<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Justifiable homicide and can you explain it in depth? [/INST] The concept of justifiable homicide in criminal law is a defense to culpable homicide (criminal or negligent homicide).  Generally, there is a burden of production of exculpatory evidence in the legal defense of justification.  In most countries, a homicide is justified when there is sufficient evidence to disprove (under the "beyond a reasonable doubt" standard for criminal charges, and "preponderance of evidence" standard for claims of wrongdoing, i.e. civil liability) the alleged criminal act or wrongdoing.  The key to this legal defense is that it was reasonable for the subject to believe that there was an imminent and otherwise unavoidable danger of death or grave bodily harm to the innocent by the deceased when they committed the homicide. A homicide in this instance is blameless.

Common excusing conditions
Potentially excusing conditions common to multiple jurisdictions include the following.

Capital punishment in places that it is legal.
Where a state is engaged in a war with a legitimate casus belli, a combatant may lawfully kill an enemy combatant so long as that combatant is not hors de combat. This principle is embedded in public international law and has been respected by most states around the world.
In most countries, it is lawful for a citizen to repel violence with violence to protect someones life or destruction of property.The scope of self-defense varies; some jurisdictions have a duty to retreat rule that disallows this defense if it was safe to flee from potential violence. In some jurisdictions, the castle doctrine allows the use of deadly force in self-defense against an intruder in ones home. Other jurisdictions have stand-your-ground laws that allow use of deadly force in self-defense in a vehicle or in public, without a duty to retreat.
Where the persons death is inflicted by the effecting of lawful arrest or prevention of lawfully detained persons escape, quelling riot or insurrection when the use of force is "no more than absolutely necessary".
The doctrine of necessity allows, for example, a surgeon to separate conjoined twins, killing the weaker twin to allow the stronger twin to survive. (This is not recognized, for example, in England and Wales).
In the United States, the 2005 Unborn Victims of Violence Act changed the legal definition of human fetuses to "unborn children", formally defining feticide as murder (under USC §1111).  However, the law retains explicit exceptions which prohibit the prosecution "of any person for conduct relating to an abortion," "of any person for any medical treatment," or "of any woman with respect to her unborn child," thereby preserving the right to an abortion stemming from Roe v. Wade. However, Roe v. Wade was overturned in 2022 by Dobbs v. Jackson Womens Health Organization.
Several countries, such as the Netherlands, Belgium, Switzerland, Japan, Canada, and the U.S. states of Oregon and Washington allow both active and passive euthanasia by law, if justified.
The "heat of the moment" defense for crimes of passion: death results from a situation where the defendant is deemed to have lost control. This may be considered a part of the defense of provocation against charges of murder. Based on the idea that all individuals may suddenly and unexpectedly lose control when words are spoken or events occur, jurisdictions differ on whether this should be allowed to excuse liability or merely mitigate to a lesser offense such as manslaughter, and under which circumstances this defense can be used. In many common law jurisdictions, provocation is a partial defense that converts what would have been murder into manslaughter.
A few jurisdictions do not prosecute (Iran, Iraq) or have a lesser penalty (Kuwait, Egypt) for honor killings.

European Convention on Human Rights
Article 2 Paragraph 2 of the European Convention On Human Rights provides that death resulted from defending oneself or others, arresting a suspect or fugitive, or suppressing riots or insurrections, will not contravene the Article when the use of force involved is "no more than absolutely necessary":

2. Deprivation of life shall not be regarded as inflicted in contravention of this Article when it results from the use of force which is no more than absolutely necessary:
(a) in defence of any person from unlawful violence;
(b) in order to effect a lawful arrest or to prevent the escape of a person lawfully detained;
(c) in action lawfully taken for the purpose of quelling a riot or insurrection.

Example of Criminal Procedure Act in South Africa
In South Africa, §49 Criminal Procedure Act used to provide:

(2) Where the person concerned is to be arrested for an offense referred to in Schedule 1 or is to be arrested on the ground of having committed such an offense, and the person authorized under this Act to arrest or to assist in arresting him cannot arrest him or prevent him from fleeing by other means than killing him, the killing shall be deemed to be justifiable homicide.
This has now been amended by §7 Judicial Matters Second Amendment Act 122 of 1998:
(2) If any arrestor attempts to arrest a suspect and the suspect resists the attempt, or flees, or resists the attempt and flees, when it is clear that an attempt to arrest him or her is being made, and the suspect cannot be arrested without the use of force, the arrestor may, in order to effect the arrest, use such force as may be reasonably necessary and proportional in the circumstances to overcome resistance or to prevent the suspect from fleeing: Provided that the arrester is justified in terms of this section in using deadly force that is intended or is likely to cause death or grievous bodily harm to a suspect, only if he believes on reasonable grounds-
(a) that the force is immediately necessary for the purpose of protecting the arrestor, any person lawfully assisting the arrestor or any other person from imminent or future death or grievous bodily harm;
(b) that there is a substantial risk that the suspect will cause imminent or future death or grievous bodily harm if the arrest is delayed; or
(c) that the offence for which the arrest is sought is in progress and is of a forcible and serious nature and involves the use of life threatening violence or a strong likelihood that it will cause grievous bodily harm.

Circumstances which justify homicide in the United States
A non-criminal homicide ruling, usually committed in self-defense or in defense of another, exists under United States law. A homicide may be considered justified if it is done to prevent a very serious crime, such as rape, armed robbery, manslaughter or murder. The victim must reasonably believe, under the totality of the circumstances, that the assailant intended to commit a criminal act that would likely result in the death or life-threatening injury of an innocent person. A homicide performed out of vengeance, or retribution for action in the past, or in pursuit of a "fleeing felon" (except under specific circumstances) would not be considered justifiable.
In many states, given a case of self-defense, the defendant is expected to obey a duty to retreat if it is possible to do so. In the states of Alabama, Alaska, Arizona, California, Colorado, Connecticut, Florida, Georgia, Hawaii, Indiana, Kansas, Kentucky, Louisiana, Maine, Maryland, Massachusetts, Michigan, Mississippi, Missouri, Montana, New Jersey, North Carolina, Ohio, Oklahoma, Oregon, Pennsylvania, Rhode Island, South Carolina, Tennessee, Texas, West Virginia, Washington, Wyoming and other Castle Doctrine states, there is no duty to retreat in certain situations (depending on the state, this may apply to ones home, business, or vehicle, or to any public place where a person is lawfully present). Preemptive self-defense, in which one kills another on suspicion that the victim might eventually become dangerous, is not justifiable.
In the U.S. Supreme Court ruling of District of Columbia v. Heller, the majority held that the Constitution protected the right to the possession of firearms for the purpose of self-defense "and to use that arm for traditionally lawful purposes, such as self-defense within the home".Two other forms of justifiable homicide are unique to the prison system: the death penalty and preventing prisoners from escaping. To quote the California State Penal Code (state law) that covers justifiable homicide:

196.  Homicide is justifiable when committed by public officers and those acting by their command in their aid and assistance, either--1. In obedience to any judgment of a competent Court; or,2. When necessarily committed in overcoming actual resistance to the execution of some legal process, or in the discharge of any other legal duty; or3. When necessarily committed in retaking felons who have been rescued or have escaped, or when necessarily committed in arresting persons charged with felony, and who are fleeing from justice or resisting such arrest.Although the above text is from California law, many other jurisdictions, like Florida, have similar laws to prevent escapes from custody. Examples include self defense, prevention of criminal act, trespassers, and defense of another person.

Notable cases involving justifiable homicide
Killing of MaKhia Bryant. Her shooting, which prevented her from stabbing another girl, was later deemed a justifiable homicide with prosecutors noting "Under Ohio law the use of deadly force by a police officer is justified when there exists an immediate or imminent threat of death or serious bodily injury to the officer or another."
Sam Cooke. After an inquest and investigation, the courts ruled Cookes death to be a justifiable homicide.
John Dillinger. When BOI agents moved to arrest Dillinger as he exited the theater, he tried to flee </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Birth injury and can you explain it in depth? [/INST] Birth injury refers to damage or injury to the child before, during, or just after the birthing process. "Birth trauma" refers specifically to mechanical damage sustained during delivery (such as nerve damage and broken bones).The term "birth injury" may be used in two different ways:

the ICD-10 uses "birth injury" and "birth trauma" interchangeably to refer to mechanical injuries sustained during delivery;
the legal community uses "birth injury" to refer to any damage or injury sustained during pregnancy, during delivery, or just after delivery, including injuries caused by trauma.Birth injuries must be distinguished from birth defects. "Birth defect" refers to damage that occurs while the fetus is in the womb, which may be caused by genetic mutations, infections, or exposure to toxins. There are more than 4,000 types of birth defects.

Causes
Difficult labor (dystocia)
Difficult labor, also known as dystocia or obstructed labor, occurs when the child cannot easily pass through the birth canal. This can result in fetal distress or physical trauma to the child, especially broken clavicles and damage to the brachial plexus nerves. It can also deprive the child of oxygen as the umbilical cord is pinched, potentially causing brain damage or death.Difficult labor may occur because the baby is abnormally large (macrosomia), because the mothers pelvis or birth canal is small or deformed, or because the baby is in an abnormal presentation for the birth (such as breech or transverse presentation).

External causes
Fetal malformations and birth injuries may occur as a result of exposure to environmental toxins such as mercury or lead. Many medications can also affect the development of the fetus, as can alcohol, tobacco, and illicit drugs.See Environmental toxins and fetal development.
See Drugs in pregnancy.

Genetic mutations
Genetic mutations can cause a wide variety of fetal malformations, ranging from relatively mild cleft lips to severe and even fatal deformities.

Infection
Maternal infection may be transmitted to the fetus; this is called a vertically transmitted infection. The fetus has a weak immune system, so infections that are relatively minor in adults can be very serious in a developing fetus. In addition, some studies suggest that maternal infections increase the risk of neurodevelopmental disorders, including schizophrenia, in the child.

Intrauterine hypoxia
Intrauterine hypoxia, or oxygen deprivation in the womb, can cause serious brain damage in the fetus. It most commonly occurs because of damage to or malformation of the umbilical cord or placenta.  Intrauterine hypoxia can cause brain damage, including cerebral palsy and other neurological and psychiatric disorders.

Maternal health issues
Certain maternal health issues can cause birth injuries. Gestational diabetes can cause premature birth, macrosomia, or stillbirth.

Pregnancy complications
Complications such as placenta previa, placental abruption,  Placenta accreta, Retained placenta, Placental insufficiency, Placental infarcts, anemia, and preeclampsia can limit the supply of oxygen and nutrients to the fetus, increasing the risk of birth defects. Severe cases may be fatal to the fetus.

Common types of birth injury
Brachial plexus injury
The brachial plexus is the plexus of nerves that lies between the neck and axilla and controls the motion of the arm and hand. The brachial plexus may be stretched and damaged during a difficult delivery </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Fasciolopsiasis and can you explain it in depth? [/INST] Fasciolopsiasis results from an infection by the trematode Fasciolopsis buski, the largest intestinal fluke of humans (up to 7.5 cm in length).

Signs and symptoms
Most infections are light, almost asymptomatic. In heavy infections, symptoms can include abdominal pain, chronic diarrhea, anemia, ascites, toxemia, allergic responses, sensitization caused by the absorption of the worms allergenic metabolites can lead to intestinal obstruction and may eventually cause death of the patient.

Cause
The parasite infects an amphibic snail (Segmentina nitidella, Segmentina hemisphaerula, Hippeutis schmackerie, Gyraulus, Lymnaea, Pila, Planorbis (Indoplanorbis)) after being released by infected mammalian feces; metacercaria released from this intermediate host encyst on aquatic plants like water spinach, which are eaten raw by pigs and humans. Water itself can also be infective when drunk unboiled ("Encysted cercariae exist not only on aquatic plants, but also on the surface of the water.")

Diagnosis
Microscopic identification of eggs, or more rarely of the adult flukes, in the stool or vomitus is the basis of specific diagnosis. The eggs are indistinguishable from those of the very closely related Fasciola hepatica liver fluke, but that is largely inconsequential since treatment is essentially identical for both.

Prevention
Infection can be prevented by immersing vegetables in boiling water for a few seconds to kill the infective metacercariae,  avoiding the use of untreated feces ("nightsoil") as a fertilizer, and maintenance of proper sanitation and good hygiene. Additionally, snail control should be attempted.

Treatment
Praziquantel is the drug of choice for treatment. Treatment is effective in early or light infections. Heavy infections are more difficult to treat. Studies of the effectiveness of various drugs for treatment of children with F. buski have shown tetrachloroethylene as capable of reducing faecal egg counts by up to 99%. Other anthelmintics that can be used include thiabendazole, mebendazole, levamisole and pyrantel pamoate. Oxyclozanide, hexachlorophene and nitroxynil are also highly effective.

Epidemiology
F. buski is endemic in Asia including China, Taiwan, Southeast Asia, Indonesia, Malaysia, and India. It has an up to 60% prevalence in worst-affected communities in southern and eastern India and mainland China and has an estimated 10 million human infections. Infections occur most often in school-aged children or in impoverished areas with a lack of proper sanitation systems.A study from 1950s found that F. buski was endemic in central Thailand, affecting about 2,936 people due to infected aquatic plants called water caltrops and the snail hosts which were associated with them. The infection, or the eggs which hatch in the aquatic environment, were correlated with the water pollution in different districts of Thailand such as Ayuthaya Province. The high incidence of infection was prevalent in females and children ages 10–14 years of age.

References
Further reading
Graczyk TK, Gilman RH, Fried B (2001). "Fasciolopsiasis: is it a controllable food-borne disease?". Parasitol. Res. 87 (1): 80–3. doi:10.1007/s004360000299 </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Sneeze and can you explain it in depth? [/INST] A sneeze (also known as sternutation) is a semi-autonomous, convulsive expulsion of air from the lungs through the nose and mouth, usually caused by foreign particles irritating the nasal mucosa. A sneeze expels air forcibly from the mouth and nose in an explosive, spasmodic involuntary action. This action allows for mucus to escape through the nasal cavity. Sneezing is possibly linked to sudden exposure to bright light, sudden change (fall) in temperature, breeze of cold air, a particularly full stomach, exposure to allergens, or viral infection. Because sneezes can spread disease through infectious aerosol droplets, it is recommended to cover ones mouth and nose with the forearm, the inside of the elbow, a tissue or a handkerchief while sneezing. In addition to covering the mouth, looking down is also recommended in order to change the direction of the droplets spread and avoid high concentration in the human breathing heights.
The function of sneezing is to expel mucus containing foreign particles or irritants and cleanse the nasal cavity. During a sneeze, the soft palate and palatine uvula depress while the back of the tongue elevates to partially close the passage to the mouth, creating a venturi (similar to a carburetor) due to Bernoullis principle so that air ejected from the lungs is accelerated through the mouth and thus creating a low pressure point at the back of the nose. This way air is forced in through the front of the nose and the expelled mucus and contaminants are launched out the mouth. Sneezing with the mouth closed does expel mucus through the nose but is not recommended because it creates a very high pressure in the head and is potentially harmful.
Sneezing cannot occur during sleep due to REM atonia – a bodily state where motor neurons are not stimulated and reflex signals are not relayed to the brain. Sufficient external stimulants, however, may cause a person to wake from sleep to sneeze, but any sneezing occurring afterwards would take place with a partially awake status at minimum.

Description
Sneezing typically occurs when foreign particles or sufficient external stimulants pass through the nasal hairs to reach the nasal mucosa. This triggers the release of histamines, which irritate the nerve cells in the nose, resulting in signals being sent to the brain to initiate the sneeze through the trigeminal nerve network. The brain then relates this initial signal, activates the pharyngeal and tracheal muscles and creates a large opening of the nasal and oral cavities, resulting in a powerful release of air and bioparticles. The powerful nature of a sneeze is attributed to its involvement of numerous organs of the upper body – it is a reflexive response involving the face, throat, and chest muscles.
Sneezing is also triggered by sinus nerve stimulation caused by nasal congestion and allergies.
The neural regions involved in the sneeze reflex are located in the brainstem along the ventromedial part of the spinal trigeminal nucleus and the adjacent pontine-medullary lateral reticular formation. This region appears to control the epipharyngeal, intrinsic laryngeal and respiratory muscles, and the combined activity of these muscles serve as the basis for the generation of a sneeze.The sneeze reflex involves contraction of a number of different muscles and muscle groups throughout the body, typically including the eyelids. The common suggestion that it is impossible to sneeze with ones eyes open is, however, inaccurate. Other than irritating foreign particles, allergies or possible illness, another stimulus is sudden exposure to bright light – a condition known as photic sneeze reflex (PSR). Walking out of a dark building into sunshine may trigger PSR, or the ACHOO (autosomal dominant compulsive helio-ophthalmic outbursts of sneezing) syndrome as its also called. The tendency to sneeze upon exposure to bright light is an autosomal dominant trait and affects 18-35% of the human population. A rarer trigger, observed in some individuals, is the fullness of the stomach immediately after a large meal. This is known as snatiation and is regarded as a medical disorder passed along genetically as an autosomal dominant trait.

Epidemiology
While generally harmless in healthy individuals, sneezes spread disease through the infectious aerosol droplets, commonly ranging from 0.5 to 5 µm. A sneeze can produce 40,000 droplets. To reduce the possibility of thus spreading disease (such as the flu), one holds the forearm, the inside of the elbow, a tissue or a handkerchief in front of ones mouth and nose when sneezing. Using ones hand for that purpose has recently fallen into disuse as it is considered inappropriate, since it promotes spreading germs through human contact (such as handshaking) or by commonly touched objects (most notably doorknobs).
Until recently, the maximum visible distance over which the sneeze plumes (or puffs) travel was observed at 0.6 metres (2.0 ft), and the maximum sneeze velocity derived was 4.5 m/s (about 10 mph). In 2020, sneezes were recorded generating plumes of up to 8 meters (26 ft).

Prevention
Proven methods to reduce sneezing generally advocate reducing interaction with irritants, such as keeping pets out of the house to avoid animal dander; ensuring the timely and continuous removal of dirt and dust particles through proper housekeeping; replacing filters for furnaces and air-handling units; air filtration devices and humidifiers; and staying away from industrial and agricultural zones. Tickling the roof of the mouth with the tongue can stop a sneeze. Some people, however, find sneezes to be pleasurable and would not want to prevent them.Holding in sneezes, such as by pinching the nose or holding ones breath, is not recommended as the air pressure places undue stress on the lungs and airways. One computer simulation suggests holding in a sneeze results in a burst of air pressure of 39 kPa, approximately 24 times that of a normal sneeze.

History
In Ancient Greece, sneezes were believed to be prophetic signs from the gods. In 401 BC, for instance, the Athenian general Xenophon gave a speech exhorting his fellow soldiers to fight against the Persians. A soldier underscored his conclusion with a sneeze. Thinking that this sneeze was a favorable sign from the gods, the soldiers were impressed. Another divine moment of sneezing for the Greeks occurs in the story of Odysseus. His waiting wife Penelope, hearing Odysseus may be alive, says that he and his son would take revenge on the suitors if he were to return. At that moment, their son sneezes loudly and Penelope laughs with joy, reassured that it is a sign from the gods (Odyssey 17: 541-550). It may be because this belief survived through the centuries, that in certain parts of Greece today, when someone is asserting something and the listener sneezes promptly at the end of the assertion, the former responds "bless you and I am speaking the truth", or "bless you and here is the truth" ("γεια σου κι αλήθεια λέω", ya sou ki alithia leo, or "γεια σου και να κι η αλήθεια", ya sou ke na ki i alithia). A similar practice is also followed in India. If either the person just having made a not most obvious statement in Flemish, or some listener sneezes, often one of the listeneners will say "It is beniesd", literally "Its sneezed upon", as if a proof of truth – usually self-ironically recalling this old superstitious habit, without either suggesting doubt or intending an actual confirmation, but making any apology by the sneezer for the interruption superfluous as the remark is received by smiles.In Europe, principally around the early Middle Ages, it was believed that ones life was in fact tied to ones breath – a belief reflected in the word "expire" (originally meaning "to exhale") gaining the additional meaning of "to come to an end" or "to die". This connection, coupled with the significant amount of breath expelled from the body during a sneeze, had likely led people to believe that sneezing could easily be fatal. Such a theory could explain the reasoning behind the traditional English phrase, "God bless you", in response to a sneeze, the origins of which are not entirely clear (see "Traditional Responses To A Sneeze" below for alternative explanations). Sir Raymond Henry Payne Crawfurd, for instance, the registrar of the Royal College of Physicians, in his 1909 book, "The Last Days of Charles II", states that, when the controversial monarch was on his deathbed, his medical attendants administered a concoction of cowslips and extract of ammonia to promote sneezing. However, it is not known if this promotion of sneezing was done to hasten his death (as coup de grâce) or as an ultimate attempt at treatment.
In certain parts of Eastern Asia, particularly in Chinese culture, Korean culture, Japanese culture and Vietnamese culture, a sneeze without an obvious cause was generally perceived as a sign that someone was talking about the sneezer at that very moment. This can be seen in the Book of Songs (a collection of Chinese poems) in ancient China as early as 1000 BC, and in Japan this belief is still depicted in present-day manga and anime. In China, Vietnam, South Korea, and Japan, for instance, there is a superstition that if talking behind someones back causes the person being talked about to sneeze; as such, the sneezer can tell if something good is being said (one sneeze), someone is thinking about you (two sneezes in a row), even if someone is in love with you (three sneezes in a row) or if this is a sign that they are about to catch a cold (multiple sneezes).Parallel beliefs are known to exist around the world, particularly in contemporary Greek, Slavic, Celtic, English, French, and Indian cultures. Similarly, in Nepal, sneezers are believed to be remembered by someone at that particular moment.In English, the onomatopoeia for sneezes is usually spelled achoo and it is similar to that of different cultures.

Culture
In Indian culture, especially in northern parts of India, Bengali (Bangladesh and Bengal of India) culture and also in Iran, it has been a common superstition that a sneeze taking place before the start of any work was a sign of impending bad interruption. It was thus customary to pause in order to drink water or break any work rhythm before resuming the job at hand in order to prevent any misfortune from occurring.
Contrarily, in Polish culture, especially in the Kresy Wschodnie borderlands, a popular belief persists that sneezes may be an inauspicious sign that, depending on the local version, either someone unspecified or ones mother-in-law speaks ill of the person sneezing at that moment. In other regions, however, this superstition concerns hiccups rather than sneezing. As with other Catholic countries, such as Mexico, Italy, or Ireland, the remnants of pagan culture are fostered in Polish peasant idiosyncratic superstitions.

The practice among Islamic culture, in turn, has largely been based on various prophetic traditions and the teachings of the prophet Muhammad. An example of this is Al-Bukhaaris narrations from Abu Hurayrah that Muhammad once said:
When one of you sneezes, let him say, "Al-hamdu-Lillah" (Praise be to God), and let his brother or companion say to him, "Yarhamuk Allah" (May God have mercy on you). If he says, "Yarhamuk-Allah", then let [the sneezer] say, "Yahdeekum Allah wa yuslihu baalakum" (May God guide you and rectify your condition).

Verbal responses
In English-speaking countries, one common verbal response to another persons sneeze is "[May God] bless you".
Another less common verbal response in the United States and Canada to anothers sneeze is "Gesundheit", which is a German word that means, appropriately, "good health".
Several hypotheses exist for why the custom arose of saying "bless you" or "God bless you" in the context of sneezing:

Some say it came into use during the plague pandemics of the 14th century. Blessing the individual after showing such a symptom was thought to prevent possible impending death due to the lethal disease.
In Renaissance times, a superstition was formed claiming ones heart stopped for a very brief moment during the sneeze; saying bless you was a sign of prayer that the heart would not fail.
It has also been stated that one says "(God) bless you" so that one does not catch the flu, cold, or any other forms of sickness.Other cultures have similar traditions:

In China, after a person sneezes they often say "百岁!" which translates to "may you live one hundred years!" the pronunciation is similar to "bless you" in English. pronunciation: [Bai Sui]
In Iran, it is common to respond to sneezing with the Persian phrase عافیت باشه âfiyat bâše, which translates to "health", similar to common European expressions.
Indian culture is to respond with Krishna, similar to a blessing in western cultures.
In Italy after a person sneezes the people present respond with the word "salute" (meaning: health). The louder the sneeze the more emphatic the response.
In Slovakia, after a person sneezes, it is proper to say "Na zdravie!" which means "For health!"; a proper response should be "Ďakujem" which means "Thanks". This is also the case in Finland where "terveydeksi" means "for health". Likewise in Russian or Ukrainian, "будь здоров" (bud zdorov), translates as "be healthy".
In Tamil, a reciprocation to someones sneeze is "ஆயுசு நூறு" (aa-yu-su noo-ru) or "ஆயுள் நூறு" (aa-yul noo-ru) which, in direct translation, means "100 years-long life". It is a particularly endearing expression often used by elderly when a young child sneezes, wishing upon them good health, as a sort of blessing. Some may say "Dheergaiyish", meaning "may you live long", but that is more closely related to Sanskrit.
In Turkey, after a person sneezes, it is proper to say "Çok yaşa" which means "Live long"; a proper response should be "Sen de gör" which means "May you see too [that I lived long enough]".
In Telugu, a reciprocation to someones sneeze is "chiranjeeva sataish" (చిర౦జీవ) which means "may you live long" (from Sanskrit).
In Japanese and Chinese entertainment, such as anime or dramas, a characters sneeze usually means that someone is talking about the character.
In the Netherlands and Flanders, the usual verbal response is "Gezondheid!" which has the same meaning as the also occasionally used German word "Gesundheit!". This is usually met with a "Dankjewel" as a response, which means "Thank you".
In Sweden, Norway and Denmark after a person sneezes, it is proper to say "Prosit", which has latin roots, and loosely translates to "Be well" or "May it do you good".

Sexuality
Some people may sneeze during the initial phases of sexual arousal </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Brain death and can you explain it in depth? [/INST] Brain death is the permanent, irreversible, and complete loss of brain function which may include cessation of involuntary activity necessary to sustain life. It differs from persistent vegetative state, in which the person is alive and some autonomic functions remain. It is also distinct from comas as long as some brain and bodily activity and function remain, and it is also not the same as the condition locked-in syndrome. A differential diagnosis can medically distinguish these differing conditions.
Brain death is used as an indicator of legal death in many jurisdictions, but it is defined inconsistently and often confused by the public. Various parts of the brain may keep functioning when others do not anymore, and the term "brain death" has been used to refer to various combinations. For example, although one major medical dictionary considers "brain death" to be synonymous with "cerebral death" (death of the cerebrum), the US National Library of Medicine Medical Subject Headings (MeSH) system defines brain death as including the brainstem. The distinctions are medically significant because, for example, in someone with a dead cerebrum but a living brainstem, spontaneous breathing may continue unaided, whereas in whole-brain death (which includes brainstem death), only life support equipment would maintain ventilation. In certain countries, patients classified as brain-dead may legally have their organs surgically removed for organ donation.

Medicolegal history
Differences in operational definitions of death have obvious medicolegal implications (in medical jurisprudence and medical law). Traditionally, both the legal and medical communities determined death through the permanent end of certain bodily functions in clinical death, especially respiration and heartbeat. With the increasing ability of the medical community to resuscitate people with no respiration, heartbeat, or other external signs of life, the need for another definition of death occurred, raising questions of legal death. This gained greater urgency with the widespread use of life support equipment and the rising capabilities and demand for organ transplantation.
Since the 1960s, laws governing the determination of death have been implemented in all countries that have active organ transplantation programs. The first European country to adopt brain death as a legal definition (or indicator) of death was Finland in 1971, while in the United States, the state of Kansas had enacted a similar law earlier.An ad hoc committee at Harvard Medical School published a pivotal 1968 report to define irreversible coma. The Harvard criteria gradually gained consensus toward what is now known as brain death. In the wake of the 1976 Karen Ann Quinlan case, state legislatures in the United States moved to accept brain death as an acceptable indication of death. In 1981, a presidential commission issued a landmark report entitled Defining Death: Medical, Legal, and Ethical Issues in the Determination of Death, which rejected the "higher-brain" approach to death in favor of a "whole-brain" definition. This report formed the basis for the Uniform Determination of Death Act, since enacted in 39 states. Today, both the legal and medical communities in the US use "brain death" as a legal definition of death, allowing a person to be declared legally dead even if life support equipment maintains the bodys metabolic processes.In the UK, the Royal College of Physicians reported in 1995, abandoning the 1979 claim that the tests published in 1976 sufficed for the diagnosis of brain death, and suggesting a new definition of death based on the irreversible loss of brain-stem function alone. This new definition, the irreversible loss of the capacity for consciousness and for spontaneous breathing, and the essentially unchanged 1976 tests held to establish that state, have been adopted as a basis of death certification for organ transplant purposes in subsequent Codes of Practice. The Australia and New Zealand Intensive Care Society (ANZICS) states that the "determination of brain death requires that there is unresponsive coma, the absence of brain-stem reflexes and the absence of respiratory centre function, in the clinical setting in which these findings are irreversible. In particular, there must be definite clinical or neuro-imaging evidence of acute brain pathology (e.g. traumatic brain injury, intracranial haemorrhage, hypoxic encephalopathy) consistent with the irreversible loss of neurological function."  In Brazil, the Federal Council of Medicine revised its regulations in 2017, including "a requirement for the patient to meet specific physiological prerequisites and for the physician to provide optimized care to the patient before starting the procedures for diagnosing brain death and to perform complementary tests, as well as the need for specific training for physicians who make this diagnosis."
In 2020, an international panel of experts, the World Brain Death Project, published a guideline that:provides recommendations for the minimum clinical standards for determination of brain death/death by neurologic criteria (BD/DNC) in adults and children with clear guidance for various clinical circumstances. The recommendations have widespread international society endorsement and can serve to guide professional societies and countries in the revision or development of protocols and procedures for determination of brain death/death by neurologic criteria, leading to greater consistency within and between countries.

Medical criteria
Natural movements also known as the Lazarus sign or Lazarus reflex can occur on a brain-dead person whose organs have been kept functioning by life support. The living cells that can cause these movements are not living cells from the brain or brain stem; these cells come from the spinal cord. Sometimes these body movements can cause false hope for family members.
A brain-dead individual has no clinical evidence of brain function upon physical examination. This includes no response to pain and no cranial nerve reflexes. Reflexes include pupillary response (fixed pupils), oculocephalic reflex, corneal reflex, no response to the caloric reflex test, and no spontaneous respirations.
Brain death can sometimes be difficult to differentiate from other medical states such as barbiturate overdose, acute alcohol poisoning, sedative overdose, hypothermia, hypoglycemia, coma, and chronic vegetative states. Some comatose patients can recover to pre-coma or near pre-coma level of functioning, and some patients with severe irreversible neurological dysfunction will nonetheless retain some lower brain functions, such as spontaneous respiration, despite the losses of both cortex and brain stem functionality. Such is the case with anencephaly.
Brain electrical activity can stop completely, or drop to such a low level as to be undetectable with most equipment. An EEG will therefore be flat, though this is sometimes also observed during deep anesthesia or cardiac arrest. Although in the United States a flat EEG test is not required to certify death, it is considered to have confirmatory value. In the UK it is not considered to be of value because any continuing activity it might reveal in parts of the brain above the brain stem is held to be irrelevant to the diagnosis of death on the Code of Practice criteria.The diagnosis of brain death is often required to be highly rigorous, in order to be certain that the condition is irreversible. Legal criteria vary, but in general require neurological examinations by two independent physicians. The exams must show complete and irreversible absence of brain function (brain stem function in UK), and may include two isoelectric (flat-line) EEGs 24 hours apart (less in other countries where it is accepted that if the cause of the dysfunction is a clear physical trauma there is no need to wait that long to establish irreversibility). The patient should have a normal temperature and be free of drugs that can suppress brain activity if the diagnosis is to be made on EEG criteria.

Also, a radionuclide cerebral blood flow scan that shows complete absence of intracranial blood flow must be considered with other exams – temporary swelling of the brain, particularly within the first 72 hours, can lead to a false positive test on a patient that may recover with more time.CT angiography is neither required nor sufficient test to make the diagnosis.Confirmatory testing is only needed under the age of 1. For children and adults, testing is optional.  Other situations possibly requiring confirmatory testing include severe facial trauma where determination of brainstem reflexes will be difficult, pre-existing pupillary abnormalities, and patients with severe sleep apnea and/or pulmonary disease </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Bullous pemphigoid and can you explain it in depth? [/INST] Bullous pemphigoid (type of pemphigoid) is an autoimmune pruritic skin disease which typically occurs in people aged over 60, that may involve the formation of blisters (bullae) in the space between the epidermal and dermal skin layers. It is classified as a type II hypersensitivity reaction, which involves formation of anti-hemidesmosome antibodies, causing a loss of keratinocytes to basement membrane adhesion.

Signs and symptoms
Clinically, the earliest lesions may appear as a hives-like red raised rash, but could also appear dermatitic, targetoid, lichenoid, nodular, or even without a rash (essential pruritus). Tense bullae eventually erupt, most commonly at the inner thighs and upper arms, but the trunk and extremities are frequently both involved. Any part of the skin surface can be involved. Oral lesions are present in a minority of cases. The disease may be acute, but can last from months to years with periods of exacerbation and remission. Several other skin diseases may have similar symptoms. However, milia are more common with epidermolysis bullosa acquisita, because of the deeper antigenic targets.  A more ring-like configuration with a central depression or centrally collapsed bullae may indicate linear IgA disease. Nikolskys sign is negative, unlike pemphigus vulgaris, where it is positive.

Causes
In most cases of bullous pemphigoid, no clear precipitating factors are identified. Potential precipitating events that have been reported include exposure to ultraviolet light and radiation therapy. Onset of pemphigoid has also been associated with certain drugs, including furosemide, nonsteroidal anti-inflammatory agents, DPP-4 inhibitors, captopril, penicillamine, and antibiotics.

Pathophysiology
The bullae are formed by an immune reaction, initiated by the formation of IgG autoantibodies targeting dystonin, also called bullous pemphigoid antigen 1, and/or type XVII collagen, also called bullous pemphigoid antigen 2, which is a component of hemidesmosomes. A different form of dystonin is associated with neuropathy. Following antibody targeting, a cascade of immunomodulators results in a variable surge of immune cells, including neutrophils, lymphocytes and eosinophils coming to the affected area.  Unclear events subsequently result in a separation along the dermoepidermal junction and eventually stretch bullae.

Diagnosis
Diagnosis consist of at least 2 positive results out of 3 criteria (2-out-of-3 rule): (1) pruritus and/or predominant cutaneous blisters, (2) linear IgG and/or C3c deposits (in an n- serrated pattern) by direct immunofluorescence microscopy (DIF) on a skin biopsy specimen, and (3) positive epidermal side staining by indirect immunofluorescence microscopy on human salt-split skin (IIF SSS) on a serum sample. Routine H&E staining or ELISA tests do not add value to initial diagnosis.

Treatment
Treatments include topical steroids such as clobetasol, and halobetasol which in some studies have proven to be equally effective as systemic, or pill, therapy and somewhat safer </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Sleepwalking and can you explain it in depth? [/INST] Sleepwalking, also known as somnambulism or noctambulism, is a phenomenon of combined sleep and wakefulness. It is classified as a sleep disorder belonging to the parasomnia family. It occurs during slow wave stage of sleep, in a state of low consciousness, with performance of activities that are usually performed during a state of full consciousness. These activities can be as benign as talking, sitting up in bed, walking to a bathroom, consuming food, and cleaning, or as hazardous as cooking, driving a motor vehicle, violent gestures and grabbing at hallucinated objects.Although sleepwalking cases generally consist of simple, repeated behaviors, there are occasionally reports of people performing complex behaviors while asleep, although their legitimacy is often disputed. Sleepwalkers often have little or no memory of the incident, as their consciousness has altered into a state in which memories are difficult to recall. Although their eyes are open, their expression is dim and glazed over. This may last from 30 seconds to 30 minutes.Sleepwalking occurs during slow-wave sleep (N3) of non-rapid eye movement sleep (NREM sleep) cycles. It typically occurs within the first third of the night when slow-wave sleep is most prominent. Usually, it will occur once in a night, if at all.

Signs and symptoms
Sleepwalking is characterized by:
partial arousal during non-rapid eye movement (NREM) sleep, typically during the first third of the night
dream content that may or may not be recalled when awake
dream-congruent motor behavior that may be simple or complex
impaired perception of the environment
impaired judgement, planning and problem-solving.Despite how it is portrayed in many cultures (eyes closed and walking with arms outstretched), the sleepwalkers eyes are open but may appear as a glassy-eyed stare or blank expression and pupils are dilated. They are often disoriented, consequent to awakening: the sleepwalker may be confused and perplexed, and might not know why or how they got out of bed; however, the disorientation will fade within minutes.  They may talk while sleepwalking, but the talk typically does not make sense to the observer.  There are varying degrees of amnesia associated with sleepwalking, ranging from no memory at all, vague memories or a narrative.

Associated disorders
In the study "Sleepwalking and Sleep Terrors in Prepubertal Children" it was found that, if a child had another sleep disorder – such as restless leg syndrome (RLS) or sleep-disorder breathing (SDB) – there was a greater chance of sleepwalking. The study found that children with chronic parasomnias may often also present SDB or, to a lesser extent, RLS. Furthermore, the disappearance of the parasomnias after the treatment of the SDB or RLS periodic limb movement syndrome suggests that the latter may trigger the former. The high frequency of SDB in family members of children with parasomnia provided additional evidence that SDB may manifest as parasomnias in children. Children with parasomnias are not systematically monitored during sleep, although past studies have suggested that patients with sleep terrors or sleepwalking have an elevated level of brief EEG arousals. When children receive polysomnographies, discrete patterns (e.g., nasal flow limitation, abnormal respiratory effort, bursts of high or slow EEG frequencies) should be sought; apneas are rarely found in children. Childrens respiration during sleep should be monitored with nasal cannula or pressure transducer system or esophageal manometry, which are more sensitive than the thermistors or thermocouples currently used in many laboratories. The clear, prompt improvement of severe parasomnia in children who are treated for SDB, as defined here, provides important evidence that subtle SDB can have substantial health-related significance. Also noteworthy is the report of familial presence of parasomnia. Studies of twin cohorts and families with sleep terror and sleepwalking suggest genetic involvement of parasomnias. RLS and SDB have been shown to have familial recurrence. RLS has been shown to have genetic involvement.
Sleepwalking may also accompany the related phenomenon of night terrors, especially in children. In the midst of a night terror, the affected person may wander in a distressed state while still asleep, and examples of sufferers attempting to run or aggressively defend themselves during these incidents have been reported in medical literature.In some cases, sleepwalking in adults may be a symptom of a psychological disorder. One study suggests higher levels of dissociation in adult sleepwalkers, since test subjects scored unusually high on the hysteria portion of the "Crown-Crisp Experiential Index". Another suggested that "A higher incidence [of sleepwalking events] has been reported in patients with schizophrenia, hysteria and anxiety neuroses". Also, patients with migraine headaches or Tourette syndrome are 4–6 times more likely to sleepwalk.

Consequences
Most sleepwalkers get injuries at some point during sleepwalking, often minor injuries such as cuts or bruises. In rare occasions, however, sleepwalkers have fractured bones and died as the result of a fall. Sleepwalkers may also face embarrassment of being found naked in public.

Causes
The cause of sleepwalking is unknown. A number of, as yet unproven, hypotheses are suggested for why it might occur, including: delay in the maturity of the central nervous system, increased slow wave sleep, sleep deprivation, fever, and excessive tiredness.  There may be a genetic component to sleepwalking. One study found that sleepwalking occurred in 45% of children who have one parent who sleepwalked, and in 60% of children if both parents sleepwalked. Thus, heritable factors may predispose an individual to sleepwalking, but expression of the behavior may also be influenced by environmental factors. Genetic studies using common fruit flies as experimental models reveal a link between night sleep and brain development mediated by evolutionary conserved transcription factors such as AP-2 Sleepwalking may be inherited as an autosomal dominant disorder with reduced penetrance. Genome-wide multipoint parametric linkage analysis for sleepwalking revealed a maximum logarithm of the odds score of 3.14 at chromosome 20q12-q13.12 between 55.6 and 61.4 cM.Sleepwalking has been hypothesized to be linked to the neurotransmitter serotonin, which also appears to be metabolized differently in migraine patients and people with Tourette syndrome, both populations being four to nine times more likely to experience an episode of sleepwalking. Hormonal fluctuations have been found to contribute to sleepwalking episodes in women, with the likeliness to sleepwalk being higher before the onset of menstruation. It also appears that hormonal changes during pregnancy decrease the likelihood of engaging in sleepwalking Medications, primarily in four classes—benzodiazepine receptor agonists and other GABA modulators, antidepressants and other serotonergic agents, antipsychotics, and β-blockers— have been associated with sleepwalking. The best evidence of medications causing sleepwalking is for Zolpidem and sodium oxybate; all other reports are based on associations noted in case reports.A number of conditions, such as Parkinsons disease, are thought to trigger sleepwalking in people without a previous history of sleepwalking.

Diagnosis
Polysomnography is the only accurate assessment of a sleepwalking episode. Because this is costly and sleepwalking episodes are usually infrequent, other measures commonly used include self-, parent-, or partner-report. Three common diagnostic systems that are generally used for sleepwalking disorders are International Classification of Diseases (ICD-10), the International Classification of Sleep Disorders (ICSD-3), and the Diagnostic and Statistical Manual.The Diagnostic and Statistical Manual defines two subcategories of sleepwalking, although sleepwalking does not need to involve either behaviours:

sleepwalking with sleep-related eating.
sleepwalking with sleep-related sexual behavior (sexsomnia).Sleep eating involves consuming food while asleep. These sleep eating disorders are more often than not induced for stress related reasons. Another major cause of this sleep eating subtype of sleepwalking is sleep medication, such as Ambien for example (Mayo Clinic). There are a few others, but Ambien is a more widely used sleep aid. Because many sleep eaters prepare the food they consume, there are risks involving burns and such with ovens and other appliances. As expected, weight gain is also a common outcome of this disorder, because food that is frequently consumed contains high carbohydrates. As with sleepwalking, there are ways that sleep eating disorders can be maintained. There are some medications that calm the sleeper so they can get longer and better-quality rest, but activities such as yoga can also be introduced to reduce the stress and anxiety causing the action.

Differential diagnoses
Sleepwalking should not be confused with alcohol- or drug-induced blackouts, which can result in amnesia for events similar to sleepwalking. During an alcohol-induced blackout (drug-related amnesia), a person is able to actively engage and respond to their environment (e.g. having conversations or driving a vehicle), however the brain does not create memories for the events. Alcohol-induced blackouts can occur with blood alcohol levels higher than 0.06g/dl. A systematic review of the literature found that approximately 50% of drinkers have experienced memory loss during a drinking episode and have had associated negative consequences similar to sleepwalkers, including injury and death.Other differential diagnoses include Rapid eye movement sleep behavior disorder, confusional arousals, and night terrors.

Assessment
An assessment of sleepwalking via polysomnography poses the problem that sleepwalking is less likely to occur in the sleep laboratory, and if an episode occurs, it is usually less complex than what the patient experiences at home. Therefore, the diagnosis can often be made by assessment of sleep history, time-course and content of the sleep related behaviors. Sometimes, home videos can provide additional information and should be considered in the diagnostic process.Some features that should always be assessed include:
Age of onset
When the episode occurs during the sleep period
How often these episodes occur (frequency) and how long they last (duration)
Description of the episode, including behavior, emotions, and thoughts during and after the event
How responsive the patient is to external stimuli during the episode
How conscious or aware the patient is, when awakened from an episode
If the episode is remembered afterwards
The triggers or precipitating factors
Sleep–wake pattern and sleep environment
Daytime sleepiness
Other sleep disorders that might be present
Family history for NREM parasomnias and other sleep disorders
Medical, psychiatric, and neurological history
Medication and substance use historyThe assessment should rule out differential diagnoses.

Treatment
There have been no clinical trials to show that any psychological or pharmacological intervention is effective in preventing sleepwalking episodes. Despite this, a wide range of treatments have been used with sleepwalkers. Psychological interventions have included psychoanalysis, hypnosis, scheduled or anticipatory waking, assertion training, relaxation training, managing aggressive feelings, sleep hygiene, classical conditioning (including electric shock), and play therapy. Pharmacological treatments have included tricyclic antidepressants (imipramine), an anticholinergic (biperiden), antiepileptics (carbamazepine, valproate), an antipsychotic (quetiapine), benzodiazepines (clonazepam, diazepam, flurazepam and triazolam), melatonin, a selective serotonin reuptake inhibitor (paroxetine), a barbiturate (sodium amytal) and herbs.There is no evidence to show that waking sleepwalkers is harmful or not, though the sleepwalker is likely to be disoriented if awakened as sleepwalking occurs during the deepest stage of sleep.Unlike other sleep disorders, sleepwalking is not associated with daytime behavioral or emotional problems. This may be because the sleepwalkers sleep is not disturbed—unless they are woken, they are still in a sleep state while sleepwalking.Maintaining the safety of the sleepwalker and others and seeking treatment for other sleep problems is recommended. Reassurance is recommended if sleepwalking is not causing any problems.  However, if it causes distress or there is risk of harm, hypnosis and scheduled waking are recommended as treatments.

Safety planning
For those whose sleepwalking episodes are hazardous, a door alarm may offer a measure of protection. There are various kinds of door alarms that can attach to a bedroom door and when the door is opened, the alarm sounds. The intention is that the sound will fully awaken the person and interrupt the sleepwalking episode, or if the sleepwalker lives with others, the sound will prompt them to check on the person.
Sleepwalkers should aim to have their bedrooms on the ground floor of a home, apartment, dorm, hotel, etc.
Sleepwalkers should not have easily accessible weapons (loaded guns, knives) in the bedroom or any room of the house for that matter. If there are weapons, they should be locked away with keys secluded from the sleepwalker.For partners of sleepwalkers who are violent or disturb their sleep, sleeping in another room may lead to better sleep quality and quantity.

Epidemiology
The lifetime prevalence of sleepwalking is estimated to be 4.6%–10.3%.  A meta-analysis of 51 studies, that included more than 100,000 children and adults, found that sleepwalking is more common in children with an estimated 5%, compared with 1.5% of adults, sleepwalking at least once in the previous 12 months. The rate of sleepwalking has not been found to vary across ages during childhood.

History
Sleepwalking has attracted a sense of mystery, but was not seriously investigated and diagnosed until the 19th century. The German chemist and parapsychologist Baron Karl Ludwig von Reichenbach (1788–1869) made extensive studies of sleepwalkers and used his discoveries to formulate his theory of the Odic force.Sleepwalking was initially thought to be a dreamer acting out a dream. For example, in one study published by the Society for Science & the Public in 1954, this was the conclusion: "Repression of hostile feelings against the father caused the patients to react by acting out in a dream world with sleepwalking, the distorted fantasies they had about all authoritarian figures, such as fathers, officers and stern superiors." This same group published an article twelve years later with a new conclusion: "Sleepwalking, contrary to most belief, apparently has little to do with dreaming. In fact, it occurs when the sleeper is enjoying his most oblivious, deepest sleep—a stage in which dreams are not usually reported." More recent research has discovered that sleepwalking is actually a disorder of NREM (non-rapid eye movement) arousal. Acting out a dream is the basis for a REM (rapid eye movement) sleep disorder called REM Behavior Disorder (or REM Sleep Behavior Disorder). More accurate data about sleep is due to the invention of technologies, such as the electroencephalogram (EEG) by Hans Berger in 1924 and BEAM by Frank Duffy in the early 1980s.In 1907, Sigmund Freud spoke about sleepwalking to the Vienna Psychoanalytic Society (Nunberg and Federn). He believed that sleepwalking was connected to fulfilling sexual wishes and was surprised that a person could move without interrupting their dream. At that time, Freud suggested that the essence of this phenomenon was the desire to go to sleep in the same area as the individual had slept in childhood. Ten years later, he speculated about somnambulism in the article "A Metapsychological Supplement to the Theory of Dreams" (1916–17 [1915]). In this essay, he clarified and expanded his hypothetical ideas on dreams. He described the dream as a fragile equilibrium that is destabilized by the repressed unconscious impulses of the unconscious system, which does not obey the wishes of the ego. Certain preconscious daytime thoughts can be resistant and these can retain a part of their cathexis as well. Unconscious impulses and day residues can come together and result in a conflict. Freud then wondered about the outcome of this wishful impulse: an unconscious instinctual demand that becomes a dream wish in the preconscious. Freud stated that this unconscious impulse could be expressed as mobility during sleep. This would be what is observed in somnambulism, though what actually makes it possible remains unknown.As of 2002, sleepwalking has not been detected in non-human primates.
It is unclear whether it simply hasnt been observed yet, or whether sleepwalking is a uniquely human phenomenon.

Society and culture
Opera
Vincenzo Bellinis 1831 Italian opera semiseria, La sonnambula, the plot of which is centered on the question of the innocence of the betrothed and soon-to-be married Amina, who, upon having been discovered in the bedchamber of a stranger, and despite the assurances of that stranger that Amina was entirely innocent, has been rejected by her enraged fiancé, Elvino — who, then, decides to marry another. In fact, when stressed, Amina was susceptible to somnambulism; and had come to be in the strangers bedchamber by sleep-walking along a high parapet (in full view of the operas audience). Elvino, who later observes the (exhausted by all the fuss) Amina, sleep-walking across a very high, very unstable, and very rickety bridge at the local mill, realizes his mistake, abandons his plans of marriage to the other woman, and re-unites with Amina.

Jenny Lind and James Braid
In August 1847, the famous soprano Jenny Lind visited Manchester, and gave two performances as Amina. The outstanding difference between Lind and her contemporaries was that, "whilst the beauty of her voice was far greater than any other in living memory (thus, the Swedish Nightingale), what really set her apart was her outstanding ability to act"; and, moreover, in performing as Amina, rather than walking along a wide and well-protected walkway (as the others did), she routinely acrobatically balanced her way along narrow planks.While she was in Manchester—on the basis that, at the time, many characterized "hypnotism" as "artificial somnambulism", and that, from a rather different perspective, her stage performance could also be described as one of "artificial" (rather than spontaneous) somnambulism—her friends arranged for her to visit the local surgeon James Braid, who had discovered hypnotism in 1841:
"Mr. Braid, surgeon, whose discoveries in hypnotism are well known, having invited the fair impersonator of a somnambulist to witness some of the abnormal feats of a real somnambulist, artificially thrown into that state, it was arranged that a private séance should take place [on Friday, 3 September 1847]." Manchester Guardian, 8 September 1847.

Drama
The sleepwalking scene (Act V Scene 1) from William Shakespeares tragic play Macbeth (1606) is one of the most famous scenes in all of literature.
In Walley Chamberlain Oultons two act farce The Sleep-Walker; or, Which is the Lady (1812), "Somno", a histrionic failed-actor-turned-manservant relives his wished-for roles when sleepwalking.

Literature
In Bram Stokers novel Dracula, the character Lucy Westenra is described as a sleepwalker. It is while sleepwalking that Count Dracula lures and attacks her.

Sleepwalking as a legal defense
As sleepwalking behaviours occur without volition, sleepwalking can be used as a legal defense, as a form of legal automatism. An individual can be accused of non-insane or insane automatism. The first is used as a defense for temporary insanity or involuntary conduct, resulting in acquittal. The latter results in a "special verdict of not guilty by reason of insanity." This verdict of insanity can result in a court order to attend a mental institution.In the 1963 case Bratty v A-G for Northern Ireland, Lord Morris stated, "Each set of facts must require a careful examination of its own circumstances, but if by way of taking an illustration it were considered possible for a person to walk in his sleep and to commit a violent crime while genuinely unconscious, then such a person would not be criminally liable for that act." While the veracity of the cases are disputed, there have been acts of homicide where the prime suspect may have committed the act while sleepwalking.
Alternative explanations to homicidal or violent sleepwalking include malingering, drug-induced amnesia, and other disorders in which sleep-related violence may occur, such as REM Sleep Behavior Disorder, fugue states, and episodic wandering.

Historical cases
1846, Albert Tirrell used sleepwalking as a defense against charges of murdering Maria Bickford, a prostitute living in a Boston brothel.
1961, Sergeant Willis Boshears confessed to strangling a local woman named Jean Constable in the early hours on New Years Day 1961, but claimed that he was asleep and only woke to realize what he had done. He pled not guilty on the basis of being asleep at the time he committed the offence and was acquitted.
In 1981, Steven Steinberg of Scottsdale, Arizona was accused of killing his wife and acquitted on the grounds of temporary insanity.
1991, R v Burgess: Burgess was accused of hitting his girlfriend on the head with a wine bottle and then a video tape recorder. He was found not guilty at Bristol Crown Court, by reason of insane automatism.
1992, R. v. Parks: Parks was accused of killing his mother-in-law and attempting to kill his father-in-law. He was acquitted by the Supreme Court of Canada.
1994, Pennsylvania v. Ricksgers: Ricksgers was accused of killing his wife. He was sentenced to life in prison without parole.
1999, Arizona v. Falater: Scott Falater, of Phoenix, Arizona, was accused of killing his wife. The court concluded that the murder was too complex to be committed while sleepwalking. Falater was convicted of first-degree murder and sentenced to life with no possibility of parole.
2001, California v </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Polycystic kidney disease and can you explain it in depth? [/INST] Polycystic kidney disease (PKD or PCKD, also known as polycystic kidney syndrome) is a genetic disorder in which the renal tubules become structurally abnormal, resulting in the development and growth of multiple cysts within the kidney. These cysts may begin to develop in utero, in infancy, in childhood, or in adulthood. Cysts are non-functioning tubules filled with fluid pumped into them, which range in size from microscopic to enormous, crushing adjacent normal tubules and eventually rendering them non-functional as well.
PKD is caused by abnormal genes that produce a specific abnormal protein; this protein has an adverse effect on tubule development. PKD is a general term for two types, each having their own pathology and  genetic cause: autosomal dominant polycystic kidney disease (ADPKD) and autosomal recessive polycystic kidney disease (ARPKD). The abnormal gene exists in all cells in the body; as a result, cysts may occur in the liver, seminal vesicles, and pancreas. This genetic defect can also cause aortic root aneurysms, and aneurysms in the circle of Willis cerebral arteries, which if they rupture, can cause a subarachnoid hemorrhage.
Diagnosis may be suspected from one, some, or all of the following: new onset flank pain or red urine; a positive family history; palpation of enlarged kidneys on physical exam; an incidental finding on abdominal sonogram; or an incidental finding of abnormal kidney function on routine lab work (BUN, serum creatinine, or eGFR). Definitive diagnosis is made by abdominal CT exam.
Complications include hypertension due to the activation of the renin–angiotensin–aldosterone system (RAAS), frequent cyst infections, urinary bleeding, and declining renal function. Hypertension is treated with angiotensin converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs). Infections are treated with antibiotics. Declining renal function is treated with renal replacement therapy (RRT): dialysis and/or transplantation.  Management from the time of the suspected or definitive diagnosis is by a board-certified nephrologist.

Signs and symptoms
Signs and symptoms include high blood pressure, headaches, abdominal pain, blood in the urine, and excessive urination. Other symptoms include pain in the back, and cyst formation (renal and other organs).

Cause
PKD is caused by abnormal genes which produce a specific abnormal protein which has an adverse effect on tubule development. PKD is a general term for two types, each having their own pathology and  genetic cause: autosomal dominant polycystic kidney disease (ADPKD) and autosomal recessive polycystic kidney disease (ARPKD).

Autosomal dominant
Autosomal dominant polycystic kidney disease (ADPKD) is the most common of all the inherited cystic kidney diseases with an incidence of 1:500 live births. Studies show that 10% of end-stage kidney disease (ESKD) patients being treated with dialysis in Europe and the U.S. were initially diagnosed and treated for ADPKD.Genetic mutations in any of the three genes PKD1, PKD2, and PKD3 have similar phenotypical presentations.
Gene PKD1 is located on chromosome 16 and codes for a protein involved in regulation of cell cycle and intracellular calcium transport in epithelial cells, and is responsible for 85% of the cases of ADPKD.
Gene PKD2 is identified, using genetic linkage study, on chromosome 4. A group of voltage-linked cation channels, with inward selectivity for K>Na>>Ca and outward selectivity for Ca2+ ≈ Ba2+ > Na+ ≈ K+, are coded for by PKD2 on chromosome 4.
PKD3 recently appeared in research papers as a postulated third gene. Fewer than 10% of cases of ADPKD appear in non-ADPKD families. Cyst formation begins in utero from any point along the nephron, although fewer than 5% of nephrons are thought to be involved. As the cysts accumulate fluid, they enlarge, separate entirely from the nephron, compress the neighboring kidney parenchyma, and progressively compromise kidney function.

Autosomal recessive
Autosomal recessive polycystic kidney disease (ARPKD) (OMIM #263200) is the less common of the two types of PKD, with an incidence of 1:20,000 live births and is typically identified in the first few weeks after birth. Unfortunately, the kidneys are often underdeveloped resulting in a 30% death rate in newborns with ARPKD. PKHD1 is involved.

Mechanism
Both autosomal dominant and autosomal recessive polycystic kidney disease cyst formation are tied to abnormal cilia-mediated signaling. The polycystin-1 and polycystin-2 proteins appear to be involved in both autosomal dominant and recessive polycystic kidney disease due to defects in both proteins. Both proteins have communication with calcium channel proteins, and causes reduction in resting (intracellular) calcium and endoplasmic reticulum storage of calcium.The disease is characterized by a ‘second hit’ phenomenon, in which a mutated dominant allele is inherited from a parent, with cyst formation occurring only after the normal, wild-type gene sustains a subsequent second genetic ‘hit’, resulting in renal tubular cyst formation and disease progression.PKD results from defects in the primary cilium, an immotile, hair-like cellular organelle present on the surface of most cells in the body, anchored in the cell body by the basal body. In the kidney, primary cilia have been found to be present on most cells of the nephron, projecting from the apical surface of the renal epithelium into the tubule lumen. The cilia were believed to bend in the urine flow, leading to changes in signalling, however this has since been shown to be an experimental error (the bending of cilia was an artifact of focal plane compensation, and also the actual effect on micturition by severe hypertension and cardiac arrest) and that bending of cilia does not contribute to alterations in Ca flux. While it is not known how defects in the primary cilium lead to cyst development, it is thought to possibly be related to disruption of one of the many signaling pathways regulated by the primary cilium, including intracellular calcium, Wnt/β-catenin, cyclic adenosine monophosphate (cAMP), or planar cell polarity (PCP). Function of the primary cilium is impaired, resulting in disruption of a number of intracellular signaling cascades which produce differentiation of cystic epithelium, increased cell division, increased apoptosis, and loss of resorptive capacity.

Diagnosis
Polycystic kidney disease can be ascertained via a CT scan of abdomen, as well as, an MRI and ultrasound of the same area </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Dysgeusia and can you explain it in depth? [/INST] Dysgeusia, also known as parageusia, is a distortion of the sense of taste. Dysgeusia is also often associated with ageusia, which is the complete lack of taste, and hypogeusia, which is a decrease in taste sensitivity. An alteration in taste or smell may be a secondary process in various disease states, or it may be the primary symptom. The distortion in the sense of taste is the only symptom, and diagnosis is usually complicated since the sense of taste is tied together with other sensory systems. Common causes of dysgeusia include chemotherapy, asthma treatment with albuterol, and zinc deficiency. Liver disease, hypothyroidism, and rarely certain types of seizures can also lead to dysgeusia. Different drugs could also be responsible for altering taste and resulting in dysgeusia. Due to the variety of causes of dysgeusia, there are many possible treatments that are effective in alleviating or terminating the symptoms of dysgeusia. These include artificial saliva, pilocarpine, zinc supplementation, alterations in drug therapy, and alpha lipoic acid.

Signs and symptoms
The alterations in the sense of taste, usually a metallic taste, and sometimes smell are the only symptoms.

Causes
Chemotherapy
A major cause of dysgeusia is chemotherapy for cancer. Chemotherapy often induces damage to the oral cavity, resulting in oral mucositis, oral infection, and salivary gland dysfunction. Oral mucositis consists of inflammation of the mouth, along with sores and ulcers in the tissues. Healthy individuals normally have a diverse range of microbial organisms residing in their oral cavities; however, chemotherapy can permit these typically non-pathogenic agents to cause serious infection, which may result in a decrease in saliva. In addition, patients who undergo radiation therapy also lose salivary tissues. Saliva is an important component of the taste mechanism. Saliva both interacts with and protects the taste receptors in the mouth. Saliva mediates sour and sweet tastes through bicarbonate ions and glutamate, respectively. The salt taste is induced when sodium chloride levels surpass the concentration in the saliva. It has been reported that 50% of chemotherapy patients have had either dysgeusia or another form of taste impairment. Examples of chemotherapy treatments that can lead to dysgeusia are cyclophosphamide, cisplatin, vismodegib, and etoposide. The exact mechanism of chemotherapy-induced dysgeusia is unknown.

Taste buds
Distortions in the taste buds may give rise to dysgeusia. In a study conducted by Masahide Yasuda and Hitoshi Tomita from Nihon University of Japan, it has been observed that patients with this taste disorder have fewer microvilli than normal. In addition, the nucleus and cytoplasm of the taste bud cells have been reduced. Based on their findings, dysgeusia results from loss of microvilli and the reduction of Type III intracellular vesicles, all of which could potentially interfere with the gustatory pathway.  Radiation to head and neck also results in direct destruction of taste buds, apart from effects of altered salivary output.

Zinc deficiency
Another primary cause of dysgeusia is zinc deficiency. While the exact role of zinc in dysgeusia is unknown, it has been cited that zinc is partly responsible for the repair and production of taste buds. Zinc somehow directly or indirectly interacts with carbonic anhydrase VI, influencing the concentration of gustin, which is linked to the production of taste buds. It has also been reported that patients treated with zinc experience an elevation in calcium concentration in the saliva. In order to work properly, taste buds rely on calcium receptors. Zinc “is an important cofactor for alkaline phosphatase, the most abundant enzyme in taste bud membranes; it is also a component of a parotid salivary protein important to the development and maintenance of normal taste buds.”

Drugs
There are also a wide variety of drugs that can trigger dysgeusia, including zopiclone, H1-antihistamines, such as azelastine and emedastine. Approximately 250 drugs affect taste, including Paxlovid, a drug used to treat COVID-19. Some describe so-called "Paxlovid mouth" as like a "mouthful of dirty pennies and rotten soymilk," according to the Wall Street Journal.The sodium channels linked to taste receptors can be inhibited by amiloride, and the creation of new taste buds and saliva can be impeded by antiproliferative drugs. Saliva can have traces of the drug, giving rise to a metallic flavor in the mouth; examples include lithium carbonate and tetracyclines. Drugs containing sulfhydryl groups, including penicillamine and captopril, may react with zinc and cause deficiency. Metronidazole and chlorhexidine have been found to interact with metal ions that associate with the cell membrane. Drugs that act by blocking the renin - angiotensin - aldosterone system, for example by antagonizing the angiotensin II receptor (as eprosartan does), have been linked to dysgeusia. There are few case reports claiming calcium channel blockers like Amlodipine also cause dysguesia by blocking calcium sensitive taste buds.

Pregnancy
Changes in hormone levels during pregnancy, such as estrogen, can affect the sense of taste. A study found that 93 percent of pregnant women reported some change in taste during pregnancy.

Miscellaneous causes
Xerostomia, also known as dry mouth syndrome, can precipitate dysgeusia because normal salivary flow and concentration are necessary for taste. Injury to the glossopharyngeal nerve can result in dysgeusia. In addition, damage done to the pons, thalamus, and midbrain, all of which compose the gustatory pathway, can be potential factors. In a case study, 22% of patients who were experiencing a bladder obstruction were also experiencing dysgeusia. Dysgeusia was eliminated in 100% of these patients once the obstruction was removed. Although it is uncertain what the relationship between bladder relief and dysgeusia entails, it has been observed that the areas responsible for urinary system and taste in the pons and cerebral cortex in the brain are close in proximity.Dysgeusia often occurs for unknown reasons. A wide range of miscellaneous factors may contribute to this taste disorder, such as gastric reflux, lead poisoning, and diabetes mellitus. A minority of pine nuts can apparently cause taste disturbances, for reasons which are not entirely proven. Certain pesticides can have damaging effects on the taste buds and nerves in the mouth. These pesticides include organochloride compounds and carbamate pesticides. Damage to the peripheral nerves, along with injury to the chorda tympani branch of the facial nerve, also cause dysgeusia. A surgical risk for laryngoscopy and tonsillectomy include dysgeusia. Patients with the burning mouth syndrome, most likely menopausal women, often have dysgeusia as well.

Normal function
The sense of taste is based on the detection of chemicals by specialized taste cells in the mouth. The mouth, throat, larynx, and esophagus all have taste buds, which are replaced every ten days. Each taste bud contains receptor cells. Afferent nerves make contact with the receptor cells at the base of the taste bud. A single taste bud is innervated by several afferent nerves, while a single efferent fiber innervates several taste buds. Fungiform papillae are present on the anterior portion of the tongue while circumvallate papillae and foliate papillae are found on the posterior portion of the tongue. The salivary glands are responsible for keeping the taste buds moist with saliva.A single taste bud is composed of four types of cells, and each taste bud has between 30 and 80 cells. Type I cells are thinly shaped, usually in the periphery of other cells. They also contain high amounts of chromatin. Type II cells have prominent nuclei and nucleoli with much less chromatin than Type I cells. Type III cells have multiple mitochondria and large vesicles. Type I, II, and III cells also contain synapses. Type IV cells are normally rooted at the posterior end of the taste bud. Every cell in the taste bud forms microvilli at the ends.

Diagnosis
In general, gustatory disorders are challenging to diagnose and evaluate. Because gustatory functions are tied to the sense of smell, the somatosensory system, and the perception of pain (such as in tasting spicy foods), it is difficult to examine sensations mediated through an individual system. In addition, gustatory dysfunction is rare when compared to olfactory disorders.Diagnosis of dysgeusia begins with the patient being questioned about salivation, swallowing, chewing, oral pain, previous ear infections (possibly indicated by hearing or balance problems), oral hygiene, and stomach problems. The initial history assessment also considers the possibility of accompanying diseases such as diabetes mellitus, hypothyroidism, or cancer. A clinical examination is conducted and includes an inspection of the tongue and the oral cavity. Furthermore, the ear canal is inspected, as lesions of the chorda tympani have a predilection for this site.

Gustatory testing
In order to further classify the extent of dysgeusia and clinically measure the sense of taste, gustatory testing may be performed. Gustatory testing is performed either as a whole-mouth procedure or as a regional test. In both techniques, natural or electrical stimuli can be used. In regional testing, 20 to 50 µL of liquid stimulus is presented to the anterior and posterior tongue using a pipette, soaked filter-paper disks, or cotton swabs. In whole mouth testing, small quantities (2-10 mL) of solution are administered, and the patient is asked to swish the solution around in the mouth.Threshold tests for sucrose (sweet), citric acid (sour), sodium chloride (salty), and quinine or caffeine (bitter) are frequently performed with natural stimuli. One of the most frequently used techniques is the "three-drop test." In this test, three drops of liquid are presented to the subject. One of the drops is of the taste stimulus, and the other two drops are pure water. Threshold is defined as the concentration at which the patient identifies the taste correctly three times in a row.Suprathreshold tests, which provide intensities of taste stimuli above threshold levels, are used to assess the patients ability to differentiate between different intensities of taste and to estimate the magnitude of suprathreshold loss of taste. From these tests, ratings of pleasantness can be obtained using either the direct scaling or magnitude matching method and may be of value in the diagnosis of dysgeusia. Direct scaling tests show the ability to discriminate among different intensities of stimuli and whether a stimulus of one quality (sweet) is stronger or weaker than a stimulus of another quality (sour). Direct scaling cannot be used to determine if a taste stimulus is being perceived at abnormal levels. In this case, magnitude matching is used, in which a patient is asked to rate the intensities of taste stimuli and stimuli of another sensory system, such as the loudness of a tone, on a similar scale. For example, the Connecticut Chemosensory Clinical Research Center asks patients to rate the intensities of NaCl, sucrose, citric acid and quinine-HCl stimuli, and the loudness of 1000 Hz tones.Other tests include identification or discrimination of common taste substances. Topical anesthesia of the tongue has been reported to be of use in the diagnosis of dysgeusia as well, since it has been shown to relieve the symptoms of dysgeusia temporarily. In addition to techniques based on the administration of chemicals to the tongue, electrogustometry is frequently used. It is based on the induction of gustatory sensations by means of an anodal electrical direct current. Patients usually report sour or metallic sensations similar to those associated with touching both poles of a live battery to the tongue. Although electrogustometry is widely used, there seems to be a poor correlation between electrically and chemically induced sensations.

Diagnostic tools
Certain diagnostic tools can also be used to help determine the extent of dysgeusia. Electrophysiological tests and simple reflex tests may be applied to identify abnormalities in the nerve-to-brainstem pathways. For example, the blink reflex may be used to evaluate the integrity of the trigeminal nerve–pontine brainstem–facial nerve pathway, which may play a role in gustatory function.Structural imaging is routinely used to investigate lesions in the taste pathway. Magnetic resonance imaging allows direct visualization of the cranial nerves. Furthermore, it provides significant information about the type and cause of a lesion. Analysis of mucosal blood flow in the oral cavity in combination with the assessment of autonomous cardiovascular factors appears to be useful in the diagnosis of autonomic nervous system disorders in burning mouth syndrome and in patients with inborn disorders, both of which are associated with gustatory dysfunction. Cell cultures may also be used when fungal or bacterial infections are suspected.In addition, the analysis of saliva should be performed, as it constitutes the environment of taste receptors, including transport of tastes to the receptor and protection of the taste receptor. Typical clinical investigations involve sialometry and sialochemistry. Studies have shown that electron micrographs of taste receptors obtained from saliva samples indicate pathological changes in the taste buds of patients with dysgeusia and other gustatory disorders.

Treatments
Artificial saliva and pilocarpine
Because medications have been linked to approximately 22% to 28% of all cases of dysgeusia, researching a treatment for this particular cause has been important. Xerostomia, or a decrease in saliva flow, can be a side effect of many drugs, which, in turn, can lead to the development of taste disturbances such as dysgeusia. Patients can lessen the effects of xerostomia with breath mints, sugarless gum, or lozenges, or physicians can increase saliva flow with artificial saliva or oral pilocarpine. Artificial saliva mimics the characteristics of natural saliva by lubricating and protecting the mouth but does not provide any digestive or enzymatic benefits. Pilocarpine is a cholinergic drug meaning it has the same effects as the neurotransmitter acetylcholine. Acetylcholine has the function of stimulating the salivary glands to actively produce saliva. The increase in saliva flow is effective in improving the movement of tastants to the taste buds.

Zinc deficiency
Zinc supplementation
Approximately one half of drug-related taste distortions are caused by a zinc deficiency. Many medications are known to chelate, or bind, zinc, preventing the element from functioning properly. Due to the causal relationship of insufficient zinc levels to taste disorders, research has been conducted to test the efficacy of zinc supplementation as a possible treatment for dysgeusia. In a randomized clinical trial, fifty patients with idiopathic dysgeusia were given either zinc or a lactose placebo. The patients prescribed the zinc reported experiencing improved taste function and less severe symptoms compared to the control group, suggesting that zinc may be a beneficial treatment. The efficacy of zinc, however, has been ambiguous in the past. In a second study, 94% of patients who were provided with zinc supplementation did not experience any improvement in their condition. This ambiguity is most likely due to small sample sizes and the wide range of causes of dysgeusia. A recommended daily oral dose of 25–100 mg, as zinc gluconate, appears to be an effective treatment for taste dysfunction provided that there are low levels of zinc in the blood serum. There is not a sufficient amount of evidence to determine whether or not zinc supplementation is able to treat dysgeusia when low zinc concentrations are not detected in the blood.A Cochrane Review in 2017 assessed the effects of different interventions for the management of taste disturbances. There was very low-quality evidence to support the role of zinc supplementation in the improvement of taste acuity and taste discrimination in patients with zinc deficiency or idiopathic taste disorders. Further research is required to improve the quality of evidence for zinc supplementation as an effective intervention for the management of dysgeusia.

Zinc infusion in chemotherapy
It has been reported that approximately 68% of cancer patients undergoing chemotherapy experience disturbances in sensory perception such as dysgeusia. In a pilot study involving twelve lung cancer patients, chemotherapy drugs were infused with zinc in order to test its potential as a treatment. The results indicated that, after two weeks, no taste disturbances were reported by the patients who received the zinc-supplemented treatment while most of the patients in the control group who did not receive the zinc reported taste alterations. A multi-institutional study involving a larger sample size of 169 patients, however, indicated that zinc-infused chemotherapy did not have an effect on the development of taste disorders in cancer patients. An excess amount of zinc in the body can have negative effects on the immune system, and physicians must use caution when administering zinc to immunocompromised cancer patients. Because taste disorders can have detrimental effects on a patients quality of life, more research needs to be conducted concerning possible treatments such as zinc supplementation.

Altering drug therapy
The effects of drug-related dysgeusia can often be reversed by stopping the patients regimen of the taste altering medication. In one case, a forty-eight-year-old woman who had hypertension was being treated with valsartan. Due to this drugs inability to treat her condition, she began taking a regimen of eprosartan, an angiotensin II receptor antagonist. Within three weeks, she began experiencing a metallic taste and a burning sensation in her mouth that ceased when she stopped taking the medication. When she began taking eprosartan on a second occasion, her dysgeusia returned. In a second case, a fifty-nine-year-old man was prescribed amlodipine in order to treat his hypertension. After eight years of taking the drug, he developed a loss of taste sensation and numbness in his tongue. When he ran out of his medication, he decided not to obtain a refill and stopped taking amlodipine. Following this self-removal, he reported experiencing a return of his taste sensation. Once he refilled his prescription and began taking amlodipine a second time, his taste disturbance reoccurred. These two cases suggest that there is an association between these drugs and taste disorders. This link is supported by the "de-challenge" and "re-challenge" that took place in both instances. It appears that drug-induced dysgeusia can be alleviated by reducing the drugs dose or by substituting a second drug from the same class.

Alpha lipoic acid
Alpha lipoic acid (ALA) is an antioxidant that is made naturally by human cells. It can also be administered in capsules or can be found in foods such as red meat, organ meats, and yeast. Like other antioxidants, it functions by ridding the body of harmful free radicals that can cause damage to tissues and organs. It has an important role in the Krebs cycle as a coenzyme leading to the production of antioxidants, intracellular glutathione, and nerve-growth factors. Animal research has also uncovered the ability of ALA to improve nerve conduction velocity. Because flavors are perceived by differences in electric potential through specific nerves innervating the tongue, idiopathic dysgeusia may be a form of a neuropathy. ALA has proven to be an effective treatment for burning mouth syndrome spurring studies in its potential to treat dysgeusia. In a study of forty-four patients diagnosed with the disorder, one half was treated with the drug for two months while the other half, the control group, was given a placebo for two months followed by a two-month treatment of ALA. The results reported show that 91% of the group initially treated with ALA reported an improvement in their condition compared to only 36% of the control group. After the control group was treated with ALA, 72% reported an improvement. This study suggests that ALA may be a potential treatment for patients and supports that full double blind randomized studies should be performed.

Managing dysgeusia
In addition to the aforementioned treatments, there are also many management approaches that can alleviate the symptoms of dysgeusia. These include using non-metallic silverware, avoiding metallic or bitter tasting foods, increasing the consumption of foods high in protein, flavoring foods with spices and seasonings, serving foods cold in order to reduce any unpleasant taste or odor, frequently brushing ones teeth and utilizing mouthwash, or using sialogogues such as chewing sugar-free gum or sour-tasting drops that stimulate the productivity of saliva. When taste is impeded, the food experience can be improved through means other than taste, such as texture, aroma, temperature, and color.

Psychological impacts
People with dysgeusia are also forced to manage the impact that the disorder has on their quality of life. An altered taste has effects on food choice and intake and can lead to weight loss, malnutrition, impaired immunity, and a decline in health </s>