<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 Argininosuccinic aciduria and explain in detail? [/INST] Argininosuccinic aciduria is an inherited disorder that causes the accumulation of argininosuccinic acid (also known as "ASA") in the blood and urine. Some patients may also have an elevation of ammonia, a toxic chemical, which can affect the nervous system. Argininosuccinic aciduria may become evident in the first few days of life because of high blood ammonia, or later in life presenting with "sparse" or "brittle" hair, developmental delay, and tremors.
An infant with argininosuccinic aciduria may seem lethargic or be unwilling to eat, have poorly controlled breathing rate or body temperature, experience seizures or unusual body movements, or go into a coma. Complications from argininosuccinic aciduria may include developmental delay and mental retardation. Progressive liver damage, skin lesions, and brittle hair may also be seen. Immediate treatment and lifelong management (following a strict diet and using appropriate supplements) may prevent many of these complications.
Occasionally, an individual may inherit a mild form of the disorder in which ammonia accumulates in the bloodstream only during periods of illness or other stress.

Genetics
Mutations in the ASL gene cause argininosuccinic aciduria. Argininosuccinic aciduria belongs to a class of genetic diseases called urea cycle disorders. The urea cycle is a sequence of reactions in the cells of the liver. It processes excess nitrogen, generated when protein is used by the body, to make a compound called urea that is excreted by the kidneys.In argininosuccinic aciduria, the enzyme argininosuccinate lyase, involved in the conversion of arginino succinate to arginine within the urea cycle, is damaged or missing. The urea cycle cannot proceed normally, and nitrogen accumulates in the bloodstream in the form of ammonia. Ammonia is especially damaging to the nervous system, so argininosuccinic aciduria causes neurological problems as well as eventual damage to the liver.This condition is inherited in an autosomal recessive pattern, which means two copies of the gene in each cell are altered. Most often, the parents of an individual with an autosomal recessive disorder are carriers of one copy of the altered gene but do not show signs and symptoms of the disorder.

Diagnosis
Diagnosis is based mainly on clinical findings and laboratory test results. Plasma concentrations of ammonia (>150 μmol/L) and citrulline (200-300 μmol/L) are elevated. Elevated levels of argininosuccinic acid (5-110 μmol/L) in the plasma or urine are diagnostic. Molecular genetic testing confirms diagnosis. Newborn screening for ASA is available in the U.S. and parts of Australia, and is considered in several European countries

Treatment
During an acute hyperammonemic episode, oral proteins must be avoided and intravenous (I.V.) lipids, glucose and insulin (if needed) should be given to promote anabolism. I.V. nitrogen scavenging therapy (with sodium benzoate and/or sodium phenylacetate) should normalize ammonia levels, but if unsuccessful, hemodialysis is recommended. Long-term management involves dietary protein restriction as well as arginine supplementation. In those with frequent episodes of metabolic decompensation or with hyperammonemia even when following a protein-restricted diet, daily oral nitrogen scavenging therapy may be successful. Orthotopic liver transplantation offers long-term relief of hyperammonemia but does not seem to sufficiently correct neurological complications. Arterial hypertension can be treated by restoring nitric oxide deficiency

Prognosis
Due to the rarity of the disease, it is hard to estimate mortality rates or life expectancy. One 2003 study which followed 88 cases receiving two different kinds of treatment found that very few persons lived beyond age 20 and none beyond age 30.

Incidence
Argininosuccinic aciduria occurs in approximately 1 in 70,000 live births. Many patients can now be detected on the newborn screen if their blood citrulline is elevated.

References
Literature
Kleijer WJ, Garritsen VH, Linnebank M, Mooyer P, Huijmans JG, Mustonen A, Simola KO, Arslan-Kirchner M, Battini R, Briones P, Cardo E, Mandel H, Tschiedel E, Wanders RJ, Koch HG (2002). "Clinical, enzymatic, and molecular genetic characterization of a biochemical variant type of argininosuccinic aciduria: prenatal and postnatal diagnosis in five unrelated families". J Inherit Metab Dis. 25 (5): 399–410. doi:10.1023/A:1020108002877. PMID 12408190. S2CID 11129281.
Lee B, Goss J (2001). "Long-term correction of urea cycle disorders". J Pediatr. 138 (1 Suppl): S62–71. doi:10.1067/mpd.2001.111838. PMID 11148551.
Reid Sutton V, Pan Y, Davis EC, Craigen WJ (2003). "A mouse model of argininosuccinic aciduria: biochemical characterization". Mol Genet Metab. 78 (1): 11–6. doi:10.1016/S1096-7192(02)00206-8. PMID 12559843.
Scaglia F, Brunetti-Pierri N, Kleppe S, Marini J, Carter S, Garlick P, Jahoor F, OBrien W, Lee B (2004). "Clinical consequences of urea cycle enzyme deficiencies and potential links to arginine and nitric oxide metabolism". J Nutr. 134 (10 Suppl): 2775S–2782S, discussion 2796S–2797S. doi:10.1093/jn/134.10.2775S. PMID 15465784. Full text
Stadler S, Gempel K, Bieger I, Pontz BF, Gerbitz KD, Bauer MF, Hofmann S (2001). "Detection of neonatal argininosuccinate lyase deficiency by serum tandem mass spectrometry" </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 Pulmonary atresia with ventricular septal defect and explain in detail? [/INST] Pulmonary atresia with ventricular septal defect is a rare birth defect characterized by pulmonary valve atresia occurring alongside a defect on the right ventricular outflow tract.It is a type of congenital heart disease/defect, and one of the two recognized subtypes of pulmonary atresia, the other being pulmonary atresia with intact ventricular septum.

Signs and symptoms
The condition consists of atresia affecting the pulmonary valve and a hypoplastic right ventricular outflow tract. The ventricular septal defect doesnt impede the in and outflowing of blood in the ventricular septum, which helps it form during fetal life.The spectrum of symptoms exhibited by children with this condition depends on the severity of the condition, while some barely show symptoms, others might develop complications such as congestive heart failure.In symptomatic children, symptoms become apparent soon after birth, these usually consist of the following:
Cyanosis
Breathing difficulties
Feeding difficulties
Exhaustion while being fed
Heart murmur
Excessive daytime sleepiness
Sticky skinOther features can occur alongside this birth defect, including other congenital anomalies such as polydactyly, microcephaly, congenital hearing loss (sensorineural type), renal agenesis, dextrocardia, etc.The condition has been called a severe form of Tetralogy of Fallot.If deformed blood vessels coming from the thoracic aorta appear alongside this condition, the phenotype is renamed to pulmonary atresia with ventricular septal defect and major aortopulmonary collaterals.

Complications
Children with this condition are at a higher risk of developing the following complications:
Failure to thrive
Recurrent chest infections
Endocarditis
Epilepsy
Stroke
Arrhythmia
Heart failure
Premature deathChildren whose PAVSD is caused by DiGeorge syndrome (also known as 22q11.2 deletion syndrome) are more likely to suffer from the post-surgical complications (especially respiratory ones) associated with surgeries that treat this defect.Women with PAVSD are at a slightly higher risk of being infertile and having miscarriages or children with a congenital heart defect.Airway hyperresponsiveness is a commonly seen co-morbidity among those afflicted with PAVSD.

Pathogenesis
Pulmonary atresia in PAVSD takes place during the first 8 weeks of fetal life, when the pulmonary valve that is supposed to form, fails to form, this doesnt allow blood to flow through the pulmonary artery from the right ventricle. The ventricular septal defect associated with PAVSD lets the right ventricule form.In some cases of PAVSD, major aortopulmonary collateral arteries develop; in a normal fetus, these arteries usually develop but then start deteriorating after pulmonary arteries grow, in fetuses with PAVSD, the pulmonary arteries dont develop, and this gives a chance to the major aortopulmonary collateral arteries to develop fully.

Pathophysiology
The mildest variant of pulmonary atresia with ventricular septal defect involves pulmonary atresia with normally developed main pulmonary artery and branch pulmonary arteries, the blood that flows to the lungs from the right side of the heart goes to the left side of the heart through the ventricular septum which then flows through the patent ductus arteriosus. The most severe variant involves the presence of severely hypoplastic main pulmonary arteries and branch pulmonary arteries, alongside agenesis of the patent ductus arteriosus. Blood flow to the lungs comes from various dysplastic (malformed) blood vessels from the thoracic aorta called major aortapulmonary collateral arteries, these blood vessels narrow down as time goes on.

Causes
Although this birth defect is congenital, the exact cause is unknown, and it may vary between children with the condition, the following factors have been known to influence the risk of a baby being born with the condition:

Genetics
The molecular genetics of this condition isnt known in most people with PA(VSD), however, there have been candidate genes found to be possibly implicated in the pathogenesis of this condition:
DNAH10
DST
FAT1
HMCN1
HNRNPC
TEP1
TYK2
NDRG4
TBX5
NKX2.5
GATA4There have also been copy number variants described in the medical literature as associated with PA(VSD):
Deletion in chromosome 16p11.2
Deletion in chromosome 5q35.3
Deletion in chromosome 5p13.1
Deletion in chromosome 22q11.2
Deletion in chromosome 15q11.2
Deletion in chromosome 8p23.2
Deletion in chromosome 17p13.2
Duplication in chromosome 5q14.1
Duplication in chromosome 10p13A 1998 study done in Britain revealed that children with a mother who had a congenital heart defect (including PAVSD) had a higher risk of being born with a congenital heart defect themselves than those whose father had a congenital heart defect.

Syndromes
Some cases of PA(VSD) have been associated with genetic syndromes such as VACTERL association, Alagille syndrome, CHARGE syndrome, trisomy 13, 18, and 21.

Environmental
While congenital heart defects cant be acquired, they can also be caused by environmental factors the mother exposed herself to before and/or during pregnancy, these include:
Smoking
Certain medications (e.g. thalidomide, retinoids, or vitamin A coegers)
Alcohol consumption
Vehicle exhaust components
By-products of disinfectants
Incinerators (proximity)
Agricultural pesticides
Solvents
Landfill sites
Heavy metalsMaternal exposure to carbon monoxide from smoke (e.g. from cigarettes) has been known for having the ability of quickly crossing the placenta into the fetus, which then attaches itself to fetal haemoglobin, leaving a shortage of nutrients and oxygen as a result </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 Extrapyramidal symptoms and explain in detail? [/INST] Extrapyramidal symptoms (EPS) are symptoms that are archetypically associated with the extrapyramidal system of the brains cerebral cortex. When such symptoms are caused by medications or other drugs, they are also known as extrapyramidal side effects (EPSE). The symptoms can be acute (short-term) or chronic (long-term). They include movement dysfunction such as dystonia (continuous spasms and muscle contractions), akathisia (may manifest as motor restlessness), parkinsonism characteristic symptoms such as rigidity, bradykinesia (slowness of movement), tremor, and tardive dyskinesia (irregular, jerky movements). Extrapyramidal symptoms are a reason why subjects drop out of clinical trials of antipsychotics; of the 213 (14.6%) subjects that dropped out of one of the largest clinical trials of antipsychotics (the CATIE trial (Clinical Antipsychotic Trials for Intervention Effectiveness), which included 1460 randomized subjects), 58 (27.2%) of those discontinuations were due to EPS.

Causes
Medications
Extrapyramidal symptoms are most commonly caused by typical antipsychotic drugs that antagonize dopamine D2 receptors. The most common typical antipsychotics associated with EPS are haloperidol and fluphenazine. Atypical antipsychotics have lower D2 receptor affinity or higher serotonin 5-HT2A receptor affinity which lead to lower rates of EPS.Other anti-dopaminergic drugs, like the antiemetic metoclopramide, can also result in extrapyramidal side effects. Short and long-term use of antidepressants such as selective serotonin reuptake inhibitors (SSRI), serotonin-norepinephrine reuptake inhibitors (SNRI), and norepinephrine-dopamine reuptake inhibitors (NDRI) have also resulted in EPS. Specifically, duloxetine, sertraline, escitalopram, fluoxetine, and bupropion have been linked to the induction of EPS.

Non-medication-related
Other causes of extrapyramidal symptoms can include brain damage and meningitis. However, the term "extrapyramidal symptoms" generally refers to medication-induced causes in the field of psychiatry.

Diagnosis
Since it is difficult to measure extrapyramidal symptoms, rating scales are commonly used to assess the severity of movement disorders. The Simpson-Angus Scale (SAS), Barnes Akathisia Rating Scale (BARS), Abnormal Involuntary Movement Scale (AIMS), and Extrapyramidal Symptom Rating Scale (ESRS) are rating scales frequently used for such assessment and are not weighted for diagnostic purposes; these scales can help clinicians weigh the benefit/expected benefit of a medication against the degree of distress which the side effects are causing the patient, aiding in the decision to maintain, reduce, or discontinue the causative medication(s).

Classification
Acute dystonic reactions: painful, muscular spasms of neck, jaw, back, extremities, eyes, throat, and tongue; highest risk in young men.Oculogyric crisis is a kind of acute dystonic reaction that involves the prolonged involuntary upward deviation of the eyes.
Akathisia: A feeling of internal motor restlessness that can present as tension, nervousness, or anxiety. Clinical manifestations include pacing and an inability to sit still.
Pseudoparkinsonism: drug-induced parkinsonism (rigidity, bradykinesia, tremor, masked facies, shuffling gait, stooped posture, sialorrhoea, and seborrhoea; greater risk in the elderly). Although Parkinsons disease is primarily a disease of the nigrostriatal pathway and not the extrapyramidal system, loss of dopaminergic neurons in the substantia nigra leads to dysregulation of the extrapyramidal system. Since this system regulates posture and skeletal muscle tone, a result is the characteristic bradykinesia of Parkinsons.
Tardive dyskinesia: involuntary muscle movements in the lower face and distal extremities; this can be a chronic condition associated with long-term use of antipsychotics.

Treatment
Medications are used to reverse the symptoms of extrapyramidal side effects caused by antipsychotics or other drugs, either by directly or indirectly inhibiting dopaminergic neurotransmission. The treatment varies by the type of the EPS, but may involve anticholinergic agents such as procyclidine, benztropine, diphenhydramine, and trihexyphenidyl, and (rarely) dopamine agonists like pramipexole.If the EPS are induced by an antipsychotic, EPS may be reduced by decreasing the dose of the antipsychotic or by switching from a typical antipsychotic to an (or to a different) atypical antipsychotic, such as aripiprazole, ziprasidone, quetiapine, olanzapine, risperidone, or clozapine. These medications possess an additional mode of action that is believed to mitigate their effect on the nigrostriatal pathway, which means they are associated with fewer extrapyramidal side-effects than "conventional" antipsychotics (chlorpromazine, haloperidol, etc.)

Dystonia
Anticholinergic medications are used to reverse acute dystonia </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 Exhibitionism and explain in detail? [/INST] Exhibitionism is the act of exposing in a public or semi-public context ones intimate parts – for example, the breasts, genitals or buttocks. The practice may arise from a desire or compulsion to expose themselves in such a manner to groups of friends or acquaintances, or to strangers for their amusement or sexual satisfaction, or to shock the bystander. Exposing oneself only to an intimate partner is normally not regarded as exhibitionism. In law, the act of exhibitionism may be called indecent exposure, "exposing ones person", or other expressions.

History
Public exhibitionism by women has been recorded since classical times, often in the context of women shaming groups of men into committing, or inciting them to commit, some public action. The ancient Greek historian Herodotus gives an account of exhibitionistic behaviors from the fifth century BC in The Histories. Herodotus writes that: When people travel to Bubastis for the festival, this is what they do. Every baris carrying them there overflows with people, a huge crowd of them, men and women together. Some of the women have clappers, while some of the men have pipes which they play throughout the voyage. The rest of the men and women sing and clap their hands. When in the course of their journey they reach a community — not the city of their destination, but somewhere else — they steer the bareis close to the bank. Some of the women carry on doing what I have already described them as doing, but others shout out scornful remarks to the women in the town, or dance, or stand and pull up their clothes to expose themselves. Every riverside community receives this treatment.
A case of what appears to be exhibitionism in a clinical sense was recorded in a report by the Commission against Blasphemy in Venice in 1550.In the UK the 4th draft of the revised Vagrancy Act of 1824 included an additional clause or openly and indecently exposing their persons which gave rise to difficulties because of its ill-defined scope. During the course of a subsequent debate on the topic in Parliament, the then Home Secretary, Mr Peel, observed that there was not a more flagrant offence than that of indecently exposing the person which had been carried to an immense extent in the parks...wanton exposure was a very different thing from accidental exposure.The development of new technologies such as smartphones and tablets has permitted some exhibitionists to reorient their methods such as with nude selfies.

Psychological aspects
The term exhibitionist was first used in 1877 by French physician and psychiatrist Charles Lasègue. Various earlier medical-forensic texts discuss genital self-exhibition, however.When exhibitionistic sexual interest is acted on with a non-consenting person or interferes with a persons quality of life or normal functioning, it can be diagnosed as exhibitionistic disorder in the Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5). The DSM states that the highest possible prevalence for exhibitionistic disorder in men is 2% to 4%. It is thought to be much less common in women. In a Swedish survey, 2.1% of women and 4.1% of men admitted to becoming sexually aroused from the exposure of their genitals to a stranger.A research team asked a sample of 185 exhibitionists, "How would you have preferred a person to react if you were to expose your privates to him or her?" The most common response was "Would want to have sexual intercourse" (35.1%), followed by "No reaction necessary at all" (19.5%), "To show their privates also" (15.1%), "Admiration" (14.1%), and "Any reaction" (11.9%) </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 Trichostasis spinulosa 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 Sibling rivalry and explain in detail? [/INST] Sibling rivalry is a type of competition or animosity among siblings, whether blood-related or not.
Siblings generally spend more time together during childhood than they do with parents. The sibling bond is often complicated and is influenced by factors such as parental treatment, birth order, personality, and people and experiences outside the family. Sibling rivalry is particularly intense when children are very close in age and of the same gender and/or where one or both children are intellectually gifted.

Throughout the lifespan
According to observational studies by Judith Dunn, children are sensitive from the age of one year to differences in parental treatment. From 18 months, siblings can understand family rules and know how to comfort and be kind to each other. By the age of 3, children have a sophisticated grasp of social rules, can evaluate themselves in relation to their siblings, and know how to adapt to circumstances within the family.Sibling rivalry often continues throughout childhood and can be very frustrating and stressful to parents. Adolescents fight for the same reasons younger children fight, but they are better equipped to physically, intellectually, and emotionally hurt and be intellectually and emotionally hurt by each other. Physical and emotional changes cause pressures in the teenage years, as do changing relationships with parents and friends. Fighting with siblings as a way to get parental attention may increase in adolescence. One study found that the age group 10 to 15 reported the highest level of competition between siblings.Sibling rivalry can continue into adulthood, and sibling relationships can change dramatically over the years. Events, such as a parent’s illness, may bring siblings closer together, whereas marriage may drive them apart, particularly if the in-law relationship is strained. Approximately one-third of adults describe their relationship with siblings as rivalrous or distant. However, rivalry often lessens over time. At least 80 percent of siblings over the age of 60 enjoy close ties.

Causes
According to Kyla Boyse from the University of Michigan, each child in a family competes to define who it is as an individual and wants to show that it is separate from its siblings.  Children may feel they are getting unequal amounts of their parents’ attention, discipline, and responsiveness. Children fight most in families where there is neither any understanding that fighting is not an acceptable way to resolve conflicts nor any alternative way of handling such conflicts; in families in which physical fighting is forbidden but no method of non-physical conflict resolution (e.g., verbal argument) is permitted, the conversion and accumulation of everyday disputes into long-simmering hostilities can have an effect nearly as corrosive.  Stress in the parents’ and children’s lives can create more conflict and increase sibling rivalry. Some research indicates that changes in the weather can increase the likelihood of children exhibiting deviant behavior.

Other psychological approaches
Alfred Adler saw siblings as "striving for significance" within the family and felt that birth order was an important aspect of personality development. In fact, psychologists and researchers today endorse the influence of birth order, as well as age and gender constellations, on sibling relationships. However, parents are seen as capable of having an important influence on whether they are competitive or not.David Levy introduced the term "sibling rivalry" in 1941, claiming that for an older sibling "the aggressive response to the new baby is so typical that it is safe to say it is a common feature of family life." Researchers today generally endorse this view, noting that parents can ameliorate this response by being vigilant to favoritism and by taking appropriate preventative steps. In fact, the ideal time to lay the groundwork for a lifetime of supportive relationships between siblings is during the months prior to the new babys arrival.

Prevention
Parents can reduce the opportunity for rivalry by refusing to compare or typecast their children, planning fun family activities together, and making sure each child has enough time and space of their own. They can also give each child individual attention, encourage teamwork, refuse to hold up one child (such as the oldest) as a role model for the others (such as the younger children), and avoid favoritism. Teaching the children positive ways to ask for attention from parents when they need it can also make it less likely that they will resort to aggressive attention-getting strategies. Eileen Kennedy-Moore notes that this remedy also requires that parents "catch children being good" by responding to childrens kind, helpful, and creative bids for attention. Additionally, by being proactive about teaching children emotional intelligence, problem solving skills, negotiation skills, and encouraging them to look for win-win solutions, parents can help children resolve conflicts that arise as a normal part of growing up together in the same household. A concerted effort by parents to reduce competitiveness while nurturing bonding can further help alleviate sibling rivalry.
However, according to Sylvia Rimm, although sibling rivalry can be reduced, it is unlikely to be entirely eliminated. In moderate doses, rivalry may be a healthy indication that each child is assertive enough to express his or her differences with other siblings.Vernon Weihe suggests that four criteria should be used to determine if questioned and/or questionable behavior is rivalry or sibling abuse. First, given that children use different conflict-resolution tactics during various developmental stages, one must rule out the possibility that the questioned behavior is in fact age-appropriate for the child exhibiting it. Second, one must determine whether the behavior is an isolated incident or instead part of an enduring pattern: abuse is, by definition, a long-term pattern rather than occasional disagreements. Third, one must determine if there is an "aspect of victimization" to the behavior: rivalry tends to be incident-specific, reciprocal, and obvious to others, while abuse is characterized by secrecy and an imbalance of power. Fourth, one must determine the goal of the questioned and/or questionable behavior: while rivalry is motivated entirely or primarily by aspects of a childs self-interest in which the interests of others, including the childs rival, do not play a role, in scenarios featuring abuse, the perpetrators ultimate interests tend to include domination, humiliation, or at least embarrassment of the victim.

Animals
Sibling rivalry is common among various animal species, in the form of competition for food and parental attention. An extreme type of sibling rivalry occurs when young animals kill their siblings. For example, a black eagle mother lays two eggs, and the first-hatched chick pecks the younger one to death within the first few days. In the blue-footed booby, there is always the emergence of a brood hierarchy. The dominant chick will attack the subordinate one in times of food scarcity, often pecking it repeatedly or driving it from the nest. Among spotted hyenas, sibling competition begins as soon as the second cub is born, and 25% of cubs are killed by their siblings.Sibling relationships in animals are not always competitive. For example, among wolves, older siblings help to feed and guard the young.

Famous instances
In religion
The Book of Genesis in the Bible contains several examples of sibling rivalry: the story of Cain and Abel tells of one brothers jealousy after God appears to favour his sibling, and the jealousy ultimately leads to murder. Esau was jealous of his brother Jacobs inheritance and blessing; sisters Leah and Rachel compete for the love of Jacob; Josephs brothers are so jealous that they effectively sell him into slavery. These stories are also present in the Quran.
Another example is provided in the myth of Romulus and Remus, wherein twin brothers Romulus and Remus fight for control over Rome, and which ends with the death of Remus at the hands of his brother.

In folk and fairy tales
Sibling rivalry, bitter jealousy, and envy are notable in several fairy tales around the world. In some tales, the jealousy escalates to outright murder of the successful sibling.
Some tale types, according to the Aarne-Thompson-Uther Index, heavily feature sibling and step-sibling rivalry as part of the plot:

ATU 301, "The Three Stolen Princesses" or "Jean de lOurs": a hero, born with strong powers, descends to an underworld realm to rescue three princesses. He sends the three maidens to the upper realm with the help of his brothers (or companions), but they cut the rope and trap him in the subterranean realm.
ATU 361, "Bearskin": a man makes a deal with devil: must not pray or bathe for a certain number of years. Later, the man meets a father with his three daughters; only the youngest sister promises to marry the man. After the time is up, the man grooms himself and goes to meet his bride, explaining the whole story. Her sisters seethe with rage and explode with jealousy; the devil takes two souls, instead of one.
ATU 403, "The Black and the White Bride": a woman, dispised by her (step)family, marries a prince. Later, her step-mother conspires to replace the woman with her (step)sibling.
ATU 432, "The Bird Lover" or "The Prince as Bird": a maiden is visited at night by a bird, which is a prince in disguise. Her family  begin to suspect something and set up a trap by her window: they put spikes (nails, broken glass, thorns) to hurt the bird. The bird prince thinks her beloved betrayed him and flees, which prompts the heroine to seek him in parts unknown.
ATU 480, "The Kind and Unkind Girls" or "The Spinning-Woman by the Spring": two sisters or stepsisters, one diligent and the other lazy, meet a supernatural entity in the woods or in a magical realm. The diligent sibling acts kindly and obeys the entitys orders, and is rewarded; the lazy one disobeys and is punished.
ATU 510A, "Cinderella": the heroine is maltreated by her stepmother and stepsiblings.
ATU 511, "One-Eye, Two-Eyes, and Three-Eyes": two women (the first one-eyed and the other three-eyed) mistreat their sibling, a woman with two eyes.
ATU 530, "The Princess on the Glass Hill": a father sends his three sons to guard his crops or to hold a vigil on his grave. The older ones disobey and/or feel frightened, so they send their youngest brother, whom they call a fool or stupid, to fulfill their fathers orders. The foolish brother acquires three magical horses and uses them to reach a princess atop a glass hill for three times.
ATU 530A, "The Pig With Golden Bristles": as a continuation of the story of The Glass Mountain, after the wedding, the tsar/king sends his sons-in-law on a quest for some creatures with marvellous attributes. The older brothers want to go on the quest to impress their father-in-law and further humiliate their youngest brother.
ATU 550, "The Golden Bird": a king sends his three sons to find the golden bird and bring it home. The older ones fail, but the youngest is successful, capturing the bird and a horse and bringing with him a maiden as his wife. Spurred by intense jealousy, they murder their sibling or toss them in a ditch and take the prizes of the quest for themselves.
ATU 551, "The Water of Life": a king is dying or blind, so he sends his sons for a magical cure (a magical bird, the water of life, etc.), which can only be found in a distant realm, in the hands of a princess or maiden. The youngest is successful and returns with the prize, but his brothers drop him in a ditch. The youngest prince survives and returns incognito to the city. The foreign maiden comes after the person who stole her property.
ATU 554, "The Grateful Animals": in some variants, the youngest brother protects or helps three animals of different species, much to his brothers chagrin, who wanted to hunt them. When the three brothers are assigned tasks by a king, the youngest accomplishes the feats with the animals help.
ATU 707, "The Dancing Water, the Singing Apple, and the Speaking Bird": one night, the prince (king, tsar, sultan) hears three sisters talking, the youngest promising that, if she were to marry the king, would bear him children (twins, triplets) with wonderful attributes. Her sisters are married to lowly officials or servants of the kings court and, bearing an intense jealousy toward the newly crowned queen, decide to get rid of the royal children.
ATU 709, "Snow White": in some regional variants of the tale type, the rivalry isnt between mother and daughter or between step-mother and step-daughter. Instead, it is the heroines older sisters who get jealous over the youngests beauty and charm and conspire to kill her.
ATU 780, "The Singing Bone": a person murders their sibling (brother or sister) and buries them in a shallow grave. A tree sprouts from it. Its wood is used to create an instrument (fiddle, violin, flute) that reveals the murder.

In literature
A number of Shakespeares plays display the incidences of sibling rivalry. King Lear provokes rivalry among his three daughters by asking them to describe their love for him; in the same play, Edmund contrives to force his half-brother Edgar into exile. In The Taming of the Shrew, sisters Kate and Bianca are shown fighting bitterly. In Richard III, the title character is at least partially motivated by rivalry with his brother, King Edward. In As You Like It, there is obvious sibling rivalry and antagonism between Orlando and Oliver, and also between Duke Frederick and Duke Senior.
Most adaptations of Sherlock Holmes depict sibling rivalry with his brother, Mycroft Holmes.
In John Steinbecks East of Eden, the brothers Cal and Aron Trask are counterparts to Cain and Abel of the Bible story.
A Song of Ice and Fire contains numerous examples, such as that between Stannis Baratheon and Renly Baratheon. After their eldest brother Robert Baratheons death they contend for the Iron Throne, Stannis finally killing Renly through dark magic on the night before Renly intends to kill Stannis in battle, though it is left unclear whether he is aware of his role in Renlys death. The history of Westeros also contains "The Dance of the Dragons", in which Princess Rhaenyra Targaryen and her half-brother Aegon II Targaryen fought over the Iron Throne after their Father Viserys I Targaryens death, Aegon eventually killing Rhaenyra, but being poisoned shortly after, leading to Rhaenyras son Aegon III becoming king.

In film and television
Sibling rivalry is a common theme in media that features child characters, reflecting the importance of this issue in early life. These issues can include jealousy on the birth of a new baby, different sibling roles, frequent arguments, competitiveness for mothers affection, and tensions between step-siblings.
Adult siblings can also be portrayed with a rivalrous relationship, often a continuation of childhood conflicts. Situation comedies exploit this to comic effect. Sibling relationships may be shown as alternately loving and argumentative. Brothers or sisters in a similar line of work may display professional rivalry </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 Hepatitis B and explain in detail? [/INST] Hepatitis B is an infectious disease caused by the Hepatitis B virus (HBV) that affects the liver; it is a type of viral hepatitis. It can cause both acute and chronic infection.Many people have no symptoms during an initial infection. For others, symptoms may appear 30 to 180 days after becoming infected and can include a rapid onset of sickness with nausea, vomiting, yellowish skin, fatigue, dark urine, and abdominal pain. Symptoms during acute infection typically last for a few weeks, though some people may feel sick for up to six months. Deaths resulting from acute stage HBV infections are rare. An HBV infection lasting longer than six months is usually considered chronic. The likelihood of developing chronic hepatitis B is higher for those who are infected with HBV at a younger age. About 90% of those infected during or shortly after birth develop chronic hepatitis B, while less than 10% of those infected after the age of five develop chronic cases. Most of those with chronic disease have no symptoms; however, cirrhosis and liver cancer eventually develop in about 25% of those with chronic HBV.The virus is transmitted by exposure to infectious blood or body fluids. In areas where the disease is common, infection around the time of birth or from contact with other peoples blood during childhood are the most frequent methods by which hepatitis B is acquired. In areas where the disease is rare, intravenous drug use and sexual intercourse are the most frequent routes of infection. Other risk factors include working in healthcare, blood transfusions, dialysis, living with an infected person, travel in countries with high infection rates, and living in an institution. Tattooing and acupuncture led to a significant number of cases in the 1980s; however, this has become less common with improved sterilization. The hepatitis B viruses cannot be spread by holding hands, sharing eating utensils, kissing, hugging, coughing, sneezing, or breastfeeding. The infection can be diagnosed 30 to 60 days after exposure. The diagnosis is usually confirmed by testing the blood for parts of the virus and for antibodies against the virus. It is one of five main hepatitis viruses: A, B, C, D, and E. During an initial infection, care is based on a persons symptoms. In those who develop chronic disease, antiviral medication such as tenofovir or interferon may be useful; however, these drugs are expensive. Liver transplantation is sometimes recommended for cases of cirrhosis or hepatocellular carcinoma.Hepatitis B infection has been preventable by vaccination since 1982. As of 2022, the hepatitis B vaccine is between 98% and 100% effective in preventing infection. The vaccine is administered in several doses; after an initial dose, two or three more vaccine doses are required at a later time for full effect. The World Health Organization (WHO) recommends infants receive the vaccine within 24 hours after birth when possible. National programs have made the hepatitis B vaccine available for infants in 190 countries as of the end of 2021. To further prevent infection, the WHO recommends testing all donated blood for hepatitis B before using it for transfusion. Using antiviral prophylaxis to prevent mother-to-child transmission is also recommended, as is following safe sex practices, including the use of condoms In 2016, the WHO set a goal of eliminating viral hepatitis as a threat to global public health by 2030. Achieving this goal would require the development of therapeutic treatments to cure chronic hepatitis B, as well as preventing its transmission and using vaccines to prevent new infections.An estimated 296 million people, or 3.8% of the global population, had chronic hepatitis B infections as of 2019. Another 1.5 million developed acute infections that year, and 820,000 deaths occurred as a result of HBV. Cirrhosis and liver cancer are responsible for most HBV-related deaths. The disease is most prevalent in Africa (affecting 7.5% of the continent’s population) and in the Western Pacific region (5.9%). Infection rates are 1.5% in Europe and 0.5% in the Americas. According to some estimates, about a third of the worlds population has been infected with hepatitis B at one point in their lives. Hepatitis B was originally known as "serum hepatitis".

Signs and symptoms
Acute infection with hepatitis B virus is associated with acute viral hepatitis, an illness that begins with general ill-health, loss of appetite, nausea, vomiting, body aches, mild fever, and dark urine, and then progresses to development of jaundice. The illness lasts for a few weeks and then gradually improves in most affected people. A few people may have a more severe form of liver disease known as fulminant hepatic failure and may die as a result. The infection may be entirely asymptomatic and may go unrecognized.Chronic infection with hepatitis B virus may be asymptomatic or may be associated with chronic inflammation of the liver (chronic hepatitis), leading to cirrhosis over a period of several years. This type of infection dramatically increases the incidence of hepatocellular carcinoma (HCC; liver cancer). Across Europe, hepatitis B and C cause approximately 50% of hepatocellular carcinomas. Chronic carriers are encouraged to avoid consuming alcohol as it increases their risk for cirrhosis and liver cancer. Hepatitis B virus has been linked to the development of membranous glomerulonephritis (MGN).Symptoms outside of the liver are present in 1–10% of HBV-infected people and include serum-sickness–like syndrome, acute necrotizing vasculitis (polyarteritis nodosa), membranous glomerulonephritis, and papular acrodermatitis of childhood (Gianotti–Crosti syndrome). The serum-sickness–like syndrome occurs in the setting of acute hepatitis B, often preceding the onset of jaundice. The clinical features are fever, skin rash, and polyarteritis. The symptoms often subside shortly after the onset of jaundice but can persist throughout the duration of acute hepatitis B. About 30–50% of people with acute necrotizing vasculitis (polyarteritis nodosa) are HBV carriers. HBV-associated nephropathy has been described in adults but is more common in children. Membranous glomerulonephritis is the most common form. Other immune-mediated hematological disorders, such as essential mixed cryoglobulinemia and aplastic anemia have been described as part of the extrahepatic manifestations of HBV infection, but their association is not as well-defined; therefore, they probably should not be considered etiologically linked to HBV.

Cause
Transmission
Transmission of hepatitis B virus results from exposure to infectious blood or body fluids containing blood. HBV is 50 to 100 times more infectious than human immunodeficiency virus (HIV). HBV can be transmitted through several routes of infection. In vertical transmission, HBV is passed from mother to child (MTCT) during childbirth. Without intervention, a mother who is positive for HBsAg has a 20% risk of passing the infection to her offspring at the time of birth. This risk is as high as 90% if the mother is also positive for HBeAg.Early life horizontal transmission can occur through bites, lesions, certain sanitary habits, or other contact with secretions or saliva containing HBV. Adult horizontal transmission is known to occur through sexual contact, blood transfusions and transfusion with other human blood products, re-use of contaminated needles and syringes. Breastfeeding after proper immunoprophylaxis does not appear to contribute to mother-to-child-transmission (MTCT) of HBV.

Virology
Structure
Hepatitis B virus (HBV) is a member of the hepadnavirus family. The virus particle (virion) consists of an outer lipid envelope and an icosahedral nucleocapsid core composed of core protein. These virions are 30–42 nm in diameter. The nucleocapsid encloses the viral DNA and a DNA polymerase that has reverse transcriptase activity. The outer envelope contains embedded proteins that are involved in viral binding of, and entry into, susceptible cells. The virus is one of the smallest enveloped animal viruses.  The 42 nm virions, which are capable of infecting liver cells known as hepatocytes, are referred to as "Dane particles". In addition to the Dane particles, filamentous and spherical bodies lacking a core can be found in the serum of infected individuals.   These particles are not infectious and are composed of the lipid and protein that forms part of the surface of the virion, which is called the surface antigens (HBsAg), and is produced in excess during the life cycle of the virus.

Genome
The genome of HBV is made of circular DNA, but it is unusual because the DNA is not fully double-stranded. One end of the full length strand is linked to the viral DNA polymerase. The genome is 3020–3320 nucleotides long (for the full-length strand) and 1700–2800 nucleotides long (for the short length-strand). The negative-sense (non-coding) is complementary to the viral mRNA. The viral DNA is found in the nucleus soon after infection of the cell. The partially double-stranded DNA is rendered fully double-stranded by completion of the (+) sense strand and removal of a protein molecule from the (−) sense strand and a short sequence of RNA from the (+) sense strand. Non-coding bases are removed from the ends of the (−) sense strand and the ends are rejoined. There are four known genes encoded by the genome, called C, X, P, and S. The core protein is coded for by gene C (HBcAg), and its start codon is preceded by an upstream in-frame AUG start codon from which the pre-core protein is produced. HBeAg is produced by proteolytic processing of the pre-core protein. In some rare strains of the virus known as Hepatitis B virus precore mutants, no HBeAg is present.
The DNA polymerase is encoded by gene P. Gene S is the gene that codes for the surface antigen (HBsAg). The HBsAg gene is one long open reading frame but contains three in frame "start" (ATG) codons that divide the gene into three sections, pre-S1, pre-S2, and S. Because of the multiple start codons, polypeptides of three different sizes called large (the order from surface to the inside: pre-S1, pre-S2, and S ), middle (pre-S2, S), and small (S) are produced. There is a myristyl group, which plays an important role in infection, on the amino-terminal end of the preS1 part of the large (L) protein. In addition to that, N terminus of the L protein have virus attachment and capsid binding sites. Because of that, the N termini of half of the L protein molecules are positioned outside the membrane and the other half positioned inside the membrane.The function of the protein coded for by gene X is not fully understood but it is associated with the development of liver cancer. It stimulates genes that promote cell growth and inactivates growth regulating molecules.

Pathogenesis
The life cycle of hepatitis B virus is complex. Hepatitis B is one of a few known pararetroviruses: non-retroviruses that still use reverse transcription in their replication process. The virus gains entry into the cell by binding to NTCP on the surface and being endocytosed. Because the virus multiplies via RNA made by a host enzyme, the viral genomic DNA has to be transferred to the cell nucleus by host proteins called chaperones. The partially double-stranded viral DNA is then made fully double stranded by a viral polymerase and transformed into covalently closed circular DNA (cccDNA). This cccDNA serves as a template for transcription of four viral mRNAs by host RNA polymerase. The largest mRNA, (which is longer than the viral genome), is used to make the new copies of the genome and to make the capsid core protein and the viral DNA polymerase. These four viral transcripts undergo additional processing and go on to form progeny virions that are released from the cell or returned to the nucleus and re-cycled to produce even more copies. The long mRNA is then transported back to the cytoplasm where the virion P protein (the DNA polymerase) synthesizes DNA via its reverse transcriptase activity.

Serotypes and genotypes
The virus is divided into four major serotypes (adr, adw, ayr, ayw) based on antigenic epitopes presented on its envelope proteins, and into eight major genotypes (A–H). The genotypes have a distinct geographical distribution and are used in tracing the evolution and transmission of the virus. Differences between genotypes affect the disease severity, course and likelihood of complications, and response to treatment and possibly vaccination. There are two other genotypes I and J but they are not universally accepted as of 2015. The diversity of genotypes is not shown equally in the world. For example, A, D, and E genotypes have been seen in Africa prevalently while B and C genotypes are observed in Asia as widespread.Genotypes differ by at least 8% of their sequence and were first reported in 1988 when six were initially described (A–F). Two further types have since been described (G and H). Most genotypes are now divided into subgenotypes with distinct properties.

Mechanisms
Hepatitis B virus primarily interferes with the functions of the liver by replicating in hepatocytes. A functional receptor is NTCP. There is evidence that the receptor in the closely related duck hepatitis B virus is carboxypeptidase D. The virions bind to the host cell via the preS domain of the viral surface antigen and are subsequently internalized by endocytosis. HBV-preS-specific receptors are expressed primarily on hepatocytes; however, viral DNA and proteins have also been detected in extrahepatic sites, suggesting that cellular receptors for HBV may also exist on extrahepatic cells.During HBV infection, the host immune response causes both hepatocellular damage and viral clearance. Although the innate immune response does not play a significant role in these processes, the adaptive immune response, in particular virus-specific cytotoxic T lymphocytes(CTLs), contributes to most of the liver injury associated with HBV infection. CTLs eliminate HBV infection by killing infected cells and producing antiviral cytokines, which are then used to purge HBV from viable hepatocytes. Although liver damage is initiated and mediated by the CTLs, antigen-nonspecific inflammatory cells can worsen CTL-induced immunopathology, and platelets activated at the site of infection may facilitate the accumulation of CTLs in the liver.

Diagnosis
The tests, called assays, for detection of hepatitis B virus infection involve serum or blood tests that detect either viral antigens (proteins produced by the virus) or antibodies produced by the host. Interpretation of these assays is complex.The hepatitis B surface antigen (HBsAg) is most frequently used to screen for the presence of this infection. It is the first detectable viral antigen to appear during infection. However, early in an infection, this antigen may not be present and it may be undetectable later in the infection as it is being cleared by the host. The infectious virion contains an inner "core particle" enclosing viral genome. The icosahedral core particle is made of 180 or 240 copies of the core protein, alternatively known as hepatitis B core antigen, or HBcAg. During this window in which the host remains infected but is successfully clearing the virus, IgM antibodies specific to the hepatitis B core antigen (anti-HBc IgM) may be the only serological evidence of disease.  Therefore, most hepatitis B diagnostic panels contain HBsAg and total anti-HBc (both IgM and IgG).Shortly after the appearance of the HBsAg, another antigen called hepatitis B e antigen (HBeAg) will appear. Traditionally, the presence of HBeAg in a hosts serum is associated with much higher rates of viral replication and enhanced infectivity; however, variants of the hepatitis B virus do not produce the e antigen, so this rule does not always hold true. During the natural course of an infection, the HBeAg may be cleared, and antibodies to the e antigen (anti-HBe) will arise immediately afterwards. This conversion is usually associated with a dramatic decline in viral replication.

If the host is able to clear the infection, eventually the HBsAg will become undetectable and will be followed by IgG antibodies to the hepatitis B surface antigen and core antigen (anti-HBs and anti HBc IgG). The time between the removal of the HBsAg and the appearance of anti-HBs is called the window period. A person negative for HBsAg but positive for anti-HBs either has cleared an infection or has been vaccinated previously.
Individuals who remain HBsAg positive for at least six months are considered to be hepatitis B carriers. Carriers of the virus may have chronic hepatitis B, which would be reflected by elevated serum alanine aminotransferase (ALT) levels and inflammation of the liver, if they are in the immune clearance phase of chronic infection. Carriers who have seroconverted to HBeAg negative status, in particular those who acquired the infection as adults, have very little viral multiplication and hence may be at little risk of long-term complications or of transmitting infection to others. However, it is possible for individuals to enter an "immune escape" with HBeAg-negative hepatitis.

PCR tests have been developed to detect and measure the amount of HBV DNA, called the viral load, in clinical specimens. These tests are used to assess a persons infection status and to monitor treatment. Individuals with high viral loads, characteristically have ground glass hepatocytes on biopsy.

Prevention
Vaccine
Vaccines for the prevention of hepatitis B have been routinely recommended for babies since 1991 in the United States. The first dose is generally recommended within a day of birth. The hepatitis B vaccine was the first vaccine capable of preventing cancer, specifically liver cancer.Most vaccines are given in three doses over a course of days. A protective response to the vaccine is defined as an anti-HBs antibody concentration of at least 10 mIU/ml in the recipients serum. The vaccine is more effective in children and 95 percent of those vaccinated have protective levels of antibody. This drops to around 90% at 40 years of age and to around 75 percent in those over 60 years. The protection afforded by vaccination is long lasting even after antibody levels fall below 10 mIU/ml. For newborns of HBsAg-positive mothers: hepatitis B vaccine alone, hepatitis B immunoglobulin alone, or the combination of vaccine plus hepatitis B immunoglobulin, all prevent hepatitis B occurrence. Furthermore, the combination of vaccine plus hepatitis B immunoglobulin is superior to vaccine alone. This combination prevents HBV transmission around the time of birth in 86% to 99% of cases.Tenofovir given in the second or third trimester can reduce the risk of mother to child transmission by 77% when combined with hepatitis B immunoglobulin and the hepatitis B vaccine, especially for pregnant women with high hepatitis B virus DNA levels. However, there is no sufficient evidence that the administration of hepatitis B immunoglobulin alone during pregnancy, might reduce transmission rates to the newborn infant. No randomized control trial has been conducted to assess the effects of hepatitis B vaccine during pregnancy for preventing infant infection.All those with a risk of exposure to body fluids such as blood should be vaccinated, if not already. Testing to verify effective immunization is recommended and further doses of vaccine are given to those who are not sufficiently immunized.In 10- to 22-year follow-up studies there were no cases of hepatitis B among those with a normal immune system who were vaccinated. Only rare chronic infections have been documented. Vaccination is particularly recommended for high risk groups including: health workers, people with chronic kidney failure, and men who have sex with men.Both types of the hepatitis B vaccine, the plasma-derived vaccine (PDV) and recombinant vaccine (RV) are of similar effectiveness in preventing the infection in both healthcare workers and chronic kidney failure groups. With one difference noticed among health worker group, that the RV intramuscular route is significantly more effective compared with RV intradermal route of administration.

Other
In assisted reproductive technology, sperm washing is not necessary for males with hepatitis B to prevent transmission, unless the female partner has not been effectively vaccinated. In females with hepatitis B, the risk of transmission from mother to child with IVF is no different from the risk in spontaneous conception.Those at high risk of infection should be tested as there is effective treatment for those who have the disease. Groups that screening is recommended for include those who have not been vaccinated and one of the following: people from areas of the world where hepatitis B occurs in more than 2%, those with HIV, intravenous drug users, men who have sex with men, and those who live with someone with hepatitis B. Screening during pregnancy is recommended in the United States.

Treatment
Acute hepatitis B infection does not usually require treatment and most adults clear the infection spontaneously. Early antiviral treatment may be required in fewer than 1% of people, whose infection takes a very aggressive course (fulminant hepatitis) or who are immunocompromised. On the other hand, treatment of chronic infection may be necessary to reduce the risk of cirrhosis and liver cancer. Chronically infected individuals with persistently elevated serum alanine aminotransferase, a marker of liver damage, and HBV DNA levels are candidates for therapy. Treatment lasts from six months to a year, depending on medication and genotype. Treatment duration when medication is taken by mouth, however, is more variable and usually longer than one year.Although none of the available medications can clear the infection, they can stop the virus from replicating, thus minimizing liver damage. As of 2018, there are eight medications licensed for the treatment of hepatitis B infection in the United States. These include antiviral medications lamivudine, adefovir, tenofovir disoproxil, tenofovir alafenamide, telbivudine, and entecavir, and the two immune system modulators interferon alpha-2a and PEGylated interferon alpha-2a. In 2015 the World Health Organization recommended tenofovir or entecavir as first-line agents. Those with current cirrhosis are in most need of treatment.The use of interferon, which requires injections daily or thrice weekly, has been supplanted by long-acting PEGylated interferon, which is injected only once weekly. However, some individuals are much more likely to respond than others, and this might be because of the genotype of the infecting virus or the persons heredity. The treatment reduces viral replication in the liver, thereby reducing the viral load (the amount of virus particles as measured in the blood). Response to treatment differs between the genotypes. Interferon treatment may produce an e antigen seroconversion rate of 37% in genotype A but only a 6% seroconversion in type D. Genotype B has similar seroconversion rates to type A while type C seroconverts only in 15% of cases. Sustained e antigen loss after treatment is ~45% in types A and B but only 25–30% in types C and D.It seems unlikely that the disease will be eliminated by 2030, the goal set in 2016 by WHO. However, progress is being made in developing therapeutic treatments. In 2010, the Hepatitis B Foundation reported that 3 preclinical and 11 clinical-stage drugs were under development, based on largely similar mechanisms. In 2020, they reported that there were 17 preclinical- and 32 clinical-stage drugs under development, using diverse mechanisms.

Prognosis
Hepatitis B virus infection may be either acute (self-limiting) or chronic (long-standing). Persons with self-limiting infection clear the infection spontaneously within weeks to months.
Children are less likely than adults to clear the infection. More than 95% of people who become infected as adults or older children will stage a full recovery and develop protective immunity to the virus. However, this drops to 30% for younger children, and only 5% of newborns that acquire the infection from their mother at birth will clear the infection. This population has a 40% lifetime risk of death from cirrhosis or hepatocellular carcinoma. Of those infected between the age of one to six, 70% will clear the infection.Hepatitis D (HDV) can occur only with a concomitant hepatitis B infection, because HDV uses the HBV surface antigen to form a capsid. Co-infection with hepatitis D increases the risk of liver cirrhosis and liver cancer. Polyarteritis nodosa is more common in people with hepatitis B infection.

Cirrhosis
A number of different tests are available to determine the degree of cirrhosis present. Transient elastography (FibroScan) is the test of choice, but it is expensive. Aspartate aminotransferase to platelet ratio index may be used when cost is an issue.

Reactivation
Hepatitis B virus DNA remains in the body after infection, and in some people, including those that do not have detectable HBsAg, the disease recurs. Although rare, reactivation is seen most often following alcohol or drug use, or in people with impaired immunity. HBV goes through cycles of replication and non-replication. Approximately 50% of overt carriers experience acute reactivation. Males with baseline ALT of 200 UL/L are three times more likely to develop a reactivation than people with lower levels. Although reactivation can occur spontaneously, people who undergo chemotherapy have a higher risk. Immunosuppressive drugs favor increased HBV replication while inhibiting cytotoxic T cell function in the liver. The risk of reactivation varies depending on the serological profile; those with detectable HBsAg in their blood are at the greatest risk, but those with only antibodies to the core antigen are also at risk. The presence of antibodies to the surface antigen, which are considered to be a marker of immunity, does not preclude reactivation. Treatment with prophylactic antiviral drugs can prevent the serious morbidity associated with HBV disease reactivation.

Epidemiology
At least 296 million people, or 3.8% of the worlds population, had chronic HBV infection as of 2019. Another 1.5 million cases of acute HBV infection also occurred that year. Regional prevalences across the globe range from around 7.5% in Africa to 0.5% in the Americas.The primary method of HBV transmission and the prevalence of chronic HBV infection in specific regions often correspond with one another. In populations where HBV infection rates are 8% or higher, which are classified as high prevalence, vertical transmission (usually occurring during birth) is most common, though rates of early childhood transmission can also be significant among these populations. In 2021, 19 African countries had infection rates ranging between 8-19%, placing them in the high prevalence category.In moderate prevalence areas where 2–7% of the population is chronically infected, the disease is predominantly spread horizontally, often among children, or vertically. China’s HBV infection rate is at the higher end of the moderate prevalence classification with an infection rate of 6.89% as of 2019. HBV prevalence in India is also moderate, with studies placing India’s infection rate between 2-4%.Countries with low HBV prevalence include Australia (0.9%), those in the WHO European Region (which average 1.5%), and most countries in North and South America (which average 0.28%).
In the United States, an estimated 0.26% of the population was living with HBV infection as of 2018.

History
Findings of HBV DNA in ancient human remains have shown that HBV has infected humans since at least ten millennia, both in Eurasia and in the Americas. This disproved the belief that hepatitis B originated in the New World and spread to Europe around 16th century. Hepatitis B virus subgenotype C4 is exclusively present in Australian aborigines, suggesting an ancient origin as much as 50,000 years old. However, analyses of ancient HBV genomes suggested that the most recent common ancestor of all known human HBV strains was dated to between 20,000 and 12,000 years ago, pointing to a more recent origin for all HBV genotypes. The evolution of HBV in humans was shown to reflect known events of human history such as the first peopling of the Americas during the late Pleistocene and the Neolithic transition in Europe. Ancient DNA studies have also showed that some ancient hepatitis viral strains still infect humans, while other became extinct.The earliest record of an epidemic caused by hepatitis B virus was made by Lurman in 1885 </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 Omphalomesenteric duct cyst 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 Abdomen and explain in detail? [/INST] The abdomen (colloquially called the belly, tummy, midriff, tucky or stomach) is the part of the body between the thorax (chest) and pelvis, in humans and in other vertebrates. The abdomen is the front part of the abdominal segment of the torso. The area occupied by the abdomen is called the abdominal cavity. In arthropods it is the posterior tagma of the body; it follows the thorax or cephalothorax.In humans, the abdomen stretches from the thorax at the thoracic diaphragm to the pelvis at the pelvic brim. The pelvic brim stretches from the lumbosacral joint (the intervertebral disc between L5 and S1) to the pubic symphysis and is the edge of the pelvic inlet. The space above this inlet and under the thoracic diaphragm is termed the abdominal cavity. The boundary of the abdominal cavity is the abdominal wall in the front and the peritoneal surface at the rear.
In vertebrates, the abdomen is a large body cavity enclosed by the abdominal muscles, at front and to the sides, and by part of the vertebral column at the back. Lower ribs can also enclose ventral and lateral walls. The abdominal cavity is continuous with, and above, the pelvic cavity. It is attached to the thoracic cavity by the diaphragm. Structures such as the aorta, inferior vena cava and esophagus pass through the diaphragm. Both the abdominal and pelvic cavities are lined by a serous membrane known as the parietal peritoneum. This membrane is continuous with the visceral peritoneum lining the organs. The abdomen in vertebrates contains a number of organs belonging to, for instance, the digestive system, urinary system, and muscular system.

Contents
The abdominal cavity contains most organs of the digestive system, including the stomach, the small intestine, and the colon with its attached appendix. Other digestive organs are known as the accessory digestive organs and include the liver, its attached gallbladder, and the pancreas, and these communicate with the rest of the system via various ducts. The spleen, and organs of the urinary system including the kidneys, and adrenal glands also lie within the abdomen, along with many blood vessels including the aorta and inferior vena cava. The urinary bladder, uterus, fallopian tubes, and ovaries may be seen as either abdominal organs or as pelvic organs. Finally, the abdomen contains an extensive membrane called the peritoneum. A fold of peritoneum may completely cover certain organs, whereas it may cover only one side of organs that usually lie closer to the abdominal wall. This is called the retroperitoneum, and the kidneys and ureters are known as retroperitoneal organs.
Abdominal organs can be highly specialized in some animals. For example, the stomach of ruminants, (a suborder of mammals that includes cattle and sheep), is divided into four chambers – rumen, reticulum, omasum and abomasum.

Muscles
There are three layers of muscles in the abdominal wall. They are, from the outside to the inside: external oblique, internal oblique, and transverse abdominal. The first three layers extend between the vertebral column, the lower ribs, the iliac crest and pubis of the hip. All of their fibers merge towards the midline and surround the rectus abdominis in a sheath before joining up on the opposite side at the linea alba. Strength is gained by the criss-crossing of fibers, such that the external oblique runs downward and forward, the internal oblique upward and forward, and the transverse abdominal horizontally forward.The transverse abdominal muscle is flat and triangular, with its fibers running horizontally. It lies between the internal oblique and the underlying transverse fascia. It originates from the inguinal ligament, costal cartilages 7-12, the iliac crest and thoracolumbar fascia. Inserts into the conjoint tendon, xiphoid process, linea alba and the pubic crest.
The rectus abdominis muscles are long and flat. The muscle is crossed by three fibrous bands called the tendinous intersections. The rectus abdominis is enclosed in a thick sheath, formed as described above, by fibers from each of the three muscles of the lateral abdominal wall. They originate at the pubis bone, run up the abdomen on either side of the linea alba, and insert into the cartilages of the fifth, sixth, and seventh ribs. In the region of the groin, the inguinal canal, is a passage through the layers. This gap is where the testes can drop through the wall and where the fibrous cord from the uterus in the female runs. This is also where weakness can form, and cause inguinal hernias.The pyramidalis muscle is small and triangular. It is located in the lower abdomen in front of the rectus abdominis. It originates at the pubic bone and is inserted into the linea alba halfway up to the navel.

Function
Functionally, the human abdomen is where most of the digestive tract is placed and so most of the absorption and digestion of food occurs here. The alimentary tract in the abdomen consists of the lower esophagus, the stomach, the duodenum, the jejunum, ileum, the cecum and the appendix, the ascending, transverse and descending colons, the sigmoid colon and the rectum. Other vital organs inside the abdomen include the liver, the kidneys, the pancreas and the spleen.
The abdominal wall is split into the posterior (back), lateral (sides), and anterior (front) walls.

Movement, breathing and other functions
The abdominal muscles have different important functions. They assist as muscles of exhalation in the breathing process during forceful exhalation. Moreover, these muscles serve as protection for the inner organs. Furthermore, together with the back muscles they provide postural support and are important in defining the form. When the glottis is closed and the thorax and pelvis are fixed, they are integral in the cough, urination, defecation, childbirth, vomit, and singing functions. When the pelvis is fixed, they can initiate the movement of the trunk in a forward motion. They also prevent hyperextension. When the thorax is fixed, they can pull up the pelvis and finally, they can bend the vertebral column sideways and assist in the trunks rotation.

Posture
The transverse abdominis muscle is the deepest muscle, therefore, it cannot be touched from the outside. It can greatly affect the bodys posture. The internal obliques are also deep and also affect body posture. Both of them are involved in rotation and lateral flexion of the spine and are used to bend and support the spine from the front. The external obliques are more superficial and they are also involved in rotation and lateral flexion of the spine. Also they stabilize the spine when upright. The rectus abdominis muscle is not the most superficial abdominal muscle. The tendonous sheath extending from the external obliques cover the rectus abdominis. The rectus abdominis is the muscle that very fit people develop into the 6-pack ab look. Although it should really be a 10 pack as there are 5 vertical sections on each side. The 2 bottom sections are just above the pubic bone and usually not visible, hence, the 6 pack abs. The rectus abdominals function is to bend ones back forward (flexion). The main work of the abdominal muscles is to bend the spine forward when contracting concentrically.

Society and culture
Social and cultural perceptions of the outward appearance of the abdomen has varying significance around the world. Depending on the type of society, excess weight can be perceived as an indicator of wealth and prestige due to excess food, or as a sign of poor health due to lack of exercise. In many cultures, bare abdomens are distinctly sexualized and perceived similarly to breast cleavage.

Exercise
Being key elements of spinal support, and contributors to good posture, it is important to properly exercise the abdominal muscles together with the back muscles because when these are weak or overly tight they can suffer painful spasms and injuries. When properly exercised, abdominal muscles contribute to improved posture and balance, reduce the likelihood of back pain episodes, reduce the severity of back pain, protect against injury by responding efficiently to stresses, help avoid some back surgeries, and help with the healing of back problems, or after spine surgery. When strengthened, the abdominal muscles provide flexibility as well. The abdominal muscles can be worked by practicing disciplines of general body strength such as Pilates, yoga, Tai chi, and jogging. There are also specific routines which target each of these muscles.

Clinical significance
Abdominal obesity is a condition where abdominal fat or visceral fat, has built up excessively between the abdominal organs. This is associated with a higher risk of heart disease, asthma and type 2 diabetes.
Abdominal trauma is an injury to the abdomen and can involve damage to the abdominal organs. There is an associated risk of severe blood loss and infection. Injury to the lower chest can cause injuries to the spleen and liver.A scaphoid abdomen is when the abdomen is sucked inwards. In a newborn, it may represent a diaphragmatic hernia. In general, it is indicative of malnutrition.

Disease
Many gastrointestinal diseases affect the abdominal organs. These include stomach disease, liver disease, pancreatic disease, gallbladder and bile duct disease; intestinal diseases include enteritis, coeliac disease, diverticulitis, and IBS.

Examination
Different medical procedures can be used to examine the organs of the gastrointestinal tract. These include endoscopy, colonoscopy, sigmoidoscopy, enteroscopy, oesophagogastroduodenoscopy and virtual colonoscopy. There are also a number of medical imaging techniques that can be used. Surface landmarks are important in the examination of the abdomen.

Surface landmarks
In the mid-line a slight furrow extends from the xiphoid process above to the pubic symphysis below, representing the linea alba in the abdominal wall. At about its midpoint sits the umbilicus or navel. The rectus abdominis on each side of the linea alba stands out in muscular people. The outline of these muscles is interrupted by three or more transverse depressions indicating the tendinous intersections. There is usually one about the xiphoid process, one at the navel, and one in between. It is the combination of the linea alba and the tendinous intersections which form the abdominal "six-pack" sought after by many people.
The upper lateral limit of the abdomen is the subcostal margin (at or near the subcostal plane) formed by the cartilages of the false ribs (8, 9, 10) joining one another. The lower lateral limit is the anterior crest of the ilium and Pouparts ligament, which runs from the anterior superior spine of the ilium to the spine of the pubis. These lower limits are marked by visible grooves. Just above the pubic spines on either side are the external abdominal rings, which are openings in the muscular wall of the abdomen through which the spermatic cord emerges in the male, and through which an inguinal hernia may rupture.
One method by which the location of the abdominal contents can be appreciated is to draw three horizontal and two vertical lines.

Horizontal lines
The highest of the former is the transpyloric line of C. Addison, which is situated halfway between the suprasternal notch and the top of the pubic symphysis, and often cuts the pyloric opening of the stomach an inch to the right of the mid-line. The hilum of each kidney is a little below it, while its left end approximately touches the lower limit of the spleen. It corresponds to the first lumbar vertebra behind.
The second line is the subcostal line, drawn from the lowest point of the subcostal arch (tenth rib). It corresponds to the upper part of the third lumbar vertebra, and it is an inch or so above the umbilicus. It indicates roughly the transverse colon, the lower ends of the kidneys, and the upper limit of the transverse (3rd) part of the duodenum.
The third line is called the intertubercular line, and runs across between the two rough tubercles, which can be felt on the outer lip of the crest of the ilium about two and a half inches (64 mm) from the anterior superior spine. This line corresponds to the body of the fifth lumbar vertebra, and passes through or just above the ileo-caecal valve, where the small intestine joins the large intestine.

Vertical lines
The two vertical or mid-Poupart lines are drawn from the point midway between the anterior superior spine and the pubic symphysis on each side, vertically upward to the costal margin.

The right one is the most valuable, as the ileo-caecal valve is situated where it cuts the intertubercular line. The orifice of the appendix lies an inch lower, at McBurneys point. In its upper part, the vertical line meets the transpyloric line at the lower margin of the ribs, usually the ninth, and here the gallbladder is situated.
The left mid-Poupart line corresponds in its upper three-quarters to the inner edge of the descending colon.The right subcostal margin corresponds to the lower limit of the liver, while the right nipple is about half an inch above its upper limit.

Quadrants and regions
The abdomen can be divided into quadrants or regions to describe the location of an organ or structure. Classically, quadrants are described as the left upper, left lower, right upper, and right lower. Quadrants are also often used in describing the site of an abdominal pain.The abdomen can also be divided into nine regions.

These terms stem from "hypo" meaning "below" and "epi" means "above", while "chondron" means "cartilage" (in this case, the cartilage of the rib) and "gaster" means stomach. The reversal of "left" and "right" is intentional, because the anatomical designations reflect the patients own right and left.)
The "right iliac fossa" (RIF) is a common site of pain and tenderness in patients who have appendicitis. The fossa is named for the underlying iliac fossa of the hip bone, and thus is somewhat imprecise. Most of the anatomical structures that will produce pain and tenderness in this region are not in fact in the concavity of the ileum </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 Solitary fibrous tumor and explain in detail? [/INST] Solitary fibrous tumor (SFT), also known as fibrous tumor of the pleura, is a rare mesenchymal tumor originating in the pleura or at virtually any site in the soft tissue including seminal vesicle. Approximately 78% to 88% of SFTs are benign and 12% to 22% are malignant. The World Health Organization (2020) classified SET as specific type of tumor in the category of malignant fibroblastic and myofibroblastic tumors.

Signs and symptoms
About 80% of pleural SFTs originate in the visceral pleura, while 20% arise from parietal pleura. Although they are often very large tumors (up to 40 cm </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 Spastic hemiplegia and explain in detail? [/INST] Spastic hemiplegia is a neuromuscular condition of spasticity that results in the muscles on one side of the body being in a constant state of contraction. It is the "one-sided version" of spastic diplegia. It falls under the mobility impairment umbrella of cerebral palsy. About 20–30% of people with cerebral palsy have spastic hemiplegia. Due to brain or nerve damage, the brain is constantly sending action potentials to the neuromuscular junctions on the affected side of the body. Similar to strokes, damage on the left side of the brain affects the right side of the body and damage on the right side of the brain affects the left side of the body. Other side can be effected for lesser extent.
The affected side of the body is rigid, weak and has low functional abilities. In most cases, the upper extremity is much more affected than the lower extremity. This could be due to preference of hand usage during early development. If both arms are affected, the condition is referred to as double hemiplegia. Some patients with spastic hemiplegia only experience minor impairments, where in severe cases one side of the body could be completely paralyzed. The severity of spastic hemiplegia is dependent upon the degree of the brain or nerve damage.

Presentation
Complications
The muscle spasticity can cause gait patterns to be awkward and jerky. The constant spastic state of the muscle can lead to bone and tendon deformation, further complicating the patients mobility. Many patients with spastic hemiplegia are subjected to canes, walkers and even wheelchairs. Due to the decrease in weight bearing, patients are at a higher risk of developing osteoporosis. An unhealthy weight can further complicate mobility. Patients with spastic hemiplegia are a high risk for experiencing seizures. Oromotor dysfunction puts patients at risk for aspiration pneumonia. Visual field deficits can cause impaired two-point discrimination. Many patients experience the loss of sensation in the arms and legs on the affected side of the body.  Nutrition is essential for the proper growth and development for a child with spastic hemiplegia.

Causes
There are many different brain dysfunctions that can account for the cause for spastic hemiplegia. Spastic hemiplegia occurs either at birth or in the womb. The cause can be all types of strokes, cerebral palsy head injuries, hereditary diseases, brain injuries and infections. Malformations of the veins or arteries in any part of the body can lead to spastic hemiplegia. The artery most commonly affected is the middle cerebral artery. Unborn and newborn babies are susceptible to strokes. Leukodystrophies are a group of hereditary diseases that are known to cause spastic hemiplegia. Brain infections that cause spastic hemiplegia are meningitis, multiple sclerosis, and encephalitis. The spasticity occurs when the afferent pathways in the brain are compromised and the communication between the brain to the motor fibers is lost. When the inhibitory signals to deactivate the stretch reflex is lost the muscle remains in a constantly contracted state. With spastic hemiplegia, one upper extremity and one lower extremity is affected, so cervical, lumbar and sacral segments of the spinal column can be affected.

Diagnosis
Infants with spastic hemiplegia may develop a hand preference earlier than is typical.

Treatment
There is no known cure for cerebral palsy, however, there is a large array of treatments proven effective at improving quality of life and relieving some of the symptoms associated with CP, especially SHCP.  Some treatments are aimed at improving mobility, strengthening muscle and improving coordination. Although CP is due to permanent damage and is not progressive in nature, without treatment the symptoms can become worse, intensifying in pain and severity, and create complications that were not initially present. Some treatments are preventative measures to help prevent further complications, such as complete paralysis of the arm due to non-use and subsequent worsening hypertonia and joint contracture. Others forms of treatment are corrective in nature. Many treatments target symptoms that are indirectly related to or caused by the SHCP. Many of these treatments are common for other forms of CP as well. Treatment is individualized based on each case and the specific needs of the patient. Treatments are often combined with other forms of treatment and a long-term treatment plan is created and continuously evaluated. Treatment can include the following:

Physical therapy – Physical therapy is the most common form of treatment (source needed). It may include sensory stimulation, stretching, strengthening and positioning. Constraint-induced movement therapy is a newer form of physical therapy for SHCP that involves casting or splinting the unaffected arm to promote the use of the affected arm (Taub). The theory behind constraint-induced movement therapy is that new neural pathways are created. Alternative forms of physical therapy include yoga and dance. Physical therapy may also include the use of braces while not actively involved with the therapist.
Occupational therapy – Occupational therapy evaluates and treats patients through selected activities in order to enable people to function as effectively and independently as possible in daily life. Occupational therapy is geared toward the individual to achieve optimal results and performance while learning to cope with their disability.
Speech therapy – Due to difficulties in speech, speech therapy is often necessary. Aside from helping with understanding language and increasing communication skills, speech therapists can also assist children that have difficulty eating and drinking.
Behavioral therapy —  Psychotherapy and counseling are heavily used in the treatment of individuals with SHPD to help them cope emotionally with their needs and frustrations. Counseling through social work can be very beneficial for social issues and adjustments to society. Psychotherapy becomes a more important aspect of therapy when more serious issues such as depression become problematic. Play therapy is a common treatment for all young children with or without disabilities but can be very useful in helping children with SHCP. This therapy again is individualized geared to improve emotional and social development; reduce aggression; improve cooperation with others; assist a child in processing a traumatic event or prepare for an upcoming event such as surgery.
Surgery – Although surgery may become necessary in some cases, physical therapy and the consistent use of braces can help mitigate the need for surgery. Surgical procedures are painful with long and difficult recoveries and do not cure the condition. Most common is a surgery that effectively lengthens the muscle. This type of surgery is usually performed on the legs, but can be performed on the arms as well. Surgeries also may be necessary to realign joints. Other, less popular surgical techniques try to reduce spasticity by severing selected overactive nerves that control muscles. This procedure, known as selective dorsal root rhizotomy, is still somewhat controversial and is generally used only on the lower extremities of severe cases. Other experimental surgical techniques are also being investigated. The benefits of surgery can also be negated or reversed if the patient does not participate in physical therapy and braces (or casts) are not worn regularly.
Medicinal – Medication targeting symptoms associated with spasticity is also a relatively new treatment that is utilized but is still in the early stages of development. Drugs such as baclofen, benzodiazepines (e.g., diazepam), tizanidine, and sometimes dantrolene have shown promise in the effort to diminish spasticity. Botulinum toxin ("Botox") type A may reduce spasticity a few months at a time and has frequently been considered a beneficial treatment for children with SHCP and other forms of CP. Botox has been shown to be especially beneficial to reducing spasticity in the gastrocnemius (calf) muscle. This therapy can improve range of motion, reduce deformity, improve response to occupational and physical therapy, and delay the need for surgery </s>