Metal fume fever is due to the inhalation of certain metals, either as fine dust or most commonly as fumes. Simple metal compounds such as oxides are equally capable of causing it. The effects of particularly toxic compounds, such as nickel carbonyl, are not considered merely metal fume fever.

Exposure usually arises through hot metalworking processes, such as smelting and casting of zinc alloys, welding of galvanized metals, brazing, or soldering. If the metal concerned is particularly high-risk, the residue from cold sanding processes may also cause fume fever, even if the dose is lower. It may also be caused by electroplated surfaces or metal-rich anti-corrosion paint, such as cadmium passivated steel or zinc chromate primer on aluminium aircraft parts. Exposure has also been reported in use of lead-free ammunition, by the harder steel core stripping excess metal from the jacket of the bullet and barrel of the rifle.

The most plausible metabolic source of the symptoms is a dose-dependent release of certain cytokines, an event which occurs by inhaling metal oxide fumes that injure the lung cells. This is not an allergic reaction, though allergic reactions to metal fumes can occur.

Treatment of mild metal fume fever consists of bedrest, keeping the patient well hydrated, and symptomatic therapy (e.g. aspirin for headaches) as indicated. In the case of non-allergic acute lung injury, standard or recommended approaches to treatment have not been defined.

The consumption of large quantities of cow's milk, either before or immediately after exposure is a traditional remedy. However, the United Kingdom Health and Safety Executive challenges this advice, warning, "Don’t believe the stories about drinking milk before welding. It does not prevent you getting metal fume fever."

Since lead has been used widely for centuries, the effects of exposure are worldwide. Environmental lead is ubiquitous, and everyone has some measurable blood lead level. Atmospheric lead pollution increased dramatically beginning in the 1950s as a result of the widespread use of leaded gasoline. Lead is one of the largest environmental medicine problems in terms of numbers of people exposed and the public health toll it takes. Lead exposure accounts for about 0.2% of all deaths and 0.6% of disability adjusted life years globally.

Although regulation reducing lead in products has greatly reduced exposure in the developed world since the 1970s, lead is still allowed in products in many developing countries. In all countries that have banned leaded gasoline, average blood lead levels have fallen sharply. However, some developing countries still allow leaded gasoline, which is the primary source of lead exposure in most developing countries. Beyond exposure from gasoline, the frequent use of pesticides in developing countries adds a risk of lead exposure and subsequent poisoning. Poor children in developing countries are at especially high risk for lead poisoning. Of North American children, 7% have blood lead levels above 10 μg/dL, whereas among Central and South American children, the percentage is 33 to 34%. About one fifth of the world's disease burden from lead poisoning occurs in the Western Pacific, and another fifth is in Southeast Asia.

In developed countries, people with low levels of education living in poorer areas are most at risk for elevated lead. In the US, the groups most at risk for lead exposure are the impoverished, city-dwellers, and immigrants. African-American children and those living in old housing have also been found to be at elevated risk for high blood lead levels in the US. Low-income people often live in old housing with lead paint, which may begin to peel, exposing residents to high levels of lead-containing dust.

Risk factors for elevated lead exposure include alcohol consumption and smoking (possibly because of contamination of tobacco leaves with lead-containing pesticides). Adults with certain risk factors might be more susceptible to toxicity; these include calcium and iron deficiencies, old age, disease of organs targeted by lead (e.g. the brain, the kidneys), and possibly genetic susceptibility.

Differences in vulnerability to lead-induced neurological damage between males and females have also been found, but some studies have found males to be at greater risk, while others have found females to be.

In adults, blood lead levels steadily increase with increasing age. In adults of all ages, men have higher blood lead levels than women do. Children are more sensitive to elevated blood lead levels than adults are. Children may also have a higher intake of lead than adults; they breathe faster and may be more likely to have contact with and ingest soil. Children of ages one to three tend to have the highest blood lead levels, possibly because at that age they begin to walk and explore their environment, and they use their mouths in their exploration. Blood levels usually peak at about 18–24 months old. In many countries including the US, household paint and dust are the major route of exposure in children.

Outcome is related to the extent and duration of lead exposure. Effects of lead on the physiology of the kidneys and blood are generally reversible; its effects on the central nervous system are not. While peripheral effects in adults often go away when lead exposure ceases, evidence suggests that most of lead's effects on a child's central nervous system are irreversible. Children with lead poisoning may thus have adverse health, cognitive, and behavioral effects that follow them into adulthood.

Estrogen birth control pills may increase the amount of copper in humans, but was not shown to increase absorption. Copper Intrauterine devices (IUDs) have been questioned anecdotally, with people claiming copper toxicity, but there is currently no scientific evidence to substantiate this claim. Estrogen increases the absorption of copper, making women more likely to carry excess copper even when no birth control is used.

The amount of estrogen (or copper) contained in these modern forms of contraception are generally considered safe, and the former restrictions for estrogen use (not to be used by women older than 40, 35 for smokers) were lifted in 1989.

There are conditions in which an individual's copper metabolism is compromised to such an extent that birth control may cause an issue with copper accumulation. They include toxicity or just increased copper from other sources, as well as the increased copper level of the individual's mother via the placenta before birth. The two hormones commonly used in birth control, estrogen and progestin, protect from each other's complications, so a combination method may work best. At least when existing imbalances have been treated.

Too much copper in water may damage marine and freshwater organisms such as fish and molluscs. Fish species vary in their sensitivity to copper, with the LD50 for 96-h exposure to copper sulphate reported to be in the order of 58 mg per litre for Tilapia ("Oreochromis niloticus") and 70 mg per litre for catfish ("Clarias gariepinus") The chronic effect of sublethal concentrations of copper on fish and other creatures is damage to gills, liver, kidneys and the nervous system. It also interferes with the sense of smell in fish, thus preventing them from choosing good mates or finding their way to mating areas.

Copper-based paint is a common marine antifouling agent. In the United States, copper-based paint replaced tributyltin, which was banned due to its toxicity, as a way for boats to control organic growth on their hulls. In 2011, Washington state became the first U.S. state to ban the use of copper-based paint for boating, although it only applied to recreational boats. California has also pursued initiatives to reduce the effect of copper leaching, with the U.S. EPA pursuing research.

Erysipelas is an acute infection typically with a skin rash, usually on any of the legs and toes, face, arms, and fingers. It is an infection of the upper dermis and superficial lymphatics, usually caused by beta-hemolytic group A "Streptococcus" bacteria on scratches or otherwise infected areas. Erysipelas is more superficial than cellulitis, and is typically more raised and demarcated. The term is from Greek ἐρυσίπελας, meaning "red skin".

Most cases of erysipelas are due to "Streptococcus pyogenes" (also known as beta-hemolytic group A streptococci), although non-group A streptococci can also be the causative agent. Beta-hemolytic, non-group A streptococci include "Streptococcus agalactiae", also known as group B strep or GBS. Historically, the face was most affected; today, the legs are affected most often. The rash is due to an exotoxin, not the "Streptococcus" bacteria, and is found in areas where no symptoms are present; e.g., the infection may be in the nasopharynx, but the rash is found usually on the upper dermis and superficial lymphatics.

Erysipelas infections can enter the skin through minor trauma, insect bites, dog bites, eczema, athlete's foot, surgical incisions and ulcers and often originate from streptococci bacteria in the subject's own nasal passages. Infection sets in after a small scratch or abrasion spreads, resulting in toxaemia.

Erysipelas does not affect subcutaneous tissue. It does not release pus, only serum or serous fluid. Subcutaneous edema may lead the physician to misdiagnose it as cellulitis, but the style of the rash is much more well circumscribed and sharply marginated than the rash of cellulitis.

Gueules cassées (broken faces) is a French expression for facially disfigured servicemen which originated in World War I. Colonel Yves Picot is said to have coined the term when he was refused passing a checkpoint to a party.

When properly treated, people with malaria can usually expect a complete recovery. However, severe malaria can progress extremely rapidly and cause death within hours or days. In the most severe cases of the disease, fatality rates can reach 20%, even with intensive care and treatment. Over the longer term, developmental impairments have been documented in children who have suffered episodes of severe malaria. Chronic infection without severe disease can occur in an immune-deficiency syndrome associated with a decreased responsiveness to "Salmonella" bacteria and the Epstein–Barr virus.

During childhood, malaria causes anemia during a period of rapid brain development, and also direct brain damage resulting from cerebral malaria. Some survivors of cerebral malaria have an increased risk of neurological and cognitive deficits, behavioural disorders, and epilepsy. Malaria prophylaxis was shown to improve cognitive function and school performance in clinical trials when compared to placebo groups.

Chimney sweep's cancer, also called soot wart, is a squamous cell carcinoma of the skin of the scrotum. It has the distinction of being the first reported form of occupational cancer, and was initially identified by Percivall Pott in 1775. It was initially noticed as being prevalent amongst chimney sweeps.

Chimney sweeps' carcinoma is a squamous cell carcinoma of the skin of the scrotum. Warts caused by the irritation from soot particles, if not excised, developed into a scrotal cancer. This then invaded the dartos, enlarged the testicle, and proceeded up the spermatic cord into the abdomen where it proved fatal.

The WHO estimates that in 2015 there were 214 million new cases of malaria resulting in 438,000 deaths. Others have estimated the number of cases at between 350 and 550 million for falciparum malaria The majority of cases (65%) occur in children under 15 years old. About 125 million pregnant women are at risk of infection each year; in Sub-Saharan Africa, maternal malaria is associated with up to 200,000 estimated infant deaths yearly. There are about 10,000 malaria cases per year in Western Europe, and 1300–1500 in the United States. About 900 people died from the disease in Europe between 1993 and 2003. Both the global incidence of disease and resulting mortality have declined in recent years. According to the WHO and UNICEF, deaths attributable to malaria in 2015 were reduced by 60% from a 2000 estimate of 985,000, largely due to the widespread use of insecticide-treated nets and artemisinin-based combination therapies. In 2012, there were 207 million cases of malaria. That year, the disease is estimated to have killed between 473,000 and 789,000 people, many of whom were children in Africa. Efforts at decreasing the disease in Africa since the turn of millennium have been partially effective, with rates of the disease dropping by an estimated forty percent on the continent.

Malaria is presently endemic in a broad band around the equator, in areas of the Americas, many parts of Asia, and much of Africa; in Sub-Saharan Africa, 85–90% of malaria fatalities occur. An estimate for 2009 reported that countries with the highest death rate per 100,000 of population were Ivory Coast (86.15), Angola (56.93) and Burkina Faso (50.66). A 2010 estimate indicated the deadliest countries per population were Burkina Faso, Mozambique and Mali. The Malaria Atlas Project aims to map global endemic levels of malaria, providing a means with which to determine the global spatial limits of the disease and to assess disease burden. This effort led to the publication of a map of "P. falciparum" endemicity in 2010. As of 2010, about 100 countries have endemic malaria. Every year, 125 million international travellers visit these countries, and more than 30,000 contract the disease.

The geographic distribution of malaria within large regions is complex, and malaria-afflicted and malaria-free areas are often found close to each other. Malaria is prevalent in tropical and subtropical regions because of rainfall, consistent high temperatures and high humidity, along with stagnant waters in which mosquito larvae readily mature, providing them with the environment they need for continuous breeding. In drier areas, outbreaks of malaria have been predicted with reasonable accuracy by mapping rainfall. Malaria is more common in rural areas than in cities. For example, several cities in the Greater Mekong Subregion of Southeast Asia are essentially malaria-free, but the disease is prevalent in many rural regions, including along international borders and forest fringes. In contrast, malaria in Africa is present in both rural and urban areas, though the risk is lower in the larger cities.

Also termed "lip dermatitis", eczematous cheilitis is a diverse group of disorders which often have an unknown cause. Chronic eczematous reactions account for the majority of chronic cheilitis cases.

It is divided into endogenous (due to an inherent characteristic of the individual), and exogenous (where it is caused by an external agent). The main cause of endogenous eczematous cheilitis is atopic cheilitis (atopic dermatitis), and the main causes of exogenous eczematous cheilitis is irritant contact cheilitis ("e.g.", caused by a lip-licking habit) and allergic contact cheilitis. The latter is characterized by a dryness, fissuring, edema, and crusting. It affects females more commonly than males, in a ratio of about 9:1.

The most common causes of allergic contact cheilitis is lip cosmetics, including lipsticks and lip balm, followed by toothpastes. A lipstick allergy can be difficult to diagnose in some cases as it is possible that cheilitis can develop without the person even wearing lipstick. Instead, small exposure such as kissing someone who is wearing lipstick is enough to cause the condition.

Allergy to Balsam of Peru can manifest as cheilitis. Allergies to metal, wood, or other components can cause cheilitis reactions in musicians, especially players of woodwind and brass instruments, "e.g.", the so-called "clarinetist's cheilitis", or "flutist's cheilitis". "Pigmented contact cheilitis" is one type of allergic cheilitis in which a brown-black discoloration of the lips develops. Patch testing is used to identify the substance triggering allergic contact cheilitis.

Hemoglobin Hopkins-2 (Hb Hop-2) is a mutation of the protein hemoglobin, which is responsible for the transportation of oxygen through the blood from the lungs to the musculature of the body in vertebrates. Generally, the mutation causes two abnormal α chains in the protein's structure. Within the chains, the mutation is the result of hemoglobin's histidine amino acid being replaced with aspartic acid in the protein's genetic sequence. This amino acid structure change occurs at residue 112. Additionally, within one of the mutated alpha chains, there are substitutes at 114 and 118, two points on the amino acid chain. This mutation can cause sickle cell anemia.

Following the initial discovery of hemoglobin, two researchers working at Johns Hopkins Hospital in the mid-twentieth century, Ernest W. Smith and J.V. Torbert, discovered the Hopkins-2 mutation of hemoglobin. Work by Harvey A. Itano and Elizabeth A. Robinson in 1960 confirmed Smith's and Torbert's finding and emphasized the importance of the alpha loci in the mutation. Later in the twentieth century, Samuel Charache, another Hopkins affiliated scientist and doctor, studied the physiological impacts of the variant on health. His findings suggest that the variant plays no effect clinically.

Trench warfare protected the bodies but left the heads exposed. Ironically, the introduction of the steel helmet in 1915 made head shots more 'survivable', but this reduction of mortality meant a mutilated life for thousands.

At the start of the war those wounded to the head were generally not considered able to survive and they would not usually be 'helped first'. This changed in the course of the war, as progress was made in medical practices like oral and maxillofacial surgery and most notably in the new field of plastic surgery. Surgeons conducted experiments with bone, cartilage and tissue transplants and the likes of Hippolyte Morestin, Harold Gillies and Léon Dufourmentel made enormous advances. Because of the experimental character of this surgery some chose to remain as they were and others could just not be helped yet. Some of the latter were helped by all kinds of new prosthetics to make them look more or less 'normal'.

Angular cheilitis (angular stomatitis) is inflammation of one or both of the corners (angles) of the mouth. It is a fairly common condition, and often affects elderly people.

There are many possible causes, including nutritional deficiencies (iron, B vitamins, folate), contact allergy, infection ("Candida albicans", "Staphylococcus aureus" or β-hemolytic streptococci) and edentulism (often with overclosure of the mouth and concomitant denture-related stomatitis), and others.

The subject of mouthpiece pressure is closely related to the issue of embouchure collapse/embouchure overuse.

It has long been argued that excessive mouthpiece pressure is a cause of embouchure problems and can be a factor in causing embouchure collapse. However, the pressure of the mouthpiece is not static during playing: it increases the higher in the register a player plays and the louder volume level. Also, a little mouthpiece pressure is essential to provide a seal between the player's embouchure and the instrument; without this, all the air would escape before entering the instrument and no sound would be emitted (brass instruments are dependent on an airflow to produce sound).

Embouchure collapse is far more common among trumpet and horn players. Both of these instruments have mouthpieces with a small circumference, and therefore the pressure is presumably greater, as the force of the mouthpiece on the face is more concentrated. This is in accordance with the principle of physics that pressure is the amount of force divided by the area on which the force is exerted.

As a result of a lack of scientific evidence (no scientific study into mouthpiece pressure as a cause of embouchure collapse has ever been done), the equally valid argument that all brass players can suffer embouchure collapse, and the subjective (not static) nature of mouthpiece pressure, knowledge of mouthpiece pressure as a cause of embouchure collapse is limited.

Embouchure collapse caused by focal dystonia can be diagnosed medically; embouchure collapse caused by embouchure overuse, however, is generally speaking not considered to be a specifically medical issue. A difficulty in diagnosis is that when a brass player describes the symptoms to a doctor or dentist (as is often the case), the medical practitioner does not fully understand what the patient means. This is because brass players learn their embouchure by "feel," and therefore words have a limited ability to describe embouchure problems, especially if the person listening to the description is not a brass player and has a limited knowledge of the embouchure.

Also, in less severe cases, the player may only be able to feel what is wrong while playing. Many players with an embouchure problem will, once they have realized that it is more than a simple case of tired lips, wish to refrain from playing. The fact that around 24 muscles are employed in forming a brass embouchure, and that each will change slightly as a player struggles to play when experiencing embouchure problems, mean that what players describe as being wrong will have not only worsened their condition when they play, but will be different each time they do so.

In the severest cases, the pain caused by embouchure overuse can be felt even when not playing; in some cases, other symptoms will manifest, such as loss of tissue and damaged nerves. This, however, occurs only in the rarest and most extreme circumstances and usually signals the end of the player's career.

There was a study on a three year old that was a carrier of the hemoglobin variant of Hopkins-2. The child had mild anemia and reticulocytosis, which is commonly seen in anemia. There were, however, no sickled cells found in the blood and they had no symptoms relating to sickle cell. There was also a reduced mean corpuscular volume (MCV), which is the average volume of red blood cell count.

"Jerusalem syndrome as a discrete form, uncompounded by previous mental illness." This describes the best-known type, whereby a previously mentally balanced person becomes psychotic after arriving in Jerusalem. The psychosis is characterised by an intense religious character and typically resolves to full recovery after a few weeks or after being removed from the locality. It shares some features with the diagnostic category of a "brief psychotic episode", although a distinct pattern of behaviors has been noted:

1. Anxiety, agitation, nervousness and tension, plus other unspecified reactions.

2. Declaration of the desire to split away from the group or the family and to tour Jerusalem alone. Tour guides aware of the Jerusalem syndrome and of the significance of such declarations may at this point refer the tourist to an institution for psychiatric evaluation in an attempt to preempt the subsequent stages of the syndrome. If unattended, these stages are usually unavoidable.

3. A need to be clean and pure: obsession with taking baths and showers; compulsive fingernail and toenail cutting.

4. Preparation, often with the aid of hotel bed-linen, of a long, ankle-length, toga-like gown, which is always white.

5. The need to shout psalms or verses from the Bible, or to sing hymns or spirituals loudly. Manifestations of this type serve as a warning to hotel personnel and tourist guides, who should then attempt to have the tourist taken for professional treatment. Failing this, the two last stages will develop.

6. A procession or march to one of Jerusalem's holy places, ex:The Western Wall.

7. Delivery of a sermon in a holy place. The sermon is typically based on a plea to humankind to adopt a more wholesome, moral, simple way of life. Such sermons are typically ill-prepared and disjointed.

8. Paranoid belief that a Jerusalem syndrome agency is after the individual, causing their symptoms of psychosis through poisoning and medicating.

Bar-El et al. reported 42 such cases over a period of 13 years, but in no case were they able to actually confirm that the condition was temporary.

"Jerusalem syndrome imposed on a previous psychotic illness." This refers to individuals already diagnosed as having a psychotic illness before their visit to Jerusalem. They have typically gone to the city because of the influence of religious ideas, often with a goal or mission in mind that they believe needs to be completed on arrival or during their stay. For example, an affected person may believe himself to be an important historical religious figure or may be influenced by important religious ideas or concepts (such as causing the coming of the Messiah or the second coming of Christ).

Samuel Taylor Coleridge (21 October 1772–25 July 1834) was an English poet, critic, and philosopher who was, along with his friend William Wordsworth, one of the founders of the Romantic Movement in England and one of the Lake Poets. He wrote the poems "The Rime of the Ancient Mariner" and "Kubla Khan", as well as the prose "Biographia Literaria".

Coleridge was widely known to have been a regular user of opium as a relaxant, analgesic, antidepressant, and treatment for numerous health concerns. "Kubla Khan" was apparently written under the drug's influence, but the degree to which he used the drug as a creative enhancement is not clear. Although Coleridge largely kept his addiction as hidden as possible from those close to him, it became public knowledge with the 1822 publication of "Confessions of an English Opium Eater" by his close friend Thomas de Quincey. The "Confessions" painted a rather negative picture of Coleridge and his reputation suffered accordingly.

Where Coleridge first developed his opium habit is an issue of some scholarly dispute but it clearly dates from a fairly youthful period in his life. Coleridge’s own explanation is clearly laid out in a letter to Joseph Cottle;

However, most scholars agree that Coleridge had resorted to the use of Laudanum (the tincture form of opium) before this date, particularly during times of nervousness and stress. Because Laudanum was widely available and widely used as an analgesic as well as a general sedative, many people were given the drug for all sorts of medical and nervous complaints. Coleridge was probably given the drug numerous times in his youth during several bouts of rheumatic illness. Small medicinal dosages seldom lead to full-blown addiction but for Coleridge, who experienced the painful return of the symptoms many times in his life, it surely introduced him to the use of the drug much earlier than his story to Cottle admits.

Regardless of when and where Coleridge’s opium addiction began, it is clear that the more reliant on the drug he became, the more his work suffered, the less he was able to focus and concentrate, and the more strained his relations became. In fact, it is arguable that any analysis of Coleridge’s life must be done against the constant background of opium usage. But as important as the issue of opium is in Coleridge’s life, it is never a straightforward issue because he often hid it from public and familial view and at other times he exaggerated its importance to his work. In the 1816 publication of his major ‘opium’ poems Coleridge purposely drew a connection between his creative work and his opium usage. Desperate for some financial success with his poetry, Coleridge intentionally attempted to portray himself as a dreamy opium eater because he, perhaps rightly, believed that it would draw a morbid fascination to his work. Opium played an interesting role in the public image of Romantic literature. There was, for a long time, a kind of cult glamorization of the drug and a morose allure to stories of its usage for respectable members of the bourgeoisie who were titillated by such taboo subjects. It was with this in mind that Coleridge generated an image of himself as dreamy poet who created drug induced fantasies.

This dreamy image of himself began even before he was widely known to have been addicted to opium. In one of a series of biographical letters written to his friend Thomas Poole, Coleridge painted this picture of himself, a picture that would always endure. Coleridge writes:

This slothful image was one that endured even with some of Coleridge’s close friends and may have been consciously created by Coleridge in the earlier part of his career in order to draw attention away from his addiction. It was only later that Coleridge perceived an advantage to drawing attention not to himself as simply a slothful scholar but a dreamy opium eater.

The most popular story that connects Coleridge’s work with his opium usage was told by Coleridge in his well-known preface to the poem Kubla Khan. Coleridge wrote:

The sleep of this story is said by Coleridge to be a sleep of opium, and Kubla Khan may be read as an early poetic description of this drug experience. The fact that the poem is generally regarded as one of Coleridge's best is one of the reasons for the continuing interest and debate about the role that opium may have played in his creative output, and in Romanticism in general.

Coleridge, in his lucid moments, understood the problems with which he struggled better than most. In an 1814 letter to his friend John Morgan, Coleridge wrote about his difficulties.

In some respects, Coleridge's life bears a resemblance to that of a modern opiate addict. Unfortunately, as much as Coleridge had some grasp of his addictions and its results, as well as an unusually sharp sense of how this addiction might be treated, many of his closest friends and peers did not understand. The people who might have served him best, like Southey and Wordsworth, were far too willing to maintain his image as slothful and selfish; this despite the professional help that he constantly bestowed upon them. Men like Robert Southey, naturally conservative in outlook were not forward looking enough to comprehend the possibility of Coleridge’s addiction being a largely physical dependence, despite the fact that Coleridge himself, as well as a growing number of professionals like his friend Gillman, were aware of the physical aspect of drug reliance. On more than one occasion Coleridge pointed to the fact that physical restraint might eventually lead to a cure, and on several occasions under the treatment of Dr. Gillman, he was led thus to the edge of freedom from the drug on which he had formed such a dependence. Southey wrote from the position of moral indignation and explicitly denied the physical aspect of the drug issue. Southey wrote to Cottle:

Juche (; ; ), usually left untranslated, or translated as "self-reliance", is the official state ideology of North Korea, described by the government as Kim Il-sung's "original, brilliant and revolutionary contribution to national and international thought". It postulates that "man is the master of his destiny", that the North Korean masses are to act as the "masters of the revolution and construction", and that by becoming self-reliant and strong a nation can achieve true socialism.

Kim Il-sung (1912–1994) developed the ideology, originally viewed as a variant of Marxism–Leninism until it became distinctly "Korean" in character, whilst incorporating the historical materialist ideas of Marxism–Leninism and strongly emphasising the individual, the nation state and its sovereignty. Consequently, "Juche" was adopted into a set of principles that the North Korean government has used to justify its policy decisions from the 1950s onwards. Such principles include moving the nation towards claimed ""jaju"" (independence), through the construction of ""jarip"" (national economy) and an emphasis upon ""jawi"" (self-defence), in order to establish socialism.

The Practice is firmly rooted in the ideals of sustainability through agricultural independence and a lack of dependency.

The "Juche" ideology has been criticized by many scholars and observers as a mechanism for sustaining the totalitarian rule of the North Korean regime, and justifying the country's heavy-handed isolationism and oppression of the North Korean people. It has also been described as a form of Korean ethnic nationalism, but one which promotes the Kim family as the saviours of the "Korean Race" and acts as a foundation of the subsequent personality cult surrounding them.

Hyperkinesia, also known as hyperkinesis, refers to an increase in muscular activity that can result in excessive abnormal movements, excessive normal movements, or a combination of both. The word hyperkinesis comes from the Greek "hyper", meaning "increased," and "kinein", meaning "to move." Hyperkinesia is a state of excessive restlessness which is featured in a large variety of disorders that affect the ability to control motor movement, such as Huntington's disease. It is the opposite of hypokinesia, which refers to decreased bodily movement, as commonly manifested in Parkinson's disease. Many hyperkinetic movements are the result of improper regulation of the basal ganglia-thalamocortical circuitry. Overactivity of a direct pathway combined with decreased activity of an indirect pathway results in activation of thalamic neurons and excitation of cortical neurons, resulting in increased motor output. Often, hyperkinesia is paired with hypotonia, a decrease in muscle tone. Many hyperkinetic disorders are psychological in nature and are typically prominent in childhood. Depending on the specific type of hyperkinetic movement, there are different treatment options available to minimize the symptoms, including different medical and surgical therapies.