Persius/hicric huggingface dataset:
Ampicillin indications and usage

# Indications and Usage
Ampicillin for Injection, USP is indicated in the treatment of infections caused by susceptible strains of the designated organisms in the following conditions:
- Respiratory tract Infections caused by S. pneumoniae (formerly D. pneumoniae). Staphylococcus aureus (penicillinase and nonpenicillinase-producing), H. influenzae, and Group A beta-hemolytic Streptococci.
- Bacterial Meningitis caused by E. coli, Group B Streptococci, and other Gram-negative bacteria (Listeria monocytogenes, N. meningitidis). The addition of an aminoglycoside with ampicillin may increase its effectiveness against Gram-negative bacteria.
- Septicemia and Endocarditis caused by susceptible Gram-positive organisms including Streptococcus sp., penicillin G-susceptible staphylococci, and enterococci. Gram-negative sepsis caused by E. coli, Proteus mirabilis and Salmonella sp. respond to ampicillin. Endocarditis due to enterococcal strains usually respond to intravenous therapy. The addition of an aminoglycoside may enhance the effectiveness of ampicillin when treating streptoccoccal endocarditis.
- Urinary Tract Infections caused by sensitve strains of E. coli and Proteus mirabilis.
- Gastrointestinal Infections caused by Salmonella typhosa (typhoid fever), other Salmonella sp., and Shigella sp. (dysentery) usually respond to oral or intravenous therapy.
Bacteriology studies to determine the causative organisms and their susceptibility to ampicillin should be performed. Therapy may be instituted prior to obtaining results of susceptibility testing.
It is advisable to reserve the parenteral form of this drug for moderately severe and severe infections and for patients who are unable to take the oral forms. A change to oral ampicillin may be made as soon as appropriate.
To reduce the development of drug-resistant bacteria and maintain the effectiveness of Ampicillin for Injection, USP and other antibacterial drugs, Ampicillin for Injection, USP should be used only to treat or prevent infections that are proven or strongly suspected to be caused by susceptible bacteria. When culture and susceptibility information are available, they should be considered in selecting or modifying antibacterial therapy. In the absence of such data, local epidemiology and susceptibility patterns may contribute to the empiric selection of therapy.
Indicated surgical procedures should be performed.
Aortic stenosis surgery overview

# Overview
Surgical intervention may be a necessary component of treatment for symptomatic severe aortic stenosis. Aortic valve replacement is the mainstay of treatment of symptomatic aortic stenosis, as it improves both the symptoms and life expectancy in aortic stenosis patients, in contrast to medical therapy alone which may improve the symptoms without prolonging life expectancy. Intervention methods may include: a) Aortic valve replacement, mechanical and device based therapies such as bileaflet mechanical aortic valves; b) Aortic Balloon Valvotomy, aortic valvuloplasty (aortic valve repair).
Percutaneous aortic valve replacement is in its infancy and thus aortic valvuloplasty can offer palliation of symptoms and potentially prolong survival for these high risk patients in class III-IV heart failure. It can be performed emergently in patients with end-stage heart failure due to aortic stenosis, patients in cardiogenic shock, as a bridge to aortic valve replacement, patients with critical aortic stenosis needing emergent non-cardiac surgery, poor surgical candidates and nonagenerians, patients with congenital or rheumatic aortic stenosis. Valvuloplasty tends to alleviate heart failure symptoms and improve hemodynamics but rarely does it alleviate angina.
In open surgery, the surgeon makes a large cut in the sternum to reach the heart.
Minimally invasive aortic valve surgery is done through much smaller surgical cuts than the large cuts needed for open surgery.

# Epidemiology and Demographics
The number of patients undergoing aortic valve replacement surgery to treat aortic stenosis has increased progressively over the past 10 years.  The surgery is usually performed in elderly patients with preserved ejection fractions.  Transcatheter aortic valve implantation (TAVI) represents a new option in patients with no surgical options.

# Indications
Aortic stenosis requires aortic valve replacement if medical management does not successfully control symptoms.
According to a prospective, single-center, nonrandomized study of 25 patients, percutaneous implantation of an aortic valve prosthesis in high risk patients with aortic stenosis results in marked hemodynamic and clinical improvement when successfully completed.

# Treatment

## Procedure
The procedure can be done either by the traditional open heart surgery or by the minimally invasive surgery. Before the surgery, the patient will receive general anesthesia. This will make the patient asleep and pain-free during the entire procedure. Other than the aortic valve replacement surgery; aortic stenosis could be treated by: percutaneous aortic balloon valvotomy or transcatheter aortic valve implantation.
Ear pain resident survival guide
Synonyms and keywords:

# Overview
Ear pain or otalgia maybe it is a pain that originates outside the ear or the pain that originates from the ear, and the etiology can be difficult to establish because of the complex innervation of the ear. Branches of the fifth, seventh, ninth, and tenth cranial nerve along with cervical nerves 1, 2, and 3 all contribute to sensation in the middle ear, external auditory canal, auricle, and peri-auricular tissues. Irritation of any portion of these cranial nerves can result in otalgia.otalgia can be the manifestation of myocardial ischemia (ie, an angina equivalent) because the vagus nerve provides sensory innervations for both structures. Intermittent pain is much more likely to be associated, for example, with musculoskeletal conditions as temporomandibular joint (TMJ) dysfunction and other myofascial pain dysfunction syndromes.otalgia classified as primary, which originated from the ear, and secondary, which originated outside the ear. When the ear examination is abnormal, the source of the pain from the ear (primary otalgia); when the ear examination is typically normal, the pain source is not the ear(secondary otalgia) .Examination should be carried out including inspection of nasal cavity, oral cavity, neck, and possibly the larynx.

# Causes

## Life Threatening Causes
Otalgia is not life-threatening, but some characteristics make a serious diagnosis more likely in patients with Otalgia. As patients who are 50 years or older have coronary artery disease, have diabetes, or are immunocompromised are at higher risk. Also, patients who smoke, drink alcohol, or lose weight unintentionally should undergo more scrutiny. Otalgia may also be the first sign of:
- Temporal arteritis
- Myocardial infarction
- Thoracic aneurysms
- Subdural hematoma
- lung cancer
- Central line placement
- Carotid artery aneurysm
- Pott puffy tumor
- Malignant neoplasms

## Common Causes
Common causes for  Primary Otalgia
- Otitis media
- Otitis externa
- Barotrauma
- Eustachian tube dysfunction
- Foreign object
- Cellulitis of auricle
- Cholesteatoma
Common causes for Secondary Otalgia
- Bell palsy
- Carotidynia
- Cervical adenopathy
- Cervical spine arthritis
- Cricoarytenoid arthritis
- Dental infections
- Gastroesophageal reflux
- Head and neck tumors
- Temporomandibular joint syndrome
- Myofascial pain
- Neuralgias (trigeminal, glossopharyngeal, geniculate, sphenopalatine)
- Oral aphthous ulcers
- Pharyngitis or tonsillitis
- Salivary gland disorders
- Sinusitis
- thyroiditis

# Diagnosis
Shown below is an algorithm summarizing the diagnosis of Ear pain according to the American Family Physician AFP 2008 guidelines.

# Treatment
Shown below is an algorithm summarizing the treatment of Ear pain according the the American Family Phsyician guidelines.
Ara Darzi, Baron Darzi of Denham
Ara Darzi, Baron Darzi of Denham, KBE (born May 7, 1960), is one of the world's leading surgeons, specialising in the field of minimally invasive and robot-assisted surgery, having pioneered many new techniques and technologies.
Lord Darzi is of Armenian origin, however he spent much of his childhood in Ireland after moving there from Iraq where he was born. He is an Irish citizen. In 2002 he became a British citizen and was awarded a knighthood for his services to medicine and surgery. He is married to Wendy with whom he shares two children, Freddie and Nina.
Darzi joined Imperial College London in 1994, becoming Head of Division in 1998. He is a consultant surgeon at St. Mary's Hospital and Royal Marsden NHS trust with a large clinical practice Keyhole surgery. Professor Darzi and his team are internationally respected for their innovative work in the advancement of minimal invasive surgery and in the development and use of allied technologies including surgical robots and image-guided surgery. This work has received international recognition including the Hamdan Award for Medical Research Excellence in 2004. Professor Darzi is a Fellow of the Royal College of Surgeons of England, Ireland, Edinburgh. He is also Fellow of the American College of Surgeons, Fellow of the Academy of Medical Sciences, and more recently awarded an Honorary Fellow of the Royal Academy of Engineering for his research contibution to Bioengineering research.
The innovative work of Professor Lord Darzi and his team in education and assessment of surgeons, including the use of simulations and virtual reality, is internationally recognised as showing the way forward for surgical education. They were awarded in 2001 the Queens Anniversary Prize for Excellence in Higher and Further Education in recognition for achievements in pioneering new technologies to address training requirements for trainee surgeons, surgeons in post and other professionals.
On 29 June 2007 Darzi was appointed Parliamentary Under-Secretary at the Department of Health by the Prime Minister, Gordon Brown. He was created a life peer on 12 July as Baron Darzi of Denham, of Gerrards Cross in the County of Buckinghamshire.
Asystole resident survival guide

# Overview
Asystole is a state of no cardiac electrical activity, hence no contractions of the myocardium and no cardiac output or blood flow.  Asystole is also known as a cardiac arrest rhythm in which there is no distinct electrical activity on ECG.  A (flat line) is another acronym for asystole. In asystole, the heart will not respond to defibrillation because it is already depolarized.

# Causes

## Life Threatening Causes
Asystole is a life-threatening condition and must be treated as such irrespective of the causes.  Life-threatening conditions  can result in death or permanent disability within 24 hours if left untreated.

## Common Causes
- Hydrogen ions (Acidosis)
- Hyperkalemia or Hypokalemia
- Hypoglycemia
- Hypothermia
- Hypovolemia
- Hypoxia
- Cardiac Tamponade
- Tablets or Toxins (Drug overdose)
- Tension pneumothorax
- Thrombosis (Myocardial infarction)
- Thrombosis (Pulmonary embolism)
- Trauma (Hypovolemia from blood loss)

# Management
Below is an algorithm summarizing the approach to a patient with asystole. Based on the 2010 American heart association ACLS algorithm for asystole

# Do's
- Efficiency of CPR can be determined by
Monitoring of chest compression rate and depth
Adequacy of chest wall relaxation
Length and duration of pauses in compression and number and depth of ventilations delivered
Physiologic parameters; partial pressure of end-tidal CO2 , arterial pressure during the relaxation phase of chest compressions, central venous oxygen saturation 
- Monitoring of chest compression rate and depth
- Adequacy of chest wall relaxation
- Length and duration of pauses in compression and number and depth of ventilations delivered
- Physiologic parameters; partial pressure of end-tidal CO2 , arterial pressure during the relaxation phase of chest compressions, central venous oxygen saturation 
- Remember that the foundation of successful ACLS is good BLS , represented in prompt high-quality CPR with minimal interruptions.
- A new class I recommendation is the use of quantitative waveform capnography for confirmation and monitoring of endotracheal tube placement.
- Supraglottic advanced airways continues to be an alternative to endotracheal intubation for airway management during CPR.

# Don'ts
- Don't routinely use cricoid pressure during airway management of patients in cardiac arrest.
- Don't routinely administer atropine in the management of pulseless asystole.
Atazanavir indications and usage

# Indications and Usage
REYATAZ (atazanavir sulfate) is indicated in combination with other antiretroviral agents for the treatment of HIV-1 infection. This indication is based on analyses of plasma HIV-1 RNA levels and CD4+ cell counts from controlled studies of 96 weeks duration in antiretroviral-naive and 48 weeks duration in antiretroviral-treatment-experienced adult and pediatric patients at least 6 years of age.
The following points should be considered when initiating therapy with REYATAZ:
In Study AI424-045, REYATAZ/ritonavir and lopinavir/ritonavir were similar for the primary efficacy outcome measure of time-averaged difference in change from baseline in HIV RNA level. This study was not large enough to reach a definitive conclusion that REYATAZ/ritonavir and lopinavir/ritonavir are equivalent on the secondary efficacy outcome measure of proportions below the HIV RNA lower limit of detection .
The number of baseline primary protease inhibitor mutations affects the virologic response to REYATAZ/ritonavir.
Atovaquone proguanil description

# Description
MALARONE (atovaquone and proguanil hydrochloride) Tablets (adult strength) and MALARONE (atovaquone and proguanil hydrochloride) Pediatric Tablets, for oral administration, contain a fixeddose combination of the antimalarial agents atovaquone and proguanil hydrochloride.
The chemical name of atovaquone is trans-2--3-hydroxy-1,4-naphthalenedione. Atovaquone is a yellow crystalline solid that is practically insoluble in water. It has a molecular weight of 366.84 and the molecular formula C22H19ClO3. The compound has the following structural formula:
The chemical name of proguanil hydrochloride is 1-(4-chlorophenyl)-5-isopropyl-biguanide hydrochloride. Proguanil hydrochloride is a white crystalline solid that is sparingly soluble in water. It has a molecular weight of 290.22 and the molecular formula C11H16ClN5HCl. The compound has the following structural formula:
Each MALARONE Tablet (adult strength) contains 250 mg of atovaquone and 100 mg of proguanil hydrochloride and each MALARONE Pediatric Tablet contains 62.5 mg of atovaquone and 25 mg of proguanil hydrochloride. The inactive ingredients in both tablets are lowsubstituted hydroxypropyl cellulose, magnesium stearate, microcrystalline cellulose, poloxamer 188, povidone K30, and sodium starch glycolate. The tablet coating contains hypromellose, polyethylene glycol 400, polyethylene glycol 8000, red iron oxide, and titanium dioxide.
Autoimmune disease and the heart

# Overview
The cardiovascular manifestations of underlying autoimmune diseases may go unrecognized and this may contribute to excess morbidity and mortality in these patients.  Below is a list of autoimmune diseases which may have cardiovascular manifestations.

# List of Autoimmune Diseases Associated with Heart Disease in Some Studies
Diseases listed below in alphabetical order:              
The Heart in Ankylosing Spondylitis
The Heart in Antiphospholipid Syndrome
The Heart in Behcet's disease
The Heart in Celiac Disease
The Heart in Chagas' disease
The Heart in Crohn's Disease
The Heart in Essential Mixed Cryoglobulinemia
The Heart in Grave's Disease (Overactive Thyroid)
The Heart in Guillain Barre Syndrome
The Heart in Hashimoto's Thyroiditis (Underactive Thyroid)
The Heart in Juvenile Rheumatoid Arthritis
The Heart in Kawasaki Disease
The Heart in Kohlmeier-Degos Disease
The Heart in Mixed Connective Tissue Disorders
The Heart in Polyarteritis Nodosa
The Heart in Polychondritis
The Heart in Polymyositis and Dermatomyositis
The Heart in Progressive Systemic Sclerosis (Scleroderma)
The Heart in Psoriasis
The Heart in Reiter's Syndrome
The Heart in Rheumatic Fever
The Heart in Rheumatoid Arthritis
The Heart in Sarcoidosis
The Heart in Sjogrens Syndrome
The Heart in Systemic Lupus Erythematosus (SLE)
The Heart in Takayasu Arteritis
The Heart in Temporal Arteritis / Giant Cell Arteritis
The Heart in Ulcerative colitis
The Heart in Wegener's Granulomatosis
The Heart in Wilson's Disease
Baker-Venkataraman rearrangement
The Baker-Venkataraman rearrangement is the chemical reaction of 2-acetoxyacetophenones with base to form 1,3-diketones.
This rearrangement reaction proceeds via enolate formation followed by acyl transfer.
The Baker-Venkataraman rearrangement is often used to synthesize chromones and flavones.
Central nervous system infection

# Overview
Central nervous system infections are those infections of the central nervous system (CNS).
There are four main causes of infections of the nervous system: bacterial, viral, fungal and protozoal.
Bacterial infections can be pyogenic infections (e.g., meningitis; brain abscess; subdural and epidural abscesses), tuberculosis, neurosyphilis, or leprosy.
Viral infections may be meningitis, encephalitis, poliomyelitis, slow virus infections, acquired immune deficiency syndrome (AIDS), and post-infectious syndromes.
Fungal infections may be meningitis or meningoencephalitis, brain abscess, or spinal epidural infection.
Protozoal infections include toxoplasmosis, malaria or amoebic infection.

# Related Chapters
- Meningitis
- Encephalitis
Beta-carotene 15,15'-dioxygenase
In enzymology, -carotene 15,15'-dioxygenase (EC 1.13.11.63) is an enzyme with systematic name beta-carotene:oxygen 15,15'-dioxygenase (bond-cleaving). In human it is encoded by the BCO1 gene. This enzyme catalyses the following chemical reaction
This is a cleavage reaction which cleaves -carotene, utilizes molecular oxygen, is enhanced by the presence of bile salts and thyroxine, and generates two molecules of retinal. In humans, the enzyme is present in the small intestine and liver. It can also cleave beta-cryptoxanthin, apocarotenal, 4'-apo--carotenal, alpha-carotene and -carotene in decreasing order, all subtrates greater than C30 with at least one unsubstituted -ionone ring.
This enzyme belongs to the family of oxidoreductases, specifically those acting on paired donors, with O2 as oxidant and incorporation or reduction of oxygen. Other names in common use include -carotene 15,15'-monooxygenase and -carotene dioxygenase. Its previous EC numbers include 1.13.11.21 (1975), 1.14.99.36 (2001).
In general, carnivores are poor converters of ionone-containing carotenoids, and pure carnivores such as cats and ferrets lack beta-carotene 15,15'-monooxygenase and cannot convert any carotenoids to retinal (resulting in none of the carotenoids being forms of vitamin A for these species). They must have preformed vitamin A in their diet.
Beta-carotene 15,15'-dioxygenase contains Fe2+.
Beta-hydroxy beta-methylbutyrate
Beta-hydroxy beta-methylbutyrate (HMB) is a metabolite of the amino acid leucine and is synthesized in the human body.  It plays a part in protein synthesis and was discovered by Dr. Steve Nissen in scientific studies to purportedly increase muscle mass and decrease muscle breakdown. It should be noted however that Nissen held the original patent on the metabolite as a nutritional supplement.  It can be found, in small quantities, in grapefruit, alfalfa, and catfish.
Research published in the Journal of Applied Physiology and other peer reviewed publications has shown that HMB may have an effect on increasing muscle weight and strength. There are, however, numerous studies published that failed to find any increase in strength or performance, and these should be included in any assessment of efficacy. Three grams of HMB per day may help muscles combat protein breakdown, assist in muscle repair and support increased endurance.  Studies suggest its benefits may be greater for the untrained.  Also, well-controlled scientific studies have found increases in muscle mass and decreases in body fat in 70 year old men.  It has helped patients with chronic obstructive pulmonary disease in hospital intensive care units, muscle wasting associated with HIV or AIDS and with cancer, and trauma victims with severe injuries.
The human body produces about 0.2-0.4 grams per day.  Standard doses in research studies have been 1.5 to 3.0 grams per day, usually divided into two doses.
Isosorbide dinitrate/hydralazine
Isosorbide dinitrate/hydralazine is a fixed dose combination drug treatment specifically indicated for African Americans with congestive heart failure. It is a combination of hydralazine (an antihypertensive) and isosorbide dinitrate (a vasodilator). It is the first race-based prescription drug in the United States. The combination preparation is marketed in the United States by Nitromed under the trade name BiDil.
Originally rejected by the Food and Drug Administration (FDA) in 1997, the combination preparation was approved by the FDA in June 2005 for African American-use only based on the results of a study by Taylor et al. (2004). It was already known that African Americans with congestive heart failure (CHF) respond less effectively to conventional CHF treatments (particularly ACE inhibitors) than Caucasians. (Exner, 2001) The study by Taylor et al. demonstrated that isosorbide dinitrate with hydralazine reduced mortality by 43%, reduced hospitalizations by 39%, and quality of life markers in African Americans patients with CHF.
Some argue that because the combination preparation comprises two generically-available drugs, widely available at a small fraction of the cost, BiDil is a marketing breakthrough, rather than a medical one but the 43% mortality benefit is striking statistic. Others argue that the combination reduces the "pill burden" for patients, which improves compliance and therefore the medical outcome. Moreover, the FDA issued a letter in May, 2006 stating that there is no bioequivalent, generic substitute to BiDil. With the 2005 FDA approval and with the issuance of a patent, BiDil is unique and no alternative therapy exists for this disproportionately burdened patient population. In 2006, the Heart Failure Society of America included the use of the fixed dose combination of isosorbide dinitrate/hydralazine as the standard of care in the treatment of heart failure in blacks. In 2007, at the American College of Cardiology annual scientific meeting in New Orleans, data was presented demonstrating a pharmacokenetic distinction between the fixed dose combination and the component agents that may account for the superior clinical benefit in mortality shown in the African American Heart Failure Trial.
It has also been pointed out that the FDA has only approved use of this drug for African Americans, implying that there is some fundamental physiological difference between black and white Americans. There is also some concern over how the implications of this alleged difference may be used to promote racist thinking. It has also been argued that the drug could also be beneficial to whites and other ethnic groups but no such tests have been done yet.