Persius/hicric huggingface dataset:
Nitrifying bacteria
Nitrifying bacteria are chemoautotrophic bacteria that grow at the expense of inorganic nitrogen compounds.  Many species of nitrifying bacteria have complex internal membrane systems that are the location for key enzymes in nitrification: ammonia monooxygenase which oxidizes ammonia to hydroxylamine, and nitrite oxidoreductase, which oxidizes nitrite to nitrate.

# Ecology
Nitrifying bacteria are widespread in soil and water, and are found in highest numbers where considerable amounts of ammonia are present (areas with extensive protein decomposition, and sewage treatment plants).  Nitrifying bacteria thrive in lakes and streams high imputs of sewage and wastewater because of the high ammonia content.

# Oxidation of ammonia to nitrate
Nitrification in nature is the result of actions of two groups of organisms, the nitrosifyers (ammonia-oxidizing bacteria) and nitrifying bacteria (nitrite-oxidizing, nitrate producing bacteria)
Nitrosifying bacteria
1. NH3 + O2 + 2e- + 2H+  NH2OH + H2O
2. NH2OH + H2O + 1/2 O2  NO2- +2 H2O + H+
Nitrifying bacteria
NO2- + 1/2 O2  NO3-
Nocturnal myoclonus

# Overview
Periodic Limb Movement Disorder (PLMD), also called nocturnal myoclonus, is a sleep disorder where the patient moves limbs involuntarily during sleep and has symptoms or problems related to the movement.  If the patient moves limbs during sleep but there are no consequences, it is simply called periodic limb movements of sleep (PLMS).  Not all patients with PLMS have PLMD (in fact, most people with PLMS do not have a disorder requiring any treatment).
PLMS is diagnosed with the aid of a polysomnogram or PSG.  PLMD is diagnosed by first finding PLMS on a PSG, then integrating that information with a detailed history from the patient and/or bed partner.  PLMS can range from a small amount of movement in the ankles and toes, to wild flailing of all four limbs. These movements, which are more common in the legs than arms, occur for between 0.5 and 5 seconds, recurring at intervals of 5 to 90 seconds. A formal diagnosis of PLMS requires three periods during the night, lasting from a few minutes to an hour or more, each containing at least 30 movements followed by partial arousal or awakening.
PLMS can cause insomnia and daytime sleepiness. The incidence of this disorder increases with age. It is estimated to occur in 5% of people age 30 to 50 and in 44% of people over the age of 65 (which means it is a normal observation in most individuals). As many as 12.2% of patients suffering from insomnia and 3.5% of patients suffering from excessive daytime sleepiness may experience PLMS.
PLMS is related to restless leg syndrome (RLS) in that 80% of people with RLS also have PLMS. However, most people with PLMS do not experience RLS.
PLMS has made its way into popular culture, being referred to as "jimmy legs" and "jimmy arms" in an episode of Seinfeld, and has been known to cause couples to sleep in separate beds.  In both examples, one subject suffers from PLMS severely enough to disturb the sleep of the other subject.

# Treatment
Nocturnal myoclonus was discovered by Mary Jane Stout. Nocturnal myoclonus is treated by medications aimed at reducing or eliminating the leg jerks or the arousals. Non-ergot derived dopaminergic drugs (pramipexole and ropinirole) are preferred. Other dopaminergic agents such as co-careldopa, co-beneldopa, pergolide, or lisuride may also be used. These drugs decrease or eliminate both the leg jerks and the arousals. These medications are also successful for the treatment of RLS restless leg syndrome.
In one study, co-careldopa was superior to dextropropoxyphene in decreasing the number of leg kicks and the number of arousals per hour of sleep. However, co-careldopa and, to a lesser extent, pergolide may shift the leg movements from the nighttime to the daytime.
Clonazepam, (Klonopin), in doses from 2 to 8 mg at bedtime, has been shown to significantly reduce leg kicks in a patient who had nocturnal myoclonus to the degree that leg and knee pain persisted throughout the next day.
Noncovalent bonding
A noncovalent bond is a type of chemical bond, typically between macromolecules, that does not involve the sharing of pairs of electrons, but rather involves more dispersed variations of electromagnetic interactions.  The noncovalent bond is the dominant type of bond between supermolecules in supermolecular chemistry. Noncovalent bonds are critical in maintaining the three-dimensional structure of large molecules, such as proteins and nucleic acids, and are involved in many biological processes in which large molecules bind specifically but transiently to one another. The energy released in the formation of noncovalent bonds is on the order of 1-5 kcal per mol. There are four main types of non-covalent bonds: hydrogen bonding, ionic interactions, Van der Waals interactions, and hydrophobic bonds. Examples of noncovalent bonds include: those binding interactions which hold the two strands DNA in the DNA double helix together, those which fold polypeptides into such secondary structures as the alpha helix and the beta conformation, those which enable enzymes to bind to their substrate, and those which enable antibodies to bind to their antigen.

# Overview
In general, noncovalent bonding refers to a variety of interactions that are not covalent in nature between molecules or parts of molecules that provide force to hold the molecules or parts of molecules together, usually in a specific orientation or conformation.  Noncovalent bonding is the dominant type of bonding in supramolecular chemistry.  These noncovalent interactions include: ionic bonds, hydrophobic interactions, hydrogen bonds, Van der Waals forces, i.e. "London dispersion forces", and Dipole-dipole bonds.
The terms "noncovalent bonding," "noncovalent interactions," and "noncovalent forces" all refer to these forces as a whole without specifying or distinguishing which specific forces are involved: noncovalent interactions often involve several of these forces working in concert. Noncovalent bonds are weak by nature and must therefore work together to have a significant effect. In addition, the combined bond strength is greater than the sum of the individual bonds. This is because the free energy of multiple bonds between two molecules is greater than the sum of the enthalpies of each bond due to entropic effects.

# Examples

## Protein structure
Main article: Protein structure
Intramolecular noncovalent interactions are largely responsible for the secondary and tertiary structure of proteins and therefore the protein's function in the mechanisms of life. Intermolecular noncovalent interactions are responsible for protein complexes (quaternary structure) where two or more proteins function in a coherent mechanism.

## Pharmaceuticals
Most drugs work by noncovalently interacting with biomolecules such as proteins or RNA. Relatively few drugs actually form covalent bonds with the biomolecules they interact with; instead, they interfere with or activate some biological mechanism through noncovalently interacting in very specific locations on specific biomolecules which present the perfect combination of noncovalent binding partners in just the right geometry.
Non-rebreather mask
A non-rebreather mask, or NRB, is a device used in medical emergencies that require oxygen therapy. An NRB requires that the patient can breathe unassisted, but unlike a nasal cannula, the NRB allows for the delivery of higher concentrations of oxygen.

# Design
The non-rebreather mask covers both the nose and mouth of the patient and attaches with the use of an elastic cord around the back of the patient's head. The NRB has an attached reservoir bag, typically 1.5 liters, that connects to an external oxygen tank. Before a NRB is placed on the patient, the reservoir bag is inflated to greater than two-thirds full of oxygen, at a rate between 8-15 liters per minute (lpm). Approximately 1/3 of the air from the reservoir is depleted as the patient breathes, which is then re-inflated by the flow from the O2 tank. If the bag becomes completely deflated, the patient will no longer have a source of air to breathe.
Exhaled air is directed through a one-way valve in the mask, which prevents the inhalation of room air and the re-inhalation of exhaled air. The valve, along with a sufficient seal around the patient's nose and mouth, allows for the administration of high concentrations of oxygen, between 60-90% O2.
Strictly, "non-rebreather" masks are "partial-rebreather" (PRB) masks; ideally, a non-rebreather mask would not permit air from the surrounding environment to be inhaled. However, since not all of the exhaled is completely removed by the one-way valve and the seal created by the mask is not perfect, intake of outside air is unavoidable.

# Usage
The non-rebreather mask is utilized for patients with physical trauma, chronic airway limitation/chronic obstructive pulmonary diseases, smoke inhalation, and carbon monoxide poisoning, or any other patient who requires high-flow oxygen, but does not require breathing assistance. Patients uncomfortable with having a mask on on their face, such as those with claustrophobia, or patient's with injuries to the mouth are more likely to benefit from a nasal cannula. Patient's who are unable to breathe on their own would require an active breathing device, such as a bag valve mask.
Noninvasive glucose
Noninvasive glucose refers to the measurement of blood glucose levels (required by people with diabetes to prevent both chronic and acute complications from the disease) without drawing blood, puncturing the skin, or causing pain or trauma. The search for a successful technique began in about 1975 and has continued to the present without a clinically or commercially viable product(1).
Hundreds of millions of dollars have been invested in companies who have sought the solution to this long-standing problem, and the search has been peppered with false starts, premature announcements of success and outright chicanery on the part of some investigators. However, most of the researchers in this field have been genuinely interested in helping those with diabetes find a less painful and more convenient way to measure their blood glucose.
Approaches that have been tried include near infrared spectroscopy (measuring glucose throught the skin using light of slightly longer wavelengths than the visible region), transdermal measurement (attempting to pull glucose through the skin using either chemicals, electricity or ultrasound), measuring the amount that polarized light is rotated by glucose in the front chamber of the eye (containing the "aqueous humor"), and many others.
A comprehensive compilation of companies pursuing this goal is maintained on a website by a long-time writer who has diabetes(2).
Normochromic anemia

# Overview
Normocytic anemia is a common issue that occurs for men and women typically over 85 years old. Its prevalence increases with age, reaching 44 percent in men older than 85 years. Normocytic anemia is the most frequently encountered type of anemia.

# Causes
The issue is thought of as representing any of the following:
- a decreased production of normal-sized red blood cells (e.g., anemia of chronic disease, aplastic anemia);
- an increased destruction or loss of red blood cells (e.g., hemolysis, posthemorrhagic anemia);
- an uncompensated increase in plasma volume (e.g., pregnancy, fluid overload);
- or a mixture of conditions producing microcytic and macrocytic anemia.

# Differentiating Normochromic Anemia from Other Diseases
To review the differential diagnosis of anemia, click here.
Novartis Foundation
The Novartis Foundation is a scientific and educational charity, formed in 1949 by the Swiss company Ciba, now Novartis. It was the direct successor to the Ciba Foundation, and the changed name (Novartis Foundation) reflected the new name of Ciba, after merging with Sandoz.
The Foundation was the brainchild of Robert Kappeli, Managing Director (and later President) of ].
Although Novartis provides financial support to the foundation, it is not represented on the Board of Trustees and occupies only a minority of seats on the Executive Council.
The foundation has its headquarters at 41 Portland Place in central London, UK.
O'nyong'nyong virus

# Overview
The O'nyong'nyong virus or O'nyong-nyong virus was a virus first isolated by the Uganda Virus Research Institute in Entebbe, Uganda in 1959.  It is a togavirus (family Togaviridae), genus Alphavirus and is closely related to Chikungunya and Igbo Ora viruses. The name comes from the Nilotic language of Uganda and Sudan and means weakening of the joints.
O'nyong'nyong virus is transmitted by bites from an infected mosquito.  It is the only virus whose primary vectors are anopheline mosquitoes (Anopheles funestus and Anopheles gambiae).
Common symptoms of infection with the virus are polyarthritis, rash and fever. Other symptoms include eye pain, chest pain, lymphadenitis and lethargy. No fatalities due to infection are known.
There have been two epidemics of Onyongnyong fever. The first occurred from 1959-1962 spreading from Uganda to Kenya, Tanzania, Zaire (Democratic Republic of the Congo), Malawi and Mozambique, and affecting over two million people. This was one of the largest arbovirus epidemics recorded. The first virus isolates were obtained during this outbreak from mosquitoes and human blood samples collected from Gulu in northern Uganda in 1959.
The second epidemic in 1996-1997 affected 400 people and was confined to Uganda. The 35-year hiatus between the two outbreaks and evidence of an outbreak in 1904-1906 in Uganda indicates a 30-50 year cycle for epidemics.
O-Desmethyltramadol
O-Desmethyltramadol (M1) is an opioid analgesic which is made in the body from tramadol.
(+)-O-Desmethyltramadol is the most important metabolite of tramadol produced in the liver after tramadol is consumed. This metabolite is considerably more potent as a  opioid agonist than the parent compound, and indeed is so much more potent that tramadol can to some extent be regarded as a prodrug for O-desmethyltramadol in the same way that codeine is a prodrug for morphine.
Tramadol is demethylated by the liver enzyme CYP2D6 in the same way as codeine, and so similarly to the variation in effects seen with codeine, individuals who have a less active form of CYP2D6 ("poor metabolisers") will tend to get reduced analgesic effects from tramadol.
The two enantiomers of O-desmethyltramadol show quite distinct pharmacological profiles; both (+) and (-)-O-desmethyltramadol are inactive as serotonin reuptake inhibitors, but (-)-O-desmethyltramadol retains activity as a dopamine and noradrenaline reuptake inhibitor and so the mix of metabolites produced contributes significantly to the complex pharmacological profile of tramadol.
Observational error
Observational error is the difference between a measured value of quantity and its true value. In statistics, an error is not a "mistake".  Variability is an inherent part of things being measured and of the measurement process.
When either randomness or uncertainty modeled by probability theory is attributed to such errors, they are "errors" in the sense in which that term is used in statistics; see errors and residuals in statistics.
Every time we repeat a measurement with a sensitive instrument, we obtain slightly different results. The common statistical model we use is that the error has two additive parts:
- systematic error which always occurs (with the same value) when we use the instrument in the same way, and
- random error which may vary from observation to observation.
The systematic error is sometimes called statistical bias. It is controlled by very carefully standardized procedures. Part of the education in every science is how to use the standard instruments of the discipline.
The random error (or random variation) is due to factors which we cannot (or do not) control. It may be too expensive or we may be too ignorant of these factors to control them each time we measure. It may even be that whatever we are trying to measure is changing in time (see dynamic models), or is fundamentally probablistic (as is the case in quantum mechanics -- see Measurement in quantum mechanics). Random error often occurs when instruments are pushed to their limits. For example, it is common for digital balances to exhibit random error in their least significant digit. Three measurements of a single object might read something like 0.9111g, 0.9110g, and 0.9112g.
Occipital neuralgia
Occipital neuralgia,  also known as C2 neuralgia, is a medical condition characterized by chronic pain in the upper neck, back of the head and behind the ears. These areas correspond to the locations of the lesser and greater occipital nerves.

# Causes
Occipital neuralgia is caused by damage to these nerves. Ways in which they can be damaged include trauma (usually concussive), physical stress on the nerve, repetitious neck contraction, flexion or extension, and as a result of medical complications (such as osteochondroma, a benign tumour of the bone).

# Symptoms
The only direct symptom of this condition is essentially a chronic headache. Commonly described as back of head and around or over the top of head, sometimes up to the eyebrow. Because chronic headaches are a common symptom for numerous conditions, occipital neuralgia is often misdiagnosed at first, most commonly as tension headache or a migraine leading to treatment failure or addiction.

# Treatment
Once diagnosed, occipital neuralgia can be treated in several ways. These include local nerve block, peripheral nerve stimulation, steroids, rhizotomy, phenol injections, antidepressants, and Occipital Cryoneurolysis.
Other less common forms of surgical neurolysis or microdecompression are also used to treat the condition when conservative measures fail.
Chiropractic is an alternative method to treating mechanical conditions such as Greater Occipital Neuralgia.  The C2 nerve root exits the spine between C1 and C2.  Irritation between these two vertebrae will cause this pain.

# Prognosis
Occipital neuralgia is not a life-threatening or otherwise health-threatening condition.
Chiropractic is  the best way to treat this condition.
Occupational cancer

# Overview
Occupational cancer is cancer caused by occupational hazards. Several cancers have been directly tied to occupational hazards, including chimney sweeps' carcinoma, mesothelioma, and others.

# Carcinogens
Carcinogens are chemicals known to cause cancer with some kind of exposure. When a person is exposed to a carcinogen in the workplace, it may cause mutations that allow cells to grow out of control, causing cancer. Carcinogens in the workplace may include chemicals like anilines, chromates, dinitrotoluenes, arsenic and inorganic arsenic compounds, beryllium and beryllium compounds, cadmium compounds, nickel compounds, crystalline forms of silica, coal tar pitch volatiles, coke oven emissions, diesel exhaust and environmental tobacco smoke.

# Occupations
- Painters are at risk for mesothelioma (due to potential asbestos exposure while working on a building), other lung cancer, and bladder cancer. The causative agent is unknown. Painters have a low rate of respirator and glove use.

# Epidemiology
An estimated 48,000 cancers are diagnosed yearly in the US that come from occupational causes; this represents approximately 4-10% of total cancer in the United States.
Ocular hypertension

# Overview
Ocular hypertension (OHT) is intraocular pressure higher than normal in the absence of optic nerve damage or visual field loss.
Current consensus in ophthalmology defines normal introcular pressure (IOP) as that between 10 mmHg and 21 mmHg. Elevated IOP is the most important risk factor for glaucoma, so those with ocular hypertension are frequently considered to have a greater chance of developing the condition.
Intraocular pressure can increase when a patient lies down. There is evidence that some glaucoma patients (e.g., normal tension glaucoma patients) with normal IOP while sitting or standing may have intraocular pressure that is elevated enough to cause problems when they are lying down.

# Treatment

## Medication
Ocular hypertension are mostly treated with pilocarpine, timolol, acetazolamide and clonidine. There are also other, less commonly used, alternatives. Eye drops may initially be started either in one or in both eyes.

# Causes

## Common Causes
- Acute angle-closure glaucoma
- Axenfeld-rieger syndrome
- Chandler iris naevus syndrome
- Congenital glaucoma
- Corneal arcus
- Essential iris atrophy
- Excessive aqueous production
- Glaucoma
- Hyphema
- Inadequate aqueous drainage
- Pigment dispersion syndrome
- Posner-schlossman syndrome
- Pseudoexfoliation syndrome
- Refractive ocular surgery

## Causes by Organ System

## Causes in Alphabetical Order
- Acute angle-closure glaucoma
- Alpha-l-iduronidase deficiency
- Amyloidosis
- Antipsychotic agents
- Atropine
- Axenfeld-rieger syndrome
- Chandler iris naevus syndrome
- Chlorpromazine
- Cocaine
- Congenital glaucoma
- Corneal arcus
- Cystathionine beta-synthase deficiency
- Essential iris atrophy
- Excessive aqueous production
- Fahr disease
- Glaucoma
- Glucocorticoids
- Hereditary onycho-osteodysplasia
- Hyphema
- Inadequate aqueous drainage
- Iridogoniodysgenesis type 1
- Levomepromazine
- Lowe syndrome
- Moore-federman syndrome
- Ocular trauma
- Perazine
- Phenelzine
- Pigment dispersion syndrome
- Pipothiazine
- Pizotifen
- Posner-schlossman syndrome
- Prednisolone
- Pseudoexfoliation syndrome
- Ranibizumab
- Refractive ocular surgery
- Steroids
- Sturge-weber syndrome
- Topiramate
- Tropicamide
- Weill-marchesani syndrome
Olanzapine overdose

# Overdosage topics
Manifestations
Lethal dosage
Treatment

## Manifestation
Among less commonly reported symptoms were the
following potentially medically serious events: aspiration, cardiopulmonary arrest, cardiac arrhythmias (such as
supraventricular tachycardia and one patient experiencing sinus pause with spontaneous resumption of normal rhythm),
delirium, possible neuroleptic malignant syndrome, coma, respiratory depression/arrest, convulsion, hypertension, and
hypotension.

## Lethal dosage
The amount of acutely ingested olanzapine was reported to be possibly as low as 450 mg; however, in
another case, a patient was reported to survive an acute olanzapine ingestion of 1500 mg

## Treatment
The possibility of multiple drug involvement should be considered. In case of acute overdosage, establish and maintain
an airway and ensure adequate oxygenation and ventilation, which may include intubation. Gastric lavage (after intubation,
if patient is unconscious) and administration of activated charcoal together with a laxative should be considered. The
possibility of obtundation, seizures, or dystonic reaction of the head and neck following overdose may create a risk of
aspiration with induced emesis. Cardiovascular monitoring should commence immediately and should include continuous
electrocardiographic monitoring to detect possible arrhythmias.
There is no specific antidote to olanzapine. Therefore, appropriate supportive measures should be initiated. Hypotension
and circulatory collapse should be treated with appropriate measures such as intravenous fluids and/or sympathomimetic
agents. (Do not use epinephrine, dopamine, or other sympathomimetics with beta-agonist activity, since beta stimulation
may worsen hypotension in the setting of olanzapine-induced alpha blockade.) Close medical supervision and monitoring
should continue until the patient recovers.
Adapted from the FDA Package Insert.