T/J=0 4,0 7$ and $1 3$  As we expect, 
 $\mbox{err}_J$  decreases as $M$ increases  This effect was observed also with mean-field inference techniques on the same model\cite{Tyagi15} 

To better understand the performances of the algorithms, in Fig  \ref{PL-varTP-Jor1} we show several True Positive (TP) curves obtained for various values of $M$ at three different temperatures $T$  As $M$ is large and/or temperature is not too small,  we are able to reconstruct correctly all the couplings present in the system (see bottom plots) 
The True Positive curve displays how many times the inference method finds a true link of the original network  as a function of the index of the vector of sorted absolute value of reconstructed couplings $J_{ij}^{\rm inf}$  
The index $n_{(ij)}$ represents the related spin couples $(ij)$  The TP curve is obtained as follows: 
first  the values $|J^{\rm inf}_{ij}|$ are sorted in descending order and  the spin pairs $(ij)$ are ordered according to the sorting position of $|J^{\rm inf}_{ij}|$  Then,
     	a cycle over the ordered set of pairs $(ij)$, indexed by $n_{(ij)}$, is performed, comparing with the original network coupling $J^{\rm true}_{ij}$ and verifying whether it is zero or not  The true positive curve is computed as
\begin{equation}
\mbox{TP}[n_{(ij)}]= \frac{\mbox{TP}\left[n_{(ij)}-1\right] (n_{ij}-1)+ 1 -\delta_{J^{\rm true}_{ij},0}}{n_{(ij)}}
\end{equation}
As far as $J^{\rm true}_{ij} \neq 0$, TP$=1$  As soon as the true coupling of a given $(ij)$ couple in the sorted list is zero, the TP curve departs from one  
In our case, where the connectivity per spin of the original system is  $c=4$ and there are $N=64$ spins, we know that we will have  $256$ non-zero couplings   
     	If the inverse problem is successful, hence, we expect a steep decrease of the TP curve when  $n_{ij}=256$ is overcome 

In Fig  \ref{PL-varTP-Jor1}
it is  shown that,  almost independently of $T/J$, the TP score improves as $M$ increases  Results are plotted for three different temperatures, $T=0 4,1$ and $2 2$, with increasing number of samples $M = 64, 128,512$ and $1024$ (clockwise)  
We can clearly appreciate the improvement in temperature if the size of the data-set is not very large: for small $M$, $T=0 4$ performs better  
When $M$ is high enough (e g , $M=1024$), instead, the TP curves do not appear to be strongly influenced by the temperature 

\begin{figure}[t!]
	\centering
	\includegraphics[width=1\linewidth]{Jor11_2D_l2_TPJR_varT_varM}
	\caption{TP  curves  for 2D short-range ordered $XY$ model with $N=64$ spins at three different values of $T/J$ with increasing - clockwise from top - $M$ }
	\label{PL-varTP-Jor1} 
\end{figure} 

\subsection{$XY$ model with complex-valued couplings}
For the complex $XY$ we have to contemporary  infer $2$ apart coupling matrices,  $J^R_{i j}$ and $J^I_{i j}$   As before, a system of $N=64$ spins is considered on a 2D lattice 
For the couplings we have considered both ordered and bimodal disordered cases 
In Fig  \ref{PL-Jor3}, a single row of the matrix $J$ (top) and the whole sorted couplings (bottom) are displayed for the ordered model (same legend as in Fig  \ref{PL-Jor1}) for the real, $J^R$ (left column), and the imaginary part, $J^I$   

\begin{figure}[t!]
	\centering
\includegraphics[width=1\linewidth]{Jor3_l2_JRJI_soJRJI_TPJRJI}
	\caption{Results related to the ordered complex XY model with $N=64$ spins on a  2D lattice  Top: instances of  single site reconstruction for the real, JR (left column), and
		the imaginary, JI (right column), part of $J_{ij}$  Bottom: sorted values of JR (left) and JI (right) }
		
	\label{PL-Jor3}
\end{figure}
 
 
  \section{PLM with Decimation}
 \label{sec:res_dec}
 

\begin{figure}[t!]
   	\centering
   	\includegraphics[width=1\linewidth]{Jor1_dec_tPLF_varT_varM}
    	\caption{Tilted Pseudolikelyhood, ${\cal L}_t$, plotted as a function of decimated couplings  Top: Different ${\cal L}_t$ curves obtained for different values of $M$ plotted on top of each other  Here $T=1 3$  The black line indicates the expected number of decimated couplings, $x^*=(N (N-1) - N c)/2=1888$  As we can see, as $M$ increases, the maximum point of ${\cal L}_t$ approaches $x^*$  Bottom: Different ${\cal L}_t$ curves obtained for different values of T with $M=2048$  We can see that, with this value of $M$, no differences can be appreciated on the maximum points of the different  ${\cal L}_t$ curves }
   	\label{var-$t$PLF}
   \end{figure}

\begin{figure}[t!]
    \centering
    \includegraphics[width=1\linewidth]{Jor1_dec_tPLF_peak_statistics_varM_prob eps}
    	\caption{Number of most likely decimated couplings, estimated by the maximum point of $\mathcal{L}_t$, as a function of the number of samples $M$  We can clearly see that the maximum point of $\mathcal{L}_t$ tends toward $x^*$, which is the right expected number of zero couplings in the system }  
    	\label{PLF_peak_statistics}
    \end{figure}
      
      For the ordered real-valued XY model we show in Fig  \ref{var-$t$PLF}, top panel, the outcome on the tilted pseudolikelyhood, $\mathcal{L}_t$ Eq  \eqref{$t$PLF}, of the progressive decimation: from a fully connected lattice  down to an empty lattice  The figure shows the behaviour of $\mathcal{L}_t$ for three different data sizes $M$  A clear data size dependence of the maximum point of  $\mathcal{L}_t$, signalling the most likely value for decimation, is shown  For small $M$ the most likely number of  couplings is overestimated and for increasing $M$ it tends to the true value, as displayed in Fig  \ref{PLF_peak_statistics}   In the bottom panel of Fig  \ref{var-$t$PLF} we display instead different 
 $\mathcal{L}_t$ curves obtained for three different values of $T$ 
  Even though the values of $\mathcal{L}_t$ decrease with increasing temperature, the value of the most likely number of decimated couplings appears to be quite independent on $T$ with $M=2048$ number of samples 
In Fig  \ref{fig:Lt_complex} we eventually display the tilted pseudolikelyhood for a 2D network with complex valued ordered couplings, where the decimation of the real and imaginary coupling matrices proceeds in parallel, that is, 
when a real coupling is small enough to be decimated its imaginary part is also decimated, and vice versa 
One can see that though the apart errors for the real and imaginary parts are different in absolute values, they display the same dip, to be compared with the maximum point of $\mathcal{L}_t$ 
     
       \begin{figure}[t!]
    	\centering
      	\includegraphics[width=1\linewidth]{Jor3_dec_tPLF_new}
      	\caption{Tilted Pseudolikelyhood, ${\cal L}_t$, plotted with the reconstruction errors for the XY model with $N=64$ spins on a 2D lattice  These results refer to the case of  ordered and complex valued couplings  The full (red) line indicates ${\cal L}_t$  The dashed (green) 
      		and the dotted (blue) lines show the reconstruction errors (Eq  \eqref{eq:errj}) obtained for the real and the imaginary couplings respectively  We can see that both ${\rm err_{JR}}$ and ${\rm err_{JI}}$ have a minimum at $x^*$ }
          	\label{fig:Lt_complex}
    \end{figure}

\begin{figure}[t!]
   	\centering
   	\includegraphics[width=1\linewidth]{Jor1_dec_JR_soJR_TPJR}
   	\caption{XY model on a 2D lattice with $N=64$ sites and real valued couplings  The graphs show the inferred (dashed black lines) and true couplings (full green lines) plotted on top of each other  The left and right columns refer to the
   		 cases of ordered and bimodal disordered couplings, respectively  Top figures: single site reconstruction, i e , one row of the matrix $J$  Bottom figures: couplings are plotted sorted in descending order }  
   	\label{Jor1_dec}
   \end{figure}
   
\begin{figure}[t!]
    	\centering
    	\includegraphics[width=1\linewidth]{Jor3_dec_JRJI_soJRJI_TPJRJI}
    	\caption{XY model on a 2D lattice with $N=64$ sites and ordered complex-valued couplings 
    		The inferred and true couplings are plotted on top of each other  The left and right columns show the real and imaginary parts, respectively, of the couplings  Top figures refer to a single site reconstruction, i e , one row of the matrix $J$  Bottom figures report the couplings sorted in descending order }
    	\label{Jor3_dec}
    \end{figure}
    
       







       \begin{figure}[t!]
     	\centering
     	\includegraphics[width=1\linewidth]{MF_PL_Jor1_2D_TPJR_varT}
     	\caption{True Positive curves obtained with the three techniques: PLM with decimation, (blue) dotted line,  PLM with $l_2$ regularization, (greed) dashed line, and mean-field, (red) full line   These results refer to real valued ordered couplings with $N=64$ spins on a 2D lattice  The temperature is here $T=0 7$ while the four graphs refer to different sample sizes: $M$ increases clockwise }
     	\label{MF_PL_TP}
     \end{figure}
    
    \begin{figure}[t!]
    	\centering
    	\includegraphics[width=1\linewidth]{MF_PL_Jor1_2D_errJ_varT_varM}
    	\caption{Variation of reconstruction error, ${\rm err_J}$, with respect to temperature as obtained with the three different techniques, see Fig  \ref{MF_PL_TP}, for four different sample size:  clockwise from top   $M=512,1024, 2048$ and $4096$ } 
    	\label{MF_PL_err}
    \end{figure}
    
     Once the most likely network has been identified through the decimation procedure, we perform the same analysis displayed in Fig  \ref{Jor1_dec}  for ordered and then quenched disordered real-valued couplings
and in Fig  \ref{Jor3_dec} for  complex-valued ordered couplings   In comparison to the results shown in Sec  \ref{sec:res_reg},
  the PLM with decimation leads to rather cleaner results  In Figs  \ref{MF_PL_err} and \ref{MF_PL_TP} we compare the performances of the PLM with decimation in respect to ones of the PLM with $l_2$-regularization  These two techniques are also analysed in respect to a mean-field technique previously implemented on the same XY systems\cite{Tyagi15} 
  
    For what concerns the network of connecting links, in Fig  \ref{MF_PL_TP} we compare the TP curves obtained with the three techniques  The results refer to the case of ordered and real valued couplings, but similar behaviours were obtained for the other cases analysed  
  The four graphs are related to different sample sizes, with $M$ increasing clockwise  When $M$ is high enough, all techniques reproduce the true network  
  However, for lower values of $M$ the performances of the PLM with $l_2$ regularization and with decimation drastically overcome those ones of the previous mean field technique  
  In particular, for $M=256$ the PLM techniques still reproduce the original network while the mean-field method fails to find more than half of the couplings  
  When $M=128$, the network is clearly reconstructed only through the PLM with decimation while the PLM with $l_2$ regularization underestimates the couplings  
  Furthermore, we notice that the PLM method with decimation is able to clearly infer the network of interaction even when $M=N$ signalling that it could be considered also in the under-sampling regime $M<N$   
 
 
In Fig  \ref{MF_PL_err} we compare the temperature behaviour of the reconstruction error 
In can be observed that for all temperatures and for all sample sizes  the reconstruction error, ${\rm err_J}$, (plotted here in log-scale) obtained with the PLM+decimation is always smaller than 
that one obtained with the other techniques  The temperature behaviour of ${\rm err_J}$ agrees with the one already observed for Ising spins in \cite{Nguyen12b} and for XY spins  in \cite{Tyagi15} with a mean-field approach:  ${\rm err_J}$ displays a minimum around $T\simeq 1$ and then it increases for very lower $T$; however,
 the error obtained with the PLM with decimation is several times smaller  than the error estimated by the other methods 



 
 

     
     \section{Conclusions}
     \label{sec:conc}


Different statistical inference methods have been applied to the inverse problem of the XY model 
After a short review of techniques based on pseudo-likelihood and their formal generalization to the model we have tested their performances against data generated by means of Monte Carlo numerical simulations of known instances
with diluted, sparse, interactions 

The main outcome is that the best performances are obtained by means of the  pseudo-likelihood method combined with decimation  Putting to zero (i e , decimating) very weak bonds, this technique turns out to be very precise for  problems whose real underlying interaction network is sparse, i e , the number of couplings per variable does not scale with number of variables 
The PLM + decimation method is compared to the PLM + regularization method, with $\ell_2$ regularization and to a mean-field-based method  The behavior of the quality of the network reconstruction is analyzed by looking at the overall sorted couplings and at the single site couplings, comparing them with the real network, and at the true positive curves in all three approaches  In the PLM +decimation method, moreover, the identification of the number of decimated bonds at which the tilted pseudo-likelihood is maximum allows for a precise estimate of the total number of bonds  Concerning this technique, it is also shown that the network with the most likely number of bonds is also the one of least reconstruction error, where not only the prediction of the presence of a bond is estimated but also its value 

The behavior of the inference quality in temperature and in the size of data samples is also investigated, basically confirming the low $T$ behavior hinted by Nguyen and Berg \cite{Nguyen12b} for the Ising model  In temperature, in particular, the reconstruction error curve displays a minimum at a low temperature, close to the critical point in those cases in which a critical behavior occurs, and a sharp increase as temperature goes to zero  The decimation method, once again, appears to enhance this minimum of the reconstruction error of almost an order of magnitude with respect to other methods 
 
The techniques displayed and the results obtained in this work can be of use in any of the many systems whose theoretical representation is given by Eq  \eqref{eq:HXY} or Eq  \eqref{eq:h_im}, some of which are recalled in Sec  \ref{sec:model}  In particular, a possible application can be the field of light waves propagation through random media and the corresponding problem of the  reconstruction of an object seen through an opaque medium or a disordered optical fiber \cite{Vellekoop07,Vellekoop08a,Vellekoop08b, Popoff10a,Akbulut11,Popoff11,Yilmaz13,Riboli14} 

 	



ground_truth: According to the globin that is affected (alpha or beta).