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Pages with broken file links, Animal behavior, Scientific classification,
Zoological nomenclature
Botanical nomenclature
Family (biology)
Error: Image is invalid or non-existent.
The hierarchy of biological classification's major eight taxonomic ranks. An order contains one or more families. Intermediate minor rankings are not shown.
In biological classification, family (Latin: familia, plural familiae) is a taxonomic rank. Exact details of formal nomenclature depend on the Nomenclature Code which applies.
History of the concept[edit | edit source]
Family, as a rank intermediate between order and genus, is a relatively recent invention.
The term familial was coined by French botanist Pierre Magnol in his Prodromus historiae generalis plantarum, in quo familiae plantarum per tabulas disponuntur (1689) where he called families (familiae) the seventy-six groups of plants he recognised in his tables. The concept of rank at that time was still in statu nascendi, and in the preface to the Prodromus Magnol spoke of uniting his families into larger genera, which is far from how the term is used today.
Since the beginning of the 20th century, however, the term has been consistently used in its modern sense. Its usage and characteristic ending of the names belonging to this category are defined in the Codes of botanical and zoological nomenclature.
Almost all families are named for a type genus, adding the ending idae (animals) or aceae (plants) to the stem of the genus name. Exceptions are:
Caprifoliaceae, Aquifoliaceae, and Fabaceae, named for their type species Lonicera caprifolium, Ilex aquifolia, and Vicia faba.
Theaceae, named for Thea, a synonym of Camellia.
Eight families of plants with alternate names. Fabaceae is also called Leguminosae, Poaceae Gramineae, etc.
Elapidae. The type genus is Homoroselaps, which was originally named Elaps but was temporarily moved to a different family and the name changed as a result.
Systematics - the study of the diversity of life
Cladistics - the classification of organisms by their order of branching in an evolutionary tree
List of families - list of family names in the taxonomy of biology
Phylogenetics - the study of evolutionary relatedness among various groups of organisms
Compare Family
Rank (botany)
Rank (zoology)
Virus classification
Taxonomic ranks
Magnorder
Domain/Superkingdom Superphylum/Superdivision Superclass Superorder Superfamily Superspecies
Kingdom Phylum/Division Class Legion Order Family Tribe Genus Species
Subkingdom Subphylum Subclass Cohort Suborder Subfamily Subtribe Subgenus Subspecies
Infrakingdom/Branch Infraphylum Infraclass Infraorder Alliance Infraspecies
Microphylum Parvclass Parvorder
Retrieved from "https://psychology.wikia.org/wiki/Family_(biology)?oldid=83713"

redpajama_set_name: RedPajamaCommonCrawl


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Syntomium ist eine Gattung der Käfer aus der Familie der Kurzflügler (Staphylinidae) innerhalb der Unterfamilie Omaliinae. Sie kommt in Europa nur mit Syntomium aeneum vor, welcher auch in Mitteleuropa heimisch ist.

Merkmale
Die Käfer haben stark metallisch glänzende Körper. Die Gattung ist durch ihre Augenhöcker, die sich sehr nahe an den Facettenaugen befinden und durch die darunter befindlichen Fühlereinlenkungen und durch das Fehlen von Punktaugen (Ocelli) charakterisiert.

Vorkommen und Lebensweise
Die Tiere leben in Moos an Bäumen und an Erdwällen und auch in Mooren.

Arten (Europa)
Syntomium aeneum (P. Müller 1821)

Quellen

Einzelnachweise

Literatur
 Karl Wilhelm Harde, Frantisek Severa und Edwin Möhn: Der Kosmos Käferführer: Die mitteleuropäischen Käfer. Franckh-Kosmos Verlags-GmbH & Co KG, Stuttgart 2000, ISBN 3-440-06959-1.
 Edmund Reitter: Fauna Germanica – Die Käfer des Deutschen Reiches. 5 Bände, Stuttgart K. G. Lutz 1908–1916, Digitale Bibliothek Band 134, Directmedia Publishing GmbH, Berlin 2006, ISBN 3-898-53534-7.

Kurzflügler
Staphylinidae

redpajama_set_name: RedPajamaWikipedia


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eMoneyHub Limited successfully close a fourth round of fundraising. Investors include a strategic Chinese investor active in the Asian P2P marketplace and the former Global Principal of Google's financial comparison team.
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Donnchad mac Domnaill Remair (mort en 1089), connu également sous le nom de Donnchadh mac Domhnall Reamhair, est un souverain de la fin du  siècle qui règne sur les royaumes de  Leinster et Dublin. Il est le fils de Domnall Remar mac Máel na mBó. Donnchad est tué en 1089.

Biographie
En 1071, les Annales des quatre maîtres révèlent qu'un conflit éclate entre les  Uí Cheinnselaigh, ces sources indiquent que Donnchad combat son cousin germain, Domnall mac Murchada meic Diarmata (mort en 1075).

L'année suivante, immédiatement après la mort de l'oncle de  Donnchad, Diarmait mac Máel na mBó, roi de Leinster, Toirdelbach Ua Briain, roi de Munster (mort en 1086) submerge le Leinster, et attaque Dublin.
C'est  dans ce royaume côtier qu'il capture les fils de  Domnall Remar, dont Donnchad lui-même. Si l'on en croit les Annales d'Inisfallen, les habitants de Dublin remettent le royaume entre les mains de Toirdelbach.Pour un temps Toirdelbach tolère apparemment que Dublin soit gouverné pour son compte par  Gofraid mac Amlaíb meic Ragnaill, roi de Dublin (mort en 1075). Toutefois le premier expulse le second en 1075 et gouverne seul. Toirdelbach nomme ensuite  Domnall comme roi de
Dublin, et il attribue le Leinster à Donnchad. Malheureusement pour  Toirdelbach, Domnall meurt peu après, et Toirdelbach le remplace par son propre fils, Muirchertach (mort en 1119).

Donnchad  s'empare du contrôle de Dublin en 1086, à la suite de la mort de Toirdelbach, et règen conjointement sur Dublin et le Leinster jusqu'en 1089. En 1087, Muirchertach, devenu roi de  Munster, décide de rétablir le contrôle des Uí Briain sur Dublin, et obtient une victoire
à Ráith Etair, au nord de la Liffey. Deux ans après Muirchertach lui succède en prenant la cité, comme les  Annales des quatre maitres notent la mort de  Donnchad tué par Conchobar Ua Conchobair Failge, roi des
Uí Failge. Muirchertach lui-même est dans l'incapacité de tenir la ville très longtemps, et doit l'abandonner à Gofraid Crobán, roi des Îles (mort en 1095) deux ans plus tard.

Notes et références

Sources primaires

Sources secondaires

Décès en 1089
Donnchad mac Domnaill Remair
Donnchad mac Domnaill Remair


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The beloved 1992 street drama Juice was a collision of first-time film talents. It was the directorial debut of Ernest R. Dickerson, Spike Lee's longtime director of photography. It was the feature film debut of Omar Epps, who starred as Q, an aspiring DJ lured into a life of crime. And it was the first screen acting gig for rapper Tupac Shakur (not counting a cameo as part of Digital Underground in 1991's Nothing but Trouble), who delivered an explosive, scene-stealing performance as the hot-tempered, trigger-happy Bishop.
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NASA Orbiter Reveals Big Changes in Mars' Atmosphere
9:20 PM Gabriella Brianna , Posted in NASA News , 0 Comments
NASA's Mars Reconnaissance Orbiter has discovered the total amount of atmosphere on Mars changes dramatically as the tilt of the planet's axis varies. This process can affect the stability of liquid water, if it exists on the Martian surface, and increase the frequency and severity of Martian dust storms.
Researchers using the orbiter's ground-penetrating radar identified a large, buried deposit of frozen carbon dioxide, or dry ice, at the Red Planet's south pole. The scientists suspect that much of this carbon dioxide enters the planet's atmosphere and swells the atmosphere's mass when Mars' tilt increases. The findings are published in this week's issue of the journal Science.
The newly found deposit has a volume similar to Lake Superior's nearly 3,000 cubic miles (about 12,000 cubic kilometers). The deposit holds up to 80 percent as much carbon dioxide as today's Martian atmosphere. Collapse pits caused by dry ice sublimation and other clues suggest the deposit is in a dissipating phase, adding gas to the atmosphere each year. Mars' atmosphere is about 95 percent carbon dioxide, in contrast to Earth's much thicker atmosphere, which is less than .04 percent carbon dioxide.
"We already knew there is a small perennial cap of carbon-dioxide ice on top of the water ice there, but this buried deposit has about 30 times more dry ice than previously estimated," said Roger Phillips of Southwest Research Institute in Boulder, Colo. Phillips is deputy team leader for the Mars Reconnaissance Orbiter's Shallow Radar instrument and lead author of the report.
"We identified the deposit as dry ice by determining the radar signature fit the radio-wave transmission characteristics of frozen carbon dioxide far better than the characteristics of frozen water," said Roberto Seu of Sapienza University of Rome, team leader for the Shallow Radar and a co-author of the new report. Additional evidence came from correlating the deposit to visible sublimation features typical of dry ice.
"When you include this buried deposit, Martian carbon dioxide right now is roughly half frozen and half in the atmosphere, but at other times it can be nearly all frozen or nearly all in the atmosphere," Phillips said.
An occasional increase in the atmosphere would strengthen winds, lofting more dust and leading to more frequent and more intense dust storms. Another result is an expanded area on the planet's surface where liquid water could persist without boiling. Modeling based on known variation in the tilt of Mars' axis suggests several-fold changes in the total mass of the planet's atmosphere can happen on time frames of 100,000 years or less.
The changes in atmospheric density caused by the carbon-dioxide increase also would amplify some effects of the changes caused by the tilt. Researchers plugged the mass of the buried carbon-dioxide deposit into climate models for the period when Mars' tilt and orbital properties maximize the amount of summer sunshine hitting the south pole. They found at such times, global, year-round average air pressure is approximately 75 percent greater than the current level.
"A tilted Mars with a thicker carbon-dioxide atmosphere causes a greenhouse effect that tries to warm the Martian surface, while thicker and longer-lived polar ice caps try to cool it," said co-author Robert Haberle, a planetary scientist at NASA's Ames Research Center in Moffett Field, Calif. "Our simulations show the polar caps cool more than the greenhouse warms. Unlike Earth, which has a thick, moist atmosphere that produces a strong greenhouse effect, Mars' atmosphere is too thin and dry to produce as strong a greenhouse effect as Earth's, even when you double its carbon-dioxide content."
The Shallow Radar, one of the Mars Reconnaissance Orbiter's six instruments, was provided by the Italian Space Agency, and its operations are led by the Department of Information Engineering, Electronics and Telecommunications at Sapienza University of Rome. NASA's Jet Propulsion Laboratory, a division of the California Institute of Technology in Pasadena, manages the Mars Reconnaissance Orbiter project for NASA's Science Mission Directorate at the agency's headquarters in Washington. Lockheed Martin Space Systems in Denver built the spacecraft.
For more information visit http://www.nasa.gov/mission_pages/MRO/news/mro20110421.html
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Personal Testimony of an Israeli Refusenik /
Personal Testimony of an Israeli Refusenik
Asaf Oron
Editor's Note: Asaf Oron, a Sergeant Major in the Giv'ati Brigade, is one of the original 53 Israeli soldiers who signed the "Fighters' Letter" declaring that from now on they will refuse to serve in the Occupied territories. He is signer #8 and one of the first in the list to include a statement explaining his action. (There are 251 signers as of February 17, 2002.) Below is the translation of Oron's statement by Ami Kronfeld of Jewish Peace News.
On February 5, 1985, I got up, left my home, went to the Compulsory Service Center on Rashi Street in Jerusalem, said goodbye to my parents, boarded the rickety old bus going to the Military Absorption Station and turned into a soldier.
Exactly seventeen years later, I find myself in a head to head confrontation with the army, while the public at large is jeering and mocking me from the sidelines. Right wingers see me as a traitor who is dodging the holy war that's just around the corner. The political center shakes a finger at me self-righteously and lectures me about undermining democracy and politicizing the army.
And the left? The square, establishment, "moderate" left that only yesterday was courting my vote now turns its back on me as well. Everyone blabbers about what is and what is not legitimate, exposing in the process the depth of their ignorance of political theory and their inability to distinguish a real democracy from a third world regime in the style of Juan Peron.
Almost no one asks the main question: why would a regular guy get up one morning in the middle of life, work, the kids and decide he's not playing the game anymore? And how come he is not alone but there are fifty... I beg your pardon, a hundred... beg your pardon again, now almost two hundred regular, run of the mill guys like him who've done the same thing?
Our parents' generation lets out a sigh: we've embarrassed them yet again. But isn't it all your fault? What did you raise us on? Universal ethics and universal justice, on the one hand: peace, liberty and equality to all. And on the other hand: "the Arabs want to throw us into the sea," "They are all crafty and primitive. You can't trust them."
On the one hand, the songs of John Lennon, Pete Seeger, Bob Dylan, Bob Marely, Pink Floyd. Songs of peace and love and against militarism and war. On the other hand, songs about a sweetheart riding the tank after sunset in the field: "The tank is yours and you are ours." [allusions to popular Israeli songs - AK]. I was raised on two value systems: one was the ethical code and the other the tribal code, and I naïvely believed that the two could coexist.
This is the way I was when I was drafted. Not enthusiastic, but as if embarking on a sacred mission of courage and sacrifice for the benefit of society. But when, instead of a sacred mission, a 19 year old finds himself performing the sacrilege of violating human beings' dignity and freedom, he doesn't dare ask - even himself - if it's OK or not. He simply acts like everyone else and tries to blend in. As it is, he's got enough problems, and boy is the weekend far off.
You get used to it in a hurry, and many even learn to like it. Where else can you go out on patrol - that is, walk the streets like a king, harass and humiliate pedestrians to your heart's content, and get into mischief with your buddies - and at the same time feel like a big hero defending your country? The Gaza Exploits became heroic tales, a source of pride for Giv'ati, then a relatively new brigade suffering from low self esteem.
For a long time, I could not relate to the whole "heroism" thing. But when, as a sergeant, I found myself in charge, something cracked inside me. Without thinking, I turned into the perfect occupation enforcer. I settled accounts with "upstarts" who didn't show enough respect. I tore up the personal documents of men my father's age. I hit, harassed, served as a bad example - all in the city of Kalkilia, barely three miles from grandma and grandpa's home-sweet-home. No. I was no "aberration." I was exactly the norm.
Having completed my compulsory service, I was discharged, and then the first Intifada began (how many more await us?) Ofer, a comrade in arms who remained in the service has become a hero: the hero of the second Giv'ati trial. He commanded a company that dragged a detained Palestinian demonstrator into a dark orange grove and beat him to death.
As the verdict stated, Ofer was found to have been the leader in charge of the whole business. He spent two months in jail and was demoted - I think that was the most severe sentence given an Israeli soldier through the entire first Intifada, in which about a thousand Palestinians were killed. Ofer's battalion commander testified that there was a order from the higher echelons to use beatings as a legitimate method of punishment, thereby implicating himself.
On the other hand, Efi Itam, the brigade commander, who had been seen beating Arabs on numerous occasions, denied that he ever gave such an order and consequently was never indicted. Today he lectures us on moral conduct on his way to a new life in politics. (In the current Intifada, incidentally, the vast majority of incidents involving Palestinian deaths are not even investigated. No one even bothers.)
And in the meantime, I was becoming more of a civilian. A copy of The Yellow Wind [a book on life in the Occupied Territories by the Israeli writer David Grossman, available in English -AK] which had just come out, crossed my path. I read it, and suddenly it hit me. I finally understood what I had done over there. What I had been over there.
I began to see that they had cheated me: They raised me to believe there was someone up there taking care of things. Someone who knows stuff that is beyond me, the little guy. And that even if sometimes politicians let us down, the "military echelon" is always on guard, day and night, keeping us safe, each and every one of their decisions the result of sacred necessity.
Yes, they cheated us, the soldiers of the Intifadas, exactly as they had cheated the generation that was beaten to a pulp in the War of Attrition and in the Yom Kippur War, exactly as they had cheated the generation that sank deep into the Lebanese mud during the Lebanon invasions. And our parents' generation continues to be silent.
Worse still, I understood that I was raised on two contradictory value systems. I think most people discover even at an earlier age they must choose between two value systems: an abstract, demanding one that is no fun at all and that is very difficult to verify, and another which calls to you from every corner - determining who is up and who is down, who is king and who - pariah, who is one of us and who is our enemy. Contrary to basic common sense, I picked the first. Because in this country the cost-effective analysis comparing one system to another is so lopsided, I can't blame those who choose the second.
I picked the first road, and found myself volunteering in a small, smoke-filled office in East Jerusalem, digging up files about deaths, brutality, bureaucratic viciousness or simply daily harassments. I felt I was atoning, to some extent, for my actions during my days with the Giv'ati brigade. But it also felt as if I was trying to empty the ocean out with a teaspoon.
Out of the blue, I was called up for the very first time for reserve duty in the Occupied Territories. Hysterically, I contacted my company commander. He calmed me down: We will be staying at an outpost overlooking the Jordan river. No contacts with the local population is expected. And that indeed was what I did, but some of my friends provided security for the Damia Bridge terminal [where Palestinians cross from Jordan to Israel and vice versa - AK].
This was in the days preceding the Gulf War and a large number of Palestinian refugees were flowing from Kuwait to the Occupied Territories (from the frying pan into the fire). The reserve soldiers - mostly right wingers - cringed when they saw the female consscripts stationed in the terminal happily ripping open down-comforters and babies' coats to make sure they didn't contain explosives. I too cringed when I heard their stories, but I was also hopeful: reserve soldiers are human after all, whatever their political views.
Such hopes were dashed three years later, when I spent three weeks with a celebrated reconnaissance company in the confiscated ruins of a villa at the outskirts of the Abasans (if you don't know where this is, it's your problem). This is where it became clear to me that the same humane reserve soldier could also be an ugly, wretched macho undergoing a total regression back to his days as a young conscript.
Already on the bus ride to the Gaza strip, the soldiers were competing with each other: whose "heroic" tales of murderous beatings during the Intifada were better (in case you missed this point: the beatings were literally murderous: beating to death).
Going on patrol duty with these guys once was all that I could take. I went up to the placement officer and requested to be given guard duty only. Placement officers like people like me: most soldiers can't tolerate staying inside the base longer than a couple of hours.
Thus began the nausea and shame routine, a routine that lasted three tours of reserve duty in the Occupied Territories: 1993, 1995, and 1997. The "pale-gray" refusal routine.
For several weeks at a time I would turn into a hidden "prisoner of conscience," guarding an outpost or a godforsaken transmitter on top of some mountain, a recluse. I was ashamed to tell most of my friends why I chose to serve this way. I didn't have the energy to hear them get on my case for being such a "wishy washy" softy.
I was also ashamed of myself: This was the easy way out. In short, I was ashamed all over. I did "save my own soul." I was not directly engaged in wrongdoing - only made it possible for others to do so while I kept guard.
Why didn't I refuse outright? I don't know. It was partly the pressure to conform, partly the political process that gave us a glimmer of hope that the whole occupation business would be over soon. More than anything, it was my curiosity to see actually what was going on over there.
And precisely because I knew so well, first hand, from years of experience what was going on over there, what reality was like over there, I had no trouble seeing, through the fog of war and the curtain of lies, what has been taking place over there since the very first days of the second Intifada.
For years, the army had been feeding on lines like "We were too nice in the first Intifada," and "If we had only killed a hundred in the very first days, everything would have been different." Now the army was given license to do things its way. I knew full well that [former Prime Minister] Ehud Barak was giving the army free hand, and that [current Chief of Staff] Shaul Mofaz was taking full advantage of this to maximize the bloodshed.
By then, I had two little kids, boys, and I knew from experience that no one - not a single person in the entire world - will ever make sure that my sons won't have to serve in the Occupied Territories when they reach 18. No one, that is, except me. And no one but me will have to look them in the eye when they're all grown up and tell them where dad was when all that happened. It was clear to me: this time I was not going.
Initially, this was a quiet decision, still a little shy, something like "I am just a bit weird, can't go and can't talk about it too much either." But as time went by, as the level of insanity, hatred, and incitement kept rising, as the generals were turning the Israeli Defense Forces into a terror organization, the decision was turning into an outcry: "If you can't see that this is one big crime leading us to the brink of annihilation, then something is terribly wrong with you!"
And then I discovered that I was not alone. Like discovering life on another planet.
The truth is that I understand why everyone is mad at us. We spoiled the neat little order of things. The holy Status Quo states that the Right holds the exclusive rights to celebrate the blood and ask for more. The role of the Left, on the other hand, is to wail while sitting in their armchairs sipping wine and waiting for the Messiah to come and with a single wave of his magic wand make the Right disappear along with the settlers, the Arabs, the weather, and the entire Middle East. That's how the world is supposed to work. So why are you causing such a disturbance? What's your problem? Bad boys!
Woe to you, dear establishment left! You haven't been paying attention! That Messiah has been here already. He waved his magic wand, saw things aren't that simple, was abandoned in the midst of battle, lost altitude, and finally was assassinated, with the rest of us (yes, me too) watching from the comfort of our armchairs. Forget it. A messiah doesn't come around twice! There is no such thing as a free lunch.
Don't you really see what we are doing, why it is that we stepped out of line? Don't you get the difference between a low key, personal refusal and an organized, public one? (and make no mistake about it, the private refusal is the easier choice.) You really don't get it? So let me spell it out for you.
First, we declare our commitment to the first value system. The one that is elusive, abstract, and not profitable. We believe in the moral code generally known as God (and my atheist friends who also signed this letter would have to forgive me - we all believe in God, the true one, not that of the Rabbis and the Ayatollahs). We believe that there is no room for the tribal code, that the tribal code simply camouflages idolatry, an idolatry of a type we should not cooperate with. Those who let such a form of idol worship take over will end up as burnt offerings themselves.
Second, we (as well as some other groups who are even more despised and harassed) are putting our bodies on the line, in the attempt to prevent the next war. The most unnecessary, most idiotic, cruel and immoral war in the history of Israel.
We are the Chinese young man standing in front of the tank. And you? If you are nowhere to be seen, you are probably inside the tank, advising the driver.


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Q: Add text on certain lines of a file, with the added text depending on the output of a command that takes a substring from the line I'm trying to make a shell script to take an input file (thousands of lines) and produce an output file that is the same except that on certain lines there will be added text.  When the text is added to the (middle of) the line, the exact added text will depend on a substring on the line.  The correlation between the substring and the added text is complex and comes from an external program that I can call in the shell.  I don't have the source for this converter program nor any control over how the mapping is done.
To explain further...
I have an input file of this general format:
Blah Blah Unimportant
Something Something
FIELD_INFO(field_name_1, output_1),
  FIELD_INFO(field_name_2, output_2),
Yadda Yadda

The whole file needs to be copied, with added text, but the only important parts for me are the field names (e.g. field_name_1, field_name_2).  I have a command line program called "converter" that can take a file of field names and output a list of corresponding actions.  Converter cannot operate directly on the input file.  The input to converter needs to be just field names and the output of converter has extra information I don't need:
converter_field_name_1 "action1" /* Use this action for field_name_1 */
converter_field_name_2 "action2" /* use this action for field_name_2 */

The desire is to create a second file that looks like this:
Blah Blah Unimportant
Something Something
FIELD_INFO(field_name_1, action1, output_1),
  FIELD_INFO(filed_name_2, action2, output_2),
Yadda Yadda

Here is the script I'm working on, but I've hit a wall (or two):
#!/bin/bash

filename="input_file"

# Let's create an array of the field names to feed to the converter program
field_array=($(sed -e '/^\s*FIELD_INFO/ s/FIELD_INFO(\(.*\),.*),/\1/' -e 't' -e 'd' < ${filename}))

# Save the array to a file, to be able to use the converter's file option
printf "%s\n" "${field_array[@]}" > script_field_names.txt

# Use converter on the whole file and extract only the actions into another array
action_array=($(converter -f script_field_names.txt | cut -d'"' -f 2))

# I will make and use an associative array and try to use
# sed to do the substitution
declare -A mapper
for i in ${!field_array[*]}
do
mapper[${field_array[i]}]=${action_array[i]}
done

#Now go back through the file and add action names (source file unchanged)
sed -e "s/FIELD_INFO(\(.*\),\(.*?),\)/FIELD_INFO(\1, ${mapper[\1], \2}/" < ${filename}

I know now that I can't use the sed group capture "\1" as an index into the mapper array like this. It is not working as a key and the output looks like this:
Blah Blah Unimportant
Something Something
FIELD_INFO(field_name_1, ,  output_1),
  FIELD_INFO(field_name_2, ,  output_2),
Yadda Yadda

My actual script has debug statements scattered throughout and I know the field array, action array, and mapper array are all getting created correctly.  But my idea of using the group capture substring from sed as the index into the mapper array is not working because I now know that sed expands the variables before running in the sub-shell, so the mapper[] array is not seeing the substring as an index.
What should I be doing instead?  This script may only be used once, but it's too time consuming and error prone to do the addition of the action strings by hand.  I want to come up with a way to make this work but I can't tell if I'm close or completely on the wrong path.

A: Why not try,
sed -n -e 's/^[ ]*FIELD_INFO(\(.*\),.*,/\1/p' -- input_file > script_field_names.txt
printf '/^[ ]*FIELD_INFO(%s,/ s/(\\(.[^,]*\\), \\(.[^)]*\\))/(\\1, %s, \\2)/\n' \
    $(converter -f script_field_names.txt | cut -d'"' -f 2 |
      paste -- script_field_names.txt -) |
    sed -f /dev/stdin -- input_file

where

*

*paste emits the map of fields (from file) and actions (from stdin)

*printf emits a script read by sed from stdin

*each script line becomes: /^[ ]*FIELD_INFO(fieldnameN,/ s/(\(.[^,]*\), \(.[^)]*\))/(\1, actionN, \2)/

A:
sed -e "s/FIELD_INFO(\(.*\),\(.*?),\)/FIELD_INFO(\1, ${mapper[\1], \2}/" < ${filename}
[...]
I now know that sed expands the variables before running in the sub-shell, so the mapper[] array is not seeing the substring as an index.

Good job identifying the problem.  Also, the non-greedy quantifier .*? does not work with sed and ${mapper[\1], \2} should probably be ${mapper[\1]}, \2.
If you want to keep your current approach I see two options.

*

*Do the replacement line by line in bash, either by creating a giant sed command string that lists the action for each line, or by executing sed inside a loop for each line while creating the command strings on the fly.

*Instead of the array mapper, create a file that lists the actions to be inserted in the order from the file. Then use GNU sed's R filename command. This command inserts the next line from filename. You can use this to insert the correct action each time you come across a filed. However, the linebreak is inserted too. So you have to fiddle with the hold space and so on to remove these linebreaks afterwards.

Both options are not that great. Therefore I'd switch to awk to insert the actions:

sed -En 's/^\s*FIELD_INFO\(([^,]*).*/\1/p' "$filename" > fields
converter -f fields | cut -d\" -f2 > actions
awk '/^\s*FIELD_INFO\(/ {getline a < "actions"; sub(",", ", " a ",")} 1' "$filename"

With GNU grep you can simplify the first line to
grep -Po '^\s*FIELD_INFO\(\K[^,]*' "$filename" > fields

redpajama_set_name: RedPajamaStackExchange


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10 key things to know ahead of Liverpool vs. Lyon in Dubai Super Cup
Liverpool play French side Lyon in the Dubai Super Cup on Sunday afternoon – here's everything you need to know about the winter friendly.
Liverpool vs. Lyon
Dubai Super Cup | Al-Maktoum Stadium
December 11, 2022 | 2pm GMT / 6pm local
1. It will go to penalties!
No, we're not predicting a draw between the two sides – in this tournament all four matches will have a penalty shootout after full-time, with the team who wins on penalties receiving an extra point.
If the match is drawn, each side gets two points. With the usual three points for a win.
With such a small number of games in the 'tournament', it's a different way of ensuring a winner.
2. Lyon have already been in action
Strangely, Lyon have already played in this tournament, while the other side, AC Milan, don't play their first game until next Tuesday.
Lyon lost 3-0 to Arsenal on Thursday night (plus 2-1 on penalties), with Gabriel, Eddie Nketiah and Fabio Vieira scoring for the Londoners.
3. Some familiar names in Lyon squad
One of the familiar faces in the Lyon squad is former Arsenal captain Alexandre Lacazette, who is partnered up front by Moussa Dembele – the former Celtic man who was linked with Liverpool for a time.
Another oft-linked player is midfielder Houssem Aouar.
Lyon are currently managed by former France World Cup-winning defender Laurent Blanc, who had a brief stint at Man United at the end of his playing career.
4. Liverpool's squad
Liverpool took 33 players to Dubai for this winter training camp, although not all are fit and Luis Diaz has since departed with a recurrence of his knee injury.
The available squad for Sunday looks like:
Goalkeepers: Kelleher, Adrian, Davies, Mrozek
Defenders: Gomez, Matip, Phillips, Quansah, Robertson, Tsimikas, Ramsay, Chambers
Midfielders: Thiago, Elliott, Milner, Oxlade-Chamberlain, Keita, Bajcetic, Cain, Corness
Forwards: Salah, Firmino, Carvalho, Clark, Doak, Frauendorf, Stewart
Diaz is definitely ruled out, Curtis Jones is unlikely after training separately in the week and there are doubts over Thiago and Joel Matip, too.
5. What Klopp's said
Speaking to the club's official website ahead of the tie, Jurgen Klopp spoke about using the time in Dubai to emerge "fighting for each inch":
"It's really good fun to be together with them, to see them.
"We all want to strike back – that's the reality. We don't accept things like this.
"But it's difficult in a season to change things because you play every three days and if you have a problem then you try to sort it and then you create another problem – that happens very often.
"We came through a difficult spell and now I think we are sixth in the table or whatever – yes, there's some distance but I don't know where it will end up but I want to see us fighting for each inch, to be honest.
"That's what we try to create here."
6. The stadium
All matches in this four-team, four-game tournament are taking place at the 15,000-seater Al-Maktoum Stadium in Dubai, home to local side Al Nasr SC.
It's a modern stadium, renovated in 2018 after initially being opened in 1995, with a mosque built into one of the stands making it unique.
7. Not our first friendly vs. Lyon
Liverpool have only played Lyon twice in competitive games in their history, both coming in the group stage of the Champions League in 2009/10.
The Reds took a 1-1 draw from Stade de Gerland, before suffering a 2-1 defeat at Anfield as they were knocked out of the group in Rafa Benitez's final season.
There was, however, a friendly between the two sides during pre-season in 2019, with goals from Roberto Firmino, Harry Wilson and an own goal from Joachim Andersen handing Liverpool a 3-1 victory in Geneva.
8. A chance for youth
Klopp called up a total of 13 academy youngsters to his squad for the trip to Dubai, and some of those will be in line for minutes on Sunday.
That includes the exciting likes of Stefan Bajcetic, Ben Doak, Bobby Clark, Luke Chambers, Melkamu Frauendorf and Jarell Quansah.
Layton Stewart, Jake Cain and Dominic Corness are slightly more experienced faces among the group, while Harvey Davies and Fabian Mrozek bolster the goalkeeping ranks.
Marcelo Pitaluga and Kaide Gordon are not in contention, however, as they recover from long-term injuries.
9. When are the other games in this tournament?
After this one, both Arsenal and Liverpool play against Italian side AC Milan, with the Reds' match being next Friday (December 16) – timed again to avoid clashing with any World Cup fixtures.
From there, Liverpool will head back to Merseyside and begin preparations for the return to competitive action against Man City on December 22.
10. How to watch
The match kicks off at 2pm GMT (6pm local time in the UAE), and is live exclusively on LFCTV.
LFCTV is available to live stream here.
Jack Sear will be running This Is Anfield's matchday live blog from 1.15pm, with updates and analysis throughout.
This Is Anfield's coverage of Liverpool FC in Dubai is brought to you in association with LFCRetail UAE – the Reds' official retailer in the United Arab Emirates.
Dubai 2022, Dubai Super Cup, Liverpool vs Lyon, Lyon


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You are here: Posts > Industry News > BG pay deal criticised
BG pay deal criticised
The Institute of Directors (IoD) has criticised the recent pay deal agreed for the new executive of the oil and gas group BG.
Helge Lund will be given £25 million for his appointment at the leading energy firm, but Simon Walker, head of the IoD, believes the move sends the wrong message ahead of next year's general election.
He has raised concerns it could undermine attempts made by the business community to gain the trust of the public and could put executive pay back on the political agenda.
"It is excessive, inflammatory and contrary to the principles of good corporate governance," said Mr Walker.
He added: "The Institute of Directors is always reluctant to criticise an individual company. However we do have a responsibility to criticise an action that brings the whole of British business into disrepute and threatens already fragile attitudes to corporate Britain."
Mr Lund's deal includes a £12 million 'golden hello', as well as annual earnings of around £13.5 million if he meets certain targets.
BG will put the new pay deal to its shareholders next month because it will require a change in the company's current pay policies - something which the IoD has raised concerns about.
Mr Walker explained: "It will damage the legitimacy and integrity of corporate Britain as a whole by seeking to unpick binding votes cast by the owners of the company. It cannot be right to put fund managers in a position where, unless they approve excessive pay way beyond agreed policy, their shares will fall in value."
He called on BG shareholders to consider the impact the pay deal could have on the whole business community and therefore, they should consider rejecting it.
A spokeswoman for BG said: "We believe Helge Lund is the right person to lead BG Group. His proposed remuneration is competitive in the international oil and gas industry. We are talking to our shareholders and will continue to do so until EGM on 15th December."
Norwegian-born Mr Lund played a key role in the advancement of Statoil and its expansion into the lucrative markets in the Gulf of Mexico and Russian Arctic.


text:
Fabrizio Ricci
University of Studies G. d'Annunzio Chieti and Pescara, Italy
Theo Pezel
Hôpital Lariboisière, France
Dominik Buckert
Ulm University Medical Center, Germany
Jérôme Garot
Institut Cardiovasculaire Paris Sud, France
Front. Cardiovasc. Med., 17 November 2021
Sec. Cardiovascular Imaging
Volume 8 - 2021 | https://doi.org/10.3389/fcvm.2021.765961
Fast-Strain Encoded Cardiac Magnetic Resonance During Vasodilator Perfusion Stress Testing
Henning Steen1, Moritz Montenbruck2, Sebastian Kelle3,4,5, Sebastian Esch2, Arne Kristian Schwarz2, Sorin Giusca6,7 and Grigorios Korosoglou6,7*
1Medneo, Hamburg, Germany
2Cardiology/Cardiac Imaging, Marien Hospital, Hamburg, Germany
3Department of Internal Medicine/Cardiology, Deutsches Herzzentrum Berlin, Berlin, Germany
4Department of Internal Medicine and Cardiology, Charité—Universitätsmedizin Berlin, Campus Virchow-Klinikum, Berlin, Germany
5Deutsches Zentrum für Herz-Kreislauf-Forschung (DZHK) (German Centre for Cardiovascular Research), Berlin, Germany
6Department of Cardiology, Vascular Medicine and Pneumology, Gesundheitszentren Rhein-Neckar (GRN) Hospital Weinheim, Weinheim, Germany
7Cardiac Imaging Center Weinheim, Hector Foundation, Weinheim, Germany
Background: Cardiac magnetic resonance perfusion imaging during vasodilator stress is an established modality in patients with suspected and known coronary artery disease (CAD).
Aim: This study aimed to evaluate the performance of fast-Strain-Encoded-MRI (fast-SENC) for the diagnostic classification and risk stratification of patients with ischemic heart disease.
Methods: Perfusion and fast-SENC cardiac magnetic resonance (CMR) images were retrospectively analyzed in 111 patients who underwent stress CMR. The average myocardial perfusion score index, global and segmental longitudinal and circumferential strain (GLS and GCS and SLS and SCS, respectively), were measured at rest and during stress. The combination of SLS and SCS was referred to as segmental aggregate strain (SAS). Segments exhibiting perfusion defects or SAS impairment during stress were defined as "ischemic." All-cause mortality, non-fatal infarction, and urgent revascularization were deemed as our combined clinical endpoint.
Results: During adenosine stress testing, 44 of 111 (39.6%) patients exhibited inducible perfusion abnormalities. During a mean follow-up of 1.94 ± 0.65 years, 25 (22.5%) patients reached the combined endpoint (death in n = 2, infarction in n = 3 and urgent revascularization in n = 20). Inducible perfusion defects were associated with higher number of segments with inducible SAS reduction ≥6.5% (χ2 = 37.8, AUC = 0.79, 95% CI = 0.71–0.87, p < 0.001). In addition, patients with inducible perfusion defects or SAS impairment exhibited poorer outcomes (AUCPerf = 0.81 vs. AUCSAS = 0.74, p = NS vs. each other, and χ2 = 30.8, HR = 10.3 and χ2 = 9.5, HR = 3.5, respectively, p < 0.01 for both).
Conclusion: Purely quantitative strain analysis by fast-SENC during vasodilator stress was related to the diagnosis of ischemia by first-pass perfusion and is non-inferior for the risk stratification of patients with ischemic heart disease. This may bear clinical implications, especially in patients with contraindications for contrast agent administration.
Cardiovascular diseases are the main cause of morbidity and death in the world, annually claiming more lives than all forms of cancer together (1). Non-invasive anatomical imaging of coronary arteries by cardiac computed tomography and functional stress testing like cardiac magnetic resonance (CMR) is currently recommended as first-line diagnostic techniques in patients with suspected or known coronary artery disease (CAD) (2, 3). In this regard, stress CMR is a well-established method for the diagnostic classification and risk stratification of such patients (4–8). Especially vasodilator stress CMR is widely used due to its excellent safety profile and superior accuracy compared with scintigraphy (5, 8, 9).
Currently, the detection of inducible ischemia during vasodilator stress CMR is mostly based on the visual assessment of perfusion defects (5–8), which is subjective and depends on the experience of the readers. In this regard, fast-Strain-Encoded-MRI (fast-SENC) has been utilized for the objective assessment of longitudinal and circumferential myocardial strain (LS and CS) in previous studies [summarized in (10)]. The ability of this technique to diagnose relevant CAD during inotropic stress and predict future adverse events has been previously demonstrated (11, 12). However, limited data are available on the value of fast-SENC to accurately identify perfusion defects and to provide risk stratification in patients who undergo vasodilator stress CMR.
Therefore, we sought to determine the diagnostic and prognostic value of SENC during vasodilator stress in patients with known or suspected CAD. Global LS (GLS) and CS (GCS) and average global strain (GS), as well as segmental LS (SLS) and CS (SCS) and combined information from SLS or SCS, referred to as segmental aggregate strain (SAS) were compared with perfusion data.
Our patient cohort consisted of patients who underwent adenosine stress CMR between September 2017 and July 2019 in the Marien Hospital Hamburg, Hamburg, Germany and had verified follow-up outcomes. Patients were referred for stress CMR due to known or suspected CAD based on current guidelines (2). CMR was performed as part of standard institutional protocols. All patients were above 18 years old and gave written informed consent. The study was conducted in concordance with the Declaration of Helsinki. Patients were excluded from the study in case of claustrophobia, contraindications to adenosine, such as the history of asthma, low blood pressure, clinical instability, advanced atrioventricular block, or sinus bradycardia, known allergy to gadolinium-based contrast agents, renal failure with a glomerular filtration rate (GFR) < 30 ml/kg/min or inability to give informed consent. All patients were deferred from consuming caffeine-containing beverages and food for 24 h before the examination. If this was not the case the examination was postponed to a later timepoint. Prior to the examination, demographic data, including the presence of arterial hypertension, hyperlipidemia, diabetes mellitus, and previous CAD were acquired.
Cardiac Magnetic Resonance Examination
Examinations were performed using a 1.5 T MR system (Achieva, Philips Healthcare, Best, The Netherlands) equipped with cardiac phased-array receiver coils. Data acquisition was triggered on the R-wave using a 4-lead vector ECG. Cine images were obtained using a breath-hold segmented-k-space balanced fast-field echo sequence (SSFP), employing retrospective ECG gating in long-axis planes (2-, 4-, and 3-chamber views) and contiguous short-axis slices covering the whole ventricles, with typically reconstructed 30 phases per cardiac cycle with 50 and 67% acquired heart phases, respectively, for short and long-axis images.
Adenosine Stress CMR Protocol and Image Acquisitions
A standard protocol for adenosine stress CMR was used, which is described in detail elsewhere (13). In short, patients received a continuous infusion of adenosine. The dose was varied between 140 and 210 μg/kg/min depending on heart rate change and clinical symptoms. During the infusion, patients were continuously monitored for heart rate and oxygen saturation, and blood pressure was measured every minute. The stress perfusion acquisition was started after at least 3–4 min of the adenosine infusion and when two criteria were met: increase in heart rate of at least 10–15 beats per minute and/or the blood pressure fall of at least 10 mmHg or both and the occurrence of symptoms related to the adenosine infusion. In case of no heart rate or blood pressure response, the dose of the adenosine infusion was increased to 175 or 210 μg/kg body weight/min until a response was observed. In addition, the presence of splenic switch-off was verified according to current recommendations (14). Stress acquisitions were performed using a gadolinium-based contrast agent (Dotarem®- gadoterate meglumine in a dosage of 0.05 mmol/kg). Three short-axis slices were acquired using a single-shot saturation recovery gradient echo sequence (FOV 320 mm, slice thickness = 8 mm, TE = 1.02 ms, TR = 226 ms, TI = 140 ms, Flip angle = 50°). Fast-SENC acquisitions were performed at baseline, and repeated acquisitions were performed in identical planes during infusion of adenosine after meeting the criteria mentioned above and before the administration of gadolinium for the acquisitions of first-pass perfusion scans. The rest perfusion was performed after 10 min using identical planes and the same dosage of the contrast agent. Afterward, late gadolinium enhancement (LGE) acquisitions were performed in three long-axis and multiple short axes, covering the entire left ventricle.
Evaluation of Myocardial Perfusion
All analyses were performed on a commercially available workstation (CVI 42, Circle Cardiovascular Imaging Inc., Calgary, Canada). Results for ventricular volumes, left- and right-ventricular (LV and RV) ejection fraction (%), and myocardial mass were derived from short-axis slices. The presence of myocardial perfusion defects was performed visually in three short-axis images. A perfusion defect was defined as a region in the myocardium exhibiting hypo-enhancement by visual criteria that persists after peak myocardium enhancement for at least 4 RR intervals and corresponds to a coronary territory (15). In addition, semiquantitative perfusion analysis was performed by using a 3-point grading scale (16):
1 = Normal Perfusion,
2 = Perfusion Deficits With <50% Transmurality and
3 = Perfusion Deficits With ≥50% Transmurality During Adenosine Stress
Corresponding images in a patient with normal perfusion during stress, with a subendocardial and with a transmural perfusion defect during vasodilator stress are provided in our Supplementary Figure 1. Based on this grading system, an average perfusion score index was built for analysis by patients, by calculating the mean score in 17 myocardial segments, as recommended by the AHA (17). Images were analyzed by experienced operators with more than 10 years of experience in cardiovascular imaging and acquired level 3 certification by the German Society of Cardiology (HS & MM).
Single Heartbeat Fast-SENC Acquisitions
As described previously, fast-SENC is based on the acquisition of high- and low-tuning image sequences with different frequency modulation. Fast-SENC image sequences were analyzed using the MyoStrain software (Myocardial Solutions, Inc., Morrisville, North Carolina, USA), as described previously (18).
With fast-SENC, bright regions in the two frequency modulation images represented static and fully contracted tissues, respectively. Circumferential and longitudinal strain within a range from 5 to −30% were encoded, with negative values translating into active myocardial contraction. In our study, a single heartbeat, a fast-SENC variant with single-shot spiral readouts was employed. Typical imaging parameters were as follows: field-of-view = 256 × 256 mm, slice thickness = 10 mm, voxel size = 4 × 4 × 10 mm, reconstructed resolution = 1 × 1 × 10 mm, single-shot spiral readout with acquisition time TA = 10 ms, flip angle = 30°, effective echo time (TE) = 0.7 ms, repetition time (TR) = 12 ms, temporal resolution = 36 ms, the typical number of acquired heart phases = 22, spectrally selective fat suppression (SPIR), and total acquisition time per slice < 1 s. Data were acquired in three long-axis (four-, three-, and two-chamber) views, and three short-axis views of the LV (basal, mid-ventricular, and apical).
Global circumferential strain by fast-SENC is extracted from 3 long-axis views, whereas GLS is extracted from the 3 short-axis images. The endocardial and epicardial borders were drawn at the end-systolic cardiac phase and are traced throughout the cardiac cycle, using an automatic tissue tracking algorithm. Tracking is then verified and manually corrected if necessary. A 16-segment model was used for the GLS and a 21-segment model for the GCS. For the analysis, GLS and GCS were expressed as the average value of all 16 and 21 segments, respectively. In addition, a GS was calculated by averaging LS and CS in all available segments (19, 20).
Global circumferential strain, GLS, and GS were measured both at baseline and during adenosine stress. In addition, segments with relevant segmental LS and/or CS strain (SAS) impairment during stress were defined as ischemic. The number of such "ischemic" segments was calculated for SLS, SCS, and SLS or SCS which was referred to as SAS in each patient.
Because myocardial shortening occurred in both longitudinal and circumferential directions during systole, the strain values were consequently negative and were so reported. However, throughout the text, and in keeping with most of the literature on the subject, we refer to the absolute values, i.e., higher strain values meaning more deformation and consequently more "negative" values.
Definition of Study Endpoints
Personnel unaware of the CMR results contacted all patients or relatives of patients who underwent stress CMR studies during follow-up. All-cause mortality, the occurrence of non-fatal myocardial infarction, and urgent coronary revascularization by PCI or CABG were selected as the combined primary endpoint of our study. We used all-cause and not only cardiovascular mortality as an endpoint since the prior is free of potential subjectivity, clinically compelling, and therefore most relevant to the patients (21). In addition, urgent revascularization was fulfilled only if patients were hospitalized unexpectedly because of persisting or increasing chest pain and revascularization was performed urgently within the same hospitalization (22).
Data were presented as M ± SD for continuous variables and as absolute values and percentages for categorical values. A paired t-test was used to compare two groups of normally distributed values. The ANOVA test was used for comparing three or more normally distributed groups with the Scheffé test for post-hoc analysis (23). The Mann-Whitney test was used to compare ordinal variables and the Fisher test to compare nominal variables. A Pearson correlation test was employed to test the relation between strain and perfusion variables. A receiver operator characteristics (ROC) analysis was used to identify the best parameter that identifies the presence of perfusion abnormalities or cardiac endpoints. Comparison of the areas under the curve (AUC) of paired data ROC curves was performed using the DeLong method (24). Survival curves were estimated by the Kaplan-Meier method and compared by log-rank tests. In addition, a hierarchic logistic regression model was used to assess the incremental value of myocardial perfusion and strain to clinical variables (age, diabetes mellitus, and history of CAD) for the prediction of the combined endpoint by calculating the corresponding total χ2 values. Inter- and intra-observer variabilities for strain values were assessed by repeated analysis of 40 randomly selected patients and were calculated as the ratio of the standard deviation to the mean. Based on a statistical power of 90%, a two-sided type I error of 0.05, and the expected SD of the results, as well as the expected margins of error (pre-specified non-inferiority margin), we calculated that a minimum of 70 patients would be necessary for our study for a comparison between strain and conventional first-pass perfusion imaging. The MedCalc software version 20.009 (MedCalc, Ostend, Belgium, 2019) was used throughout. All p < 0.05 were considered statistically significant.
Demographic, CMR, and Outcome Data
Complete CMR and follow-up data were available in 111 individuals who underwent vasodilator stress perfusion CMR for clinical reasons. Demographic, clinical, and CMR data are provided in Table 1. Mean age was 62.6 ± 11.8 years old whereas 28 (25%), 84 (76%), and 16 (14%) patients had diabetes mellitus, hyperlipidemia, and previous infarction, respectively.
Table 1. Demographic, clinical, and CMR data from our patient cohort.
During the adenosine stress test, 44 of 111 (39.6%) patients exhibited inducible perfusion abnormalities. Patients with inducible perfusion abnormalities had similar demographic and baseline CMR data to those with negative stress results, except for LV-mass, which was increased in patients with inducible perfusion abnormalities. However, significant differences were observed with the average perfusion score index and for global strain parameters during stress in patients with vs. without perfusion abnormalities (Table 1).
Association Between Myocardial Strain and Perfusion
Patients with inducible perfusion defects had significantly lower GLS, GCS, and GS during stress (p < 0.05 for all) compared with patients without perfusion defects, whereas all baseline strain values were similar between the 2 groups (Figures 1A–C).
Figure 1. Patients with inducible perfusion abnormalities had significantly lower global longitudinal and circumferential myocardial strain (GLS and GCS, respectively), as well as global strain (GS) during stress compared to patients with negative stress results (p < 0.05 for all), whereas baseline strain values were similar for all markers between the two groups (A–C).
Based on a priori ROC analysis, a cut-off value of 6.5% for absolute segmental strain (SLS, SCS, and SAS) reduction during vasodilator stress was selected as best indicative for the presence of segmental myocardial ischemia by perfusion analysis. Thus, the number of ischemic segments with inducible SLS, SCS, or SAS decrease ≥6.5% were all indicative for the presence of inducible perfusion defects, with SAS exhibiting the highest accuracy, followed by SCS and SLS (AUCSCS = 0.78, 95% CI = 0.69–0.84, AUCSAS = 0.79, 95% CI = 0.71–0.87 and AUCSLS = 0.58, 95% CI = 0.49–0.68; p < 0.05 for SLS vs. SAS and SCS, Figure 2A). Therefore, SAS values deriving information both from longitudinal and circumferential deformation were used for further analysis. Corresponding sensitivities and specificities are provided in Table 2A.
Figure 2. The presence of inducible strain decrease ≥6.5% by segmental LS (SLS), segmental CS (SCS), and segmental aggregate strain (SAS) during stress were all indicative for the presence of inducible perfusion abnormalities, with SCS and SAS exhibiting higher accuracies (A). Patients with inducible perfusion abnormalities exhibited a higher number of ischemic segments by SAS (B) and higher absolute SAS decrease during stress (C). A moderate inverse correlation was observed between the perfusion score index and inducible SAS decrease (D).
Table 2. Sensitivities, specificities, and accuracy values for (A) detection of inducible perfusion abnormalities by strain and (B) Prediction of outcomes using perfusion and strain parameters.
Patients with inducible perfusion defects exhibited a higher number of segments with inducible SAS decrease ≥6.5% (χ2 = 37.8, p < 0.001) and significantly higher absolute SAS decrease during adenosine stress (p < 0.001) (Figures 2B,C). In addition, a weak inverse correlation was observed between the average perfusion score and the SAS decrease during stress (r = −0.34, p < 0.01; Figure 2D). On a segmental level, a slight absolute SLS decrease and a blunted SLS increase were noticed in segments with subendocardial and transmural perfusion defects, respectively, compared with segments with normal perfusion during stress, exhibiting a slight SLS increase (Supplementary Figure 2A). The same patterns were observed after the exclusion of segments with LGE (Supplementary Figure 2B). Additional correlations between perfusion and strain parameters are provided in Table 3.
Table 3. Correlations between the average perfusion score index and strain parameters during stress.
Association With Perfusion and SAS With Clinical Endpoints
During a mean follow-up duration of 1.94 ± 0.65 years, 2 patients died, 3 had a non-fatal myocardial infarction and 20 underwent urgent coronary revascularization by PCI (n = 15) or CABG (n = 5).
A significant association was observed between inducible perfusion abnormalities and the combined endpoint (χ2 = 31.7, contingency coefficient = 0.47, p < 0.001). The perfusion score index was significantly higher in patients with vs. without cardiac endpoints (Figure 3A).
Figure 3. The average perfusion score index was significantly higher in patients with future cardiac endpoints (A). Similarly, patients with cardiac endpoints had significantly higher absolute SAS decrease during stress (B) and a higher number of ischemic segments by SAS (C). In addition, a strong association was present between ischemic segments by SAS and future cardiac events (D).
In addition, patients with cardiac endpoints exhibited higher SAS decrease and higher number of ischemic segments by SAS during stress compared with those without cardiac endpoints (p < 0.001 for both; Figures 3B,C). A strong association also was present between the presence of ischemic segments by SAS and future events (χ2 = 15.2, p < 0.001; Figure 3D).
Prediction of Endpoints by Perfusion and Segmental Strain
Both visual perfusion and quantitative SAS analysis predicted the combined cardiac endpoint with similar accuracy rates (AUC = 0.81, 95% CI = 0.72–0.88 vs. 0.74, 95% CI = 0.65–0.82; ΔAUC =0.065, p = NS). Similarly, the perfusion score index performed as well as the number of ischemic segments by SAS, predicting the combined endpoint (AUC = 0.82, 95% CI = 0.73–0.88 vs.0.74, 95% CI = 0.65–0.82; ΔAUC = 0.075, p = NS; Figures 4A,B). The corresponding sensitivity and specificity values and Kaplan-Maier curves are provided in Table 2B and Figures 4C,D, respectively.
Figure 4. The presence of perfusion abnormalities or at least one ischemic segment by SAS, the average perfusion score, and the number of ischemic segments by SAS all predicted the combined cardiac endpoint with similar accuracy rates (A,B). The corresponding Kaplan-Maier curves are provided in (C,D).
The independent association of perfusion and SAS with cardiac outcomes were confirmed by multivariable regression analysis (Table 4). In addition, the presence of impaired SAS during stress exhibited incremental value to perfusion imaging and clinical data for the prediction of the combined endpoint, as shown by the acquired χ2 values (Figure 5).
Table 4. Multiple regression analysis for the prediction of the combined endpoint death, non-fatal myocardial infarction, and urgent coronary revascularization during follow-up.
Figure 5. The presence of strain abnormalities added incremental value to perfusion imaging and clinical data for the prediction of the combined endpoint.
Intra and Interobserver Variabilities
Intra- and interobserver variabilities for LS, CS were 1.5 and 1.6% and 2.1 and 2.3%, respectively. Total acquisition time was <15 s per patient, whereas the time spent required for quantitative analysis of LS, CS, and SAS was 304 ± 125 s (5.1 ± 2.1 min) per patient.
Patient Case Example
A 58-year-old female patient with arterial hypertension, hyperlipidemia and suspected CAD due to atypical angina underwent adenosine stress CMR, which did not show abnormal findings (not shown). Normal strain response was seen by fast-SENC in the short axis views (Figures 6A–F). However, abnormal strain response was detected in the corresponding 3 chamber view fast-SENC images (Figures 6G,H) with a significant inducible strain decrease in the apical cap (red arrow in Figure 6H and the corresponding bull's eye maps in Figure 6I). Due to the absence of a perfusion defect cardiac catheterization was deferred. However, after 1 year the patient underwent urgent revascularization by PCI and stent placement in the LAD.
Figure 6. Adenosine stress cardiovascular magnetic resonance (CMR) showed normal findings in a 58-year-old female patient with suspected coronary artery disease (CAD) due to atypical angina (not shown). A normal strain response was also seen by fast-SENC in the short axis views (A–F). However, abnormal strain response was detected in the corresponding 3 chamber view fast-SENC images (G,H) with a significant inducible strain decrease in the apical cap [red arrow in (H) and the corresponding bull's eye maps in (I)].
In this analysis of 111 patients with complete perfusion, segmental strain analysis, and follow-up outcomes, we found that:
I. Myocardial perfusion abnormalities during vasodilator administration were associated with clinical outcomes.
II. Evaluation of segmental myocardial strain during baseline and vasodilator stress using fast-SENC was feasible with high reproducibility and within reasonable time-spent.
III. An inducible absolute SAS decrease ≥6.5% during adenosine stress in one or more myocardial segments was associated with inducible perfusion abnormalities during first-pass perfusion imaging.
IV. Perfusion and strain abnormalities during vasodilator stress predicted future cardiac outcomes in patients with ischemic heart disease. Overall, perfusion defects showed numerically higher predictive values for future events, which was an expected finding since perfusion is a well-established marker for the prediction of future events (4, 7). However, segmental strain measures exhibited independent and incremental value for the prediction of outcomes.
Previous Studies
We and others had previously described the incremental value of SENC both for the diagnostic classification and for the risk stratification of patients with suspected and known CAD (11, 12). Quantitative strain analysis enabled the identification of myocardial ischemia already during intermediate stages of inotropic stress, thus exhibiting enhanced sensitivity for the detection of CAD (12). In addition, the incremental value of SENC was demonstrated for the prediction of clinical outcomes during inotropic stress (11). Despite the presence of wide evidence for the diagnostic and prognostic value of inotropic strain in patients with ischemic heart disease, most of the clinical stress CMR studies are currently performed using vasodilator stress with adenosine or regadenoson. In this direction, the study of Romano et al. recently demonstrated the incremental value of longitudinal strain during vasodilator stress for the risk stratification of patients with CAD (25). Thus, using regadenoson perfusion stress CMR, GLS was measured at baseline and during stress in the 2-chamber long-axis cine view. GLS ≥ −19 during vasodilator stress was independently associated with worse cardiac outcomes, independent of clinical variables, perfusion abnormalities, and LGE data. This study reinforced the incremental value of strain assessment during vasodilator stress CMR. However, the strain was assessed by feature tracking imaging in this study, which was shown to have limitations, such as low reproducibility especially on a regional level and with less experienced operators (26–28). This, along with the fact that analysis was performed only in the 2-chamber long-axis view limits the interpretation of the obtained results (29). In this regard, fast-SENC provides an alternative to FTI and allows for a very quick, single heartbeat and comprehensive evaluation of regional and global myocardial strain with high reproducibility (18). In our study, SENC enabled the comprehensive assessment of myocardial strain with single heartbeat acquisitions with high reproducibility. Worsening myocardial strain during vasodilator stress CMR offered the precise detection of perfusion defects and was also associated with worse ischemic outcomes during follow-up. This may be a particular advantage in patients with contraindications for gadolinium-based contrast agents. Changes in SAS were much more sensitive than global strain (GLS, GCS, and GS) both for the detection of regional ischemia by perfusion analysis and for the prediction of outcomes. This is not striking since ischemia usually occurs regionally in one or two of three perfusion territories and not in all three simultaneously. In contrast to the study by Romano et al. (25) SCS and SAS were more strongly associated with perfusion abnormalities and predictive of outcomes compared with SLS. This may be attributed to methodological differences between FTI and SENC, the latter allowing for more comprehensive and reproducible measures of strain, especially on a regional level, which is decisive for the detection of ischemic heart disease (18, 26–31). Generally, CS is believed to be a more sensitive marker for subtle myocardial dysfunction in asymptomatic patients without any history of cardiovascular disease (32) and a more accurate marker of regional ischemic myocardial dysfunction, which is supported by the results of our study (33).
Implementation of Our Findings Into the Current Clinical Context
Functional stress testing has been the non-invasive gold standard for the diagnostic work-up of patients with suspected and known CAD within the last decades, whereas its role in the diagnostic classification and risk stratification is widely accepted in patients with chronic coronary syndromes (CCS) based on current guidelines (2). Particularly CMR is currently acknowledged by clinicians as the clinical gold standard technique for the assessment of myocardial function, ischemia, and viability, if required all within a single examination, non-invasively and without radiation exposure for the patients. The amount of evidence for the applicability of dobutamine and vasodilator stress CMR for the detection of ischemia and the risk stratification of patients with CAD is large and has been highlighted in previous meta-analyses (6, 7). Based on the recent ISCHEMIA study, however, the role of coronary revascularization guided by the presence of myocardial ischemia has been questioned, since patients with stable coronary disease and moderate or severe ischemia, may not always profit in terms of outcomes from a primary revascularization strategy (34). However, patients with angina at baseline due to obstructive CAD improved in terms of limiting symptoms such as angina and exertional dyspnea from invasive strategies, which is an important cornerstone in the treatment of CAD (35). Furthermore, a recent meta-analysis demonstrated that patients with CCS randomized to elective revascularization vs. optimal medical treatment exhibited benefits in terms of cardiac survival, which improved with longer follow-up durations and were associated with fewer spontaneous myocardial infarctions (36). In addition, the MR-Inform study reinforced the role of vasodilator stress CMR in patients with stable angina and risk factors for CAD, being non-inferior to a primary invasive approach with X-Ray angiography and fractional flow reserve (FFR) measures with respect to clinical outcomes in patients with CCS (37).
From a pathophysiologic point of view, myocardial strain is more sensitive to disturbances of the myocardial metabolism or perfusion, which may be seen in the early stages of many cardiovascular disorders, including CAD and heart failure (38). In this regard, we recently demonstrated that even in patients at risk for heart failure and without coronary or structural heart disease, the impaired myocardial strain may be present as an early sign of subclinical cardiac dysfunction (19). In the present study, reduced strain response was seen in patients with myocardial ischemia during vasodilator stress, compared with those without perfusion abnormalities. Since hyperemic stress leads to redistribution of myocardial blood flow between the endocardium and epicardium (39), it is conceivable that endocardial strain is reduced due to impaired oxygen supply of the endocardium in regions with inducible ischemia, resulting in lower strain values in such regions. Thus, such individuals may have early damage of the sub-endocardial or mid-myocardial layers and therefore experience worse outcomes during follow-up. However, at present, it is not clear whether impaired strain during hyperemic stress requires a specific treatment, which merits further investigation in future studies.
Our cohort was relatively small and heterogeneous with a high percentage of patients with known CAD. This limits the extrapolation of our findings to lower risk cohorts. In addition, the follow-up duration was quite short and only 25 endpoints were recorded. Especially the small number of hard endpoints such as death and non-fatal myocardial infarction and the inclusion of only patients with CMR and complete follow-up data are limitations, that need to be accounted for when interpreting our results. In addition, patients who underwent elective revascularization within the first 90 days after abnormal stress perfusion by CMR were excluded from analysis, and no repeated CMR was performed after the revascularization procedures, which would have helped define the impact of residual ischemia on clinical outcomes. Furthermore, the cut-off value of SS decrease ≥6.5% during vasodilator stress was selected by a priori ROC analysis, as best indicative for the presence of myocardial ischemia by perfusion analysis, which may overestimate the association between perfusion defects and strain. However, the same cut-off was then independently applied for the prediction of cardiac events, exhibiting significant prognostic value. In addition, a certain overlap was observed for strain values in patients with and without perfusion abnormalities, so that average strain values may not be useful on an individual scale. However, by a selection of a cut-off value for the strain on a segmental level, clinically acceptable accuracy rates could be achieved for the estimation of perfusion abnormalities and clinical endpoints on a patient-by-patient level. Furthermore, we cannot evaluate the accuracy of strain or perfusion abnormalities for CAD detection by comparing these variables to invasive data in conjunction with FFR measures. However, most of our patients had negative stress test results, which helped defer invasive angiography, and this is clinically meaningful.
Fast-SENC during vasodilator stress was non-inferior compared with standard visual perfusion analysis for the diagnosis of ischemia and the risk stratification of patients with ischemic heart disease. This may bear clinical implications since fast-SENC relies on purely quantitative analysis, which is reproducible and can be performed within reasonable time-spent. Thus, fast-SENC can obviate the need for contrast agent injections in this regard, in the interest of time and costs and potentially patient safety. Now prospective larger-scale trials are warranted to test the ability of fast-SENC to predict hard cardiac outcomes.
The raw data supporting the conclusions of this article will be made available by the authors, without undue reservation.
The studies involving human participants were reviewed and approved by Ethics Committee of the General Medical Council Hamburg. The patients/participants provided their written informed consent to participate in this study.
GK and HS designed the study, performed the analysis, wrote and reviewed the manuscript, and provided important intellectual input. MM performed the acquisitions, reviewed the manuscript, and provided important intellectual input. SK, SE, AS, and SG reviewed the manuscript and provided important intellectual input. All authors contributed to the article and approved the submitted version.
HS, SK, and GK received research grants from Myocardial Solutions. SK owns stock options of Myocardial Solutions.
The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
We thank Birgit Hoerig, Kirsten Falk, Ute Pfeiffer, and Silke Morgenstern for their excellent technical assistance with the acquisitions of all CMR scans.
The Supplementary Material for this article can be found online at: https://www.frontiersin.org/articles/10.3389/fcvm.2021.765961/full#supplementary-material
Supplementary Figure 1. Corresponding mid short axis images in (i) a patient with normal perfusion during stress [(A,B), note the asterisk, pointing to a dark rim artifact during resting perfusion], (ii) a patient with a subendocardial defect [(C,D), red arrow in (D), pointing to an inducible subendocardial perfusion defect of the septal wall] and (iii) a patient with a transmural perfusion defect [(E,F), red arrow in (F), pointing to an inducible transmural perfusion defect of the inferior-septal wall] during vasodilator stress are provided in this figure.
Supplementary Figure 2. On a segmental level, a slight absolute SLS decrease and a blunted SLS increase was observed in segments with subendocardial and transmural perfusion defects, respectively, vs. segments with normal perfusion during stress, which showed a slight SLS increase (A). The same patterns were observed after exclusion of segments with LGE (B).
Supplementary Table 1. Hemodynamic data during vasodilator stress.
AUC, area under the curve; BMI, body mass index; CABG, coronary artery bypass graft; CMR, cardiovascular magnetic resonance; CAD, coronary artery disease; CCS, chronic coronary syndromes; CS, circumferential strain; Fast-SENC, fast strain encoded sequence; GCS, global circumferential strain; GFR, glomerular filtration rate; GLS, global longitudinal strain; GS, global strain; LGE, late gadolinium enhancement; LS, longitudinal strain; LV, left ventricle; PCI, percutaneous coronary intervention; RV, right ventricle; SCS, segmental circumferential strain; SCS, segmental circumferential strain; SAS, segmental aggregate strain.
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Keywords: fast strain-encoded CMR (fast-SENC), average perfusion score index, adenosine, late gadolinium enhancement, cardiac outcomes
Citation: Steen H, Montenbruck M, Kelle S, Esch S, Schwarz AK, Giusca S and Korosoglou G (2021) Fast-Strain Encoded Cardiac Magnetic Resonance During Vasodilator Perfusion Stress Testing. Front. Cardiovasc. Med. 8:765961. doi: 10.3389/fcvm.2021.765961
Received: 27 August 2021; Accepted: 11 October 2021;
Published: 17 November 2021.
Fabrizio Ricci, University of Studies G. d'Annunzio Chieti and Pescara, Italy
Theo Pezel, Hôpital Lariboisière, France
Jérôme Garot, Institut Cardiovasculaire Paris Sud, France
Dominik Buckert, Ulm University Medical Center, Germany
Copyright © 2021 Steen, Montenbruck, Kelle, Esch, Schwarz, Giusca and Korosoglou. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Grigorios Korosoglou, gkorosoglou@hotmail.com
Insights in Cardiovascular Imaging: 2021


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