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Spinal Muscular Atrophy Type 3

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Last Updated: 02 July 2021

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This information sheet briefly explains the cause, effects, and management of Spinal Muscular Atrophy Type 3. It includes sources of further information and support. It is written for families of children diagnosed with SMA Type 3. It may also be useful for healthcare and other professionals. Sma Type 3 is a complex condition; there is a lot of information to take in, and every child with SMA is different. Your children's medical team will always be happy to go over any of this with you. Sma Type 3 is sometimes called Kugelberg - Welander disease. Symptoms of muscle weakness and floppiness usually appear after 18 months of age, but the actual age of onset is very variable and may not appear until late childhood or early adulthood. Each child with SMA Type 3 is different, but the onset of muscle weakness is gradual and children are generally able to walk until late childhood and sometimes into adolescence 3. Sometimes doctors try to indicate the degree of severity within SMA Type 3 by using decimal classification 4, for example, 3. 1 3. 2 3. 5 3. 9 If you have any queries regarding this, please speak to your children's medical team. Life expectancy for children diagnosed with SMA Type 3 is usually normal 5 and most people live long, fulfilling, and productive lives. A doctor will diagnose SMA Type 3 after taking medical history, physically examining your child, and by taking blood samples for DNA testing. Blood sample is tested for deletion mutation in survival motor neurone 1 gene on chromosome 5. The result of this test is usually available within 2 - 4 weeks. There may be uncertainty about diagnosis, so further observations and muscle tests such as electromyogram or muscle biopsy may be needed, which can take time. Is there treatment or cure for SMA Type 3? There is one approved treatment for SMA, Spinraza. Its availability varies from country to country and SMA types. If Spinraza is not available in your country, symptoms can be managed so that your child can achieve their maximum mobility, independence, and quality of life. This section describes the effects of SMA Type 3 in general terms. But, it is important to remember that each child with SMA Type 3 is affected differently and the severity of condition varies from child to child. Children's muscle weakness is usually the same on both sides of their body. Muscles closest to the centre of the body are usually more severely affected than muscles furthest from the centre of the body. Generally, children with SMA Type 3 find that their legs are weaker than their arms. As your child grows, it may be difficult for their muscles to keep up with their daily activities. If your child has been able to, for example, walk or climb stairs, they may lose this ability as they get older. Some children may fall more easily as a result of their muscle weakness.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

IMPORTANT SAFETY INFORMATION

In several forms of SMA, respiratory muscle weakness is a significant problem. Its most common cause of death in chromosome 5 SMA types 1 and 2, though not the only cause. When respiratory muscles weaken, air doesnt move into and out of lungs very well, with subsequent adverse effects on general health. Signs of weakening respiratory muscles include headaches, difficulty sleeping at night, frequent yawning or sighing during the day, excess sleepiness during the day, poor concentration, difficulty lying flat, chest infections, and, eventually, heart damage and respiratory failure. Often, in infantile - onset SMA, muscles between affect baby's ribs are very weak, while diaphragm muscle stay fairly strong. This causes child to appear to be breathing by moving their belly rather than their chest. The body can also appear to be pear - shaped. In recent years, availability of portable, effective ventilation devices has created more options for newborns with SMA, and in some cases, has greatly extended life. Assist ventilation also helps children and adults with different forms of SMA. Many physicians advise starting out with noninvasive ventilation, which generally means that air is delivered under pressure through a mask or mouthpiece. This kind of system comes in many forms and can be used as many hours of day and / or night as necessary. It can easily be removed for eating, drinking, and talking. When noninvasive ventilation isnt sufficient, ventilation assistance can be delivered through tracheostomy surgical hole in the trachea, or windpipe. Air under pressure is then delivered through a tube in tracheostomy site. After a period of adjustment, it is usually possible for people to eat, drink, and talk with a tracheostomy tube. Other necessary aspects of respiratory care in SMA include clearance of respiratory secretions, sometimes also achieved with mechanical device, and prevention of infection. Insufflator - exsufflator is one type of device that can assist with clearing respiratory secretions from the airway. The device applies positive pressure to the airway and then rapidly reverses to negative pressure, mimicking natural cough. The Coughassist, made by Philips Respironics, is an example of this type of device. Another type of airway clearance aid is the high - frequency chest wall oscillation device. This device is a vest that rapidly inflates and deflates, vibrating chest and creating mini - coughs that dislodge mucus from small airways, moving it toward larger airways from which it can be more easily coughed out. The Incourage system, made by Philips Respironics, is an example. To prevent respiratory infections, almost everyone with SMA should get a flu shot every year. Other precautions include staying away from crowds and getting adequate rest and nutrition. The Mda Care Center team can advise you about respiratory care, flu shots, and related matters. Swallowing problems occur when muscles of the mouth and throat are weak. Babies with infantile - onset SMA usually have trouble swallowing and sucking. Sucking weakness can lead to dehydration and poor nutrition, while swallowing weakness can lead to obstruction of the airway and respiratory infections from inhaling food or liquids.


What causes SMA?

The most common form of SMA is caused by defects in both copies of survival motor neuron 1 gene on chromosome 5q. This gene produces survival motor neuron protein which maintains health and normal function of motor neurons. Individuals with SMA have insufficient levels of SMN protein, which leads to loss of motor neurons in the spinal cord, producing weakness and wasting of skeletal muscles. This weakness is often more severe in trunk and upper leg and arm muscles than in the muscles of hands and feet. There are many types of spinal muscular atrophy that are caused by changes in same genes. Less common forms of SMA are caused by mutations in other genes, including the VAPB gene located on chromosome 20, DYNC1H1 gene on chromosome 14, BICD2 gene on chromosome 9, and UBA1 gene on X chromosome. Types differ in age of onset and severity of muscle weakness; however, there is overlap between types.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

What is SMA type 3?

This is the most common type of SMA. Itas sometimes called infantile onset or Werdnig - Hoffmann disease. Babies with type 1 have symptoms that start at birth up to 6 months of age. Most show signs of disease by the time they are 3 months old. A baby with type 1 SMA may not be able to hold their head up without help. They may have floppy arms and legs, and a hard time eating and swallowing. Babies with this type of ca sit without support. Type 1 SMA can progress very quickly. Weak muscles can lead to respiratory infections and trouble breathing. Many children with type 1 SMA do live past 2 years old.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Symptoms

Symptoms vary a lot, depending on type of SMA: type 0. This is the rarest and most severe form of SMA and develops while you are still pregnant. Babies with this type of SMA move less in the womb and are born with joint problems, weak muscle tone, and weak muscles for breathing. They often do not survive due to breathing problems. Type 1. This is also a severe type of SMA. A child may not be able to support their head or sit without help. They may have floppy arms and legs and problems swallowing. The biggest concern is weakness in muscles that control breathing. Most children with type 1 SMA don't live past age 2 because of breathing problems. Keep in touch with your medical team, family members, clergy, and others who can help give you emotional support you need while your child fights this disease. Type 2. This affects children 6 - 18 months old. Symptoms range from moderate to severe and usually involve legs more than arms. Your child may be able to sit and walk or stand with help.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Diagnosis

Symptoms of following disorders can be similar to those of spinal muscular atrophy. Comparisons may be useful for differential diagnosis. Following spinal Muscular atrophies are not linked to chromosome 5q but have certain signs and symptoms in common: Finkel type SMA: manifest usually after age 30 years, is inherited as autosomal dominant genetic disorder and is associated with mutations in VAPB gene. Scapuloperoneal spinal Muscular atrophies are usually autosomal dominant conditions, starting in childhood or adulthood,. The weakest muscles are the scapula and peroneal muscles. Progression is usually slow, and ambulation is not lost until the fifth decade of life. Linkage analysis of 1 large kindred has identified locus on chromosome 12q24. 1 - q24. 31. Distal spinal muscular atrophies are characterized by weakness and wasting that starts with distal muscles of upper and lower limbs and spreads later to other muscle groups. Phenotypically, affected individuals resemble patients with Charcot - Marie - Tooth Disease. More than 10 Distal SMAs have been report, each associated with a different gene. The Form of Distal spinal Muscular atrophy with respiratory distress secondary to diaphragmatic paralysis in the early months of life was first described in 1974 and linked to chromosome 11q12 - q14. 1 conditions with distinctive presenting features other than muscle weakness include: X - link spinal and bulbar Muscular atrophy, also know as Kennedy Disease, is a gradually progressive neuromuscular disorder in adult men in whom degeneration of lower motor neurons results in proximal muscle weakness, muscle atrophy, and fasciculations beginningbetween ages of 20 and 50 years. Hexosaminidase deficiency results in lysosomal storage of specific glycosphingolipid, GM2 ganglioside. Juvenile, chronic, and adult - onset variants have onset after infancy, slow progression, and variable neurologic findings, including dystonia, spinocerebellar degeneration, and lower motor neuron Disease. Diagnosis is by biochemical or molecular testing. Monomelic Muscular atrophy is predominantly cervical form of spinal muscular atrophy. Goutieres and colleagues report 5 patients with a form of spinal muscular atrophy that is present in the first few months of life, predominantly with weakness of neck flexors and extensors. Fazio - Londe Disease, motor neuron disease limited to lower cranial nerves, starts in the second decade of life and progresses to death within 1 to 5 years. Other diseases involving both anterior horn cell and other neurologic systems include spinal Muscular atrophy associated with brain atrophy and olivopontocerebellar atrophy. A mutation in the VRK1 gene in consanguineous members of family has been described as this condition. Spinal Muscular atrophy associated with congenital bone fractures was initially reported in boy,s and the disorder was speculated to be X - link, but the latest report describes a girl with the same problem. The Gene for spinal muscular atrophy, 5q13, was found to be normal. The following conditions should be considered when concerns about SMA 0 or 1 are present: Prader - Willi syndrome is a genetic disorder characterized by diminished muscle tone, feeding difficulties, and failure to grow and gain weight during infancy; short stature; genital abnormalities; and mental retardation.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Treatment

Treatments for spinal muscular atrophy will vary depending on type of diagnosis and age of onset. Most conditions that develop after the first two years of life include physical therapy in treatment plans in order to improve mobility and joint movement. Many people with Type 1 do not survive past first two years of life due to high rates of respiratory failure. Breathing difficulties can sometimes be managed through use of non - invasive ventilators and bi - level positive airway pressure support. However, tracheostomy may be needed if non - invasive methods are unable to address the issue. For patients who survive past 2 years old, treatment plan that includes regular respiratory therapy is generally needed to reduce risk of lung complications. Patients with Type I can also experience difficulty acquiring proper nutrition due to weaker sucking reflex and tendency to tire more easily. Naso - gastric or gastric tubes may be used to assist in feeding. Treatment for patients with Type 2, and those with Type 1 who live past their second year, often includes powered wheelchairs. If symptoms are less severe, other assistive devices such as vertical stander or standing wheelchair may be used. People diagnosed with spinal muscular Type III or IV are often able to walk and remain fully functional for many years before they begin to need assistance.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Outlook

Spinal muscular atrophy causes muscle wasting and weakness. It can be difficult for person with SMA to stand, walk, control their head movements, and even, in some cases, breathe and swallow. Some types of SMA are present from birth, but others appear later in life. Some types affect life expectancy. Sma affects one in every 8 000 - 10 000 people around the world, according to Genetics Home Reference. There is no cure for SMA, but new drugs, such as nusinersen and onasemnogene abeparvovec - xioi, may slow its progress. Sma is a genetic condition that can affect children or adults, depending on type. A person's outlook will depend on the severity of symptoms. Infants with severe SMA may experience respiratory disease because muscles that support breathing are weak. This complication can be fatal in some cases. Many people with milder forms of SMA can expect to live as long as person without SMA, although some may need extensive medical support. It is not possible to prevent SMA, but medication, physical therapy, and other strategies can help person live a full and active life. As researchers learn more about SMA, new and experimental treatment options are showing promise for treating, preventing, or even curing the condition in the future. People with a family history of SMA who are planning to start a family may wish to seek genetic counseling first.


What is spinal muscular atrophy (SMA)?

Spinal muscular atrophy is a group of genetic diseases that cause weakness and wasting in voluntary muscles of infants and children and, more rarely, in adults. It is one of the most common genetic conditions affecting children. It is estimated that one in every 6 000 to 10 000 babies worldwide is born with SMA. In more than 95 percent of cases, SMA is caused by inadequate production of protein called survival motor neuron protein that is essential to motor neurons. Smn is produced by SMN1 and to a lesser extent by SMN2. These genes are on chromosome 5. Typically, people have two copies of SMN1 gene and up to two copies of SMN2 gene in each of their motor neuron cells. In people with spinal muscular atrophy, both copies of the SMN1 gene are altered or missing. Having additional copies of SMN2 gene is associated with milder disease by partially compensating for missing SMN1. Rarely, SMA caused by mutations in genes other than SMN. Motor neurons lie on the anterior horn of the spinal cord and directly control body skeletal muscles. Without adequate SMN protein, spinal cord motor neurons begin to shrink and die. As this happen, children's brain is unable to control the body's voluntary muscles, especially those in the arms and legs and in the head and neck. Muscles begin to weaken and waste away. This affects movements such as walking, crawling, head and neck control, swallowing, and breathing.


Treatment

There are two pharmaceutical treatments now available for people with SMA. Nusinersen is approved by the Food and Drug Administration for use in children and adults. Medication is injected into fluid surrounding the spinal cord. It improves head control and ability to crawl or walk, among other mobility milestones in infants and others with certain types of SMA. Another FDA - approved treatment is onasemnogene abeparvovec. It is intended for children under 2 years old with the most common types of SMA. Intravenous medication, works by delivering functional copy of SMN1 gene into children target motor neuron cells. This leads to better muscle function and mobility. The first four doses of Spinraza are administered over a period of 72 days. Afterward, maintenance doses of medication are administered every four months. Children on Zolgensma receive one - time dose of medication. Talk with your children's doctor to determine whether either medication is right for them. Other treatments and therapies that may bring relief from SMA include muscle relaxers and mechanical, or assist, ventilation.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Kugelberg Welander Syndrome

Kugelberg Welander syndrome is a milder type of Spinal Muscular atrophy. It is a rare inherited neuromuscular disorder characterized by wasting and weakness in muscles of arms and legs, leading to walking difficulties and eventual loss of ambulation. Symptoms of Kugelberg Welander syndrome occur after 12 months of age. Patients learn to walk, may fall frequently and may have trouble walking up and down stairs at 2 - 3 years of age; some patients will not show functional changes until their teens. Legs are more severely affected than arms. Long - term prognosis depends on the degree of motor function attained as child. Kugelberg Welander syndrome is inherited autosomal recessive trait. Molecular genetic testing has revealed that all types of autosomal recessive SMA are caused by mutations in the SMN gene on chromosome 5. Deletion of NAIP gene that is close to SMN gene is also associated with SMA. More patients with Werdnig Hoffman disease than other types of SMA have NAIP deletions. The relationship between specific mutations in SMN gene and nearby genes and severity of SMA is still being investigated, so classification of SMA subdivisions is based on age of onset of symptoms and maximum function achieved as opposed to genetic profile.


SMA TYPE II, SMA TYPE III

Most patients with SMA types II and III are normal at birth. In series of 19 infants who were later classified as having SMA Type II, all were found to be normal at birth. 18 onset of disease, however, is before the age of 18 months. 19 Patients can sit unsupported but never stand. Survival to ages 5 and 25 years is 98. 5% and 68. 5%, respectively. Many patients with SMA Type III achieve normal gross motor milestones early on and often into later childhood. The onset of symptoms is usually after the age of 18 months, and patients can stand alone; lifespan is almost normal. The Sma phenotype is determine, at least in part, by the number of copies of centromeric copy of SMN gene, know as SMN2; Patients with milder phenotypes tend to have more copies of SMN2. Most patients with SMA Type I have one or two copies of SMN2, most patients with SMA Type II have two or three copies, and the vast majority of patients with SMA Type III have three or four copies of SMN2.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Causes

Following resources from Cure SMA provide descriptions of symptoms, as well as videos to assist with early diagnosis: SMA type 0 is the most severe form of disease and is characterized by decreased fetal movement, joint abnormalities, difficulty swallowing and respiratory failure. Sma type 1 is the most common type of SMA and is also a severe form of the disease. Infants with SMA type 1 experience severe weakness before 6 months of age and never sit independently. Muscle weakness, lack of motor development and poor muscle tone are major clinical manifestations of SMA type I. Infants with gravest prognosis have problems sucking or swallowing. Some show abdominal breathing in the first few months of life. Muscle weakness occurs on both sides of the body and ocular muscles are not affect. Twitching of tongue is often see. Intelligence is normal. Most affected children die before two years of age but survival may be dependent on degree of respiratory function. For more information about SMA type 1, choose Werdnig Hoffman Disease as your search term in Rare Disease Database. The Onset of weakness in SMA type 2 patients is usually between 6 and 12 months. Affected children are able to sit independently early in development but are unable to walk even 10 feet independently. Trembling of fingers is almost always seen in SMA type 2. Approximately 70% of those affected do not have deep tendon reflexes. Those affected with SMA type 2 are usually not able to sit independently by mid - teens or later. Patients with SMA type 3 learn to walk but fall frequently and have trouble walking up and down stairs at 2 - 3 years of age. Legs are more severely affected than arms. Long - term prognosis depends on the degree of motor function attained as child. For more information about SMA3, choose Kugelberg Welander syndrome as your search term in Rare Disease Database. The Onset of muscle weakness for those with SMA type 4 is after age 10 years; these patients usually are ambulatory until age 60 years. Complications of SMA include scoliosis, joint contractures, pneumonia and metabolic abnormalities such as severe metabolic acidosis and dicarboxylic aciduria.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Related Disorders

Symptoms of following disorders can be similar to those of Kugelberg Welander syndrome. Comparisons may be useful for differential Diagnosis: Duchenne Muscular dystrophy, hereditary degenerative disease of skeletal muscles, is considered the most prevalent form of childhood muscular dystrophy. The disorder typically is recognized from approximately three to five years; Patients with DMD usually lose ambulatory abilities by 12 years of age. Duchenne Muscular dystrophy is initially characterized by muscle weakness within the pelvic area that may be followed by involvement of shoulder muscles. With disease progression, muscle weakness and atrophy affect trunk and forearms and gradually progress to involve most major muscles of the body. For more information about this disorder, choose Muscular dystrophy, Duchenne as your search in Rare Disease Database. Myotubular myopathy is a rare muscle wasting disorder that occurs in three forms. The most severe form is present at birth, inherited as an X - link genetic trait, and presented with severe respiratory muscle weakness. A less severe form is present at birth or early childhood, progresses slowly and is inherited as an autosomal recessive genetic trait. The least severe of three forms is inherited as an autosomal dominant genetic trait, presented between the first and third decades of life and is slowly progressive. For more information on this disorder, choose myotubular myopathy as your search term in Rare Disease Database. Nemaline myopathy is a rare inherited neuromuscular disease that is usually apparent at birth and characterized by extreme muscle weakness but may manifest itself after age 1 year. Laboratory examination of muscle tissue samples from people with nemaline myopathy revealed the presence of fine fibrous threads know as nemaline rods that interfere with muscle function. For more information on this disorder, choose nemaline myopathy as your search term in Rare Disease Database. Glycogen storage diseases are a group of hereditary disorders caused by lack of one or more enzymes involved in glycogen synthesis or breakdown and characterized by deposition of abnormal amounts or types of glycogen in tissues. Gait disorder secondary to glycogen accumulation in muscles May start after age 1 year.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Standard Therapies

Since the introduction of new drug treatments for SMA, we have observed disease trajectories that differ significantly from the known natural history of disease. These new phenotypes now also cross traditional subtypes of SMA. For example, patients with onset before six months of age might achieve independent sitting if treatment is initiated early. It is now more appropriate to rely on a combination of age of onset, number of SMN2 copies, and age at start of Drug Treatment rather than traditional subtypes to define the clinical phenotype of SMA. These new disease trajectories also mean we must modify and adapt to clinical approach For example, longer survival without ventilatory support following initiation of Drug Treatment needs to be considered when counseling parents of patients with early - onset types of SMA. On one end of the spectrum, namely in very severe cases entailing prenatal onset, drug treatment is not likely to lead to any relevant improvement in motor function, nor will it prevent the need for permanent ventilation; it might therefore be inadvisable. On the other hand, initiating treatment in presymptomatic patient might result in almost normal motor development. Additional organ involvement, including occurrence of cardiac defects, autonomic dysregulation or abnormal fatty acid metabolism has been reported in SMA. Smn protein is known to be highly expressed prenatally in most organs, so that significant role in organogenesis has been discuss. Further research is needed to understand if systemic treatment of SMN deficiency is of clinical benefit compared to restricted treatment of the central nervous system. In the context of rare diseases, it is almost inevitable that drug approval will be based on weaker evidence than is the case with drugs for common diseases. This issue concerns disease spectrums investigated in clinical trials, patient numbers, and observation periods. For example, nusinersen was approved for all types and disease stages of SMA despite the fact that two randomized control trials covered only a small proportion of the total SMA population, namely infants and young children presenting relatively early disease stage. Several centers publish their experiences with nusinsersen Treatment of SMA Type 1 patients of different age groups in early - Access Program and deliver similar results: Age at beginning of Treatment is the most important factor that determines motor response to Treatment. Interestingly, no marked difference in motor response between patients with 2 or 3 copies of SMN2 was observe. In contrast to clinical trials, patient cohorts were heterogeneous regarding ventilation - dependency, need for nutritional support and age; data on patients up to 19 years of age were analyzed in Italian cohort. More conflicting than data on motor response are findings regarding ventilation and nutritional support: in both German and French cohorts, significant proportion of patients exhibiting motor improvement had started permanent ventilation or undergone tracheostomy or placement of feeding tube.


How is spinal muscular atrophy diagnosed?

Spinal muscular atrophy is a genetic neuromuscular disease. Large motor nerves of the spinal cord are abnormal in people with SMA because a gene is missing or alter. Without gene,ss or with damaged gene, nerves do not have specific protein that allows them to control muscles. Decrease of SMN1 protein results in improper functioning, and eventually death of motor nerve cells in the spinal cord. Severity of SMA is related to the amount of SMN1 protein that is absent in motor nerve cells. The severity of the disease ranges from mild muscle weakness, to total paralysis and need for support to breathe.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Sources

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

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