Persius/hicric huggingface dataset:
Pleural Empyema pathophysiology

# Overview
The process leading to the formation of empyema involves  migration of organisms into the pleural cavity.  Lung parenchymal infection stimulates local pleural immune activation, neutrophil migration and release of inflammatory cellular components and toxic oxygen species, such as IL-6, IL-8 and tumour necrosis factor (TNF)-.
These mediators promotes endothelial injury resulting in increased pleural membrane permeability and increased osmotic pressure. With persistent inflammation, increased permeability of vascular and mesothelial membranes results in increased plasma leakage into the pleural cavity. Coagulation cascade when activated within the pleural cavity contributes to the development of a fibrinopurulent or complicated parapneumonic effusion. Fibrin is deposited over the pleural surfaces with fibrinous septae producing loculated effusions.

# Pathophysiology

## Pathogenesis
The process leading to the formation of empyema involves  migration of organisms into the pleural cavity. This may be via direct extension/contiguous route. Lung parenchymal infection stimulates local pleural immune activation, neutrophil migration and release of inflammatory cellular components and toxic oxygen species, such as IL-6, IL-8 and tumour necrosis factor (TNF)-.
These mediators promotes endothelial injury resulting in increased pleural membrane permeability and increased osmotic pressure.  The resultant empyema may spontaneously burrowed through the parietal pleura into the chest wall to form a subcutaneous abscess that may eventually rupture through the skin leading to formation of empyema necessitans. Mesothelial cells release TNF- and concurrently antifibrinolytic mediator function is enhance, example plasminogen activator inhibitor-1 and -2.
Mycobacteria bacille CalmetteGuerin infection of pleural cells lead to enhanced VEGF release.  Mycobacteria bacille CalmetteGuerin  (BCG) and S. aureus infections increase permeability across the mesothelial membrane, partly via downregulation of -catenin. 

## Genetics
S. aureus infection of the pleura have been found to result in pleural mesothelial cells expression of early response genes c-fos and c-jun, followed by the expression of pro-apoptotic genes Bak and Bad during later stage of infection. This results in apoptosis of mesothelial tissue and impaired membrane integrity, which may contribute to loss of the normal fibrinolytic function of the pleura.

## Microscopic Pathology
With persistent inflammation, increased permeability of vascular and mesothelial membranes results in increased plasma leakage into the pleural cavity. Coagulation cascade when activated within the pleural cavity contributes to the development of a fibrinopurulent or complicated parapneumonic effusion. Fibrin is deposited over the pleural surfaces with fibrinous septae producing loculated effusions.
Entecavir indications and usage

# Indications And Usage
BARACLUDE (entecavir) is indicated for the treatment of chronic hepatitis B virus infection in adults with evidence of active viral replication and either evidence of persistent elevations in serum aminotransferases (ALT or AST) or histologically active disease.
The following points should be considered when initiating therapy with BARACLUDE:
- This indication is based on histologic, virologic, biochemical, and serologic responses in nucleoside-treatment-naive and lamivudine-resistant adult subjects with HBeAg-positive or HBeAg-negative chronic HBV infection and compensated liver disease .
- Virologic, biochemical, serologic, and safety data are available from a controlled study in adult subjects with chronic HBV infection and decompensated liver disease .
- Virologic, biochemical, serologic, and safety data are available for a limited number of adult subjects with HIV/HBV co-infection who have received prior lamivudine therapy .
Epidermodysplasia verruciformis

# Overview
Epidermodysplasia verruciformis (also called Lewandowsky-Lulz dysplasia or  Lulz-Lewandowsky epidermodysplasia verruciformis) is an extremely rare skin disease characterized by the growth of scaly macules and papules, particularly on the hands. Named after doctors Felix Lewandowsky and Wilhelm Lulz, the condition usually begins in childhood and has no known cure.
It is believed to be caused by the human papillomavirus and is most strongly associated with strains 5 and 8, although others may also contribute. Genetic predisposition is also thought to partly explain why the disease is so rare, as EV papillomaviruses are often found (15-20%) in normal skin with no increased incidence of cancer.

# Diagnosis

## Physical Examination

### Skin
- Epidermodysplasia verruciformis. Adapted from Dermatology Atlas.
- Epidermodysplasia verruciformis. Adapted from Dermatology Atlas.
- Epidermodysplasia verruciformis. Adapted from Dermatology Atlas.
- Epidermodysplasia verruciformis. Adapted from Dermatology Atlas.
- Epidermodysplasia verruciformis. Adapted from Dermatology Atlas.
- Epidermodysplasia verruciformis. Adapted from Dermatology Atlas.
- Epidermodysplasia verruciformis. Adapted from Dermatology Atlas.

# Notable cases
In March 2007, a Romanian man was diagnosed with this condition.  The man, patient of dermatologist Dr. Carmen Madeleine Curea, quickly became an internet meme, his pictures appearing on numerous blogs and Romanian press sources.  Dr. Curea works out of Spitalului Clinic Colentina in Bucharest, Romania.  Stephen Stone, past president of the American Academy of Dermatology, confirms this is Lewandowsky-Lutz.

# Further reading
- H. Sadakane, Y. Yabe. The Virus of Epidermodysplasia Verruciformis: Electron Microscopic and Fluorescent Antibody Studies. Journal of Investigative Dermatology (1975) 65, 324330 
- F. Lewandowsky, W. Lulz. Ein Fall einer bisher noch nicht beschriebener Hauterkrankung (Epidermodysplasia verruciformis). Archiv fur Dermatologie und Syphilis (1922) 141, 193-202.
Ertapenem indications and usage

# Indications and Usage
To reduce the development of drug-resistant bacteria and maintain the effectiveness of INVANZ and other antibacterial drugs, INVANZ 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.

## Treatment
INVANZ is indicated for the treatment of adult patients and pediatric patients (3 months of age and older) with the following moderate to severe infections caused by susceptible isolates of the designated microorganisms .

### Complicated Intra-Abdominal Infections
INVANZ is indicated for the treatment of complicated intra-abdominal infections due to Escherichia coli, Clostridium clostridioforme, Eubacterium lentum, Peptostreptococcus species, Bacteroides fragilis, Bacteroides distasonis,Bacteroides ovatus, Bacteroides thetaiotaomicron, or Bacteroides uniformis.

### Complicated Skin and Skin Structure Infections, Including Diabetic Foot Infections without Osteomyelitis
INVANZ is indicated for the treatment of complicated skin and skin structure infections, including diabetic foot infections without osteomyelitis due to Staphylococcus aureus (methicillin susceptible isolates only), Streptococcus agalactiae,Streptococcus pyogenes, Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, Bacteroides fragilis,Peptostreptococcus species, Porphyromonas asaccharolytica, or Prevotella bivia. INVANZ has not been studied in diabetic foot infections with concomitant osteomyelitis .

### Community Acquired Pneumonia
INVANZ is indicated for the treatment of community acquired pneumonia due to Streptococcus pneumoniae (penicillin susceptible isolates only) including cases with concurrent bacteremia, Haemophilus influenzae (beta-lactamase negative isolates only), or Moraxella catarrhalis.

### Complicated Urinary Tract Infections Including Pyelonephritis
INVANZ is indicated for the treatment of complicated urinary tract infections including pyelonephritis due to Escherichia coli, including cases with concurrent bacteremia, or Klebsiella pneumoniae.

### Acute Pelvic Infections Including Postpartum Endomyometritis, Septic Abortion and Post Surgical Gynecologic Infections
INVANZ is indicated for the treatment of acute pelvic infections including postpartum endomyometritis, septic abortion and post surgical gynecological infections due to Streptococcus agalactiae, Escherichia coli, Bacteroides fragilis, Porphyromonas asaccharolytica, Peptostreptococcus species, or Prevotella bivia.

## Prevention

### Prophylaxis of Surgical Site Infection Following Elective Colorectal Surgery
INVANZ is indicated for the prevention of surgical site infection following elective colorectal surgery.
Estrogen-related receptor gamma
Estrogen-related receptor gamma (ERR-gamma), also known as NR3B3 (nuclear receptor subfamily 3, group B, member 3), is a nuclear receptor that in humans is encoded by the ESRRG (EStrogen Related Receptor Gamma) gene. It behaves as a constitutive activator of transcription.
This protein is a member of nuclear hormone receptor  family of steroid hormone receptors. No physiological activating ligand is known for this orphan receptor, but 4-hydroxytamoxifen and diethylstilbestrol act as inverse agonists and deactivate ESRRG. It also seems to be the target of bisphenol A (see below).

# Bisphenol A binding
There is evidence that bisphenol A functions as an endocrine disruptor by binding strongly to ERR-. BPA as well as its nitrated and chlorinated metabolites seems to binds strongly to ERR- (dissociation constant = 5.5 nM), but not to the estrogen receptor (ER)., BPA binding to ERR- preserves its basal constitutive activity. It can also protect it from deactivation from the selective estrogen receptor modulator 4-hydroxytamoxifen.
Different expression of ERR- in different parts of the body may account for variations in bisphenol A effects. For instance, ERR- has been found in high concentration in the placenta, explaining reports of high bisphenol A accumulation there.
Excitation-contraction coupling

# Introduction
Excitation-contraction (EC) coupling is a term coined in 1952 to describe the physiological process of converting an electrical stimulus to mechanical response . This process is fundamental to muscle physiology, whereby the electrical stimulus is usually an action potential and the mechanical response is contraction.  EC coupling can be dysregulated in many disease conditions.
Though EC coupling has been known for over half a century, it is still an active area of biomedical research.  The general scheme is that an action potential arrives to depolarise the cell membrane.  By mechanisms specific to the muscle type, this depolarisation results in an increase in cytosolic calcium that is called a calcium transient.  This increase in calcium activates calcium-sensitive contractile proteins that then use ATP to cause cell shortening.

# Skeletal Muscle
1. Acetylcholine released by axon of motor neuron crosses cleft and binds to receptors/channels on motor end plate
2. Action potential generated in response to binding of acetylcholine and subsequent end plate potential is propagated across surface membrane and down T tubules of muscle cell
3. Action potential in T tubule triggers Ca2+ (calcium) release from sarcoplasmic reticulum
4. Calcium ions released from lateral sacs bind to troponin on actin filaments; leads to tropomyosin being physically moved aside to uncover cross-bridge binding sites on actin
5. Myosin cross bridges attach to actin and bend, pulling actin filaments toward center of sarcomere; powered by energy provided by ATP
6. Ca2+ actively taken up by sarcoplasmic reticulum when there is no longer local action potential
7. With Ca2+ no longer bound to troponin, tropomyosin slips back to its blocking position over binding sites on actin; contraction ends; actin slides back to original resting position

# Cardiac Muscle

# Smooth Muscle
Extensor hallucis longus muscle

# Overview
The Extensor hallucis longus is a thin muscle, situated between the Tibialis anterior and the Extensor digitorum longus that functions to extend the big toe, dorsiflex the foot, and assists with foot inversion.
It arises from the anterior surface of the fibula for about the middle two-fourths of its extent, medial to the origin of the Extensor digitorum longus; it also arises from the interosseous membrane to a similar extent.
The anterior tibial vessels and deep peroneal nerve lie between it and the Tibialis anterior.
The fibers pass downward, and end in a tendon, which occupies the anterior border of the muscle, passes through a distinct compartment in the cruciate crural ligament, crosses from the lateral to the medial side of the anterior tibial vessels near the bend of the ankle, and is inserted into the base of the distal phalanx of the great toe.
Opposite the metatarsophalangeal articulation, the tendon gives off a thin prolongation on either side, to cover the surface of the joint.
An expansion from the medial side of the tendon is usually inserted into the base of the proximal phalanx.

# Variations
Occasionally united at its origin with the Extensor digitorum longus.
Extensor ossis metatarsi hallucis, a small muscle, sometimes found as a slip from the Extensor hallucis longus, or from the Tibialis anterior, or from the Extensor digitorum longus, or as a distinct muscle; it traverses the same compartment of the transverse ligament with the Extensor hallucis longus.

# Additional images
- The mucous sheaths of the tendons around the ankle. Medial aspect.
- Deep nerves of the front of the leg.
- Nerves of the dorsum of the foot.
- File:Extensor hallucis longus.png
Extensor pollicis longus muscle
The Extensor pollicis longus is much larger than the Extensor pollicis brevis muscle, the origin of which it partly covers.

# Origin and insertion
It arises from the lateral part of the middle third of the dorsal surface of the body of the ulna below the origin of the Abductor pollicis longus, and from the interosseous membrane.
It ends in a tendon, which passes through a separate compartment in the dorsal carpal ligament, lying in a narrow, oblique groove on the back of the lower end of the radius.
It then crosses obliquely the tendons of the Extensores carpi radialis longus and brevis, and is separated from the Extensor brevis pollicis by a triangular interval, the anatomical snuff box in which the radial artery is found; and is finally inserted into the base of the last phalanx of the thumb.

# Relations
The radial artery is crossed by the tendons of the Abductor pollicis longus and of the Extensores pollicis longus and brevis.

# Action
The  extends the proximal phalanx, and the
Extensor pollicis longus extends the terminal phalanx of the thumb; in combination with the Extensor pollicis brevis, it helps to extend and abduct the wrist.

# Additional images
- Anatomical snuff box
Anatomical snuff box
- Bones of left forearm. Posterior aspect.
- Bones of the left hand. Dorsal surface.
- Tendons of forefinger and vincula tendina.
- Cross-section through the middle of the forearm.
- Posterior surface of the forearm. Superficial muscles.
- Posterior surface of the forearm. Deep muscles.
Posterior surface of the forearm. Deep muscles.
- Transverse section across the wrist and digits.
- Arteries of the back of the forearm and hand.
Facial nerve paralysis overview

# Overview
Facial nerve paralysis and Bell's palsy is due to a loss of voluntary movement of the muscles on one side of the face due to abnormal function of the facial nerve(s). A Peripheral palsy affects all ipsilateral muscles of facial expression (paralysis results on the entire ipsilateral side). A supranuclear palsy involves the lower part of the face.
Facial nerve paralysis is a common problem that involves the paralysis of any structures innervated by the facial nerve. The pathway of the facial nerve is long and relatively convoluted, and so there are a number of causes that may result in facial nerve paralysis. The most common is Bell's palsy, an idiopathicdisease that may only be diagnosed by exclusion.
A thorough medical history and physical examination are the first steps in making a diagnosis.
During the physical examination, a distinction must first be made between paralysis and paresis (incomplete paralysis). Not surprisingly, paralysis is far more serious and requires immediate treatment. It must also be determined whether the forehead is involved in the motor defect or not. This is usually accomplished by assessing how well a patient can raise her eyebrows. The question is an important one because it helps determine if the lesion is in the upper motor neuroncomponent of the facial nerve, or in its lower motor neuron component.
Laboratory investigations include an audiogram, nerve conduction studies (ENoG), computed tomography (CT) ormagnetic resonance (MR) imaging.
Fair Packaging and Labeling Act
The Fair Packaging and Labeling Act is a US law that applies to labels on many consumer products. It requires the label to state:
- The identity of the product;
- The name and place of business of the manufacturer, packer, or distributor; and
- The net quantity of contents.
The contents statement must include both metric and U.S. customary units.
Passed under Lyndon B. Johnson in 1966, the law first took effect on July 1, 1967. The metric labeling requirement was added in 1992 and took effect on February 14, 1994. The law is codified as Template:Usc.
Currently, there is a strong effort underway by industry to amend the FPLA to allow manufacturers to use metric-only labeling. In light of a January 1 2010 European Union deadline that will no longer allow dual-unit product labeling, an amendment to the FPLA to allow metric-only labeling would allow manufacturers, both importers and exporters, to avoid the significant costs associated with the potential necessity of producing two distinct package types.
Famotidine detailed information
Famotidine (INN) (Template:PronEng) is a histamine H2-receptor antagonist that inhibits stomach acid production, and is commonly used in the treatment of  peptic ulcer disease (PUD) and gastroesophageal reflux disease (GERD/GORD). It is commonly marketed by J&J/Merck under the trade names Pepcidine and Pepcid.

# Clinical use
Main article: H2-receptor antagonist
Certain preparations of famotidine are available over the counter (OTC) in various countries. In the United States, preparations of 10 mg and 20 mg tablets, sometimes in combination with a more traditional antacid, are available OTC. Larger doses still require a prescription.
Famotidine is given to surgery patients before operations to prevent post-operation nausea and to reduce the risk of aspiration pneumonitis.

# History and development
Famotidine was developed by Merck & Co. and is marketed by a joint venture between Merck and Johnson & Johnson. The imidazole-ring of cimetidine was replaced with a 2-guanidinothiazole ring. Famotidine proved to be 30 times more active than cimetidine.
It was first marketed in 1985. Pepcid RPD orally-disintegrating tablets (that are not swallowed) was released in 1999. Generic preparations became available in 2001, e.g. Fluxid (Schwarz) or Quamatel (Gedeon Richter Ltd.). In the United States, a product called Pepcid Complete is available that combines famotidine with an antacid in a chewable tablet to ameliorate the relatively slow onset of effects. In the UK, this product is known as Pepcidtwo.
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High-molecular-weight kininogen
High-molecular-weight kininogen (HMWK or HK) is a circulating plasma protein which participates in the initiation of blood coagulation, and in the generation of the vasodilator bradykinin via the kallikrein-kinin system. HMWK is inactive until it either adheres to binding proteins beneath an endothelium disrupted by injury, thereby initiating coagulation; or it binds to intact endothelial cells or platelets for functions other than coagulation.

# Other names
In the past, HMWK has been called HMWK-kallikrein factor, Flaujeac factor (1975), Fitzgerald factor (1975), and Williams-Fitzgerald-Flaujeac factor, - the eponyms being for people first reported to have HMWK deficiency. Its current accepted name is to contrast it with low molecular weight kininogen (LMWK) which has a similar function to HMWK in the tissue (as opposed to serum) kinin-kallikrein system.

# Structure and function
HMWK is an alpha-globulin with six functional domains. It circulates as a single-chain 626 amino acid polypeptide . The heavy chain contains domains 1, 2, and 3; the light chain, domains 5 and 6. Domain 4 links the heavy and light chains.
The domains contain the following functional sites:
- Domain 1 - calcium binding
- Domain 2 - cysteine protease inhibition
- Domain 3 - cysteine protease inhibition; platelet and endothelial cell binding
- Domain 4 - bradykinin generation
- Domain 5 - heparin and cell binding; antiangiogenic properties; binding to negatively charged surfaces
- Domain 6 - prekallikrein and factor XI binding (amino acids 420 to 510)(histidine rich)
HMWK is one of four proteins which interact to initiate the contact activation pathway (also called the intrinsic pathway) of coagulation: the other three are Factor XII, Factor XI and prekallikrein. HMWK is not enzymatically active, and functions only as a cofactor for the activation of kallikrein and factor XII. It is also necessary for the activation of factor XI by factor XIIa.
HMWK is also a precursor of bradykinin; this vasodilator is released through positive feedback by kallikrein.
HMWK is a strong inhibitor of cysteine proteinases. Responsible for this activity are domains 2 and 3 on its heavy chain.

# Genetics
The gene for both LMWK and HMWK is located on the 3rd chromosome (3q26).

# Measurement
Measurement of HMWK is usually done with mixing studies, in which plasma deficient in HMWK is mixed with the patient's sample and a partial thromboplastin time (PTT) is determined. Results are expressed in % of normal - a value under 60% indicates a deficiency.

# Clinical features
The existence of HMWK was hypothesised in 1975 when several patients were described with a deficiency of a class of plasma protein and a prolonged bleeding time and PTT. 
There is no increased risk of bleeding or any other symptoms, so the deficiency is a trait, not a disease.
Flunitrazepam contraindications

# Overview
Flunitrazepam/Rohypnol is a prescription drug - the only sedative that has been used in many date rapes in the US. Rohypnol's medical use is a preoperation anesthetic or strong sleeping pill, but stronger doses can bring on amnesia. It takes effect very quickly - sometimes as quick as 10 minutes after taken - and reaches its peak eight hours later when it can render a patient totally unconscious. 
Rohypnol comes as a pill that can diissolve in liquids. Some are round , small and white. Newer pills are oval and green-grey in colour. When slipped into a drink , a dye in these new pills makes clear liquids turn blue and the dark drinks turn cloudy. But this colour change might br hard to see in a dark drink, or in a dark room.Also the pills with no dye are available. these pills may be grounded up into a powder.

# Contraindications
Flunitrazepam is contraindicated in conditions like Myasthenia gravis, Respiratory depression, Acute pulmonary insufficiency, Sleep apnea syndrome.