Persius/hicric huggingface dataset:
Dorothy Nyswander
Dorothy Bird Nyswander (1894-1988), was an American health educator. She graduated with masters and bachelors degrees from the University of Nevada and a Ph.D. in Psychology from the University of California, Berkeley. She is considered the Mother of Health education.

# Professional life and vision
Her career spanned over six decades and several continents.  During this time, Nyswander was an advocate for community health and rights. As a single mother, she taught in high school while earning her doctorate.  She worked for the Works Progress Administration during the Great Depression; advocated working mothers child care while employed with the Federal Works Agency; and promoted preventive school health as the director of Queens City Health Center.
In 1943, Nyswander became instrumental in founding the Berkeley School of Public Health.  In 1946 she became a full-time professor at UC Berkeley and remained there for nearly 12 years. Following her retirement, in 1957, and at age 62, Dorothy Nyswander then began a 16-year career with the World Health Organization travelling to Jamaica, Turkey, Brazil, the South Seas, and India developing health education programs. She is said to have regretted not getting into politics.  However, in her words "but you don't get to do everything you want in this life" Template:Harvard citation .
Dr. Nyswander was committed to an "Open Society.  In 1966 she defined an open society as "one where justice is the same for every ; where dissent is taken seriously as an index of something wrong or something needed; where diversity is expected; . . . where the best of health care is available to all; where poverty is a community disgrace not an individuals weakness;  where desires for power over  become satisfaction with the use of power for people  Template:Harvard citation.

# SOPHE
In 1996, two years prior to her death, the California Chapter of the Society for Public Health Education (NC-SOPHE) began awarding the Dorothy B. Nyswander Award for Leadership in Health Education for health educators who have demonstrated the professional standards set forth by Nsywander.  The first recipient was Helen Ross, former Chair of the San Jose State University MPH Program. Subsequent recipients include Kathleen Roe, former MPH Program Director and chair of the SJSU Health Science Department since 2002; Meredith Minkler, Professor of Health and Social Behavior at UC Berkeley, and Kate Lorig, Professor, in the Stanford University Department of Medicine
and Director of Patient Education Research Center. In 2005, the national Society for Public Health Education created the Open Society Award to honor Dorothy's legacy. The award is given each year to recognize an individual or group who embodies and promotes an Open Society, through research, practice, and/or teaching. The first recipient of this award was the San Jose University Department of Health Science Master of Public Health Program.
Ductus arteriosus

# Overview
In the developing fetus, the ductus arteriosus (DA) is a shunt connecting the pulmonary artery to the aortic arch that allows most of the blood from the right ventricle to bypass the fetus' fluid-filled lungs. During fetal development, this shunt protects the lungs from being overworked and allows the right ventricle to strengthen.  There are two other fetal shunts, the ductus venosus and the foramen ovale.

# Eponym
The ductus arteriosus is sometimes called the ductus Botalli, after Leonardo Botallo, although the discovery should have been attributed to Giulio Cesare Aranzi, to whom (less commonly) the ductus venosus is named.

# Closure at birth
When the newborn takes its very first breath, pulmonary vascular resistance falls due to physical opening of the pulmonary capillaries and attenuation of intrauterine hypoxic pulmonary vasoconstriction. Decreased pulmonary vascular resistance increases pulmonary blood flow while pulmonary vascular pressure falls below aortic pressure. At the same time, the lungs release bradykinin (vasodilator) and falling prostaglandin levels cause constriction of the smooth muscle in wall of the DA, reducing flow. Bradykinin works by acting on eNOS to increase NO produced, thus inducing vasodilatation. ACE breaks down bradykinin and therefore, ACE inhibitors aid in prolonging the action of vasodilatation by bradykinin. Additionally, because of reduced pulmonary resistance, more blood flows from the pulmonary arteries to the lungs and thus the lungs deliver more oxygenated blood to the left heart. This further increases aortic pressure so that flow in DA may transiently reverse.
Usually, the DA begins to close when breathing is established, and is completely sealed after four to ten days. A cord-like vestige of the DA, called the ligamentum arteriosum, remains to connect the exterior of the left pulmonary artery to the exterior of the aortic arch.
When the ligamentum arteriosum forms it traps the left branch of the recurrent left vagus nerve in the thorax.

# Patent ductus arteriosus
Failure of a child's DA to close after birth results in a condition called patent ductus arteriosus and the generation of a left-to-right shunt. If left uncorrected, patency leads to pulmonary hypertension and possibly congestive heart failure and cardiac arrhythmias. Closure may be induced with a drug class known as NSAIDs such as indomethacin or ibuprofen because these drugs inhibit prostaglandin synthesis. Prostaglandins are responsible for maintaining the ductus arteriosus.
Duplex ultrasound
Duplex ultrasound is a form of ultrasound that incorporates two elements:
1) B-mode, pulsed-doppler display to visualize the blood flow within a vessel;
2) Color-doppler display to visualize the structure and hemodynamics within a vessel.
Both displays are presented on the same screen ("duplex") to facilitate interpretation.
Vascular ultrasound is the main branch of radiology that uses duplex.  Vascular ultrasound, a subspeciality within ultrasound, helps determine multiple factors within the circulatory system.  It can evaluate central (abdominal) and peripheral arteries and veins, it helps determine the amount of vascular stenosis (narrowing) or occlusion (complete blockage) within an artery, it assists in ruling out aneurysmal disease as well as being the main aid to rule out thrombotic events.  Duplex is an inexpensive, non-invasive way to determine pathology.  Duplex evaluation is usually done prior to any invasive testing or surgical procedure.
Duret haemorrhage
Duret haemorrhage (also spelled, Duret hemorrhages) are small areas of bleeding in the ventral and paramedian parts of the upper brainstem, (midbrain and pons). They are secondary to raised intracranial pressure with formation of a transtentorial pressure cone in which the cerebellar tonsils are impacted in the foramen magnum by the high pressure. Kernohans notch is a groove in the cerebral peduncle caused by this displacement of the brainstem against the incisura of the tentorium in some cases. The resulting ipsilateral hemiparesis is a false localising sign (Collier 1904), known as the Kernohan-Woltman syndrome. This may succeed or accompany temporal lobe (uncal) herniation and subfalcial herniation secondary to a supratentorial mass.

# Causes
The common causes are an acute haematoma, oedema following trauma, abscess, or tumour. The Duret haemorrhage is demonstrated at CT or MRI. It usually indicates a fatal outcome. The mechanism is uncertain but is probably caused by the displacement of the brainstem stretching and lacerating pontine perforating branches of the basilar artery; venous infarction may play a role.

# Sources
- Collier, J. The false localizing signs of intracranial tumour. Brain 27:490-508, 1904.
- J. W. Kernohan JW, Woltman HW. Incisura of the crus due to contralateral brain tumor. Archives of Neurology and Psychiatry, Chicago, 1929, 21: 274287.
- Fisher, C.M. Brain herniation: a revision of classical concepts. Can J Neurol Sci. 1995, 22(2):83-91
Dyslexia overview

# Overview
Dyslexia is a  learning disability that manifests primarily as a difficulty with written language, particularly with reading and spelling. It is separate and distinct from reading difficulties resulting from other causes, such as a non-neurological deficiency with vision or hearing, or from poor or inadequate reading instruction. 
Evidence suggests that dyslexia results from differences in how the brain processes written and/or verbal language. Although dyslexia is the result of a neurological difference, it is not an intellectual disability. Dyslexia occurs at all levels of intelligence; sub-average, average, above average, and highly gifted.

# Causes
Developmental reading disorder (DRD), or dyslexia, occurs when there is a problem in areas of the brain that help interpret language. It is not caused by vision problems. The disorder is a specific information processing problem that does not interfere with one's ability to think or to understand complex ideas. Most people with DRD have normal intelligence, and many have above-average intelligence.
DRD may appear in combination with developmental writing disorder and developmental arithmetic disorder. All of these involve using symbols to convey information. These conditions may appear alone or in any combination.
DRD often runs in families.

# Diagnosis

## MRI
Functional MRI (fMRI) studies have shown changes in the brains of dyslexic children and adults with phonics tutoring, along with improved performance on tests of phonemic awareness and text decoding.
Functional MRI studies have also shown changes in the brain and spelling improvement of dyslexic children taughtspelling phonetically in an orthographic manner. 
One factor that characterises the field of dyslexia treatment is the incessant flow of alternative therapeutic approaches. These controversial treatments include sensory, dietary, and movement-based approaches as well as many others. 

# Treatment

## Primary Prevention
Learning disorders, such as DRD, tend to run in families. Affected families should make every effort to recognize existing problems early. Early intervention will provide the best possible outcome.
Ejection fraction

# Overview
In cardiovascular physiology, ejection fraction (Ef) is the fraction of blood pumped out of a ventricle with each heart beat. The term ejection fraction applies to both the right and left ventricles; one can speak equally of the left ventricular ejection fraction (LVEF) and the right ventricular ejection fraction (RVEF). Without a qualifier, the term ejection fraction refers specifically to that of the left ventricle.
By definition, the volume of blood within a ventricle immediately before a contraction is known as the end-diastolic volume. Similarly, the volume of blood left in a ventricle at the end of contraction is end-systolic volume. The difference between end-diastolic and end-systolic volumes is the stroke volume, the volume of blood ejected with each beat. Ejection fraction (Ef) is the fraction of the end-diastolic volume that is ejected with each beat; that is, it is stroke volume (SV) divided by end-diastolic volume (EDV):

# Normal values
In a healthy 70-kg (154-lb) man, the SV is approximately 70 ml and the left ventricular EDV is 120 ml, giving an ejection fraction of 70/120, or 58%. Right ventricular volumes being roughly equal to those of the left ventricle, the ejection fraction of the right ventricle is normally equal to that of the left ventricle within narrow limits.
Healthy individuals typically have ejection fractions greater than 0.55. However, normal values depend upon the modality being used to calculate the ejection fraction.  Damage to the muscle of the heart (myocardium), such as that sustained during myocardial infarction or in cardiomyopathy, impairs the heart's ability to eject blood and therefore reduces ejection fraction. This reduction in the ejection fraction can manifest itself clinically as heart failure.  The ejection fraction is one of the most important predictors of prognosis; those with significantly reduced ejection fractions typically have a poorer prognoses.

# Measurement
Ejection fraction is commonly measured by echocardiography, in which the volumes of the heart's chambers are measured during the cardiac cycle. Ejection fraction can then be obtained by dividing stroke volume by end-diastolic volume as described above.
Other methods of measuring ejection fraction include cardiac MRI, fast scan cardiac computed axial tomography (CT) imaging, ventriculography, Gated SPECT, and the MUGA scan. A MUGA scan involves the injection of a radioisotope into the blood and detecting its flow through the left ventricle. The historical gold standard for the measurement of ejection fraction is ventriculography.

# ACC/AHA/ESC 2006 Guidelines (DO NOT EDIT) 

## Left Ventricular Function and Imaging Recommendations
EMT-Critical Care
- A level of EMS certification unique to New York State.
- Very similar in education and scope of practice to the National Standard EMT-Intermediate.
- May perform Intubation, Intravenous therapy, Cardiac monitoring, Electrical Therapies, Needle thoracotomy, Cricothyrotomy, Administration of medications.
- Generally has less diagnostic capability and thus less standing orders than paramedics but is trained in all the same procedures.
ESC 2012 schedule
Here is the page we will use to coordinate the TV events at ESC 2012. Open time slots are indicated below in red.
Filming location TBD.

# Click on Date for Detailed Schedule
Saturday August 25, 2012
Sunday August 26, 2012

# Saturday August 25, 2012

## 11:00 AM
11:00 AM - 11:30 AM
- Interviewee: Dr. Matthew Roe and Dr. Magnus Ohman
- Topic: TRILOGY-ACS: Prasugrel versus clopidogrel for patients with unstable angina/NSTEMI who are medically managed without revascularization
- Embargo lift: Sunday, August 26, 2012 at 11:45 AM

## 1:00 PM
1:00 PM - 1:30 PM
- Interviewee: Dr. Holger Thiele
- Topic: IABP-SHOCK II: Randomized comparision of intra-aortic balloon counterpulsation versus optimal medical therapy in addition to early revascularization in acute myocardial infarction complicated by cardiogenic shock
- Embargo lift: Monday, August 27, 2012 at 11:00 AM

## 1:30 PM
OPEN TIME SLOT

## 2:00 PM
OPEN TIME SLOT

## 2:30 PM
OPEN TIME SLOT

## 3:00 PM
OPEN TIME SLOT

## 3:30 PM
OPEN TIME SLOT

## 4:00 PM
4:00 PM - 4:30 PM
- Interviewee: Dr. Jur ten Berg and Dr. Willem JM Dewilde
- Topic: WOEST: First randomised trial that compares two different regimens with and without aspirin in patients on oral anticoagulant therapy (OAC) undergoing coronary stent placement (PCI).
- Embargo lift: Tuesday, August 28, 2012 at 11:15 AM

# Sunday August 26, 2012

## 8:15 AM
8:15 AM - 9:15 AM
- Interviewee: Prof. Ken Okumura
- Topic: Update in ESC: Dabigatran among OAC - Efficacy and Safety and its positioning
- Embargo lift:

## 10:30 AM
OPEN TIME SLOT

## 1:00 PM
1:00 PM - 1:30 PM
- Interviewee: Dr. Bernard De Bruyne
- Topic: FAME II:Fractional Flow Reserve-Guided Percutaneous Coronary Intervention plus Optimal Medical Treatment versus Optimal Medical Treatment Alone in Patients with Stable Coronary Artery Disease
- Embargo lift: Tuesday, August 28, 2012 at 12:15 pm

## 1:30 PM
OPEN TIME SLOT

## 2:00 PM
2:00 PM - 2:30 PM
- Interviewee: Dr. Wolfgang Shillinger
- Topic: ACCESS-EUROPE: An Observational Study of the MitraClip System in Europe
- Embargo lift: Monday, August 27, 2012 at 11:45 am
Ohtahara syndrome
Synonyms and keywords: Early Infantile Epileptic Encephalopathy with Burst-Suppression (EIEE)

# Overview
Ohtahara Syndrome  (OS) is the earliest-developing age-related epileptic encephalopathy.  It is an extremely debilitating progressive neurological disorder, involving intractable seizures and severe mental retardation.  No single cause has been identified, although in many cases structural brain damage is present. The syndrome is outwardly characterized by tonic spasms and partial seizures, and receives its more elaborate name from the pattern of burst activity in an EEG.

# Pathophysiology

## Pathology
There is severe atrophy of both hemispheres of the brain.

# Causes
No single cause of OS has been identified.  Less often, the root of the disorder is an underlying metabolic syndrome. No genetic connection has been established.

# Epidemiology and Demographics

## Age
Seizure onset within the first three months (and often first 10 days) of life.

# Natural History, Complications and Prognosis

## Complications
- Mental retardation
- Infections

## Prognosis
Infants with Ohtahara syndrome make very little developmental progress. They remain totally dependent on others and often feed poorly. They often die within the first two years of life because of repeated chest infections. Those who do survive will be severely disabled.

# Diagnosis

## Symptoms
- Excessive sleepiness
- Seizures - generalised tonic clonic type
- Age-related epileptic encephalophy, with seizure onset occurring within the first three months (and often first 10 days) of life.  Many, but not all, cases of OS evolve into other seizure disorders, namely West Syndrome and Lennox-Gastaut Syndrome.

## Physical Examination

### Appearance of the Patient
Infant is very floppy and excessively sleepy.

### Neurologic
- Generalized seizures
- Tonic seizures (a generalized seizure involving a sudden stiffening of the limbs).
- Partial seizures
- Myoclonic seizures
- Profound mental and physical retardation
- Encephalopathy

## Laboratory Findings

### EEG
- OS is characterized by a burst suppression pattern
- High voltage spike wave discharge followed by little brain wave activity.

# Treatment
Treatment outlook is poor. Anti-epileptic drugs and steroids may be used to try to control the seizures, but their effectiveness is limited. Most therapies are related to symptoms and day-to-day living. Few infants with focal lesions can have surgery to correct underlying abnormality.
Reston ebolavirus

# Overview
Ebola Reston is a strain of the Ebola virus. In 1989 crab-eating macaques imported from the Philippines ended up in the Hazleton Research Products facility at 1946 Isaac Newton Sq W, Reston, Virginia where the outbreak occurred.
This specific strain of the Ebola virus caused a rather large panic, but after containment, it was discovered that although closely resembling Ebola Zaire, it proved fatal to only non-human primates. However, four of the Reston primate handlers tested positive for antibodies to the virus, suggesting that they had been infected but were asymptomatic.
The physical building in which the outbreak occurred was demolished on 5/30/1995 and a new building constructed in its place.  This facility, which is part of an office park, became a Kindercare and is a Mulberry Child Care and preschool center as of 2007.
Ebola Reston is indistinguishable under an electron microscope from other Human-type Ebola, yet deadly to the monkeys that were in the Reston research facility. It has been hypothesized that the reason that this strain of Ebola is deadly to non-human primates but harmless to humans lies in a minute genetic mutation of the virus. This strain is spread via airborne means, a supporting fact of gentic mutation as the original Ebola strain was not capable of infecting organisms through airborne contact. The surviving monkeys were euthanized as a precautionary measure.
The outbreak was the subject of Richard Preston's best selling 1994 book, The Hot Zone.

# Possible Mutation
A crossing of the Ebola Reston strain, which can infect humans but doesn't harm them and therefore is not dangerous for humans, and one of the other Ebola strains (like Ebola Zaire), for example in a subject infected with both strains, could potentially result in a new, for humans deadly, over-the-air infectious Ebola strain mutation. At first it was believed that Ebola Reston is such an Ebola strain and caused panic until it was discovered that it is only dangerous for non-human primates. A new mutation resulting in an Ebola strain which combines the deadliness of Ebola Zaire (or another Ebola strain) and the airborne infectious possibility of Ebola Reston would probably again cause such a panic. The real danger of such a mutation or new Ebola strain would rely on the effectiveness of that strain in airborne infections, the deadliness within humans and the length of incubation period (the incubation period of all curently known lethal Ebola variants being brief enough as to make outbreaks self-limiting by exhausting the availability of potential hosts before the outbreak can spread further).

# External link
- Ebola Reston Outbreaks
- Recent Outbreaks
Ectopic pacemaker
An ectopic pacemaker or ectopic focus is an excitable group of cells that causes a premature heart beat outside the normally functioning SA node of the human heart.  Acute occurrence is usually non-life threatening, but chronic occurrence can progress into ventricular fibrillation.

# Etiology
Ectopic pacemakers can occur within healthy hearts in response to various stimulating events, such as:
- Elevated sympathetic nervous system input
- Overstimulation from drugs such as caffeine.
- Cardiac Ischemia (particularly ventricular ischemia) - The membranes of apoptotic (dying) cells become "leaky" and cause surrounding tissue to become hyperkalemic or hypercalcemic (high concentration of potassium/calcium), causing random excitation.

# Physiology
An ectopic pacemaker can reside within a part of the conduction system of the heart, or within the muscle cells of the atria or ventricles.  When an ectopic pacemaker initiates a beat, premature contraction occurs.  A premature contraction will not follow the normal signal transduction pathway, and can render the heart refractory or incapable of transmitting the normal signal from the SA node.

# Diagnosis
On an ECG, the QRS complex will be abnormally shaped. It can be perceived as a skipped beat on both the ECG and through normal pulse-taking.
Edman degradation

# Overview
Edman degradation, developed by Pehr Edman, is a method of sequencing amino acids in a peptide. In this method, the amino-terminal residue is labeled and cleaved from the peptide without disrupting the peptide bonds between other amino acid residues.

## Mechanism for Edman Degradation
Phenylisothiocyanate is reacted with an uncharged terminal amino group, under mildly alkaline conditions, to form a phenylthiocarbamoyl derivative. Then, under acidic conditions, this derivative of the terminal amino acid is cleaved as a thiazolinone derivative. The thiazolinone amino acid is then selectively extracted into an organic solvent and treated with acid to form the more stable phenylthiohydantoin (PTH)- amino acid derivative that can be identified by using chromatography or electrophoresis. This procedure can then be repeated again to identify the next amino acid. A major drawback to this technique is that the peptides being sequenced in this manner cannot have more than 50 to 60 residues. This is because the Edman degradation reaction is not 100% efficient, meaning that the cleavage step does not occur every time. However, this problem can be resolved by cleaving large peptides into smaller peptides before proceeding with the reaction. It is able to accurately sequence up to 30 amino acids with 98% efficiency per amino acid. An advantage of the Edman degradation is that it only uses 10 - 100 picomoles of peptide for the sequencing process. Edman degradation reaction is automated to speed up the process. 

# Bergmann Degradation
An older related method for the stepwise degradation of polypeptides involving azides is the Bergmann Degradation  .