Persius/hicric huggingface dataset:
Pandemic Preparedness and Response Act
The Pandemic Preparedness and Response Act is a bill introduced on October 5, 2005 by U.S. Senators Harry Reid, Evan Bayh, Dick Durbin, Ted Kennedy, Barack Obama, and Tom Harkin in response to the growing threat of an outbreak of avian influenza. The bill calls for:
- Preparing for a pandemic by finalizing, implementing and funding pandemic preparedness and response plans.
- Improving surveillance and international partnerships to monitor the spread of avian flu and detect the emergence of a flu strain with pandemic potential immediately.
- Protecting Americans through the development, production and distribution of an effective vaccine.
- Planning ahead for a pandemic by stockpiling antivirals, vaccines and other essential medications and supplies.
- Strengthening the public health infrastructure.
- Increasing awareness and education about pandemic flu.
- Devoting adequate resources to pandemic preparedness. ()
Paroxysmal AV Block Intrinsic AV Block

# Overview
- Intrinsic paroxysmal AV block (I-AVB) is an AV block secondary to an innate anatomical defect. Given the presence of such a defect it's prognosis, compared to extrinsic paroxysmal vagal AV block and extrinsic paroxysmal idiopathic  AV block is poor. It may have a bradycardia or tachycardia component associated with it and is characterized by atrial/ventricular premature beats prior to the period of asystole.

# Pathophysiology
- Intrinsic AV block (I-AVB) is an AV block secondary to an innate anatomical defect.
- It is hugely recognized on an ECG as an atrial premature beat (APB) or ventricular premature beat (VPB) before and after a variable period of complete AV block/asystole.
Sinus rate increase/ decrease prior to the VPB/APB or during the period of asystole further divides it into Tachycardia Dependent AV block (TD-AVB) and Pause/Bradycardia dependent AV block (PD- AVB).
- Sinus rate increase/ decrease prior to the VPB/APB or during the period of asystole further divides it into Tachycardia Dependent AV block (TD-AVB) and Pause/Bradycardia dependent AV block (PD- AVB).
- Normal cardiac myocytes are associated with a more negative resting membrane potential, an increased amplitude of action potential and a fast depolarizing sodium current.
- An exact opposite is seen in diseased myocytes responsible for TD- PAVB. An imbalance between inward depolarizing sodium and calcium currents and outward repolarizing potassium currents causes an increase in recovery time and leads to a phenomenon called post-repolarization refractoriness.
- Despite repolarization being complete, a stimulus would not be able to induce an action potential. 
- A hypothetical line of thinking that could be attributed to both PD-AVB and TD-AVB is a concealed conduction in the intra His Bundle which serves as a source of a delayed escape rhythm, thereby disrupting  the refractoriness and recovery time of the surrounding myocytes. This predisposes the patient to fatal complications such as syncope, presyncope, sudden cardiac death and atrial fibrillation with a rapid ventricular response rate.
- Certain studies hypothesize that ventricular or supraventricular impulses reach this concealed conduction at a time when there is a local phase 4 block (when sodium channels are inactive.) This subsequent long pause is reflected by the increased H-H interval in EPS studies and confirms an intra His Bundle block (an entity commonly missed and mislabeled as an infra-His Bundle block or AV block on electrophysiological studies) 
- Much debate surrounds this as it has also been documented that TD- AV/ PD-AV blocks are not related to phase 3 or phase 4 conduction defects, as previously hypothesized. It is related to myocardial ischemia, Mobitz type II block, RBBB and Intra His bundle conduction defects, retrograde ventricular premature beats and anterograde atrial premature beats; all factors that are independent of local phase 4 blocks.
Perelman's Pocket Cyclopedia of Cigars
The Perelman's Pocket Cyclopedia of Cigars is an annually published and updated reference of cigar brands available in the U.S., (And as such, currently does not include information on Cuban Cigars (see: Cuban Embargo)), including specifications and information regarding each cigar, as well as basic cigar knowledge in general, such as wrapper colours and shapes and sizes. There is also an 'Almanac' section which includes a list of new brands and those that have been discontinued since the last edition, details about 'ancient' brands that are still in production, a list unusual cigars(with multicoloured wrappers, for example), a list of the smallest and largest cigars available (by length and ring gauge), and more.
It was first published in 1995, and contained 370 brands, but the latest edition(2007) includes information on 1,233 brands (1,074 Handmade, 94 Machine made and 65 Small cigars/cigarillos).

### Cyclopedia of Havana Cigars
There is a companion edition, the Perelman's Pocket Cyclopedia of Havana Cigars which is similar, but includes information solely on the Cuban cigar brands. It is currently in its third edition (published 2005), but is not published every year(the 2nd edition was in 1998), and also includes information about how cigars are made in Cuba, a history of tobacco and Cuban brands, and details on vitolas.
Both editions are written by Richard B. Perelman.

# References/External Links
- Richard B. Perelman, Perelman's Pocket Cyclopedia of Cigars(2007), ISBN 1-893273-08-3
- Richard B. Perelman, Perelman's Pocket Cyclopedia of Havana Cigars, Third edition (2005), ISBN 1-893273-06-7
- Official Site
Pineocytoma diagnostic study of choice

# Overview

# Diagnostic Study of Choice

## Study of choice
 is the gold standard test for the diagnosis of .
OR
The following result of  is confirmatory of :
OR
 must be performed when:
- The patient presents with , , and .
- A  is positive for , , and  in the patient.
OR
 is the gold standard test for the diagnosis of .
OR
The diagnostic study of choice for  is .
OR
There is no single diagnostic study of choice for the diagnosis of .
OR
There is no single diagnostic study of choice for the diagnosis of , but  can be diagnosed based on  and .
OR
 is primarily diagnosed based on the clinical presentation.
OR
Investigations:
- Among the patients who present with clinical signs of , the  is the most specific test for the diagnosis.
- Among the patients who present with clinical signs of , the  is the most sensitive test for diagnosis.
- Among the patients who present with clinical signs of , the  is the most efficient test for diagnosis.

### The comparison of various diagnostic studies for 
 is the preferred investigation based on the sensitivity and specificity
The following finding(s) on performing  is(are) confirmatory for :
The  must be performed when:
- The patient presented with symptoms/signs 1, 2, and 3 as the first step of diagnosis.
- A positive  is detected in the patient, to confirm the diagnosis.
OR
The various investigations must be performed in the following order:

## Name of Diagnostic Criteria
It is recommended that you include the criteria in a table. Make sure you always cite the source of the content and whether the table has been adapted from another source.
 is primarily diagnosed based on clinical presentation. There are no established criteria for the diagnosis of .
OR
There is no single diagnostic study of choice for , though  may be diagnosed based on  established by .
OR
The diagnosis of  is made when at least  of the following  diagnostic criteria are met: , , , and .
OR
The diagnosis of  is based on the  criteria, which includes , , and .
OR
 may be diagnosed at any time if one or more of the following criteria are met:
- Criteria 1
- Criteria 2
- Criteria 3
OR
IF there are clear, established diagnostic criteria
The diagnosis of  is made when at least  of the following  diagnostic criteria are met: , , , and .
OR
The diagnosis of  is based on the  criteria, which include , , and .
OR
The diagnosis of  is based on the  definition, which includes , , and .
OR
IF there are no established diagnostic criteria
There are no established criteria for the diagnosis of .
Posaconazole dosage and administration

# Dosage and Administration

## General
The prescriber should follow the specific dosing instructions for each formulation. The delayed-release tablet and oral suspension are not to be used interchangeably due to the differences in the dosing of each formulation.
Noxafil delayed-release tablets should be swallowed whole, and not be divided, crushed, or chewed. Noxafil delayed-release tablets should be taken with food
Noxafil oral suspension should be administered with a full meal or with a liquid nutritional supplement or an acidic carbonated beverage (e.g., ginger ale) in patients who cannot eat a full meal.
Coadministration of drugs that can decrease the plasma concentrations of posaconazole should generally be avoided unless the benefit outweighs the risk. If such drugs are necessary, patients should be monitored closely for breakthrough fungal infections
Patients who have severe diarrhea or vomiting should be monitored closely for breakthrough fungal infections.

## Instructions for use with Noxafil Delayed-Release Tablets
Noxafil is recommended that the spoon is rinsed with water after each administration and before storage.

## Administration Information
To enhance the oral absorption of Noxafil and optimize plasma concentrations:
Noxafil delayed-release tablets should be administered with food.
Each dose of Noxafil oral suspension should be administered during or immediately (i.e., within 20 minutes) following a full meal.
For patients who cannot eat a full meal, Noxafil delayed-release tablets should be used instead of Noxafil oral suspension. Noxafil delayed-release tablets should be used only for the prophylaxis indication. Noxafil delayed-release tablets provide higher plasma drug exposures than Noxafil oral suspension under fasted conditions.
In patients who cannot eat a full meal and for whom Noxafil delayed-release tablets are not an option, each dose of Noxafil oral suspension should be administered with a liquid nutritional supplement or an acidic carbonated beverage.
For patients who cannot eat a full meal or tolerate an oral nutritional supplement or an acidic carbonated beverage and who do not have the option of taking Noxafil delayed-release tablets, an alternative antifungal therapy should be considered or patients should be monitored closely for breakthrough fungal infections.
Posterior fascial compartment of thigh
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The posterior fascial compartment of the thigh contains the knee flexors and hip extensors.
It consists of the following muscles:
- biceps femoris
- semitendinosus
- semimembranosus
The muscles here (except for the short head of the biceps femoris) are the hamstrings.
Protein kinase, AMP-activated, alpha 1
5'-AMP-activated protein kinase catalytic subunit alpha-1 is an enzyme that in humans is encoded by the PRKAA1 gene.
The protein encoded by this gene belongs to the serine/threonine protein kinase family. It is the catalytic subunit of the 5'-prime-AMP-activated protein kinase (AMPK). AMPK is a cellular energy sensor conserved in all eukaryotic cells. The kinase activity of AMPK is activated by the stimuli that increase the cellular AMP/ATP ratio. AMPK regulates the activities of a number of key metabolic enzymes through phosphorylation. It protects cells from stresses that cause ATP depletion by switching off ATP-consuming biosynthetic pathways. Alternatively spliced transcript variants encoding distinct isoforms have been observed.

# Interactions
Protein kinase, AMP-activated, alpha 1 has been shown to interact with TSC2.
Pterygoid branches of maxillary artery
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The pterygoid branches of the maxillary artery, irregular in their number and origin, supply the lateral pterygoid muscle and  medial pterygoid muscle.
Pyrazinamide dosage and administration

# Dosage and Administration
Pyrazinamide should always be administered with other effective antituberculous drugs. It is administered for the initial 2 months of a 6-month or longer treatment regimen for drug-susceptible patients. Patients who are known or suspected to have drug-resistant disease should be treated with regimens individualized to their situation.
Pyrazinamide frequently will be an important component of such therapy.
Patients with concomitant HIV infection may require longer courses of therapy. Physicians treating such patients should be alert to any revised recommendations from CDC for this group of patients.
Usual dose: Pyrazinamide is administered orally, 15 to 30 mg/kg once daily. Older regimens employed 3 or 4 divided doses daily, but most current recommendations are for once a day. Three grams per day should not be exceeded. The CDC recommendations do not exceed 2 g per day when given as a daily regimen (see table).
Alternatively, a twice weekly dosing regimen (50 to 75 mg/kg twice weekly based on lean body weight) has been developed to promote patient compliance with a regimen on an outpatient basis. In studies evaluation the twice weekly regimen, doses of pyrazinamide in excess of 3 g twice weekly have been administered. This exceeds the recommended maximum 3 g/daily dose. However, an increased incidence of adverse reactions has not been reported.
This table is taken from the CDC-American Thoracic Society joint recommendations.
Quick Start Guide - Introduce yourself

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Radial artery cathetarization overview

# Overview
The first introduction to the use of radial artery for cardiac catheterization was made by Radner in 1948.
Subsequently, a Canadian Cardiologist, Lucian Campeau, in 1989 re-introduced the practice. There have been a gradual increase in its preference over the femoral approach internationally; with United States experiencing a 10-fold increase (1 in every 6 PCIs performed) in the adoption of transradial procedures between 2007 and 2012, largely as a result of reduced major bleeding, vascular complications, length of hospital stay and cost, and increased patient satisfaction and quality of care.
The rationale for the choice of radial access include:
- Decreased risk of limb ischemia - The hand has a dual arterial supply i.e., radial and ulnar arteries, which unites to form the superficial and deep palmer arches.  Therefore, the radial artery is not an end artery like the femoral artery, thus decreasing the risk of arterial occlusion post PCI.
- Decreased risk of bleeding - The superficial course of the distal radial artery allows for easy compressibility in order to minimize hemorrhage post PCI.
Rapidly progressing glomerulonephritis
Rapidly Progressing Glomerulonephritis (RPGN, also known as Crescentic Glomerulonephritis) is a form of acute Glomerulonephritis that results in severe injury to kidney glomerulus.  The damage inflicted causes leakage of plasma proteins into the glomerulus which stimulate parietal epithelial cells lining Bowman's space along with infiltrating monocytes to form a crescent-shaped scar.  As more and more glomeruli become disfunctional due to scarring, other glomeruli become larger (hypertrophy) to pick up the slack and maintain the glomerular filtration rate.  This stresses the remaining glomeruli, causing them to become damaged, leading to a downwards spiral into acute renal failure.

# Types of RPGN

## Type I RPGN - Anti-GBM Disease
RPGN caused by auto-antibodies to glomerular basement membrane (GBM), possible the noncollagenous domain of Type IV collagen.  If there is concurrent pulmonary alveolar disease, the disease is known as Goodpasture's syndrome.

## Type II RPGN - Immune Complex Mediated Disease
RPGN caused by the glomerular deposition of massive amounts of immune complexes, usually generated by sever bouts of other diseases such as SLE, post-strep glomerulonephritis, MPGN, or IgA nephropathy.

## Type III RPGN - Pauci-Immune Disease
Also known as non-immune deposit (NID) RPGN, is a type of RPGN that does not show glomerular deposition of antibodies or immune complexes.  Instead, the glomeruli are damaged in an undefined manner, perhaps through the activation of PMNs in response to Anti-Neutrophil Cytoplasmic Antibodies (ANCA), releasing free radicals.  This type of RPGN can be isolated, or associated with vascular diseases such as Microscopic polyangiitis, Wegener's granulomatosis, or Churg-Strauss syndrome.

# Aetiology and Pathogenesis
- 1. may follow acute diffuse proliferative GN. This is more common in adults
- 2. Idiopathic (unknown cause)
- 3. RPGN may occur in association with systemic diseases e.g. SLE, PAN, Scleroadenoma Honoch Sholein purpura and Goodpasture's syndrome.

# Clinical Picture
- 1. Severe Oliguria or Anuria
- 2. Proteinuria is mild or moderate
- 3. Haematuria
- 4. Hypertention and oedema
When the cause is Goodpasture's syndrome or vasculitic disease (such as Wegener's granulomatosis), the patient may also get lung and even upper airway involvement, with: cough, haemoptysis, dyspnoea, nasal bleeding/obstruction/sinusitis.

# Fate
- 1. It is rapidly progressive and fatal due to acute renal failure or hypertension
- 2. Chronic glomerulonephritis
de:Rasch progressive Glomerulonephritis
Rizatriptan dosage forms and strengths

# Dosage Forms and Strengths

### MAXALT Tablets
5 mg tablets are pale pink, capsule-shaped, compressed tablets coded MRK on one side and 266 on the other.
10 mg tablets are pale pink, capsule-shaped, compressed tablets coded MAXALT on one side and MRK 267 on the other.

### MAXALT-MLT Orally Disintegrating Tablets
5 mg orally disintegrating tablets are white to off-white, round lyophilized tablets debossed with a modified triangle on one side.
10 mg orally disintegrating tablets are white to off-white, round lyophilized tablets debossed with a modified square on one side.
Spondyloepiphyseal dysplasia congenita

# Overview
Spondyloepiphyseal dysplasia congenita (abbreviated to SED more often than SDC) is a rare disorder of bone growth that results in dwarfism, characteristic skeletal abnormalities, and occasionally problems with vision and hearing. The name of the condition indicates that it affects the bones of the spine (spondylo-) and the ends of bones (epiphyses), and that it is present from birth (congenital). The signs and symptoms of spondyloepiphyseal dysplasia congenita are similar to, but milder than, the related skeletal disorders achondrogenesis type 2 and hypochondrogenesis. Spondyloepiphyseal dysplasia congenita is a subtype of collagenopathy, types II and XI.

# Presentation
People with spondyloepiphyseal dysplasia are short-statured from birth, with a very short trunk and neck and shortened limbs. Their hands and feet, however, are usually average-sized. Adult height ranges from 0.9 metres to just over 1.4 metres. Curvature of the spine (kyphoscoliosis and lordosis) progresses during childhood and can cause problems with breathing. Changes in the spinal bones (vertebrae) in the neck may also increase the risk of spinal cord damage. Other skeletal signs include flattened vertebrae (platyspondyly), a hip joint deformity in which the upper leg bones turn inward (coxa vara), and an inward- and downward-turning foot (called clubfoot). Decreased joint mobility and arthritis often develop early in life.
Medical texts often state a mild and variable change to facial features, although this appears to be unfounded. The cheekbones close to the nose may appear flattened. Some infants are born with an opening in the roof of the mouth, which is called a cleft palate. Severe nearsightedness (high myopia) is sometimes present, as are other eye problems that can affect vision such as detached retinas. About one-quarter of people with this condition have hearing loss.

# Causes
Spondyloepiphyseal dysplasia congenita is one of a spectrum of skeletal disorders caused by mutations in the COL2A1 gene. The protein made by this gene forms type II collagen, a molecule found mostly in cartilage and in the clear gel that fills the eyeball (the vitreous). Type II collagen is essential for the normal development of bones and other connective tissues. Mutations in the COL2A1 gene interfere with the assembly of type II collagen molecules, which prevents bones from developing properly and causes the signs and symptoms of this condition.
Spondyloepiphyseal dysplasia congenita is inherited in an autosomal dominant pattern, which means one copy of the altered gene is sufficient to cause the disorder.

# Diagnosis

# Notable cases
Actor Warwick Davis's dwarfism has been attributed to spondyloepiphyseal dysplasia congenita. The condition of late actor Michael Dunn has been attributed to spondyloepiphyseal dysplasia, type unspecified.
Seattle Institute of Oriental Medicine
The Seattle Institute of Oriental Medicine (SIOM) is a post-graduate college located in Seattle, Washington's Roosevelt neigborhood.  It is accredited by the Accreditation Commission for Acupuncture and Oriental Medicine and authorized by the Washington Higher Education Coordinating Board to award the degree of Master of Acupuncture and Oriental Medicine. SIOM's clinic-based educational program trains future practioners in acupuncture, tui na, traditional chinese medicine, Chinese herbal medicine, and Chinese language.
SIOM operates a teaching clinic and herbal dispensary where graduate students observe experienced practitioners or practice under their supervision. More than 50 patients are treated each week at SIOM's clinic.

# Notes
-  *Accreditation Commission for Acupuncture and Oriental Medicine: Accredited Programs
-  Washington Higher Education Coordinating Board. Washington Degree-granting Colleges and Universities
-  Seattle Institute of Oriental Medicine: Accreditation and Approvals
-  Seattle Institute of Oriental Medicine