Persius/hicric huggingface dataset:
Papillary muscle

# Overview
In anatomy, the papillary muscles of the heart serve to limit the movements of the mitral and tricuspid valves. These muscles contract to tighten the chordae tendineae, which in turn prevent inversion. This occurs in response to pressure gradients. Instead they brace the valves against the high pressure, preventing regurgitation of ventricular blood back into the atrial cavities.
- Image courtesy of Hartwig, Walter C., The Editor of Fundamental Anatomy, 1st Edition, 2008 and copyrighted
- Image courtesy of Hartwig, Walter C., The Editor of Fundamental Anatomy, 1st Edition, 2008 and copyrighted

# Additional images
- Section of the heart showing the ventricular septum.
- Schematic representation of the atrioventricular bundle of His.
Mycotic aneurysm

# Overview
Mycotic aneurysm is an aneurysm that results from an infectious process that involves the arterial wall.  A person with a mycotic aneurysm has a bacterial infection in the wall of an artery, resulting in the formation of an aneurysm. The most common locations include arteries in the abdomen, thigh, neck, and arm. A mycotic aneurysm can result in sepsis, or life-threatening bleeding if the aneurysm ruptures. Less than 3% of abdominal aortic aneurysms are mycotic aneurysms.

# Historical Perspective
William Osler first used the term "mycotic aneurysm" in 1885 to describe a mushroom-shaped aneurysm in a patient with subacute bacterial endocarditis. This may create considerable confusion, since "mycotic" is typically used to define fungal infections. However, mycotic aneurysm is still used for all extracardiac or intracardiac aneurysms caused by infections, except for syphilitic aortitis.
The term "infected aneurysm," proposed by Jarrett and associates is more appropriate, since few infections involve fungi. According to some authors, a more accurate term might have been endovascular infection or infective vasculitis, because mycotic aneurysms are not due to a fungal organism.

# Causes

## Life Threatening Causes
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

## Common Causes
- Salmonella 
- Staphylococcus aureus 
- Staphylococcus epidermidis
- Streptococcus pneumoniae

## Causes by Organ System

## Causes in Alphabetical Order

# Natural History, Complications, and Prognosis
Mycotic aneurysms account for 2.6% of aortic aneurysms. For the clinician, early diagnosis is the cornerstone of effective treatment. Without medical or surgical management, catastrophic hemorrhage or uncontrolled sepsis may occur. However, symptomatology is frequently nonspecific during the early stages, so a high index of suspicion is required to make the diagnosis.
Intracranial mycotic aneurysms (ICMAs) complicate about 2% to 3% of infective endocarditis (IE) cases, although as many as 15% to 29% of patients with IE have neurologic symptoms.

# Diagnosis

## Imaging Studies

# Medical Therapy

## Antimicrobial Regimen
- Empiric antimicrobial therapy
- Preferred regimen: Vancomycin 15 mg/kg IV divided q12h (trough of 15-20 mcg/mL) for 6 weeks AND (Ceftriaxone 2 g IV q24h for 6 weeks OR Piperacillin-Tazobactam 3.375 g IV q6h for 6 weeks OR Ciprofloxacin 400 mg IV q12h for 6 weeks)
- Note: For critically ill patients, start with a vancomycin loading dose of 25 mg/kg.
N-myc-interactor
N-myc-interactor also known as N-myc and STAT interactor is a protein that in humans is encoded by the NMI gene.

# Function
NMYC interactor (NMI) interacts with NMYC and CMYC (two members of the oncogene Myc family), and other transcription factors containing a Zip, HLH, or HLH-Zip motif. The NMI protein also interacts with all STATs except STAT2 and augments STAT-mediated transcription in response to cytokines IL-2 and IFN-gamma. The NMI mRNA has low expression levels in all human fetal and adult tissues tested except brain and has high expression in cancer cell line-myeloid leukemias.

# Interactions
NMI (gene) has been shown to interact with BRCA1, IFI35, Myc, and STAT5A, and TUBA3C.
Neonatal malaria
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# Overview
Although malaria is still common in endemic regions, Neonatal Malaria remains very rare in both endemic as well non- endemic regions.

# Pathophysiology
The vertical transmission of malarial parasites mostly occurs at time of delivery.

# Epidemiology and Demographics
Malaria is still responsible for a significant burden of disease, estimated to cause more than 300,000 fetal and infant deaths and 2,500 deaths of pregnant women worldwide annually.

# Natural History, Complications and Prognosis
Malaria during pregnancy can result in premature labour, Intrauterine Growth Retardation, high perinatal mortality, anaemia, miscarriage, and low birth weight.
Nephronophthisis
Nephronophthisis is a genetic disorder of the kidneys which affects children. It is classified as a medullary cystic kidney disease.
The disorder is inherited in an autosomal recessive fashion and, although rare, is the most common genetic cause of childhood kidney failure.

# Symptoms
Infantile, juvenile, and adolescent forms of nephronophthisis have been identified. Although the range of characterizations is broad, patients typically present with polyuria (production of large volume of urine), polydipsia (excessive liquid intake), and mild proteinuria (the abnormal appearance of protein in the urine), and after several months to years, end-stage kidney disease, a condition necessitating either dialysis or a kidney transplant in order to survive.
Approximately 10% of individuals of with nephronophthisis also have so-called "extra-renal symptoms" which can include blindness, liver problems, mental retardation, and neurologic involvement in which the cerebellum is affected.

# Histology
Histologically, nephronophthisis is characterized by fibrosis and the formation of cysts in a specific region of the kidney.  In contrast to other cystic diseases of the kidney in which the kidneys are larger than usual, in nephronophthisis the kidneys are small to normal in size.

# Pathophysiology
From sequencing the DNA of individuals and families with nephronophthisis, scientists have identified thus far 8 different genes in which mutations can cause the disease.  These genes are called NPHP1, NPHP2, NPHP3, NPHP4, NPHP5, NPHP6, NPHP7, and NPHP8, and the proteins for which they encode are known as the nephrocystins.  Although the biological function of these proteins is not yet known, they all localize at least in part to an organelle in the cell called the primary cilia.

## Relation to other rare genetic disorders
Recent findings in genetic research have suggested that a large number of genetic disorders, both genetic syndromes and genetic diseases, that were not previously identified in the medical literature as related, may be, in fact, highly related in the genetypical root cause of the widely-varying, phenotypically-observed disorders.  Thus, Nephronophthisis is a ciliopathy.  Other known ciliopathies include primary ciliary dyskinesia, Bardet-Biedl syndrome, polycystic kidney and liver disease, Alstrom syndrome, Meckel-Gruber syndrome and some forms of retinal degeneration..
Vestibular nerve

# Overview
The vestibular nerve is one of the two branches of the Vestibulocochlear nerve (the cochlear nerve being the other). It goes to the semicircular canals via the vestibular ganglion. It receives positional information.
Axons of the vestibular nerve synapse in the vestibular nucleus on the lateral floor and wall of the fourth ventricle in the pons and medulla.
It arises from bipolar cells in the vestibular ganglion, ganglion of Scarpa, which is situated in the upper part of the outer end of the internal auditory meatus.

# Branches
The peripheral fibers divide into three branches:
- the superior branch passes through the foramina in the area vestibularis superior and ends in the utricle and in the ampullae of the superior and lateral semicircular ducts;
- the fibers of the inferior branch traverse the foramina in the area vestibularis inferior and end in the saccule;
- the posterior branch runs through the foramen singulare and supplies the ampulla of the posterior semicircular duct.
Nesidioblastosis

# Overview
Nesidioblastosis is a controversial medical term for hyperinsulinemic hypoglycemia attributed to excessive function of pancreatic beta cells with an abnormal microscopic appearance.

# Historical Perspective
The term was coined in the first half of the 20th century. The abnormal histologic aspects of the tissue included the presence of islet cell enlargement, islet cell dysplasia, beta cells budding from ductal epithelium, and islets in apposition to ducts.
By the 1970s, nesidioblastosis was primarily used to describe the pancreatic dysfunction associated with persistent congenital hyperinsulinism and in most cases from the 1970s until the 1970s, it was used as a synonym for what is now referred to as congenital hyperinsulinism. Most congenital hyperinsulinism is caused by different mechanisms than excessive proliferation of beta cells in a fetal pattern and the term fell into disfavor after it was recognized in the late 1980s that the characteristic tissue features were sometimes seen in pancreatic tissue from normal infants and even adults, and is not consistently associated with hyperinsulinemic hypoglycemia.
However, the term has been resurrected in recent years to describe a form of acquired hyperinsulinism with beta cell hyperplasia found in adults, especially after gastrointestinal surgery.

# Related Chapters
- Congenital hyperinsulinism
Neurogenic shock
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Ayan Sen, M.D, Henry Ford Hospital, Detroit MI, USA

# Overview
Neurogenic shock is shock caused by the sudden loss of the sympathetic nervous system signals to the smooth muscle in vessel walls. This can result from severe central nervous system (brain and spinal cord) damage. With the sudden loss of background sympathetic stimulation, the vessels suddenly relax resulting in a sudden decrease in peripheral vascular resistance and decreased blood pressure.

# Causes
- Spinal cord injury / Ischemia
- Regional Anesthesia
- Drugs
- Neurological Disorders

# History and Symptoms
The classic presentation of a patient in neurogenic shock is almost the opposite to that found in other shock states. In hypovolaemic shock the patient presents with cold, clammy, and pale or cyanotic peripheries. In neurogenic shock, the extremities may remain pink, warm and well perfused. Due to the loss of sympathetic function, he is unable to initiate the vasoconstriction required to divert blood to the central vital organs; and thus it pools in the peripheral vascular compartments.
Similarly, a hypovolaemic patient typically presents with tachycardia and hypotension; the increased heart rate represents an early and sustained attempt to support the failing circulation, and maintain central perfusion. In neurogenic shock, the cardiovascular system cannot stimulate compensatory changes in the same way; and thus the patient may present with a normal heart rate. As vital signs and physical assessment do not indicate shock, this factor may also mask other underlying causes of the shock state, such as hypovolemia.
Symptoms of neurogenic shock may include:
- Hypotension
- Bradycardia
- Warm, dry extremities
- Peripheral vasodilation
- Venous pooling
- Poikilothermia
- Priapism Due to PNS stimulation
- Decreased cardiac output (with cervical or high thoracic injury)

# Treatment

## Medical Therapy
- Large volumes of fluid may be needed to restore normal hemodynamics
- Vasopressors (Norepinephrine)
- Atropine (this vagolytic reduces vagal tone, increases heart rate and increases cardiac output)
Nezelof syndrome

# Overview
Nezelof syndrome (also known as "Thymic dysplasia with normal immunoglobulins":85) is an autosomal recessive congenital immunodeficiency condition due to underdevelopment of the thymus. An association with CD44 has been proposed.
The defect is a type of purine nucleoside phosphorylase deficiency with inactive phosphorylase. This results in an accumulation of deoxy-GTP which inhibits ribonucleotide reductase.  Ribonucleotide reductase catalyzes the formation of deoxyribonucleotides from ribonucleotides.  Thus, DNA replication is inhibited and cells cannot replicate.

# Historical Perspective
The disorder was characterized in 1964. It is considered to be a form of combined immunodeficiency in ICD-10 but a deficiency of cell-mediated immunity in ICD-9.

# Classification

# Pathophysiology

# Causes

# Differentiating Nezelof syndrome from Other Diseases

# Epidemiology and Demographics

# Risk Factors

# Screening

# Natural History, Complications, and Prognosis

## Natural History

## Complications

## Prognosis

# Diagnosis
It causes severe infections and malignancies. it is characterized by elevated immunoglobulins that function poorly.

## History and Symptoms

## Physical Examination

## Laboratory Findings

## Imaging Findings

## Other Diagnostic Studies

# Treatment

## Medical Therapy
Treatment includes antimicrobial therapy, IV immunoglobulin, bone marrow transplantation, thymus transplantation and thymus factors.

## Surgery

## Prevention
No-reflow case 1

# No-Reflow

## Pre-intervention
Shown below is a pre-intervention angiogram with occlusion in the proximal part of SVG (saphenous vein graft) to the RCA.

## Intervention
Shown below is an angiogram with ongoing intervention on the occlusion described above.

## Post-intervention
Shown below is a post-intervention angiogram with acute reduction in blood flow (TIMI flow grade 1) in the absence of dissection, thrombus, spasm, or high-grade residual stenosis in the SVG (saphenous vein graft) depicting no-reflow.
Shown below is a post-intervention angiogram with a complete restoration of blood flow (TIMI flow grade 3) after transient no-reflow as depicted above.
Nodule of vermis

# Overview
The nodule (nodular lobe), or anterior end of the inferior vermis, abuts against the roof of the fourth ventricle, and can only be distinctly seen after the cerebellum has been separated from the medulla oblongata and pons.
On either side of the nodule is a thin layer of white substance, named the posterior medullary velum.
It is semilunar in form, its convex border being continuous with the white substance of the cerebellum; it extends on either side as far as the flocculus.
Nuclear envelope

# Overview
The nuclear envelope (also known as the perinuclear envelope, nuclear membrane, nucleolemma or karyotheca) is the double membrane of the nucleus that encloses genetic material in eukaryotic cells. It separates the contents of the nucleus (DNA in particular) from the cytosol (cytoplasm).
Numerous nuclear pores are present on the nuclear envelope to facilitate and regulate the exchange of materials (for example, proteins and RNA) between the nucleus and the cytoplasm.
The space between the two membranes that make up the nuclear envelope is called the perinuclear space (also called the perinuclear cisterna), and is usually about 20 - 40 nm wide. Each of the two membranes is composed of a lipid bilayer.  The outer membrane is continuous with the rough endoplasmic reticulum.
The inner membrane is erected upon the nuclear lamina, a network of intermediate filaments made of lamin, that plays a role in mitosis and meiosis. The type of lamins present are A, B1, B2, and C.
The nuclear envelope may also play a role in the disposition of chromatin inside the nucleus. The lamina acts as a site of attachment for chromosomes. It also acts like a shield for the nucleus.

# Disintegration during mitosis in metazoans
During prophase in mitosis, the chromatids begin condensing to form chromosomes, and the nuclear envelope begins to disintegrate. During metaphase, the nuclear envelope is completely disintegrated, and the chromosomes can be pulled apart as chromatids by the spindle fibers.  Other eukaryotes such as yeast undergo closed mitosis, where the chromosomes segregate within the nuclear envelope, which then buds as the two daughter cells divide.
Nucleus ambiguus
The nucleus ambiguus (literally "ambiguous nucleus") is a region of histologically disparate cells located just dorsal (posterior) to the inferior olivary nucleus in the lateral portion of the upper (rostral) medulla.
This nucleus gives rise to the efferent motor fibers of the vagus nerve (CN X) terminating in the laryngeal and pharyngeal muscles, as well as to the efferent motor fibers of the glossopharyngeal nerve (CN IX) terminating in the stylopharyngeus.

# Areas supplied
The muscles supplied by the vagus (included with this is the cranial part of the accessory nerve), such as levator veli palatini, are also necessary to swallow properly through integration by the nucleus of the solitary tract. The vagus also supplies the upper part of the esophagus, and other parts of the pharynx and larynx.
As well as motor functions, nucleus ambiguus also contains the preganglionic neurons for the heart.

# Additional images
- Section of the medulla oblongata at about the middle of the olive.
- The cranial nerve nuclei schematically represented; dorsal view. Motor nuclei in red; sensory in blue.
- Nuclei of origin of cranial motor nerves schematically represented; lateral view.
- Primary terminal nuclei of the afferent (sensory) cranial nerves schematically represented; lateral view.
- The formatio reticularis of the medulla oblongata, shown by a transverse section passing through the middle of the olive.
Solitary nucleus
The solitary nucleus and tract are structures in the brainstem that carry and receive visceral sensation and taste from the facial (VII), glossopharyngeal (IX), vagus (X) cranial nerves, as well as the cranial part of the accessory nerve (XI).

# Anatomy
The nucleus is located along the length of the medulla (with a small portion in the lower pons). The solitary tract runs in the middle of the nucleus, creating a speck of white matter (axons of the tract), surrounded by grey matter (the nucleus). This stands out on a stained section, which is where the name solitary comes from.
The solitary nucleus is divided into a rostral (towards the top) gustatory nucleus and caudal (towards the bottom) cardiorespiratory nucleus. The cardiorespiratory nucleus can be further divided into a cardiovascular center, which sits at the midline of the nucleus, and a respiratory center, which is located laterally.

# Inputs to the solitary nucleus
In addition to afferent taste information from nerves VII, IX and X, the solitary nucleus also handles primary afferent signals from a variety of visceral regions and organs. These afferents include chemoreceptors in the carotid (via IX) and aortic bodies (via X) as well as stretch receptors from the aorta and carotid arteries called arterial baroreceptors. In addition, chemically and mechanically sensitive neurons with endings located in the heart, lungs, airways, gastrointestinal system, liver and other viscera send axons via cranial nerves (IX and X) chiefly that directly enter the brainstem to form synapses within the caudal third of the solitary nucleus. Neurons that synapse in this nucleus mediate the gag reflex, the carotid sinus reflex, the aortic reflex, the cough reflex, the baroreceptor and chemoreceptor reflexes, several respiratory reflexes and reflexes within the gastrointestinal system regulating motility and secretion. Information about the gut wall, as well as stretch of the lungs and dryness of mucous membranes, also synapses at the solitary nucleus. These first central neurons within the solitary nucleus can participate in autonomic reflexes that may be as simple as two central neurons with the second neuron being an efferent or motor neuron that projects back directly to the organ such as the heart forming some of the simplest reflex pathways in the brain.

# Outputs from the solitary nucleus
Most information goes from the solitary nucleus to the hypothalamus and cingulate gyrus, as well as to other nuclei in the brainstem (such as visceral motor or respiratory centers).

# Additional images
- Section of the medulla oblongata at about the middle of the olive.
- Nuclei of origin of cranial motor nerves schematically represented; lateral view.
- Primary terminal nuclei of the afferent (sensory) cranial nerves schematically represented; lateral view.
O-Acetylpsilocin
O-Acetylpsilocin or 4-acetoxy-N,N-dimethyltryptamine (4-AcO-DMT) is a psychedelic (hallucinogenic).  It is the acetylated form of the psychedelic mushroom alkaloid psilocin, and is a lower homologue of 4-Acetoxy-DET and 4-Acetoxy-DIPT. It may also be considered an analogue of psilocin and DMT, which are Schedule 1 Drugs under the Controlled Substances Act of the USA.

# History
O-Acetylpsilocin is a newer psychedelic with a limited history.

# Chemistry
O-Acetylpsilocin can be obtained by acetylation of psilocin under strongly acidic or under alkaline conditions.  It is a synthetic compound. O-Acetylpsilocin is more resistant than psilocin to oxidation under basic conditions due to its acetoxy group.

# Pharmacology
In the body 4-acetylpsilocin is evidently rapidly desacetylated to psilocin by acetylases and therefore has identical pharmacological properties to psilocin.

# Dosage
A dose of O-acetylpsilocin is 8 mg - 30 mg.  These are slightly lower than that of the free phenol, psilocin.  Some report very strong effects with 15 mg.  The duration of 4-acetylpsilocin is usually slightly longer than that of psilocin at about 4-7 hours.
Obesity overview

# Overview
Obesity  is a condition in which the natural energy reserve, stored in the fatty tissue of humans and other mammals, is increased to a point where it is associated with certain health conditions or increased mortality.
Although obesity is an individual clinical condition, it is increasingly viewed as a serious and growing public health problem: excessive body weight has been shown to predispose to various diseases, particularly cardiovascular diseases, diabetes  mellitus type 2, sleep apnea and osteoarthritis.
Obesity is characterized as a state of excess adipose mass with abnormal increase of fat on the subcutaneous connective tissue. Obesity is generally gauged by the Body Mass Index(BMI). A high BMI is associated with a higher risk for potentially lethal medical problems.

# Historical Perspective

# Classification

# Pathophysiology

# Causes

# Differentiating Obesity from other Diseases

# Epidemiology and Demographics

# Risk Factors

# Screening

# Natural History, Complications and Prognosis

# Diagnosis

## History and Symptoms

## Physical Examination

## Laboratory Findings
Blood tests may be done to look for thyroid or hormone problems that could lead to weight gain.

## Electrocardiogram

## Chest X Ray

## CT

## MRI

## Echocardiography or Ultrasound

## Other Imaging Findings

## Other Diagnostic Studies

# Treatment

## Surgery

## Medical Therapy

## Primary Prevention

## Secondary Prevention

## Cost-Effectiveness of Therapy

## Future or Investigational Therapies

# Case Studies

## Case #1