<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 Congenital myopathy and explain in detail? [/INST] Congenital myopathy is a very broad term for any muscle disorder present at birth. This defect primarily affects skeletal muscle fibres and causes muscular weakness and/or hypotonia. Congenital myopathies account for one of the top neuromuscular disorders in the world today, comprising approximately 6 in 100,000 live births every year. As a whole, congenital myopathies can be broadly classified as follows:

A distinctive abnormality in skeletal muscle fibres on the cellular level; observable via light microscope
Symptoms of muscle weakness and hypotonia
Is a congenital disorder, meaning it occurs during development and symptoms present themselves at birth or in early life.
Is a genetic disorder.

Classification
Myopathies with inclusion bodies and abnormal protein accumulation
Congenital myopathies with inclusion bodies and protein accumulation is a broad category, and some congenital myopathies that fall within this group are well understood, such as nemaline myopathy (see below). Typically, the development error in this category occurs when muscle proteins aggregate and build up in the sarcoplasm, which leads to muscle dysfunction.

Myopathies with cores
Core myopathies such as multicore myopathy and central core disease are characterized by sharply-demarcated areas devoid of oxidative enzymes NADH, SDH, and COX, in muscle fibres.

Myopathies with central nuclei
Myopathies with central nuclei, such as myotubular myopathy, involves an error in the gene involved in vesicle movement throughout the cell. This creates problems in vesicles reaching the plasma membrane with the cellular components necessary to fuse myoblast, a major step in the formation of the skeletal muscle. This creates structural problems throughout the skeletal muscle and in the Z line of the sarcomere, creating the weakness in the muscle.

Myopathies with fiber size variation
Myopathies with varying fiber size, such as congenital fiber type disproportion,
occurs when type 1 fibers, the slow twitch fibers involved in sustaining activity, are smaller than type 2 fibers, the fast twitch fibers involved in quick activity.  Since smaller type 1 fibers is not associated with nemaline myopathy, the most common type of congenital myopathy, it has not been studied in as great detail as many of the others. However, the smaller type 1 fibers explains why patients typically can participate in activities for shorter periods of time, but struggle with extended activity.

Cause
Diagnosis
There are rarely any specific tests for the congenital myopathies except for muscle biopsy. Tests can be run to check creatine kinase in the blood, which is often normal or mildly elevated in congenital myopathies. Electromyography can be run to check the electrical activity of the muscle. Diagnosis heavily relies on muscle pathology, where a muscle biopsy is visualised on the cellular level. Diagnosis usually relies on this method, as creatine kinase levels and electromyography can be unreliable and non-specific. Since congenital myopathies are genetic, there have been advancements in prenatal screenings.

Types
The conditions included under the term "congenital myopathy" can vary. One source includes nemaline myopathy, myotubular myopathy, central core myopathy, congenital fiber type disproportion, and multicore myopathy. The term can also be used more broadly, to describe conditions present from birth.

Nemaline myopathy
Nemaline myopathy was first described in 1963 and is the most common congenital myopathy. It is characterized by generalized muscle weakness and low muscle tone. In its severest form, affected babies often die from respiratory failure. To date, 9 gene mutations have been found to cause nemaline myopathy. 6 of the identified genes are associated with the actin filament, which is the basis for muscle contraction. Histologically, nemaline rods stain red with Gomoris trichrome and are mostly seen in the subsarcolemmal region of muscle fibres. Nemaline rods have also been observed in the intermyofibrillar region of muscle fibres and within the nucleus. Nemaline myopathy is an autosomal dominant and sometimes an autosomal recessive genetic disorder. Sporadic cases have also been described.

Myotubular myopathy
Myotubular myopathy, also known as centeronuclear myopathy, is recognized by pain during exercise and difficulty walking. People affected by this disease typically are wheelchair-reliant by middle adulthood, have weakness in the muscles involved in eye movement, nerve function disorders, and some form of intellectual disability. Myotubular myopathy is very rare, with less than 50 families currently affected.
Genetically, myotubular myopathy can have two causes: autosomal dominant and autosomal recessive. When caused by a mutation in the DNM2 gene, the disorder is autosomal dominant, meaning it can be passed on by one mutated gene. When the mutation takes place in the BIN1 gene, the disease is instead autosomal recessive, and both genes must be mutated for the disease to be inherited. Autosomal recessive onset is most common.

Central core disease
Central core disease or central core myopathy was first described in 1956 and usually presents in infancy or early childhood as non-progressive mild proximal weakness that persists throughout life. Central core disease is believed to be more prevalent than currently reported, as it is hard to recognize and often misdiagnosed in early childhood. Central core disease has been found to be allelic with malignant hyperthermia, which is a life-threatening anesthetic reaction that causes a rise in body temperature, muscular rigidity and muscular breakdown, grossly elevated creatine kinase, and acidosis. Central core disease is caused by a mutation in the RYR1 gene.

Congenital fiber type disproportion
Congenital fiber type disproportion affects skeletal muscle, typically causing weakness in the shoulders, upper arms, thighs, and hips. Skeletal muscle is made up of two kinds of fiber, type 1 and type 2. In congenital fiber type disproportion, type 1 fibers are not only smaller but often more abundant than type 2 fibers. This leads to affected individuals being able to maintain an active lifestyle, though they usually have lower levels of stamina.
Severity with this disease varies greatly, but people typically present symptoms by the age of one. Individuals do not usually worsen with time, and cases have even been reported of improvements.

Multicore myopathy
Multicore myopathy also referred to as minicore myopathy, is associated with small areas of decreased oxidative activities, resulting in areas that appear in this histology as "cores". These appear through microscopy very similar to central core, however the cores are typically smaller in multicore myopathy. As with congenital fiber type disproportion, patients have a greater number of type 1 fibers. Overall, approximately half of diagnosed individuals report no progression of muscle weakness, while half report a very slow progression.

Cylindrical spirals myopathy
Cylindrical spirals myopathy is very rare with only 18 individual cases described as of 2013. The majority of cases are sporadic, and has been observed in only 3 families. It is characterized by the presence of cylindrical spirals as the main pathological finding in muscle biopsies. Cylindrical spirals are unusual membrane structures that have a spiral pattern </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 Foot drop and explain in detail? [/INST] Foot drop is a gait abnormality in which the dropping of the forefoot happens due to weakness, irritation or damage to the deep fibular nerve (deep peroneal), including the sciatic nerve, or paralysis of the muscles in the anterior portion of the lower leg. It is usually a symptom of a greater problem, not a disease in itself. Foot drop is characterized by inability or impaired ability to raise the toes or raise the foot from the ankle (dorsiflexion). Foot drop may be temporary or permanent, depending on the extent of muscle weakness or paralysis and it can occur in one or both feet.  In walking, the raised leg is slightly bent at the knee to prevent the foot from dragging along the ground.
Foot drop can be caused by nerve damage alone or by muscle or spinal cord trauma, abnormal anatomy, atoxins, or disease. Toxins include organophosphate compounds which have been used as pesticides and as chemical agents in warfare. The poison can lead to further damage to the body such as a neurodegenerative disorder called organophosphorus induced delayed polyneuropathy. This disorder causes loss of function of the motor and sensory neural pathways.  In this case, foot drop could be the result of paralysis due to neurological dysfunction. Diseases that can cause foot drop include trauma to the posterolateral neck of fibula, stroke, amyotrophic lateral sclerosis, muscular dystrophy, poliomyelitis, Charcot Marie Tooth disease, multiple sclerosis, cerebral palsy, hereditary spastic paraplegia, Guillain–Barré syndrome, Welander distal myopathy, Friedreichs ataxia and Chronic Compartment Syndrome . It may also occur as a result of hip replacement surgery or knee ligament reconstruction surgery.

Signs and symptoms
Foot drop is characterized by steppage gait.  While walking, people suffering the condition drag their toes along the ground or bend their knees to lift their foot higher than usual to avoid the dragging. This serves to raise the foot high enough to prevent the toe from dragging and prevents the slapping. To accommodate the toe drop, the patient may use a characteristic tiptoe walk on the opposite leg, raising the thigh excessively, as if walking upstairs, while letting the toe drop. Other gaits such as a wide outward leg swing (to avoid lifting the thigh excessively or to turn corners in the opposite direction of the affected limb) may also indicate foot drop.Patients with painful disorders of sensation (dysesthesia) of the soles of the feet may have a similar gait but do not have foot drop. Because of the extreme pain evoked by even the slightest pressure on the feet, the patient walks as if walking barefoot on hot sand.

Pathophysiology
The causes of foot drop, as for all causes of neurological lesions, should be approached using a localization-focused approach before etiologies are considered. Most of the time, foot drop is the result of neurological disorder; only rarely is the muscle diseased or nonfunctional. The source for the neurological impairment can be central (spinal cord or brain) or peripheral (nerves located connecting from the spinal cord to an end-site muscle or sensory receptor).Foot drop is rarely the result of a pathology involving the muscles or bones that make up the lower leg. The anterior tibialis is the muscle that picks up the foot. Although the anterior tibialis plays a major role in dorsiflexion, it is assisted by the fibularis tertius, extensor digitorum longus and the extensor hallucis longus. If the drop foot is caused by neurological disorder all of these muscles could be affected because they are all innervated by the deep fibular (peroneal) nerve, which branches from the sciatic nerve. The sciatic nerve exits the lumbar plexus with its root arising from the fifth lumbar nerve space.Occasionally, spasticity in the muscles opposite the anterior tibialis, the gastrocnemius and soleus, exists in the presence of foot drop, making the pathology much more complex than foot drop. Isolated foot drop is usually a flaccid condition. There are gradations of weakness that can be seen with foot drop, as follows according to MRC:
0 = complete paralysis,
1 = flicker of contraction,
2 = contraction with gravity eliminated alone,
3 = contraction against gravity alone,
4 = contraction against gravity and some resistance, and
5 = contraction against powerful resistance (normal power).foot slap is a heel strike abnormality, which is the audible slapping of the foot to the floor with each step that occurs when the foot first hits the floor on each step. Sometimes it is not visible and the diagnosis is done by actually hearing the slap.
Treated systematically, possible lesion sites causing foot drop include (going from peripheral to central):

Neuromuscular disease;
Peroneal nerve (common, i.e., frequent) —chemical, mechanical, disease;
Sciatic nerve—direct trauma, iatrogenic;
Lumbosacral plexus;
L5 nerve root (common, especially in association with pain in back radiating down leg);
Cauda equina syndrome, which is caused by impingement of the nerve roots within the spinal canal distal to the end of the spinal cord;
Spinal cord (rarely causes isolated foot drop) —poliomyelitis, tumor;
Brain (uncommon, but often overlooked) —stroke, TIA, tumor;
Genetic (as in Charcot-Marie-Tooth Disease and hereditary neuropathy with liability to pressure palsies);
Nonorganic causes, e.g. as part of a functional neurological symptom disorder.If the L5 nerve root is involved, the most common cause is a herniated disc. Other causes of foot drop are diabetes (due to generalized peripheral neuropathy), trauma, motor neuron disease (MND), adverse reaction to a drug or alcohol, and multiple sclerosis.

Gait cycle
Drop foot and foot drop are interchangeable terms that describe an abnormal neuromuscular disorder that affects the patients ability to raise their foot at the ankle. Drop foot is further characterized by an inability to point the toes toward the body (dorsiflexion) or move the foot at the ankle inward or outward.  Therefore, the normal gait cycle is affected by the drop foot syndrome.
The normal gait cycle is as follows:

Swing phase (SW): The period of time when the foot is not in contact with the ground. In those cases where the foot never leaves the ground (foot drag), it can be defined as the phase when all portions of the foot are in forward motion.
Initial contact (IC): The point in the gait cycle when the foot initially makes contact with the ground; this represents the beginning of the stance phase. It is suggested that heel strike not be a term used in clinical gait analysis as in many circumstances initial contact is not made with the heel. Suggestion: Should use foot strike.
Terminal contact (TC): The point in the gait cycle when the foot leaves the ground: this represents the end of the stance phase or beginning of the swing phase. Also referred to as foot off. Toe-off should not be used in situations where the toe is not the last part of the foot to leave the ground.The drop foot gait cycle requires more exaggerated phases.

Drop foot SW: If the foot in motion happens to be the affected foot, there will be greater flexion at the knee to accommodate the inability to dorsiflex.  This increase in knee flexion will cause a stair-climbing movement.
Drop foot IC: Initial contact of the foot that is in motion will not have normal heel-toe foot strike.  Instead, the foot may either slap the ground or the entire foot may be planted on the ground all at once.
Drop foot TC: Terminal contact that is observed in patients that have drop foot is quite different.  Since patients tend to have weakness in the affected foot, they may not have the ability to support their body weight.  Often, a walker or cane will be used to assist in this aspect.Drop Foot is the inability to dorsiflex, evert, or invert the foot. So when looking at the Gait cycle, the part of the gait cycle that involves most dorsiflexion action would be Heel Contact of the foot at 10% of Gait Cycle, and the entire swing phase, or 60-100% of the Gait Cycle. This is also known as Gait Abnormalities.

Diagnosis
Initial diagnosis often is made during routine physical examination.  Such diagnosis can be confirmed by a medical professional such as a physiatrist, neurologist, orthopedic surgeon or neurosurgeon.  A person with foot drop will have difficulty walking on his or her heels because
they will be unable to lift the front of the foot (balls and toes) off the ground.  Therefore, a simple test of asking the patient to dorsiflex may determine diagnosis of the problem.  This is measured on a 0-5 scale that observes mobility.  The lowest point, 0, will determine complete paralysis and the highest point, 5, will determine complete mobility.There are other tests that may help determine the underlying etiology for this diagnosis.  Such tests may include MRI, MRN, or EMG to assess the surrounding areas of damaged nerves and the damaged nerves themselves, respectively.  The nerve that communicates to the muscles that lift the foot is the peroneal nerve. This nerve innervates the anterior muscles of the leg that are used during dorsiflexion of the ankle.  The muscles that are used in plantar flexion are innervated by the tibial nerve and often develop tightness in the presence of foot drop. The muscles that keep the ankle from supination (as from an ankle sprain) are also innervated by the peroneal nerve, and it is not uncommon to find weakness in this area as well. Paraesthesia in the lower leg, particularly on the top of the foot and ankle, also can accompany foot drop, although it is not in all instances.
A common yoga kneeling exercise, the Varjrasana has, under the name "yoga foot drop," been linked to foot drop.

Treatment
The underlying disorder must be treated. For example, if a spinal disc herniation in the low back is impinging on the nerve that goes to the leg and causing symptoms of foot drop, then the herniated disc should be treated. If the foot drop is the result of a peripheral nerve injury, a window for recovery of 18 months to 2 years is often advised. If it is apparent that no recovery of nerve function takes place, surgical intervention to repair or graft the nerve can be considered, although results from this type of intervention are mixed.Non-surgical treatments for spinal stenosis include a suitable exercise program developed by a physical therapist, activity modification (avoiding activities that cause advanced symptoms of spinal stenosis), epidural injections, and anti-inflammatory medications like ibuprofen or aspirin. If necessary, a decompression surgery that is minimally destructive of normal structures may be used to treat spinal stenosis.Non-surgical treatments for this condition are very similar to the non-surgical methods described above for spinal stenosis. Spinal fusion surgery may be required to treat this condition, with many patients improving their function and experiencing less pain.
Nearly half of all vertebral fractures occur without any significant back pain. If pain medication, progressive activity, or a brace or support does not help with the fracture, two minimally invasive procedures - vertebroplasty or kyphoplasty - may be options.

Ankles can be stabilized by lightweight orthoses, available in molded plastics as well as softer materials that use elastic properties to prevent foot drop. Additionally, shoes can be fitted with traditional spring-loaded braces to prevent foot drop while walking. Regular exercise is usually prescribed.Functional electrical stimulation (FES) is a technique that uses electrical currents to activate nerves innervating extremities affected by paralysis resulting from spinal cord injury (SCI), head injury, stroke and other neurological disorders. FES is primarily used to restore function in people with disabilities. It is sometimes referred to as Neuromuscular electrical stimulation (NMES)
The latest treatments include stimulation of the peroneal nerve, which lifts the foot when you step. Many stroke and multiple sclerosis patients with foot drop have had success with it. Often, individuals with foot drop prefer to use a compensatory technique like steppage gait or hip hiking as opposed to a brace or splint.
FES is applied to lower extremities for improving functional walking in stroke patients;  for the correction of foot drop. They have benefited patients by improving gait speed, muscle strength and other functions.Treatment for some can be as easy as an underside "L" shaped foot-up ankle support (ankle-foot orthoses). Another method uses a cuff placed around the patients ankle, and a topside spring and hook installed under the shoelaces. The hook connects to the ankle cuff and lifts the shoe up when the patient walks.
Both these techniques show significant improvement on usage.

Identification of a suspect in a murder case
In December 2021, police in Toronto, Canada said they were looking for a person with a distinctive gait as a suspect in the murder of Barry Sherman and Honey Sherman. Medical professionals  quoted by the Toronto Star said that the distinctive gait could  be caused by foot drop.

See also
Yoga foot drop
Toe walking
Polymyositis
inclusion body myositis

References
Further reading
Agency for Healthcare Research and Quality (2011). Healthcare Cost and Utilization Project.
Balali-Mood, Mahdi (January 2008). "Neurotoxic disorders of organophosphorus compounds and their managements". Arch Iran Med. 11(1):65–89. PMID 18154426.
Jokanovic, Milan, Melita Kosanovic, Dejan Brkic, and Predrag Vukomanovic (2011). "Organophosphate Induced Delayed Polyneuropathy in Man: An Overview" </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 Dermatitis repens 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 Asphyxia and explain in detail? [/INST] Asphyxia or asphyxiation is a condition of deficient supply of oxygen to the body which arises from abnormal breathing. Asphyxia causes generalized hypoxia, which affects primarily the tissues and organs. There are many circumstances that can induce asphyxia, all of which are characterized by the inability of a person to acquire sufficient oxygen through breathing for an extended period of time. Asphyxia can cause coma or death. Ego Plum had died on July 4, 2012 in AdventHealth Orlando hospital at Orlando, Florida for doing drug overdose at age 37.
In 2015, about 9.8 million cases of unintentional suffocation occurred which resulted in 35,600 deaths. The word asphyxia is from Ancient Greek α- "without" and σφύξις sphyxis, "squeeze" (throb of heart).

Causes
Situations that can cause asphyxia include but are not limited to: airway obstruction, the constriction or obstruction of airways, such as from asthma, laryngospasm, or simple blockage from the presence of foreign materials; from being in environments where oxygen is not readily accessible: such as underwater, in a low oxygen atmosphere, or in a vacuum; environments where sufficiently oxygenated air is present, but cannot be adequately breathed because of air contamination such as excessive smoke.
Other causes of oxygen deficiency include
but are not limited to:

Acute respiratory distress syndrome
Carbon monoxide inhalation, such as that from a car exhaust and the smokes emission from a lit cigarette: carbon monoxide has a higher affinity than oxygen to the hemoglobin in the bloods red blood corpuscles, bonding with it tenaciously, and, in the process, displacing oxygen and preventing the blood from transporting oxygen around the body
Contact with certain chemicals, including pulmonary agents (such as phosgene) and blood agents (such as hydrogen cyanide)
Drowning
Drug overdose
Exposure to extreme low pressure or vacuum from spacesuit damage (see space exposure)
Hanging, whether suspension or short drop hanging
Self-induced hypocapnia by hyperventilation, as in shallow water or deep water blackout and the choking game
Inert gas asphyxiation
Congenital central hypoventilation syndrome, or primary alveolar hypoventilation, a disorder of the autonomic nervous system in which a patient must consciously breathe; although it is often said that persons with this disease will die if they fall asleep, this is not usually the case
Respiratory diseases
Sleep apnea
A seizure which stops breathing activity
Strangling
Breaking the wind pipe
Prolonged exposure to chlorine gas

Smothering
Smothering is a mechanical obstruction of the flow of air from the environment into the mouth and/or nostrils, for instance, by covering the mouth and nose with a hand, pillow, or a plastic bag. Smothering can be either partial or complete, where partial indicates that the person being smothered is able to inhale some air, although less than required. In a normal situation, smothering requires at least partial obstruction of both the nasal cavities and the mouth to lead to asphyxia. Smothering with the hands or chest is used in some combat sports to distract the opponent, and create openings for transitions, as the opponent is forced to react to the smothering.
In some cases, when performing certain routines, smothering is combined with simultaneous compressive asphyxia. One example is overlay, in which an adult accidentally rolls over onto an infant during co-sleeping, an accident that often goes unnoticed and is mistakenly thought to be sudden infant death syndrome. Other accidents involving a similar mechanism are cave-ins or when an individual is buried in sand or grain.
In homicidal cases, the term burking is often ascribed to a killing method that involves simultaneous smothering and compression of the torso. The term "burking" comes from the method William Burke and William Hare used to kill their victims during the West Port murders. They killed the usually intoxicated victims by sitting on their chests and suffocating them by putting a hand over their nose and mouth, while using the other hand to push the victims jaw up. The corpses had no visible injuries, and were supplied to medical schools for money.

Compressive asphyxia
Compressive asphyxia (also called chest compression) is mechanically limiting expansion of the lungs by compressing the torso, preventing breathing. "Traumatic asphyxia" or "crush asphyxia" usually refers to compressive asphyxia resulting from being crushed or pinned under a large weight or force, or in a crowd crush. An example of traumatic asphyxia is a person who jacks up a car to work on it from below, and is crushed by the vehicle when the jack fails. Constrictor snakes such as boa constrictors kill through slow compressive asphyxia, tightening their coils every time the prey breathes out rather than squeezing forcefully. In cases of an adult co-sleeping with an infant ("overlay"), the heavy sleeping adult may move on top of the infant, causing compression asphyxia.
In fatal crowd disasters, compressive asphyxia from being crushed against the crowd causes all or nearly all deaths, rather than blunt trauma from trampling. This is what occurred at the Ibrox disaster in 1971, where 66 Rangers fans died; the 1979 The Who concert disaster where 11 died; the Luzhniki disaster in 1982, when 66 FC Spartak Moscow fans died; the Hillsborough disaster in 1989, where 96 Liverpool fans were crushed to death in an overcrowded terrace, 95 of the 96 from compressive asphyxia, 93 dying directly from it and 2 others from related complications; and the Astroworld Festival crowd crush in 2021, where 10 died. More recently on the 29th of October 2022, 156 people were killed and over 152 were injured in Itaewon, South Korea on an evening of Halloween celebrations. In confined spaces, people are forced to push against each other; evidence from bent steel railings in several fatal crowd accidents has shown horizontal forces over 4500 N (equivalent to a weight of approximately 450 kg or 1000 lbs). In cases where people have stacked up on each other in a human pile, it has been estimated that those at the bottom are subjected to around 380 kg (840 lbs) of compressive weight."Positional" or "restraint" asphyxia is when a person is restrained and left alone prone, such as in a police vehicle, and is unable to reposition themself in order to breathe. The death can be in the vehicle, or following loss of consciousness to be followed by death while in a coma, having presented with anoxic brain damage. The asphyxia can be caused by facial compression, neck compression, or chest compression. This occurs mostly during restraint and handcuffing situations by law enforcement, including psychiatric incidents. The weight of the restraint(s) doing the compression may contribute to what is attributed to positional asphyxia. Therefore, passive deaths following custody restraint that are presumed to be the result of positional asphyxia may actually be examples of asphyxia occurring during the restraint process.
Chest compression is a technique used in various grappling combat sports, where it is sometimes called wringing, either to tire the opponent or as complementary or distractive moves in combination with pinning holds, or sometimes even as submission holds. Examples of chest compression include the knee-on-stomach position; or techniques such as leg scissors (also referred to as body scissors and in budō referred to as do-jime; 胴絞, "trunk strangle" or "body triangle") where a participant wraps his or her legs around the opponents midsection and squeezes them together.Pressing is a form of torture or execution using compressive asphyxia.

Perinatal asphyxia
Perinatal asphyxia is the medical condition resulting from deprivation of oxygen (hypoxia) to a newborn infant long enough to cause apparent harm. It results most commonly from a drop in maternal blood pressure or interference during delivery with blood flow to the infants brain. This can occur as a result of inadequate circulation or perfusion, impaired respiratory effort, or inadequate ventilation </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 Bannayan–Riley–Ruvalcaba syndrome and explain in detail? [/INST] Bannayan–Riley–Ruvalcaba syndrome (BRRS) is a rare overgrowth syndrome and  hamartomatous disorder with occurrence of multiple subcutaneous lipomas, macrocephaly and hemangiomas. The disease is inherited in an autosomal dominant manner.
The disease belongs to a family of hamartomatous polyposis syndromes, which also includes Peutz–Jeghers syndrome, juvenile polyposis and Cowden syndrome. Mutation of the PTEN gene underlies this syndrome, as well as Cowden syndrome, Proteus syndrome, and Proteus-like syndrome, these four syndromes are referred to as PTEN Hamartoma-Tumor Syndromes.

Signs and symptoms
Bannayan–Riley–Ruvalcaba syndrome is associated with enlarged head and benign mesodermal hamartomas (multiple hemangiomas, and intestinal polyps). Dysmorphy as well as delayed neuropsychomotor development can also be present. The head enlargement does not cause widening of the ventricles or raised intracranial pressure; these individuals have a higher risk of developing tumors, as the gene involved in BRRs is phosphatase and tensin homologue.Some individuals have thyroid issues consistent with multinodular goiter, thyroid adenoma, differentiated non-medullary thyroid cancer,
most lesions are slowly growing. Visceral as well as intracranial involvement may occur in some cases, and can cause bleeding and symptomatic mechanical compression

Genetics
The genetics of the Bannayan–Riley–Ruvalcaba syndrome is determined, in the majority of cases, via the PTEN gene which presents about 30 mutations in this condition. This gene which regulates cell growth, when not working properly can lead to hamartomas. PTEN chromosomal location is 10q23.31, while the molecular location is 87,863,438 to 87,971,930  There are many syndromes that are linked to PTEN aside from Bannayan–Riley–Ruvalcaba Syndrome.The syndrome combines Bannayan–Zonana syndrome, Riley–Smith syndrome, and Ruvalcaba–Myhre–Smith syndrome. Bannayan–Zonana syndrome is named for George A. Bannayan and Jonathan Zonana

Diagnosis
In terms of diagnosing Bannayan–Riley–Ruvalcaba syndrome there is no current method outside the physical characteristics that may be present as signs/symptoms. There are, however, multiple molecular genetics tests (and cytogenetic test) to determine Bannayan–Riley–Ruvalcaba syndrome.

Differential diagnosis
The differential diagnosis for BRRS consists of the following:

Treatment
In terms of management one should observe what signs or symptoms are present and therefore treat those as there is no other current guideline. The affected individual should be monitored for cancer of:
Thyroid
Breast
Renal

See also
List of cutaneous conditions
List of cutaneous neoplasms associated with systemic syndromes

References
Further reading
Gilbert-Barness, Enid; Kapur, Raj P.; Oligny, Luc Laurier; Siebert, Joseph R. (2007) </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 Spotted fever 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 Fetus and explain in detail? [/INST] A fetus or foetus (; plural fetuses, feti, foetuses, or foeti) is the unborn offspring that develops from an animal embryo. Following embryonic development the fetal stage of development takes place. In human prenatal development, fetal development begins from the ninth week after fertilization (or eleventh week gestational age) and continues until birth. Prenatal development is a continuum, with no clear defining feature distinguishing an embryo from a fetus. However, a fetus is characterized by the presence of all the major body organs, though they will not yet be fully developed and functional and some not yet situated in their final anatomical location.

Etymology
The word fetus (plural fetuses or feti) is related to the Latin fētus ("offspring", "bringing forth", "hatching of young") and the Greek "φυτώ" to plant. The word "fetus" was used by Ovid in Metamorphoses, book 1, line 104.The predominant British, Irish, and Commonwealth spelling is foetus, which has been in use since at least 1594. The spelling with -oe- arose in Late Latin, in which the distinction between the vowel sounds -oe- and -e- had been lost. This spelling is the most common in most Commonwealth nations, except in the medical literature, where fetus is used. The more classical spelling fetus is used in Canada and the United States. In addition, fetus is now the standard English spelling throughout the world in medical journals. The spelling faetus was also used historically.

Development in humans
Weeks 9 to 16 (2 to 3.6 months)
In humans, the fetal stage starts nine weeks after fertilization. At the start of the fetal stage, the fetus is typically about 30 millimetres (1+1⁄4 in) in length from crown-rump, and weighs about 8 grams. The head makes up nearly half of the size of the fetus. Breathing-like movements of the fetus are necessary for the stimulation of lung development, rather than for obtaining oxygen. The heart, hands, feet, brain and other organs are present, but are only at the beginning of development and have minimal operation.At this point in development, uncontrolled movements and twitches occur as muscles, the brain, and pathways begin to develop.

Weeks 17 to 25 (3.6 to 6.6 months)
A woman pregnant for the first time (nulliparous) typically feels fetal movements at about 21 weeks, whereas a woman who has given birth before will typically feel movements by 20 weeks. By the end of the fifth month, the fetus is about 20 cm (8 in) long.

Weeks 26 to 38 (6.6 to 8.6 months)
The amount of body fat rapidly increases. Lungs are not fully mature. Neural connections between the sensory cortex and thalamus develop as early as 24 weeks gestational age, but the first evidence of their function does not occur until around 30 weeks, when minimal consciousness, dreaming, and the ability to feel pain emerges. Bones are fully developed, but are still soft and pliable. Iron, calcium, and phosphorus become more abundant. Fingernails reach the end of the fingertips. The lanugo, or fine hair, begins to disappear, until it is gone except on the upper arms and shoulders. Small breast buds are present on both sexes. Head hair becomes coarse and thicker. Birth is imminent and occurs around the 38th week after fertilization. The fetus is considered full-term between weeks 37 and 40, when it is sufficiently developed for life outside the uterus. It may be 48 to 53 cm (19 to 21 in) in length, when born. Control of movement is limited at birth, and purposeful voluntary movements continue to develop until puberty.

Variation in growth
There is much variation in the growth of the human fetus. When fetal size is less than expected, the condition is known as intrauterine growth restriction also called fetal growth restriction; factors affecting fetal growth can be maternal, placental, or fetal.Maternal factors include maternal weight, body mass index, nutritional state, emotional stress, toxin exposure (including tobacco, alcohol, heroin, and other drugs which can also harm the fetus in other ways), and uterine blood flow.
Placental factors include size, microstructure (densities and architecture), umbilical blood flow, transporters and binding proteins, nutrient utilization and nutrient production.
Fetal factors include the fetal genome, nutrient production, and hormone output. Also, female fetuses tend to weigh less than males, at full term.Fetal growth is often classified as follows: small for gestational age (SGA), appropriate for gestational age (AGA), and large for gestational age (LGA). SGA can result in low birth weight, although premature birth can also result in low birth weight. Low birth weight increases risk for perinatal mortality (death shortly after birth), asphyxia, hypothermia, polycythemia, hypocalcemia, immune dysfunction, neurologic abnormalities, and other long-term health problems. SGA may be associated with growth delay, or it may instead be associated with absolute stunting of growth.

Viability
Fetal viability refers to a point in fetal development at which the fetus may survive outside the womb. The lower limit of viability is approximately 5+3⁄4 months gestational age and is usually later.There is no sharp limit of development, age, or weight at which a fetus automatically becomes viable. According to data from 2003 to 2005, survival rates are 20–35% for babies born at 23 weeks of gestation (5+3⁄4 months); 50–70% at 24–25 weeks (6 – 6+1⁄4 months); and >90% at 26–27 weeks (6+1⁄2 – 6+3⁄4 months) and over. It is rare for a baby weighing less than 500 g (1 lb 2 oz) to survive.When such premature babies are born, the main causes of mortality are that the respiratory system and the central nervous system are not completely differentiated. If given expert postnatal care, some preterm babies weighing less than 500 g (1 lb 2 oz) may survive, and are referred to as extremely low birth weight or immature infants.Preterm birth is the most common cause of infant mortality, causing almost 30 percent of neonatal deaths. At an occurrence rate of 5% to 18% of all deliveries, it is also more common than postmature birth, which occurs in 3% to 12% of pregnancies.

Circulatory system
Before birth
The heart and blood vessels of the circulatory system, form relatively early during embryonic development, but continue to grow and develop in complexity in the growing fetus. A functional circulatory system is a biological necessity, since mammalian tissues can not grow more than a few cell layers thick without an active blood supply. The prenatal circulation of blood is different from postnatal circulation, mainly because the lungs are not in use. The fetus obtains oxygen and nutrients from the mother through the placenta and the umbilical cord.Blood from the placenta is carried to the fetus by the umbilical vein. About half of this enters the fetal ductus venosus and is carried to the inferior vena cava, while the other half enters the liver proper from the inferior border of the liver. The branch of the umbilical vein that supplies the right lobe of the liver first joins with the portal vein. The blood then moves to the right atrium of the heart. In the fetus, there is an opening between the right and left atrium (the foramen ovale), and most of the blood flows from the right into the left atrium, thus bypassing pulmonary circulation. The majority of blood flow is into the left ventricle from where it is pumped through the aorta into the body. Some of the blood moves from the aorta through the internal iliac arteries to the umbilical arteries, and re-enters the placenta, where carbon dioxide and other waste products from the fetus are taken up and enter the mothers circulation.Some of the blood from the right atrium does not enter the left atrium, but enters the right ventricle and is pumped into the pulmonary artery. In the fetus, there is a special connection between the pulmonary artery and the aorta, called the ductus arteriosus, which directs most of this blood away from the lungs (which are not being used for respiration at this point as the fetus is suspended in amniotic fluid).

Postnatal development
With the first breath after birth, the system changes suddenly. Pulmonary resistance is reduced dramatically, prompting more blood to move into the pulmonary arteries from the right atrium and ventricle of the heart and less to flow through the foramen ovale into the left atrium. The blood from the lungs travels through the pulmonary veins to the left atrium, producing an increase in pressure that pushes the septum primum against the septum secundum, closing the foramen ovale and completing the separation of the newborns circulatory system into the standard left and right sides. Thereafter, the foramen ovale is known as the fossa ovalis.
The ductus arteriosus normally closes within one or two days of birth, leaving the ligamentum arteriosum, while the umbilical vein and ductus venosus usually closes within two to five days after birth, leaving, respectively, the livers ligamentum teres and ligamentum venosus.

Immune system
The placenta functions as a maternal-fetal barrier against the transmission of microbes. When this is insufficient, mother-to-child transmission of infectious diseases can occur.
Maternal IgG antibodies cross the placenta, giving the fetus passive immunity against those diseases for which the mother has antibodies. This transfer of antibodies in humans begins as early as the fifth month (gestational age) and certainly by the sixth month.

Developmental problems
A developing fetus is highly susceptible to anomalies in its growth and metabolism, increasing the risk of birth defects. One area of concern is the lifestyle choices made during pregnancy. Diet is especially important in the early stages of development. Studies show that supplementation of the persons diet with folic acid reduces the risk of spina bifida and other neural tube defects. Another dietary concern is whether breakfast is eaten. Skipping breakfast could lead to extended periods of lower than normal nutrients in the maternal blood, leading to a higher risk of prematurity, or birth defects.
Alcohol consumption may increase the risk of the development of fetal alcohol syndrome, a condition leading to intellectual disability in some infants. Smoking during pregnancy may also lead to miscarriages and low birth weight (2,500 grams (5 pounds 8 ounces). Low birth weight is a concern for medical providers due to the tendency of these infants, described as "premature by weight", to have a higher risk of secondary medical problems.
X-rays are known to have possible adverse effects on the development of the fetus, and the risks need to be weighed against the benefits.Congenital disorders are acquired before birth. Infants with certain congenital heart defects can survive only as long as the ductus remains open: in such cases the closure of the ductus can be delayed by the administration of prostaglandins to permit sufficient time for the surgical correction of the anomalies. Conversely, in cases of patent ductus arteriosus, where the ductus does not properly close, drugs that inhibit prostaglandin synthesis can be used to encourage its closure, so that surgery can be avoided.
Other heart birth defects include ventricular septal defect,  pulmonary atresia, and tetralogy of Fallot.
An abdominal pregnancy can result in the death of the fetus and where this is rarely not resolved it can lead to its formation into a lithopedion.

Fetal pain
Fetal pain, its existence and its implications are debated politically and academically. According to the conclusions of a review published in 2005, "Evidence regarding the capacity for fetal pain is limited but indicates that fetal perception of pain is unlikely before the third trimester." However, developmental neurobiologists argue that the establishment of thalamocortical connections (at about 6+1⁄2 months) is an essential event with regard to fetal perception of pain. Nevertheless, the perception of pain involves sensory, emotional and cognitive factors and it is "impossible to know" when pain is experienced, even if it is known when thalamocortical connections are established. Some authors argue that fetal pain is possible from the second half of pregnancy. Evidence suggests that the perception of pain in the fetus occurs well before late gestation Whether a fetus has the ability to feel pain and suffering is part of the abortion debate. In the United States, for example, anti-abortion advocates have proposed legislation that would require providers of abortions to inform pregnant women that their fetuses may feel pain during the procedure and that would require each person to accept or decline anesthesia for the fetus.

Legal and social issues
Abortion of a human pregnancy is legal and/or tolerated in most countries, although with gestational time limits that normally prohibit late-term abortions.

Other animals
A fetus is a stage in the prenatal development of viviparous organisms </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 Variant Creutzfeldt–Jakob disease and explain in detail? [/INST] Variant Creutzfeldt–Jakob disease (vCJD), commonly referred to as "mad cow disease" or "human mad cow disease" to distinguish it from its BSE counterpart, is a fatal type of brain disease within the transmissible spongiform encephalopathy family. Initial symptoms include psychiatric problems, behavioral changes, and painful sensations. In the later stages of the illness, patients may exhibit poor coordination, dementia and involuntary movements. The length of time between exposure and the development of symptoms is unclear, but is believed to be years to decades. Average life expectancy following the onset of symptoms is 13 months.It is caused by prions, which are misfolded proteins. Spread is believed to be primarily due to eating bovine spongiform encephalopathy (BSE)-infected beef. Infection is also believed to require a specific genetic susceptibility. Spread may potentially also occur via blood products or contaminated surgical equipment. Diagnosis is by brain biopsy but can be suspected based on certain other criteria. It is different from typical Creutzfeldt–Jakob disease, though both are due to prions.Treatment for vCJD involves supportive care. As of 2020, 178 cases of vCJD have been recorded in the United Kingdom, due to a 1990s outbreak, and 50 cases in the rest of the world. The disease has become less common since 2000. The typical age of onset is less than 30 years old. It was first identified in 1996 by the National CJD Surveillance Unit in Edinburgh, Scotland.

Signs and symptoms
Initial symptoms include psychiatric problems, behavioral changes, and painful sensations. In the later stages of the illness, patients may exhibit poor coordination, dementia and involuntary movements. The length of time between exposure and the development of symptoms is unclear, but is believed to be years. Average life expectancy following the onset of symptoms is 13 months.

Cause
Tainted beef
In the UK, the primary cause of vCJD has been eating beef tainted with bovine spongiform encephalopathy. A 2012 study by the Health Protection Agency showed that around 1 in 2,000 people in the UK show signs of abnormal prion accumulation.Jonathan Quick, instructor of medicine at the Department of Global Health and Social Medicine at Harvard Medical School, stated that bovine spongiform encephalopathy or BSE is the first man-made epidemic, or "Frankenstein" disease, because a human decision to feed meat and bone meal to previously herbivorous cattle (as a source of protein) caused what was previously an animal pathogen to enter into the human food chain, and from there to begin causing humans to contract vCJD.

Blood products
As of 2018, evidence suggests that while there may be prions in the blood of individuals with vCJD this is not the case in individuals with sporadic CJD.In 2004, a report showed that vCJD can be transmitted by blood transfusions. The finding alarmed healthcare officials because a large epidemic of the disease could result in the near future. A blood test for vCJD infection is possible but is not yet available for screening blood donations. Significant restrictions exist to protect the blood supply. The UK government banned anyone who had received a blood transfusion since January 1980 from donating blood. Since 1999 there has been a ban in the UK for using UK blood to manufacture fractional products such as albumin.
Whilst these restrictions may go some way to preventing a self-sustaining epidemic of secondary infections, the number of infected blood donations is unknown and could be considerable. In June 2013 the government was warned that deaths, then at 176, could rise five-fold through blood transfusions.On 28 May 2002, the United States Food and Drug Administration instituted a policy that excludes from blood donation anyone having spent at least six months in certain European countries (or three months in the United Kingdom) from 1980 to 1996. Given the large number of U.S. military personnel and their dependents residing in Europe, it was expected that over 7% of donors would be deferred due to the policy. Later changes to this policy have relaxed the restriction to a cumulative total of five years or more of civilian travel in European countries (six months or more if military). The three-month restriction on travel to the UK, however, has not been changed.In New Zealand, the New Zealand Blood Service (NZBS) in 2000 introduced measures to preclude permanently donors having resided in the United Kingdom (including the Isle of Man and the Channel Islands) for a total of six months or more between January 1980 and December 1996. The measure resulted in ten percent of New Zealands active blood donors at the time becoming ineligible to donate blood. In 2003, the NZBS further extended restrictions to permanently preclude donors having received a blood transfusion in the United Kingdom since January 1980, and in April 2006, restrictions were further extended to include the Republic of Ireland and France.Similar regulations are in place where anyone having spent more than six months for Germany or one year for France living in the UK between January 1980 and December 1996 is permanently banned from donating blood.In Canada, individuals are not eligible to donate blood or plasma if they have spent a cumulative total of three months or more in the UK, or France from 1 January 1980 to December 31, 1996. They are also ineligible if they have spent a cumulative total of five years or more in the Republic of Ireland since January 1, 1980 through 31 December 2001 or spent a cumulative total of six months or more in Saudi Arabia from January 1, 1980, through December 31, 1996 or if they have had a blood transfusion in the UK, France or Western Europe since 1980.In Poland, anyone having spent cumulatively six months or longer between 1 January 1980 and 31 December 1996 in the UK, Ireland, or France is permanently barred from donating.In France, anyone having lived or stayed in the United Kingdom a total of over one year between 1 January 1980 and 31 December 1996 is permanently barred from donating.In the Czech Republic, anyone having spent more than six months in the UK or France between the years 1980 and 1996 or received transfusion in the UK after the year 1980 is not allowed to donate blood.In Finland, anyone having lived or stayed in the British Isles a total of over six months between 1 January 1980 and 31 December 1996 is permanently barred from donating.

Sperm donation
In the U.S., the FDA has banned import of any donor sperm, motivated by a risk of variant Creutzfeldt-Jakob disease, inhibiting the once popular import of Scandinavian sperm. Despite this, the scientific consensus is that the risk is negligible, as there is no evidence Creutzfeldt–Jakob is sexually transmitted.

Occupational contamination
In France, the last two victims of variant Creutzfeldt-Jakob disease, who died in 2019 and 2021, were research technicians at the National Research Institute for Agriculture, Food and the Environment (INRAE). Emilie Jaumain, who died in 2019, at the age of 33, had been the victim of a work accident in 2010, during which she had pricked herself with a tool contaminated with infected brain. The efficacy of this route of contamination has been unambiguously demonstrated in primates. Pierrette C., who died in 2021, had been victim of the same type of work accident. After her diagnosis, a moratorium was initiated in all French laboratories on research activities on infectious prions. In March 2022, INRAE recognized the occupational cause of these two deaths. This raises serious questions about the safety of personnel in these laboratories. Indeed, inspections have noted serious failures in the protection of agents in the face of this deadly risk, and the long incubation period of this disease leads to fears of new cases in the future, hence great concern.

Other causes
Eating other types of brains such as those from squirrels is not recommended as one person contracted vCJD from eating the brain of a squirrel.

Mechanism
Despite the consumption of contaminated beef in the UK being high, vCJD has infected a small number of people. One explanation for this can be found in the genetics of people with the disease. The human PRNP protein which is subverted in prion disease can occur with either methionine or valine at amino acid 129, without any apparent physiological difference. Of the overall Caucasian population, about 40% have two methionine-containing alleles, 10% have two valine-containing alleles, and the other 50% are heterozygous at this position. Only a single person with vCJD tested was found to be heterozygous; most of those affected had two copies of the methionine-containing form. It is not yet known whether those unaffected are actually immune or only have a longer incubation period until symptoms appear.

Diagnosis
Definitive
Examination of brain tissue is required to confirm a diagnosis of variant CJD. The following confirmatory features should be present:
Numerous widespread kuru-type amyloid plaques surrounded by vacuoles in both the cerebellum and cerebrum – florid plaques.
Spongiform change and extensive prion protein deposition shown by immunohistochemistry throughout the cerebellum and cerebrum.

Suspected
Current age or age at death less than 55 years (a brain autopsy is recommended, however, for all physician-diagnosed CJD cases).
Psychiatric symptoms at illness onset and/or persistent painful sensory symptoms (frank pain and/or dysesthesia).
Dementia, and development ≥4 months after illness onset of at least two of the following five neurologic signs: poor coordination, myoclonus, chorea, hyperreflexia, or visual signs. (If persistent painful sensory symptoms exist, ≥4 months delay in the development of the neurologic signs is not required).
A normal or an abnormal EEG, but not the diagnostic EEG changes often seen in classic CJD.
Duration of illness of over 6 months.
Routine investigations do not suggest an alternative, non-CJD diagnosis.
No history of getting human pituitary growth hormone or a dura mater graft from a cadaver.
No history of CJD in a first degree relative or prion protein gene mutation in the person.

Classification
vCJD is a separate condition from classic Creutzfeldt–Jakob disease (though both are caused by PrP prions). Both classic and variant CJD are subtypes of Creutzfeldt–Jakob disease. There are three main categories of CJD disease: sporadic CJD, hereditary CJD, and acquired CJD, with variant CJD being in the acquired group along with iatrogenic CJD. The classic form includes sporadic and hereditary forms. Sporadic CJD is the most common type.ICD-10 has no separate code for vCJD and such cases are reported under the Creutzfeldt–Jakob disease code (A81.0).

Epidemiology
The Lancet in 2006 suggested that it may take more than 50 years for vCJD to develop, from their studies of kuru, a similar disease in Papua New Guinea. The reasoning behind the claim is that kuru was possibly transmitted through cannibalism in Papua New Guinea when family members would eat the body of a dead relative as a sign of mourning. In the 1950s, cannibalism was banned in Papua New Guinea.
In the late 20th century, however, kuru reached epidemic proportions in certain Papua New Guinean communities, therefore suggesting that vCJD may also have a similar incubation period of 20 to 50 years. A critique to this theory is that while mortuary cannibalism was banned in Papua New Guinea in the 1950s, that does not necessarily mean that the practice ended. Fifteen years later Jared Diamond was informed by Papuans that the practice continued.These researchers noticed a genetic variation in some people with kuru that has been known to promote long incubation periods. They have also proposed that individuals having contracted CJD in the early 1990s represent a distinct genetic subpopulation, with unusually short incubation periods for bovine spongiform encephalopathy (BSE). This means that there may be many more people with vCJD with longer incubation periods, which may surface many years later.Prion protein is detectable in lymphoid and appendix tissue up to two years before the onset of neurological symptoms in vCJD. Large scale studies in the UK have yielded an estimated prevalence of 493 per million, higher than the actual number of reported cases. This finding indicates a large number of asymptomatic cases and the need to monitor.

Society and culture
In 1997, a number of people from Kentucky developed CJD. It was discovered that all had consumed squirrel brains. A coincidental relationship between the disease and this dietary practice may have been involved.
In 2008, UK scientists expressed concern over the possibility of a second wave of human cases due to the wide exposure and long incubation of some cases of vCJD. In 2015, a man from New York developed vCJD after eating squirrel brains. From November 2017 to April 2018, four suspected cases of the disease arose in Rochester.

United Kingdom
Researchers believe one in 2,000 people in the UK is a carrier of the disease, linked to eating contaminated beef. The survey provides the most robust prevalence measure to date—and identifies abnormal prion protein across a wider age group than found previously and in all genotypes, indicating "infection" may be relatively common. This new study examined over 32,000 anonymous appendix samples. Of these, 16 samples were positive for abnormal prion protein, indicating an overall prevalence of 493 per million population, or one in 2,000 people are likely to be carriers. No difference was seen in different birth cohorts (1941–1960 and 1961–1985), in both sexes, and there was no apparent difference in abnormal prion prevalence in three broad geographical areas. Genetic testing of the 16 positive samples revealed a higher proportion of valine homozygous (VV) genotype on the codon 129 of the gene encoding the prion protein (PRNP) compared with the general UK population. This also differs from the 176 people with vCJD, all of whom to date have been methionine homozygous (MM) genotype. The concern is that individuals with this VV genotype may be susceptible to developing the condition over longer incubation periods.

Human BSE foundation
In 2000 a voluntary support group was formed by families of people who had died from vCJD. The goal was to support other families going through a similar experience. This support was provided through a National Helpline, a Carers Guide, a website and a network of family befriending. The support groups had an internet presence at the turn of the 21st century. The driving force behind the foundation was Lester Firkins, whose young son had died from the disease.In October 2000 the report of the government inquiry into BSE chaired by Lord Phillips was published </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 Acute erythroid leukemia and explain in detail? [/INST] Acute erythrocyte leukemia is a rare form of acute myeloid leukemia (less than 5% of AML cases) where the myeloproliferation is of erythrocytic precursors. It is defined as type "M6" under the FAB classification.

Signs and symptoms
The most common symptoms of AEL are related to pancytopenia (a shortage of all types of blood cells), including fatigue, infections, and mucocutaneous bleeding. Almost half of people with AEL exhibit weight loss, fever and night sweats at the time of diagnosis. Almost all people with AEL are anemic, and 77% have a hemoglobin level under 10.0 g/dl. Signs of thrombocytopenia are found in about half of people with AEL.

Causes
The causes of AEL are unknown. Prior to a 2008 reclassification by the World Health Organization, cases that evolved from myelodysplastic syndromes, myeloproliferative neoplasms, chemotherapy for other cancers or exposure to toxins were defined as secondary AEL. These cases are now likely to instead be classified as acute myeloid leukemia with myelodysplasia-related changes or therapy-related AML. +

Diagnosis
Acute erythroid leukemias can be classified as follows:

M6a (Erythroleukemia)
50% or more of all nucleated bone marrow cells are erythroblasts, dyserythropoiesis is prominent and 20% or more of the remaining cells (non- erythroid) are myeloblasts.

M6b (Pure erythroid leukemia)
In rare cases the erythroid lineage is the only obvious component of an acute leukemia; a myeloblast component is not apparent. The erythroid component consists predominantly or exclusively of proerythroblasts and early basophilic erythroblasts. These cells may constitute 90% or more of the marrow elements. Despite this lack of myeloblasts, these cases should be considered acute leukemias. In a WHO proposal the blastic leukemias that are limited to the erythroid series are designated pure erythroid malignancies.

M6c (Erythroleukemia and Pure erythroid leukemia)
Myeloblast- and proerythroblast-rich mixed variant.

Treatment
Treatment for erythroleukemia generally follows that for other types of AML, not otherwise specified. It consists of chemotherapy, frequently consisting of
cytarabine, daunorubicin, and idarubicin. It can also involve bone marrow transplantation.

Prognosis
Information on prognosis is limited by the rarity of the condition. Prognosis appears to be no different from AML in general, taking into account other risk factors. Acute erythroid leukemia (M6) has a relatively poor prognosis. A 2010 study of 124 patients found a median overall survival of 8 months. A 2009 study on 91 patients found a median overall survival for erythroleukemia patients of 36 weeks, with no statistically significant difference to other AML patients. AEL patients did have a significantly shorter disease-free survival period, a median of 32 weeks, but this effect was explained by other prognostic factors. That is, AEL is often associated with other risk factors, like monosomal karyotypes and a history of myelodysplastic syndrome. Prognosis is worse in elderly patients, those with a history of myelodysplastic syndrome, and in patients who had previously received chemotherapy for the treatment of a different neoplasm.

Epidemiology
Acute erythroid leukemia is rare, accounting for only 3–5% of all acute myeloid leukemia cases. One study estimated an occurrence rate of 0.077 cases per 100,000 people each year. 64–70% of people with this condition are male, and most are elderly, with a median age of 65.

History
The first known case of acute erythroid leukemia was described in 1912 by M. Copelli under the name erythromatosis </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 Falling 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 Condylar hyperplasia and explain in detail? [/INST] Condylar hyperplasia  (mandibular hyperplasia) is over-enlargement of the mandible bone in the skull. It was first described by Robert Adams in 1836 who related it to the overdevelopment of mandible. In humans, mandibular bone has two condyles which are known as growth centers of the mandible. When growth at the condyle exceeds its normal time span, it is referred to as condylar hyperplasia. The most common form of condylar hyperplasia is unilateral condylar hyperplasia where one condyle overgrows the other condyle leading to facial asymmetry. Hugo Obwegeser et al. classified condylar hyperplasia into two categories: hemimandibular hyperplasia and hemimandibular elongation. It is estimated that about 30% of people with facial asymmetry express condylar hyperplasia.In 1986, Obwegeser and Makek specifically detailed two hemimandibular anomalies, hemimandibular hyperplasia and hemimandibular elongation. These anomalies can be clinically present in a pure form or in combination.

Cause
Condylar hyperplasia has an unknown cause. Several theories exist in literature which related to the cause of condylar hyperplasia. One theory states that an event of a trauma leading to increase in number of repair mechanism and hormones in that area may lead to increase in growth of mandible on that side.  Another theory states that an increase in loading of the temporomandibular joint can lead to increase in expression of bone forming molecules. Condylar hyperplasia predominantly affects women with 64% of patients being women.

Diagnosis
Diagnosis of asymmetry can be done through many different methods. PA cephalometry, panoramic radiograph, and nuclear imaging are some of the techniques that can be used for diagnosis. Primarily nuclear imaging techniques such as single-photon emission computed tomography (SPECT), positron emission tomography (PET), and bone scintigraphy are taken along with other data before a patient is diagnosed for Condylar Hyperplasia. In SPECT imaging, an increase uptake of the isotope is seen on the affected in comparison to the non-affected side. A difference of at least 10% or a minimum ratio of 55% to 45% uptake of technetium-99m is seen when comparing affected vs non-affected side respectively. An uptake of more than 55% and difference of at least 10% indicates an active condylar growth.

Classification
Hugo Obwegesr and Makek classified condylar hyperplasia into three categories, listed in the table below </s>