Myasthenia gravis is an autoimmune disorder where antibodies are formed against acetylcholine receptors at the neuromuscular junction, reducing their numbers and causing muscle weakness. There are two major forms: ocular and generalized. It is treatable with medications like anticholinesterases, immunosuppressants, plasmapheresis, and thymectomy. The autoimmune attack is believed to be caused by an acquired immune reaction producing anti-acetylcholine receptor antibodies, though the exact trigger is unknown. Diagnosis involves examining for easily fatigable muscles that improve with rest.
Myasthenia Gravis is a neuromuscular junction disorder characterized by skeletal muscle weakness and fatigability. It is caused by antibodies that interfere with acetylcholine receptor function, reducing the efficiency of nerve impulse transmission and causing muscle weakness. Symptoms include weakness of eye muscles, facial muscles, and limbs which worsens with repeated use and improves with rest. Diagnosis involves tests like repetitive nerve stimulation, blood tests for antibodies, and response to medication. Treatment options include anticholinesterase medications, immunosuppressants, plasmapheresis, IVIG, and sometimes thymectomy. With current treatments prognosis is generally good though exacerbations can occasionally cause life-threatening crises requiring respiratory support.
Myasthenia gravis is an autoimmune disease that causes muscle weakness. It is caused by antibodies that block signals from nerves to muscles. The main symptoms are drooping eyelids, blurred vision, difficulty speaking and swallowing, and weakness in the limbs. Diagnosis involves tests like tensilon tests, EMGs, and checking for antibodies against acetylcholine receptors or related proteins. Treatment focuses on medications to enhance nerve signaling, immunosuppressants, and sometimes surgery to remove the thymus gland. Crises can occur where weakness suddenly worsens and ventilator support may be needed.
This document provides guidelines for the management of myasthenia gravis (MG). It discusses the various subtypes of MG, diagnostic testing, and treatment options. For treatment, it recommends pyridostigmine as initial therapy in most cases, with corticosteroids or immunosuppressive drugs for those who do not respond adequately. It provides guidance on immunosuppressive agents, intravenous immunoglobulin and plasma exchange, treatment of myasthenic crisis and thymectomy. The guidelines aim to optimize treatment based on the subtype and severity of MG.
This document summarizes diagnostic testing and treatment approaches for myasthenia gravis (MG). It describes that anti-striated muscle antibody tests are 90% sensitive for generalized MG and 50-70% for ocular MG. Positive results in those under 40 should prompt searching for thymoma. Half of seronegative MG patients may test positive for anti-MuSK or anti-LRP4 antibodies. Repetitive nerve stimulation and single-fiber electromyography can help diagnose MG. An edrophonium test involves injecting the drug to see if symptoms improve. Treatment includes pyridostigmine, steroids, azathioprine, thymectomy, plasmapheresis, and intravenous immunoglob
Neurology 14th diseases of the neuromuscular junction and myopathiesRamiAboali
This document discusses Myasthenia Gravis (MG), a chronic autoimmune neuromuscular disease characterized by varying degrees of muscle weakness. MG is caused by autoantibodies that block neuromuscular transmission, reducing acetylcholine receptors. Symptoms include fatigable weakness of the eyes, face, neck, and limbs. Diagnosis involves tests like the Tensilon test, repetitive nerve stimulation, and antibody tests. Treatment includes anticholinesterases, immunosuppressants, plasma exchange, and sometimes thymectomy. The document also briefly discusses other myopathies and neuromuscular junction disorders like Lambert-Eaton myasthenic syndrome.
Mysthenia gravis is an autoimmune neuromuscular disease caused by antibodies blocking or reducing acetylcholine receptors at the neuromuscular junction, resulting in fluctuating muscle weakness that worsens with activity and improves with rest. It can affect any muscle and occur at any age or gender. Symptoms may include ptosis, difficulty swallowing or speaking, and weakness of facial or eye muscles. Diagnosis involves testing for acetylcholine receptor antibodies and imaging for potential thymoma. Treatment options include acetylcholinesterase inhibitors to increase acetylcholine levels, immunosuppressants to reduce antibody levels, plasma exchange to remove antibodies, and immunoglobulins for crisis situations.
Disorders of the neuromuscular junction include Myasthenia gravis, Lambert-Eaton myasthenic syndrome, Botulism, Tetanus, Strychnine intoxication, Organophosphates poisoning and neuromyotonia. Pharmacology of the NMJ is also reviewed in brief.
Myasthenia Gravis is a neuromuscular junction disorder characterized by skeletal muscle weakness and fatigability. It is caused by antibodies that interfere with acetylcholine receptor function, reducing the efficiency of nerve impulse transmission and causing muscle weakness. Symptoms include weakness of eye muscles, facial muscles, and limbs which worsens with repeated use and improves with rest. Diagnosis involves tests like repetitive nerve stimulation, blood tests for antibodies, and response to medication. Treatment options include anticholinesterase medications, immunosuppressants, plasmapheresis, IVIG, and sometimes thymectomy. With current treatments prognosis is generally good though exacerbations can occasionally cause life-threatening crises requiring respiratory support.
Myasthenia gravis is an autoimmune disease that causes muscle weakness. It is caused by antibodies that block signals from nerves to muscles. The main symptoms are drooping eyelids, blurred vision, difficulty speaking and swallowing, and weakness in the limbs. Diagnosis involves tests like tensilon tests, EMGs, and checking for antibodies against acetylcholine receptors or related proteins. Treatment focuses on medications to enhance nerve signaling, immunosuppressants, and sometimes surgery to remove the thymus gland. Crises can occur where weakness suddenly worsens and ventilator support may be needed.
This document provides guidelines for the management of myasthenia gravis (MG). It discusses the various subtypes of MG, diagnostic testing, and treatment options. For treatment, it recommends pyridostigmine as initial therapy in most cases, with corticosteroids or immunosuppressive drugs for those who do not respond adequately. It provides guidance on immunosuppressive agents, intravenous immunoglobulin and plasma exchange, treatment of myasthenic crisis and thymectomy. The guidelines aim to optimize treatment based on the subtype and severity of MG.
This document summarizes diagnostic testing and treatment approaches for myasthenia gravis (MG). It describes that anti-striated muscle antibody tests are 90% sensitive for generalized MG and 50-70% for ocular MG. Positive results in those under 40 should prompt searching for thymoma. Half of seronegative MG patients may test positive for anti-MuSK or anti-LRP4 antibodies. Repetitive nerve stimulation and single-fiber electromyography can help diagnose MG. An edrophonium test involves injecting the drug to see if symptoms improve. Treatment includes pyridostigmine, steroids, azathioprine, thymectomy, plasmapheresis, and intravenous immunoglob
Neurology 14th diseases of the neuromuscular junction and myopathiesRamiAboali
This document discusses Myasthenia Gravis (MG), a chronic autoimmune neuromuscular disease characterized by varying degrees of muscle weakness. MG is caused by autoantibodies that block neuromuscular transmission, reducing acetylcholine receptors. Symptoms include fatigable weakness of the eyes, face, neck, and limbs. Diagnosis involves tests like the Tensilon test, repetitive nerve stimulation, and antibody tests. Treatment includes anticholinesterases, immunosuppressants, plasma exchange, and sometimes thymectomy. The document also briefly discusses other myopathies and neuromuscular junction disorders like Lambert-Eaton myasthenic syndrome.
Mysthenia gravis is an autoimmune neuromuscular disease caused by antibodies blocking or reducing acetylcholine receptors at the neuromuscular junction, resulting in fluctuating muscle weakness that worsens with activity and improves with rest. It can affect any muscle and occur at any age or gender. Symptoms may include ptosis, difficulty swallowing or speaking, and weakness of facial or eye muscles. Diagnosis involves testing for acetylcholine receptor antibodies and imaging for potential thymoma. Treatment options include acetylcholinesterase inhibitors to increase acetylcholine levels, immunosuppressants to reduce antibody levels, plasma exchange to remove antibodies, and immunoglobulins for crisis situations.
Disorders of the neuromuscular junction include Myasthenia gravis, Lambert-Eaton myasthenic syndrome, Botulism, Tetanus, Strychnine intoxication, Organophosphates poisoning and neuromyotonia. Pharmacology of the NMJ is also reviewed in brief.
Myasthenia gravis is an autoimmune disorder where antibodies are formed against acetylcholine receptors in the neuromuscular junction, reducing their numbers and causing muscle weakness that worsens with repeated use and improves with rest. It most commonly affects the eye muscles and muscles of the face, throat, and limbs. While idiopathic in most cases, it has associations with certain genes and tumors of the thymus gland. Diagnosis involves testing muscle fatigue and response to medication, and treatment focuses on immunosuppressants, thymectomy, and supporting respiratory function to prevent crisis. Nurses monitor symptoms and respiratory status, educate on triggers and crisis response, and carefully manage medications and nutrition.
This document summarizes Myasthenia Gravis (MG), a disorder of the neuromuscular junction caused by autoantibodies against acetylcholine receptors. It presents with fatigable weakness, especially of eye, face, neck and bulbar muscles. Diagnosis involves tests like tensilon/ice pack tests and repetitive nerve stimulation. Treatment includes acetylcholinesterase inhibitors, immunosuppression with steroids/azathioprine, plasma exchange and thymectomy. Prognosis varies but is generally good if confined to eye muscles and in young females after thymectomy. Other related conditions like Lambert-Eaton myasthenic syndrome and various muscular dystrophies are also briefly discussed.
The document summarizes myasthenia gravis (MG), an autoimmune disorder causing muscle weakness. MG results from antibodies blocking acetylcholine receptors at the neuromuscular junction, inhibiting nerve signal transmission. Signs and symptoms include weakness of eye, facial, swallowing, and respiratory muscles. Diagnosis involves testing for acetylcholine receptor antibodies. Treatment includes anticholinesterases, immunosuppressants, plasmapheresis, IV immunoglobulins, and sometimes thymectomy. While the immune system's role is clear, further research is still needed to develop more effective medical treatments without adverse effects.
Myasthenia Gravis is a neuromuscular disorder primarily characterized by muscle weakness and muscle fatigue. Although the disorder usually becomes apparent during adulthood, symptom onset may occur at any age.
Myasthenia gravis (MG) is a long-term neuromuscular disease that leads to varying degrees of skeletal muscle weakness. The most commonly affected muscles are those of the eyes, face, and swallowing.
This document discusses disorders of the neuromuscular junction, focusing on Myasthenia Gravis and Lambert-Eaton Myasthenic Syndrome. It covers the pathophysiology, clinical features, diagnostic tests, and treatment for each condition. Myasthenia Gravis is an autoimmune disorder causing weakness through antibodies against acetylcholine receptors. It is treated with anticholinesterases, immunosuppressants, thymectomy, plasmapheresis or IVIg. Lambert-Eaton Myasthenic Syndrome features impaired acetylcholine release associated with cancer; it is treated by addressing any tumors plus immunosuppression or 3,4-diaminopyridine. Both can potentially cause respiratory failure requiring
This document summarizes key information about Myasthenia Gravis (MG), an autoimmune disorder characterized by muscle weakness and fatigue. It discusses the epidemiology of MG, noting peaks in incidence among younger females. The pathophysiology involves antibodies interacting with acetylcholine receptors at the neuromuscular junction, reducing receptor numbers. Diagnosis involves testing for antibodies and response to cholinesterase inhibitors. Treatment focuses on immunomodulation including plasmapheresis, IVIG, thymectomy and immunosuppressive drugs.
Myasthenia gravis is an autoimmune disorder causing fatigue and weakness of voluntary muscles. It is usually caused by antibodies against acetylcholine receptors at the neuromuscular junction, impairing signal transmission. Most patients have thymic hyperplasia or thymoma. Diagnosis involves tests like the Tensilon test and checking for acetylcholine receptor antibodies. Treatment focuses on acetylcholinesterase inhibitors and immunosuppression with corticosteroids, azathioprine or plasma exchange to reduce antibodies. Prognosis depends on factors like age of onset and presence of thymoma.
Myasthenia gravis is an autoimmune neuromuscular disorder characterized by weakness and fatigability of skeletal muscles. It results from antibodies that block or destroy acetylcholine receptors at the neuromuscular junction, reducing signal transmission from nerves to muscles. Common symptoms include ptosis, diplopia, and weakness of proximal limb muscles or bulbar muscles. Diagnosis involves history, physical exam, electrodiagnostic testing showing decremental response to repetitive nerve stimulation, and presence of acetylcholine receptor antibodies. Treatment options include anticholinesterase medications, immunosuppression, plasmapheresis, IVIg, and thymectomy.
This document provides information about Myasthenia Gravis (MG), including its epidemiology, clinical presentation, immunopathology, diagnostic procedures, treatment, and management of different subtypes. Some key points include:
- MG is an autoimmune disorder causing muscle weakness due to antibodies interfering with acetylcholine receptors at the neuromuscular junction.
- It can present with symptoms like ptosis, diplopia, limb or swallowing weakness.
- Diagnosis involves tests like repetitive nerve stimulation, serum acetylcholine receptor antibody levels, and single fiber electromyography.
- Treatment includes pyridostigmine, corticosteroids, immunosuppressants, IVIG, plasma exchange,
Neuromuscular junction diseases interfere with the transmission of signals from nerves to muscles and can be acquired or inherited. Myasthenia gravis is an acquired autoimmune disorder where antibodies induce acetylcholine receptor deficiency at the neuromuscular junction, causing weakness that fluctuates with activity. Symptoms are tested using drugs like edrophonium, and treatment includes anticholinesterases, immunosuppressants, thymectomy, and plasmapheresis. Lambert-Eaton myasthenic syndrome is another autoimmune condition where antibodies affect calcium channels, and is associated with lung cancer. Certain drugs can also induce myasthenic syndrome symptoms.
Myasthenia Gravis is an autoimmune disorder that causes muscle weakness. It occurs when antibodies block or destroy acetylcholine receptors in the neuromuscular junction, inhibiting muscle contraction. Common signs include drooping eyelids, double vision, difficulty speaking and swallowing. While its exact cause is unknown, it is associated with thymic abnormalities. Treatment involves anticholinesterase medications to improve transmission in the neuromuscular junction, immunosuppressants to reduce antibody production, and sometimes thymectomy.
Myasthenia gravis is a disorder of the neuromuscular junction caused by autoantibodies that block signal transmission. It causes progressive weakness of voluntary muscles, especially those of the eyes, face, neck, and limbs. Symptoms worsen with activity and improve with rest. Diagnosis involves tests like the Tensilon test and repetitive nerve stimulation. Treatment focuses on improving acetylcholine activity and suppressing the immune response, using medications, thymectomy, or other immunotherapies. Prognosis depends on which muscles are affected, with ocular-only forms having an excellent prognosis.
This document provides information on Myasthenia Gravis (MG), an autoimmune neuromuscular disease caused by antibodies against postsynaptic muscle membranes. It discusses the prevalence and classification of MG, clinical features including weakness and fatigability, diagnostic testing such as repetitive nerve stimulation and edrophonium testing, treatment including acetylcholinesterase inhibitors and immunotherapies, and management of symptoms. Key points covered include the fluctuating muscle weakness that worsens with exertion seen in MG, different classifications based on symptoms and severity, and first line treatment involving pyridostigmine and corticosteroids.
Myasthenia gravis is a disease characterized by fluctuating muscle weakness that worsens with exertion and improves with rest. It results from impaired signaling at the neuromuscular junction due to antibodies against acetylcholine receptors. Symptoms vary depending on the affected muscle groups but commonly involve eye and facial muscles. While the root cause is unknown, it is considered an autoimmune disease associated with changes in the thymus gland. Treatment aims to improve muscle strength and prevent worsening through acetylcholinesterase inhibitors, immunosuppressants, plasmapheresis, and in some cases thymectomy.
Pregnancy in a young girl with Myasthenia Gravis.Anita Aggarwal
This document describes the case of a 31-year-old woman with a history of myasthenia gravis who presented with amenorrhea. Myasthenia gravis is an autoimmune disorder causing muscle weakness due to antibodies against acetylcholine receptors at the neuromuscular junction. The patient had been experiencing symptoms of myasthenia gravis for 9 years and underwent thymectomy in 2008. She became pregnant after 6 months of marriage and had an uneventful pregnancy while continuing medication for myasthenia gravis. She delivered a baby girl via cesarean section due to failure to progress in labor. Both mother and baby were discharged in good condition.
Myasthenia gravis is an autoimmune disorder causing muscle weakness and fatigability due to antibodies interfering with signal transmission at the neuromuscular junction. It is classified based on severity and affected muscle groups. Symptoms include drooping eyelids and difficulties with eye movement, facial expression, swallowing, talking and breathing. The condition occurs when antibodies disrupt acetylcholine receptor signaling, commonly due to thymic abnormalities. Diagnosis involves physical exams, blood tests, imaging and response to medication. Treatment includes acetylcholinesterase inhibitors, immunosuppressants, plasmapheresis and sometimes thymectomy.
Myasthenia gravis is an autoimmune disorder where antibodies attack acetylcholine receptors at the neuromuscular junction, reducing their numbers. This causes fluctuating muscle weakness in certain muscle groups. It occurs more often in young women. Symptoms include drooping eyelids, blurred or double vision, weakness of face muscles and limbs. Diagnosis involves testing for antibodies, electromyography, the Tensilon test to confirm improvement of symptoms with edrophonium. Treatment consists of anticholinesterase medications, corticosteroids, immunosuppressants. Thymectomy may be done if thymus tumors are present. Nursing care focuses on monitoring breathing and nutrition due to respiratory and swallowing weakness
This document provides an overview of myasthenia gravis (MG), including its pathophysiology, clinical presentation, diagnosis, and treatment. MG is an autoimmune disorder caused by antibodies against acetylcholine receptors at the neuromuscular junction. This results in impaired signal transduction and muscle weakness/fatigability. Diagnosis involves testing for specific antibodies and demonstrating improvement of weakness with medication challenges like edrophonium (Tensilon test). Treatment includes acetylcholinesterase inhibitors, immunosuppression, plasmapheresis, IVIG, and sometimes thymectomy.
The document summarizes the biography of Dr. Dubravka Savic, an Associate Professor of plant physiology at the University of Belgrade. It describes her early interest in plants as a child growing up in Serbia and her decision to study plant physiology in school and university. It outlines her career path, including graduate studies focusing on plant physiology, getting a job teaching vegetable production, and conducting research on topics related to photosynthesis, plant growth, and productivity. It also discusses her mentors and collaborations with institutions in other countries, as well as her ongoing work in teaching, research, and training on topics at the intersection of plant physiology and vegetable production.
Myasthenia gravis is an autoimmune disorder where antibodies are formed against acetylcholine receptors in the neuromuscular junction, reducing their numbers and causing muscle weakness that worsens with repeated use and improves with rest. It most commonly affects the eye muscles and muscles of the face, throat, and limbs. While idiopathic in most cases, it has associations with certain genes and tumors of the thymus gland. Diagnosis involves testing muscle fatigue and response to medication, and treatment focuses on immunosuppressants, thymectomy, and supporting respiratory function to prevent crisis. Nurses monitor symptoms and respiratory status, educate on triggers and crisis response, and carefully manage medications and nutrition.
This document summarizes Myasthenia Gravis (MG), a disorder of the neuromuscular junction caused by autoantibodies against acetylcholine receptors. It presents with fatigable weakness, especially of eye, face, neck and bulbar muscles. Diagnosis involves tests like tensilon/ice pack tests and repetitive nerve stimulation. Treatment includes acetylcholinesterase inhibitors, immunosuppression with steroids/azathioprine, plasma exchange and thymectomy. Prognosis varies but is generally good if confined to eye muscles and in young females after thymectomy. Other related conditions like Lambert-Eaton myasthenic syndrome and various muscular dystrophies are also briefly discussed.
The document summarizes myasthenia gravis (MG), an autoimmune disorder causing muscle weakness. MG results from antibodies blocking acetylcholine receptors at the neuromuscular junction, inhibiting nerve signal transmission. Signs and symptoms include weakness of eye, facial, swallowing, and respiratory muscles. Diagnosis involves testing for acetylcholine receptor antibodies. Treatment includes anticholinesterases, immunosuppressants, plasmapheresis, IV immunoglobulins, and sometimes thymectomy. While the immune system's role is clear, further research is still needed to develop more effective medical treatments without adverse effects.
Myasthenia Gravis is a neuromuscular disorder primarily characterized by muscle weakness and muscle fatigue. Although the disorder usually becomes apparent during adulthood, symptom onset may occur at any age.
Myasthenia gravis (MG) is a long-term neuromuscular disease that leads to varying degrees of skeletal muscle weakness. The most commonly affected muscles are those of the eyes, face, and swallowing.
This document discusses disorders of the neuromuscular junction, focusing on Myasthenia Gravis and Lambert-Eaton Myasthenic Syndrome. It covers the pathophysiology, clinical features, diagnostic tests, and treatment for each condition. Myasthenia Gravis is an autoimmune disorder causing weakness through antibodies against acetylcholine receptors. It is treated with anticholinesterases, immunosuppressants, thymectomy, plasmapheresis or IVIg. Lambert-Eaton Myasthenic Syndrome features impaired acetylcholine release associated with cancer; it is treated by addressing any tumors plus immunosuppression or 3,4-diaminopyridine. Both can potentially cause respiratory failure requiring
This document summarizes key information about Myasthenia Gravis (MG), an autoimmune disorder characterized by muscle weakness and fatigue. It discusses the epidemiology of MG, noting peaks in incidence among younger females. The pathophysiology involves antibodies interacting with acetylcholine receptors at the neuromuscular junction, reducing receptor numbers. Diagnosis involves testing for antibodies and response to cholinesterase inhibitors. Treatment focuses on immunomodulation including plasmapheresis, IVIG, thymectomy and immunosuppressive drugs.
Myasthenia gravis is an autoimmune disorder causing fatigue and weakness of voluntary muscles. It is usually caused by antibodies against acetylcholine receptors at the neuromuscular junction, impairing signal transmission. Most patients have thymic hyperplasia or thymoma. Diagnosis involves tests like the Tensilon test and checking for acetylcholine receptor antibodies. Treatment focuses on acetylcholinesterase inhibitors and immunosuppression with corticosteroids, azathioprine or plasma exchange to reduce antibodies. Prognosis depends on factors like age of onset and presence of thymoma.
Myasthenia gravis is an autoimmune neuromuscular disorder characterized by weakness and fatigability of skeletal muscles. It results from antibodies that block or destroy acetylcholine receptors at the neuromuscular junction, reducing signal transmission from nerves to muscles. Common symptoms include ptosis, diplopia, and weakness of proximal limb muscles or bulbar muscles. Diagnosis involves history, physical exam, electrodiagnostic testing showing decremental response to repetitive nerve stimulation, and presence of acetylcholine receptor antibodies. Treatment options include anticholinesterase medications, immunosuppression, plasmapheresis, IVIg, and thymectomy.
This document provides information about Myasthenia Gravis (MG), including its epidemiology, clinical presentation, immunopathology, diagnostic procedures, treatment, and management of different subtypes. Some key points include:
- MG is an autoimmune disorder causing muscle weakness due to antibodies interfering with acetylcholine receptors at the neuromuscular junction.
- It can present with symptoms like ptosis, diplopia, limb or swallowing weakness.
- Diagnosis involves tests like repetitive nerve stimulation, serum acetylcholine receptor antibody levels, and single fiber electromyography.
- Treatment includes pyridostigmine, corticosteroids, immunosuppressants, IVIG, plasma exchange,
Neuromuscular junction diseases interfere with the transmission of signals from nerves to muscles and can be acquired or inherited. Myasthenia gravis is an acquired autoimmune disorder where antibodies induce acetylcholine receptor deficiency at the neuromuscular junction, causing weakness that fluctuates with activity. Symptoms are tested using drugs like edrophonium, and treatment includes anticholinesterases, immunosuppressants, thymectomy, and plasmapheresis. Lambert-Eaton myasthenic syndrome is another autoimmune condition where antibodies affect calcium channels, and is associated with lung cancer. Certain drugs can also induce myasthenic syndrome symptoms.
Myasthenia Gravis is an autoimmune disorder that causes muscle weakness. It occurs when antibodies block or destroy acetylcholine receptors in the neuromuscular junction, inhibiting muscle contraction. Common signs include drooping eyelids, double vision, difficulty speaking and swallowing. While its exact cause is unknown, it is associated with thymic abnormalities. Treatment involves anticholinesterase medications to improve transmission in the neuromuscular junction, immunosuppressants to reduce antibody production, and sometimes thymectomy.
Myasthenia gravis is a disorder of the neuromuscular junction caused by autoantibodies that block signal transmission. It causes progressive weakness of voluntary muscles, especially those of the eyes, face, neck, and limbs. Symptoms worsen with activity and improve with rest. Diagnosis involves tests like the Tensilon test and repetitive nerve stimulation. Treatment focuses on improving acetylcholine activity and suppressing the immune response, using medications, thymectomy, or other immunotherapies. Prognosis depends on which muscles are affected, with ocular-only forms having an excellent prognosis.
This document provides information on Myasthenia Gravis (MG), an autoimmune neuromuscular disease caused by antibodies against postsynaptic muscle membranes. It discusses the prevalence and classification of MG, clinical features including weakness and fatigability, diagnostic testing such as repetitive nerve stimulation and edrophonium testing, treatment including acetylcholinesterase inhibitors and immunotherapies, and management of symptoms. Key points covered include the fluctuating muscle weakness that worsens with exertion seen in MG, different classifications based on symptoms and severity, and first line treatment involving pyridostigmine and corticosteroids.
Myasthenia gravis is a disease characterized by fluctuating muscle weakness that worsens with exertion and improves with rest. It results from impaired signaling at the neuromuscular junction due to antibodies against acetylcholine receptors. Symptoms vary depending on the affected muscle groups but commonly involve eye and facial muscles. While the root cause is unknown, it is considered an autoimmune disease associated with changes in the thymus gland. Treatment aims to improve muscle strength and prevent worsening through acetylcholinesterase inhibitors, immunosuppressants, plasmapheresis, and in some cases thymectomy.
Pregnancy in a young girl with Myasthenia Gravis.Anita Aggarwal
This document describes the case of a 31-year-old woman with a history of myasthenia gravis who presented with amenorrhea. Myasthenia gravis is an autoimmune disorder causing muscle weakness due to antibodies against acetylcholine receptors at the neuromuscular junction. The patient had been experiencing symptoms of myasthenia gravis for 9 years and underwent thymectomy in 2008. She became pregnant after 6 months of marriage and had an uneventful pregnancy while continuing medication for myasthenia gravis. She delivered a baby girl via cesarean section due to failure to progress in labor. Both mother and baby were discharged in good condition.
Myasthenia gravis is an autoimmune disorder causing muscle weakness and fatigability due to antibodies interfering with signal transmission at the neuromuscular junction. It is classified based on severity and affected muscle groups. Symptoms include drooping eyelids and difficulties with eye movement, facial expression, swallowing, talking and breathing. The condition occurs when antibodies disrupt acetylcholine receptor signaling, commonly due to thymic abnormalities. Diagnosis involves physical exams, blood tests, imaging and response to medication. Treatment includes acetylcholinesterase inhibitors, immunosuppressants, plasmapheresis and sometimes thymectomy.
Myasthenia gravis is an autoimmune disorder where antibodies attack acetylcholine receptors at the neuromuscular junction, reducing their numbers. This causes fluctuating muscle weakness in certain muscle groups. It occurs more often in young women. Symptoms include drooping eyelids, blurred or double vision, weakness of face muscles and limbs. Diagnosis involves testing for antibodies, electromyography, the Tensilon test to confirm improvement of symptoms with edrophonium. Treatment consists of anticholinesterase medications, corticosteroids, immunosuppressants. Thymectomy may be done if thymus tumors are present. Nursing care focuses on monitoring breathing and nutrition due to respiratory and swallowing weakness
This document provides an overview of myasthenia gravis (MG), including its pathophysiology, clinical presentation, diagnosis, and treatment. MG is an autoimmune disorder caused by antibodies against acetylcholine receptors at the neuromuscular junction. This results in impaired signal transduction and muscle weakness/fatigability. Diagnosis involves testing for specific antibodies and demonstrating improvement of weakness with medication challenges like edrophonium (Tensilon test). Treatment includes acetylcholinesterase inhibitors, immunosuppression, plasmapheresis, IVIG, and sometimes thymectomy.
The document summarizes the biography of Dr. Dubravka Savic, an Associate Professor of plant physiology at the University of Belgrade. It describes her early interest in plants as a child growing up in Serbia and her decision to study plant physiology in school and university. It outlines her career path, including graduate studies focusing on plant physiology, getting a job teaching vegetable production, and conducting research on topics related to photosynthesis, plant growth, and productivity. It also discusses her mentors and collaborations with institutions in other countries, as well as her ongoing work in teaching, research, and training on topics at the intersection of plant physiology and vegetable production.
The document summarizes the biography of Dr. Dubravka Savic, an Associate Professor of plant physiology at the University of Belgrade. It describes her early interest in plants as a child growing up in Serbia and her decision to study plant physiology in school and university. It outlines her career path, including graduate studies focusing on plant physiology, getting a job teaching vegetable production, and conducting research on topics related to photosynthesis, plant growth, and productivity. It also discusses her mentors and collaborations with institutions in other countries, as well as her ongoing work in teaching, research, and training on topics at the intersection of plant physiology and vegetable production.
Myasthenia gravis is an autoimmune disorder where antibodies are formed against acetylcholine receptors at the neuromuscular junction, reducing their numbers and causing muscle weakness. There are two major forms: ocular and generalized. It is treatable with medications like anticholinesterases, immunosuppressants, plasmapheresis, and thymectomy. The autoimmune attack is believed to be caused by an acquired immune reaction producing anti-acetylcholine receptor antibodies, though the exact trigger is unknown. Diagnosis involves examining for easily fatigable muscles that improve with rest.
The document provides instructions for creating a multimedia website using Wix.com that covers text, graphics, sound, and video. Under each main heading, it lists subheadings and topics that must be researched and explained, such as font types, image file formats, embedding sound and dealing with file sizes, and factors that affect video quality like connection speed. Students are also directed to additional online resources for researching these topics and told to include examples and descriptions in their website.
If you grew up in east vancouver share2LoriEnglish
Lorraine Mahovlic Gargaro started a Facebook page called "If You Grew Up in East Vancouver Share Memories" in July 2011. Many people from East Vancouver have thanked Lorraine for creating the group, as it has allowed them to reconnect with old friends and neighbors, share memories and photos, and make new friends. The group has brought much joy to its members as they reminisce about their childhoods and lives in East Vancouver.
The document provides guidance on various aspects of a minor project including selecting and justifying processes and equipment, creating a Gantt chart to plan the project timeline, developing a finance plan to track project costs, and creating final concept drawings and storyboards to illustrate the planned presentation layout and incorporate audio/video elements. Key tasks to be documented in the Gantt chart and financed include developing concepts, making selections and justifications, time planning, finance planning, and producing presentation deliverables like video, audio, and the final presentation.
La historia habla sobre una mujer que le cuenta a su hija cómo conoció a su padre Miguel. Ellos se conocieron cuando eran adolescentes en una fiesta y con el tiempo se enamoraron, aunque luego se separaron. Más tarde, Miguel terminó su relación con su mejor amiga y él y la mujer volvieron a unirse, no sorprendiendo a sus amigos que siempre supieron que terminarían juntos.
La historia habla sobre una mujer que recuerda su niñez y los momentos que pasaba jugando con sus dos mejores amigos, Nicolás y Cristóbal. A ellos les encantaba usar cajas de cartón para crear mundos imaginarios y un día encontraron una caja gigante con la que decidieron crear una máquina del tiempo. Pasaron un día imaginando que viajaban al pasado hasta que la caja se arruinó con la lluvia. Los tres amigos sintieron respeto por la caja que les había permitido crear tantas aventuras y esperaron a que se la l
Here are brief responses to your questions:
1. Myasthenia Gravis (MG) is a rare autoimmune neuromuscular disease that causes weakness in the skeletal muscles.
2. MG is specifically an autoimmune disorder where the immune system produces antibodies that attack the nicotinic acetylcholine receptors at the neuromuscular junction.
3. In MG, antibodies activate the complement system at the neuromuscular junction, leading to membrane attack complex formation and destruction of the postsynaptic membrane.
4. In MG, acetylcholine receptors are affected as antibodies bind to receptors and block acetylcholine binding/action, accelerate receptor turnover, and activate complement-mediated destruction of receptors.
Myasthenia gravis (MG) is the neuromuscular disorder that causes muscle weakness. It affects muscles that a person can generally control consciously. Muscles which are most commonly affected are those controlling the eyelids, eye movement, breathing and swallowing, as well as the facial and shoulder muscles. The weakness tends to temporarily worsen with the activity and improve with rest. MG is an autoimmune disorder. This means the body’s immune system mistakenly attacks the connection between the nerves and muscle. In MG, the muscle cells have problems responding to the nerve impulses that normally signal them to contract and these results in weakness
Myasthenia gravis is an autoimmune disease characterized by weakness and fatigability of skeletal muscles caused by a decrease in acetylcholine receptors at the neuromuscular junction. Autoantibodies develop against acetylcholine receptors, impairing nerve conduction and ultimately destroying receptors. Symptoms include painless weakness that increases with activity and improves with rest, often affecting eye muscles first and sometimes spreading to other muscles. Diagnosis involves testing for acetylcholine receptor antibodies and responding to medication like Tensilon. Treatment options include anticholinesterase medications, immunosuppressants, thymectomy, plasmapheresis, IVIG, and in severe cases respiratory support.
Myasthenia gravis is an autoimmune disease characterized by weakness and fatigability of skeletal muscles caused by a decrease in acetylcholine receptors at the neuromuscular junction. Autoantibodies develop against acetylcholine receptors, impairing nerve conduction and ultimately destroying receptors. Symptoms include painless weakness that increases with activity and improves with rest, often affecting eye muscles first before spreading to other muscles. Diagnosis involves testing for acetylcholine receptor antibodies and responding to medication like Tensilon. Treatment options include anticholinesterase medications, immunosuppressants, thymectomy, plasmapheresis, IVIG, and steroids.
This document provides information on myasthenia gravis (MG), including:
- MG is an autoimmune neuromuscular junction disorder causing muscle weakness.
- Treatment involves immunomodulation with pyridostigmine, corticosteroids, immunosuppressants like azathioprine and mycophenolate, IVIG, or plasma exchange.
- Diagnosis is based on symptoms, serologic testing for acetylcholine receptor (AChR) or muscle-specific kinase (MuSK) antibodies, and electrodiagnostic testing showing decremental response on repetitive nerve stimulation.
1) Myasthenia gravis is an autoimmune disorder characterized by muscle weakness and fatigability caused by antibodies against acetylcholine receptors at the neuromuscular junction.
2) These antibodies interfere with nerve impulses to muscles, causing fatigue and weakness of muscles under voluntary control.
3) Treatment involves immunosuppressant drugs to reduce antibody levels, acetylcholinesterase inhibitors, plasmapheresis, intravenous immunoglobulin and sometimes thymectomy.
1. Myasthenia gravis is an autoimmune disorder characterized by weakness of skeletal muscles caused by antibodies against acetylcholine receptors at the neuromuscular junction.
2. Clinical features include weakness of ocular, facial, bulbar, and limb muscles that worsens with activity and improves with rest.
3. Treatment involves anticholinesterase medications to enhance neuromuscular transmission, thymectomy to remove the thymus gland which is often abnormal, immunosuppressive drugs as long-term therapy, and short-term immunotherapies like plasmapheresis and IVIG during crisis.
This document provides a mini review of autoimmune encephalitis. It begins by introducing autoimmune encephalitis as an inflammatory central nervous system disorder that was previously underrecognized. Autoimmune encephalitis is believed to be the third leading cause of encephalitis. The review discusses the clinical presentations of autoimmune encephalitis and how it can affect the gray matter of the brain. It describes the different classifications of autoimmune encephalitis based on whether it is paraneoplastic or non-paraneoplastic, and based on the targets of antibodies in the body. Specific types of autoimmune encephalitis are discussed like anti-NMDA receptor antibody limbic encephalitis. The review concludes that autoimmune en
Myasthenia gravis is a disorder of the neuromuscular junction that causes muscle weakness. It occurs when antibodies are produced that attack proteins in the neuromuscular junction. The classic presentation is a fluctuating weakness that is more prominent in the afternoon and involves the eyes, face, throat, and limbs. Diagnosis involves testing for antibodies, repetitive nerve stimulation tests, edrophonium tests, and sometimes imaging. Treatment focuses on symptomatic relief and management of symptoms.
- Myasthenia gravis is an autoimmune disorder where antibodies target acetylcholine receptors at the neuromuscular junction, impairing signal transmission.
- Three proposed mechanisms for receptor impairment are: accelerated receptor degradation, blockade of acetylcholine binding sites, and complement-mediated membrane damage.
- Early studies found a reduction in acetylcholine receptors at the neuromuscular junction in myasthenia gravis patients, correlating with impaired signal transmission. This helped establish the autoimmune nature and antibody-mediated mechanisms of the disorder.
This presentation provides an overview of demyelinating diseases, focusing on multiple sclerosis (MS). It defines demyelinating diseases as those that cause myelin destruction while sparing other nervous system elements. MS is described as an autoimmune, inflammatory demyelinating disease of the central nervous system (CNS) that is more common in women. The presentation covers the pathology, clinical features, investigations, and treatment approaches for MS.
This document summarizes disorders of the neuromuscular junction, including myasthenia gravis and other myasthenic syndromes. It describes the definition, aetiology, clinical features, investigations, management, and prognosis of myasthenia gravis. It also discusses other myasthenic syndromes such as Lambert-Eaton myasthenic syndrome and compares it to myasthenia gravis. The document further summarizes diseases of muscles including muscular dystrophies, spinal muscular atrophies, and neurofibromatosis.
A 49-year-old female presented with voice changes for 1 month. She had a history of total thymectomy 7 years ago for low-grade thymoma. On examination, she had signs of vocal fatigue and weakness. Tests confirmed bulbar myasthenia gravis with strongly positive anti-acetylcholine receptor antibodies. Bulbar myasthenia can develop years after thymectomy, possibly due to residual mature T-cells released from the thymoma persisting in the periphery and stimulating autoantibody production. While rare, postoperative myasthenia generally responds well to treatment and has a good prognosis.
Actualización en la etiología, clasificación y manejo de las glomerulopatías.pdfjhinner eloy
This document provides an overview of recent updates in the classification and management of various glomerular diseases. It discusses how new genetic discoveries have led to changes in classifications, such as membranoproliferative glomerulonephritis now being divided into C3 glomerulopathy and immunoglobulin/C3 positive categories. Treatment options for diseases like minimal change disease, membranous nephropathy, and focal segmental glomerulosclerosis have expanded with the use of rituximab and complement inhibitors. Rapidly progressive glomerulonephritis is now classified based on etiology into anti-glomerular basement membrane antibody disease, ANCA-associated vasculitis, and immune complex disorders.
Myasthenia gravis (MG) is a neuromuscular disorder characterized by weakness and fatigability of skeletal muscles.
The underlying defect is a decrease in the number of available acetylcholine receptors (AChRs) at neuromuscular junctions due to an antibody-mediated autoimmune attack
Myasthenia Gravis is an autoimmune disorder of the neuromuscular junction where antibodies block neuromuscular transmission, reducing acetylcholine receptors. Clinical features include weakness of the eye muscles, face, neck, and limb muscles that worsens with activity and improves with rest. Diagnosis involves fatigue testing, pharmacological testing with edrophonium, electrical studies showing decremental responses, and serological testing for antibodies. Treatment includes anticholinesterases, steroids, immunosuppressants, IVIG, and plasmapheresis. Thymectomy may be considered for some patients.
This document discusses paraneoplastic syndromes of the nervous system. It defines paraneoplastic syndromes as disorders that accompany benign or malignant tumors but are not directly caused by tumor invasion or mass effects. It then lists and describes various paraneoplastic syndromes that can affect the central nervous system, peripheral nervous system, neuromuscular junction, and muscles. The document discusses the pathogenesis of paraneoplastic syndromes and antibodies associated with different syndromes. It provides information on incidence, diagnostic criteria, treatment approaches, prognosis, and testing considerations for paraneoplastic syndromes.
Myasthenia gravis (MG) is a chronic autoimmune disorder of the postsynaptic membrane at the neuromuscular junction (NMJ) in skeletal muscle. Circulating antibodies against the nicotinic acetylcholine receptor (achr) and associated proteins impair neuromuscular transmission
Paraneoplastic disorders of the peripheral nervous systemElectrodx Inr
Manifestaciones diversas en sistema nervioso periférico con relación a proceso oncológicos o su tratamiento, síndromes paraneoplásicos. Banderas rojas y alertas sobre su detección.
Myasthenia gravis is an either autoimmune or congenital neuromuscular disease that leads to fluctuating muscle weakness and fatigue. In the most common cases, muscle weakness is caused by circulating antibodies that block acetylcholine receptors at the postsynaptic neuromuscular junction, inhibiting the excitatory effects of the neurotransmitter acetylcholine on nicotinic receptors at neuromuscular junctions. Alternatively, in a much rarer form, muscle weakness is caused by a genetic defect in some portion of the neuromuscular junction, that is inherited at birth as opposed to developing it through autoimmunity later in life or through passive transmission by the mother's immune system at birth.
Connector Corner: Seamlessly power UiPath Apps, GenAI with prebuilt connectorsDianaGray10
Join us to learn how UiPath Apps can directly and easily interact with prebuilt connectors via Integration Service--including Salesforce, ServiceNow, Open GenAI, and more.
The best part is you can achieve this without building a custom workflow! Say goodbye to the hassle of using separate automations to call APIs. By seamlessly integrating within App Studio, you can now easily streamline your workflow, while gaining direct access to our Connector Catalog of popular applications.
We’ll discuss and demo the benefits of UiPath Apps and connectors including:
Creating a compelling user experience for any software, without the limitations of APIs.
Accelerating the app creation process, saving time and effort
Enjoying high-performance CRUD (create, read, update, delete) operations, for
seamless data management.
Speakers:
Russell Alfeche, Technology Leader, RPA at qBotic and UiPath MVP
Charlie Greenberg, host
Your One-Stop Shop for Python Success: Top 10 US Python Development Providersakankshawande
Simplify your search for a reliable Python development partner! This list presents the top 10 trusted US providers offering comprehensive Python development services, ensuring your project's success from conception to completion.
Monitoring and Managing Anomaly Detection on OpenShift.pdfTosin Akinosho
Monitoring and Managing Anomaly Detection on OpenShift
Overview
Dive into the world of anomaly detection on edge devices with our comprehensive hands-on tutorial. This SlideShare presentation will guide you through the entire process, from data collection and model training to edge deployment and real-time monitoring. Perfect for those looking to implement robust anomaly detection systems on resource-constrained IoT/edge devices.
Key Topics Covered
1. Introduction to Anomaly Detection
- Understand the fundamentals of anomaly detection and its importance in identifying unusual behavior or failures in systems.
2. Understanding Edge (IoT)
- Learn about edge computing and IoT, and how they enable real-time data processing and decision-making at the source.
3. What is ArgoCD?
- Discover ArgoCD, a declarative, GitOps continuous delivery tool for Kubernetes, and its role in deploying applications on edge devices.
4. Deployment Using ArgoCD for Edge Devices
- Step-by-step guide on deploying anomaly detection models on edge devices using ArgoCD.
5. Introduction to Apache Kafka and S3
- Explore Apache Kafka for real-time data streaming and Amazon S3 for scalable storage solutions.
6. Viewing Kafka Messages in the Data Lake
- Learn how to view and analyze Kafka messages stored in a data lake for better insights.
7. What is Prometheus?
- Get to know Prometheus, an open-source monitoring and alerting toolkit, and its application in monitoring edge devices.
8. Monitoring Application Metrics with Prometheus
- Detailed instructions on setting up Prometheus to monitor the performance and health of your anomaly detection system.
9. What is Camel K?
- Introduction to Camel K, a lightweight integration framework built on Apache Camel, designed for Kubernetes.
10. Configuring Camel K Integrations for Data Pipelines
- Learn how to configure Camel K for seamless data pipeline integrations in your anomaly detection workflow.
11. What is a Jupyter Notebook?
- Overview of Jupyter Notebooks, an open-source web application for creating and sharing documents with live code, equations, visualizations, and narrative text.
12. Jupyter Notebooks with Code Examples
- Hands-on examples and code snippets in Jupyter Notebooks to help you implement and test anomaly detection models.
"Frontline Battles with DDoS: Best practices and Lessons Learned", Igor IvaniukFwdays
At this talk we will discuss DDoS protection tools and best practices, discuss network architectures and what AWS has to offer. Also, we will look into one of the largest DDoS attacks on Ukrainian infrastructure that happened in February 2022. We'll see, what techniques helped to keep the web resources available for Ukrainians and how AWS improved DDoS protection for all customers based on Ukraine experience
Fueling AI with Great Data with Airbyte WebinarZilliz
This talk will focus on how to collect data from a variety of sources, leveraging this data for RAG and other GenAI use cases, and finally charting your course to productionalization.
Driving Business Innovation: Latest Generative AI Advancements & Success StorySafe Software
Are you ready to revolutionize how you handle data? Join us for a webinar where we’ll bring you up to speed with the latest advancements in Generative AI technology and discover how leveraging FME with tools from giants like Google Gemini, Amazon, and Microsoft OpenAI can supercharge your workflow efficiency.
During the hour, we’ll take you through:
Guest Speaker Segment with Hannah Barrington: Dive into the world of dynamic real estate marketing with Hannah, the Marketing Manager at Workspace Group. Hear firsthand how their team generates engaging descriptions for thousands of office units by integrating diverse data sources—from PDF floorplans to web pages—using FME transformers, like OpenAIVisionConnector and AnthropicVisionConnector. This use case will show you how GenAI can streamline content creation for marketing across the board.
Ollama Use Case: Learn how Scenario Specialist Dmitri Bagh has utilized Ollama within FME to input data, create custom models, and enhance security protocols. This segment will include demos to illustrate the full capabilities of FME in AI-driven processes.
Custom AI Models: Discover how to leverage FME to build personalized AI models using your data. Whether it’s populating a model with local data for added security or integrating public AI tools, find out how FME facilitates a versatile and secure approach to AI.
We’ll wrap up with a live Q&A session where you can engage with our experts on your specific use cases, and learn more about optimizing your data workflows with AI.
This webinar is ideal for professionals seeking to harness the power of AI within their data management systems while ensuring high levels of customization and security. Whether you're a novice or an expert, gain actionable insights and strategies to elevate your data processes. Join us to see how FME and AI can revolutionize how you work with data!
zkStudyClub - LatticeFold: A Lattice-based Folding Scheme and its Application...Alex Pruden
Folding is a recent technique for building efficient recursive SNARKs. Several elegant folding protocols have been proposed, such as Nova, Supernova, Hypernova, Protostar, and others. However, all of them rely on an additively homomorphic commitment scheme based on discrete log, and are therefore not post-quantum secure. In this work we present LatticeFold, the first lattice-based folding protocol based on the Module SIS problem. This folding protocol naturally leads to an efficient recursive lattice-based SNARK and an efficient PCD scheme. LatticeFold supports folding low-degree relations, such as R1CS, as well as high-degree relations, such as CCS. The key challenge is to construct a secure folding protocol that works with the Ajtai commitment scheme. The difficulty, is ensuring that extracted witnesses are low norm through many rounds of folding. We present a novel technique using the sumcheck protocol to ensure that extracted witnesses are always low norm no matter how many rounds of folding are used. Our evaluation of the final proof system suggests that it is as performant as Hypernova, while providing post-quantum security.
Paper Link: https://eprint.iacr.org/2024/257
Conversational agents, or chatbots, are increasingly used to access all sorts of services using natural language. While open-domain chatbots - like ChatGPT - can converse on any topic, task-oriented chatbots - the focus of this paper - are designed for specific tasks, like booking a flight, obtaining customer support, or setting an appointment. Like any other software, task-oriented chatbots need to be properly tested, usually by defining and executing test scenarios (i.e., sequences of user-chatbot interactions). However, there is currently a lack of methods to quantify the completeness and strength of such test scenarios, which can lead to low-quality tests, and hence to buggy chatbots.
To fill this gap, we propose adapting mutation testing (MuT) for task-oriented chatbots. To this end, we introduce a set of mutation operators that emulate faults in chatbot designs, an architecture that enables MuT on chatbots built using heterogeneous technologies, and a practical realisation as an Eclipse plugin. Moreover, we evaluate the applicability, effectiveness and efficiency of our approach on open-source chatbots, with promising results.
Dandelion Hashtable: beyond billion requests per second on a commodity serverAntonios Katsarakis
This slide deck presents DLHT, a concurrent in-memory hashtable. Despite efforts to optimize hashtables, that go as far as sacrificing core functionality, state-of-the-art designs still incur multiple memory accesses per request and block request processing in three cases. First, most hashtables block while waiting for data to be retrieved from memory. Second, open-addressing designs, which represent the current state-of-the-art, either cannot free index slots on deletes or must block all requests to do so. Third, index resizes block every request until all objects are copied to the new index. Defying folklore wisdom, DLHT forgoes open-addressing and adopts a fully-featured and memory-aware closed-addressing design based on bounded cache-line-chaining. This design offers lock-free index operations and deletes that free slots instantly, (2) completes most requests with a single memory access, (3) utilizes software prefetching to hide memory latencies, and (4) employs a novel non-blocking and parallel resizing. In a commodity server and a memory-resident workload, DLHT surpasses 1.6B requests per second and provides 3.5x (12x) the throughput of the state-of-the-art closed-addressing (open-addressing) resizable hashtable on Gets (Deletes).
[OReilly Superstream] Occupy the Space: A grassroots guide to engineering (an...Jason Yip
The typical problem in product engineering is not bad strategy, so much as “no strategy”. This leads to confusion, lack of motivation, and incoherent action. The next time you look for a strategy and find an empty space, instead of waiting for it to be filled, I will show you how to fill it in yourself. If you’re wrong, it forces a correction. If you’re right, it helps create focus. I’ll share how I’ve approached this in the past, both what works and lessons for what didn’t work so well.
For the full video of this presentation, please visit: https://www.edge-ai-vision.com/2024/06/how-axelera-ai-uses-digital-compute-in-memory-to-deliver-fast-and-energy-efficient-computer-vision-a-presentation-from-axelera-ai/
Bram Verhoef, Head of Machine Learning at Axelera AI, presents the “How Axelera AI Uses Digital Compute-in-memory to Deliver Fast and Energy-efficient Computer Vision” tutorial at the May 2024 Embedded Vision Summit.
As artificial intelligence inference transitions from cloud environments to edge locations, computer vision applications achieve heightened responsiveness, reliability and privacy. This migration, however, introduces the challenge of operating within the stringent confines of resource constraints typical at the edge, including small form factors, low energy budgets and diminished memory and computational capacities. Axelera AI addresses these challenges through an innovative approach of performing digital computations within memory itself. This technique facilitates the realization of high-performance, energy-efficient and cost-effective computer vision capabilities at the thin and thick edge, extending the frontier of what is achievable with current technologies.
In this presentation, Verhoef unveils his company’s pioneering chip technology and demonstrates its capacity to deliver exceptional frames-per-second performance across a range of standard computer vision networks typical of applications in security, surveillance and the industrial sector. This shows that advanced computer vision can be accessible and efficient, even at the very edge of our technological ecosystem.
Northern Engraving | Nameplate Manufacturing Process - 2024Northern Engraving
Manufacturing custom quality metal nameplates and badges involves several standard operations. Processes include sheet prep, lithography, screening, coating, punch press and inspection. All decoration is completed in the flat sheet with adhesive and tooling operations following. The possibilities for creating unique durable nameplates are endless. How will you create your brand identity? We can help!
For the full video of this presentation, please visit: https://www.edge-ai-vision.com/2024/06/temporal-event-neural-networks-a-more-efficient-alternative-to-the-transformer-a-presentation-from-brainchip/
Chris Jones, Director of Product Management at BrainChip , presents the “Temporal Event Neural Networks: A More Efficient Alternative to the Transformer” tutorial at the May 2024 Embedded Vision Summit.
The expansion of AI services necessitates enhanced computational capabilities on edge devices. Temporal Event Neural Networks (TENNs), developed by BrainChip, represent a novel and highly efficient state-space network. TENNs demonstrate exceptional proficiency in handling multi-dimensional streaming data, facilitating advancements in object detection, action recognition, speech enhancement and language model/sequence generation. Through the utilization of polynomial-based continuous convolutions, TENNs streamline models, expedite training processes and significantly diminish memory requirements, achieving notable reductions of up to 50x in parameters and 5,000x in energy consumption compared to prevailing methodologies like transformers.
Integration with BrainChip’s Akida neuromorphic hardware IP further enhances TENNs’ capabilities, enabling the realization of highly capable, portable and passively cooled edge devices. This presentation delves into the technical innovations underlying TENNs, presents real-world benchmarks, and elucidates how this cutting-edge approach is positioned to revolutionize edge AI across diverse applications.
Have you ever been confused by the myriad of choices offered by AWS for hosting a website or an API?
Lambda, Elastic Beanstalk, Lightsail, Amplify, S3 (and more!) can each host websites + APIs. But which one should we choose?
Which one is cheapest? Which one is fastest? Which one will scale to meet our needs?
Join me in this session as we dive into each AWS hosting service to determine which one is best for your scenario and explain why!
1. Myasthenia gravis (MG) is a relatively rare autoimmune disorder of peripheral nerves in which
antibodies form against acetylcholine (ACh) nicotinic postsynaptic receptors at the neuromuscular
junction (NMJ). The basic pathology is a reduction in the number of ACh receptors (AChR) at the
postsynaptic muscle membrane brought about by an acquired autoimmune reaction producing anti-
AChR antibodies. MG is broken down into 2 major clinical forms: ocular MG and generalized MG.
The reduction in the number of AChRs results in a characteristic pattern of progressively reduced
muscle strength with repeated use and recovery of muscle strength after a period of rest. The bulbar
muscles are affected most commonly and most severely, but most patients also develop some degree
of fluctuating generalized weakness.[1] The most important aspect of MG in emergency situations is
detection and management of the 2 crises: myasthenic and cholinergic.
MG is one of the most treatable neurologic disorders. Pharmacologic therapy includes
anticholinesterase medication and immunosuppressive agents, such as corticosteroids, azathioprine,
cyclosporine, plasmapheresis, and intravenous immune globulin (IVIg). Plasmapheresis and
thymectomy are also employed to treat MG. Thymectomy is an especially important option if a
thymoma is present. Patients with MG require close follow-up care in cooperation with the primary
care physician.
Etiology
MG is idiopathic in most patients. Although the main cause behind its development remains
speculative, the end result is a derangement of immune system regulation. MG is clearly an
autoimmune disease in which the specific antibody has been characterized completely. In as many as
90% of generalized cases, IgG to AChR is present.[7] Even in patients who do not develop clinical
myasthenia, anti-AChR antibodies can sometimes be demonstrated.
Patients who are negative for anti-AChR antibodies may be seropositive for antibodies against MuSK.
Muscle biopsies in these patients show myopathic signs with prominent mitochondrial abnormalities,
as opposed to the neurogenic features and atrophy frequently found in MG patients positive for anti-
AChR. The mitochondrial impairment could explain the oculobulbar involvement in anti-MuSK–
positive MG.[8]
Numerous findings have been associated with MG. For example, females and people with certain
human leukocyte antigen (HLA) types have a genetic predisposition to autoimmune diseases. The
histocompatibility complex profile includes HLA-B8, HLA-DRw3, and HLA-DQw2 (though these have
not been shown to be associated with the strictly ocular form of MG). Both SLE and RA may be
associated with MG.
Sensitization to a foreign antigen that has cross-reactivity with the nicotinic ACh receptor has been
proposed as a cause of myasthenia gravis, but the triggering antigen has not yet been identified.
Various drugs may induce or exacerbate symptoms of MG, including the following:
Antibiotics (eg, aminoglycosides, polymyxins, ciprofloxacin, erythromycin, and ampicillin)
Penicillamine - This can induce true myasthenia, with elevated anti-AChR antibody titers seen in
90% of cases; however, the weakness is mild, and full recovery is achieved weeks to months after
discontinuance of the drug
Beta-adrenergic receptor blocking agents (eg, propranolol and oxprenolol)
Lithium
Magnesium
Procainamide
Verapamil
Quinidine
Chloroquine
Prednisone
Timolol (ie, a topical beta-blocking agent used for glaucoma)
Anticholinergics (eg, trihexyphenidyl)
Neuromuscular blocking agents (eg, vecuronium and curare) - These should be used cautiously in
myasthenic patients to avoid prolonged neuromuscular blockade
2. Nitrofurantoin has also been linked to the development of ocular MG in 1 case report; discontinuance
of the drug resulted in complete recovery.
Thymic abnormalities are common: Of patients with MG, 75% have thymic disease, 85% have thymic
hyperplasia, and 10-15% havethymoma. Extrathymictumors may include small cell lung cancer and
Hodgkin disease. Hyperthyroidism is present in 3-8% of patients with MG and has a particular
association with ocular MG.
Pathophysiology
With every nerve impulse, the amount of ACh released by the presynaptic motor neuron normally
decreases because of a temporary depletion of the presynaptic ACh stores (a phenomenon referred
to as presynaptic rundown).
In MG, there is a reduction in the number of AChRs available at the muscle endplate and flattening of
the postsynaptic folds. Consequently, even if a normal amount of ACh is released, fewer endplate
potentials will be produced, and they may fall below the threshold value for generation of an action
potential. The end result of this process is inefficient neuromuscular transmission.
Inefficient neuromuscular transmission together with the normally present presynaptic rundown
phenomenon results in a progressive decrease in the amount of nerve fibers being activated by
successive nerve fiber impulses. This explains the fatigability seen in MG patients.
Patients become symptomatic once the number of AChRs is reduced to approximately 30% of
normal. The cholinergic receptors of smooth and cardiac muscle have a different antigenicity than
skeletal muscle and are not affected by the disease.
The decrease in the number of postsynaptic AChRs is believed to be due to an autoimmune process
whereby anti-AChR antibodies are produced and block the target receptors, cause an increase the
turnover of the receptors, and damage the postsynaptic membrane in a complement-mediated
manner.
Clinical observations support the idea that immunogenic mechanisms play important roles in the
pathophysiology of MG. Such observations include the presence of associated autoimmune disorders
(eg, autoimmune thyroiditis, systemic lupus erythematosus [SLE], and rheumatoid arthritis [RA]) in
patients with MG.
Moreover, infants born to myasthenic mothers can develop a transient myasthenialike syndrome.
Patients with MG will have a therapeutic response to various immunomodulating therapies, including
plasmapheresis, corticosteroids, intravenous immunoglobulin (IVIg), other immunosuppressants, and
thymectomy.
Anti-AChR antibody is found in approximately 80-90% of patients with MG. Experimental observations
supporting an autoimmune etiology of MG include the following:
Induction of a myasthenialike syndrome in mice by injecting a large quantity of immunoglobulin G
(IgG) from MG patients (ie, passive transfer experiments)
Demonstration of IgG and complement at the postsynaptic membrane in patients with MG
Induction of a myasthenialike syndrome in rabbits immunized against AChR by injecting them with
AChR isolated from Torpedo californica (the Pacific electric ray)
The exact mechanism of loss of immunologic tolerance to AChR, a self-antigen, is not understood.
MG can be considered a B cell–mediated disease, in that it derives from antibodies (a B cell product)
against AChR. However, the importance of T cells in the pathogenesis of MG is becoming
increasingly apparent. The thymus is the central organ in T cell–mediated immunity, and thymic
abnormalities such as thymic hyperplasia or thymoma are well recognized in myasthenic patients.
Antibody response in MG is polyclonal. In an individual patient, antibodies are composed of different
subclasses of IgG. In most instances, 1 antibody is directed against the main immunogenic region
(MIR) on the alpha subunit. The alpha subunit is also the site of ACh binding, though the binding site
for ACh is not the same as the MIR. Binding of AChR antibodies to AChR results in impairment of
neuromuscular transmission in several ways, including the following:
3. Cross-linking 2 adjacent AChRs with anti-AChR antibody, thus accelerating internalization and
degradation of AChR molecules
Causing complement-mediated destruction of junctional folds of the postsynaptic membrane
Blocking the binding of ACh to AChR
Decreasing the number of AChRs at the NMJ by damaging the junctional folds on the postsynaptic
membrane, thereby reducing the surface area available for insertion of newly synthesized AChRs
Patients without anti-AChR antibodies are recognized as having seronegative MG (SNMG). Many
patients with SNMG have antibodies against muscle-specific kinase (MuSK). MuSK plays a critical
role in postsynaptic differentiation and clustering of AChRs. Patients with anti-MuSK antibodies are
predominantly female, and respiratory and bulbar muscles are frequently involved. Another group has
reported patients who exhibit prominent neck, shoulder, and respiratory weakness. [5, 6]
The role of the thymus in the pathogenesis of MG is not entirely clear, but 75% of patients with MG
have some degree of thymus abnormality (eg, hyperplasia or thymoma). Histopathologic studies have
shown prominent germinal centers. Epithelial myoid cells normally present in the thymus do resemble
skeletal muscle cells and possess AChRs on their surface membrane. These cells may become
antigenic and unleash an autoimmune attack on the muscular endplate AChRs by molecular mimicry.
The question of why MG afflicts the extraocular muscles first and predominantly remains unanswered.
The answer probably has to do with the physiology and antigenicity of the muscles in question.
Diagnosis
MG can be a difficult diagnosis, as the symptoms can be subtle and hard to distinguish from both
[4]
normal variants and other neurological disorders. A thorough physical examination can reveal easy
fatigability, with the weakness improving after rest and worsening again on repeat of the exertion
testing. Applying ice to weak muscle groups characteristically leads to improvement in strength of
those muscles. Additional tests are often performed, as mentioned below. Furthermore, a good
response to medication can also be considered a sign of autoimmune pathology.
[edit]Physical examination
[11]
Muscle fatigability can be tested for many muscles. A thorough investigation includes:
looking upward and sidewards for 30 seconds: ptosis and diplopia
looking at the feet while lying on the back for 60 seconds
keeping the arms stretched forward for 60 seconds
ten deep knee bends
walking 30 steps on both the toes and the heels
five situps, lying down and sitting up completely
"Peek sign": after complete initial apposition of the lid margins, they quickly (within 30 seconds)
[4]
start to separate and the sclera starts to show
[edit]Blood tests
If the diagnosis is suspected, serology can be performed in a blood test to identify certain antibodies:
[4]
One test is for antibodies against the acetylcholine receptor. The test has a
reasonable sensitivity of 80–96%, but in MG limited to the eye muscles (ocular myasthenia) the
test may be negative in up to 50% of the cases.
A proportion of the patients without antibodies against the acetylcholine receptor have antibodies
[12]
against the MuSK protein.
4. In specific situations (decreased reflexes which increase on facilitation, coexisting autonomic
features, suspected presence of neoplasm, especially of the lung, presence of increment or
facilitation on repetitive EMG testing) testing is performed for Lambert-Eaton syndrome, in which
other antibodies (against a voltage-gated calcium channel) can be found.
[edit]Electrodiagnostics
Muscle fibers of patients with MG are easily fatigued, and thus do not respond as well as muscles in
healthy individuals to repeated stimulation. By stimulating a nerve-muscle motor unit with short
sequences of rapid, regular electrical impulses, before and after exercising the motor unit, the
fatiguability of the muscle can be measured. This is called the repetitive nerve stimulation test. In
single fiber electromyography (SFEMG), which is considered to be the most sensitive (although not
[4]
the most specific) test for MG, a thin needle electrode is inserted into different areas of a particular
muscle to record the action potentials from several samplings of different individual muscle fibers.
Two muscle fibers belonging to the same motor unit are identified and the temporal variability in their
firing patterns are measured. Frequency and proportion of particular abnormal action potential
patterns, "jitter" and "blocking," are diagnostic. Jitter refers to the abnormal variation in the time
interval between action potentials of adjacent muscle fibers in the same motor unit. Blocking refers to
the failure of nerve impulses to elicit action potentials in adjacent muscle fibers of the same motor
[13]
unit.
[edit]Edrophonium test
Photograph of a patient showing right partial ptosis (left picture), the left lid shows compensatory pseudo lid retraction
because of equal innervation of the levatorpalpabraesuperioris (Hering's law of equal innervation). Right picture: after
an edrophonium test, note the improvement in ptosis.
The "edrophonium test" is infrequently performed to identify MG; its application is limited to the
situation when other investigations do not yield a conclusive diagnosis. This test requires
the intravenous administration of edrophonium chloride (Tensilon, Reversol) or neostigmine
(Prostigmin), drugs that block the breakdown of acetylcholine by cholinesterase (acetylcholinesterase
inhibitors) and temporarily increases the levels of acetylcholine at theneuromuscular junction. In
people with myasthenia gravis involving the eye muscles, edrophonium chloride will briefly relieve
[14]
weakness.
[edit]Imaging
A chest CT-scan showing a thymoma (red circle)
5. A chest X-ray is frequently performed; it may point towards alternative diagnoses (e.g. Lambert-Eaton
syndrome due to a lung tumor) and comorbidity. It may also identify widening of
the mediastinum suggestive of thymoma, but computed tomography (CT) or magnetic resonance
imaging (MRI) are more sensitive ways to identify thymomas, and are generally done for this
[15]
reason. MRI of the cranium and orbits is also performed to exclude compressive and inflammatory
[16]
lesions of the cranial nerves and ocular muscles.
[edit]Pulmonary function test
Spirometry (lung function testing) may be performed for the assessing of respiratory function if there
are concerns about a patient's ability to breathe adequately. The forced vital capacity may be
monitored at intervals so as not to miss a gradual worsening of muscular weakness. Acutely, negative
inspiratory force may be used to determine adequacy of ventilation. Severe myasthenia may
[17]
cause respiratory failure due to exhaustion of the respiratory muscles.
[edit]Pathological findings
Muscle biopsy is only performed if the diagnosis is in doubt and a muscular condition is
suspected. Immunofluorescence shows IgG antibodies on the neuromuscular junction. (The antibody
which causes myasthenia gravis does not fluoresce, but rather a secondary antibody directed against
it.) Muscle electron microscopy shows receptor infolding and loss of the tips of the folds, together with
widening of the synaptic clefts. Both these techniques are currently used for research rather than
[7]
diagnostically.