document_title: Neuroimaging

question_text: a technique for studying brain structure that uses high-resolution x-rays is known as

text: Neuroimaging

text: History[edit]

text: The first chapter of the history of neuroimaging traces back to the Italian neuroscientist Angelo Mosso who invented the 'human circulation balance', which could non-invasively measure the redistribution of blood during emotional and intellectual activity.[2] However, even if only briefly mentioned by William James in 1890, the details and precise workings of this balance and the experiments Mosso performed with it have remained largely unknown until the recent discovery of the original instrument as well as Mosso’s reports by Stefano Sandrone and colleagues.[3]

text: In 1918 the American neurosurgeon Walter Dandy introduced the technique of ventriculography. X-ray images of the ventricular system within the brain were obtained by injection of filtered air directly into one or both lateral ventricles of the brain. Dandy also observed that air introduced into the subarachnoid space via lumbar spinal puncture could enter the cerebral ventricles and also demonstrate the cerebrospinal fluid compartments around the base of the brain and over its surface. This technique was called pneumoencephalography.

text: In 1927 Egas Moniz introduced cerebral angiography, whereby both normal and abnormal blood vessels in and around the brain could be visualized with great precision.

text: In the early 1970s, Allan McLeod Cormack and Godfrey Newbold Hounsfield introduced computerized axial tomography (CAT or CT scanning), and ever more detailed anatomic images of the brain became available for diagnostic and research purposes. Cormack and Hounsfield won the 1979 Nobel Prize for Physiology or Medicine for their work. Soon after the introduction of CAT in the early 1980s, the development of radioligands allowed single photon emission computed tomography (SPECT) and positron emission tomography (PET) of the brain.

text: More or less concurrently, magnetic resonance imaging (MRI or MR scanning) was developed by researchers including Peter Mansfield and Paul Lauterbur, who were awarded the Nobel Prize for Physiology or Medicine in 2003. In the early 1980s MRI was introduced clinically, and during the 1980s a veritable explosion of technical refinements and diagnostic MR applications took place. Scientists soon learned that the large blood flow changes measured by PET could also be imaged by the correct type of MRI. Functional magnetic resonance imaging (fMRI) was born, and since the 1990s, fMRI has come to dominate the brain mapping field due to its low invasiveness, lack of radiation exposure, and relatively wide availability.

text: In the early 2000s the field of neuroimaging reached the stage where limited practical applications of functional brain imaging have become feasible. The main application area is crude forms of brain-computer interface.

text: Indications[edit]

text: Neuroimaging follows a neurological examination in which a physician has found cause to more deeply investigate a patient who has or may have a neurological disorder.

text: One of the more common neurological problems which a person may experience is simple syncope.[4][5] In cases of simple syncope in which the patient's history does not suggest other neurological symptoms, the diagnosis includes a neurological examination but routine neurological imaging is not indicated because the likelihood of finding a cause in the central nervous system is extremely low and the patient is unlikely to benefit from the procedure.[5]

text: Neuroimaging is not indicated for patients with stable headaches which are diagnosed as migraine.[6] Studies indicate that presence of migraine does not increase a patient's risk for intracranial disease.[6] A diagnosis of migraine which notes the absence of other problems, such as papilledema, would not indicate a need for neuroimaging.[6] In the course of conducting a careful diagnosis, the physician should consider whether the headache has a cause other than the migraine and might require neuroimaging.[6]

text: Another indication for neuroimaging is CT-, MRI- and PET-guided stereotactic surgery or radiosurgery for treatment of intracranial tumors, arteriovenous malformations and other surgically treatable conditions.[7][8][9][10]

text: Brain imaging techniques[edit]

text: Computed axial tomography[edit]

text: Computed tomography (CT) or Computed Axial Tomography (CAT) scanning uses a series of x-rays of the head taken from many different directions. Typically used for quickly viewing brain injuries, CT scanning uses a computer program that performs a numerical integral calculation (the inverse Radon transform) on the measured x-ray series to estimate how much of an x-ray beam is absorbed in a small volume of the brain. Typically the information is presented as cross sections of the brain.[11]

text: Diffuse optical imaging[edit]

text: Diffuse optical imaging (DOI) or diffuse optical tomography (DOT) is a medical imaging modality which uses near infrared light to generate images of the body. The technique measures the optical absorption of haemoglobin, and relies on the absorption spectrum of haemoglobin varying with its oxygenation status. High-density diffuse optical tomography (HD-DOT) has been compared directly to fMRI using response to visual stimulation in subjects studied with both techniques, with reassuringly similar results.[12] HD-DOT has also been compared to fMRI in terms of language tasks and resting state functional connectivity.[13]

text: Event-related optical signal[edit]

text: Event-related optical signal (EROS) is a brain-scanning technique which uses infrared light through optical fibers to measure changes in optical properties of active areas of the cerebral cortex. Whereas techniques such as diffuse optical imaging (DOT) and near infrared spectroscopy (NIRS) measure optical absorption of haemoglobin, and thus are based on blood flow, EROS takes advantage of the scattering properties of the neurons themselves, and thus provides a much more direct measure of cellular activity. EROS can pinpoint activity in the brain within millimeters (spatially) and within milliseconds (temporally). Its biggest downside is the inability to detect activity more than a few centimeters deep. EROS is a new, relatively inexpensive technique that is non-invasive to the test subject. It was developed at the University of Illinois at Urbana-Champaign where it is now used in the Cognitive Neuroimaging Laboratory of Dr. Gabriele Gratton and Dr. Monica Fabiani.

text: Magnetic resonance imaging[edit]

text: Magnetic resonance imaging (MRI) uses magnetic fields and radio waves to produce high quality two- or three-dimensional images of brain structures without use of ionizing radiation (X-rays) or radioactive tracers.

text: Functional magnetic resonance imaging[edit]

text: Functional magnetic resonance imaging (fMRI) and arterial spin labeling (ASL) relies on the paramagnetic properties of oxygenated and deoxygenated hemoglobin to see images of changing blood flow in the brain associated with neural activity. This allows images to be generated that reflect which brain structures are activated (and how) during performance of different tasks or at resting state. According to the oxygenation hypothesis, changes in oxygen usage in regional cerebral blood flow during cognitive or behavioral activity can be associated with the regional neurons as being directly related to the cognitive or behavioral tasks being attended.

text: Most fMRI scanners allow subjects to be presented with different visual images, sounds and touch stimuli, and to make different actions such as pressing a button or moving a joystick. Consequently, fMRI can be used to reveal brain structures and processes associated with perception, thought and action. The resolution of fMRI is about 2-3 millimeters at present, limited by the spatial spread of the hemodynamic response to neural activity. It has largely superseded PET for the study of brain activation patterns. PET, however, retains the significant advantage of being able to identify specific brain receptors (or transporters) associated with particular neurotransmitters through its ability to image radiolabelled receptor "ligands" (receptor ligands are any chemicals that stick to receptors).

text: As well as research on healthy subjects, fMRI is increasingly used for the medical diagnosis of disease. Because fMRI is exquisitely sensitive to oxygen usage in blood flow, it is extremely sensitive to early changes in the brain resulting from ischemia (abnormally low blood flow), such as the changes which follow stroke. Early diagnosis of certain types of stroke is increasingly important in neurology, since substances which dissolve blood clots may be used in the first few hours after certain types of stroke occur, but are dangerous to use afterwards. Brain changes seen on fMRI may help to make the decision to treat with these agents. With between 72% and 90% accuracy where chance would achieve 0.8%,[14] fMRI techniques can decide which of a set of known images the subject is viewing.[15]

text: Magnetoencephalography[edit]

text: Magnetoencephalography (MEG) is an imaging technique used to measure the magnetic fields produced by electrical activity in the brain via extremely sensitive devices such as superconducting quantum interference devices (SQUIDs) or spin exchange relaxation-free[16] (SERF) magnetometers. MEG offers a very direct measurement of neural electrical activity (compared to fMRI for example) with very high temporal resolution but relatively low spatial resolution. The advantage of measuring the magnetic fields produced by neural activity is that they are likely to be less distorted by surrounding tissue (particularly the skull and scalp) compared to the electric fields measured by electroencephalography (EEG). Specifically, it can be shown that magnetic fields produced by electrical activity are not affected by the surrounding head tissue, when the head is modeled as a set of concentric spherical shells, each being an isotropic homogeneous conductor. Real heads are non-spherical and have largely anisotropic conductivities (particularly white matter and skull). While skull anisotropy has negligible effect on MEG (unlike EEG), white matter anisotropy strongly affects MEG measurements for radial and deep sources.[17] Note, however, that the skull was assumed to be uniformly anisotropic in this study, which is not true for a real head: the absolute and relative thicknesses of diploë and tables layers vary among and within the skull bones. This makes it likely that MEG is also affected by the skull anisotropy,[18] although probably not to the same degree as EEG.

text: There are many uses for MEG, including assisting surgeons in localizing a pathology, assisting researchers in determining the function of various parts of the brain, neurofeedback, and others.

text: Positron emission tomography[edit]

text: Positron emission tomography (PET) measures emissions from radioactively labeled metabolically active chemicals that have been injected into the bloodstream. The emission data are computer-processed to produce 2- or 3-dimensional images of the distribution of the chemicals throughout the brain.[19]:57 The positron emitting radioisotopes used are produced by a cyclotron, and chemicals are labeled with these radioactive atoms. The labeled compound, called a radiotracer, is injected into the bloodstream and eventually makes its way to the brain. Sensors in the PET scanner detect the radioactivity as the compound accumulates in various regions of the brain. A computer uses the data gathered by the sensors to create multicolored 2- or 3-dimensional images that show where the compound acts in the brain. Especially useful are a wide array of ligands used to map different aspects of neurotransmitter activity, with by far the most commonly used PET tracer being a labeled form of glucose (see Fludeoxyglucose (18F) (FDG)).

text: The greatest benefit of PET scanning is that different compounds can show blood flow and oxygen and glucose metabolism in the tissues of the working brain. These measurements reflect the amount of brain activity in the various regions of the brain and allow to learn more about how the brain works. PET scans were superior to all other metabolic imaging methods in terms of resolution and speed of completion (as little as 30 seconds), when they first became available. The improved resolution permitted better study to be made as to the area of the brain activated by a particular task. The biggest drawback of PET scanning is that because the radioactivity decays rapidly, it is limited to monitoring short tasks.[19]:60 Before fMRI technology came online, PET scanning was the preferred method of functional (as opposed to structural) brain imaging, and it continues to make large contributions to neuroscience.

text: PET scanning is also used for diagnosis of brain disease, most notably because brain tumors, strokes, and neuron-damaging diseases which cause dementia (such as Alzheimer's disease) all cause great changes in brain metabolism, which in turn causes easily detectable changes in PET scans. PET is probably most useful in early cases of certain dementias (with classic examples being Alzheimer's disease and Pick's disease) where the early damage is too diffuse and makes too little difference in brain volume and gross structure to change CT and standard MRI images enough to be able to reliably differentiate it from the "normal" range of cortical atrophy which occurs with aging (in many but not all) persons, and which does not cause clinical dementia.

text: Single-photon emission computed tomography[edit]

text: Single-photon emission computed tomography (SPECT) is similar to PET and uses gamma ray-emitting radioisotopes and a gamma camera to record data that a computer uses to construct two- or three-dimensional images of active brain regions.[20] SPECT relies on an injection of radioactive tracer, or "SPECT agent," which is rapidly taken up by the brain but does not redistribute. Uptake of SPECT agent is nearly 100% complete within 30 to 60 seconds, reflecting cerebral blood flow (CBF) at the time of injection. These properties of SPECT make it particularly well-suited for epilepsy imaging, which is usually made difficult by problems with patient movement and variable seizure types. SPECT provides a "snapshot" of cerebral blood flow since scans can be acquired after seizure termination (so long as the radioactive tracer was injected at the time of the seizure). A significant limitation of SPECT is its poor resolution (about 1 cm) compared to that of MRI. Today, SPECT machines with Dual Detector Heads are commonly used, although Triple Detector Head machines are available in the marketplace. Tomographic reconstruction, (mainly used for functional "snapshots" of the brain) requires multiple projections from Detector Heads which rotate around the human skull, so some researchers have developed 6 and 11 Detector Head SPECT machines to cut imaging time and give higher resolution.[21][22]

text: Like PET, SPECT also can be used to differentiate different kinds of disease processes which produce dementia, and it is increasingly used for this purpose. Neuro-PET has a disadvantage of requiring use of tracers with half-lives of at most 110 minutes, such as FDG. These must be made in a cyclotron, and are expensive or even unavailable if necessary transport times are prolonged more than a few half-lives. SPECT, however, is able to make use of tracers with much longer half-lives, such as technetium-99m, and as a result, is far more widely available.

text: Cranial ultrasound[edit]

text: Cranial ultrasound is usually only used in babies, whose open fontanelles provide acoustic windows allowing ultrasound imaging of the brain. Advantages include absence of ionising radiation and the possibility of bedside scanning, but the lack of soft-tissue detail means MRI may be preferred for some conditions.

text: Advantages and Concerns of Neuroimaging Techniques[edit]

text: Functional Magnetic Resonance Imaging (fMRI)[edit]

text: fMRI is commonly classified as a minimally-to-moderate risk due to its non-invasiveness compared to other imaging methods. fMRI uses blood oxygenation level dependent (BOLD)-contrast in order to produce its form of imaging. BOLD-contrast is a naturally occurring process in the body so fMRI is often preferred over imaging methods that require radioactive markers to produce similar imaging.[23] A concern in the use of fMRI is its use in individuals with medical implants or devices and metallic items in the body. The magnetic resonance (MR) emitted from the equipment can cause failure of medical devices and attract metallic objects in the body if not properly screened for. Currently, the FDA classifies medical implants and devices into three categories, depending on MR-compatibility: MR-safe (safe in all MR environments), MR-unsafe (unsafe in any MR environment), and MR-conditional (MR-compatible in certain environments, requiring further information).[24]

text:
FDA MR safety labels for implants and devices

MR Safe[25]

MR Conditional

MR Unsafe

text: Computed Tomography (CT) Scan[edit]

text: The CT scan was introduced in the 1970s and quickly became one of the most widely used methods of imaging. A CT scan can be performed in under a second and produce rapid results for clinicians, with its ease of use leading to an increase in CT scans performed in the United States from 3 million in 1980 to 62 million in 2007. Clinicians oftentimes take multiple scans, with 30% of individuals undergoing at least 3 scans in one study of CT scan usage[26]. CT scans can expose patients to levels of radiation 100-500 times higher than traditional x-rays, with higher radiation doses producing better resolution imaging.[27] While easy to use, increases in CT scan use, especially in asymptomatic patients, is a topic of concern since patients are exposed to significantly high levels of radiation[26].

text: Positron Emission Tomography (PET)[edit]

text: In PET scans, imaging does not rely on intrinsic biological processes, but relies on a foreign substance injected into the blood stream traveling to the brain. Patients are injected with radioisotopes that are metabolized in the brain and emit positrons to produce a visualization of brain activity.[23] The amount of radiation a patient is exposed to in a PET scan is relatively small, comparable to the amount of environmental radiation an individual is exposed to across a year. PET radioisotopes have limited exposure time in the body as they commonly have very short half-lives (~2 hours) and decay rapidly.[28] Currently, fMRI is a preferred method of imaging brain activity compared to PET, since it does not involve radiation, has a higher temporal resolution than PET, and is more readily available in most medical settings.[23]

text: Magnetoencephalography (MEG) & Electroencephalography (EEG)[edit]

text: The high temporal resolution of MEG and EEG allow these methods to measure brain activity down to the millisecond. Both MEG and EEG do not require exposure of the patient to radiation to function. EEG electrodes detect electrical signals produced by neurons to measure brain activity and MEG uses oscillations in magnetic field produced by these electrical currents to measure activity. A barrier in widespread usage of MEG is due to pricing, as MEG systems can cost millions of dollars. EEG is a much more widely used method to achieve such temporal resolution as EEG systems cost much less than MEG systems. A disadvantage of EEG and MEG is that both methods have poor spatial resolution when compared to fMRI.[23]

text: Criticism and cautions[edit]

text: Some scientists have criticized the brain image-based claims made in scientific journals and the popular press, like the discovery of "the part of the brain responsible" for functions like talents, specific memories, or generating emotions such as love. Many mapping techniques have a relatively low resolution, including hundreds of thousands of neurons in a single voxel. Many functions also involve multiple parts of the brain, meaning that this type of claim is probably both unverifiable with the equipment used, and generally based on an incorrect assumption about how brain functions are divided. It may be that most brain functions will only be described correctly after being measured with much more fine-grained measurements that look not at large regions but instead at a very large number of tiny individual brain circuits. Many of these studies also have technical problems like small sample size or poor equipment calibration which means they cannot be reproduced - considerations which are sometimes ignored to produce a sensational journal article or news headline. In some cases the brain mapping techniques are used for commercial purposes, lie detection, or medical diagnosis in ways which have not been scientifically validated.[29]


document_title: I Was Jack (You Were Diane)

question_text: who wrote i was jack you were diane

question_tokens: who wrote i was jack you were diane

root

text: I Was Jack (You Were Diane)

text:
"I Was Jack (You Were Diane)"

Single by Jake Owen

from the EP Jake Owen

Released
March 12, 2017 (2017-03-12)

Format
Digital download

Length
3:08

Label
Big Loud

Songwriter(s)

Tommy Cecil
David Ray
Jody Stevens
Craig Wiseman
John Mellencamp

Producer(s)
Joey Moi

Jake Owen singles chronology

"Good Company"
(2017)
"I Was Jack (You Were Diane)"
(2017)

tag: table

text: "I Was Jack (You Were Diane)" is a song written by David Ray, Tommy Cecil, Jody Stevens, Craig Wiseman, and John Mellencamp and recorded by American country music singer Jake Owen. This was Owen's first single release for Big Loud Records.

tag: p

text: Content[edit]

text: The song is a tribute to John Mellencamp's 1982 single "Jack & Diane", and credits Mellencamp as a co-writer for incorporating that song's guitar riff. Rolling Stone writer Chris Parton described the song as "Owen's updated version highlights the original's impact on present-day America, while a regular Joe reminisces about falling in love to the tune years before."[1] Owen said that he asked Mellencamp personally for permission to incorporate portions of "Jack & Diane" into the song, and recorded it after receiving Mellencamp's permission. Owen said that he wanted to record it because of the feelings of nostalgia that the lyrics evoked in him.[2]

text: The song is Owen's first release on Big Loud Records, following a decade on RCA Records Nashville.[3]

text: Charts[edit]

text:
Chart (2018)
Peak
position

Canada Country (Billboard)[4]
32

US Bubbling Under Hot 100 Singles (Billboard)[5]
1

US Country Airplay (Billboard)[6]
11

US Hot Country Songs (Billboard)[7]
17


document_title: I Have a Dream (song)

question_text: who wrote the song i have a dream

question_tokens: who wrote the song i have a dream

text: I Have a Dream (song)

text: Overview[edit]

text: The song was written by Benny Andersson and Bjorn Ulvaeus and was taken from the group's 1979 album, Voulez-Vous. Anni-Frid Lyngstad sang the lead vocals. It was released as a single in December 1979 with a live version of "Take a Chance on Me" as the B-side. The recording is notable for being the only ABBA song to include vocalists other than the four band members; the final chorus features a children's choir from the International School of Stockholm. In the UK, "I Have a Dream" was held off the No. 1 spot by Pink Floyd's "Another Brick in the Wall" which also features a children's choir. "I Have a Dream" is included on the ABBA Gold: Greatest Hits album, as well as in the Mamma Mia! musical.

text: In the UK, the single was issued in a lavish gatefold sleeve, intended as a souvenir for UK fans who had attended the Wembley concerts (the live recording of "Take a Chance on Me" being from one of them). The inner gatefold made use of the pyramid/mountain/iceberg designs similar to those used in the inner sleeve of Greatest Hits Vol. 2. The inner gatefold was effectively an advert for ABBA's existing albums released in the UK, but the back cover featured a message from ABBA themselves regarding the Wembley concerts, together with their signatures. The front cover used the same live photo of ABBA as the worldwide release, but artwork and fonts were different. This was only Epic's second picture sleeve for an ABBA single.

text: The live version of "Take a Chance on Me" on the B-side was one of three mixes of the same recording to be issued. Released soon after the concerts, this version is thought to be the genuine recording. A very slightly extended version, featuring spoken introductions from the group, was used as the B-side in Australia. This extended version has been released internationally on the deluxe edition of ABBA: The Album. Finally, a third mix was included on ABBA Live issued in 1986.

text: Chart performance[edit]

text:
Chart (1979/1980)
Position

Australia (ARIA)[1]
64

Austria (Ö3 Austria Top 40)[2]
1

Belgium (Ultratop 50 Flanders)[3]
1

Canada Adult Contemporary Chart[4]
1

Netherlands (Dutch Top 40)[5]
1

Netherlands (Single Top 100)[6]
1

Ireland (IRMA)[7]
2

Switzerland (Schweizer Hitparade)[8]
1

UK Singles (Official Charts Company)[9]
2

text: Westlife version[edit]

text:
"I Have a Dream"

Single by Westlife

from the album Coast to Coast

A-side

"Seasons in the Sun"
(double A-side)

Released
6 December 1999 (1999-12-06)

Format

CD single
cassette single

Recorded
1999

Studio
PWL, London

Genre
Teen pop

Length
4:06

Label
BMG

Songwriter(s)

Benny Andersson
Björn Ulvaeus

Producer(s)

Dan Frampton
Pete Waterman

Westlife singles chronology

"Flying Without Wings"
(1999)
"I Have a Dream"
(1999)
"Fool Again"
(1999)

Music video

"I Have a Dream" on YouTube

text: Irish boy band Westlife released a cover of "I Have a Dream" in December 1999, twenty years after ABBA's original release. The song became the group's fourth UK number-one single. The release was a double A-side, also featuring "Seasons in the Sun", another cover. The release became the UK's Christmas number-one single of 1999, beating Cliff Richard's charity single "The Millennium Prayer" into the No. 2 spot. Westlife's version of "I Have a Dream" was later included on their second studio album Coast to Coast in 2000. It then extended its peak into January 2000 and spending seventeen weeks in the UK chart.[10] The song was the 26th best-selling single of 1999 in the UK and it was also the final number one single of the 1990s.

text: In 2001, as part of a UNICEF fund-raising campaign, the song was re-recorded with additional vocals by Indonesian child singer, Sinna Sherina Munaf. The song has received a Platinum sales certification in the UK for over 650,000 copies sold.[11]

text: Music video[edit]

text: The music video for the Westlife version of "I Have a Dream" features the band exiting out of a car and into a dark street where a group of children are. The children start singing with the band members and play with toys lying nearby before the band head back to the car and drive away.

text: As of 2017, the video has reached 23 million views on YouTube.[12]

text: Track listing[edit]

text:
"I Have a Dream" (Single Remix) – 4:06
"Seasons in the Sun" (Single Remix) – 4:10
"On the Wings of Love" – 3:22

tag: ol

text: Chart performance[edit]

text:
Country (1999-2000)
Peak
position

Denmark (Tracklisten)[13]
11

Europe (Eurochart Hot 100)[14]
7

Finland (Suomen virallinen lista)[15]
10

Germany (Official German Charts)[16]
24

Ireland (IRMA)[17]
1

New Zealand (Recorded Music NZ)[18]
10

Norway (VG-lista)[19]
10

Scotland (Official Charts Company)[20]
1

Sweden (Sverigetopplistan)[21]
15

Switzerland (Schweizer Hitparade)[22]
18

UK Singles (Official Charts Company)[23]
1

text: End-of-year charts[edit]

text:
End-of-year chart (1999)
Position

UK Singles Chart
26

text:
Preceded by
"Goodbye" by Spice Girls
UK Singles Chart Christmas number-one single (Westlife version)
1999
Succeeded by
"Can We Fix It?" by Bob the Builder

Preceded by
"I Try" by Macy Gray
Irish IRMA number one single
18 December 1999 (5 weeks)
Succeeded by
"Born to Make You Happy" by Britney Spears

Preceded by
"Kiss (When the Sun Don't Shine)" by Vengaboys
Scottish Singles Chart
18 December 1999 (4 weeks)
Succeeded by
"The Masses Against the Classes" by Manic Street Preachers

Preceded by
"The Millennium Prayer" by Cliff Richard
UK Singles Chart number-one single (Westlife version)
18 December 1999 – 8 January 2000 (4 weeks)
Succeeded by
"The Masses Against the Classes" by Manic Street Preachers

text: Other cover versions[edit]

text: This section needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (February 2014) (Learn how and when to remove this template message)

text:
In 1981, American country-gospel music singer, Cristy Lane recorded a cover of the song and released it as a single to the Billboard Country Chart, peaking at Number 17 that year.
In 1983, Greek singer Nana Mouskouri recorded a French cover of this song entitled "Chanter La Vie" for her album Quand on revient. She also recorded an English version, which was released as a single in 1986 and included on her 1990 album Alone,as well as a German version of the song, "Ich leb´im Traum" - "I live in a dream".
In 1985, Croatian singer Tereza Kesovija recorded a cover of the song entitled "Pronađi put" with lyrics in Croatian by Željko Sabol for her album of the same name
In 1987, a recording by the dansband Streaplers, with lyrics in Swedish by Ingela Forsman, "Jag har en dröm", was Number 1 on the Swedish Svensktoppen radio chart for 17 weeks from 31 May – 6 December of that year.[24]
In 1994, Hawaiian singers the Makaha Sons covered this song on their album Ke Alaulau
Swiss chef/singer Dan Daniell recorded a cover as a duet with original ABBA member Anni-Frid Lyngstad for his album Lieber Gott[25]
In 2004, Irish singer Daniel O'Donnell covered the song for his double album Songs of Inspiration/I Believe
In 2005, Irish folk music duo Foster & Allen have covered the song for their album Sing The Number 1's
In 2005, a duet version was recorded by German celebrity Barbara Schöneberger and American singer Sydney Youngblood for the German ABBA Mania compilation, which coincided with a TV special
In 2006, Italian-American singer Al Martino included a cover of the song for his album Come Share The Wine
In 2006, German AC/DC tribute band Riff Raff recorded a cover in AC/DC style for their album Rock 'N' Roll Mutation Vol. 1: Riff Raff Performs ABBA
In 2007, Connie Talbot covered the song on Over The Rainbow
In 2008, the song was covered in a jazz/lounge music style by American group BNB on the album Bossa Mia: Songs of ABBA[26]
The song is featured in the Mamma Mia! musical as a recurring musical theme sung by the character of Sophie. It is also featured in the trailer for the film based on the musical. At the beginning of the musical, the context of the song is interpreted that Sophie dreams about her real father coming to the wedding when she sends the invitations, to her potential fathers, away. At the end of the musical, Sophie sings this song when she and Sky set off the Island to go around the world. The context of the song is used in this case as Sophie, now knowing what she really wants, hopes to achieve her dream as she goes around the world with Sky. The song is included on the 2008 movie soundtrack and is sung by actress Amanda Seyfried.
The song features prominently in episode 2, season 1 of the British TV show "Black Mirror."

tag: ul


document_title: Heart sounds

question_text: when is the second sound of the heartbeat produced

text: Heart sounds

text: Primary heart sounds[edit]

text: Normal heart sounds are associated with heart valves closing:

text: The first heart sound, or S1, forms the "lub" of "lub-dub" and is composed of components M1 (mitral valve closure) and T1 (tricuspid valve closure). Normally M1 precedes T1 slightly. It is caused by the closure of the atrioventricular valves, i.e. tricuspid and mitral (bicuspid), at the beginning of ventricular contraction, or systole. When the ventricles begin to contract, so do the papillary muscles in each ventricle. The papillary muscles are attached to the cusps or leaflets of the tricuspid and mitral valves via chordae tendineae (heart strings). When the papillary muscles contract, the chordae tendineae become tense and thereby prevent the backflow of blood into the lower pressure environment of the atria. The chordae tendineae act a bit like the strings on a parachute, and allow the leaflets of the valve to balloon up into the atria slightly, but not so much as to evert the cusp edges and allow back flow of blood. It is the pressure created from ventricular contraction that closes the valve, not the papillary muscles themselves. The contraction of the ventricle begins just prior to AV valves closing and prior to the semilunar valves opening. The sudden tensing of the chordae tendineae and the squeezing of the ventricles against closed semilunar valves, sends blood rushing back toward the atria, and the parachute-like valves catch the rush of blood in their leaflets causing the valve to snap shut. The S1 sound results from reverberation within the blood associated with the sudden block of flow reversal by the valves. The delay of T1 even more than normally causes the split S1 which is heard in a right bundle branch blockage.

text: The second heart sound, or S2, forms the "dub" of "lub-dub" and is composed of components A2 (aortic valve closure) and P2 (pulmonary valve closure). Normally A2 precedes P2 especially during inspiration where a split of S2 can be heard. It is caused by the closure of the semilunar valves (the aortic valve and pulmonary valve) at the end of ventricular systole and the beginning of ventricular diastole. As the left ventricle empties, its pressure falls below the pressure in the aorta. Aortic blood flow quickly reverses back toward the left ventricle, catching the pocket-like cusps of the aortic valve, and is stopped by aortic valve closure. Similarly, as the pressure in the right ventricle falls below the pressure in the pulmonary artery, the pulmonary valve closes. The S2 sound results from reverberation within the blood associated with the sudden block of flow reversal.

text: Splitting of S2, also known as physiological split, normally occurs during inhalation because the decrease in intrathoracic pressure increases the time needed for pulmonary pressure to exceed that of the right ventricular pressure. A widely split S2 can be associated with several different cardiovascular conditions, including left bundle branch block, pulmonary stenosis, and atrial septal defect.

text: Extra heart sounds[edit]

text: The rarer extra heart sounds form gallop rhythms and are heard in both normal and abnormal situations.

text: Rarely, there may be a third heart sound also called a protodiastolic gallop, ventricular gallop, or informally the "Kentucky" gallop as an onomatopoeic reference to the rhythm and stress of S1 followed by S2 and S3 together (S1=Ken; S2=tuck; S3=y).[1]

text: "lub-dub-ta" or "slosh-ing-in" If new, indicates heart failure or volume overload.

text: It occurs at the beginning of diastole after S2 and is lower in pitch than S1 or S2 as it is not of valvular origin. The third heart sound is benign in youth, some trained athletes, and sometimes in pregnancy but if it re-emerges later in life it may signal cardiac problems, such as a failing left ventricle as in dilated congestive heart failure (CHF). S3 is thought to be caused by the oscillation of blood back and forth between the walls of the ventricles initiated by blood rushing in from the atria. The reason the third heart sound does not occur until the middle third of diastole is probably that during the early part of diastole, the ventricles are not filled sufficiently to create enough tension for reverberation.

text: It may also be a result of tensing of the chordae tendineae during rapid filling and expansion of the ventricle. In other words, an S3 heart sound indicates increased volume of blood within the ventricle. An S3 heart sound is best heard with the bell-side of the stethoscope (used for lower frequency sounds). A left-sided S3 is best heard in the left lateral decubitus position and at the apex of the heart, which is normally located in the 5th left intercostal space at the midclavicular line. A right-sided S3 is best heard at the lower-left sternal border. The way to distinguish between a left and right-sided S3 is to observe whether it increases in intensity with inhalation or exhalation. A right-sided S3 will increase on inhalation, while a left-sided S3 will increase on exhalation.

text: S3 can be a normal finding in young patients but is generally pathologic over the age of 40. The most common cause of pathologic S3 is congestive heart failure.

text: S4 when audible in an adult is called a presystolic gallop or atrial gallop. This gallop is produced by the sound of blood being forced into a stiff or hypertrophic ventricle.

text: "ta-lub-dub" or "a-stiff-wall"

text: It is a sign of a pathologic state, usually a failing or hypertrophic left ventricle, as in systemic hypertension, severe valvular aortic stenosis, and hypertrophic cardiomyopathy. The sound occurs just after atrial contraction at the end of diastole and immediately before S1, producing a rhythm sometimes referred to as the "Tennessee" gallop where S4 represents the "Ten-" syllable.[1] It is best heard at the cardiac apex with the patient in the left lateral decubitus position and holding his breath. The combined presence of S3 and S4 is a quadruple gallop, also known as the "Hello-Goodbye" gallop. At rapid heart rates, S3 and S4 may merge to produce a summation gallop, sometimes referred to as S7.

text: Atrial contraction must be present for production of an S4. It is absent in atrial fibrillation and in other rhythms in which atrial contraction does not precede ventricular contraction.

text: Murmurs[edit]

text: Heart murmurs are produced as a result of turbulent flow of blood strong enough to produce audible noise. They are usually heard as a whooshing sound. The term murmur only refers to a sound believed to originate within blood flow through or near the heart; rapid blood velocity is necessary to produce a murmur. Most heart problems do not produce any murmur and most valve problems also do not produce an audible murmur.

text: Murmurs can be heard in many situations in adults without major congenital heart abnormalities:

text:
Regurgitation through the mitral valve is by far the most commonly heard murmur, producing a pansystolic/holosystolic murmur which is sometimes fairly loud to a practiced ear, even though the volume of regurgitant blood flow may be quite small. Yet, though obvious using echocardiography visualization, probably about 20% of cases of mitral regurgitation do not produce an audible murmur.
Stenosis of the aortic valve is typically the next most common heart murmur, a systolic ejection murmur. This is more common in older adults or in those individuals having a two-leaflet, not a three-leaflet, aortic valve.
Regurgitation through the aortic valve, if marked, is sometimes audible to a practiced ear with a high quality, especially electronically amplified, stethoscope. Generally, this is a very rarely heard murmur, even though aortic valve regurgitation is not so rare. Aortic regurgitation, though obvious using echocardiography visualization, usually does not produce an audible murmur.
Stenosis of the mitral valve, if severe, also rarely produces an audible, low frequency soft rumbling murmur, best recognized by a practiced ear using a high quality, especially electronically amplified, stethoscope.
Other audible murmurs are associated with abnormal openings between the left ventricle and right heart or from the aortic or pulmonary arteries back into a lower pressure heart chamber.

text:
Gradations of Murmurs[1]
(Defined based on use of an acoustic, not a high-fidelity amplified electronic stethoscope)

Grade
Description

Grade 1
Very faint, heard only after listener has "tuned in"; may not be heard in all positions. Only heard if the patient "bears down" or performs the Valsalva maneuver.

Grade 2
Quiet, but heard immediately after placing the stethoscope on the chest.

Grade 3
Moderately loud.

Grade 4
Loud, with palpable thrill (a tremor or vibration felt on palpation)[2]

Grade 5
Very loud, with thrill. May be heard when stethoscope is partly off the chest.

Grade 6
Very loud, with thrill. May be heard with stethoscope entirely off the chest.

text: Though several different cardiac conditions can cause heart murmurs, the murmurs can change markedly with the severity of the cardiac disease. An astute physician can sometimes diagnose cardiac conditions with some accuracy based largely on the murmur, related physical examination, and experience with the relative frequency of different heart conditions. However, with the advent of better quality and wider availability of echocardiography and other techniques, heart status can be recognized and quantified much more accurately than formerly possible with only a stethoscope, examination, and experience. Another advantage to the use of the echocardiogram is that the devices can be hand held.[3]

text: Effects of breathing[edit]

text: Inhalation decreases intrathoracic pressure which allows more venous blood to return to the right heart (pulling blood into the right side of the heart via a vacuum-like effect). Therefore, right-sided heart murmurs generally increase in intensity with inhalation. The decreased (more negative) intrathoracic pressure has an opposite effect on the left side of the heart, making it harder for the blood to exit into circulation. Therefore, left-sided murmurs generally decrease in intensity during inhalation. Increasing venous blood return to the right side of the heart by raising a patient's legs to a 45-degree while lying supine produces similar effect which occurs during inhalation. Inhalation can also produce a non-pathological split S2 which will be heard upon auscultation.

text: With exhalation, the opposite haemodynamic changes occur: left-sided murmurs generally increase in intensity with exhalation.

text: Interventions that change murmurs[edit]

text: There are a number of interventions that can be performed that alter the intensity and characteristics of abnormal heart sounds. These interventions can differentiate the different heart sounds to more effectively obtain a diagnosis of the cardiac anomaly that causes the heart sound.

text: Other abnormal sounds[edit]

text: Clicks – Heart clicks are short, high-pitched sounds that can be appreciated with modern non-invasive imaging techniques.

text: Rubs – The pericardial friction rub can be heard in pericarditis, an inflammation of the pericardium, the sac surrounding the heart. This is a characteristic scratching, creaking, high-pitched sound emanating from the rubbing of both layers of inflamed pericardium. It is the loudest in systole, but can often be heard at the beginning and at the end of diastole. It is very dependent on body position and breathing, and changes from hour to hour.

text: Surface anatomy[edit]

text: The aortic area, pulmonic area, tricuspid area and mitral area are areas on the surface of the chest where the heart is auscultated. Heart sounds result from reverberation within the blood associated with the sudden block of flow reversal by the valves closing. Because of this, auscultation to determine function of a valve is usually not performed at the position of the valve, but at the position to where the sound waves reverberate.

text:
Aortic valve (to aorta)
right second intercostal space
upper right sternal border

Pulmonary valve (to pulmonary trunk)
left second intercostal space
upper left sternal border

Erb's point
Left third intercostal space
left sternal border

Tricuspid valve (to right ventricle)
left fourth, fifth intercostal spaces
lower left sternal border

Mitral valve (to left ventricle)
left fifth intercostal space
left midclavicular line

text: Recording heart sounds[edit]

text: Using electronic stethoscopes, it is possible to record heart sounds via direct output to an external recording device, such as a laptop or MP3 recorder. The same connection can be used to listen to the previously recorded auscultation through the stethoscope headphones, allowing for more detailed study of murmurs and other heart sounds, for general research as well as evaluation of a particular patient's condition.


document_title: Eternity ring

question_text: when do you traditionally buy an eternity ring

text: Eternity ring

text: This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (May 2018) (Learn how and when to remove this template message)

text: An eternity ring, also known as an infinity ring, is a woman's ring, worn on the hand, comprising a band of precious metal (usually gold) set with a continuous line of identically cut gemstones (usually diamonds)[1] to symbolize never-ending love, usually given by a spouse to his or her wife on the occasion of a significant anniversary, typically after 1 or more years of marriage date[citation needed] Because the presence of stones all the way round the eternity ring can make it cumbersome to wear, the alternative is to have the stones across the face of the ring only. This is sometimes referred to as a "half-eternity" ring rather than a "full" eternity ring.

text: Eternity rings featuring paste gems, white topaz or a mix of stones appeared in the 18th century.[2]

text: History[edit]

text: The concept of the diamond eternity ring was created in the 1960s by diamond merchant De Beers.[3][4] American investigative journalist Edward Jay Epstein stated that at the time the company had a secret agreement with the Soviet Union which, in return for the creation of a "single channel" controlling the world's supply of diamonds, 'required' the purchase of 90-95% of the uncut gem diamonds produced by Russia.[4] The prevailing fashion at the time, particularly for engagement rings, was for them to be set with a single, large diamond. The Soviet gems, however, were small, often less than 0.25 Carats.[3] To avoid stockpiling, De Beers embarked on a campaign of promotion of jewelry containing a number of small diamonds culminating in the eternity ring, which was aimed at older, married women.[3] One campaign slogan, aimed at husbands, was "She married you for richer or poorer. Let her know how it’s going."[5]


document_title: Architect of the Capitol

question_text: who is credited with being the principal architect of the united states capitol

text: Architect of the Capitol

text: Overview[edit]

text: The Architect of the Capitol sits on the Capitol Police Board, which has jurisdiction over the United States Capitol Police, and on the United States Capitol Guide Board, which has jurisdiction over the United States Capitol Guide Service.

text: Until 1989, the position of Architect of the Capitol was filled by appointment from the President of the United States for an indefinite term. Legislation enacted in 1989 provides that the Architect is to be appointed for a term of ten years by the President, with the advice and consent of the Senate, from a list of three candidates recommended by a congressional commission. Upon confirmation by the Senate, the Architect becomes an official of the legislative branch as an officer and agent of Congress;[citation needed] he is eligible for reappointment after completion of his term.

text: Responsibility[edit]

text: The Architect of the Capitol is responsible to the United States Congress and the Supreme Court for the maintenance, operation, development, and preservation of 17.4 million square feet of buildings and more than 553 acres (224 ha) of land throughout Capitol Hill.[2] The Architect’s Office is also responsible for the upkeep and improvement of the Capitol Grounds, and the arrangement of inaugural ceremonies and other ceremonies held in the building or on the grounds. Legislation has been enacted over the years to place additional buildings and grounds under the jurisdiction of the Architect of the Capitol.

text: The Capitol Complex includes the following facilities:[2]

text:
the Capitol
the Capitol Visitor Center
the seven congressional office buildings

Cannon
Ford
Longworth
Rayburn
Russell
Dirksen
Hart

the Library of Congress buildings
the United States Supreme Court Building
the United States Botanic Garden
the Thurgood Marshall Federal Judiciary Building
the Capitol Power Plant
the House and Senate page dormitories
the United States Capitol Police headquarters and K9 division facilities
other facilities

text: Architects of the Capitol[edit]

text:
Architect of the Capitol
Term of Office
Deputy Architect
Assistant Architect
Appointing President
Notes

William Thornton
1793-1802
9999 !
—

9999 !
—

Washington
Honored as the "first architect" for his design of the U.S. Capitol.

Benjamin Henry Latrobe
March 6, 1803 –
July 1, 1811
9999 !
—

9999 !
—

Jefferson
Latrobe was appointed twice. President Jefferson appointed him to take over work on the building in 1803 and construction was halted in 1811. During the War of 1812, the Capitol was burned by British troops, prompting President Madison to reappoint Latrobe as Architect of the Capitol and conduct repairs.

April 6, 1815 –
November 20, 1817
Madison

Charles Bulfinch
January 8, 1818 –
June 25, 1829
9999 !
—

9999 !
—

Monroe

Thomas U. Walter
(Engineer-in-charge:
Montgomery C. Meigs)
June 11, 1851 –
May 26, 1865
9999 !
—

Edward Clark
Fillmore
Walter and Meigs shared responsibility for the Capitol and the construction of its additions.

Edward Clark
August 30, 1865 –
January 6, 1902
9999 !
—

Elliott Woods
A. Johnson

Elliott Woods
February 19, 1902 –
May 22, 1923
9999 !
—

9999 !
—

T. Roosevelt

David Lynn
August 22, 1923 –
September 30, 1954
9999 !
—

Horace Rouzer (1930-1946)
Arthur Cook (1946-1959)

Coolidge

J. George Stewart
October 1, 1954 –
May 24, 1970
9999 !
—

Arthur Cook (1946-1959)
Mario Campioli, FAIA (1959-1980)

Eisenhower

George M. White, FAIA
January 27, 1971 –
November 21, 1995
9999 !
—

Mario Campioli, FAIA (1959-1980)
William L. Ensign, FAIA (1980-1997)

Nixon
Ensign acted as Architect after White's retirement until a replacement was appointed

Alan M. Hantman, FAIA
January 6, 1997 –
February 2, 2007
Stephen T. Ayers, AIA

(Deputy: October 2005-February 2007)
(Acting Architect: February 2, 2007 – May 11, 2010)

Michael G. Turnbull, FAIA
(June 1998 – present)

Clinton
Hantman was the first Architect of the Capitol appointed under the legislation passed in 1989 providing for a fixed, renewable ten-year term for the Architects of the Capitol. On August 1, 2006, Hantman announced he would not seek a second term when his term expired in 2007.

Stephen T. Ayers, AIA, LEED AP
May 12, 2010–Present
Christine A. Merdon, PE, CCM (2011–Present)
Michael G. Turnbull, FAIA (1998–Present)
Obama
Ayers is the second Architect of the Capitol appointed under the legislation passed in 1989 providing for a fixed, renewable ten-year term for the Architects of the Capitol. Ayers was appointed acting Architect of the Capitol from February 2007- May 2010, and unanimously confirmed as Architect of the Capitol May 12, 2010.


document_title: Rh blood group system

question_text: where does the rh negative factor come from

text: Rh blood group system

text: Rh factor[edit]

text: An individual either has, or does not have, the "Rh factor" on the surface of their red blood cells. This term strictly refers only to the most immunogenic D antigen of the Rh blood group system, or the Rh− blood group system. The status is usually indicated by Rh positive (Rh+ does have the D antigen) or Rh negative (Rh− does not have the D antigen) suffix to the ABO blood type. However, other antigens of this blood group system are also clinically relevant. These antigens are listed separately (see below: Rh nomenclature). In contrast to the ABO blood group, immunization against Rh can generally only occur through blood transfusion or placental exposure during pregnancy in women.

text: History of discoveries[edit]

text: The rhesus blood type named after the rhesus monkey was first discovered in 1937 by Karl Landsteiner and Alexander S. Wiener. The significance of the discovery was not immediately apparent and was only realized in 1940, after subsequent findings by Philip Levine and Rufus Stetson.[1] This serum that led to the discovery was produced by immunizing rabbits with red blood cells from a rhesus macaque. The antigen that induced this immunization was designated by them as Rh factor to indicate that rhesus blood had been used for the production of the serum.[2]

text: In 1939, Phillip Levine and Rufus Stetson published in a first case report the clinical consequences of non-recognized Rh factor, hemolytic transfusion reaction and hemolytic disease of the newborn in its most severe form.[3] It was recognized that the serum of the reported woman agglutinated with red blood cells of about 80% of the people although the then known blood groups, in particular ABO were matched. No name was given to this agglutinin when described. In 1940, Karl Landsteiner and Alexander S. Wiener made the connection to their earlier discovery, reporting a serum that also reacted with about 85% of different human red blood cells.[4]

text: Based on the serologic similarities Rh factor was later also used for antigens, and anti-Rh for antibodies, found in humans such as the previously described by Levine and Stetson. Although differences between these two sera were shown already in 1942 and clearly demonstrated in 1963, the already widely used term "Rh" was kept for the clinically described human antibodies which are different from the ones related to the rhesus monkey. This real factor found in rhesus macaque was classified in the Landsteiner-Wiener antigen system (antigen LW, antibody anti-LW) in honor of the discoverers. [5][6]

text: It was recognized that the Rh factor was just one in a system of various antigens. Based on different models of genetic inheritance, two different terminologies were developed; both of them are still in use.

text: The clinical significance of this highly immunizing D antigen (i.e. Rh factor) was soon realized. Some keystones were to recognize its importance for blood transfusion (including reliable diagnostic tests), hemolytic disease of the newborn (including exchange transfusion), and very importantly the prevention of it by screening and prophylaxis.

text: The discovery of fetal cell-free DNA in maternal circulation by Holzgrieve et al. led to the noninvasive genotyping of fetal Rh genes in many countries.

text: Rh nomenclature[edit]

text:
Rh haplotype notation

Fisher-Race
Wiener

Dce
R0

DCe
R1

DcE
R2

DCE
RZ

dce
r

dCe
r′

dcE
r″

dCE
rY

text: The Rh blood group system has two sets of nomenclatures: one developed by Ronald Fisher and R.R. Race, the other by Wiener. Both systems reflected alternative theories of inheritance. The Fisher-Race system, which is more commonly in use today, uses the CDE nomenclature. This system was based on the theory that a separate gene controls the product of each corresponding antigen (e.g., a "D gene" produces D antigen, and so on). However, the d gene was hypothetical, not actual.

text: The Wiener system used the Rh–Hr nomenclature. This system was based on the theory that there was one gene at a single locus on each chromosome, each contributing to production of multiple antigens. In this theory, a gene R1 is supposed to give rise to the “blood factors” Rh0, rh′, and rh″ (corresponding to modern nomenclature of the D, C and E antigens) and the gene r to produce hr′ and hr″ (corresponding to modern nomenclature of the c and e antigens).[7]

text: Notations of the two theories are used interchangeably in blood banking (e.g., Rho(D) meaning RhD positive). Wiener’s notation is more complex and cumbersome for routine use. Because it is simpler to explain, the Fisher-Race theory has become more widely used.

text: DNA testing has shown that both are partially correct.[citation needed] There are in fact two linked genes, the RHD gene which produces a single immune specificity (anti-D) and the RHCE gene with multiple specificities (anti-C, anti-c, anti-E, anti-e). Thus, Wiener’s postulate that a gene could have multiple specificities (something many did not give credence to originally) has been proven correct. On the other hand, Wiener’s theory that there is only one gene has proven incorrect, as has the Fischer-Race theory that there are three genes, rather than the 2. The CDE notation used in the Fisher-Race nomenclature is sometimes rearranged to DCE to more accurately represent the co-location of the C and E encoding on the RhCE gene, and to make interpretation easier.

text: Rh system antigens[edit]

text: The proteins which carry the Rh antigens are transmembrane proteins, whose structure suggest that they are ion channels.[8] The main antigens are D, C, E, c and e, which are encoded by two adjacent gene loci, the RHD gene which encodes the RhD protein with the D antigen (and variants)[9] and the RHCE gene which encodes the RhCE protein with the C, E, c and e antigens (and variants).[10] There is no d antigen. Lowercase "d" indicates the absence of the D antigen (the gene is usually deleted or otherwise nonfunctional).

text: Rh phenotypes are readily identified by identifying the presence or absence of the Rh surface antigens. As can be seen in the table below, most of the Rh phenotypes can be produced by several different Rh genotypes. The exact genotype of any individual can only be identified by DNA analysis. Regarding patient treatment, only the phenotype is usually of any clinical significance to ensure a patient is not exposed to an antigen they are likely to develop antibodies against. A probable genotype may be speculated on, based on the statistical distributions of genotypes in the patient’s place of origin.

text: R0 (cDe) is today most common in Africa. The allele was thus often assumed in early blood group analyses to have been typical of populations on the continent; particularly in areas below the Sahara. Given the presence of high R0 percentages among Sephardim and Ashkenazim Jews compared to native European populations and the relative genetic isolation of Ashkenazim, Ottensooser et al. (1963) therefore suggested that high R0 frequencies were likely characteristic of the ancient Palestine Jews, who had emigrated from Egypt prior to their dispersal throughout the Mediterranean Basin and Europe.[11] However, more recent studies have found R0 frequencies as low as 24.3% among some Afroasiatic-speaking groups in the Horn of Africa,[12] as well as higher R0 frequencies among certain other Afroasiatic speakers in North Africa (37.3%)[13] and among some Palestinians in the Levant (30.4%).[14]

text:
Rh phenotypes and genotypes

Phenotype expressed on cell
Genotype expressed in DNA
Prevalence
(%) †

Fisher-Race notation
Wiener notation

D+ C+ E+ c+ e+ (RhD+)
Dce/DCE
R0RZ
0.0125

Dce/dCE
R0rY
0.0003

DCe/DcE
R1R2
11.8648

DCe/dcE
R1r″
0.9992

DcE/dCe
R2r′
0.2775

DCE/dce
RZr
0.1893

D+ C+ E+ c+ e− (RhD+)
DcE/DCE
R2RZ
0.0687

DcE/dCE
R2rY
0.0014

DCE/dcE
RZr″
0.0058

D+ C+ E+ c− e+ (RhD+)
DCe/dCE
R1rY
0.0042

DCE/dCe
RZr′
0.0048

DCe/DCE
R1RZ
0.2048

D+ C+ E+ c− e− (RhD+)
DCE/DCE
RZRZ
0.0006

DCE/dCE
RZrY
< 0.0001

D+ C+ E− c+ e+ (RhD+)
Dce/dCe
R0r′
0.0505

DCe/dce
R1r
32.6808

DCe/Dce
R1R0
2.1586

D+ C+ E− c− e+ (RhD+)
DCe/DCe
R1R1
17.6803

DCe/dCe
R1r′
0.8270

D+ C− E+ c+ e+ (RhD+)
DcE/Dce
R2R0
0.7243

Dce/dcE
R0r″
0.0610

DcE/dce
R2r
10.9657

D+ C− E+ c+ e− (RhD+)
DcE/DcE
R2R2
1.9906

DcE/dcE
R2r″
0.3353

D+ C− E− c+ e+ (RhD+)
Dce/Dce
R0R0
0.0659

Dce/dce
R0r
1.9950

D− C+ E+ c+ e+ (RhD−)
dce/dCE
rrY
0.0039

dCe/dcE
r′r″
0.0234

D− C+ E+ c+ e− (RhD−)
dcE/dCE
r″rY
0.0001

D− C+ E+ c− e+ (RhD−)
dCe/dCE
r′rY
0.0001

D− C+ E+ c− e− (RhD−)
dCE/dCE
rYrY
< 0.0001

D− C+ E− c+ e+ (RhD−)
dce/dCe
rr′
0.7644

D− C+ E− c− e+ (RhD−)
dCe/dCe
r′r′
0.0097

D− C− E+ c+ e+ (RhD−)
dce/dcE
rr″
0.9235

D− C− E+ c+ e− (RhD−)
dcE/dcE
r″r″
0.0141

D− C− E− c+ e+ (RhD−)
dce/dce
rr
15.1020

text: † Figures taken from a study performed in 1948 on a sample of 2000 people in the United Kingdom.[15]

text:
Rh phenotypes in patients and donors in Turkey[16]

Rh Phenotype
CDE
Patients (%)
Donors (%)

R1r
CcDe
37.4
33.0

R1R2
CcDEe
35.7
30.5

R1R1
CDe
5.7
21.8

rr
ce
10.3
11.6

R2r
cDEe
6.6
10.4

R0R0
cDe
2.8
2.7

R2R2
cDE
2.8
2.4

rr″
cEe
–
0.98

RZRZ
CDE
–
0.03

rr′
Cce
0.8
–

text: Hemolytic disease of the newborn[edit]

text: The hemolytic condition occurs when there is an incompatibility between the blood types of the mother and the fetus. There is also potential incompatibility if the mother is Rh negative and the father is positive. When any incompatibility is detected, the mother often receives an injection at 28 weeks gestation and at birth to avoid the development of antibodies toward the fetus. These terms do not indicate which specific antigen-antibody incompatibility is implicated. The disorder in the fetus due to Rh D incompatibility is known as erythroblastosis fetalis.

text:
Hemolytic comes from two words: "hemo" (blood) and "lysis" (destruction) or breaking down of red blood cells
Erythroblastosis refers to the making of immature red blood cells
Fetalis refers to the fetus.

text: When the condition is caused by the Rh D antigen-antibody incompatibility, it is called Rh D Hemolytic disease of the newborn or Rh disease. Here, sensitization to Rh D antigens (usually by feto-maternal transfusion during pregnancy) may lead to the production of maternal IgG anti-D antibodies which can pass through the placenta. This is of particular importance to D negative females at or below childbearing age, because any subsequent pregnancy may be affected by the Rh D hemolytic disease of the newborn if the baby is D positive. The vast majority of Rh disease is preventable in modern antenatal care by injections of IgG anti-D antibodies (Rho(D) Immune Globulin). The incidence of Rh disease is mathematically related to the frequency of D negative individuals in a population, so Rh disease is rare in old-stock populations of Africa and the eastern half of Asia, and the Indigenous peoples of Oceania and the Americas, but more common in other genetic groups, most especially Western Europeans, but also other West Eurasians, and to a lesser degree, native Siberians, as well as those of mixed-race with a significant or dominant descent from those (e.g. the vast majority of Latin Americans and Central Asians).

text:
Symptoms and signs in the fetus:

Enlarged liver, spleen, or heart and fluid buildup in the fetus' abdomen seen via ultrasound.

Symptoms and signs in the newborn:

Anemia that creates the newborn’s pallor (pale appearance).
Jaundice or yellow discoloration of the newborn’s skin, sclera or mucous membrane. This may be evident right after birth or after 24–48 hours after birth. This is caused by bilirubin (one of the end products of red blood cell destruction).
Enlargement of the newborn’s liver and spleen.
The newborn may have severe edema of the entire body.
Dyspnea or difficulty breathing.

text: Population data[edit]

text: The frequency of Rh factor blood types and the RhD neg allele gene differs in various populations.

text:
Population data for the Rh D factor and RhD neg allele[17]

Population
Rh(D) Neg
Rh(D) Pos
Rh(D) Neg alleles

African Americans
∼ 7%
93%
∼ 26%

Asian (Republic of Korea)
∼ 10%
> 90%
1%

Basques[18]
21%-36%
65%
∼ 60%

Britain[19]
17%
83%

China[19]
<1%
<99%

Ethiopians[19]
1%-21%
99%-79%

Europeans (others)
16%
84%
40%

India[19]
0.6%-8.4%
99.4%-91.6%

Indonesia[19]
<1%
<99%

Japan[19]
<1%
<99%

Madagascar[19]
1%
99%

Moroccans[19]
29%
71%

Native Americans
∼ 1%
99%
∼ 10%

Saudi Arabia[19]
29%
71%

Subequatorial Africa[19]
1%-3%
99%-97%

United States[19]
15%
85%

text: Inheritance[edit]

text: If both of a child’s parents are Rh negative, the child will definitely be Rh negative. Otherwise the child may be Rh positive or Rh negative, depending on the parents' specific genotypes.[20]

text: The D antigen is inherited as one gene (RHD) (on the short arm of the first chromosome, p36.13–p34.3) with various alleles. Though very much simplified, one can think of alleles that are positive or negative for the D antigen. The gene codes for the RhD protein on the red cell membrane. D− individuals who lack a functional RHD gene do not produce the D antigen, and may be immunized by D+ blood.

text: The epitopes for the next 4 most common Rh antigens, C, c, E and e are expressed on the highly similar RhCE protein that is genetically encoded in the RHCE gene, also found on chromosome 1. It has been shown that the RHD gene arose by duplication of the RHCE gene during primate evolution.[citation needed] Mice have just one RH gene.[21]

text: The RHAG gene, responsible for encoding Rh-associated glycoprotein (RhAG) is found on chromosome 6a.

text: The polypeptides produced from the RHD and RHCE genes form a complex on the red blood cell membrane with the Rh-associated glycoprotein.[22]

text: Function[edit]

text: On the basis of structural homology it has been proposed that the product of RHD gene, the RhD protein, is a membrane transport protein of uncertain specificity (CO2 or NH3) and unknown physiological role.[23][24] The three-dimensional structure of the related RHCG protein and biochemical analysis of the RhD protein complex indicates that the RhD protein is one of three subunits of an ammonia transporter.[25][26] Three recent studies[27][28][29] have reported a protective effect of the RhD-positive phenotype, especially RhD heterozygosity, against the negative effect of latent toxoplasmosis on psychomotor performance in infected subjects. RhD-negative compared to RhD-positive subjects without anamnestic titres of anti-Toxoplasma antibodies have shorter reaction times in tests of simple reaction times. And conversely, RhD-negative subjects with anamnestic titres (i.e. with latent toxoplasmosis) exhibited much longer reaction times than their RhD-positive counterparts. The published data suggested that only the protection of RhD-positive heterozygotes was long term in nature; the protection of RhD-positive homozygotes decreased with duration of the infection while the performance of RhD-negative homozygotes decreased immediately after the infection. The overall change in reaction times was always larger in the RhD-negative group than in the RhD-positive.

text: Origin of RHD polymorphism[edit]

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text: For a long time, the origin of RHD polymorphism was an evolutionary enigma.[30][31][32] Before the advent of modern medicine, the carriers of the rarer allele (e.g. RhD-negative women in a population of RhD positives or RhD-positive men in a population of RhD negatives) were at a disadvantage as some of their children (RhD-positive children born to preimmunised RhD-negative mothers) were at a higher risk of fetal or newborn death or health impairment from hemolytic disease. It was suggested that higher tolerance of RhD-positive heterozygotes against Toxoplasma-induced impairment of reaction time [27][28] and Toxoplasma-induced increase of risk of traffic accident[29] could counterbalance the disadvantage of the rarer allele and could be responsible both for the initial spread of the RhD allele among the RhD-negative population and for a stable RhD polymorphism in most human populations. It was also suggested that differences in the prevalence of Toxoplasma infection between geographical regions (0–95%) could also explain the striking variation in the frequency of RhD-negative alleles between populations. According to some parasitologists [27] it is possible that the better psychomotor performance of RhD-negative subjects in the Toxoplasma-free population could be the reason for spreading of the “d allele” (deletion) in the European population. In contrast to the situation in Africa and certain (but not all) regions of Asia, the abundance of wild cats (definitive hosts of Toxoplasma gondii) in Europe was very low before the advent of the domestic cat.

text: Weak D[edit]

text: In serologic testing, D positive blood is easily identified. Units which are D negative are often retested to rule out a weaker reaction. This was previously referred to as Du, which has been replaced.[33]:322 By definition, weak D phenotype is characterized by negative reaction with anti-D reagent at immediate spin (IS), negative reaction after 37 °C incubation, and positive reaction at anti-human globulin (AHG) phase. Weak D phenotype can occur in several ways. In some cases, this phenotype occurs because of an altered surface protein that is more common in people of European descent. An inheritable form also occurs, as a result of a weakened form of the R0 gene. Weak D may also occur as "C in trans", whereby a C gene is present on the opposite chromosome to a D gene (as in the combination R0r', or "Dce/dCe"). The testing is difficult, since using different anti-D reagents, especially the older polyclonal reagents, may give different results.

text: The practical implication of this is that people with this sub-phenotype will have a product labeled as "D positive" when donating blood. When receiving blood, they are sometimes typed as a "D negative", though this is the subject of some debate. Most "Weak D" patients can receive "D positive" blood without complications.[33]:323 However, it is important to correctly identify the ones that have to be considered D+ or D−. This is important, since most blood banks have a limited supply of "D negative" blood and the correct transfusion is clinically relevant. In this respect, genotyping of blood groups has much simplified this detection of the various variants in the Rh blood group system.

text: Partial D[edit]

text: It is important to differentiate weak D (due to a quantitative difference in the D antigen) from partial D (due to a qualitative difference in the D antigen). Simply put, the weak D phenotype is due to a reduced number of D antigens on a red blood cell. In contrast, the partial D phenotype is due to an alteration in D-epitopes. Thus, in partial D, the number of D antigens is not reduced but the protein structure is altered. These individuals, if alloimmunized to D, can produce an anti-D antibody. Therefore, partial D patients who are donating blood should be labeled as D-positive but, if receiving blood, they should be labeled as D-negative and receive D-negative units.[22]

text: In the past, partial D was called 'D mosaic' or 'D variant.' Different partial D phenotypes are defined by different D epitopes on the outer surface of the red blood cell membrane. More than 30 different partial D phenotypes have been described.[22]

text: Rhnull phenotype[edit]

text: Rhnull individuals have no Rh antigens (no Rh or RhAG) on their red blood cells.[34] This condition is rare.[34] As a consequence of Rh antigen absence, Rhnull red blood cells also lack LW and Fy5 and show weak expression of S, s, and U antigens. Red blood cells lacking Rh/RhAG proteins have structural abnormalities (such as stomatocytosis) and cell membrane defects that can result in hemolytic anemia.[22][34]

text: Other Rh group antigens[edit]

text: Currently, 50 antigens have been described in the Rh group system; among those described here, the D, C, c, E and e antigens are the most important. The others are much less frequently encountered or are rarely clinically significant. Each is given a number, though the highest assigned number (CEST or RH57 according to the ISBT terminology) is not an accurate reflection of the antigens encountered since many (e.g. Rh38) have been combined, reassigned to other groups, or otherwise removed.[33]:324

text: Rh antibodies[edit]

text: Rh antibodies are IgG antibodies which are acquired through exposure to Rh-positive blood (generally either through pregnancy or transfusion of blood products). The D antigen is the most immunogenic of all the non-ABO antigens. Approximately 80% of individuals who are D-negative and exposed to a single D-positive unit will produce an anti-D antibody. The percentage of alloimmunization is significantly reduced in patients who are actively exsanguinating.[35]

text: All Rh antibodies except D display dosage (antibody reacts more strongly with red cells homozygous for an antigen than cells heterozygous for the antigen (EE stronger reaction vs Ee).

text: If anti-E is detected, the presence of anti-c should be strongly suspected (due to combined genetic inheritance). It is therefore common to select c-negative and E-negative blood for transfusion patients who have an anti-E. Anti-c is a common cause of delayed hemolytic transfusion reactions.[22]

text: Erythroblastosis Fetalis[edit]

text: Rh agglutinins (antibodies) are capable of causing hemolytic transfusion reactions with extravascular hemolysis. They may also result in severe hemolytic disease of the fetus and newborn (HDFN or HDN) when a Rh negative mother who has had an Rh positive baby before carries an Rh positive fetus, as the Rh agglutinogens from the fetus trigger an immune response from the mother, producing Rh agglutinins and causing the blood of the fetus to agglutinate. Symptoms in the newborn usually include an abnormally large liver or spleen, anemia or low red blood cell count, and in serious cases, swelling of the skin or internal organs.[36] Treatment of the mother with Rh-immunoglobulin (RhIg) during term may help prevent the formation of antibody directed against the D antigen, preventing HDFN in future pregnancies..