Persius/hicric huggingface dataset:
Nucleoside triphosphate
Nucleoside triphosphate (NTP) is a nucleotide with three phosphates. Natural nucleoside triphosphates include adenosine triphosphate (ATP), guanosine triphosphate (GTP), cytidine triphosphate (CTP), thymidine triphosphate (TTP) and uridine triphosphate (UTP). These terms refer to those nucleotide triphosphates that contain ribose. The nucleotide triphosphates containing deoxyribose take prefix deoxy- in their names and small d- in their abbreviations: deoxyadenosine triphosphate (dATP), deoxyguanosine triphosphate (dGTP), deoxycytidine triphosphate (dCTP), deoxythimidine triphosphate (dTTP) and deoxyuridine triphosphate. Check the entry nucleotide for table and description of these compounds.
Apart from (d)ATP, (d)GTP, (d)CTP, (d)TTP and (d)UTP, there are other less abundant NTPs, such as intermediates of nucleotide metabolism, but also "rare" natural nucleotides or even artificial nucleotides.
Nucleotide derivatives are of unparalleled importance for current natural life forms, as they are building blocks of nucleic acids and have thousands of other roles in cell metabolism and regulation. ATP is a major source of cellular energy. GTP is a very frequent cofactor of enzymes and proteins. NTPs generally provide energy and phosphate group for phosphorylations.
Generally nucleosides are nucleotides (e.g. adenine, guanine, cytosine...) that lack phosphates. However, for the sake of technical terminology, nucleotides are given classifications as nucleosides with a suffix describing the number of phosphates present in a specific unit. For example, if a nucleotide has one phosphate, it is a nucleoside monophosphate (NMP). If the nucleotide has two phosphates, then it is called a nucleoside diphosphate (NDP), and for three, it is a nucleoside triphosphate (NTP). The nucleotides that contain a ribose sugar are the monomers of RNA and those that contain a deoxyribose sugar compose DNA.
NTPs, NDPs and NMPs are ubiquitous in cell cytoplasm, nucleus and organelles. Given their multifarious functions, their levels are under fairly tight metabolic control. Most of the discussion on mutual ratios of nucleotides should belong under entry nucleotide, but concentrating strictly on the abundance of the triphosphorylated versions, we find that ATP spending is replenished by oxidative phosphorylation, while phosphorylation status of other nucleotides is regulated by NDP kinases (EC 2.7.4.6) and NMP kinases (EC 2.7.4.9) that use ATP pool as their cross-phosphorylation source.
de:Nukleosidtriphosphate
it:Nucleoside trifosfato
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Superior oblique muscle
For the abdominal muscle see: External oblique muscle

# Overview
The superior oblique muscle, or obliquus oculi superior, is a fusiform muscle in the upper, medial side of the orbit whose primary action is intorsion and whose secondary actions are to abduct (laterally rotate) and depress the eyeball (i.e. it makes the eye move outward and downward). One of the extraocular muscles, the superior oblique is the only muscle innervated by the trochlear nerve.
The primary action of the superior oblique muscle is intorsion; the secondary action is depression (primarily in the adducted position); the tertiary action is abduction.  A brief survey of neurology and physiology texts and websites reveals much confusion about the role of the superior oblique muscle, with many sources claiming that its role is to move the eye towards the nose.  In fact, because of its positioning, it is able to rotate the eye away from the nose so that when the eye is already adducted (looking directly "inwards") its rotational action turns the pupil downwards to look towards the mouth, which many texts misinterpret as its primary action.
Usually the eye muscles do not work alone, which leads to the confusion of the primary actions.  The superior oblique intorts, depresses, abducts the eye if it were to work by itself.  Normally, the superior oblique, in conjunction with the medial rectus, causes the eye to ADduct.
The origin for the superior oblique is the annulus of Zinn at the orbital apex. It loops through a pulley like structure (the trochlea of superior oblique) and inserts on the posterotemporal surface of the eyeball.
It arises immediately above the margin of the optic foramen, above and medial to the origin of the superior rectus, and, passing forward, ends in a rounded tendon, which plays in a fibrocartilaginous ring or pulley attached to the trochlear fovea of the frontal bone.
The contiguous surfaces of the tendon and ring are lined by a delicate mucous sheath, and enclosed in a thin fibrous investment.
The tendon is reflected backward, lateralward, and downward beneath the superior rectus to the lateral part of the bulb of the eye, and is inserted onto the scleral surface, behind the equator of the eyeball, the insertion of the muscle lying between the superior rectus and Rectus lateralis.

# Clinical significance
Superior oblique palsy is a common complication of closed head trauma.   Restriction of superior oblique movement is found in Brown syndrome, leading to difficulty elevating the eye in the adducted position.
Superior oblique myokymia is an uncommon neurological condition caused by vascular compression of the trochlear nerve resulting in repeated, brief, involuntary episodes of movement of the eye.
Operations of the superior oblique include tenotomy, recession, silicone expander lengthening, split tendon lengthening, tucking, and the Harada-Ito procedure.

# Additional images
- Nerves of the orbit. Seen from above.
- Dissection showing origins of right ocular muscles, and nerves entering by the superior orbital fissure.
Ocular dominance column

# Overview
Ocular dominance columns are regions of neurons in the striate cortex that synapse with axons carrying transduced signals from either the left or right eye. The columns span multiple cortical layers, producing a striped pattern when the deeper levels are stained.
Prior to birth, monocular transduction pathways are already established through a process known as fire together, wire together. Spontaneous retinal activity in one eye of the developing fetus leads to neuronal depolarization. Synapses that receive multiple inputs are more likely to propagate the signal, whereas errant connections will not be sufficient to trigger another action potential. Post-synaptic neurons that depolarize become permeable to calcium ions, if glutamate has been released by the pre-synaptic axon terminal. Calciums entry leads to a chemical process that strengthens the synapse, making it more likely to survive than other connections.
In a normally-developed visual system, the area of dominance columns for both eyes is the same, and each cortical cell responds to visual input according to its column. Monocular deprivation during early life prevents this balance from developing, and the non-deprived eye assumes control of nearly all cortical cells. These effects were identified by Torsten Wiesel and David Hubel, neuroscientists at Harvard Medical School, through studies on cats.
Odorant-binding protein
Odorant-binding proteins are abundant small soluble proteins secreted in the nasal mucus of many animal species and in the sensillar lymph of chemosensory sensilla of insects.
The olfactory receptors of terrestrial animals exist in an aqueous environment, yet detect odorants that are primarily hydrophobic. The aqueous solubility of hydrophobic odorants is greatly enhanced via odorant-binding proteins, which exist in the extracellular fluid surrounding the odorant receptors. This family is composed of pheromone binding proteins (PBP), which are male-specific and associate with pheromone-sensitive neurons and general-odorant-binding proteins (GOBP).
These proteins were initially identified on the basis of their ability to bind with moderate-affinity radioactively labeled odorants.
One and a half syndrome
The one and a half syndrome is a rare cause of ophthalmoparesis characterized by "a conjugate horizontal gaze palsy in one direction and an internuclear ophthalmoplegia in the other".  The most common manifestation of this unusual syndrome is limitation of horizontal eye movement to abduction of one eye with no horizontal movement of the other eye. Convergence is classically spared as Cranial Nerve III (oculomotor nerve) and its nucleus is spared bilaterally.

# Anatomy
The syndrome usually results from a single unilateral lesion of the paramedian pontine reticular formation which also involves the ipsilateral medial longitudinal fasciculus.  An alternative anatomical cause is a lesion of the abducens nucleus on one side, with interruption of the ipsilateral medial longitudinal fasciculus after it has crossed the midline from its site of origin in the contralateral abducens nucleus (resulting in a failure of adduction of the ipsilateral eye).

# Causes
Causes of the one and a half syndrome include pontine hemorrhage, ischemia, tumors, infective mass lesions such as tuberculomas, and demyelinating conditions like multiple sclerosis.

# Treatment
There have been cases of improvement in extra-ocular movement with botulinum toxin injection.
Ornithogalum umbellatum
Ornithogalum umbellatum (Star-of-Bethlehem), is a perennial bulbous flowering plant of the family Hyacinthaceae. It is native throughout most of southern and central Europe (north to Austria and Belgium), and in northwestern Africa and southwestern Asia.

# Description
This plant is perennial with bulbs below ground; the bulb is 15-25 mm long and 18-32 mm diameter. It has six to ten leaves, linear with a white line on upper surface, up to 30 cm long and 8 mm broad, and a scape of 10-30 cm. The flowers group in a corymbose raceme with 6-20 flowers, and are white with a green stripe outside.

# Cultivation
O. umbellatum require a lot of moisture during winter & spring, but tolerate summer droughtiness. It can be grown in the woodland garden. Semi-shade is preferable. It is hardy to hardiness zone 5, and can become weedy. The plant is toxic. Used in some herbal remedies.
Other red cell antigens
In addition to the defined Human blood group systems, there are erythrocyte antigens which do not meet the definition of a blood group system.  Most of these are either nearly universal in human blood or extremely rare and are rarely significant in a clinical setting.  Reagents to test for these antigens are difficult to find and many cannot be purchased commercially.

# Blood Group Collections
These three groups are antigens with shared characteristics but do not meet the ISBT definition of a human blood group system.  Further research may identify them as blood group systems.

## Cost
The Knops blood group system was formerly part of this collection.  All that remains are the Csa and Csb antigens.  Csa is a very high frequency (>98%) antigen and Csb is not uncommon (~34%).

## Er
The Er collection includes one high incidence (>99%) antigen, Era and one (<1%) rare antigen, Erb.

## Vel
The Vel collection includes the high incidence Vel and ABTI antigens.  Antibodies to Vel have been implicated in transfusion reactions.

# Other high-incidence antigens
These antigens are almost universally present on human red cells, but their absence has been noted in some individuals and some have been associated with transfusion reactions or other problems. Finding compatible units for transfusion to a patient that lacks one of these antigens is a major challenge and some countries maintain rare donor registries specifically for that purpose.
- Lan antigen: anti-Lan is IgG and has been associated with transfusion reactions. A weaker variant of the antigen has also been reported.
- Ata Antigen: only found in people of African descent. Associated with hemolytic transfusion reactions but not hemolytic disease of the newborn.
- Jra Antigen: mostly found in Japan. Not associated with acute transfusion reactions.
- AnWj Antigen: the receptor for Haemophilus influenzae. Implicated in severe hemolytic transfusion reactions.
- Sda Antigen: This antigen is present on cells other than red cells and is less frequent but still very common. It may be associated with transfusion reactions, but not hemolytic disease of the newborn.

# Other low incidence antigens
These antigens are extremely rare and are of little concern in selecting compatible units for transfusion.  They may be implicated in rare cases of hemolytic disease of the newborn, however.
- Batty (By)
- Biles (Bi)
- Box (Bxa)
- Christiansen (Chra)
- HJK
- HOFM
- JFV
- JONES
- Jensen (Jea)
- Katagiri (Kg)
- Livesay (Lia)
- Milne
- Oldeide (Ola)
- Peters (Pta)
- Rasmussen (RASM)
- Reid (Rea)
- REIT
- SARA
- Torkildsen (Toa)
- Bg (Bennett-Goodspeed): These are actually Human Leukocyte Antigens that cause confusing results on serological tests of erythrocytes.
Otitis interna overview

# Overview
Otitis interna is an inflammation of the inner ear and is usually considered synonymous with labyrinthitis.

# Causes
The cause of otitis interna is rarely identified, but it is thought most commonly to be derived from a viral inflammation of the vestibular labyrinth (the part of the inner ear responsible for balance).

# Diagnosis

## History and Symptoms
Labyrinthitis is an inflammation of the inner ear that typically results in severe vertigo lasting for one or more days. Patients usually present with the sudden onset of severe whirling vertigo, nausea and vomiting.

# Treatment

## Medical Therapy
The symptoms can be so severe and disabling that patients frequently go to the emergency room for care and require vestibular suppressants such as valium or meclizine in order to tolerate the vertigo. Symptoms typically subside over a few days, but may leave the patient with vague imbalance which slowly improves over weeks to months. Hearing loss rarely accompanies the vertigo in labyrinthitis. Occasionally a bacterial infection of the middle ear can spread to the inner ear and cause this disease. In this situation antibiotic treatment may be helpful.
Outcome measures in SMA
There is currently no cure for spinal muscular atrophy.  There has been great interest in identifying agents that can increase the amount of full- length SMN protein by upregulating expression of the SMN2 gene. Many clinical trials are ongoing to find the most reliable outcome measures.
Several new outcome measures have shown encouraging results and helped in designing future clinical trials. Some of them currently used in clinical trials are as follows 
- Quantitative muscle ultrasound
- The Six-Minute Walk Test (6MWT)  In case of ambulatory SMA patients.
- 10 minute walk/run test
- The Hammersmith Motor Scale
- The Hammersmith Functional Motor Scale Expanded (HFMSE)
- Knee flexor strength test
- The Children's Hospital of Philadelphia Infant Test of Neuromuscular Disorders (CHOP INTEND)
- The Gross Motor Function Measurement
- Motor unit number estimation (MUNE)
- Compound motor action potential (CMAP) amplitude
- Serologic biomarkers (SMN mRNA and protein levels)
Oxiconazole description

# Description
OXISTAT (oxiconazole nitrate) Cream, 1% and OXISTAT (oxiconazole nitrate) Lotion, 1% formulations contain the antifungal active compound oxiconazole nitrate. Both formulations are for topical dermatologic use only.
Chemically, oxiconazole nitrate is 2',4'-dichloro-2-imidazol-1-ylacetophenone (Z)-, mononitrate. The compound has the molecular formula C18H13ON3CI4HNO3, a molecular weight of 492.15, and the following structural formula:
Oxiconazole nitrate is a nearly white crystalline powder, soluble in methanol; sparingly soluble in ethanol, chloroform, and acetone; and very slightly soluble in water.
OXISTAT Cream contains 10 mg of oxiconazole per gram of cream in a white to off-white, opaque cream base of purified water USP, white petrolatum USP, stearyl alcohol NF, propylene glycol USP, polysorbate 60 NF, cetyl alcohol NF, and benzoic acid USP 0.2% as a preservative.
OXISTAT Lotion contains 10 mg of oxiconazole per gram of lotion in a white to off-white, opaque lotion base of purified water USP, white petrolatum USP, stearyl alcohol NF, propylene glycol USP, polysorbate 60 NF, cetyl alcohol NF, and benzoic acid USP 0.2% as a preservative.
Pulmonary gas pressures

# Overview
Following is a list of average partial pressures (in torr) for a human at rest:

# Factors affecting alveolar gas pressures
The alveolar oxygen pressure is lower than the atmospheric O2 partial pressure for two reasons.
- Firstly, as the air enters the lungs, it is humidified by the upper airway and thus the partial pressure of water vapour (47 mmHg) reduces the oxygen partial pressure to about 150 mmHg.
- The rest of the difference is due to the continual uptake of oxygen by the pulmonary capillaries, and the continual diffusion of CO2 out of the capillaries into the alveoli.
The factors that determine the values for alveolar PO2 and PCO2 are:
- The pressure of outside air
- The partial pressures of inspired oxygen and carbon dioxide
- The rates of total body oxygen consumption and carbon dioxide production
- The rates of alveolar ventilation and perfusion
The alveolar pO2 is not routinely measured but is calculated from blood gas measurements by the Alveolar gas equation.

# Pathology
Hypoventilation exists when the ratio of carbon dioxide production to alveolar ventilation increases above normal values.
Hyperventilation exists when the same ratio decreases.

# Related chapters
- Pulmonary alveolus
- A-a gradient
Palivizumab description

# Description
Palivizumab is a humanized monoclonal antibody (IgG1) produced by recombinant DNA technology, directed to an epitope in the A antigenic site of the F protein of RSV. Palivizumab is a composite of human (95%) and murine (5%) antibody sequences. The human heavy chain sequence was derived from the constant domains of human IgG1 and the variable framework regions of the VH genes Cor and Cess. The human light chain sequence was derived from the constant domain of C and the variable framework regions of the VL gene K104 with J -4. The murine sequences were derived from a murine monoclonal antibody, Mab 1129, in a process that involved the grafting of the murine complementarity determining regions into the human antibody frameworks. Palivizumab is composed of two heavy chains and two light chains and has a molecular weight of approximately 148,000 Daltons.
Synagis is supplied as a sterile, preservative-free liquid solution at 100 mg per mL to be administered by intramuscular injection. Thimerosal or other mercury-containing salts are not used in the production of Synagis. The solution has a pH of 6.0 and should appear clear or slightly opalescent.
Each 100 mg single-dose vial of Synagis liquid solution contains 100 mg of palivizumab and also contains chloride (0.5 mg), glycine (0.1 mg), and histidine (3.9 mg), in a volume of 1 mL.
Each 50 mg single-dose vial of Synagis liquid solution contains 50 mg of palivizumab and also contains chloride (0.2 mg), glycine (0.06 mg), and histidine (1.9 mg), in a volume of 0.5 mL.
Paroxysmal AV Block MRI

# Overview
MRI can be helpful in diagnosing infiltrative processes, including sarcoidosis, hemochromatosis, and amyloidosis.

# MRI

## 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay
- Cardiac MRI and computed tomography are particularly helpful in the diagnosis of infiltrative disorders (such as sarcoidosis and amyloidosis) that present with AV block.
Patellar tendon rupture
Patellar tendon rupture is an injury occurring in the knee.
The patellar tendon attaches to the tibial tubercle on the front of the tibia just below the front of the knee, and is connected to the bottom of the patella, above which are attached to the quadriceps tendon, followed by the quadriceps muscle, large muscles on the front of the thigh. This structure allows the knee to flex and extend, allowing use of basic functions such as walking, running, etc.

# Diagnosis
When rupture occurs, the patella loses support from the tibia and moves toward the hip when the quadriceps muscle contract, hindering the leg's ability to extend. This means that those affected cannot stand, as their knee buckles and gives way when they attempt to.
Through X-Ray scans, Patellar Tendon Rupture is diagnosed by recognizing that the patella has moved upward along the thigh.
(Images courtesy of RadsWiki)
- MRI: Patellar tendon rupture
- MRI: Patellar tendon rupture
- MRI: Patellar tendon rupture
- MRI: Patellar tendon rupture
- MRI: Patellar tendon rupture
- MRI: Patellar tendon rupture

# Treatment
Patellar tendon rupture must be treated through surgery.

## Surgery
An incision is made in the skin over the rupture, the site of which is identified. The tendons are retracted so surgeons may inspect the femur. The tendon ends are then sewn together.
A cast or brace is then put over where the operation took place. The cast or brace remains for at least 6 weeks followed by an unidentified time of rehabilitation of the knee.

## Side Effects
The usual risks of surgery are involved including: infection, stiffness, suture reaction, failure of satisfactory healing, risks of anesthesia, phlebitis, pulmonary embolus, and persistent pain or weakness after the injury and repair.

# Complications

## Patella alta
(Images courtesy of RadsWiki)
- X-ray: Patella alta secondary to patellar tendon rupture
- X-ray: Patella alta secondary to patellar tendon rupture
- MRI: Patella alta secondary to patellar tendon rupture
- MRI: Patella alta secondary to patellar tendon rupture
Pediatric endocrinology
Pediatric endocrinology (British: Paediatric)  is a medical subspecialty dealing with variations of physical growth and sexual development in childhood, as well as diabetes and other disorders of the endocrine glands.
By age, pediatric endocrinologists care for patients from infancy to late adolescence.
By disease, the most common disease of the specialty is type 1 diabetes, which usually accounts for at least 50% of a typical clinical practice. The next most common problem is growth disorders, especially those amenable to growth hormone treatment. Pediatric endocrinologists are usually the primary physicians involved in the medical care of infants and children with intersex disorders. The specialty also deals with hypoglycemia and other forms of hyperglycemia in childhood, variations of puberty, as well other adrenal, thyroid, and pituitary problems. Many pediatric endocrinologists have interests and expertise in bone metabolism, lipid metabolism, adolescent gynecology, or inborn errors of metabolism.
In the United States and Canada, pediatric endocrinology is a subspecialty of the American Board of Pediatrics, with board certification following fellowship training. It is a relatively small and primarily cognitive specialty, with few procedures and an emphasis on diagnostic evaluation.
Most pediatric endocrinologists in North America and many from around the world can trace their professional genealogy to Lawson Wilkins, who pioneered the specialty in the pediatrics department of Johns Hopkins Medical School and the Harriet Lane Home in Baltimore in between the late 1940's and the mid-1960's.
The principal North American professional association is named the Lawson Wilkins Pediatric Endocrine Society . Other longstanding pediatric endocrine associations include the European Society for Paediatric Endocrinology, the British Society for Paediatric Endocrinology, and the Japanese Society for Pediatric Endocrinology. Professional associations of the specialty continue to proliferate.
Training for pediatric endocrinology consists of a 2-3 year fellowship following completion of a 3 year pediatrics residency. The fellowship, and the specialty, are heavily research-oriented and academically based, although less exclusively now than in past decades.