<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 Dust storm and can you explain it in depth? [/INST] A dust storm, also called a sandstorm, is a meteorological phenomenon common in arid and semi-arid regions. Dust storms arise when a gust front or other strong wind blows loose sand and dirt from a dry surface. Fine particles are transported by saltation and suspension, a process that moves soil from one place and deposits it in another.
The arid regions of North Africa, the Arabian peninsula, Central Asia and China are the main terrestrial sources of airborne dust. It has been argued that poor management of Earths drylands, such as neglecting the fallow system, are increasing the size and frequency of dust storms from desert margins and changing both the local and global climate, as well as impacting local economies.The term sandstorm is used most often in the context of desert dust storms, especially in the Sahara Desert, or places where sand is a more prevalent soil type than dirt or rock, when, in addition to fine particles obscuring visibility, a considerable amount of larger sand particles are blown closer to the surface. The term dust storm is more likely to be used when finer particles are blown long distances, especially when the dust storm affects urban areas.

Causes
As the force of dust passing over loosely held particles increases, particles of sand first start to vibrate, then to move across the surface in a process called saltation. As they repeatedly strike the ground, they loosen and break off smaller particles of dust which then begin to travel in suspension. At wind speeds above that which causes the smallest to suspend, there will be a population of dust grains moving by a range of mechanisms: suspension, saltation and creep.A study from 2008 finds that the initial saltation of sand particles induces a static electric field by friction. Saltating sand acquires a negative charge relative to the ground which in turn loosens more sand particles which then begin saltating. This process has been found to double the number of particles predicted by previous theories.Particles become loosely held mainly due to a prolonged drought or arid conditions, and high wind speeds. Gust fronts may be produced by the outflow of rain-cooled air from an intense thunderstorm. Or, the wind gusts may be produced by a dry cold front: that is, a cold front that is moving into a dry air mass and is producing no precipitation—the type of dust storm which was common during the Dust Bowl years in the U.S. Following the passage of a dry cold front, convective instability resulting from cooler air riding over heated ground can maintain the dust storm initiated at the front.
In desert areas, dust and sand storms are most commonly caused by either thunderstorm outflows, or by strong pressure gradients which cause an increase in wind velocity over a wide area. The vertical extent of the dust or sand that is raised is largely determined by the stability of the atmosphere above the ground as well as by the weight of the particulates. In some cases, dust and sand may be confined to a relatively-shallow layer by a low-lying temperature inversion. In other instances, dust (but not sand) may be lifted as high as 6,000 m (20,000 ft).
Drought and wind contribute to the emergence of dust storms, as do poor farming and grazing practices by exposing the dust and sand to the wind.
One poor farming practice which contributes to dust storms is dryland farming. Particularly poor dryland farming techniques are intensive tillage or not having established crops or cover crops when storms strike at particularly vulnerable times prior to revegetation. In a semi-arid climate, these practices increase susceptibility to dust storms. However, soil conservation practices may be implemented to control wind erosion.

Physical and environmental effects
A sandstorm can transport and carry large volumes of sand unexpectedly. Dust storms can carry large amounts of dust, with the leading edge being composed of a wall of thick dust as much as 1.6 km (5,200 ft) high. Dust and sand storms which come off the Sahara Desert are locally known as a simoom or simoon (sîmūm, sîmūn). The haboob (həbūb) is a sandstorm prevalent in the region of Sudan around Khartoum, with occurrences being most common in the summer.
The Sahara desert is a key source of dust storms, particularly the Bodélé Depression and an area covering the confluence of Mauritania, Mali, and Algeria. Sahara dust is frequently emitted into the Mediterranean atmosphere and transported by the winds sometimes as far north as central Europe and Great Britain.Saharan dust storms have increased approximately 10-fold during the half-century since the 1950s, causing topsoil loss in Niger, Chad, northern Nigeria, and Burkina Faso. In Mauritania there were just two dust storms a year in the early 1960s; there are about 80 a year since 2007, according to English geographer Andrew Goudie, professor at the University of Oxford. Levels of Saharan dust coming off the east coast of Africa in June 2007 were five times those observed in June 2006, and were the highest observed since at least 1999, which may have cooled Atlantic waters enough to slightly reduce hurricane activity in late 2007.

Dust storms have also been shown to increase the spread of disease across the globe. Virus spores in the ground are blown into the atmosphere by the storms with the minute particles and interact with urban air pollution.Short-term effects of exposure to desert dust include immediate increased symptoms and worsening of the lung function in individuals with asthma, increased mortality and morbidity from long-transported dust from both Saharan and Asian dust storms suggesting that long-transported dust storm particles adversely affects the circulatory system </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 Gnathostomiasis and can you explain it in depth? [/INST] Gnathostomiasis (also known as larva migrans profundus: 436 ) is the human infection caused by the nematode (roundworm) Gnathostoma spinigerum and/or Gnathostoma hispidum, which infects vertebrates.

Symptoms and signs
A few days after ingestion epigastric pain, fever, vomiting, and loss of appetite resulting from migration of larvae through intestinal wall to the abdominal cavity will appear in the patient. Migration in the subcutaneous tissues (under the skin) causes intermittent, migratory, painful, pruritic swellings (cutaneous larva migrans). Patches of edema appear after the above symptoms clear and are usually found on the abdomen. These lesions vary in size and can be accompanied by pruritus (itchy anus), rash, and stabbing pain. Swellings may last for 1 to 4 weeks in a given area and then reappear in a different location. Migration to other tissues (visceral larva migrans), can result in cough, hematuria (blood in urine), ocular (eye) involvement, meningitis, encephalitis and eosinophilia. Eosinophilic myeloencephalitis may also result from invasion of the central nervous system by the larvae.

Causes
Human gnathostomiasis is infection by the migrating third-stage larvae of any of five species of Gnathostoma, which is type of worm (more specifically a type of nematode).  The most common cause in Asia is G. spinigerum, and the most common cause in the Americas is G. binucleatum. G. hispidium and G. doloresi occur in East and Southeast Asia; the former has also been found in Eastern Europe. G. nipponicum occurs only in Japan and China. There is one unconfirmed report of G. malaysiae causing disease in humans.

Transmission
Gnathostomiasis is transmitted by the ingestion of raw or insufficiently cooked definitive hosts such as fresh water fish, poultry, or frogs.In Thailand and Vietnam, the most common cause appears to be consumption of undercooked Asian swamp eels (Monopterus albus, also called Fluta alba) which transmit G. spinigerum. Monopterus albus is an invasive species in North America, but no Gnathostoma infections in humans have yet been conclusively identified in the US.

Hosts
Intermediate host
The primary intermediate host is the minute crustaceans of the genus Cyclops. These crustaceans are then ingested by a second intermediate host, such as frogs.

Definitive host
The definitive hosts for gnathostomiasis include cats, dogs, tigers, leopards, lions, mink, opossums, raccoons, poultry, frogs, freshwater fish, snakes or birds.

Incubation period
The incubation period for gnathostomiasis is 3–4 weeks when the larvae begin to migrate through the subcutaneous tissue of the body.

Morphology
The adult parasite is reddish-brown in color and has a globular cephalic dome that is separated from the rest of the body by constriction. The posterior portion of the nematode is smooth while the anterior half is covered with fine leaf-like spines. The head is round and contains 4 to 8 transverse rows of hooklets that are protected by a pair of fleshy lips . The males are shorter than the females, 11–25 mm (0.43–0.98 in) compared to 25–54 mm (0.98–2.13 in) respectively. Eggs are oval and have a mucoid plug at one end.

Life cycle
Life cycle in definitive hosts
Adult worms are found in a tumor located in the gastric wall of the definitive hosts and release eggs into the hosts digestive tract. The eggs are then released with feces and in about a week hatch in water to develop into first stage larva. Larvae are then ingested by minute copepods of the genus Cyclops. Once entering the copepod, the larvae penetrate the gastric wall of their intermediate host and begin to develop into second-stage and even early third-stage larvae. The copepods are then ingested by a second intermediate host such as fish, frogs, or snakes. Within this second intermediate or definitive host the larva repeat a similar pattern of penetrating the gastric wall, but then continue to migrate to muscular tissue and develop into advanced third-stage larvae. These larvae then encyst within the musculature of the new host. If the cyst containing flesh of these hosts is ingested by a definitive host, such as dogs, and cats, the cysts are ingested and the larvae escape the cysts and penetrate the gastric wall. These released larvae travel to the connective tissue and muscle as observed before and after 4 weeks they return to the gastric wall as adults. Here they form a tumor and continue to mature into adults for the next 6–8 months. Worms mate and females begin to excrete fertilized eggs with feces 8–12 months after ingestion of cysts. They are passed out in the feces and eaten by another fish.

Life cycle in humans
Infection of humans by gnathostomiasis is accidental because humans are not one of the definitive hosts of the parasite and do not allow the parasite to complete its life cycle. Infection in humans follows ingestion of raw or insufficiently cooked infected intermediate hosts. The ingested third stage larva migrates from the gastric wall and its migration results in the symptoms associated with infection by gnathostomiasis. The third stage larvae dont return to the gastric wall preventing it from maturing into adult worms, leaving the life cycle incomplete. Instead the larvae continue to migrate unpredictably unable to develop into adults, so eggs are seldom found in diagnostic tests. This also means the number of worms present in humans is a reflection of the number of third stage larvae ingested.

Diagnosis
Diagnosis of gnathostomiasis is possible (with microscopy) after removal of the worm.
The primary form of diagnosis of gnathostomiasis is the identification of larva in the tissue. Serological testing such as enzyme-linked immunosorbent assay (ELISA) or the Western blot are also reliable but may not be easily accessible in endemic areas.CT scanning or MRI can be used to help identify a soft tissue worm and when looking at CNS disease it can be used to reveal the presence of the worm. The presence of haemorrhagic tracks on gradient-echo T2-weighted MRI is characteristic and possibly diagnostic.

Prevention
The best strategies for preventing accidental infection of humans is to educate those living in endemic areas to only consume fully cooked meat. The inability of the parasite to complete its life cycle within humans means that transmission can easily be contained by adequate preparation of meat from intermediate hosts. This is especially useful because of the difficulty and lack of feasibility inherent in eliminating all intermediate hosts of gnathostomiasis. So instead, individuals in endemic areas should avoid eating raw and undercooked meat in endemic areas, but this may be difficult in these areas.
The dish ceviche is native to Peru and a favorite of Mexico. It consists of onion, cubed fish, lime or lemon juice and Andean spices including salt and chili. The ingredients are mixed together and they are allowed to marinate several hours before being served at room temperature. Then in endemic areas in Southeast Asia there are traditional dishes associated with these areas that also include raw uncooked fish, such as koipla in Thailand, goi ca song in Vietnam, sashimi and sushi in Japan.Acknowledging these cultural traditions, individuals in these cultural can be educated on methods of adapting their food preparation activities in order to remove the larvae without greatly altering these traditional dishes. For instance, meat should be marinated in vinegar for six hours or in soy sauce for 12 hours in order to successfully kill the larvae. In areas with reliable electricity, meat can be frozen at -20 degrees Celsius for 3–5 days to achieve the same results of killing the larvae present.

Treatment
Surgical removal or treatment with albendazole or ivermectin is recommended.
The most prescribed treatment for gnathostomiasis is surgical removal of the larvae but this is only effective when the worms are located in an accessible location. In addition to surgical excision, albendazole and ivermectin have been noted in their ability to eliminate the parasite. Albendazole is recommended to be administered at 400 mg daily for 21 days as an adjunct to surgical excision, while ivermectin is better tolerated as a single dose. Ivermectin can also serve as a replacement for those that cant handle albendazole 200 ug/kg p.o. as a single dose. However, ivermectin has been shown to be less effective than albendazole.

Epidemiology
Endemic areas include Asia, Mexico, India and parts of South Africa. Originally believed to be confined to Asia, in the 1970s gnathostomiasis was discovered in Mexico, and found in Australia in 2011 </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 Restless legs syndrome and can you explain it in depth? [/INST] Restless legs syndrome (RLS), also known as Willis-Ekbom disease (WED), is generally a long-term disorder that causes a strong urge to move ones legs. There is often an unpleasant feeling in the legs that improves somewhat by moving them. This is often described as aching, tingling, or crawling in nature. Occasionally, arms may also be affected. The feelings generally happen when at rest and therefore can make it hard to sleep. Due to the disturbance in sleep, people with RLS may have daytime sleepiness, low energy, irritability and a depressed mood. Additionally, many have limb twitching during sleep. RLS is not the same as habitual foot tapping or leg rocking.Risk factors for RLS include low iron levels, kidney failure, Parkinsons disease, diabetes mellitus, rheumatoid arthritis, pregnancy and celiac disease. A number of medications may also trigger the disorder including antidepressants, antipsychotics, antihistamines, and calcium channel blockers. There are two main types. One is early onset RLS which starts before age 45, runs in families and worsens over time. The other is late onset RLS which begins after age 45, starts suddenly, and does not worsen. Diagnosis is generally based on a persons symptoms after ruling out other potential causes.Restless legs syndrome may resolve if the underlying problem is addressed. Otherwise treatment includes lifestyle changes and medication. Lifestyle changes that may help include stopping alcohol and tobacco use, and sleep hygiene. Medications used include  a dopamine agonist such as pramipexole. RLS affects an estimated 2.5–15% of the American population. Females are more commonly affected than males, and it becomes increasingly common with age.

Signs and symptoms
RLS sensations range from pain or an aching in the muscles, to "an itch you cant scratch", a "buzzing sensation", an unpleasant "tickle that wont stop", a "crawling" feeling, or limbs jerking while awake. The sensations typically begin or intensify during quiet wakefulness, such as when relaxing, reading, studying, or trying to sleep.It is a "spectrum" disease with some people experiencing only a minor annoyance and others having major disruption of sleep and impairments in quality of life.The sensations—and the need to move—may return immediately after ceasing movement or at a later time. RLS may start at any age, including childhood, and is a progressive disease for some, while the symptoms may remit in others. In a survey among members of the Restless Legs Syndrome Foundation, it was found that up to 45% of patients had their first symptoms before the age of 20 years.
"An urge to move, usually due to uncomfortable sensations that occur primarily in the legs, but occasionally in the arms or elsewhere."The sensations are unusual and unlike other common sensations. Those with RLS have a hard time describing them, using words or phrases such as uncomfortable, painful, antsy, electrical, creeping, itching, pins and needles, pulling, crawling, buzzing, and numbness. It is sometimes described similar to a limb falling asleep or an exaggerated sense of positional awareness of the affected area.  The sensation and the urge can occur in any body part; the most cited location is legs, followed by arms. Some people have little or no sensation, yet still, have a strong urge to move."Motor restlessness, expressed as activity, which relieves the urge to move."Movement usually brings immediate relief, although temporary and partial. Walking is most common; however, stretching, yoga, biking, or other physical activity may relieve the symptoms. Continuous, fast up-and-down movements of the leg, and/or rapidly moving the legs toward then away from each other, may keep sensations at bay without having to walk. Specific movements may be unique to each person."Worsening of symptoms by relaxation."Sitting or lying down (reading, plane ride, watching TV) can trigger the sensations and urge to move. Severity depends on the severity of the persons RLS, the degree of restfulness, duration of the inactivity, etc."Variability over the course of the day-night cycle, with symptoms worse in the evening and early in the night."Some experience RLS only at bedtime, while others experience it throughout the day and night. Most people experience the worst symptoms in the evening and the least in the morning."restless legs feel similar to the urge to yawn, situated in the legs or arms."These symptoms of RLS can make sleeping difficult for many patients and a 2005 National Sleep Foundation poll shows the presence of significant daytime difficulties resulting from this condition.  These problems range from being late for work to missing work or events because of drowsiness.  Patients with RLS who responded reported driving while drowsy more than patients without RLS.  These daytime difficulties can translate into safety, social and economic issues for the patient and for society.RLS may contribute to higher rates of depression and anxiety disorders in RLS patients.

Primary and secondary
RLS is categorized as either primary or secondary.

Primary RLS is considered idiopathic or with no known cause. Primary RLS usually begins slowly, before approximately 40–45 years of age and may disappear for months or even years. It is often progressive and gets worse with age. RLS in children is often misdiagnosed as growing pains.
Secondary RLS often has a sudden onset after age 40, and may be daily from the beginning. It is most associated with specific medical conditions or the use of certain drugs (see below).

Causes
While the cause is generally unknown, it is believed to be caused by changes in the nerve transmitter dopamine resulting in an abnormal use of iron by the brain. RLS is often due to iron deficiency (low total body iron status). Other associated conditions may include end-stage kidney disease and hemodialysis, folate deficiency, magnesium deficiency, sleep apnea, diabetes, peripheral neuropathy, Parkinsons disease, and certain autoimmune diseases, such as multiple sclerosis. RLS can worsen in pregnancy, possibly due to elevated estrogen levels. Use of alcohol, nicotine products, and caffeine may be associated with RLS. A 2014 study from the American Academy of Neurology also found that reduced leg oxygen levels were strongly associated with restless legs Syndrome symptom severity in untreated patients.

ADHD
An association has been observed between attention deficit hyperactivity disorder (ADHD) and RLS or periodic limb movement disorder. Both conditions appear to have links to dysfunctions related to the neurotransmitter dopamine, and common medications for both conditions among other systems, affect dopamine levels in the brain. A 2005 study suggested that up to 44% of people with ADHD had comorbid (i.e. coexisting) RLS, and up to 26% of people with RLS had confirmed ADHD or symptoms of the condition.

Medications
Certain medications may cause or worsen RLS, or cause it secondarily, including:
certain antiemetics (antidopaminergic ones)
certain antihistamines (especially the sedating, first generation H1 antihistamines often in over-the-counter cold medications)
many antidepressants (both older TCAs and newer SSRIs)
antipsychotics and certain anticonvulsants
a rebound effect of sedative-hypnotic drugs such as a benzodiazepine withdrawal syndrome from discontinuing benzodiazepine tranquilizers or sleeping pills
alcohol withdrawal can also cause restless legs syndrome and other movement disorders such as akathisia and parkinsonism usually associated with antipsychotics
opioid withdrawal is associated with causing and worsening RLSBoth primary and secondary RLS can be worsened by surgery of any kind; however, back surgery or injury can be associated with causing RLS.The cause vs. effect of certain conditions and behaviors observed in some patients (ex. excess weight, lack of exercise, depression or other mental illnesses) is not well established. Loss of sleep due to RLS could cause the conditions, or medication used to treat a condition could cause RLS.

Genetics
More than 60% of cases of RLS are familial and are inherited in an autosomal dominant fashion with variable penetrance.Research and brain autopsies have implicated both dopaminergic system and iron insufficiency in the substantia nigra. Iron is well understood to be an essential cofactor for the formation of L-dopa, the precursor of dopamine.
Six genetic loci found by linkage are known and listed below. Other than the first one, all of the linkage loci were discovered using an autosomal dominant model of inheritance.

The first genetic locus was discovered in one large French Canadian family and maps to chromosome 12q. This locus was discovered using an autosomal recessive inheritance model. Evidence for this locus was also found using a transmission disequilibrium test (TDT) in 12 Bavarian families.
The second RLS locus maps to chromosome 14q and was discovered in one Italian family. Evidence for this locus was found in one French Canadian family. Also, an association study in a large sample 159 trios of European descent showed some evidence for this locus.
This locus maps to chromosome 9p and was discovered in two unrelated American families. Evidence for this locus was also found by the TDT in a large Bavarian family, in which significant linkage to this locus was found.
This locus maps to chromosome 20p and was discovered in a large French Canadian family with RLS.
This locus maps to chromosome 2p and was found in three related families from population isolated in South Tyrol.
The sixth locus is located on chromosome 16p12.1 and was discovered by Levchenko et al. in 2008.Three genes, MEIS1, BTBD9 and MAP2K5, were found to be associated to RLS.
Their role in RLS pathogenesis is still unclear. More recently, a fourth gene, PTPRD was found to be associated with RLS.There is also some evidence that periodic limb movements in sleep (PLMS) are associated with BTBD9 on chromosome 6p21.2, MEIS1, MAP2K5/SKOR1, and PTPRD. The presence of a positive family history suggests that there may be a genetic involvement in the etiology of RLS.

Mechanism
Although it is only partly understood, pathophysiology of restless legs syndrome may involve dopamine and iron system anomalies. There is also a commonly acknowledged circadian rhythm explanatory mechanism associated with it, clinically shown simply by biomarkers of circadian rhythm, such as body temperature. The interactions between impaired neuronal iron uptake and the functions of the neuromelanin-containing and dopamine-producing cells have roles in RLS development, indicating that iron deficiency might affect the brain dopaminergic transmissions in different ways.Medial thalamic nuclei may also have a role in RLS as part as the limbic system modulated by the dopaminergic system which may affect pain perception. Improvement of RLS symptoms occurs in people receiving low-dose dopamine agonists.

Diagnosis
There are no specific tests for RLS, but non-specific laboratory tests are used to rule out other causes such as vitamin deficiencies. Five symptoms are used to confirm the diagnosis:
A strong urge to move the limbs, usually associated with unpleasant or uncomfortable sensations.
It starts or worsens during inactivity or rest.
It improves or disappears (at least temporarily) with activity.
It worsens in the evening or night.
These symptoms are not caused by any medical or behavioral condition.These symptoms are not essential, like the ones above, but occur commonly in RLS patients:
genetic component or family history with RLS
good response to dopaminergic therapy
periodic leg movements during day or sleep
most strongly affected are people who are middle-aged or older
other sleep disturbances are experienced
decreased iron stores can be a risk factor and should be assessedAccording to the International Classification of Sleep Disorders (ICSD-3), the main symptoms have to be associated with a sleep disturbance or impairment in order to support RLS diagnosis. As stated by this classification, RLS symptoms should begin or worsen when being inactive, be relieved when moving, should happen exclusively or mostly in the evening and at night, not be triggered by other medical or behavioral conditions, and should impair ones quality of life. Generally, both legs are affected, but in some cases there is an asymmetry.

Differential diagnosis
The most common conditions that should be differentiated with RLS include leg cramps, positional discomfort, local leg injury, arthritis, leg edema, venous stasis, peripheral neuropathy, radiculopathy, habitual foot tapping/leg rocking, anxiety, myalgia, and drug-induced akathisia.Peripheral artery disease and arthritis can also cause leg pain but this usually gets worse with movement.There are less common differential diagnostic conditions included myelopathy, myopathy, vascular or neurogenic claudication, hypotensive akathisia, orthostatic tremor, painful legs, and moving toes.

Treatment
If RLS is not linked to an underlying cause, its frequency may be reduced by lifestyle modifications such as adopting improving sleep hygiene, regular exercise, and stopping smoking. Medications used may include dopamine agonists or gabapentin in those with daily restless legs syndrome, and opioids for treatment of resistant cases.Treatment of RLS should not be considered until possible medical causes are ruled out. Secondary RLS may be cured if precipitating medical conditions (anemia) are managed effectively.

Physical measures
Stretching the leg muscles can bring temporary relief. Walking and moving the legs, as the name "restless legs" implies, brings temporary relief. In fact, those with RLS often have an almost uncontrollable need to walk and therefore relieve the symptoms while they are moving. Unfortunately, the symptoms usually return immediately after the moving and walking ceases. A vibratory counter-stimulation device has been found to help some people with primary RLS to improve their sleep.

Iron
There is some evidence that intravenous iron supplementation moderately improves restlessness for people with RLS.

Medications
For those whose RLS disrupts or prevents sleep or regular daily activities, medication may be useful. Evidence supports the use of dopamine agonists including:  pramipexole, ropinirole, rotigotine, and cabergoline. They reduce symptoms, improve sleep quality and quality of life. Levodopa is also effective. However, pergolide and cabergoline are less recommended due to their association with increased risk of valvular heart disease. Ropinirole has a faster onset with shorter duration. Rotigotine is commonly used as a transdermal patch which continuously provides stable plasma drug concentrations, resulting in its particular therapeutic effect on patients with symptoms throughout the day. One 2008 review found pramipexole to be better than ropinirole.There are, however, issues with the use of dopamine agonists including augmentation. This is a medical condition where the drug itself causes symptoms to increase in severity and/or occur earlier in the day. Dopamine agonists may also cause rebound when symptoms increase as the drug wears off. In many cases, the longer dopamine agonists have been used the higher the risk of augmentation and rebound as well as the severity of the symptoms. Also, a recent study indicated that dopamine agonists used in restless legs syndrome can lead to an increase in compulsive gambling.
Gabapentin or pregabalin, a non-dopaminergic treatment for moderate to severe primary RLS
Opioids are only indicated in severe cases that do not respond to other measures due to their very high abuse liability and high rate of side effects, which may include constipation, fatigue and headache.One possible treatment for RLS is dopamine agonists, unfortunately patients can develop dopamine dysregulation syndrome, meaning that they can experience an addictive pattern of dopamine replacement therapy. Additionally, they can exhibit some behavioral disturbances such as impulse control disorders like pathologic gambling, compulsive purchasing and compulsive eating. There are some indications that stopping the dopamine agonist treatment has an impact on the resolution or at least improvement of the impulse control disorder, even though some people can be particularly exposed to dopamine agonist withdrawal syndrome.Benzodiazepines, such as diazepam or clonazepam, are not generally recommended, and their effectiveness is unknown. They however are sometimes still used as a second line, as add on agents. Quinine is not recommended due to its risk of serious  side effects involving the blood.

Prognosis
RLS symptoms may gradually worsen with age, although more slowly for those with the idiopathic form of RLS than for people who also have an associated medical condition. Current therapies can control the disorder, minimizing symptoms and increasing periods of restful sleep. In addition, some people have remissions, periods in which symptoms decrease or disappear for days, weeks, or months, although symptoms usually eventually reappear. Being diagnosed with RLS does not indicate or foreshadow another neurological disease, such as Parkinsons disease. RLS symptoms can worsen over time when dopamine-related drugs are used for therapy, an effect called "augmentation" which may represent symptoms occurring throughout the day and affect movements of all limbs. There is no cure for RLS.

Epidemiology
RLS affects an estimated 2.5–15% of the American population. A minority (around 2.7% of the population) experience daily or severe symptoms. RLS is twice as common in women as in men, and Caucasians are more prone to RLS than people of African descent. RLS occurs in 3% of individuals from the Mediterranean or Middle Eastern regions, and in 1–5% of those from East Asia, indicating that different genetic or environmental factors, including diet, may play a role in the prevalence of this syndrome. RLS diagnosed at an older age runs a more severe course. RLS is even more common in individuals with iron deficiency, pregnancy, or end-stage kidney disease. The National Sleep Foundations 1998 Sleep in America poll showed that up to 25 percent of pregnant women developed RLS during the third trimester. Poor general health is also linked.There are several risk factors for RLS, including old age, family history, and uremia. The prevalence of RLS tends to increase with age, as well as its severity and longer duration of symptoms. People with uremia receiving renal dialysis have a prevalence from 20% to 57%, while those having kidney transplant improve compared to those treated with dialysis.RLS can occur at all ages, although it typically begins in the third or fourth decade.
Genome‐wide association studies have now identified 19 risk loci associated with RLS. Neurological conditions linked to RLS include Parkinsons disease, spinal cerebellar atrophy, spinal stenosis, lumbosacral radiculopathy and Charcot–Marie–Tooth disease type 2.

History
The first known medical description of RLS was by Sir Thomas Willis in 1672. Willis emphasized the sleep disruption and limb movements experienced by people with RLS.  Initially published in Latin (De Anima Brutorum, 1672) but later translated to English (The London Practice of Physick, 1685), Willis wrote:

Wherefore to some, when being abed they betake themselves to sleep, presently in the arms and legs, leapings and contractions on the tendons, and so great a restlessness and tossings of other members ensue, that the diseased are no more able to sleep, than if they were in a place of the greatest torture.
The term "fidgets in the legs" has also been used as early as the early nineteenth century.Subsequently, other descriptions of RLS were published, including those by François Boissier de Sauvages (1763), Magnus Huss (1849), Theodur Wittmaack (1861), George Miller Beard (1880), Georges Gilles de la Tourette (1898), Hermann Oppenheim (1923) and Frederick Gerard Allison (1943). However, it was not until almost three centuries after Willis, in 1945, that Karl-Axel Ekbom (1907–1977) provided a detailed and comprehensive report of this condition in his doctoral thesis, restless legs: clinical study of hitherto overlooked disease. Ekbom coined the term "restless legs" and continued work on this disorder throughout his career. He described the essential diagnostic symptoms, differential diagnosis from other conditions, prevalence, relation to anemia, and common occurrence during pregnancy.Ekboms work was largely ignored until it was rediscovered by Arthur S. Walters and Wayne A. Hening in the 1980s. Subsequent landmark publications include 1995 and 2003 papers, which revised and updated the diagnostic criteria </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 Elsewhere and can you explain it in depth? [/INST]  </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 Alcoholic beverage and can you explain it in depth? [/INST] An alcoholic beverage (also called an alcoholic drink, adult beverage, or a drink) is a drink that contains ethanol, a type of alcohol that acts as a drug and is produced by fermentation of grains, fruits, or other sources of sugar. The consumption of alcoholic drinks, often referred to as "drinking", plays an important social role in many cultures. Most countries have laws regulating the production, sale, and consumption of alcoholic beverages. Regulations may require the labeling of the percentage alcohol content (as ABV or proof) and the use of a warning label. Some countries ban such activities entirely, but alcoholic drinks are legal in most parts of the world. The global alcoholic drink industry exceeded $1 trillion in 2018.Alcohol is a depressant, which in low doses causes euphoria, reduces anxiety, and increases sociability. In higher doses, it causes drunkenness, stupor, unconsciousness, or death. Long-term use can lead to an alcohol use disorder, an increased risk of developing several types of cancer, cardiovascular disease, and physical dependence.
Alcohol is one of the most widely used recreational drugs in the world, and about 33% of all humans currently drink alcohol. In 2015, among Americans, 86% of adults had consumed alcohol at some point, with 70% drinking it in the last year and 56% in the last month. Alcoholic drinks are typically divided into three classes—beers, wines, and spirits—and typically their alcohol content is between 3% and 50%.
Discovery of late Stone Age jugs suggest that intentionally fermented drinks existed at least as early as the Neolithic period (c. 10,000 BC). Several other animals are affected by alcohol similarly to humans and, once they consume it, will consume it again if given the opportunity, though humans are the only species known to produce alcoholic drinks intentionally.

Fermented drinks
Beer
Beer is a beverage fermented from grain mash. It is typically made from barley or a blend of several grains and flavored with hops. Most beer is naturally carbonated as part of the fermentation process. If the fermented mash is distilled, then the drink becomes a spirit. Beer is the most consumed alcoholic beverage in the world.

Cider
Cider or cyder ( SY-dər) is a fermented alcoholic drink made from any fruit juice; apple juice (traditional and most common), peaches, pears ("Perry" cider) or other fruit. Cider alcohol content varies from 1.2% ABV to 8.5% or more in traditional English ciders. In some regions, cider may be called "apple wine".

Fermented tea
Fermented tea (also known as post-fermented tea or dark tea) is a class of tea that has undergone microbial fermentation, from several months to many years. The tea leaves and the liquor made from them become darker with oxidation. Thus, the various kinds of fermented teas produced across China are also referred to as dark tea, not be confused with black tea. The most famous fermented tea is kombucha which is often homebrewed, pu-erh, produced in Yunnan Province, and the Anhua dark tea produced in Anhua County of Hunan Province. The majority of kombucha on the market are under 0.5% ABV.

Fermented water
Fermented water is an ethanol-based water solution with approximately 15-17% ABV without sweet reserve. Fermented water is exclusively fermented with white sugar, yeast, and water. Fermented water is clarified after the fermentation to produce a colorless or off-white liquid with no discernible taste other than that of ethanol.

Fermented sugar water
Fermented sugar water is fermented water with added refined sugar.

Mead
Mead () is an alcoholic drink made by fermenting honey with water, sometimes with various fruits, spices, grains, or hops. The alcoholic content of mead may range from as low as 3% ABV to more than 20%. The defining characteristic of mead is that the majority of the drinks fermentable sugar is derived from honey. Mead can also be referred to as "honeywine."

Pulque
Pulque is the Mesoamerican fermented drink made from the "honey water" of maguey, Agave americana. The drink distilled from pulque is tequila or mescal Mezcal.

Rice wine
Sake, huangjiu, mijiu, and cheongju are popular examples of East Asian rice wine.

Wine
Wine is a fermented beverage produced from grapes and sometimes other fruits. Wine involves a longer fermentation process than beer and a long aging process (months or years), resulting in an alcohol content of 9%–16% ABV.

Others
Fruit wines are made from fruits other than grapes, such as plums, cherries, or apples.
Sparkling wine like French Champagne, Catalan Cava or Italian Prosecco can be made by means of a secondary fermentation.

Distilled beverages
Distilled beverages (also called liquors or spirit drinks) are alcoholic drinks produced by distilling (i.e., concentrating by distillation) ethanol produced by means of fermenting grain, fruit, or vegetables. Unsweetened, distilled, alcoholic drinks that have an alcohol content of at least 20% ABV are called spirits. For the most common distilled drinks, such as whiskey and vodka, the alcohol content is around 40%. The term hard liquor is used in North America to distinguish distilled drinks from undistilled ones (implicitly weaker). Vodka, gin, baijiu, shōchū, soju, tequila, whiskey, brandy and rum are examples of distilled drinks. Distilling concentrates the alcohol and eliminates some of the congeners. Freeze distillation concentrates ethanol along with methanol and fusel alcohols (fermentation by-products partially removed by distillation) in applejack.
Fortified wine is wine, such as port or sherry, to which a distilled beverage (usually brandy) has been added. Fortified wine is distinguished from spirits made from wine in that spirits are produced by means of distillation, while fortified wine is  wine that has had a spirit added to it. Many different styles of fortified wine have been developed, including port, sherry, madeira, marsala, commandaria, and the aromatized wine vermouth.

Rectified spirit
Rectified spirit, also called "neutral grain spirit", is alcohol which has been purified by means of "rectification" (i.e. repeated distillation). The term neutral refers to the spirits lack of flavor that would have been present if the mash ingredients had been distilled to a lower level of alcoholic purity. Rectified spirit also lacks any flavoring added to it after distillation (as is done, for example, with gin). Other kinds of spirits, such as whiskey, are distilled to a lower alcohol percentage to preserve the flavor of the mash.
Rectified spirit is a clear, colorless, flammable liquid that may contain as much as 95% ABV. It is often used for medicinal purposes. It may be a grain spirit or it may be made from other plants. It is used in mixed drinks, liqueurs, and tinctures, and also as a household solvent.

Congeners
In the alcoholic drinks industry, congeners are substances produced during fermentation. These substances include small amounts of chemicals such as occasionally desired other alcohols, like propanol and 3-methyl-1-butanol, but also compounds that are never desired such as acetone, acetaldehyde and glycols. Congeners are responsible for most of the taste and aroma of distilled alcoholic drinks, and contribute to the taste of non-distilled drinks. It has been suggested that these substances contribute to the symptoms of a hangover. Tannins are congeners found in wine in the presence of phenolic compounds. Wine tannins add bitterness, have a drying sensation, taste herbaceous and are often described as astringent. Wine tannins adds balance, complexity, structure and makes a wine last longer, so they play an important role in the aging of wine.

Amount of use
The average number of people who drink as of 2016 was 39% for males and 25% for females (2.4 billion people in total). Females on average drink 0.7 drinks per day while males drink 1.7 drinks per day. The rates of drinking varies significantly in different areas of the world.

Reasons for use
Apéritifs and digestifs
An apéritif is any alcoholic beverage usually served before a meal to stimulate the appetite, while a digestif is any alcoholic beverage served after a meal for the stated purpose of improving digestion. Fortified wine, liqueurs, and dry champagne are common apéritifs. Because apéritifs are served before dining, they are usually dry rather than sweet. One example is Cinzano, a brand of vermouth. Digestifs include brandy, fortified wines and herb-infused spirits (Drambuie).

Caloric content
The USDA uses a figure of 6.93 kilocalories (29.0 kJ) per gram of alcohol (5.47 kcal or 22.9 kJ per ml) for calculating food energy. For distilled spirits, a standard serving in the United States is 44 ml (1.5 US fl oz), which at 40% ethanol (80 proof), would be 14 grams and 98 calories. For other than distille spirits, many alcoholic drinks contain carbohydrates, which adds to the calories per serving.Alcoholic drinks are considered empty calorie foods because other than food energy they contribute no essential nutrients. According to the U.S. Department of Agriculture, based on NHANES 2013–2014 surveys, women in the US ages 20 and up consume on average 6.8 grams/day and men consume on average 15.5 grams/day.Alcohol is known to potentiate the insulin response of the human body to glucose, which, in essence, "instructs" the body to convert consumed carbohydrates into fat and to suppress carbohydrate and fat oxidation. Ethanol is directly processed in the liver to acetyl CoA, the same intermediate product as in glucose metabolism. Because ethanol is mostly metabolized and consumed by the liver, chronic excessive use can lead to fatty liver. This leads to a chronic inflammation of the liver and eventually alcoholic liver disease.

Flavoring
Pure ethanol tastes bitter to humans; some people also describe it as sweet. However, ethanol is also a moderately good solvent for many fatty substances and essential oils. This facilitates the use of flavoring and coloring compounds in alcoholic drinks as a taste mask, especially in distilled drinks. Some flavors may be naturally present in the beverages raw material. Beer and wine may also be flavored before fermentation, and spirits may be flavored before, during, or after distillation. Sometimes flavor is obtained by allowing the beverage to stand for months or years in oak barrels, usually made of American or French oak. A few brands of spirits may also have fruit or herbs inserted into the bottle at the time of bottling.
Wine is important in cuisine not just for its value as an accompanying beverage, but as a flavor agent, primarily in stocks and braising, since its acidity lends balance to rich savory or sweet dishes. Wine sauce is an example of a culinary sauce that uses wine as a primary ingredient. Natural wines may exhibit a broad range of alcohol content, from below 9% to above 16% ABV, with most wines being in the 12.5–14.5% range. Fortified wines (usually with brandy) may contain 20% alcohol or more.

Alcohol measurement
Alcohol concentration
The concentration of alcohol in a beverage is usually stated as the percentage of alcohol by volume  (ABV, the number of milliliters (ml) of pure ethanol in 100 ml of beverage) or as proof. In the United States, proof is twice the percentage of alcohol by volume at 60 degrees Fahrenheit (e.g. 80 proof = 40% ABV). Degrees proof were formerly used in the United Kingdom, where 100 degrees proof was equivalent to 57.1% ABV. Historically, this was the most dilute spirit that would sustain the combustion of gunpowder.
Ordinary distillation cannot produce alcohol of more than 95.6% by weight, which is about 97.2% ABV (194.4 proof) because at that point alcohol is an azeotrope with water. A spirit which contains a very high level of alcohol and does not contain any added flavoring is commonly called a neutral spirit. Generally, any distilled alcoholic beverage of 170 US proof or higher is considered to be a neutral spirit.Most yeasts cannot reproduce when the concentration of alcohol is higher than about 18%, so that is the practical limit for the strength of fermented drinks such as wine, beer, and sake. However, some strains of yeast have been developed that can reproduce in solutions of up to 25% ABV.

Serving measures
Shot sizes
Shot sizes vary significantly from country to country. In the United Kingdom, serving size in licensed premises is regulated under the Weights and Measures Act (1985). A single serving size of spirits (gin, whisky, rum, and vodka) are sold in 25 ml or 35 ml quantities or multiples thereof. Beer is typically served in pints (568 ml), but is also served in half-pints or third-pints. In Israel, a single serving size of spirits is about twice as much, 50 or 60 mL.
The shape of a glass can have a significant effect on how much one pours. A Cornell University study of students and bartenders pouring showed both groups pour more into short, wide glasses than into tall, slender glasses. Aiming to pour one shot of alcohol (1.5 ounces or 44.3 ml), students on average poured 45.5 ml & 59.6 ml (30% more) respectively into the tall and short glasses. The bartenders scored similarly, on average pouring 20.5% more into the short glasses. More experienced bartenders were more accurate, pouring 10.3% less alcohol than less experienced bartenders. Practice reduced the tendency of both groups to over pour for tall, slender glasses but not for short, wide glasses. These misperceptions are attributed to two perceptual biases: (1) Estimating that tall, slender glasses have more volume than shorter, wider glasses; and (2) Over focusing on the height of the liquid and disregarding the width.

Standard drinks
There is no single standard, but a standard drink of 10g alcohol, which is used in the WHO AUDIT (Alcohol Use Disorders Identification Test)s questionnaire form example, have been adopted by more countries than any other amount. 10 grams is equivalent to 12.7 millilitres.
A standard drink is a notional drink that contains a specified amount of pure alcohol. The standard drink is used in many countries to quantify alcohol intake. It is usually expressed as a measure of beer, wine, or spirits. One standard drink always contains the same amount of alcohol regardless of serving size or the type of alcoholic beverage. The standard drink varies significantly from country to country. For example, it is 7.62 ml (6 grams) of alcohol in Austria, but in Japan it is 25 ml (19.75 grams).

In the United Kingdom, there is a system of units of alcohol which serves as a guideline for alcohol consumption. A single unit of alcohol is defined as 10 ml. The number of units present in a typical drink is sometimes printed on bottles. The system is intended as an aid to people who are regulating the amount of alcohol they drink; it is not used to determine serving sizes.
In the United States, the standard drink contains 0.6 US fluid ounces (18 ml) of alcohol. This is approximately the amount of alcohol in a 12-US-fluid-ounce (350 ml) glass of beer, a 5-US-fluid-ounce (150 ml) glass of wine, or a 1.5-US-fluid-ounce (44 ml) glass of a 40% ABV (80 US proof) spirit.

Laws
Alcohol laws regulate the manufacture, packaging, labelling, distribution, sale, consumption, blood alcohol content of motor vehicle drivers, open containers, and transportation of alcoholic drinks. Such laws generally seek to reduce the adverse health and social impacts of alcohol consumption. In particular, alcohol laws set the legal drinking age, which usually varies between 15 and 21 years old, sometimes depending upon the type of alcoholic drink (e.g., beer vs wine vs hard liquor or distillates). Some countries do not have a legal drinking or purchasing age, but most countries set the minimum age at 18 years. Some countries, such as the U.S., have the drinking age higher than the legal age of majority (18), at age 21 in all 50 states. Such laws may take the form of permitting distribution only to licensed stores, monopoly stores, or pubs and they are often combined with taxation, which serves to reduce the demand for alcohol (by raising its price) and it is a form of revenue for governments </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 Anosmia and can you explain it in depth? [/INST] Anosmia, also known as smell blindness, is the loss of the ability to detect one or more smells. Anosmia may be temporary or permanent. It differs from hyposmia, which is a decreased sensitivity to some or all smells.Anosmia can be due to a number of factors, including an inflammation of the nasal mucosa, blockage of nasal passages or a destruction of one temporal lobe. Inflammation is due to chronic mucosa changes in the lining of the paranasal sinus and in the middle and superior turbinates.When anosmia is caused by inflammatory changes in the nasal passageways, it is treated simply by reducing inflammation. It can be caused by chronic meningitis and neurosyphilis that would increase intracranial pressure over a long period of time, and in some cases by ciliopathy, including ciliopathy due to primary ciliary dyskinesia.The term derives from the New Latin anosmia, based on Ancient Greek ἀν- (an-) + ὀσμή (osmḗ smell; another related term, hyperosmia, refers to an increased ability to smell). Some people may be anosmic for one particular odor, a condition known as "specific anosmia". The absence of the sense of smell from birth is known as congenital anosmia.In the United States, 3% of people aged over 40 are affected by anosmia.Anosmia is a common symptom of COVID-19 and can persist as long COVID.

Definition
Anosmia is the inability to smell. It may be partial or total, and can be specific to certain smells. Reduced sensitivity to some or all smells is hyposmia.

Signs and symptoms
Anosmia can have a number of harmful effects. People with sudden onset anosmia may find food less appetizing, though congenital anosmics rarely complain about this, and none report a loss in weight. Loss of smell can also be dangerous because it hinders the detection of gas leaks, fire, and spoiled food. The common view of anosmia as trivial can make it more difficult for a patient to receive the same types of medical aid as someone who has lost other senses, such as hearing or sight.Many experience one sided loss of smell, often as a result of minor head trauma. This type of anosmia is normally only detected if both of the nostrils are tested separately. Using this method of testing each nostril separately will often show a reduced or even completely absent sense of smell in either one nostril or both, something which is often not revealed if both nostrils are simultaneously tested.Losing an established and sentimental smell memory (e.g. the smell of grass, of the grandparents attic, of a particular book, of loved ones, or of oneself) has been known to cause feelings of depression.Loss of the ability to smell may lead to the loss of libido, though this usually does not apply to loss of smell present at birth.Often people who have loss of smell at birth report that they pretended to be able to smell as children because they thought that smelling was something that older/mature people could do, or did not understand the concept of smelling but did not want to appear different from others. When children get older, they often realize and report to their parents that they do not actually possess a sense of smell, often to the surprise of their parents.

Causes
A temporary loss of smell can be caused by a blocked nose or infection. In contrast, a permanent loss of smell may be caused by death of olfactory receptor neurons in the nose or by brain injury in which there is damage to the olfactory nerve or damage to brain areas that process smell (see olfactory system). The lack of the sense of smell at birth, usually due to genetic factors, is referred to as congenital anosmia. Family members of the patient with congenital anosmia are often found with similar histories; this suggests that the anosmia may follow an autosomal dominant pattern. Anosmia may very occasionally be an early sign of a degenerative brain disease such as Parkinsons disease and Alzheimers disease.Another specific cause of permanent loss could be from damage to olfactory receptor neurons because of use of certain types of nasal spray; i.e., those that cause vasoconstriction of the nasal microcirculation. To avoid such damage and the subsequent risk of loss of smell, vasoconstricting nasal sprays should be used only when absolutely necessary and then for only a short amount of time. Non-vasoconstricting sprays, such as those used to treat allergy-related congestion, are safe to use for prescribed periods of time. Anosmia can also be caused by nasal polyps. These polyps are found in people with allergies, histories of sinusitis, and family history. Individuals with cystic fibrosis often develop nasal polyps.Amiodarone is a drug used in the treatment of arrhythmias of the heart. A clinical study demonstrated that the use of this drug induced anosmia in some patients. Although rare, there was a case in which a 66-year-old male was treated with amiodarone for ventricular tachycardia. After the use of the drug he began experiencing olfactory disturbance, however after decreasing the dosage of amiodarone, the severity of the anosmia decreased accordingly, suggesting a relationship between use of amiodarone to the development of anosmia.

COVID-19-related anosmia
Chemosensory disturbances, including loss of smell or taste, are the predominant neurological symptom of COVID-19. As many as 80% of COVID-19 patients exhibit some change in chemesthesis, including smell. Loss of smell has also been found to be more predictive of COVID-19 than all other symptoms, including fever, cough or fatigue, based on a survey of 2 million participants in the UK and US. Google searches for "smell", "loss of smell", "anosmia", and other similar terms increased since the early months of the pandemic, and strongly correlated with increases in daily cases and deaths. Research into the mechanisms underlying these symptoms is currently ongoing.Many countries list anosmia as an official COVID-19 symptom, and some have developed "smell tests" as potential screening tools.In 2020, the Global Consortium for Chemosensory Research, a collaborative research organization of international smell and taste researchers, formed to investigate loss of smell and related chemosensory symptoms.

List of causes
Diagnosis
Doctors will begin with a detailed elicitation of history. Then the doctor will ask for any related injuries in relation to anosmia which could include upper respiratory infections or head injury. Psychophysical Assessment of order and taste identification can be used to identify anosmia. A nervous system examination is performed to see if the cranial nerves are damaged. The diagnosis, as well as the degree of impairment, can now be tested much more efficiently and effectively than ever before thanks to "smell testing kits" that have been made available as well as screening tests which use materials that most clinics would readily have. Occasionally, after accidents, there is a change in a patients sense of smell. Particular smells that were present before are no longer present </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 Microcheilia and can you explain it in depth? [/INST]  </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 Field and can you explain it in depth? [/INST]  </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 Paragonimiasis and can you explain it in depth? [/INST] Paragonimiasis is a food-borne parasitic disease caused by several species of lung flukes belonging to genus Paragonimus. Infection is acquired by eating crustaceans such as crabs and crayfishes which host the infective forms called metacercariae, or by eating raw or undercooked meat of mammals harboring the metacercariae from crustaceans.More than 40 species of Paragonimus have been identified; 10 of these are known to cause disease in humans. The most common cause of human paragonimiasis is P. westermani, the oriental lung fluke.About 22 million people are estimated to be affected yearly worldwide. It is particularly common in East Asia. Paragonimiasis is easily mistaken for other diseases with which it shares clinical symptoms, such as tuberculosis and lung cancer.

Life cycle
Not all Paragonimus species infect humans. However, all of them target mammals as their final (definitive) hosts. In mammalian lung tissue, the adult flukes live as encapsulated pairs. As hermaphrodites, they produce and fertilise their own eggs that are released through the respiratory tract. The eggs are excreted to the environment either through the sputum or swallowed and passed out along the faeces.In the external environment, the eggs remain unembryonated until ideal conditions of temperature and humidity are encountered. Then, they embryonate and develop into ciliated larvae called miracidia. As the egg shells disintegrate, the motile miracidia hatch and swim to seek the first intermediate host, a snail, and penetrate its soft tissues. Each miracidium goes through several developmental stages inside the snail: firstly into a series of daughter cells called sporocysts and then into rediae, which give rise to many worm-like larvae called cercariae. The cercariae penetrate through the body of the snail, emerging into the water. Development in the snail takes about 9 to 13 weeks.The cercariae then infect the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. Encystment occurs in the liver, gills, intestine, skeletal muscles and sometimes in the heart. These cysts are the infective stage for the mammalian host. Freshwater crab species of genera Potamiscus, Potamon, Paratelphusa, Eriocheir, Geothelphusa, Barytelphusa, crayfish species of genus Camberoides and shrimps of genera Acrohrachium and Caridina commonly serve as the secondary intermediate hosts. The secondary intermediate hosts are infected either by directly eating the snail or penetration of the body by free-swimming cercariae.Human infection with P. westermani — the best understood species — occurs by eating inadequately cooked or pickled crab or crayfish that harbour metacercariae of the parasite. The metacercariae excyst in the duodenum, penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults (7.5 to 12 mm by 4 to 6 mm). Unlike most other trematodes, after they migrate from the intestine, they remain in the peritoneal cavity until they find a suitable partner. Only then do the couples enter the lung tissues to form capsules. The flukes can also reach other organs and tissues, such as the brain and skeletal muscles. However, when this takes place completion of the life cycles is not achieved, because the eggs laid cannot exit these sites. Time from infection to laying of eggs is 65 to 90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P. westermani. For other species, rodents and deer are also additional (paratenic) hosts. By consuming infected animals of these reservoir species, even animals and humans that do not eat crustaceans directly can become infected.

Background
The first human case was seen in 1879 in Taiwan. An autopsy was done and adult trematodes were found in the lungs. The adult flukes have a reddish-brown in color with an ovoid shape. They have two muscular suckers, the first an oral sucker located anteriorly and the second a ventral sucker located mid-body. The adult flukes can live up to 20 years. The eggs are golden brown in color and are asymmetrically ovoid. They have a very thick shell. As seen above, these trematodes have a very complex life cycle with seven distinct phases involving intermediate hosts and humans. These seven phases are outlined as follows: eggs reach fresh water where they develop into miracidia. These penetrate many species of aquatic snails (first intermediate host) where they go through three distinct stages: first sporocysts, then rediae, and finally cercariae, also referred to as the larvae. These larvae released into water and penetrate crabs, crayfish and other crustaceans (second intermediate host). The cercariae situate themselves into the gills, liver and muscles where they further develop into metacercariae. When the parasite-filled crustacean is eaten, the metacercariae hatch in the intestine. These young worms penetrate intestinal wall, peritoneum, the diaphragm and the pleura where they finally reach the lungs. Here they live in pairs, lay eggs that are coughed up in sputum to restart the cycle.

Geographic distribution
There are more than 30 known species of Paragonimus. Species of Paragonimus are widely distributed in Asia, Africa, and North and South America. P. westermani is found in southeast Asia and Japan, while P. kellicotti is endemic to North America. P. africanus is found in Africa and P. mexicanus is found in central and South America. Just as the species names imply, paragonimiasis  is more prominent in Asians, Africans and Hispanics because of their habitats and cultures. Prominence increases with age from older children to young adults then decreases with age. It is also higher among the female populations. This is a very common parasite of crustacean-eating mammals.

Symptoms and diagnosis
Paragonimiasis causes pneumonia with characteristic symptoms including prolonged cough, chest pain, shortness of breath, and hemoptysis. Owing to the diverse symptoms it presents, the disease is variously known as endemic haemoptysis, oriental lung fluke infection, pulmonary distomiasis, parasitical haemoptysis, and parasitare haemopte. Pulmonary paragonimiasis is the most common clinical manifestation, accounting for 76 to 90% of all infections. It has the classic symptoms of pneumonia. Extra-pulmonary infection is due to migration of the young worms away from the normal route to the lungs. In such case, any other part of the body can be infected. Cutaneous paragonimiasis is common in children and is generally indicated by skin nodules that move from one place to another. Cerebral paragonimias is most severe extra-pulmonary symptoms that affect the brain and leads to seizure, headache, visual disturbance, and motor and sensory disturbances.The acute phase (invasion and migration) may be marked by diarrhea, abdominal pain, fever, cough, urticaria, hepatosplenomegaly, pulmonary abnormalities, and eosinophilia. During the chronic phase, pulmonary manifestations include cough, expectoration of discolored sputum containing clumps of eggs, hemoptysis, and chest radiographic abnormalities. Extrapulmonary locations of the adult worms result in more severe manifestations, especially when the brain is involved. Diagnosis is based on microscopic demonstration of eggs in stool or sputum, but these are not present until 2 to 3 months after infection. (Eggs are also occasionally encountered in effusion fluid or biopsy material.) Concentration techniques may be necessary in patients with light infections. Biopsy may allow diagnostic confirmation and species identification when an adult or developing fluke is recovered.Diagnosis is done by microscopic examination of sputum and stool samples, and presence of the eggs is a confirmation. However, eggs are not always to be found. In such case, serological tests based on antibody detection using ELISA is a better method. A more arduous method like immunoblotting is also used. For brain infection, radiological examinations including plain skull x-rays, brain CT, and MR scans are used </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 Ganglion and can you explain it in depth? [/INST]  </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 Subacute thyroiditis and can you explain it in depth? [/INST] Subacute thyroiditis is a form of thyroiditis that can be a cause of both thyrotoxicosis and hypothyroidism. It is uncommon and can affect individuals of both sexes, occurring three times as often in women than in men. and people of all ages </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 Periodic fever syndrome and can you explain it in depth? [/INST] Periodic fever syndromes  are a set of disorders characterized by recurrent episodes of systemic and organ-specific inflammation. Unlike autoimmune disorders such as systemic lupus erythematosus, in which the disease is caused by abnormalities of the adaptive immune system, people with autoinflammatory diseases do not produce autoantibodies or antigen-specific T or B cells.  Instead, the autoinflammatory diseases are characterized by errors in the innate immune system.The syndromes are diverse, but tend to cause episodes of fever, joint pains, skin rashes, abdominal pains and may lead to chronic complications such as amyloidosis.Most autoinflammatory diseases are genetic and present during childhood.  The most common genetic autoinflammatory syndrome is familial Mediterranean fever, which causes short episodes of fever, abdominal pain, serositis, lasting less than 72 hours.  It is caused by mutations in the MEFV gene, which codes for the protein pyrin.Pyrin is a protein normally present in the inflammasome.  The mutated pyrin protein is thought to cause inappropriate activation of the inflammasome, leading to release of the pro-inflammatory cytokine IL-1β </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 Idiopathic interstitial pneumonia and can you explain it in depth? [/INST]  </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 Avascular necrosis and can you explain it in depth? [/INST] Avascular necrosis (AVN), also called osteonecrosis or bone infarction, is death of bone tissue due to interruption of the blood supply. Early on, there may be no symptoms. Gradually joint pain may develop which may limit the ability to move. Complications may include collapse of the bone or nearby joint surface.Risk factors include bone fractures, joint dislocations, alcoholism, and the use of high-dose steroids. The condition may also occur without any clear reason. The most commonly affected bone is the femur. Other relatively common sites include the upper arm bone, knee, shoulder, and ankle. Diagnosis is typically by medical imaging such as X-ray, CT scan, or MRI. Rarely biopsy may be used.Treatments may include medication, not walking on the affected leg, stretching, and surgery. Most of the time surgery is eventually required and may include core decompression, osteotomy, bone grafts, or joint replacement. About 15,000 cases occur per year in the United States. People 30 to 50 years old are most commonly affected. Males are more commonly affected than females.

Signs and symptoms
In many cases, there is pain and discomfort in a joint which increases over time. While it can affect any bone, about half of cases show multiple sites of damage.Avascular necrosis most commonly affects the ends of long bones such as the femur. Other common sites include the humerus, knees, shoulders, ankles and the jaw.

Causes
The main risk factors are bone fractures, joint dislocations, alcoholism, and the use of high-dose steroids. Other risk factors include radiation therapy, chemotherapy, and organ transplantation. Osteonecrosis is also associated with cancer, lupus, sickle cell disease, HIV infection, Gauchers disease, and Caisson disease (dysbaric osteonecrosis). The condition may also occur without any clear reason.Bisphosphonates are associated with osteonecrosis of the mandible. Prolonged, repeated exposure to high pressures (as experienced by commercial and military divers) has been linked to AVN, though the relationship is not well understood.In children, avascular osteonecrosis can have several causes. It can occur in the hip as part of Legg–Calvé–Perthes syndrome, and it can also occur as a result after malignancy treatment such as acute lymphoblastic leukemia and allotransplantation.

Pathophysiology
The hematopoietic cells are most sensitive to low oxygen and are the first to die after reduction or removal of the blood supply, usually within 12 hours. Experimental evidence suggests that bone cells (osteocytes, osteoclasts, osteoblasts etc.) die within 12–48 hours, and that bone marrow fat cells die within 5 days.Upon reperfusion, repair of bone occurs in 2 phases. First, there is angiogenesis and movement of undifferentiated mesenchymal cells from adjacent living bone tissue grow into the dead marrow spaces, as well as entry of macrophages that degrade dead cellular and fat debris. Second, there is cellular differentiation of mesenchymal cells into osteoblasts or fibroblasts. Under favorable conditions, the remaining inorganic mineral volume forms a framework for establishment of new, fully functional bone tissue.

Diagnosis
In the early stages, bone scintigraphy and MRI are the preferred diagnostic tools.X-ray images of avascular necrosis in the early stages usually appear normal. In later stages it appears relatively more radio-opaque due to the nearby living bone becoming resorbed secondary to reactive hyperemia. The necrotic bone itself does not show increased radiographic opacity, as dead bone cannot undergo bone resorption which is carried out by living osteoclasts. Late radiographic signs also include a radiolucency area following the collapse of subchondral bone (crescent sign) and ringed regions of radiodensity resulting from saponification and calcification of marrow fat following medullary infarcts.

Types
When AVN affects the scaphoid bone, it is known as Preiser disease. Another named form of AVN is Köhler disease, which affects the navicular bone of the foot, primarily in children. Yet another form of AVN is Kienböcks disease, which affects the lunate bone in the wrist.

Treatment
A variety of methods may be used to treat the most common being the total hip replacement (THR). However, THRs have a number of downsides including long recovery times and short life spans of the hip joints. THRs are an effective means of treatment in the older population; however, in younger people, they may wear out before the end of a persons life.Other techniques such as metal on metal resurfacing may not be suitable in all cases of avascular necrosis; its suitability depends on how much damage has occurred to the femoral head. Bisphosphonates which reduce the rate of bone breakdown may prevent collapse (specifically of the hip) due to AVN.

Core decompression
Other treatments include core decompression, where internal bone pressure is relieved by drilling a hole into the bone, and a living bone chip and an electrical device to stimulate new vascular growth are implanted; and the free vascular fibular graft (FVFG), in which a portion of the fibula, along with its blood supply, is removed and transplanted into the femoral head. A 2016 Cochrane review found no clear improvement between people who have had hip core decompression and participate in physical therapy, versus physical therapy alone. There is additionally no strong research on the effectiveness of hip core decompression for people with sickle cell disease.Progression of the disease could possibly be halted by transplanting nucleated cells from bone marrow into avascular necrosis lesions after core decompression, although much further research is needed to establish this technique.

Prognosis
The amount of disability that results from avascular necrosis depends on what part of the bone is affected, how large an area is involved, and how effectively the bone rebuilds itself </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 Side and can you explain it in depth? [/INST]  </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 Farmers lung and can you explain it in depth? [/INST] Farmers lung (not to be confused with silo-fillers disease) is a hypersensitivity pneumonitis induced by the inhalation of biologic dusts coming from hay dust or mold spores or any other agricultural products. It results in a type III hypersensitivity inflammatory response and can progress to become a chronic condition which is considered potentially dangerous.

Signs and symptoms
Acute Stage: Appears four to eight hours after exposure.  Symptoms such as headache, irritating cough, and shortness of breath upon physical exertion.
Subacute Stage: Symptoms persist without further exposure, and increase in severity. Symptoms include: shortness of breath upon exertion, chronic coughing, physical weakness, occasional fever and sweating, decrease in appetite, aches and pains.
Chronic Stage: Debilitating effects are now considered long-term. Symptoms include: severe shortness of breath, chronic coughing, physical weakness, occasional fever and sweating at night, decrease in appetite, and general aches and pains.These symptoms develop between four and eight hours after exposure to the antigens.  In acute attacks, the symptoms mimic pneumonia or flu.  In chronic attacks, there is a possibility of the victim going into shock and dying from the attack.

Causes
Permanent lung damage can arise due to ones inability to recognize the cause of symptoms. Farmers lung occurs because repeated exposure to antigens, found in the mold spores of hay, crops, and animal feed, triggers an allergic reaction within the farmers immune system. The defense mechanisms of the body present as cold and flu-like symptoms that occur in individuals who experience either acute or chronic reactions.The mold spores are inhaled and provoke the creation of IgE antibodies that circulate in the bloodstream, these types of immune response are most often initiated by exposure to thermophilic actinomycetes (most commonly Saccharopolyspora rectivirgula), which generate IgG-type antibodies. Following a subsequent exposure, IgG antibodies combined with the inhaled allergen to form immune complexes in the walls of the alveoli in the lungs. This causes fluid, protein, and cells to accumulate in the alveolar wall which slows blood-gas interchange and compromises the function of the lung.  After multiple exposures, it takes less and less of the antigens to set off the reaction in the lung.

Prevention
Farmers lung disease (FLD) is permanent and cannot be reversed, therefore in order to prevent the onset of further stages, farmers should inform their doctor of their occupation and if they have mold in their work environment. Prevention of this respiratory illness can be facilitated through the ventilation of work areas, drying of materials, and the use of a mask when working in confined areas with moldy hay or crops.

Diagnosis
Diagnoses of Farmers lung is difficult due to its similarity to cold and flu-like symptoms </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 Megaureter and can you explain it in depth? [/INST]  </s>