Persius/hicric huggingface dataset:
Health Reimbursement Account
Health Reimbursement Accounts, or Health Reimbursement Arrangements, (HRAs) are IRS-sanctioned arrangements that allow an employer, as agreed to in the HRA plan document, to reimburse for medical expenses paid by participating employees. HRAs reimburse only those items (copays, coinsurance, deductibles and services) agreed to by the employer which are not covered by the company's selected standard insurance plan (any health insurance plan, not only  high-deductible plans). These arrangements are described in IRS Section 105.
Qualified claims must be described in the HRA plan document at inception, i.e., before reimbursing employees for those medical expenses. Arrangements (medical services, dental services, co-pays, coinsurance, deductibles, participation) may vary from plan to plan, and an employer may have multiple plans in place, allowing much flexibility.
The employer is not required to prepay into a fund for reimbursements, instead, the employer reimburses employee claims as they occur. Reimbursements of qualified claims are tax-deductible for the employer.
Reimbursements claimed by the employee are tax free (not included in W2 earnings), provided they are tied to qualified health care expenses (as defined in Section 105). HRAs are initiated by the employer and serviced by a third-party administrator or plan service provider; the employee does not pay for the right to participate. The employer may provide in the HRA plan document that credit balances in an employee's HRA account can be rolled over from year to year like a savings account. The employer decides if the funds are rolled from year to year and how much rolls over (which can be either a flat amount or a percentage).
A frequent complaint regarding HRA arrangements is that they are extremely opaque in regards to their requirements. Rules pertaining to their reimbursements are perceived by member participants to be somewhat contradictory and/or even incoherent- leading some to lose contributions which are intended for healthcare but are learned (after the procedure or laboratory test) to be disallowed.
Complaints pertaining to HRA management are dealt with thru ERISA channels.
Very low density lipoprotein

# Overview

# Historical Perspective

# Classification

# Biochemistry

# Physiology

# Clinical Correlation

## High VLDL
Epidemiology and Demographics | Pathophysiology | Causes | Prognosis and Complications

## Low VLDL
Epidemiology and Demographics | Pathophysiology | Causes | Prognosis and Complications

# Treatment
Medical Therapy | Primary Prevention | Secondary Prevention | Landmark Trials | Future or Investigational Therapies
Holmes and Rahe stress scale
In 1967, psychiatrists Thomas Holmes and Richard Rahe examined the medical records of over 5,000 medical patients as a way to determine whether stressful life events might cause illnesses. Patients were asked to tally a list of 43 life events based on a relative score. A positive 0.1 correlation was found between their life events and their illnesses. Thus, the Social Readjustment Rating Scale (SRRS) or the Holmes and Rahe Stress Scale was born. However, this study can be perceived as unreliable since it asks participants to look back at their life events, making the data retrospective.

# Scale for Adults
To measure stress according to the Holmes and Rahe Stress Scale, the number of "Life Change Units" that apply to events in the past year of an individual's life are added and the final score will give a rough estimate of how stress affects health.
Score of 300+: At risk of illness.
Score of 150-299+: Risk of illness is moderate (reduced by 30% from the above risk).
Score 150-: Only have a slight risk of illness.

# Scale for minors
A modified scale has also been developed for non-adults.  Similar to the adult scale, stress points for life events in the past year are added and compared to the rough estimate of how stress affects health.
If you have kids, you've got stress in your life. And if your child has special needs, you likely have more than your share. Although stress can be protective, as in the 'fight or flight' response when threatened with immediate harm, or a positive response which spurs us to action, too much stress over a long period of time can have very negative effects on our emotions and on our health.
Although you might not be able to control the stressful events in your life, you do have control over your response to them and the effect that they have on your life. The negative effects of stress can be reduced by such things as getting enough rest, exercise, good nutrition, and taking some time for yourself.
Score of 300+: At risk of illness.
Score of 150-299+: Risk of illness is moderate. (reduced by || 30% from the above risk)
Score 150-: Slight risk of illness.

# Supporting Research
A study by Rahe (1970) was carried out to test the reliability of the stress scale as a predictor of illness. The scale was given to 2,500 US sailors and they were asked to rate scores of 'life events' over the previous six months. Over the next six months, detailed records were kept of the sailors' health.
There was a +0.118 correlation between stress scale scores and illness. This seemingly small correlation is significant and supports the hypothesis of a link between life events and illness.
Homeostatic model assessment
The homeostatic model assessment (HOMA) is a method used to quantify insulin resistance and Beta cell function. It was first described under the name HOMA by Matthews et al in 1985.

# Derivation
The HOMA authors used data from physiological studies to develop mathematical equations describing glucose regulation as a feedback loop
.  They published computer software that solves the equations, so that insulin resistance and beta-cell function can be estimated from fasting glucose and insulin levels.  They also published an equation (see below) that gave approximately the same answers as an early version of the computer software
However, the computer model has since been improved to better reflect human physiology and recalibrated to modern insulin assays, and the developers have written that they recommend the computer software be used wherever possible

# Notes
The HOMA model was originally designed as a special case of a more general model called HOMA-CIGMA 
The approximating equation for insulin resistance, in the early model, used
a fasting blood sample, and was derived by use of the insulin-glucose product, divided by a constant:
In this equation, one should use the constant 22.5 instead of 405 if the glucose is reported in mmol/L. This model correlated well with estimates using the euglycemic clamp method (r = 0.88).
The authors have tested HOMA extensively against other measures of insulin resistance (or its reciprocal, insulin sensitivity) and beta-cell function
Hospital rapid response team

# Overview
Hospital rapid response teams are "multidisciplinary team most frequently consisting of intensive care unit trained personnel who are available 24 hours per day, 7 days per week for evaluation of patients who develop signs or symptoms of severe clinical deterioration." A Medical emergency team includes a physician.

# Structure
Hospital rapid response teams have four components:
- The afferent limb identifies clinical deterioration in patients and triggers a response.
- The efferent limb "is the response, which includes both the personnel and the equipment brought to the patient."
- Patient safety and quality improvement constitute the third component, which monitors performance of the system and provides feedback.
- Administration and governance

## Afferent limb

## Efferent limb
The presence of a physician may not improve effectiveness.

# Effectiveness
The use of hospital rapid response teams may or may not be associated with reduced mortality according to meta-analyses. The only randomized controlled trial showed no benefit.
Vasquez Hurst Sotos syndrome
Synonyms and keywords: Hypogonadism - gynecomastia - X-linked intellectual deficit

# Overview
Vasquez-Hurst-Sotos syndrome is characterized by the association of X-linked intellectual deficit, hypogonadotropic hypogonadism, gynecomastia, facial dysmorphism, obesity, and short stature. 

# Pathophysiology

## Genetics
Transmission appears to be X-linked recessive.
This syndrome may belong to the group of X-linked intellectual deficit-hypotonic facies syndromes caused by mutations in the ATRX gene (Xq21.1).

# Epidemiology and Demographics
It has been described in five males from four generations of one family.
IMITREX injection overdosage

# Overdosage
No gross overdoses in clinical practice have been reported. Coronary vasospasm was observed after intravenous administration of IMITREX Injection . Overdoses would be expected from animal data (dogs at 0.1 g/kg, rats at 2 g/kg) to possibly cause convulsions, tremor, inactivity, erythema of the extremities, reduced respiratory rate, cyanosis, ataxia, mydriasis, injection site reactions (desquamation, hair loss, and scab formation), and paralysis.
The elimination half-life of sumatriptan is about 2 hours , and therefore monitoring of patients after overdose with IMITREX Injection should continue for at least 10 hours or while symptoms or signs persist.
It is unknown what effect hemodialysis or peritoneal dialysis has on the serum concentrations of sumatriptan.
Indirect pathway of movement
Indirect pathway of movement' describes the one of the pathways modulated by the striatum, the other being a direct pathway of movement.
In the indirect pathway, striatal neurons inhibit neurons in the globus pallidus externus, which in turn inhibit neurons in the subthalamic nucleus.  The direct and indirect pathways then converge at the level of the globus pallidus internus with the excitation of neurons in this region by subthalamic neurons.  Opposite of the direct pathway, globus pallidus internus neurons inhibit thalamic neurons that excite the premotor cortex.
The result of all these excitations and inhibitions is an inhibition of movement by the indirect pathway. This is why damage to the pathway, as in Parkinson's disease, causes an inability to switch to new, desired motor programs.
Inferior cerebellar peduncle

# Overview
The upper part of the posterior district of the medulla oblongata is occupied by the inferior peduncle, a thick rope-like strand situated between the lower part of the fourth ventricle and the roots of the glossopharyngeal and vagus nerves.
The inferior peduncles connect the medulla spinalis and medulla oblongata with the cerebellum, and are sometimes named the restiform bodies.

# Function
The inferior cerebellar peduncle carries many types of input and output fibers that are mainly concerned with integrating proprioceptive sensory input with motor vestibular functions such as balance and posture maintenance.
Proprioceptive information from the body is carried to the cerebellum via the posterior spinocerebellar tract.
This tract passes through the inferior cerebellar peduncle and synapses within the paleocerebellum.
Vestibular information projects onto the archicerebellum.
This peduncle also carries information directly from the Purkinje cells to the vestibular nuclei in the dorsal brainstem located at the junction between the pons and medulla.
Internal intercostal muscles

# Overview
The Intercostales interni (Internal intercostals) are eleven in number on either side. They commence anteriorly at the sternum, in the interspaces between the cartilages of the true ribs, and at the anterior extremities of the cartilages of the false ribs, and extend backward as far as the angles of the ribs, whence they are continued to the vertebral column by thin aponeuroses, the posterior intercostal membranes.
Each arises from the ridge on the inner surface of a rib, as well as from the corresponding costal cartilage, and is inserted into the upper border of the rib below.
Their fibers are also directed obliquely, but pass in a direction opposite to those of the Intercostales externi.

# Additional images
- A central rib of the left side. Inferior aspect.
- The Obliquus internus abdominis.
- Diagram of the course and branches of a typical intercostal nerve.
- Thoracic portion of the sympathetic trunk.
Interleukin 23 subunit alpha
Interleukin-23 subunit alpha is a protein that in humans is encoded by the IL23A gene.  IL-23 is produced by dendritic cells and macrophages.
Interleukin-23 is a heterodimeric cytokine composed of an IL-12p40 subunit that is shared with IL-12 and the IL-23p19 subunit. A functional receptor for IL-23 (the IL-23 receptor) has been identified and is composed of IL-12R 1 and IL-23R.

# Function
IL-23 is an important part of the inflammatory response against infection. It promotes upregulation of the matrix metalloprotease MMP9, increases angiogenesis and reduces CD8+ T-cell infiltration into tumours. IL-23 mediates its effects on both innate and adaptive arms of the immune system that express the IL-23 receptor. Th17 cells represent the most prominent T cell subset that responds to IL-23, although IL-23 has been implicated in inhibiting the development of regulatory T cell development in the intestine. Th17 cells produce IL-17, a proinflammatory cytokine that enhances T cell priming and stimulates the production of other proinflammatory molecules such as IL-1, IL-6, TNF-alpha, NOS-2, and chemokines resulting in inflammation.
The expression of IL23A is decreased after AHR knockdown in THP-1 cells and primary mouse macrophages.

# Clinical significance
Knockout mice deficient in either p40 or p19, or in either subunit of the IL-23 receptor (IL-23R and IL12R-1) develop less severe symptoms of experimental autoimmune encephalomyelitis (EAE) and inflammatory bowel disease highlighting the importance of IL-23 in the inflammatory pathway.

# Discovery
A computational search for IL-12 homologue genes found p19, a gene that encodes a cytokine chain. Experimental work revealed that p19 formed a heterodimer by binding to p40, a subunit of IL-12. This new heterodimer was named IL-23.
Knockdown of AHR decreases the expression of IL23A in THP-1 cells and primary macrophage.
Interleukin 8 receptor, beta
Interleukin 8 receptor, beta  is a chemokine receptor. IL8RB is also known as CXCR2, and CXCR2 is now the IUPHAR Committee on Receptor Nomenclature and Drug classification-recommended name.

# Function
The protein encoded by this gene is a member of the G-protein-coupled receptor family. This protein is a receptor for interleukin 8 (IL8). It binds to IL8 with high affinity, and transduces the signal through a G-protein-activated second messenger system (Gi/o-coupled). This receptor also binds to chemokine (C-X-C motif) ligand 1 (CXCL1/MGSA), a protein with melanoma growth stimulating activity, and has been shown to be a major component required for serum-dependent melanoma cell growth. In addition, it binds ligands CXCL2, CXCL3, and CXCL5.
The angiogenic effects of IL8 in intestinal microvascular endothelial cells are found to be mediated by this receptor. Knockout studies in mice suggested that this receptor controls the positioning of oligodendrocyte precursors in developing spinal cord by arresting their migration. This gene, IL8RA, a gene encoding another high affinity IL8 receptor, and IL8RBP, a pseudogene of IL8RB, form a gene cluster in a region mapped to chromosome 2q33-q36.
Mutations in CXCR2 cause                 hematological traits            .

# Senescence
Knock-down studies involving the chemokine receptor CXCR2 alleviates both replicative and oncogene-induced senescence (OIS) and diminishes the DNA-damage response. Also, ectopic expression of CXCR2 results in premature senescence via a p53-dependent mechanism.
Internuclear ophthalmoplegia
Internuclear ophthalmoplegia or INO is a physical finding, or sign, that is a particular form of eye muscle weakness or ophthalmoparesis.  It can affect either the right or left eye.  It is a disorder of conjugate lateral gaze.  The affected eye shows impairment of adduction.  The partner eye diverges from the affected eye during abduction, producing horizontal diplopia, in other words, if the affected eye is on the right, the patient will see "double" when looking to the left and the images will be side by side. During extreme abduction, compensatory nystagmus can be seen in the partner eye.

# Causes
The disorder is caused by injury or dysfunction in the medial longitudinal fasciculus (MLF), a heavily-myelinated tract that allows conjugate eye movement by connecting the paramedian pontine reticular formation (PPRF) -abducens nucleus complex of one side to the oculomotor nucleus of the opposite side.
In young patients with bilateral INO, multiple sclerosis is nearly always the cause. In older patients with one-sided lesions a stroke is a distinct possibility.
- Vestibulo-ocular reflex

# Variants
A rostral lesion within the midbrain may affect the convergence center thus causing bilateral divergence of the eyes which is known as the WEBINO syndrome ( Wall Eyed Bilateral INO) as each eye looks at the opposite "wall".
If the lesion affects the PPRF and the MLF on the same side (the MLF having crossed from the opposite side) then the "one and a half syndrome" occurs which, simply put, involves paralysis of all conjugate horizontal  eye movements other than abduction of the eye on the opposite side to the lesion.
Intramembranous ossification

# Overview
Intramembranous ossification is one of two types of bone formation and is the process responsible for the development of flat bones, especially those found in the skull and clavicles. Unlike endochondral ossification, cartilage is not involved or present in this process.

# Overview
The first step in the process is the formation of bone spicules which eventually fuse with each other and become trabeculae. The periosteum is formed and bone growth continues at the surface of trabeculae. Much like spicules, the increasing growth of trabeculae result in interconnection and this network is called woven bone. Eventually, woven bone is replaced by lamellar bone.
Process Overview
- Mesenchyme cell in the membrane become osteochondral progenitor cell
- osteochondral progenitor cell specialized to become osteoblast
- Osteoblast produce bone matrix and surrounded collagen fiber and become osteocyte
- As the result process trabeculae will develop
- Osteoblast will trap trabeculae to produce bone
- Trabeculae will join together to produce spongy cell
- Cells in the spongy cell will specialize to produce red bone marrow
- Cells surrounding the developing bone will produce periosteum
- Osteoblasts from the Periosteum on the bone matrix will produce compact bone

# Formation of bone spicules
Embryologic mesenchymal cells (MSC) condense into layers of vascularized primitive connective tissue. Certain  mesenchymal cells group together, usually near or around blood vessels, and differentiate into osteogenic cells which deposit bone matrix constitutively. These aggregates of bony matrix are called bone spicules. Separate mesenchymal cells differentiate into osteoblasts, which line up along the surface of the spicule and secrete more osteoid, which increases the size of the spicule.

# Formation of woven bone
As the spicules continue to grow, they fuse with adjacent spicules and this results in the formation of trabeculae. When osteoblasts become trapped in the matrix they secrete, they differentiate into osteocytes. Osteoblasts continue to line up on the surface which increases the size. As growth continues, trabeculae become interconnected and woven bone is formed. The term primary spongiosa is also used to refer to the initial trabecular network.

# Primary centre of ossification
The periosteum is formed around the trabeculae by differentiating mesenchymal cells. The primary centre of ossification is the area where bone growth occurs between the periosteum and the bone. Osteogenic cells that originate from the periosteum increase appositional growth and a bone collar is formed. The bone collar is eventually mineralized and lamellar bone is formed.

# Formation of osteon
Osteons are units or principal structures of compact bone. During the formation of bone spicules, cytoplasmic processes from osteoblasts interconnect. This becomes the canaliculi of osteons. Since bone spicules tend to form around blood vessels, the perivascular space is greatly reduced as the bone continues to grow. When replacement to compact bone occurs, this blood vessel becomes the central canal of the osteon.
Intraventricular hemorrhages
Intraventricular hemorrhage (or "IVH") is a bleeding of the ventricles, where the cerebrospinal fluid is produced and circulates through towards the subarachnoid space.

# In infants
This type of hemorrhage is particularly common in infants, especially premature infants or those of very low birth weight.  The cause of IVH in premature infants, unlike that in older infants, children or adults, is rarely due to trauma.  Instead it is thought to result from changes in perfusion of the delicate cellular structures that are present in the growing brain.  The lack of blood flow results in cell death and subsequent breakdown of the blood vessel walls, leading to bleeding.  While this bleeding can result in further injury, it is itself a marker for injury that has already occurred.  Most intraventricular hemorrhages occur in the first 72 hours after birth.
Images courtesy of Professor Peter Anderson DVM PhD and published with permission  PEIR, University of Alabama at Birmingham, Department of Pathology
- Brain: Intraventricular Hemorrhage In Newborn: Gross natural color separated cerebral hemispheres with removed septum pellucidum showing ventricle filled with blood
- Brain: Intraventricular Hemorrhage: Gross natural color blood filled basilar leptomeninges characteristic of external brain appearance with intraventricular hemorrhage

# In adults
Intraventricular hemorrhage is rare in adults and requires a great deal of force to cause.  Thus the hemorrhage usually does not occur without an extensive associated damage, and so the outcome is rarely good.

# Associated conditions
Brain contusions and subarachnoid hemorrhages are commonly associated with IVH.  The bleeding can involve the middle communicating artery or the posterior communicating artery.
In both adults and infants, IVH can cause dangerous increases in intracranial pressure, damage to the brain tissue, and hydrocephalus.
Kentucky School for the Deaf
The school's creation was that of General Elias Barbee, whose daughter, Lucy, was deaf. Barbee introduced a bill to the Kentucky Assembly, placing it in Danville in the hands of the Centre College Board of Trustees. John Adamson Jacobs became principal of KSD in 1825. The school has since had 14 superintendents, and today is directed by Dr. Harvey Jay Corson.
Jacobs Hall, the oldest surviving building on campus, is listed as a National Historic Landmark.

# Athletics
The team nickname is the Colonels
They have found moderate success at best. They have won at least one high school 8 man football championship.