Persius/hicric huggingface dataset:
Mucocele
Synonyms and keywords: Mucus extravasation phenomenon.

# Overview
A mucocele, also referred to as mucus extravasation phenomenon, is a swelling of connective tissue consisting of collected mucin from a ruptured salivary gland duct, which is usually caused by local trauma. The mucocele is a bluish translucent color, and is more commonly found in children and young adults.

# Locations
The most common location to find a mucocele is the surface of the lower lip. It can also be found on the inner side of the cheek (known as the buccal mucosa), on the anterior ventral tongue, and the floor of the mouth. When found on the floor of the mouth, the mucocele is referred to as a ranula. They are rarely found on the upper lip.

# Characteristics
The size of mucoceles vary from 1 mm to several centimeters. On palpation, mucoceles may appear to fluctuant but can also be firm. Their duration lasts from days to years, and may have recurrent swelling with occasional rupturing of its contents.

# Variations
A variant of a mucocele is found on the palate, retromolar pad, and posterior buccal mucosa. Known as a "superficial mucocele", this type presents as single or multiple vesicles and bursts into an ulcer. Despite healing after a few days, superficial mucoceles recur often in the same location.

# Histology
Microscopically, mucoceles appears as granulation tissue surrounding mucin. Since inflammation occurs concurrently, neutrophils and foamy histiocytes usually are present.

# Physical examination

## Gallery

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# Treatment
Some mucoceles spontaneously resolve on their own after a short time. Others are chronic and require surgical removal. Recurrence may occur, and thus the adjacent salivary gland is excised as a preventive measure.
Several types of procedures are available for the surgical removal of mucoceles. These include laser and minimally-invasive techniques which means recovery times are reduced drastically.
Mycetoma
Synonyms and keywords: Madura foot.

# Overview
Mycetoma, or Madura Foot, is an important disease in arid and semi-arid regions around the globe.  It is found in Brazil, Mexico, the Sahel, in pan-Arabia, and in semi-arid areas of India. It is found as far north as Romania.
There are two known forms of mycetoma. The two forms of mycetoma are bacterial mycetoma and fungal mycetoma: bacterial mycetoma is known as actinomycetoma while the fungal form is called eumycetoma. Even at the level of electron microscopy the two forms of mycetoma are difficult to distinguish from one another.

# Pathogenesis
The disease is usually acquired while performing agricultural work, and it generally afflicts men between 20 and 40 years old.The disease is acquired by contacting grains of bacterial or fungal spores that have been discharged onto the soil.  Infection usually involves an open area or break in the skin. Pseudoallescheria boydii is one of many fungi spp. that causes the fungal form of madura foot (see below).  The disease is characterized by a yogurt-like discharge upon maturation of the infection. Hematogenous or lymphatic spread is uncommon. Infections normally start in the foot or hand and travel up the leg or arm.

# Diagnosis
Diagnosis of mycetoma is usually accomplished by radiology, ultrasound or by fine needle aspiration of the fluid within an afflicted area of the body.

# Physical examination

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# Treatment
There are several clinical treatments available for this disease. They include surgery, Ketoconazole, Itraconazole and amputation.  There is no sure-fire treatment available at this date. Nor is there available at this date a vaccine for mycetoma.  Scientists at such institutions as The Mycetoma Research Center at The University of Khartoum in the Sudan are working on a cure.

# Causative species
Species of bacteria that cause Mycetoma include:
- Actinomadura madurae
- Actinomadura pelletierii
- Streptomyces somaliensis'
Species of fungus that cause Mycetoma include:
- Madurella myceomatis
- Scedosporium apiospermum
- Leptosphaeria sengalensis
- Madurella grisea
Myogenin
Myogenin (myogenic factor 4), also known as MYOG, is a gene.
Myogenin is a muscle-specific basic-helix-loop-helix (bHLH) transcription factor involved in the coordination of skeletal muscle development or myogenesis and repair.  Myogenin is a member of the MyoD family of transcription factors, which also includes MyoD, Myf5, and Mrf4.
In mice, myogenin is essential for the development of functional skeletal muscle. Myogenin is required for the proper differentiation of most myogenic precursor cells during the process of myogenesis. When the DNA coding for myogenin was knocked out of the mouse genome, severe skeletal muscle defects were observed.  Mice lacking both copies of myogenin (homozygous-null) suffer from perinatal lethality due to the lack of mature secondary skeletal muscle fibers throughout the body.
In cell culture, myogenin can induce myogenesis in a variety of non-muscle cell types.

# Interactions
Myogenin has been shown to interact with:
- MDFI,
- POLR2C,
- Serum response factor
- Sp1 transcription factor,  and
- TCF3.
Myositis
Synonyms and keywords:

# Overview
Myositis is a general term for inflammation of the muscles.  Many such conditions are considered likely to be caused by autoimmune conditions, rather than directly due to infection (although autoimmune conditions can be activated or exacerbated by infections.)
Elevation of creatine kinase (CK) in blood is indicative of myositis. The MM and not the MB or BB fraction of the CK will be elevated.

# Differential diagnosis of myositis
Myositis must be differentiated from the following conditions causing muscle weakness, hypotonia, or flaccid paralysis:
The following drugs or conditions may additionally need to be differentiated from myositis:
Atorvastatin
Cellulitis
Deep vein thrombosis
Dermatomyositis
Dolutegravir
Hematoma
Idiopathic inflammatory myopathies
Inclusion body myositis
Influenza myositis
Juvenile dermatomyositis
Lovastatin
Lyme myositis
Myositis ossificans
Neuromuscular complications accompanying AIDS
Osteoarthritis
Osteomyelitis
Paraneoplastic neuropathy
Peripheral vascular disease
Polymyositis
Pravastatin (less likely than other statins)
Pyomyositis
Rheumatoid arthritis
Simvastatin
Statin therapy
Systemic lupus erythematosus
Toxoplasma myositis
Trichinosis
Trypanosomiasis
Tuberculous pyomyositis
Viral myositis (including following an episode of influenza)
Wasting syndrome

## Causes

## Drug Side Effect
- Pembrolizumab
- Pergolide
- Zidovudine

# Diagnostic Findings

## MRI
(Images courtesy of RadsWiki)
- Myositis
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- Myositis
Myositis
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Myositis
Myotilin
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# Overview
Myotilin, also known as MYOT, is a human gene.
Striated muscle sarcomeres are highly organized structures composed of actin (thin) and myosin (thick) filaments that slide past each other during contraction. The integrity of sarcomeres is controlled by a set of structural proteins, among which are titin (TTN; MIM 188840), a giant molecule that contains several immunoglobulin (Ig)-like domains and associates with thin and thick filaments, and alpha-actinin (ACTN1; MIM 102575), an actin cross-linking protein. Mutations in several sarcomeric and sarcolemmal proteins have been shown to result in muscular dystrophy and cardiomyopathy.
Myotonia
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# Overview
Myotonia is a symptom of a small handful of certain neuromuscular disorders characterized by the slow relaxation of the muscles after voluntary contraction or electrical stimulation. Generally, repeated effort is needed to relax the muscles, and the condition improves after the muscles have warmed-up.  However, prolonged, rigorous exercise may also trigger the condition. Individuals with the disorder may have trouble releasing their grip on objects or may have difficulty rising from a sitting position and a stiff, awkward gait. Symptoms of myotonia are more frequently experienced in women during pregnancy.
Myotonia can affect all muscle groups, however the pattern of affected muscles can vary depending on the specific disorder involved. It may be acquired or inherited, and is caused by an abnormality in the muscle membrane. Specifically, the ion channels. Myotonia is a symptom commonly seen in patients with myotonic muscular dystrophy, of which two documented types and one speculated type exist, and in a group of disorders called channelopathies (hereditary diseases that are caused by mutations in the chloride, sodium or potassium ion transport channels in the muscle membrane), such as Myotonia Congenita (Congenital Myotonia) of which two types called Becker's Disease and Thomsen's Disease exist. There is also a disorder called Paramyotonia Congenita. Myotonia arising from channelopathies, and myotonic muscular dystrophy can be exacerbated by exposure to cold (and occasionally heat), by eating foods that are potassium-rich (such as bananas), with exertion, especially after long periods of inactivity, sudden surprises, and stressful situations.
Myotonia is not always a disease-related or abnormal phenomenon. Humans and other animals often display myotonia when placed in situations of extreme stress or fear; a resultant increase in 'fight-or-flight' hormones such as epinephrine and cortisol may cause increased muscle tension throughout the body.
People suffering from disorders involving myotonia can have a life threatening reaction to certain anaesthetics, one of these conditions occurs when the patient is under anaesthetic and is termed " Malignant Hyperthermia ". Anaesthetics cannot diagnose this condition until the patient is under anaesthetic so this condition is very life threatening.
Myxedema
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Synonyms and keywords: Myxoedema;

# Overview
Myxedema is a skin and tissue disorder usually due to severe prolonged hypothyroidism. Hypothyroidism can be caused by Hashimoto's thyroiditis, surgical removal of the thyroid, and rarer conditions. Partial forms of myxedema, especially of the lower legs (called pretibial myxedema), occasionally occur in adults with Graves' disease, a cause of hyperthyroidism; or also Hashimoto's thyroiditis without severe hypothyroidism.

# Pathophysiology
Myxedema stemming from both the hyperthyroid and hypothyroid conditions, results from the accumulation of increased amounts of hyaluronic acid and chondroitin sulfate in the dermis in both lesional and normal skin. The mechanism that causes myxedema is still not yet understood, although animal model studies suggest that thyroid hormones affect the synthesis and catabolism of mucopolysaccharides and collagen by dermal fibroblasts. The fibroblasts in the orbital and pretibial dermis share antigenic sites that underlie the autoimmune process that causes Grave's disease. This cross-reaction may contribute to the development of myxedema long after normal levels of thyroid hormones have been restored by treatment.

# Causes
- Hashimoto's thyroiditis
- Drug side effects:
- Potassium iodide

# Differentiating myxedema from other diseases
Myxedema must be differentiated from other causes of lower limb edema like chronic venous insufficiency, acute deep venous thrombosis, lipedema, lymphatic filariasis, cellulitis and causes of generalized edema.

# Diagnosis

## Symptoms
Myxedema usually presents itself with some of the following symptoms:
- Skin thickening
- Coarse skin
- Change in facial appearance
- Thickening nose
- Swollen lips
- Puffiness around the eyes
- Jelly-like infiltrations in subcutaneous tissues
- Slow speech
- Mental dullness
- Lethargy
- Mental problems
- Dry skin
- Yellow skin
- Swollen subcutaneous tissue
- Weight gain
- Constipation
- Thinning hair
- Brittle hair
- Bald patches
- Muscle pains
- Deafness
- Hearing impairment
- Carpal tunnel syndrome

# Treatment
Treatment for myxedema is difficult. Systemic or intralesional glucocorticoids, topical glucocorticoids under occlusion or high-dose intravenous immunoglobulin have been reported to offer some relief to patients.
Treatment should follow correction of the original hyperthyroidism/hypothyroidism.

# Related Chapters
- Cretinism - congenital hypothyroidism
NCLEX-PN
Assistant Editor-In-Chief: Michelle Lew

# Overview
The NCLEX-PN (National Council Licensure EXamination-Practical Nurse) is a computer-adaptive test of entry-level nursing competence. Passing the exam is required of candidates for licensure as a Licensed Practical Nurse (LPN) or Licensed Vocational Nurse (LVN) by all US state and territorial Boards of Nursing.
The NCLEX-RN and NCLEX-PN examinations are developed and owned by the National Council of State Boards of Nursing, Inc. (NCSBN). NCSBN administers these examinations on behalf of its member boards which consist of the boards of nursing in the 50 states, the District of Columbia, and four U.S. territories American Samoa, Guam, Northern Mariana Islands and the Virgin Islands.
To ensure public protection, each board of nursing requires a candidate for licensure to pass the appropriate NCLEX examination, NCLEX-RN for registered nurses and the NCLEX-PN for practical/vocational nurses. NCLEX examinations are designed to test the knowledge, skills and abilities essential to the safe and effective practice of nursing at the entry-level.
NCLEX examinations are provided in a computerized adaptive testing (CAT) format and are presently administered by Pearson VUE in their network of Pearson Professional Centers (PPC).
CAT is a method for administering tests that merges existing computer technology with modern measurement theory to increase the efficiency of the testing process. The NCLEX examination uses items with a variety of response formats, such as, single response multiple-choice, multiple response, fill-in-the-blank, drag and drop and a variety of display formats, such as, chart/exhibit displays, tables, and graphic images.
All items are developed and validated using the expertise of practicing nurses, educators and regulators from throughout the country. The content of the items of the NCLEX examinations is based on a practice analysis conducted every three years.

# Exam content
The majority of test items are written at the application or higher levels of cognition but the exam may include items at all of the cognitive levels.
The exam's content is based on client needs:
- Safe Effective Care Environment
Coordinated Care
Safety and Infection Control
- Coordinated Care
- Safety and Infection Control
- Health Promotion and Maintenance
- Psychosocial Integrity
- Physiological Integrity
Basic Care and Comfort
Pharmacological Therapies
Reduction of Risk Potential
Physiological Adaptation
- Basic Care and Comfort
- Pharmacological Therapies
- Reduction of Risk Potential
- Physiological Adaptation
NDUFA4L2
NADH dehydrogenase (ubiquinone) 1 alpha subcomplex, 4-like 2 is a protein that in humans is encoded by the NDUFA4L2 gene. The NDUFA4L2 protein is a subunit of NADH dehydrogenase (ubiquinone), which is located in the mitochondrial inner membrane and is the largest of the five complexes of the electron transport chain.

# Structure
The NDUFA4L2 gene is located on the long q arm of chromosome 12 at position 13.3 and it spans 5,860 base pairs. NDUFA4L2 is a subunit of the enzyme NADH dehydrogenase (ubiquinone), the largest of the respiratory complexes. The structure is L-shaped with a long, hydrophobic transmembrane domain and a hydrophilic domain for the peripheral arm that includes all the known redox centers and the NADH binding site. It has been noted that the N-terminal hydrophobic domain has the potential to be folded into an alpha helix spanning the inner mitochondrial membrane with a C-terminal hydrophilic domain interacting with globular subunits of Complex I. The highly conserved two-domain structure suggests that this feature is critical for the protein function and that the hydrophobic domain acts as an anchor for the NADH dehydrogenase (ubiquinone) complex at the inner mitochondrial membrane.

# Function
The human NDUFA4L2 gene codes for a subunit of Complex I of the respiratory chain, which transfers electrons from NADH to ubiquinone. Initially, NADH binds to Complex I and transfers two electrons to the isoalloxazine ring of the flavin mononucleotide (FMN) prosthetic arm to form FMNH2. The electrons are transferred through a series of iron-sulfur (Fe-S) clusters in the prosthetic arm and finally to coenzyme Q10 (CoQ), which is reduced to ubiquinol (CoQH2). The flow of electrons changes the redox state of the protein, resulting in a conformational change and pK shift of the ionizable side chain, which pumps four hydrogen ions out of the mitochondrial matrix.
Nadorite
Nadorite is a mineral with the chemical formula PbSb.
In the orthorhombic crystal system, Nadorite is brown, brownish-yellow or yellow in colour, with a white or yellowish-white streak.
With a Mohs hardness of 312 to 4, it has one perfect cleavage.
Nadorite is named after Djebel Nador in Algeria, where it was first identified in 1870. Djebel Nador and Djebel Debbar (both in the Constantine Province of Algeria) are its co-type localities.
Neem oil
Neem oil is a vegetable oil pressed from the fruits and seeds of Neem (Azadirachta indica), an evergreen tree which is endemic to the Indian sub-continent and has been introduced to many other areas in the tropics.
It is perhaps the most important of the commercially available products of neem.

# Characteristics
Neem oil is generally light to dark brown, bitter and has a rather strong odour that is said to combine the odours of peanut and garlic. It comprises mainly triglycerides and large amounts of triterpenoid compounds, which are responsible for the bitter taste. It is hydrophobic in nature and in order to emulsify it in water for application purposes, it must be formulated with appropriate surfactants.
Neem oil also contains steroids (campesterol, beta-sitosterol, stigmasterol) and a plethora of triterpenoids of which Azadirachtin is the most well known and studied. The Azadirachtin content of Neem Oil varies from 300ppm to over 2000ppm depending on the quality of the neem seeds crushed.

# Uses
Neem oil is not used for cooking purposes but, in India and Bangladesh, it is used for preparing cosmetics (soap, hair products, body hygiene creams, hand creams) and in Ayurvedic, Unani and folklore traditional medicine, in the treatment of a wide range of afflictions. The most frequently reported indications in ancient Ayurvedic writings are skin diseases, inflammations and fevers, and more recently rheumatic disorders, insect repellent and insecticide effects.
Traditional Ayurvedic uses of neem include the treatment of fever, leprosy, malaria, ophthalmia and tuberculosis. Various folk remedies for neem include use as an anthelmintic, antifeedant, antiseptic, diuretic, emmenagogue, contraceptive, febrifuge, parasiticide, pediculocide and insecticide. It has been used in traditional medicine for the treatment of tetanus, urticaria, eczema, scrofula and erysipelas. Traditional routes of administration of neem extracts included oral, vaginal and topical use. Neem oil has an extensive history of human use in India and surrounding regions for a variety of therapeutic purposes. Puri (1999) has given an account of traditional uses and therapeutic indications and pharmacological studies of this oil, in his book on neem.
Neoplasm

# Overview
Neoplasia (new growth in Greek) is the abnormal proliferation of cells, resulting in a neoplasm.   Neoplasia is the scientific term for the group of diseases commonly called tumor or cancer. 
Because neoplasia includes very different diseases, it is difficult to find a definition that describe them all. The definition of the British oncologist R.A. Willis is widely cited:
A neoplasm is an abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of the normal tissues, and persists in the same excessive manner after cessation of the stimulus which evoked the change.

# Types
A neoplasm can be benign, potentially malignant (pre-cancer) or malignant (cancer).  
- Benign neoplasms include uterine fibroids and melanocytic nevi (skin moles). They do not transform into cancer.
- Potentially malignant neoplasms include carcinoma in situ. They do not invade and destroy but, given enough time, will transform into a cancer.
- Malignant neoplasms are commonly called cancer. They invade and destroy the surrounding tissue,  may form metastases and eventually kill the host.

# Difficulty of definition
A precise and all-encompassing definition of neoplasm has proven elusive.  A neoplasm has been defined as an uncontrolled and progressive growth, although this definition is criticized because some neoplasms, such as nevi, are not progressive.
Some sources consider a neoplasm to be synonymous with a tumor or unusual mass of tissue.  This is criticized because many neoplasms form no mass, including cervical intraepithelial neoplasia, anal intraepithelial neoplasia, and leukemia.

# Biological properties of neoplastic cells
The structure of a neoplasm is less organized than that of the surrounding tissue.

## Clonality
Neoplastic tumors often contain more than one type of cell, but their initiation and continued growth is usually dependent on a single population of neoplastic cells. These cells are usually presumed to be clonal - that is, they are descended from a single progenitor cell.
The neoplastic cells typically bear common genetic or epigenetic abnormalities, an evidence of clonality. For some types of neoplasm, e.g. lymphoma and leukemia, the demonstration of clonality is now considered to be necessary (though not sufficient) to define a cellular proliferation as neoplastic.
Netrin 1
Netrin-1 is a protein that in humans is encoded by the NTN1 gene.
Netrin is included in a family of laminin-related secreted proteins.  The function of this gene has not yet been defined; however, netrin is thought to be involved in axon guidance and cell migration during development.  Mutations and loss of expression of netrin suggest that variation in netrin may be involved in cancer development.

# Interactions
NTN1 has been shown to interact with Deleted in Colorectal Cancer.