<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Fever and explain in detail? [/INST] Fever, also referred to as pyrexia, is defined as having a temperature above the normal range due to an increase in the bodys temperature set point. There is not a single agreed-upon upper limit for normal temperature with sources using values between 37.2 and 38.3 °C (99.0 and 100.9 °F) in humans. The increase in set point triggers increased muscle contractions and causes a feeling of cold or chills. This results in greater heat production and efforts to conserve heat. When the set point temperature returns to normal, a person feels hot, becomes flushed, and may begin to sweat. Rarely a fever may trigger a febrile seizure, with this being more common in young children. Fevers do not typically go higher than 41 to 42 °C (106 to 108 °F).A fever can be caused by many medical conditions ranging from non-serious to life-threatening. This includes viral, bacterial, and parasitic infections—such as influenza, the common cold, meningitis, urinary tract infections, appendicitis, Lassa, COVID-19, and malaria. Non-infectious causes include vasculitis, deep vein thrombosis, connective tissue disease, side effects of medication or vaccination, and cancer. It differs from hyperthermia, in that hyperthermia is an increase in body temperature over the temperature set point, due to either too much heat production or not enough heat loss.Treatment to reduce fever is generally not required. Treatment of associated pain and inflammation, however, may be useful and help a person rest. Medications such as ibuprofen or paracetamol (acetaminophen) may help with this as well as lower temperature. Children younger than three months require medical attention, as might people with serious medical problems such as a compromised immune system or people with other symptoms. Hyperthermia requires treatment.Fever is one of the most common medical signs. It is part of about 30% of healthcare visits by children and occurs in up to 75% of adults who are seriously sick. While fever evolved as a defense mechanism, treating a fever does not appear to improve or worsen outcomes. Fever is often viewed with greater concern by parents and healthcare professionals than is usually deserved, a phenomenon known as fever phobia.

Associated symptoms
A fever is usually accompanied by sickness behavior, which consists of lethargy, depression, loss of appetite, sleepiness, hyperalgesia, dehydration, and the inability to concentrate. Sleeping with a fever can often cause intense or confusing nightmares, commonly called "fever dreams". Mild to severe delirium (which can also cause hallucinations) may also present itself during high fevers.

Diagnosis
A range for normal temperatures has been found. Central temperatures, such as rectal temperatures, are more accurate than peripheral temperatures.
Fever is generally agreed to be present if the elevated temperature is caused by a raised set point and:

Temperature in the anus (rectum/rectal) is at or over 37.5–38.3 °C (99.5–100.9 °F) An ear (tympanic) or forehead (temporal) temperature may also be used.
Temperature in the mouth (oral) is at or over 37.2 °C (99.0 °F) in the morning or over 37.7 °C (99.9 °F) in the afternoon
Temperature under the arm (axillary) is usually about 0.6 °C (1.1 °F) below core body temperature.In adults, the normal range of oral temperatures in healthy individuals is 35.7–37.7 °C (96.3–99.9 °F) among men and 33.2–38.1 °C (91.8–100.6 °F) among women, while when taken rectally it is 36.7–37.5 °C (98.1–99.5 °F) among men and 36.8–37.1 °C (98.2–98.8 °F) among women, and for ear measurement it is 35.5–37.5 °C (95.9–99.5 °F) among men and 35.7–37.5 °C (96.3–99.5 °F) among women.Normal body temperatures vary depending on many factors, including age, sex, time of day, ambient temperature, activity level, and more.  Normal daily temperature variation has been described as 0.5 °C (0.9 °F).: 4012   A raised temperature is not always a fever.  For example, the temperature rises in healthy people when they exercise, but this is not considered a fever, as the set point is normal. On the other hand, a "normal" temperature may be a fever, if it is unusually high for that person; for example, medically frail elderly people have a decreased ability to generate body heat, so a "normal" temperature of 37.3 °C (99.1 °F) may represent a clinically significant fever.

Hyperthermia
Hyperthermia is an elevation of body temperature over the temperature set point, due to either too much heat production or not enough heat loss. Hyperthermia is thus not considered fever.: 103  Hyperthermia is not to be confused with hyperpyrexia (which is a very high fever).: 102 Clinically, it is important to distinguish between fever and hyperthermia as hyperthermia may quickly lead to death and does not respond to antipyretic medications. The distinction may however be difficult to make in an emergency setting, and is often established by identifying possible causes.: 103

Types
Various patterns of measured patient temperatures have been observed, some of which may be indicative of a particular medical diagnosis:
Continuous fever, where temperature remains above normal and does not fluctuate more than 1 °C in 24 hours (e.g. in bacterial pneumonia, typhoid, infective endocarditis, tuberculosis, or typhus.
Intermittent fever is present only for a certain period, later cycling back to normal (e.g., in malaria, leishmaniasis, pyemia, sepsis, or African trypanosomiasis.
Remittent fever, where the temperature remains above normal throughout the day and fluctuates more than 1 °C in 24 hours (e.g., in infective endocarditis or brucellosis).
Pel–Ebstein fever is a cyclic fever that is rarely seen in patients with Hodgkins lymphoma.
Undulant fever, seen in brucellosis.
Typhoid fever is a continuous fever showing a characteristic step-ladder pattern, a step-wise increase in temperature with a high plateau.Among the types of intermittent fever are ones specific to cases of malaria caused by different pathogens. These are:
Quotidian fever, with a 24-hour periodicity, typical of malaria caused by Plasmodium knowlesi (P. knowlesi);
Tertian fever, with a 48-hour periodicity, typical of later course malaria caused by P. falciparum, P. vivax, or P. ovale;
Quartan fever, with a 72-hour periodicity, typical of later course malaria caused by P. malariae.In addition, there is disagreement regarding whether a specific fever pattern is associated with Hodgkins lymphoma—the Pel–Ebstein fever, with patients argued to present high temperature for one week, followed by low for the next week, and so on, where the generality of this pattern is debated.Persistent fever that cannot be explained after repeated routine clinical inquiries is called fever of unknown origin. A neutropenic fever, also called febrile neutropenia, is a fever in the absence of normal immune system function. Because of the lack of infection-fighting neutrophils, a bacterial infection can spread rapidly; this fever is, therefore, usually considered to require urgent medical attention. This kind of fever is more commonly seen in people receiving immune-suppressing chemotherapy than in apparently healthy people.

Hyperpyrexia
Hyperpyrexia is an extreme elevation of body temperature which, depending upon the source, is classified as a core body temperature greater than or equal to 40 or 41 °C (104 or 106 °F); the range of hyperpyrexias includes cases considered severe (≥ 40 °C) and extreme (≥ 42 °C). It differs from hyperthermia in that ones thermoregulatory systems set point for body temperature is set above normal, then heat is generated to achieve it. In contrast, hyperthermia involves body temperature rising above its set point due to outside factors. The high temperatures of hyperpyrexia are considered medical emergencies, as they may indicate a serious underlying condition or lead to severe morbidity (including permanent brain damage), or to death. A common cause of hyperpyrexia is an intracranial hemorrhage. Other causes in emergency room settings include sepsis, Kawasaki syndrome, neuroleptic malignant syndrome, drug overdose, serotonin syndrome, and thyroid storm.

Differential diagnosis
Fever is a common symptom of many medical conditions:

Infectious disease, e.g., COVID-19, dengue, Ebola, gastroenteritis, HIV, influenza, Lyme disease, rocky mountain spotted fever, secondary syphilis, malaria, mononucleosis, as well as infections of the skin, e.g., abscesses and boils.
Immunological diseases, e.g., relapsing polychondritis, autoimmune hepatitis, granulomatosis with polyangiitis, Horton disease, inflammatory bowel diseases, Kawasaki disease, lupus erythematosus, sarcoidosis, and Stills disease;
Tissue destruction, as a result of cerebral bleeding, crush syndrome, hemolysis, infarction, rhabdomyolysis, surgery, etc.;
Cancers, particularly blood cancers such as leukemia and lymphomas;
Metabolic disorders, e.g., gout, and porphyria; and
Inherited metabolic disorder, e.g., Fabry disease.Adult and pediatric manifestations for the same disease may differ; for instance, in COVID-19, one metastudy describes 92.8% of adults versus 43.9% of children presenting with fever.In addition, fever can result from a reaction to an incompatible blood product.Teething is not a cause of fever.

Function
Immune function
Fever is thought to contribute to host defense, as the reproduction of pathogens with strict temperature requirements can be hindered, and the rates of some important immunological reactions are increased by temperature. Fever has been described in teaching texts as assisting the healing process in various ways, including:

increased mobility of leukocytes;: 1044
enhanced leukocyte phagocytosis;: 1030
decreased endotoxin effects;: 1029  and
increased proliferation of T cells.: 1030 : 212

Advantages and disadvantages
Having a fever response in response to an infectious disease is generally regarded as protective, whereas fever in non-infections may be maladaptive. Studies have not been consistent on whether treating fever generally worsens or improves mortality risk. Benefits or harms may depend on the type of infection, health status of the patient and other factors.  Studies using warm-blooded vertebrates suggest that they recover more rapidly from infections or critical illness due to fever. In sepsis, fever is associated with reduced mortality.

Pathophysiology of fever induction
Hypothalamus
Temperature is regulated in the hypothalamus. The trigger of a fever, called a pyrogen, results in the release of prostaglandin E2 (PGE2). PGE2 in turn acts on the hypothalamus, which creates a systemic response in the body, causing heat-generating effects to match a new higher temperature set point. There are four receptors in which PGE2 can bind (EP1-4), with a previous study showing the EP3 subtype is what mediates the fever response. Hence, the hypothalamus can be seen as working like a thermostat. When the set point is raised, the body increases its temperature through both active generation of heat and retention of heat. Peripheral vasoconstriction both reduces heat loss through the skin and causes the person to feel cold. Norepinephrine increases thermogenesis in brown adipose tissue, and muscle contraction through shivering raises the metabolic rate.If these measures are insufficient to make the blood temperature in the brain match the new set point in the hypothalamus, the brain orchestrates heat effector mechanisms via the autonomic nervous system or primary motor center for shivering. These may be:
Increased heat production by increased muscle tone, shivering (muscle movements to produce heat) and release of hormones like epinephrine; and
Prevention of heat loss, e.g., through vasoconstriction.When the hypothalamic set point moves back to baseline—either spontaneously or via medication—normal functions such as sweating, and the reverse of the foregoing processes (e.g., vasodilation, end of shivering, and nonshivering heat production) are used to cool the body to the new, lower setting.This contrasts with hyperthermia, in which the normal setting remains, and the body overheats through undesirable retention of excess heat or over-production of heat. Hyperthermia is usually the result of an excessively hot environment (heat stroke) or an adverse reaction to drugs. Fever can be differentiated from hyperthermia by the circumstances surrounding it and its response to anti-pyretic medications.In infants, the autonomic nervous system may also activate brown adipose tissue to produce heat (non-exercise-associated thermogenesis, also known as non-shivering thermogenesis).Increased heart rate and vasoconstriction contribute to increased blood pressure in fever.

Pyrogens
A pyrogen is a substance that induces fever. In the presence of an infectious agent, such as bacteria, viruses, viroids, etc., the immune response of the body is to inhibit their growth and eliminate them. The most common pyrogens are endotoxins, which are lipopolysaccharides (LPS) produced by Gram-negative bacteria such as E. coli. But pyrogens include non-endotoxic substances (derived from microorganisms other than gram-negative-bacteria or from chemical substances) as well. The types of pyrogens include internal (endogenous) and external (exogenous) to the body.The "pyrogenicity" of given pyrogens varies: in extreme cases, bacterial pyrogens can act as superantigens and cause rapid and dangerous fevers.

Endogenous
Endogenous pyrogens are cytokines released from monocytes (which are part of the immune system). In general, they stimulate chemical responses, often in the presence of an antigen, leading to a fever. Whilst they can be a product of external factors like exogenous pyrogens, they can also be induced by internal factors like damage associated molecular patterns such as cases like rheumatoid arthritis or lupus.Major endogenous pyrogens are interleukin 1 (α and β): 1237–1248  and interleukin 6 (IL-6). Minor endogenous pyrogens include interleukin-8, tumor necrosis factor-β, macrophage inflammatory protein-α and macrophage inflammatory protein-β as well as interferon-α, interferon-β, and interferon-γ.: 1237–1248  Tumor necrosis factor-α (TNF) also acts as a pyrogen, mediated by interleukin 1 (IL-1) release. These cytokine factors are released into general circulation, where they migrate to the brains circumventricular organs where they are more easily absorbed than in areas protected by the blood–brain barrier. The cytokines then bind to endothelial receptors on vessel walls to receptors on microglial cells, resulting in activation of the arachidonic acid pathway.Of these, IL-1β, TNF, and IL-6 are able to raise the temperature setpoint of an organism and cause fever. These proteins produce a cyclooxygenase which induces the hypothalamic production of PGE2 which then stimulates the release of neurotransmitters such as cyclic adenosine monophosphate and increases body temperature.

Exogenous
Exogenous pyrogens are external to the body and are of microbial origin. In general, these pyrogens, including bacterial cell wall products, may act on Toll-like receptors in the hypothalamus and elevate the thermoregulatory setpoint.An example of a class of exogenous pyrogens are bacterial lipopolysaccharides (LPS) present in the cell wall of gram-negative bacteria. According to one mechanism of pyrogen action, an immune system protein, lipopolysaccharide-binding protein (LBP), binds to LPS, and the LBP–LPS complex then binds to a CD14 receptor on a macrophage. The LBP-LPS binding to CD14 results in cellular synthesis and release of various endogenous cytokines, e.g., interleukin 1 (IL-1), interleukin 6 (IL-6), and tumor necrosis factor-alpha (TNFα). A further downstream event is activation of the arachidonic acid pathway.

PGE2 release
PGE2 release comes from the arachidonic acid pathway. This pathway (as it relates to fever), is mediated by the enzymes phospholipase A2 (PLA2), cyclooxygenase-2 (COX-2), and prostaglandin E2 synthase. These enzymes ultimately mediate the synthesis and release of PGE2.PGE2 is the ultimate mediator of the febrile response. The setpoint temperature of the body will remain elevated until PGE2 is no longer present. PGE2 acts on neurons in the preoptic area (POA) through the prostaglandin E receptor 3 (EP3). EP3-expressing neurons in the POA innervate the dorsomedial hypothalamus (DMH), the rostral raphe pallidus nucleus in the medulla oblongata (rRPa), and the paraventricular nucleus (PVN) of the hypothalamus. Fever signals sent to the DMH and rRPa lead to stimulation of the sympathetic output system, which evokes non-shivering thermogenesis to produce body heat and skin vasoconstriction to decrease heat loss from the body surface. It is presumed that the innervation from the POA to the PVN mediates the neuroendocrine effects of fever through the pathway involving pituitary gland and various endocrine organs.

= Management= =
Fever does not necessarily need to be treated, and most people with a fever recover without specific medical attention. Although it is unpleasant, fever rarely rises to a dangerous level even if untreated. Damage to the brain generally does not occur until temperatures reach 42.0 °C (107.6 °F), and it is rare for an untreated fever to exceed 40.6 °C (105.1 °F). Treating fever in people with sepsis does not affect outcomes. Small trials have shown no benefit of treating fevers of 38.5 °C (101.3 °F) or higher of critical ill patients in ICUs, and one trial was terminated early because patients receiving aggressive fever treatment were dying more often.According to the NIH, the two assumptions which are generally used to argue in favor of treating fevers have not been experimentally validated. These are that (1) a fever is noxious, and (2) suppression of a fever will reduce its noxious effect. Most of the other studies supporting the association of fever with poorer outcomes have been observational in nature. In theory, these critically ill patients and those faced with additional physiologic stress may benefit from fever reduction, but the evidence on both sides of the argument appears to be mostly equivocal.

Conservative measures
Limited evidence supports sponging or bathing feverish children with tepid water. The use of a fan or air conditioning may somewhat reduce the temperature and increase comfort. If the temperature reaches the extremely high level of hyperpyrexia, aggressive cooling is required (generally produced mechanically via conduction by applying numerous ice packs across most of the body or direct submersion in ice water). In general, people are advised to keep adequately hydrated. Whether increased fluid intake improves symptoms or shortens respiratory illnesses such as the common cold is not known.

Medications
Medications that lower fevers are called antipyretics. The antipyretic ibuprofen is effective in reducing fevers in children. It is more effective than acetaminophen (paracetamol) in children. Ibuprofen and acetaminophen may be safely used together in children with fevers. The efficacy of acetaminophen by itself in children with fevers has been questioned. Ibuprofen is also superior to aspirin in children with fevers. Additionally, aspirin is not recommended in children and young adults (those under the age of 16 or 19 depending on the country) due to the risk of Reyes syndrome.Using both paracetamol and ibuprofen at the same time or alternating between the two is more effective at decreasing fever than using only paracetamol or ibuprofen. It is not clear if it increases child comfort. Response or nonresponse to medications does not predict whether or not a child has a serious illness.With respect to the effect of antipyretics on the risk of death in those with infection, studies have found mixed results as of 2019. Animal models have found worsened outcomes with the use of antipyretics in influenza as of 2010 but they have not been studied for this use in humans.

Epidemiology
Fever is one of the most common medical signs. It is part of about 30% of healthcare visits by children, and occurs in up to 75% of adults who are seriously sick. About 5% of people who go to an emergency room have a fever.

History
A number of types of fever were known as early as 460 BC to 370 BC when Hippocrates was practicing medicine including that due to malaria (tertian or every 2 days and quartan or every 3 days). It also became clear around this time that fever was a symptom of disease rather than a disease in and of itself.Infections presenting with fever were a major source of mortality in humans for about 200,000 years. Until the late nineteenth century, approximately half of all humans died from infections before the age of fifteen.An older term, febricula (a diminutive form of the Latin word for fever), was once used to refer to a low-grade fever lasting only a few days. This term fell out of use in the early 20th century, and the symptoms it referred to are now thought to have been caused mainly by various minor viral respiratory infections.

Society and culture
Mythology
Febris (fever in Latin) is the goddess of fever  in Roman mythology. People with fevers would visit her temples.
Tertiana and Quartana are the goddesses of tertian and quartan fevers of malaria in Roman mythology.
Jvarasura (fever-demon in Hindi) is the personification of fever and disease in Hindu and Buddhist mythology.

Paediatrics
Fever is often viewed with greater concern by parents and healthcare professionals than might be deserved, a phenomenon known as fever phobia, which is based in both caregivers and parents misconceptions about fever in children. Among them, many parents incorrectly believe that fever is a disease rather than a medical sign, that even low fevers are harmful, and that any temperature even briefly or slightly above the oversimplified "normal" number marked on a thermometer is a clinically significant fever. They are also afraid of harmless side effects like febrile seizures and dramatically overestimate the likelihood of permanent damage from typical fevers. The underlying problem, according to professor of pediatrics Barton D. Schmitt, is that "as parents we tend to suspect that our childrens brains may melt." As a result of these misconceptions parents are anxious, give the child fever-reducing medicine when the temperature is technically normal or only slightly elevated, and interfere with the childs sleep to give the child more medicine.

Other species
Fever is an important metric for the diagnosis of disease in domestic animals. The body temperature of animals, which is taken rectally, is different from one species to another </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Wilson–Mikity syndrome and explain in detail? [/INST] Wilson–Mikity syndrome, a form of chronic lung disease (CLD) that exists only in premature infants, leads to progressive or immediate development of respiratory distress. This rare condition affects low birth babies and is characterized by rapid development of lung emphysema after birth, requiring prolonged ventilation and oxygen supplementation. It is closely related to bronchopulmonary dysplasia (BPD), differing mainly in the lack of prior ventilatory support. All the initial patients described with Wilson–Mikity syndrome were very low birth weight infants that had no history of mechanical ventilation, yet developed a syndrome that clinically resembled BPD. Upon the death of some of these infants, autopsies showed histologic changes similar to those seen in BPD.It was characterized by Miriam G. Wilson and Victor G. Mikity in 1960.

Symptoms and signs
The onset of respiratory difficulty occurs at the first day of life and continues up to three weeks into the infants life, at which point treatment is needed for infant survival.

Complications
Mothers who have developed chorioamnionitis during pregnancy put their infant at higher risk for development of Wilson-Mikity syndrome. It is a rare complication that requires prolonged treatment. Infection, however, is not shown to be an etiological factor, but a correlation to chorioamnionitis is identified as a risk.

Cause
The cause of Wilson-Mikity syndrome is unknown.

Diagnosis
The diagnosis of Wilson-Mikity syndrome can be made through two distinct symptoms: analogous characteristics of respiratory distress syndrome and presence of diffuse and streaky infiltrates with small cystic changes, seen through a chest X-ray. Early screening allows for the identification of a collapsed lung, cystic changes within the lung, and possible start of right-sided heart failure. Upon autopsy, alveolar collapse and alveoli rupture can be seen. This can reduce the number of capillaries within the system and lead to cyanosis. Cyanosis occurs from chronic or intermittent respiratory distress and episodes of dyspnea (or apnea). Symptoms can develop within hours post-birth or be gradual; infants will experience transient respiratory distress, causing a lapse in diagnosis by around 30 to 40 days. Dangerous recurrent apnea (or dyspnea) can occur in the first two to six weeks postpartum. This cessation of breathing can progress to cyanosis and lung collapse.
Infants display deteriorating respiratory symptoms along with early chronic lung changes which can be seen on chest radiography. These changes are diagnosed either directly upon birth or within the first month, as the premature infant requires mechanical ventilation for survival.

Treatment
When caught early enough, continuous, mechanical oxygen therapy can be used to reverse the infants poor circulation and decreased blood oxygen, a symptom known as cyanosis. Improvement is gradual; however, cases show that after the first year of treatment using oxygen therapy and mechanical ventilators, infants show normal respiratory activity and are free from chest infiltrates with small cystic changes. Absence of fever (febrile), and normal white blood cell count correspond to successful reversion and allow for a positive prognosis.When not treated properly, methods of reversion using oxygen supplementation and ventilation have the possibility to put the infant at risk for rare complications. If not enough oxygen is administered to the infant, the apnea continues and the infant is unable proper recovery. In contrast, too much oxygen administered can lead to higher risk for retrolental fibroplasia and/or oxygen toxicity within the lungs. Continued dyspnea is a sign that Wilson-Mikity syndrome is still affecting the infant. Increased ventilation to allow proper respiration is then required. Patients in recovery are slowly taken off oxygen support and eventually are able to ventilate with minimal to no respiratory distress.There is a lack of research on the long-term effects of Wilson-Mikity into adulthood.

Epidemiology
Around 75% of affected infants survive and are able to receive oxygen therapies and treatments to overcome this disease. In fatal cases, infants do not have noticeable or substantial respiratory recovery and can develop right-sided heart failure, ultimately leading to death. Patients that are not recovering will also continue to show signs of dyspnea, respiratory distress, and continued low body weight, heightening the risk of death. Infants that survive six months or longer have substantially better prognosis.

See also
Infant respiratory distress syndrome
Bronchopulmonary dysplasia
Chronic obstructive pulmonary disease
Retrolental Fibroplasia
Chorioamnionitis

References
Further reading
Hoepker, A; Seear, M; Petrocheilou, A; Hayes D Jr; Nair, A; Deodhar, J; Kadam, S; OToole, J (Oct 2008). "Wilson-Mikity syndrome: updated diagnostic criteria based on nine cases and a review of the literature". Pediatric Pulmonology </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Mediastinitis and explain in detail? [/INST] Mediastinitis is inflammation of the tissues in the mid-chest, or mediastinum.  It can be either acute or chronic. It is thought to be due to four different etiologies:direct contamination
hematogenous or lymphatic spread
extension of infection from the neck or retroperitoneum
extension from the lung or pleuraAcute mediastinitis is usually caused by bacteria and is most often due to perforation of the esophagus. As the infection can progress rapidly, this is considered a serious condition.
Chronic sclerosing (or fibrosing) mediastinitis, while potentially serious, is caused by a long-standing inflammation of the mediastinum, leading to growth of acellular collagen and fibrous tissue within the chest and around the central vessels and airways.  It has a different cause, treatment, and prognosis than acute infectious mediastinitis.
Space infections: Pretracheal space – lies anterior to trachea. Pretracheal space infection leads to mediastinitis. Here, the fascia fuses with the pericardium and the parietal pleura, which explains the occurrence of empyema and pericardial effusion in mediastinitis. However, infectious of other spaces can also lead to mediastinitis.

Symptoms
Acute
Acute mediastinitis is an infectious process and can cause fever, chills, tachycardia. Pain can occur with mediastinitis but the location of the pain depends on which part of the mediastinum is involved. When the upper mediastinum is involved, the pain is typically retro-sternal pain. When the lower mediastinum is involved, pain can be located between in the scapulae and radiate around to the chest.

Chronic
Symptoms depend on what organs of the mediastinum the disease is affecting. They might be caused by a constricted airway, constricted esophagus, or constricted blood vessels. Symptoms also depend on how mush fibrosis has occurred. There may be cough, shortness of breath, coughing up blood, pain in the chest, and difficulty in swallowing.

Causes
Acute
Esophageal perforation, a form of direct contamination, accounts for 90% of acute mediastinal infections.  Esophageal perforation can arise from vomiting, incidental trauma from a procedure or operation, external trauma, ingestion of corrosive substances, malignancy, or other esophageal disease.Other causes of acute mediastinitis include infection secondary to cervical disease which arises from dental procedures, skin infections of the neck, neck trauma, or neck procedures.Descending necrotizing mediastinitis (DNM) was first described by Herman E. Pearse Jr., M.D. in 1938 and he stated, "the term mediastinitis means little unless qualified by a description of its type and kind." Although Descending Necrotizing Mediastinitis is an acute mediastinitis, it is distinct because it does not originate from structures within the mediastinum. Therefore, the term Descending Necrotizing Mediastinitis implies that the infection of the mediastinum originated from a primary site in the head or neck and descended through fascial spaces into the mediastinum.Though rare in developed countries, acute mediastinitis can be caused by inhalation of bacterial spores such as Anthrax. Historically, this infection was referred to as Wool-sorters Disease. In the lungs, spores can spread via lymphatics to mediastinal lymph nodes, where the mature rods can release exotoxins promoting edema and tissue necrosis. Clinically, persons infected with anthrax can develop a hemorrhagic mediastinitis, which manifests as acute pulmonary hemorrhage and meningitis. Hallmark finding of disease is a widened mediastinum visualized on chest x-ray. Once clinical symptoms of anthrax induced mediastinitis appear, disease is nearly 100% fatal. Individuals with known exposure to spores may be treated prophylactically with antibiotics (fluoroquinolones or tetracycline) to prevent disease progression.

Chronic
There are two types of fibrosing mediastinitis: granulomatous and non-granulomatous. Granulomatous mediastinitis is due to a granulomatous process of the mediastinal lymph nodes leading to fibrosis and chronic abscesses in the mediastinum. The most common causes are histoplasmosis and tuberculosis infections. Non-granulomatous fibrosing mediastinitis is caused by an idiopathic reaction to drugs and radiation therapy </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Indian Institute of Infrastructure and Construction and explain in detail? [/INST] The Indian Institute of Infrastructure and Construction Kollam or IIIC-Kollam is a public institute of international standard situated at Chavara in Kollam, Kerala. The initiative has been undertaken by the Government of Kerala with the support of the Government of India. The academy is coming under the Kerala Academy for Skills Excellence (KASE) to support the skill development programmes for construction related occupations

History
The construction academy was first proposed by the LDF ministry during 2008. They started the background works for the academy and named the project as Kerala Construction Academy, proposed at Chathannoor in Kollam district. When UDF came into power, they have shifted the project from Chathannoor to chavara and renamed as Indian Institute of Infrastructure and Construction.

Campus
The institute is on a 9.02 acres (36,500 m2) campus along the NH-66, near chavara in Kollam Metropolitan Area. KASE has developed a Master Plan and detailed design for the campus with 235,100 square feet (21,800 m2) of facilities including an administrative block, training block, canteen, and substation. Foundation stone was laid by the then Chief Minister of Kerala Mr. Oommen Chandy on 15 March 2013. The campus was inaugurated for academic activities by the Hon. Chief Minister Shri. Pinarayi Vijayan in August 2018.

Courses
During the initial phase, there will be three technician and managerial level courses along with a course in supervisory level. There will be an advanced certificate programme also in plumbing engineering. Candidates with SSLC, Plus Two, ITI, diploma, degree and B.Tech qualification can join for the courses.

Significance
Kerala state depends on migrant workers for the various jobs needed. The dependence on Migrant labourers in Kerala is found mainly in the field of construction </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Stepfather and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Involvement and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Hallux rigidus and explain in detail? [/INST] Hallux rigidus or stiff big toe is degenerative arthritis and stiffness due to bone spurs that affects the metatarsophalangeal joints (MTP) at the base of the hallux (big toe).
Hallux flexus was initially described by Davies-Colley  in 1887 as a plantar flexed posture of phalanx relative to the metatarsal head. About the same time, Cotterill first used the term hallux rigidus.

Signs and symptoms
Pain and stiffness in the joint at the base of the big toe during use (walking, standing, bending, etc.)
Difficulty with certain activities (running, squatting)
Swelling and inflammation around the jointAlthough the condition is degenerative, it can occur in patients who are relatively young, particularly active sports people who have at some time suffered trauma to the joint (turf toe). A notable example is NBA star Shaquille ONeal who returned to basketball after surgery.

Causes
This condition, which occurs in adolescents and adults, can be associated with previous trauma.
The true cause is not known. Most commonly, hallux rigidus is thought to be caused by wear and tear of the first metatarsophalangeal joint.

Classification
In 1988, Hattrup and Johnson described the following radiographic classification system:

Grade I – mild changes with maintained joint space and minimal spurring.
Grade II – moderate changes with narrowing of joint space, bony proliferation on the metatarsophalangeal head and phalanx and subchondral sclerosis or cyst.
Grade III – severe changes with significant joint space narrowing, extensive bony proliferation and loose bodies or a dorsal ossicle.

Treatment
Non-surgical
Early treatment for mild cases of hallux rigidus may include prescription foot orthotics, shoe modifications (such as a pad under the joint, and/or a deeper toe box to take the pressure off the toe and/or facilitate walking), specialized footwear (rocker-sole shoes), medications (anti-inflammatory drugs) or injection therapy (corticosteroids to reduce inflammation and pain). Physical therapy programs may be recommended, although there is very limited evidence that they provide benefit for reducing pain and improving function of the joint.

Surgical
The goal of surgery is to eliminate or reduce pain. There are several types of surgery for treatment of hallux rigidus </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Orthopnea and explain in detail? [/INST] Orthopnea or orthopnoea is shortness of breath (dyspnea) that occurs when lying flat, causing the person to have to sleep propped up in bed or sitting in a chair. It is commonly seen as a late manifestation of heart failure, resulting from fluid redistribution into the central circulation, causing an increase in pulmonary capillary pressure and causing difficulty in breathing. It is also seen in cases of abdominal obesity or pulmonary disease. Orthopnea is the opposite of platypnea, shortness of breath that worsens when sitting or standing upright.

Causes
Orthopnea is often a symptom of left ventricular heart failure and/or cardiogenic pulmonary edema. It can also occur in those with asthma and chronic bronchitis, as well as those with sleep apnea or panic disorder.  It is also as associated with polycystic liver disease. From a neuromuscular perspective, orthopnea is potentially a sign of severe diaphragmatic weakness. Under such circumstances, patients may describe shortness of breath when they bend over (e.g </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Ankyloglossia and explain in detail? [/INST] Ankyloglossia, also known as tongue-tie, is a congenital oral anomaly that may decrease the mobility of the tongue tip and is caused by an unusually short, thick lingual frenulum, a membrane connecting the underside of the tongue to the floor of the mouth. Ankyloglossia varies in degree of severity from mild cases characterized by mucous membrane bands to complete ankyloglossia whereby the tongue is tethered to the floor of the mouth.

Presentation
Ankyloglossia can affect eating, especially breastfeeding, speech and oral hygiene as well as have mechanical/social effects. Ankyloglossia can also prevent the tongue from contacting the anterior palate. This can then promote an infantile swallow and hamper the progression to an adult-like swallow which can result in an open bite deformity. It can also result in mandibular prognathism; this happens when the tongue contacts the anterior portion of the mandible with exaggerated anterior thrusts.Opinion varies regarding how frequently ankyloglossia truly causes problems. Some professionals believe it is rarely symptomatic, whereas others believe it is associated with a variety of problems. The disagreement among professionals was documented in a study by Messner and Lalakea (2000).

Feeding
Messner et al. studied ankyloglossia and infant feeding. Thirty-six infants with ankyloglossia were compared to a control group without ankyloglossia. The two groups were followed for six months to assess possible breastfeeding difficulties; defined as nipple pain lasting more than six weeks, or infant difficulty latching onto or staying onto the mothers breast. Twenty-five percent of mothers of infants with ankyloglossia reported breastfeeding difficulty compared with only 3% of the mothers in the control group. The study concluded that ankyloglossia can adversely affect breastfeeding in certain infants. Infants with ankyloglossia do not, however, have such big difficulties when feeding from a bottle. Limitations of this study include the small sample size and the fact that the quality of the mothers breastfeeding was not assessed.Wallace and Clark also studied breastfeeding difficulties in infants with ankyloglossia. They followed 10 infants with ankyloglossia who underwent surgical tongue-tie division. Eight of the ten mothers experienced poor infant latching onto the breast, 6/10 experienced sore nipples and 5/10 experienced continual feeding cycles; 3/10 mothers were exclusively breastfeeding. Following a tongue-tie division, 4/10 mothers noted immediate improvements in breastfeeding, 3/10 mothers did not notice any improvements and 6/10 mothers continued breastfeeding for at least four months after the surgery. The study concluded that tongue-tie division may be a possible benefit for infants experiencing breastfeeding difficulties due to ankyloglossia and further investigation is warranted. The limitations of this study include the small sample size and the fact that there was not a control group. In addition, the conclusions were based on subjective parent report as opposed to objective measures.

Speech
Messner and Lalakea studied speech in children with ankyloglossia. They noted that the phonemes likely to be affected due to ankyloglossia include sibilants and lingual sounds such as r. In addition, the authors also state that it is uncertain as to which patients will have a speech disorder that can be linked to ankyloglossia and that there is no way to predict at a young age which patients will need treatment. The authors studied 30 children from one to 12 years of age with ankyloglossia, all of whom underwent frenuloplasty. Fifteen children underwent speech evaluation before and after surgery. Eleven patients were found to have abnormal articulation before surgery and nine of these patients were found to have improved articulation after surgery. Based on the findings, the authors concluded that it is possible for children with ankyloglossia to have normal speech in spite of decreased tongue mobility. However, according to their study, a large percentage of children with ankyloglossia will have articulation deficits that can be linked to tongue-tie and these deficits may be improved with surgery. The authors also note that ankyloglossia does not cause a delay in speech or language, but at the most, problems with enunciation. Limitations of the study include a small sample size as well as a lack of blinding of the speech-language pathologists who evaluated the subjects’ speech.
Several recent systematic reviews and randomized control trials have argued that ankyloglossia does not impact speech sound development and that there is no difference in speech sound development between children who received surgery to release tongue-tie and those who did not.Messner and Lalakea also examined speech and ankyloglossia in another study. They studied 15 patients and speech was grossly normal in all the subjects. However, half of the subjects reported that they thought that their speech was more effortful than other peoples speech.Horton and colleagues discussed the relationship between ankyloglossia and speech. They believe that the tongue-tie contributes to difficulty in range and rate of articulation and that compensation is needed. Compensation at its worst may involve a Cupids bow of the tongue.Although the tongue-tie exists, and even years following surgery, common speech abnormalities include mispronunciation of words, the most common of which is pronouncing Ls as Ws; for example, the word "lemonade" would come out as "wemonade".

Mechanical and social effects
Ankyloglossia can result in mechanical and social effects. Lalakea and Messner studied 15 people, aged 14 to 68 years old. The subjects were given questionnaires in order to assess functional complaints associated with ankyloglossia. Eight subjects noted one or more mechanical limitations which included cuts or discomfort underneath the tongue and difficulties with kissing, licking ones lips, eating an ice cream cone, keeping ones tongue clean and performing tongue tricks. In addition, seven subjects noted social effects such as embarrassment and teasing. The authors concluded that this study confirmed anecdotal evidence of mechanical problems associated with ankyloglossia and it suggests that the kinds of mechanical and social problems noted may be more prevalent than previously thought. Furthermore, the authors note that some patients may be unaware of the extent of the limitations they have due to ankyloglossia, since they have never experienced a normal tongue range of motion. A limitation of this study is the small sample size that also represented a large age range.Lalakea and Messner note that mechanical and social effects may occur even without other problems related to ankyloglossia, such as speech and feeding difficulties.  Also, mechanical and social effects may not arise until later in childhood, as younger children may be unable to recognize or report the effects. In addition, some problems, such as kissing, may not come about until later in life.

Tongue posture and mouth breathing
Ankyloglossia most often prohibits the tongue from resting in its ideal posture, at the roof of the mouth. When the tongue rests at the roof of the mouth, it enables nasal breathing. A seemingly unrelated consequence of ankyloglossia is chronic mouth breathing. Mouth breathing is correlated with other health issues such as enlarged tonsils and adenoids, chronic ear infections, and sleep-disordered breathing.

Dental issues
Ankyloglossia is correlated to grinding teeth (bruxism) and temporomandibular joint (TMJ) pain. When the tongue normally rests at the roof of the mouth, it leads to the development of an ideal "U"-shaped palate. Ankyloglossia often causes a narrow, "V"-shaped palate to develop,  which crowds teeth and increases the potential need for braces and possibly jaw surgery.

Fascia and Muscle Compensation
The lingual frenulum under the tongue is part of the bodys larger fascia network. When the tongue is restricted by an overly tight frenulum, the tightness can travel to other nearby parts of the body such as the neck causing muscle tightness and poor posture. The tongue being restricted can force other muscles in the neck and jaw to compensate causing muscle soreness.

Diagnosis
According to Horton et al., diagnosis of ankyloglossia may be difficult; it is not always apparent by looking at the underside of the tongue, but is often dependent on the range of movement permitted by the genioglossus muscles. For infants, passively elevating the tongue tip with a tongue depressor may reveal the problem.  For older children, making the tongue move to its maximum range will demonstrate the tongue tip restriction. In addition, palpation of genioglossus on the underside of the tongue will aid in confirming the diagnosis.Some signs of ankyloglossia can be difficulty speaking, difficulty eating, ongoing dental issues, jaw pain, or migraines.A severity scale for ankyloglossia, which grades the appearance and function of the tongue, is recommended for use in the Academy of Breastfeeding Medicine.

Treatment
There are varying types of intervention for ankyloglossia. Intervention for ankyloglossia does sometimes include surgery in the form of frenotomy (also called a frenectomy or frenulectomy) or frenuloplasty. This relatively common dental procedure may be done with soft-tissue lasers, such as the CO2 laser.A frenotomy can be performed as a standalone procedure or as part of another surgery. The procedure is typically quick and is performed under local anesthesia. First, the area under the tongue is numbed with an injection. Once the patient is numb, a small incision is made in the tissue and the tongue is freed from its tether. The incision is then closed with dissolvable sutures. Recovery from a frenotomy is typically quick and most patients experience little to no pain or discomfort.According to Lalakea and Messner, surgery can be considered for patients of any age with a tight frenulum, as well as a history of speech, feeding, or mechanical/social difficulties </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Out and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is 1 and explain in detail? [/INST] 1 (one, unit, unity) is a number representing a single or the only entity. 1 is also a numerical digit and represents a single unit of counting or measurement. For example, a line segment of unit length is a line segment of length 1. In conventions of sign where zero is considered neither positive nor negative, 1 is the first and smallest positive integer. It is also sometimes considered the first of the infinite sequence of natural numbers, followed by 2, although by other definitions 1 is the second natural number, following 0.
The fundamental mathematical property of 1 is to be a multiplicative identity, meaning that any number multiplied by 1 equals the same number. Most if not all properties of 1 can be deduced from this. In advanced mathematics, a multiplicative identity is often denoted 1, even if it is not a number. 1 is by convention not considered a prime number; this was not universally accepted until the mid-20th century. Additionally, 1 is the smallest possible difference between two distinct natural numbers.
The unique mathematical properties of the number have led to its unique uses in other fields, ranging from science to sports. It commonly denotes the first, leading, or top thing in a group.

Etymology
The word one can be used as a noun, an adjective, and a pronoun.It comes from the English word an, which comes from the Proto-Germanic root *ainaz. The Proto-Germanic root *ainaz comes from the Proto-Indo-European root *oi-no-.Compare the Proto-Germanic root *ainaz to Old Frisian an, Gothic ains, Danish en, Dutch een, German eins and Old Norse einn.
Compare the Proto-Indo-European root *oi-no- (which means "one, single") to Greek oinos (which means "ace" on dice), Latin unus (one), Old Persian aivam, Old Church Slavonic -inu and ino-, Lithuanian vienas, Old Irish oin and Breton un (one).

As a number
One, sometimes referred to as unity, is the first non-zero natural number. It is thus the integer after zero.
Any number multiplied by one remains that number, as one is the identity for multiplication. As a result, 1 is its own factorial, its own square and square root, its own cube and cube root, and so on. One is also the result of the empty product, as any number multiplied by one is itself. It is also the only natural number that is neither composite nor prime with respect to division, but is instead considered a unit (meaning of ring theory).

As a digit
The glyph used today in the Western world to represent the number 1, a vertical line, often with a serif at the top and sometimes a short horizontal line at the bottom, traces its roots back to the Brahmic script of ancient India, where it was a simple vertical line. It was transmitted to Europe via the Maghreb and Andalusia during the Middle Ages, through scholarly works written in Arabic.
In some countries, the serif at the top is sometimes extended into a long upstroke, sometimes as long as the vertical line, which can lead to confusion with the glyph used for seven in other countries. In styles in which the digit 1 is written with a long upstroke, the digit 7 is often written with a horizontal stroke through the vertical line, to disambiguate them. Styles that do not use the long upstroke on digit 1 usually do not use the horizontal stroke through the vertical of the digit 7 either.
While the shape of the character for the digit 1 has an ascender in most modern typefaces, in typefaces with text figures, the glyph usually is of x-height, as, for example, in .
Many older typewriters lack a separate key for 1, using the lowercase letter l or uppercase I instead. It is possible to find cases when the uppercase J is used, though it may be for decorative purposes. In some typefaces, different glyphs are used for I and 1, but the numeral 1 resembles a small caps version of I, with parallel serifs at top and bottom, with the capital I being full-height.

Mathematics
Definitions
Mathematically, 1 is:

in arithmetic (algebra) and calculus, the natural number that follows 0 and the multiplicative identity element of the integers, real numbers and complex numbers;
more generally, in algebra, the multiplicative identity (also called unity), usually of a group or a ring.Formalizations of the natural numbers have their own representations of 1. In the Peano axioms, 1 is the successor of 0. In Principia Mathematica, it is defined as the set of all singletons (sets with one element), and in the Von Neumann cardinal assignment of natural numbers, it is defined as the set {0}.
In a multiplicative group or monoid, the identity element is sometimes denoted 1, but e (from the German Einheit, "unity") is also traditional. However, 1 is especially common for the multiplicative identity of a ring, i.e., when an addition and 0 are also present. When such a ring has characteristic n not equal to 0, the element called 1 has the property that n1 = 1n = 0 (where this 0 is the additive identity of the ring). Important examples are finite fields.
By definition, 1 is the magnitude, absolute value, or norm of a unit complex number, unit vector, and a unit matrix (more usually called an identity matrix). Note that the term unit matrix is sometimes used to mean something quite different.
By definition, 1 is the probability of an event that is absolutely or almost certain to occur.
In category theory, 1 is sometimes used to denote the terminal object of a category.
In number theory, 1 is the value of Legendres constant, which was introduced in 1808 by Adrien-Marie Legendre in expressing the asymptotic behavior of the prime-counting function. Legendres constant was originally conjectured to be approximately 1.08366, but was proven to equal exactly 1 in 1899.

Properties
Tallying is often referred to as "base 1", since only one mark – the tally itself – is needed. This is more formally referred to as a unary numeral system. Unlike base 2 or base 10, this is not a positional notation.
Since the base 1 exponential function (1x) always equals 1, its inverse does not exist (which would be called the logarithm base 1 if it did exist).
There are two ways to write the real number 1 as a recurring decimal: as 1.000..., and as 0.999.... 1 is the first figurate number of every kind, such as triangular number, pentagonal number and centered hexagonal number, to name just a few.
In many mathematical and engineering problems, numeric values are typically normalized to fall within the unit interval from 0 to 1, where 1 usually represents the maximum possible value in the range of parameters. Likewise, vectors are often normalized into unit vectors (i.e., vectors of magnitude one), because these often have more desirable properties. Functions, too, are often normalized by the condition that they have integral one, maximum value one, or square integral one, depending on the application.
Because of the multiplicative identity, if f(x) is a multiplicative function, then f(1) must be equal to 1.
It is also the first and second number in the Fibonacci sequence (0 being the zeroth) and is the first number in many other mathematical sequences.
The definition of a field requires that 1 must not be equal to 0. Thus, there are no fields of characteristic 1. Nevertheless, abstract algebra can consider the field with one element, which is not a singleton and is not a set at all.
1 is the most common leading digit in many sets of data, a consequence of Benfords law.
1 is the only known Tamagawa number for a simply connected algebraic group over a number field.
The generating function that has all coefficients 1 is given by

            1

              1
              −
              x

        =
        1
        +
        x
        +

          x

            2

        +

          x

            3

        +
        …

    {\displaystyle {\frac {1}{1-x}}=1+x+x^{2}+x^{3}+\ldots }

This power series converges and has finite value if and only if

          |

        x

          |

        <
        1

    {\displaystyle |x|<1}
  .

Primality
1 is by convention neither a prime number nor a composite number, but a unit (meaning of ring theory) like −1 and, in the Gaussian integers, i and −i.
The fundamental theorem of arithmetic guarantees unique factorization over the integers only up to units. For example, 4 = 22, but if units are included, is also equal to, say, (−1)6 × 123 × 22, among infinitely many similar "factorizations".
1 appears to meet the naïve definition of a prime number, being evenly divisible only by 1 and itself (also 1). As such, some mathematicians considered it a prime number as late as the middle of the 20th century, but mathematical consensus has generally and since then universally been to exclude it for a variety of reasons (such as complicating the fundamental theorem of arithmetic and other theorems related to prime numbers) </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Ear and explain in detail? [/INST] An ear is the organ that enables hearing and, in mammals, body balance using the vestibular system. In mammals, the ear is usually described as having three parts—the outer ear, the middle ear and the inner ear. The outer ear consists of the pinna and the ear canal. Since the outer ear is the only visible portion of the ear in most animals, the word "ear" often refers to the external part alone. The middle ear includes the tympanic cavity and the three ossicles. The inner ear sits in the bony labyrinth, and contains structures which are key to several senses: the semicircular canals, which enable balance and eye tracking when moving; the utricle and saccule, which enable balance when stationary; and the cochlea, which enables hearing. The ears of vertebrates are placed somewhat symmetrically on either side of the head, an arrangement that aids sound localisation.
The ear develops from the first pharyngeal pouch and six small swellings that develop in the early embryo called otic placodes, which are derived from ectoderm.
The ear may be affected by disease, including infection and traumatic damage. Diseases of the ear may lead to hearing loss, tinnitus and balance disorders such as vertigo, although many of these conditions may also be affected by damage to the brain or neural pathways leading from the ear.
The ear has been adorned by earrings and other jewelry in numerous cultures for thousands of years, and has been subjected to surgical and cosmetic alterations.

Structure
The human ear consists of three parts—the outer ear, middle ear and inner ear. The ear canal of the outer ear is separated from the air-filled tympanic cavity of the middle ear by the eardrum. The middle ear contains the three small bones—the ossicles—involved in the transmission of sound, and is connected to the throat at the nasopharynx, via the pharyngeal opening of the Eustachian tube. The inner ear contains the otolith organs—the utricle and saccule—and the semicircular canals belonging to the vestibular system, as well as the cochlea of the auditory system.

Outer ear
The outer ear is the external portion of the ear and includes the fleshy visible pinna (also called the auricle), the ear canal, and the outer layer of the eardrum (also called the tympanic membrane).The pinna consists of the curving outer rim called the helix, the inner curved rim called the antihelix, and opens into the ear canal. The tragus protrudes and partially obscures the ear canal, as does the facing antitragus. The hollow region in front of the ear canal is called the concha. The ear canal stretches for about 1 inch (2.5 cm). The first part of the canal is surrounded by cartilage, while the second part near the eardrum is surrounded by bone. This bony part is known as the auditory bulla and is formed by the tympanic part of the temporal bone. The skin surrounding the ear canal contains ceruminous and sebaceous glands that produce protective ear wax. The ear canal ends at the external surface of the eardrum.Two sets of muscles are associated with the outer ear: the intrinsic and extrinsic muscles. In some mammals, these muscles can adjust the direction of the pinna. In humans, these muscles have little or no effect. The ear muscles are supplied by the facial nerve, which also supplies sensation to the skin of the ear itself, as well as to the external ear cavity. The great auricular nerve, auricular nerve, auriculotemporal nerve, and lesser and greater occipital nerves of the cervical plexus all supply sensation to parts of the outer ear and the surrounding skin.The pinna consists of a single piece of elastic cartilage with a complicated relief on its inner surface and a fairly smooth configuration on its posterior surface. A tubercle, known as Darwins tubercle, is sometimes present, lying in the descending part of the helix and corresponding to the ear-tip of mammals. The earlobe consists of areola and adipose tissue. The symmetrical arrangement of the two ears allows for the localisation of sound. The brain accomplishes this by comparing arrival-times and intensities from each ear, in circuits located in the superior olivary complex and the trapezoid bodies which are connected via pathways to both ears.

Middle ear
The middle ear lies between the outer ear and the inner ear. It consists of an air-filled cavity called the tympanic cavity and includes the three ossicles and their attaching ligaments; the auditory tube; and the round and oval windows. The ossicles are three small bones that function together to receive, amplify, and transmit the sound from the eardrum to the inner ear. The ossicles are the malleus (hammer), incus (anvil), and the stapes (stirrup). The stapes is the smallest named bone in the body. The middle ear also connects to the upper throat at the nasopharynx via the pharyngeal opening of the Eustachian tube.The three ossicles transmit sound from the outer ear to the inner ear. The malleus receives vibrations from sound pressure on the eardrum, where it is connected at its longest part (the manubrium or handle) by a ligament. It transmits vibrations to the incus, which in turn transmits the vibrations to the small stapes bone. The wide base of the stapes rests on the oval window. As the stapes vibrates, vibrations are transmitted through the oval window, causing movement of fluid within the cochlea.The round window allows for the fluid within the inner ear to move. As the stapes pushes the secondary tympanic membrane, fluid in the inner ear moves and pushes the membrane of the round window out by a corresponding amount into the middle ear. The ossicles help amplify sound waves by nearly 15–20 times.

Inner ear
The inner ear sits within the temporal bone in a complex cavity called the bony labyrinth. A central area known as the vestibule contains two small fluid-filled recesses, the utricle and saccule. These connect to the semicircular canals and the cochlea. There are three semicircular canals angled at right angles to each other which are responsible for dynamic balance. The cochlea is a spiral shell-shaped organ responsible for the sense of hearing. These structures together create the membranous labyrinth.The bony labyrinth refers to the bony compartment which contains the membranous labyrinth, contained within the temporal bone. The inner ear structurally begins at the oval window, which receives vibrations from the incus of the middle ear. Vibrations are transmitted into the inner ear into a fluid called endolymph, which fills the membranous labyrinth. The endolymph is situated in two vestibules, the utricle and saccule, and eventually transmits to the cochlea, a spiral-shaped structure. The cochlea consists of three fluid-filled spaces: the vestibular duct, the cochlear duct, and the tympanic duct. Hair cells responsible for transduction—changing mechanical changes into electrical stimuli are present in the organ of Corti in the cochlea.

Blood supply
The blood supply of the ear differs according to each part of the ear.
The outer ear is supplied by a number of arteries. The posterior auricular artery provides the majority of the blood supply. The anterior auricular arteries provide some supply to the outer rim of the ear and scalp behind it. The posterior auricular artery is a direct branch of the external carotid artery, and the anterior auricular arteries are branches from the superficial temporal artery. The occipital artery also plays a role.The middle ear is supplied by the mastoid branch of either the occipital or posterior auricular arteries and the deep auricular artery, a branch of the maxillary artery. Other arteries which are present but play a smaller role include branches of the middle meningeal artery, ascending pharyngeal artery, internal carotid artery, and the artery of the pterygoid canal.The inner ear is supplied by the anterior tympanic branch of the maxillary artery; the stylomastoid branch of the posterior auricular artery; the petrosal branch of middle meningeal artery; and the labyrinthine artery, arising from either the anterior inferior cerebellar artery or the basilar artery.

Function
Hearing
Sound waves travel through the outer ear, are modulated by the middle ear, and are transmitted to the vestibulocochlear nerve in the inner ear. This nerve transmits information to the temporal lobe of the brain, where it is registered as sound.
Sound that travels through the outer ear impacts on the eardrum, and causes it to vibrate. The three ossicles bones transmit this sound to a second window (the oval window) which protects the fluid-filled inner ear. In detail, the pinna of the outer ear helps to focus a sound, which impacts on the eardrum. The malleus rests on the membrane, and receives the vibration. This vibration is transmitted along the incus and stapes to the oval window. Two small muscles, the tensor tympani and stapedius, also help modulate noise. The two muscles reflexively contract to dampen excessive vibrations. Vibration of the oval window causes vibration of the endolymph within the vestibule and the cochlea.The inner ear houses the apparatus necessary to change the vibrations transmitted from the outside world via the middle ear into signals passed along the vestibulocochlear nerve to the brain. The hollow channels of the inner ear are filled with liquid, and contain a sensory epithelium that is studded with hair cells. The microscopic "hairs" of these cells are structural protein filaments that project out into the fluid. The hair cells are mechanoreceptors that release a chemical neurotransmitter when stimulated. Sound waves moving through fluid flows against the receptor cells of the organ of Corti. The fluid pushes the filaments of individual cells; movement of the filaments causes receptor cells to become open to receive the potassium-rich endolymph. This causes the cell to depolarise, and creates an action potential that is transmitted along the spiral ganglion, which sends information through the auditory portion of the vestibulocochlear nerve to the temporal lobe of the brain.The human ear can generally hear sounds with frequencies between 20 Hz and 20 kHz (the audio range). Sounds outside this range are considered infrasound (below 20 Hz) or ultrasound (above 20 kHz) Although hearing requires an intact and functioning auditory portion of the central nervous system as well as a working ear, human deafness (extreme insensitivity to sound) most commonly occurs because of abnormalities of the inner ear, rather than in the nerves or tracts of the central auditory system.

Balance
Providing balance, when moving or stationary, is also a central function of the ear. The ear facilitates two types of balance: static balance, which allows a person to feel the effects of gravity, and dynamic balance, which allows a person to sense acceleration.
Static balance is provided by two ventricles, the utricle and the saccule. Cells lining the walls of these ventricles contain fine filaments, and the cells are covered with a fine gelatinous layer. Each cell has 50–70 small filaments, and one large filament, the kinocilium. Within the gelatinous layer lie otoliths, tiny formations of calcium carbonate. When a person moves, these otoliths shift position. This shift alters the positions of the filaments, which opens ion channels within the cell membranes, creating depolarisation and an action potential that is transmitted to the brain along the vestibulocochlear nerve.Dynamic balance is provided through the three semicircular canals. These three canals are orthogonal (at right angles) to each other. At the end of each canal is a slight enlargement, known as the ampulla, which contains numerous cells with filaments in a central area called the cupula. The fluid in these canals rotates according to the momentum of the head. When a person changes acceleration, the inertia of the fluid changes. This affects the pressure on the cupula, and results in the opening of ion channels. This causes depolarisation, which is passed as a signal to the brain along the vestibulocochlear nerve. Dynamic balance also helps maintain eye tracking when moving, via the vestibulo–ocular reflex.

Development
During embryogenesis the ear develops as three distinct structures: the inner ear, the middle ear and the outer ear. Each structure originates from a different germ layer: the ectoderm, endoderm and mesenchyme.

Inner ear
After implantation, around the second to third week the developing embryo consists of three layers: endoderm, mesoderm and ectoderm. The first part of the ear to develop is the inner ear, which begins to form from the ectoderm around the 22nd day of the embryos development. Specifically, the inner ear derives from two thickenings called otic placodes on either side of the head. Each otic placode recedes below the ectoderm, forms an otic pit and then an otic vesicle. This entire mass will eventually become surrounded by mesenchyme to form the bony labyrinth.Around the 33rd day of development, the vesicles begin to differentiate. Closer to the back of the embryo, they form what will become the utricle and semicircular canals. Closer to the front of the embryo, the vesicles differentiate into a rudimentary saccule, which will eventually become the saccule and cochlea. Part of the saccule will eventually give rise and connect to the cochlear duct. This duct appears approximately during the sixth week and connects to the saccule through the ductus reuniens.As the cochlear ducts mesenchyme begins to differentiate, three cavities are formed: the scala vestibuli, the scala tympani and the scala media. Both the scala vestibuli and the scala tympani contain an extracellular fluid called perilymph. The scala media contains endolymph. A set of membranes called the vestibular membrane and the basilar membrane develop to separate the cochlear duct from the vestibular duct and the tympanic duct, respectively.Parts of the otic vesicle in turn form the vestibulocochlear nerve. These form bipolar neurons which supply sensation to parts of the inner ear (namely the sensory parts of the semicircular canals, macular of the utricle and saccule, and organ of Corti). The nerve begins to form around the 28th day.
Molecular regulationMost of the genes responsible for the regulation of inner ear formation and its morphogenesis are members of the homeobox gene family such as Pax, Msx and Otx homeobox genes. The development of inner ear structures such as the cochlea is regulated by Dlx5/Dlx6, Otx1/Otx2 and Pax2, which in turn are controlled by the master gene Shh. Shh is secreted by the notochord.

Middle ear
The middle ear and its components develop from the first and second pharyngeal arches. The tympanic cavity and auditory tube develop from the first part of the pharyngeal pouch between the first two arches in an area which will also go on to develop the pharynx. This develops as a structure called the tubotympanic recess. The ossicles (malleus, incus and stapes) normally appear during the first half of fetal development. The first two (malleus and incus) derive from the first pharyngeal arch and the stapes derives from the second. All three ossicles develop from the neural crest. Eventually cells from the tissue surrounding the ossicles will experience apoptosis and a new layer of endodermal epithelial will constitute the formation of the tympanic cavity wall.

Outer ear
Unlike structures of the inner and middle ear, which develop from pharyngeal pouches, the ear canal originates from the dorsal portion of the first pharyngeal cleft. It is fully expanded by the end of the 18th week of development. The eardrum is made up of three layers (ectoderm, endoderm and connective tissue). The pinna originates as a fusion of six hillocks. The first three hillocks are derived from the lower part of the first pharyngeal arch and form the tragus, crus of the helix, and helix, respectively. The final three hillocks are derived from the upper part of the second pharyngeal arch and form the antihelix, antitragus, and earlobe. The outer ears develop in the lower neck. As the mandible forms they move towards their final position level with the eyes.

Clinical significance
Hearing loss
Hearing loss may be either partial or total. This may be a result of injury or damage, congenital disease, or physiological causes. When hearing loss is a result of injury or damage to the outer ear or middle ear, it is known as conductive hearing loss. When deafness is a result of injury or damage to the inner ear, vestibulochoclear nerve, or brain, it is known as sensorineural hearing loss.
Causes of conductive hearing loss include an ear canal blocked by ear wax, ossicles that are fixed together or absent, or holes in the eardrum. Conductive hearing loss may also result from middle ear inflammation causing fluid build-up in the normally air-filled space, such as by otitis media. Tympanoplasty is the general name of the operation to repair the middle ears eardrum and ossicles. Grafts from muscle fascia are ordinarily used to rebuild an intact eardrum. Sometimes artificial ear bones are placed to substitute for damaged ones, or a disrupted ossicular chain is rebuilt in order to conduct sound effectively.
Hearing aids or cochlear implants may be used if the hearing loss is severe or prolonged. Hearing aids work by amplifying the sound of the local environment and are best suited to conductive hearing loss. Cochlear implants transmit the sound that is heard as if it were a nervous signal, bypassing the cochlea. Active middle ear implants send sound vibrations to the ossicles in the middle ear, bypassing any non-functioning parts of the outer and middle ear.

Congenital abnormalities
Anomalies and malformations of the pinna are common. These anomalies include chromosome syndromes such as ring 18. Children may also present cases of abnormal ear canals and low ear implantation. In rare cases no pinna is formed (atresia), or is extremely small (microtia). Small pinnae can develop when the auricular hillocks do not develop properly. The ear canal can fail to develop if it does not channelise properly or if there is an obstruction. Reconstructive surgery to treat hearing loss is considered as an option for children older than five, with a cosmetic surgical procedure to reduce the size or change the shape of the ear is called an otoplasty. The initial medical intervention is aimed at assessing the babys hearing and the condition of the ear canal, as well as the middle and inner ear. Depending on the results of tests, reconstruction of the outer ear is done in stages, with planning for any possible repairs of the rest of the ear.Approximately one out of one thousand children suffer some type of congenital deafness related to the development of the inner ear. Inner ear congenital anomalies are related to sensorineural hearing loss and are generally diagnosed with a computed tomography (CT) scan or a magnetic resonance imaging (MRI) scan. Hearing loss problems also derive from inner ear anomalies because its development is separate from that of the middle and external ear. Middle ear anomalies can occur because of errors during head and neck development. The first pharyngeal pouch syndrome associates middle ear anomalies to the malleus and incus structures as well as to the non-differentiation of the annular stapedial ligament. Temporal bone and ear canal anomalies are also related to this structure of the ear and are known to be associated with sensorineural hearing loss and conductive hearing loss.

Vertigo
Vertigo refers to the inappropriate perception of motion. This is due to dysfunction of the vestibular system. One common type of vertigo is benign paroxysmal positional vertigo, when an otolith is displaced from the ventricles to the semicircular canal. The displaced otolith rests on the cupola, causing a sensation of movement when there is none. Ménières disease, labyrinthitis, strokes, and other infective and congenital diseases may also result in the perception of vertigo.

Injury
Outer earInjuries to the external ear occur fairly frequently, and can leave minor to major deformity. Injuries include: laceration, avulsion injuries, burn and repeated twisting or pulling of an ear, for discipline or torture. Chronic damage to the ears can cause cauliflower ear, a common condition in boxers and wrestlers in which the cartilage around the ears becomes lumpy and distorted owing to persistence of a haematoma around the perichondrium, which can impair blood supply and healing. Owing to its exposed position, the external ear is susceptible to frostbite as well as skin cancers, including squamous-cell carcinoma and basal-cell carcinomas.
Middle earThe ear drum may become perforated in the event of a large sound or explosion, when diving or flying (called barotrauma), or by objects inserted into the ear. Another common cause of injury is due to an infection such as otitis media. These may cause a discharge from the ear called otorrhea, and are often investigated by otoscopy and audiometry. Treatment may include watchful waiting, antibiotics and possibly surgery, if the injury is prolonged or the position of the ossicles is affected. Skull fractures that go through the part of the skull containing the ear structures (the temporal bone) can also cause damage to the middle ear. A cholesteatoma is a cyst of squamous skin cells that may develop from birth or secondary to other causes such as chronic ear infections. It may impair hearing or cause dizziness or vertigo, and is usually investigated by otoscopy and may require a CT scan. The treatment for cholesteatoma is surgery.
Inner earThere are two principal damage mechanisms to the inner ear in industrialised society, and both injure hair cells. The first is exposure to elevated sound levels (noise trauma), and the second is exposure to drugs and other substances (ototoxicity). A large number of people are exposed to sound levels on a daily basis that are likely to lead to significant hearing loss. The National Institute for Occupational Safety and Health has recently published research on the estimated numbers of persons with hearing difficulty (11%) and the percentage of those that can be attributed to occupational noise exposure (24%). Furthermore, according to the National Health and Nutrition Examination Survey (NHANES), approximately twenty-two million (17%) US workers reported exposure to hazardous workplace noise. Workers exposed to hazardous noise further exacerbate the potential for developing noise-induced hearing loss when they do not wear hearing protection.

Tinnitus
Tinnitus is the hearing of sound when no external sound is present. While often described as a ringing, it may also sound like a clicking, hiss or roaring. Rarely, unclear voices or music are heard. The sound may be soft or loud, low pitched or high pitched and appear to be coming from one ear or both. Most of the time, it comes on gradually. In some people, the sound causes depression, anxiety, or concentration difficulties.Tinnitus is not a disease but a symptom that can result from a number of underlying causes. One of the most common causes is noise-induced hearing loss. Other causes include: ear infections, disease of the heart or blood vessels, Ménières disease, brain tumors, emotional stress, exposure to certain medications, a previous head injury, and earwax. It is more common in those with depression and anxiety.

Society and culture
The ears have been ornamented with jewelry for thousands of years, traditionally by piercing of the earlobe. In ancient and modern cultures, ornaments have been placed to stretch and enlarge the earlobes, allowing for larger plugs to be slid into a large fleshy gap in the lobe. Tearing of the earlobe from the weight of heavy earrings, or from traumatic pull of an earring (for example, by snagging on a sweater), is fairly common.Injury to the ears has been present since Roman times as a method of reprimand or punishment – "In Roman times, when a dispute arose that could not be settled amicably, the injured party cited the name of the person thought to be responsible before the Praetor; if the offender did not appear within the specified time limit, the complainant summoned witnesses to make statements.  If they refused, as often happened, the injured party was allowed to drag them by the ear and to pinch them hard if they resisted.  Hence the French expression "se faire tirer l’oreille", of which the literal meaning is "to have ones ear pulled" and the figurative meaning "to take a lot of persuading". We use the expression "to tweak (or pull) someones ears"  to mean "inflict a punishment"."The pinnae have an effect on facial appearance. In Western societies, protruding ears (present in about 5% of ethnic Europeans) have been considered unattractive, particularly if asymmetric. The first surgery to reduce the projection of prominent ears was published in the medical literature by Ernst Dieffenbach in 1845, and the first case report in 1881.

Pointy ears are a characteristic of some creatures in folklore such as the French croquemitaine, Brazilian curupira or Japanese earth spider. It has been a feature of characters on art as old as that of Ancient Greece and medieval Europe. Pointy ears are a common characteristic of many creatures in the fantasy genre, including elves, faeries, pixies, hobbits, or orcs. They are a characteristic of creatures in the horror genre, such as vampires. Pointy ears are also found in the science fiction genre; for example among the Vulcan and Romulan races of the Star Trek universe and the Nightcrawler character from the X-Men universe.Georg von Békésy was a Hungarian biophysicist born in Budapest, Hungary. In 1961, he was awarded the Nobel Prize in Physiology or Medicine for his research on the function of the cochlea in the mammalian hearing organ.The Vacanti mouse was a laboratory mouse that had what looked like a human ear grown on its back. The "ear" was actually an ear-shaped cartilage structure grown by seeding cow cartilage cells into a biodegradable ear-shaped mold and then implanted under the skin of the mouse; then the cartilage naturally grew by itself. It was developed as an alternative to ear repair or grafting procedures and the results met with much publicity and controversy in 1997.

Other animals
The pinna helps direct sound through the ear canal to the eardrum. The complex geometry of ridges on the inner surface of some mammalian ears helps to sharply focus sounds produced by prey, using echolocation signals. These ridges can be regarded as the acoustic equivalent of a fresnel lens, and may be seen in a wide range of animals, including the bat, aye-aye, lesser galago, bat-eared fox, mouse lemur and others.Some large primates such as gorillas and orang-utans (and also humans) have undeveloped ear muscles that are non-functional vestigial structures, yet are still large enough to be easily identified. An ear muscle that cannot move the ear, for whatever reason, has lost that biological function. This serves as evidence of homology between related species. In humans, there is variability in these muscles, such that some people are able to move their ears in various directions, and it has been said that it may be possible for others to gain such movement by repeated trials. In such primates, the inability to move the ear is compensated for mainly by the ability to easily turn the head on a horizontal plane, an ability which is not common to most monkeys—a function once provided by one structure is now replaced by another.In some animals with mobile pinnae (like the horse), each pinna can be aimed independently to better receive the sound. For these animals, the pinnae help localise the direction of the sound source.

The ear, with its blood vessels close to the surface, is an essential thermoregulator in some land mammals, including the elephant, the fox, and the rabbit. There are five types of ear carriage in domestic rabbits, some of which have been bred for exaggerated ear length—a potential health risk that is controlled in some countries. Abnormalities in the skull of a half-lop rabbit were studied by Charles Darwin in 1868. In marine mammals, earless seals are one of three groups of Pinnipedia.

Invertebrates
Only vertebrate animals have ears, though many invertebrates detect sound using other kinds of sense organs </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Left bundle branch block and explain in detail? [/INST] Left bundle branch block (LBBB) is a conduction abnormality in the heart that can be seen on an electrocardiogram (ECG). In this condition, activation of the left ventricle of the heart is delayed, which causes the left ventricle to contract later than the right ventricle.

Causes
Among the causes of LBBB are:
Aortic stenosis
Dilated cardiomyopathy
Acute myocardial infarction
Extensive coronary artery disease
Primary disease of the cardiac electrical conduction system
Long standing hypertension leading to aortic root dilatation and subsequent aortic regurgitation
Lyme disease

Mechanisms
Slow or absent conduction through the left bundle branch means that it takes longer than normal for the left ventricle to fully depolarise.  This can be due to a damaged bundle branch that is completely unable to conduct, but may represent intact conduction that is slower than normal.  LBBB may be fixed, present at all times, but may be intermittent for example occurring only during rapid heart rates </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Erythema toxicum neonatorum and explain in detail? [/INST] Erythema toxicum neonatorum is a common, non-threatening rash in newborns. It appears in 4-70% of newborns within the first week of life, and it typically improves within 1–2 weeks. It only occurs during the newborn period, but may appear slightly later in premature babies. The rash has a variable appearance. It typically includes blotchy red spots, often with overlying firm, yellow-white bumps or pus-filled boils. There may be only a few or many lesions. The lesions can appear almost anywhere on the body, and individual lesions may appear and disappear within hours. There are no other symptoms associated with erythema toxicum neonatorum, and the rash does not have any long-term effects on the skin. Erythema toxicum neonatorum is not harmful and does not require any treatment.

Epidemiology
The exact prevalence of erythema toxicum neonatorum is unknown, and studies estimate prevalence as low as 3.7 percent to as high as 72 percent. It is one of the most commonly diagnosed rashes in healthy babies. It is more common among infants born at higher gestational age and is rare among premature infants. Erythema toxicum neonatorum is more likely to develop in infants delivered vaginally. Higher birth weight is an additional risk factor. There may be a slightly increased risk in males, but this association is unclear. There are no known associations with race or ethnicity.

Presentation
Erythema toxicum neonatorum usually appears during the first week of life, most often on day two. It may develop several days or weeks later in premature babies.The rash has a variable appearance, ranging from a few blotchy red spots to many yellow-white bumps and boils. The classic presentation is 1–3 mm, firm, yellow-white bumps with a surrounding red halo. The rash is often described as "flea-bitten." There may be only a few or many lesions, and they may be clustered or widespread. The rash often appears on the cheeks first and may later spread throughout the face, trunk, arms, and legs. Lesions most often appear on the thighs, buttocks, and trunk. The palms and soles are not affected, likely because the skin in these areas does not have hair follicles.Individual lesions may grow and shrink over hours or days. They usually fade within a week or two. The rash may recur within the next few weeks, but this is rare.

Cause
Erythema toxicum neonatorum is related to activation of the immune system, but its exact cause is unknown. Many inflammatory factors have been detected in erythema toxicum neonatorum lesions, including IL-1alpha, IL-1beta, IL-8, and eotaxin. These molecules cause redness and swelling in the skin and attract immune cells.Eosinophils and other immune cells are found in the upper layer of the skin in erythema toxicum neonatorum lesions. Immune cells tend to cluster around hair follicles in particular. The leading hypothesis about the cause of erythema toxicum neonatorum is that bacteria activate the immune system when they enter hair follicles for the first time. This is part of a normal process in which bacteria from the environment start to grow on a babys skin. It is unknown whether the immune response that causes erythema toxicum neonatorum is helpful to the baby. Recent research indicates an association with Demodex mites infestation (demodicosis).

Diagnosis
Health professionals can diagnose erythema toxicum neonatorum with a skin exam. Most cases of erythema toxicum neonatorum can be diagnosed without further testing. If more testing is needed to make a diagnosis, the contents of a lesion can be examined under a microscope. A health professional may make a small cut into a pus-filled lesion and collect a swab of pus for testing. Lesions caused by erythema toxicum neonatorum contain eosinophils and other immune cells. These cells can be seen under a microscope when a special stain is applied to the sample.Since the appearance of erythema toxicum neonatorum varies, it may be confused with other newborn rashes. Some newborn infections cause bumps or boils, which may look like erythema toxicum neonatorum. Bacterial infections, including Staphylococcus and Streptococcus infections, almost always cause additional symptoms. These symptoms may be severe, and they are usually not limited to rash. Bacterial rashes can be diagnosed by testing pus from a lesion along with a blood sample. Bacteria can be seen under a microscope with a special stain or may be found on a culture. Fungal infection with Candida may also cause a similar rash in newborns, but it usually causes additional symptoms like thrush. Similarly, fungus can be seen under a microscope or found on a culture. Some viral infections may cause a rash with boils on a reddish base </s>