query: What is the name of the chronic neurological autoimmune disease which attacks the protein sheath that surrounds nerve cells causing a gradual loss of movement in the body?

title: Autoimmune hepatitis

text: used. The current name at present is autoimmune hepatitis (AIH). Autoimmune hepatitis Autoimmune hepatitis, formerly called lupoid hepatitis, is a chronic, autoimmune disease of the liver that occurs when the body's immune system attacks liver cells causing the liver to be inflamed. Common initial symptoms include fatigue or muscle aches or signs of acute liver inflammation including fever, jaundice, and right upper quadrant abdominal pain. Individuals with autoimmune hepatitis often have no initial symptoms and the disease is detected by abnormal liver function tests. Anomalous presentation of MHC class II receptors on the surface of liver cells, possibly due to

title: Malignant peripheral nerve sheath tumor

text: nerve sheath tumors are a rare type of cancer that arise from the soft tissue that surrounds nerves. They are a type of sarcoma. Most malignant peripheral nerve sheath tumors arise from the nerve plexuses that distribute nerves into the limbs—the brachial and lumbar plexuses—or from nerves as they arise from the trunk. Symptoms may include: Soft tissue sarcomas have been linked within families, so it is hypothesized that neurofibrosarcoma may be genetic, although researchers still do not know the exact cause of the disease. Evidence supporting this hypothesis includes loss of heterozygosity on the 17p chromosome. The p53 (a

title: Autoimmune hepatitis

text: Autoimmune hepatitis Autoimmune hepatitis, formerly called lupoid hepatitis, is a chronic, autoimmune disease of the liver that occurs when the body's immune system attacks liver cells causing the liver to be inflamed. Common initial symptoms include fatigue or muscle aches or signs of acute liver inflammation including fever, jaundice, and right upper quadrant abdominal pain. Individuals with autoimmune hepatitis often have no initial symptoms and the disease is detected by abnormal liver function tests. Anomalous presentation of MHC class II receptors on the surface of liver cells, possibly due to genetic predisposition or acute liver infection, causes a cell-mediated immune

title: Autoimmune thyroiditis

text: Autoimmune thyroiditis Autoimmune thyroiditis, (or Chronic Autoimmune thyroiditis), is a chronic disease in which the body interprets the thyroid glands and its hormone products T3, T4 and TSH as threats, therefore producing special antibodies that target the thyroid’s cells, thereby destroying it. It may present with hypothyroidism or hyperthyroidism and with or without a goiter. The symptoms may vary depending on the thyroid function, i.e. hyperthyroidism or hypothyroidism. Hyperthyroidism can cause sweating, rapid heart rate, anxiety, tremors, fatigue, difficulty sleeping, sudden weight loss, and protruding eyes. Hypothyroidism can cause weight gain, fatigue, dry skin, hair loss, intolerance to cold, and

title: Autoimmune thyroiditis

text: person has been diagnosed with thyroid cancer, and just like TPOAb, it can be associated with Hashimoto’s thyroiditis. Specialists separate autoimmune thyroiditis into two clinical categories. It can also refer to Graves' disease. If the symptoms of thyroiditis appear in women after giving birth, it is called postpartum thyroiditis. Immunosuppressants such as methotrexate, cyclophosphamide. Possible connection with depression and anxiety Autoimmune thyroiditis Autoimmune thyroiditis, (or Chronic Autoimmune thyroiditis), is a chronic disease in which the body interprets the thyroid glands and its hormone products T3, T4 and TSH as threats, therefore producing special antibodies that target the thyroid’s cells, thereby

title: Autoimmune disease

text: was challenged by the discovery of a substance in the serum of patients with paroxysmal cold hemoglobinuria that reacted with red blood cells. Autoimmune disease An autoimmune disease is a condition arising from an abnormal immune response to a normal body part. There are at least 80 types of autoimmune diseases. Nearly any body part can be involved. Common symptoms include low grade fever and feeling tired. Often symptoms come and go. The cause is generally unknown. Some autoimmune diseases such as lupus run in families, and certain cases may be triggered by infections or other environmental factors. Some common

title: Chronic kidney disease

text: Chronic kidney disease Chronic kidney disease (CKD) is a type of kidney disease in which there is gradual loss of kidney function over a period of months or years. Early on there are typically no symptoms. Later, leg swelling, feeling tired, vomiting, loss of appetite, or confusion may develop. Complications may include heart disease, high blood pressure, bone disease, or anemia. Causes of chronic kidney disease include diabetes, high blood pressure, glomerulonephritis, and polycystic kidney disease. Risk factors include a family history of the condition. Diagnosis is generally by blood tests to measure the glomerular filtration rate and urine tests

title: Autoimmune disease

text: other hand, is the presence of self-reactive immune response (e.g., auto-antibodies, self-reactive T cells), with or without damage or pathology resulting from it. This may be restricted to certain organs (e.g. in autoimmune thyroiditis) or involve a particular tissue in different places (e.g. Goodpasture's disease which may affect the basement membrane in both the lung and the kidney). There are many theories as to how an autoimmune disease state arises. Some common ones are listed below. Although it is possible for a potential autoantigen to be spatially sequestered in an immune privileged site within the body (e.g. the eye), mechanisms

title: Polyneuropathy

text: or by "classes" of polyneuropathy, in terms of which part of the nerve cell is affected mainly: the axon, the myelin sheath, or the cell body. Among the signs/symptoms of polyneuropathy, which can be divided (into sensory and hereditary) and are consistent with the following: The causes of polyneuropathy can be divided into hereditary and acquired and are therefore as follows: In regards to the pathophysiology of polyneuropathy, of course, the former depends on "which" polyneuropathy. For instance in the case of chronic inflammatory demyelinating polyneuropathy, one finds that it is a autoimmune disease. Here, T cells involvement has been

title: Autoimmune disease

text: Autoimmune disease An autoimmune disease is a condition arising from an abnormal immune response to a normal body part. There are at least 80 types of autoimmune diseases. Nearly any body part can be involved. Common symptoms include low grade fever and feeling tired. Often symptoms come and go. The cause is generally unknown. Some autoimmune diseases such as lupus run in families, and certain cases may be triggered by infections or other environmental factors. Some common diseases that are generally considered autoimmune include celiac disease, diabetes mellitus type 1, Graves' disease, inflammatory bowel disease, multiple sclerosis, psoriasis, rheumatoid arthritis,

title: Anemia of chronic disease

text: is advised either in conjunction with adequate iron replacement which in practice is intravenous, or when IV iron has proved ineffective. Anemia of chronic disease Anemia of chronic disease, or anemia of chronic inflammation, is a form of anemia seen in chronic infection, chronic immune activation, and malignancy. These conditions all produce massive elevation of Interleukin-6, which stimulates hepcidin production and release from the liver, which in turn reduces the iron carrier protein ferroportin so that access of iron to the circulation is reduced. Other mechanisms may also play a role, such as reduced erythropoiesis. Anemia of chronic inflammation is

title: Anemia of chronic disease

text: Anemia of chronic disease Anemia of chronic disease, or anemia of chronic inflammation, is a form of anemia seen in chronic infection, chronic immune activation, and malignancy. These conditions all produce massive elevation of Interleukin-6, which stimulates hepcidin production and release from the liver, which in turn reduces the iron carrier protein ferroportin so that access of iron to the circulation is reduced. Other mechanisms may also play a role, such as reduced erythropoiesis. Anemia of chronic inflammation is the preferred term since not all chronic diseases are associated with this form of anemia. Anemia is considered when RBCs count

title: Adult polyglucosan body disease

text: Adult polyglucosan body disease Adult polyglucosan body disease (APBD) is an orphan disease and a glycogen storage disorder that is caused by an inborn error of metabolism. Symptoms can emerge any time after the age of 30; early symptoms include trouble controlling urination, trouble walking, and lack of sensation in the legs. People eventually develop dementia. A person inherits loss-of-function mutations in the "GBE1" gene from each parent, and the lack of glycogen branching enzyme (the protein encoded by "GNE1") leads to buildup of unbranched glycogen in cells, which harms neurons more than other kinds of cells. Most people first

title: IL17A

text: the transcriptional factor NF-kappa B activity and interleukin-6 (IL-6) secretion in fibroblasts. IL-17RA pairs with IL-17RC to allow binding and signaling of IL-17A and IL-17F. High levels of this cytokine are associated with several chronic inflammatory diseases including rheumatoid arthritis, psoriasis and multiple sclerosis. Multiple sclerosis (MS) is a neurological disease caused by immune cells, which attack and destroy the myelin sheath that insulates neurons in the brain and spinal cord. This disease and its animal model experimental autoimmune encephalomyelitis (EAE) have historically been associated with the discovery of Th17 cells. However, elevated expression of IL-17A in multiple sclerosis (MS)

title: Autoimmune disease

text: list to 81 diseases and estimated overall cumulative US prevalence for the 81 autoimmune diseases at 5.0%, with 3.0% for males and 7.1% for females. The estimated community prevalence, which takes into account the observation that many people have more than one autoimmune disease, was 4.5% overall, with 2.7% for males and 6.4% for females. In both autoimmune and inflammatory diseases, the condition arises through aberrant reactions of the human adaptive or innate immune systems. In autoimmunity, the patient's immune system is activated against the body's own proteins. In chronic inflammatory diseases, neutrophils and other leukocytes are constitutively recruited by

title: Alexander disease

text: Alexander disease Alexander disease is one of a group of neurological conditions known as the leukodystrophies, which are ailments caused by anomalies in the myelin, which protects nerve fibers in the brain. According to the National Institute of Neurological Disorders and Stroke, the destruction of white matter is accompanied by the formation of Rosenthal fibers—abnormal clumps of protein that accumulate in astrocytes in the brain. The most common type of Alexander disease is the infantile form that usually begins during the first 2 years of life. Symptoms include mental and physical developmental delays, followed by the loss of developmental milestones,

title: Charcot–Marie–Tooth disease

text: exchange molecular signals that regulate survival and differentiation. These signals are disrupted in CMT. Demyelinating Schwann cells causes abnormal axon structure and function. They may cause axon degeneration, or they may simply cause axons to malfunction. The myelin sheath allows nerve cells to conduct signals faster. When the myelin sheath is damaged, nerve signals are slower, and this can be measured by a common neurological test, electromyography. When the axon is damaged, though, this results in a reduced compound muscle action potential. CMT can be diagnosed through symptoms, through measurement of the speed of nerve impulses (nerve conduction studies), through

title: Vitamin D and neurology

text: lack of "Nurr1" expression leads to impaired DA neuronal development. Failure to form DA neurons would lead to lower dopamine concentrations in the basal ganglia. Additionally, rats lacking "Nurr1" exhibited hypoactivity followed by death shortly after birth. Multiple sclerosis (MS) is an autoimmune disease causing demyelination within the central nervous system. In the central nervous system, there are many cells encased in a fatty coating called the myelin sheath. This sheath allows for informational signals to be transmitted at greater speeds down through the cell. In multiple sclerosis, this sheath deterioration causes a slower transmission of nerve signals. This ultimately

title: Myelin

text: further understanding of nerve fiber regeneration in the central nervous system. Demyelination is the loss of the myelin sheath insulating the nerves, and is the hallmark of some neurodegenerative autoimmune diseases, including multiple sclerosis, acute disseminated encephalomyelitis, neuromyelitis optica, transverse myelitis, chronic inflammatory demyelinating polyneuropathy, Guillain–Barré syndrome, central pontine myelinosis, inherited demyelinating diseases such as leukodystrophy, and Charcot-Marie-Tooth disease. Sufferers of pernicious anaemia can also suffer nerve damage if the condition is not diagnosed quickly. Subacute combined degeneration of spinal cord secondary to pernicious anaemia can lead to slight peripheral nerve damage to severe damage to the central nervous system,

title: Pathology of multiple sclerosis

text: the reasons why, especially in early phases of the disease, symptoms tend to decrease or disappear temporarily. Nevertheless, nerve damage and irreversible loss of neurons occur early in MS. The oligodendrocytes that originally formed a myelin sheath cannot completely rebuild a destroyed myelin sheath. However, the central nervous system can recruit oligodendrocyte stem cells capable of proliferation and migration and differentiation into mature myelinating oligodendrocytes. The newly formed myelin sheaths are thinner and often not as effective as the original ones. Repeated attacks lead to successively fewer effective remyelinations, until a scar-like plaque is built up around the damaged axons.

title: Coeliac disease

text: for Health and Clinical Excellence (NICE) recommend testing for coeliac disease in first-degree relatives of those with the disease already confirmed, in people with persistent fatigue, abdominal or gastrointestinal symptoms, faltering growth, unexplained weight loss or iron, vitamin B12 or folate deficiency, severe mouth ulcers, and with diagnoses of type 1 diabetes, autoimmune thyroid disease, and with newly diagnosed chronic fatigue syndrome and irritable bowel syndrome. Dermatitis herpetiformis is included in other recommendations. The NICE also recommend offering serological testing for coeliac disease in people with metabolic bone disease (reduced bone mineral density or osteomalacia), unexplained neurological disorders (such as

title: Vestibular nerve

text: nerve implicitly plays a role in maintaining stable blood pressure during movement, maintaining balance control, spatial memory and spatial navigation. The most common causes of damage to the vestibular nerve are exposure to ototoxic antibiotics, Ménière's disease, encephalitis and some rare autoimmune disorders. Typically, patients with a damaged nerve suffer from acute attacks of vertigo accompanied by nausea/vomiting, inability to maintain posture and horizontal nystagmus. Rapid compensation to damage of the vestibular nerve occurs within seven to ten days of receiving the damage. A small percentage of patients with damage to the vestibular nerve experience recurrent symptoms. These patients have

title: Autoimmune disease in women

text: Autoimmune disease in women Autoimmune disease in women is a description of the autoimmune diseases that affect women. Some of these differences are unique to women such as the effects during pregnancy. Women with autoimmune diseases can safely have children. There are be some risks for the mother or baby, depending on the disease and how severe it is. For instance, pregnant women with lupus have a higher risk of preterm birth and stillbirth. Pregnant women with myasthenia gravis (MG) might have symptoms that lead to trouble breathing during pregnancy. For some women, symptoms tend to improve during pregnancy, while

title: Whipple's disease

text: advanced form, malabsorption (insufficient absorption of nutrients from the diet) leads to wasting and the enlargement of lymph nodes in the abdomen. Neurological symptoms (discussed below) are more common in those with the severe form of the abdominal disease. Chronic malabsorptive diarrhea leads to the poor absorption of fat, causing steatorrhea (fatty, offensive-smelling stool), flatulence, and abdominal distension. Protein-losing enteropathy may also occur, causing depletion of albumin, a blood protein, which may lead to peripheral edema caused by the lowered oncotic pressures. Hyperpigmentation of the skin occurs in almost half; some also have skin nodules. Various eye problems, such as

title: Neurological disorder

text: problems with the blood vessels (cardiovascular system) supplying the brain; autoimmune disorders involve damage caused by the body's own immune system; lysosomal storage diseases such as Niemann-Pick disease can lead to neurological deterioration. The National Institutes of Health recommend considering the evaluation of an underlying celiac disease in people with unexplained neurological symptoms, particularly peripheral neuropathy or ataxia. In a substantial minority of cases of neurological symptoms, no neural cause can be identified using current testing procedures, and such "idiopathic" conditions can invite different theories about what is occurring. Neurological disorders can be categorized according to the primary location affected,

title: Autoimmune inner ear disease

text: tumor necrosis factor-α (TNF-α) inhibitors must be administered alongside corticosteroids to achieve a favorable outcome and eventual end to corticosteroid treatment. Recent papers have indicated that the TNF-α inhibitor, infliximab, has the potential to allow for sustained patient improvement and alleviation of symptoms. Cytotoxic agents such as cyclophosphamide and methotrexate have been used in AIED treatment in the past; however, findings have suggested limited symptom alleviation from these drugs. Autoimmune inner ear disease Autoimmune inner ear disease (AIED) was first defined by Dr. Brian McCabe in a landmark paper describing an autoimmune loss of hearing. The disease results in progressive

title: Chronic inflammatory demyelinating polyneuropathy

text: lumbar puncture to verify the presence of increased cerebrospinal fluid protein. Symptoms such as diminished or absent deep-tendon reflexes and sensory ataxia are common. Other symptoms include proximal and distal muscle weakness in the limbs. Chronic inflammatory demyelinating polyneuropathy (or polyradiculoneuropathy) is considered an autoimmune disorder destroying myelin, the protective covering of the nerves. Typical early symptoms are "tingling" (sort of electrified vibration or paresthesia) and/or numbness in the extremities, frequent (night) leg cramps, loss of reflexes (in knees), muscle fasciculations, "vibration" feelings, loss of balance, general muscle cramping and nerve pain. CIDP is extremely rare but under-recognized and under-treated

title: Neurilemma

text: function for peripheral nerve fibers. Damaged nerve fibers may regenerate if the cell body is not damaged and the neurilemma remains intact. The neurilemma forms a regeneration tube through which the growing axon re-establishes its original connection. A neurilemoma is a tumor of the neurilemma. Neurilemma Neurilemma (also known as neurolemma, sheath of Schwann, or Schwann's sheath) is the outermost nucleated cytoplasmic layer of Schwann cells (also called neurilemmocytes) that surrounds the axon of the neuron. It forms the outermost layer of the nerve fiber in the peripheral nervous system. The neurilemma is underlain by the myelin sheath (referred to

title: Sphingomyelin

text: accumulation of sphingomyelin in spleen, liver, lungs, bone marrow, and brain, causing irreversible neurological damage. Of the two types involving sphingomyelinase, type A occurs in infants. It is characterized by jaundice, an enlarged liver, and profound brain damage. Children with this type rarely live beyond 18 months. Type B involves an enlarged liver and spleen, which usually occurs in the pre-teen years. The brain is not affected. Most patients present with <1% normal levels of the enzyme in comparison to normal levels. As a result of the autoimmune disease multiple sclerosis (MS), the myelin sheath of neuronal cells in the

title: Parkinson's disease clinical research

text: and stability and allowed the nerve cells to resume normal activity. Successful long-term therapy must both protect the areas of the brain under attack and foster the repair of dopaminergic neurons damage to other brain cell populations. Astrocyte dysfunction can contribute to multiple neurological disorders. After transplantation, dopaminergic, interneurons and synaptophysin were all rescued. Interneurons play an important role in information processing and movement control and are lost in Parkinson's. Synaptophysin is a protein that is essential for communication between nerve cells. The transplanted rats recovered motor skills to normal levels, essentially reversing all symptoms. No previous therapies rescued these

title: Mucosal associated invariant T cell

text: respond against viruses upon stimulation with IL-18 and other cytokines, such as IL-12 and IFN-α/β. After receiving these cytokine signals, MAIT cells secrete anti-viral cytotoxic molecules and cytokines that aid the immune response. While MAIT cells play a crucial role in the immune system by targeting bacterially-infected cells and other pathogens, they may also attack healthy cells and play a role in certain autoimmune diseases. For individuals with the autoimmune disease multiple sclerosis (MS), the immune system attacks the myelin sheaths covering nerves, causing impaired nerve signaling. While T helper 1 (Th1) and T helper 17 (Th17) cells have been

title: Molecular mimicry

text: CNS tissue and act as autoantibodies. This contributes to many CNS complications found in AIDS patients. Theiler's murine encephalomyelitis virus (TMEV) leads to the development in mice of a progressive CD4 T cell-mediated response after these cells have infiltrated the CNS. This virus has been shown to cause CNS disease in mice that resembles multiple sclerosis, an autoimmune disease in humans that results in the gradual destruction of the myelin sheath coating axons of the CNS. The TMEV mouse virus shares a thirteen amino acid sequence (His-Cys-Leu-Gly-Lys-Trp-Leu-Gly-His-Pro-Asp-Lys-Phe) (PLP (proteolipid protein) 139-151 epitope) with that of a human myelin-specific epitope. Bystander

title: Thyroid disease

text: without causing any symptoms or clinical changes, and may not require treatment. The following medications have been linked to various forms of thyroid disease: Most thyroid disease in the United States stems from a condition where the body's immune system attacks itself. In other instances, thyroid disease comes from the body trying to adapt to environmental conditions like iodine deficiency or to new physiologic conditions like pregnancy. Autoimmune thyroid disease is a general category of disease that occurs due to the immune system targeting its own body. It is not fully understood why this occurs, but it is thought to

title: Chronic granulomatous disease

text: Minnesota, and in 1957 it was named "a fatal granulomatosus of childhood" in a publication describing their disease. The underlying cellular mechanism that causes chronic granulomatous disease was discovered in 1967, and research since that time has further elucidated the molecular mechanisms underlying the disease. Bernard Babior made key contributions in linking the defect of superoxide production of white blood cells, to the cause of the disease. In 1986, the X-linked form of CGD was the first disease for which positional cloning was used to identify the underlying genetic mutation. Classically, patients with chronic granulomatous disease will suffer from recurrent

title: Autoimmune hypophysitis

text: a rare disease and the most recent estimates as to its prevalence give it a value of around 5 per million. Autoimmune hypophysitis Autoimmune hypophysitis or lymphocytic hypophysitis is defined as inflammation of the pituitary gland due to autoimmunity. The symptoms depend on what part of the pituitary is affected. Lymphocytic adenohypophysitis (LAH) occurs when the anterior pituitary cells are affected by autoimmune inflammation resulting in either no symptoms, adrenal insufficiency (if the ACTH producing cells are affected), hypothyroidism (if the TSH producing cells are damaged), or hypogonadism (if the LH and/or FSH producing cells are involved). In some cases,

title: Autoimmune hypophysitis

text: Autoimmune hypophysitis Autoimmune hypophysitis or lymphocytic hypophysitis is defined as inflammation of the pituitary gland due to autoimmunity. The symptoms depend on what part of the pituitary is affected. Lymphocytic adenohypophysitis (LAH) occurs when the anterior pituitary cells are affected by autoimmune inflammation resulting in either no symptoms, adrenal insufficiency (if the ACTH producing cells are affected), hypothyroidism (if the TSH producing cells are damaged), or hypogonadism (if the LH and/or FSH producing cells are involved). In some cases, the presence of inflammation within the pituitary gland leads to interruption of dopamine flow from the hypothalamus into the pituitary causing

title: Alexander disease

text: older patients, bulbar or pseudobulbar symptoms and spasticity predominate. Symptoms of the adult form may also resemble multiple sclerosis. No more than 500 cases have been reported. Alexander disease Alexander disease is one of a group of neurological conditions known as the leukodystrophies, which are ailments caused by anomalies in the myelin, which protects nerve fibers in the brain. According to the National Institute of Neurological Disorders and Stroke, the destruction of white matter is accompanied by the formation of Rosenthal fibers—abnormal clumps of protein that accumulate in astrocytes in the brain. The most common type of Alexander disease is

title: Protein toxicity

text: lead to death. Most of the problems stem from the accumulation of unfiltered toxins and wastes from protein metabolism. Kidney function naturally declines with age due to the gradual loss of nephrons (filters) in the kidney. Therefore, a 90-year-old cannot safely consume the same amount of protein as a 20-year-old. Common causes of chronic kidney disease include diabetes, heart disease, long term untreated high blood pressure, as well as abuse of analgesics like ibuprofen, aspirin, and paracetamol. Kidney disease like the polycystic kidney disease can be genetic in nature and progress as the patient ages. A confirmation of kidney failure

title: Autoimmune disease in women

text: others find their symptoms tend to flare up. Also, some medicines used to treat autoimmune diseases might not be safe to use during pregnancy. Talking with a health care provider before becoming pregnant is recommended. They may suggest to wait until the disease is in remission or suggest a change in medication before becoming pregnant. There are endocrinologists that specialize in treating women with high-risk pregnancies. Some women with autoimmune diseases may have problems getting pregnant. This can happen for many reasons. Tests can tell if fertility problems are caused by an autoimmune disease or an unrelated reason. Fertility treatments

title: Autoimmune hepatitis

text: weight loss, mild right upper quadrant pain, malaise, anorexia, nausea, jaundice or arthralgia affecting the small joints. Rarely, rash or unexplained fever may appear. In women, amenorrhoea is a frequent feature. Physical examination may be normal, but it may also reveal signs and symptoms of chronic liver disease. Many people have only laboratory abnormalities as their initial presentation, as unexplained increase in transaminases and are diagnosed during an evaluation for other reasons. Others have already developed cirrhosis at diagnosis. Of note, alkaline phosphatase and bilirubin are usually normal. Autoimmune hepatitis frequently appears associated with other autoimmune conditions, mainly celiac disease,

title: Coeliac disease

text: Coeliac disease Coeliac disease or celiac disease is a long-term autoimmune disorder that primarily affects the small intestine. Classic symptoms include gastrointestinal problems such as chronic diarrhoea, abdominal distention, malabsorption, loss of appetite and among children failure to grow normally. This often begins between six months and two years of age. Non-classic symptoms are more common, especially in people older than two years. There may be mild or absent gastrointestinal symptoms, a wide number of symptoms involving any part of the body or no obvious symptoms. Coeliac disease was first described in childhood; however, it may develop at any age.

title: Composition of the human body

text: Composition of the human body Body composition may be analyzed in terms of molecular type e.g., water, protein, connective tissue, fats (or lipids), hydroxylapatite (in bones), carbohydrates (such as glycogen and glucose) and DNA. In terms of tissue type, the body may be analyzed into water, fat, muscle, bone, etc. In terms of cell type, the body contains hundreds of different types of cells, but notably, the largest "number" of cells contained in a human body (though not the largest mass of cells) are not human cells, but bacteria residing in the normal human gastrointestinal tract. Almost 99% of the

title: Composition of the human body

text: organisms. Composition of the human body Body composition may be analyzed in terms of molecular type e.g., water, protein, connective tissue, fats (or lipids), hydroxylapatite (in bones), carbohydrates (such as glycogen and glucose) and DNA. In terms of tissue type, the body may be analyzed into water, fat, muscle, bone, etc. In terms of cell type, the body contains hundreds of different types of cells, but notably, the largest "number" of cells contained in a human body (though not the largest mass of cells) are not human cells, but bacteria residing in the normal human gastrointestinal tract. Almost 99% of

title: Inclusion body disease

text: as a profound, highly severe neurological illness that is swiftly fatal. In adult boa constrictors, the disease assumes a milder, more chronic form with a wide array of extremely variable symptoms that gradually progresses to death. Clinical signs may vary, with regurgitation and neurological symptoms being the most prominent in the early and later stages of its progression. In boa constrictors, the first signs may include off-and-on regurgitation, and some develop head tremors. Abnormal shedding may occur. Some develop chronic regurgitation and anorexia (lack of appetite or refusal to feed). However, not all infected snakes may regurgitate. Boas lose weight

title: CNS demyelinating autoimmune diseases

text: CNS demyelinating autoimmune diseases CNS demyelinating autoimmune diseases are autoimmune diseases which primarily affect the central nervous system. Examples include: The brain and the spinal cord are the essential components of the central nervous system and it is responsible for the integration of the signals received from the afferent nerves and initiates action. The nerve cells, known as neurons, carry impulses throughout the body and the nerve impulses are carried along the axon. These microscopic nerve fibers, where the action potential occurs, are protected by a white, fatty tissue that surrounds and insulates it, known as the myelin sheath. This

title: Autoimmune neutropenia

text: Autoimmune neutropenia Autoimmune neutropenia is a form of neutropenia which is most common in infants and young children where the body identifies the neutrophils as enemies and makes antibody to destroy them. Primary autoimmune neutropenia (AIN) is an autoimmune disease first reported in 1975 that primarily occurs in infancy. In autoimmune neutropenia, the immune system produces autoantibodies directed against the neutrophilic protein antigens in white blood cells known as granulocytic neutrophils (granulocytes, segmented neutrophils, segs, polysegmented neutrophils, polys). These antibodies destroy granulocytic neutrophils. Consequently, patients with autoimmune neutropenia have low levels of granulocytic neutrophilic white blood cells causing a condition

title: Autoimmune regulator

text: homolog of "Aire" has created a transgenic mouse model that is used to study the mechanism of disease in human patients. Autoimmune regulator has been shown to interact with CREB binding protein. Autoimmune regulator The autoimmune regulator ("AIRE") is a protein that in humans is encoded by the "AIRE" gene. AIRE is a transcription factor expressed in the medulla (inner part) of the thymus. It is part of the mechanism which eliminates self-reactive T cells that would cause autoimmune disease. It exposes T cells to normal, healthy proteins from all parts of the body, and T cells that react to

title: Optic nerve sheath meningioma

text: Optic nerve sheath meningioma Optic nerve sheath meningiomas (ONSM) are rare benign tumors of the optic nerve. 60–70% of cases occur in middle age females, and is more common in older adults (mean age 44.7 years). It is also seen in children, but this is rare. The tumors grow from cells that surround the optic nerve, and as the tumor grows, it compresses the optic nerve. This causes loss of vision in the affected eye. Rarely, it may affect both eyes at the same time. It is typically a slow growing tumor, and has never been reported to cause death.

title: CNS demyelinating autoimmune diseases

text: acquired metabolic derangements, viral demyelination, and hypoxic-ischaemic demyelination. CNS demyelinating autoimmune diseases CNS demyelinating autoimmune diseases are autoimmune diseases which primarily affect the central nervous system. Examples include: The brain and the spinal cord are the essential components of the central nervous system and it is responsible for the integration of the signals received from the afferent nerves and initiates action. The nerve cells, known as neurons, carry impulses throughout the body and the nerve impulses are carried along the axon. These microscopic nerve fibers, where the action potential occurs, are protected by a white, fatty tissue that surrounds and

title: Signs and symptoms of HIV/AIDS

text: (PML) is a demyelinating disease, in which the gradual destruction of the myelin sheath covering the axons of nerve cells impairs the transmission of nerve impulses. It is caused by a virus called JC virus which occurs in 70% of the population in latent form, causing disease only when the immune system has been severely weakened, as is the case for AIDS patients. It progresses rapidly, usually causing death within months of diagnosis. AIDS dementia complex (ADC) is a metabolic encephalopathy induced by HIV infection and fueled by immune activation of HIV infected brain macrophages and microglia. These cells are

title: Canavan disease

text: sheath of the nerve fibers of the brain. The myelin sheath is the fatty covering that surrounds nerve cells and acts as an insulator, allowing for efficient transmission of nerve impulses. The diagnosis of neonatal/infantile Canavan disease relies on demonstration of very high concentration of N-acetylaspartic acid (NAA) in the urine. In mild/juvenile Canavan disease, NAA may only be slightly elevated; thus, the diagnosis relies on molecular genetic testing of "ASPA", the gene encoding the enzyme aspartoacylase. No cure for Canavan disease is known, nor is there a standard course of treatment. Treatment is symptomatic and supportive. Physical therapy may

title: Autoimmune regulator

text: Autoimmune regulator The autoimmune regulator ("AIRE") is a protein that in humans is encoded by the "AIRE" gene. AIRE is a transcription factor expressed in the medulla (inner part) of the thymus. It is part of the mechanism which eliminates self-reactive T cells that would cause autoimmune disease. It exposes T cells to normal, healthy proteins from all parts of the body, and T cells that react to those proteins are destroyed. Each T cell recognizes a specific antigen when it is presented in complex with a MHC molecule by an antigen presenting cell. This recognition is accomplished by the

title: CNS demyelinating autoimmune diseases

text: insulation helps the axon of a nerve cell with the conduction and speed of the signal along the axon. CNS demyelination autoimmune disease causes the myelin sheath to deteriorate since the sense of recognition of self is lost.The loss of the myelin insulation either disrupts or prevents neural conduction along the nerve cell’s axon. Since the neural impulse is inhibited it may lead to paresthesia, muscle weakness, unsteady gait, paralysis, vision loss and other motor dysfunctions. The pathogenesis of the demyelination can vary. Some of the factors that contribute to the deteriorating of the myelin are due to inflammatory processes,

title: Autoimmune neutropenia

text: been proposed. See article at BioMed Central site: Autoimmune neutropenia Autoimmune neutropenia is a form of neutropenia which is most common in infants and young children where the body identifies the neutrophils as enemies and makes antibody to destroy them. Primary autoimmune neutropenia (AIN) is an autoimmune disease first reported in 1975 that primarily occurs in infancy. In autoimmune neutropenia, the immune system produces autoantibodies directed against the neutrophilic protein antigens in white blood cells known as granulocytic neutrophils (granulocytes, segmented neutrophils, segs, polysegmented neutrophils, polys). These antibodies destroy granulocytic neutrophils. Consequently, patients with autoimmune neutropenia have low levels of

title: Wilson disease protein

text: kidney disease and neurological disease. The major cause is the malfunction of ATP7B by single base pair mutations, deletions, frame-shifts, splice errors in "ATP7B" gene. Wilson disease protein Wilson disease protein (WND), also known as ATP7B protein, is a copper-transporting P-type ATPase which is encoded by the "ATP7B" gene. The ATP7B protein is located in the trans-Golgi network of the liver and brain and balances the copper level in the body by excreting excess copper into bile and plasma. Genetic disorder of the ATP7B gene may cause Wilson's disease, a disease in which copper accumulates in tissues, leading to neurological

title: Autoimmune heart disease

text: to the post-streptococcal glomerulonephritis. Here, the anti-bacterial antibodies cross react with the heart antigens causing inflammation. Inflammatory damage leads to the following: These depend on the amount of inflammation. These are covered in their relevant articles. Intensive cardiac care and immunosuppressives including corticosteroids are helpful in the acute stage of the disease. Chronic phase has, mainly debility control and supportive care options. Autoimmune heart disease Autoimmune heart diseases are the effects of the body's own immune defense system mistaking cardiac antigens as foreign and attacking them leading to inflammation of the heart as a whole, or in parts. The commonest

title: Autoimmune inner ear disease

text: Autoimmune inner ear disease Autoimmune inner ear disease (AIED) was first defined by Dr. Brian McCabe in a landmark paper describing an autoimmune loss of hearing. The disease results in progressive sensorineural hearing loss (SNHL) that acts bilaterally and asymmetrically, and sometimes affects an individual's vestibular system. AIED is used to describe any disorder in which the inner ear is damaged as a result of an autoimmune response. Some examples of autoimmune disorders that have presented with AIED are Cogan's syndrome, relapsing polychondritis, systemic lupus erythematosus, granulomatosis with polyangiitis, polyarteritis nodosa, Sjogren's syndrome, and Lyme disease. Research has come to

title: Chronic kidney disease

text: that reduction in kidney function to this level or lower represents loss of half or more of the adult level of normal kidney function, which may be associated with a number of complications such as the development of cardiovascular disease. Protein in the urine is regarded as an independent marker for worsening of kidney function and cardiovascular disease. Hence, British guidelines append the letter "P" to the stage of chronic kidney disease if protein loss is significant. Stage 1 Slightly diminished function; kidney damage with normal or relatively high GFR (≥90 ml/min/1.73 m) and persistent albuminuria. Kidney damage is defined

title: Anemia of chronic disease

text: it allows the body to keep more iron away from bacterial pathogens in the body, while producing more immune cells to fight off infection. Almost all bacteria depend on iron to live and multiply. However, if inflammation continues, the effect of locking up iron stores is to reduce the ability of the bone marrow to produce red blood cells. These cells require iron for their massive amounts of hemoglobin which allow them to transport oxygen. Because anemia of chronic disease can be the result of non-infective causes of inflammation, future research is likely to investigate whether hepcidin antagonists might be

title: Charcot–Marie–Tooth disease

text: complex regional pain syndrome, among other diseases. Charcot–Marie–Tooth disease is caused by mutations that cause defects in neuronal proteins. Nerve signals are conducted by an axon with a myelin sheath wrapped around it. Most mutations in CMT affect the myelin sheath, but some affect the axon. The most common cause of CMT (70–80% of the cases) is the duplication of a large region on the short arm of chromosome 17 that includes the gene "PMP22". Some mutations affect the gene "MFN2", which codes for a mitochondrial protein. Cells contain separate sets of genes in their nuclei and mitochondria. In nerve

title: Wilson disease protein

text: Wilson disease protein Wilson disease protein (WND), also known as ATP7B protein, is a copper-transporting P-type ATPase which is encoded by the "ATP7B" gene. The ATP7B protein is located in the trans-Golgi network of the liver and brain and balances the copper level in the body by excreting excess copper into bile and plasma. Genetic disorder of the ATP7B gene may cause Wilson's disease, a disease in which copper accumulates in tissues, leading to neurological or psychiatric issues and liver diseases. Wilson disease protein is associated with "ATP7B" gene,approximate 80 Kb, located on human chromosome 13 and consists of 21

title: Chronic kidney disease

text: 10,000 years. The mortality rate of CKD was 10 deaths per 10,000. The breeds with the highest rates were the Bernese mountain dog, miniature schnauzer and boxer. The Swedish elkhound, Siberian husky and Finnish spitz were the breeds with the lowest rates. Currently, several compounds are in development for the treatment of CKD. These include the angiotensin receptor blocker (ARB) olmesartan medoxomil and sulodexide, a mixture of low molecular weight heparin and dermatan sulfate. Chronic kidney disease Chronic kidney disease (CKD) is a type of kidney disease in which there is gradual loss of kidney function over a period of

title: Cold agglutinin disease

text: Cold agglutinin disease Cold agglutinin disease is an autoimmune disease characterized by the presence of high concentrations of circulating antibodies, usually IgM, directed against red blood cells, causing them to agglutinate and undergo lysis. It is a form of autoimmune hemolytic anemia, specifically one in which antibodies bind red blood cells only at low body temperatures, typically 28–31 °C. Cold agglutinin disease was first described in 1957. Cold agglutinin disease can be either primary (arising spontaneously) or secondary (a result of another pathology). The primary form is caused by excessive cell proliferation of B lymphocytes. Secondary cold agglutinin disease is

title: Autoimmune retinopathy

text: antibodies. Autoimmune retinopathy Autoimmune retinopathy (AIR) is a rare disease in which the patient's immune system attacks proteins in the retina, leading to loss of eyesight. The disease is poorly understood, but may be the result of cancer or cancer chemotherapy. The disease is an autoimmune condition characterized by vision loss, blind spots, and visual field abnormalities. It can be divided into cancer-associated retinopathy (CAR) and melanoma-associated retinopathy (MAR). The condition is associated with retinal degeneration caused by autoimmune antibodies recognizing retinal proteins as antigens and targeting them. AIR's prevalence is extremely rare, with CAR being more common than MAR.

title: Autoimmune retinopathy

text: Autoimmune retinopathy Autoimmune retinopathy (AIR) is a rare disease in which the patient's immune system attacks proteins in the retina, leading to loss of eyesight. The disease is poorly understood, but may be the result of cancer or cancer chemotherapy. The disease is an autoimmune condition characterized by vision loss, blind spots, and visual field abnormalities. It can be divided into cancer-associated retinopathy (CAR) and melanoma-associated retinopathy (MAR). The condition is associated with retinal degeneration caused by autoimmune antibodies recognizing retinal proteins as antigens and targeting them. AIR's prevalence is extremely rare, with CAR being more common than MAR. It

title: Autoimmune disease in women

text: are able to help some women with autoimmune disease become pregnant. Although most autoimmune diseases cannot be cured, it is possible to manage the disease and participate in same activities that other women are able to do. Women with autoimmune diseases lead full, active lives. Seeing a specialist will assist in maintaining function and the maintenance of optimal health. Non-pharmacological treatments are effective in treating autoimmune disease and contribute to a sense of well-being. Women can: Autoimmune disease in women Autoimmune disease in women is a description of the autoimmune diseases that affect women. Some of these differences are unique

title: Autoimmune regulator

text: thymocytes to become tolerant towards peripheral organs, thereby suppressing autoimmune disease. The AIRE gene is expressed in many other tissues as well. AIRE gene is also expressed in the 33D1+ subset of dendritic cells in mouse and in human dendritic cells. The AIRE gene is mutated in the rare autoimmune syndrome Autoimmune Polyendocrinopathy Syndrome type 1 (APS-1), also known as Autoimmune Polyendocrinopathy-Candidiasis-Ectodermal Dystrophy (APECED). Disruption of "AIRE" results in the development of a range of autoimmune diseases, the most common clinical conditions in the syndrome are hypoparathyroidism, primary adrenocortical failure and chronic mucocutaneous candidiasis. A gene knockout of the murine

title: Autoimmune GFAP Astrocytopathy

text: Autoimmune GFAP Astrocytopathy Autoimmune GFAP Astrocytopathy is an autoimmune disease in which the immune system of the patient attacks a protein of the nervous system called glial fibrillary acidic protein (GFAP). It was described in 2016 by researchers of the Mayo clinic in the United States. GFAP is an intermediate filament (IF) protein that is expressed by numerous cell types of the central nervous system (CNS) including astrocytes. The destruction of astrocytes can lead to the development of a glial scar. There are multiple disorders associated with improper GFAP regulation and glial scarring is a consequence of several neurodegenerative conditions.

title: Autoimmune disease

text: an immune response in which a T or B cell component cross-recognizes self. The cross reactive immune response is responsible for the autoimmune disease state. Cross-reactive immune responses to self were first described for antibodies. According to this theory the effector function of the immune response is mediated by the glycans (polysaccharides) displayed by the cells and humoral components of the immune system. Individuals with autoimmunity have alterations in their glycosylation profile such that a proinflammatory immune response is favored. It is further hypothesized that individual autoimmune diseases will have unique glycan signatures. According to the hygiene hypothesis, high levels

title: S100 protein

text: are involved in regulation of protein phosphorylation, transcription factors, Ca homeostasis, the dynamics of cytoskeleton constituents, enzyme activities, cell growth and differentiation, and the inflammatory response. S100A7 (psoriasin) and S100A15 have been found to act as cytokines in inflammation, particularly in autoimmune skin conditions such as psoriasis. Several members of the S100 protein family are useful as markers for certain tumors and epidermal differentiation. It can be found in melanomas, 100% of schwannomas, 100% of neurofibromas (weaker than schwannomas), 50% of malignant peripheral nerve sheath tumors (may be weak and/or focal), paraganglioma stromal cells, histiocytoma and clear cell sarcomas. Further,

title: Autoimmune lymphoproliferative syndrome

text: All people with ALPS have signs of lymphoproliferation, which makes it the most common clinical manifestation of the disease. The increased proliferation of lymphoid cells can cause the size of lymphoid organs such as the lymph nodes and spleen to increase (lymphadenopathy and splenomegaly, present in respectively over 90% and over 80% of patients). The liver is enlarged (hepatomegaly in 30 - 40% of patients). Autoimmune disease is the second most common clinical manifestation and one that most often requires treatment. Autoimmune cytopenias: Most common. Can be mild to very severe. Can be intermittent or chronic. These include: Autoimmune hemolytic

title: Hirschsprung's disease

text: is 10 years of age. The first report of Hirschsprung's disease dates to 1691, when it was described by Dutch anatomist Frederik Ruysch. However, the disease is named after Harald Hirschsprung, the Danish physician who first described two infants who died of this disorder in 1888. Hirschsprung’s disease is a congenital disorder of the colon in which certain nerve cells, known as ganglion cells, are absent, causing chronic constipation. The lack of ganglion cells is in the myenteric plexus (Auerbach's plexus), which is responsible for moving food in the intestine. A barium enema is the mainstay of diagnosis of Hirschsprung’s,

title: Optic nerve

text: injuries to the optic nerve are from glaucoma, optic neuritis (especially in those younger than 50 years of age), and anterior ischemic optic neuropathy (usually in those older than 50). Glaucoma is a group of diseases involving loss of retinal ganglion cells causing optic neuropathy in a pattern of peripheral vision loss, initially sparing central vision. Glaucoma is associated with increased intraocular pressure that damages the optic nerve as it exits the eyeball. Although glaucoma does eventually damage the optic nerve, it is primarily a disease of eye not of the nerve. Optic neuritis is inflammation of the optic nerve.

title: Movement protein

text: the transport of mature virus particles. Examples of viruses that use this mechanism are cowpea mosaic virus (CPMV) and tomato spotted wilt virus (TSWV). The second mechanism by which movement proteins work is by associating with and coating the genome of the virus, causing the ribonucleoprotein complexes to be transported through plasmodesmata into neighbouring cells. TMV's 30 KDa movement protein acts via this mechanism, although it may also have other roles in infection. Movement protein Successful infection of a plant by a plant virus depends on its ability to move from the cell initially infected to neighbouring cells in order

title: Chronic liver disease

text: acute hepatitis. Toxic and drugs Paracetamol (acetaminophen) causes acute liver damage. Metabolic Autoimmune response causes Other These differ according to the type of chronic liver disease. Chronic liver disease takes several years to develop and the condition may not be recognised unless there is clinical awareness of subtle signs and investigation of abnormal liver function tests. Testing for chronic liver disease involves blood tests, imaging including ultrasound and a biopsy of the liver. The liver biopsy is a simple procedure done with a fine thin needle under local anaesthesia. The tissue sample is sent to a laboratory where it is

title: Inebilizumab

text: disease. This drug was developed by Viela Bio and MedImmune, LLC. Inebilizumab Inebilizumab (previously known as MEDI-551) is a humanized mAb that binds to and depletes CD19+ B cells including plasmablasts and plasma cells. Inebilizumab is currently being tested in a phase 2 study for treating Neuromyelitis Optica Spectrum Disorder (NMOSD). NMOSD is a rare autoimmune disorder in which immune system cells and autoantibodies attack and damage the optic nerves and spinal cord. Clinically, the disease is manifested with attacks/relapses that result in neurological impairment such as blindness, paraplegia, sensory loss, bladder dysfunction, and peripheral pain. The disability from each

title: Nerve tissue protein

text: Nerve tissue protein Nerve tissue is a biological molecule related to the function and maintenance of normal nervous tissue. An example would include, for example, the generation of myelin which insulates and protects nerves. These are typically calcium-binding proteins. There are two types of myelin the first is ogliodendrocyte- Myelin which can be found in the mammalian Central Nervous System (CNS) and the second is Schwann cells which are found in the Peripheral Nervous System (PNS). Myelination of axons by these Schwann cells are essential for normal nerve function. Peripheral nerves rely on communication between axons and Schwaan cells. Prion

title: Crohn's disease

text: loss leading to iron deficiency or by vitamin B deficiency, usually caused by ileal disease impairing vitamin B absorption. Rarely autoimmune hemolysis may occur. Ferritin levels help assess if iron deficiency is contributing to the anemia. Erythrocyte sedimentation rate (ESR) and C-reactive protein help assess the degree of inflammation, which is important as ferritin can also be raised in inflammation. Serum iron, total iron binding capacity and transferrin saturation may be more easily interpreted in inflammation. Anemia of chronic disease results in a normocytic anemia. Other causes of anemia include medication used in treatment of inflammatory bowel disease, like azathioprine,

title: Crohn's disease

text: of bowel cancer. While the cause of Crohn's disease is unknown, it is believed to be due to a combination of environmental, immune, and bacterial factors in genetically susceptible individuals. It results in a chronic inflammatory disorder, in which the body's immune system attacks the gastrointestinal tract possibly directed at microbial antigens. While Crohn's is an immune-related disease, it does not appear to be an autoimmune disease (in that the immune system is not being triggered by the body itself). The exact underlying immune problem is not clear; however, it may be an immunodeficiency state. About half of the overall

title: Prickle (protein)

text: Prickle (protein) Prickle is also known as REST/NRSF-interacting LIM domain protein, which is a putative nuclear translocation receptor. Prickle is part of the non-canonical Wnt signaling pathway that establishes planar cell polarity. A gain or loss of function of Prickle1 causes defects in the convergent extension movements of gastrulation. In epithelial cells, Prickle2 establishes and maintains cell apical/basal polarity. Prickle1 plays an important role in the development of the nervous system by regulating the movement of nerve cells. The first prickle protein was identified in "Drosophila" as a planar cell polarity protein. Vertebrate prickle-1 was first found as a rat

title: Pancreatic disease

text: due to a lack of digestive enzymes made by the pancreas. EPI is found in humans afflicted with cystic fibrosis and Shwachman–Diamond syndrome. It is caused by a progressive loss of the pancreatic cells that make digestive enzymes. Chronic pancreatitis is the most common cause of EPI in humans. Loss of digestive enzymes leads to maldigestion and malabsorption of nutrients. Cystic fibrosis, is a hereditary disease that affects the entire body, causing progressive disability and early death. It is caused by a mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. The product of this gene helps create sweat,

title: Osteonecrosis of the jaw

text: marrow content that are involved in the disease process. The first stage is an oedema of the bone marrow initiated by a bone infarct, which is itself modulated by numerous causes, leading to myelofibrosis as a result of hypoxia and gradual loss of mineral bone density characteristic of ischaemic osteoporosis. Further deterioration can be triggered by additional bone infarcts leading to anoxia and a localized areas of osteonecrosis within the osteoporotic cancellous bone. Secondary events such as dental infection, injection of local anaesthetics with vasoconstrictors, such as epinephrine, and trauma can add further complications to the disease process and chronic

title: Optic nerve sheath meningioma

text: US each year; corresponding to ~100 cases of ONSM each year in the US. The actual number of meningiomas is likely much higher as it is very common in elderly women. ONSM comprises about 2% of orbital tumors, and about 10% of optic nerve lesions. Neurofibromatosis type II (NF-2) affects around 9% of ONSM patients, where the incidence in the general population is around 0.03–0.05%. Thus NF-2 is felt to be a risk factor for the development of ONSM. Optic nerve sheath meningioma Optic nerve sheath meningiomas (ONSM) are rare benign tumors of the optic nerve. 60–70% of cases occur

title: Chronic granulomatous disease

text: from the name of the disease as children survived into adulthood. Gene therapy is currently being studied as a possible treatment for chronic granulomatous disease. CGD is well-suited for gene therapy since it is caused by a mutation in single gene which only affects one body system (the hematopoietic system). Viruses have been used to deliver a normal gp91 gene to rats with a mutation in this gene, and subsequently the phagocytes in these rats were able to produce oxygen radicals. In 2006, two human patients with X-linked chronic granulomatous disease underwent gene therapy and blood cell precursor stem cell

title: Movement protein

text: Movement protein Successful infection of a plant by a plant virus depends on its ability to move from the cell initially infected to neighbouring cells in order to spread infection. Unlike animal cells, plant cells have robust cell walls, which viruses cannot easily penetrate. A movement protein is a non-structural protein which is encoded by some plant viruses to allow their movement from one infected cell to neighbouring cells. Many, if not all, plant viruses encode a movement protein, and some express more than one. The movement protein of tobacco mosaic virus (TMV) has been most extensively studied. Plant viruses

title: Cranial nerve disease

text: Cranial nerve disease <nowiki> </nowiki> Cranial nerve disease is an impaired functioning of one of the twelve cranial nerves. Although it could theoretically be considered a mononeuropathy, it is not considered as such under MeSH. It is possible for a disorder of more than one cranial nerve to occur at the same time, if a trauma occurs at a location where many cranial nerves run together, such as the jugular fossa. A brainstem lesion could also cause impaired functioning of multiple cranial nerves, but this condition would likely also be accompanied by distal motor impairment. A neurological examination can test

title: Gastrointestinal disease

text: where the liver is unable to compensate for chronic damage, and unable to meet the metabolic demands of the body. In the acute setting, this may be a cause of hepatic encephalopathy and hepatorenal syndrome. Other causes of chronic liver disease are genetic or autoimmune disease, such as hemochromatosis, Wilson's disease, autoimmune hepatitis, and primary biliary cirrhosis. Acute liver disease rarely results in pain, but may result in jaundice. Infectious liver disease may cause a fever. Chronic liver disease may result in a buildup of fluid in the abdomen, yellowing of the skin or eyes, easy bruising, immunosuppression, and feminsation.

title: Inebilizumab

text: Inebilizumab Inebilizumab (previously known as MEDI-551) is a humanized mAb that binds to and depletes CD19+ B cells including plasmablasts and plasma cells. Inebilizumab is currently being tested in a phase 2 study for treating Neuromyelitis Optica Spectrum Disorder (NMOSD). NMOSD is a rare autoimmune disorder in which immune system cells and autoantibodies attack and damage the optic nerves and spinal cord. Clinically, the disease is manifested with attacks/relapses that result in neurological impairment such as blindness, paraplegia, sensory loss, bladder dysfunction, and peripheral pain. The disability from each attack is cumulative, making NMOSD a chronically debilitating and potentially life-threatening

title: Lyme disease microbiology

text: also play a role, by immunosuppression, in the development of chronic Lyme disease. FoxP3 is a specific marker of regulatory T cells. The signaling pathway P38 mitogen-activated protein kinases (p38 MAP kinase) has also been identified as promoting expression of proinflammatory cytokines from "Borrelia". The culmination of these new and ongoing immunological studies suggests this cell-mediated immune disruption in the Lyme patient amplifies the inflammatory process, often rendering it chronic and self-perpetuating, regardless of whether the "Borrelia" bacterium is still present in the host, or in the absence of the inciting pathogen in an autoimmune pattern. A vaccine based on

title: Sulfatide

text: of lysosomal sulfatide, which then develops into metachromatic leukodystrophy. Sulfatide plays an important role in the myelin. Myelin acts as an insulating sheath that surrounds many nerve fibers and increases the speed at which impulses are conducted. When sulfatide is not distributed properly, it can affect the normal physiological conduction of electrical impulses between nerve cells. This then results in demyelination because of the buildup of sulfatide and is the main cause of Metachromatic Leukodystrophy. However, how sulfatide buildup causes demyelination and neural degeneration is still mostly unknown. Metachromatic Leukodystrophy results in neurological manifestations that are centered on the impairment

title: E3 binding protein

text: E3 binding protein E3 binding protein also known as pyruvate dehydrogenase protein X component, mitochondrial is a protein that in humans is encoded by the "PDHX" gene. The E3 binding protein is a component of the pyruvate dehydrogenase complex found only in eukaryotes.Defects in this gene are a cause of pyruvate dehydrogenase deficiency which results in neurological dysfunction and lactic acidosis in infancy and early childhood. This protein is also a minor antigen for antimitochondrial antibodies. These autoantibodies are present in nearly 95% of patients with the autoimmune liver disease primary biliary cirrhosis (PBC). In PBC, activated T lymphocytes attack

title: Autoimmune disease

text: to "Witebsky's postulates" (first formulated by Ernest Witebsky and colleagues in 1957 and modified in 1994): Autoimmune diseases have a wide variety of different effects. They do tend to have one of three characteristic pathological effects which characterize them as autoimmune diseases: It has been estimated that autoimmune diseases are among the leading causes of death among women in the United States in all age groups up to 65 years. A substantial minority of the population suffers from these diseases, which are often chronic, debilitating, and life-threatening. There are more than 80 illnesses caused by autoimmunity. The human immune system

title: Autoimmune hemolytic anemia

text: years, the disease often follows a more chronic course, requiring long-term immunosuppression, with serious developmental consequences. The aim of therapy may sometimes be to lower the use of steroids in the control of the disease. In this case, splenectomy may be considered, as well as other immunosuppressive drugs. Infection is a serious concern in patients on long-term immunosuppressant therapy, especially in very young children (less than two years). Autoimmune hemolytic anemia Autoimmune hemolytic anemia (AIHA) occurs when antibodies directed against the person's own red blood cells (RBCs) cause them to burst (lyse), leading to an insufficient number of oxygen-carrying red

title: Chronic granulomatous disease

text: how much they are affected. A similar test uses dihydrorhodamine (DHR), in which whole blood is stained with DHR, incubated, and stimulated to produce superoxide radicals which oxidize DHR to rhodamin in cells with normal function. An advanced test called the "cytochrome C reduction assay" tells physicians how much superoxide a patient's phagocytes can produce. Once the diagnosis of CGD is established, a genetic analysis may be used to determine exactly which mutation is the underlying cause. Chronic granulomatous disease is the name for a genetically heterogeneous group of immunodeficiencies. The core defect is a failure of phagocytic cells to

title: Chronic granulomatous disease

text: transplantation to their bone marrow. Both patients recovered from their CGD, clearing pre-existing infections and demonstrating increased oxidase activity in their neutrophils. However, long-term complications and efficacy of this therapy were unknown. In 2012, a 16-year-old boy with CGD was treated at the Great Ormond Street Hospital, London with an experimental gene therapy which temporarily reversed the CGD and allowed him to overcome a life-threatening lung disease. Chronic granulomatous disease Chronic granulomatous disease (CGD) (also known as Bridges–Good syndrome, chronic granulomatous disorder, and Quie syndrome) is a diverse group of hereditary diseases in which certain cells of the immune system

title: Anemia of chronic disease

text: seen in people with chronic disease should be diagnosed as anemia of chronic disease. On the other hand, both of these examples show the complexity of this diagnosis: HIV infection itself can produce anemia of chronic disease, and renal failure can lead to inflammatory changes that also can produce anemia of chronic disease. Limiting some microbes' access to iron can reduce their virulence, thereby potentially reducing the severity of infection. Blood transfusion to patients with anemia of chronic disease is associated with a higher mortality, supporting the concept. Anemia of chronic disease is usually mild but can be severe. It

title: Tau protein

text: direct effect on the breakdown of a living cell caused by tangles that form and block nerve synapses. Tangles are clumps of Tau protein that stick together and block essential nutrients that need to be distributed to cells in the brain, causing the cells to die. Recent research suggests that tau may be released extracellularly by an exosome-based mechanism in Alzheimer's disease. Gender-specific tau gene expression across different regions of the human brain has recently been implicated in gender differences in the manifestations and risk for tauopathies. Some aspects of how the disease functions also suggest that it has some

title: Optic nerve sheath meningioma

text: will not advocate any treatment unless visual loss is present and ongoing. Reports of patients with ONSM having no change in their vision for multiple years are not uncommon. If loss of vision occurs, radiation therapy will improve vision in about ⅓ of cases, and preserve vision in about ⅓ of cases. Surgery has traditionally been associated with rapid deteroriation of vision. However, newer surgical techniques may prove better for the treatment of ONSM. About 1–2% of all meningiomas are optic nerve sheath meningiomas. Meningiomas have an incidence of ~4.18/100,000 persons each year. Thus, ~10,000 meningiomas are diagnosed in the

title: MuSK protein

text: proteins mentioned, other proteins are then gathered, to form the endplate to the neuromuscular junction. The nerve terminates onto the endplate, forming the neuromuscular junction - a structure required to transmit nerve impulses to the muscle, and thus initiating muscle contraction. Antibodies directed against this protein (Anti-MuSK autoantibodies) are found in those patients with myasthenia gravis not demonstrating antibodies to the acetylcholine receptor (sero-negative). The disease still appears to result in an autoimmune loss of acetylcholine receptor activity, but the phenotype of these patients appears to be different from those of many other myasthenic patients: more likely women, less eye

title: Myelin protein zero

text: Myelin protein zero Myelin protein zero (P0, MPZ) is a single membrane glycoprotein which in humans is encoded by the "MPZ" gene. P0 is a major structural component of the myelin sheath in the peripheral nervous system (PNS). Myelin protein zero is expressed by Schwann cells and accounts for over 50% of all proteins in the peripheral nervous system, making it the most common protein expressed in the PNS. Mutations in myelin protein zero can cause myelin deficiency and are associated with neuropathies like Charcot–Marie–Tooth disease and Dejerine–Sottas disease. In humans, the gene that encodes myelin protein zero is located