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The amino alcohol found in sphingomyelin is called sphingosine. It is a component of the sphingolipid family and plays a key role in the formation of cell membranes.
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Yes, sphingomyelin contains a fatty acid, sphingosine, and a phosphate group, but not glycerol. It is a type of sphingolipid found in cell membranes and plays a role in cell signaling and membrane structure.
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An actinoporin is a type of actinotoxin which forms pores in membranes which contain sphingomyelin.
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The lecithin to sphingomyelin ratio of 2:1 or greater is characteristic of mature fetal lungs. Fetuses delivered prior to this gestational age are at increased risk of neonatal respiratory distress syndrome.
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Sphingomyelin (SPH) is a type of sphingolipid found in animal cell membranes, especially in the membranous myelin sheath that surrounds some nerve cell axons. It usually consists of phosphorylcholine and ceramide. In humans SPH represents ~85% of all sphingolipids.
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The molecule described is sphingomyelin, which is a type of sphingolipid. It is composed of sphingosine, a fatty acid, phosphoric acid, and choline. Sphingomyelin is an important component of cell membranes and is especially abundant in the nervous system.
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SPHINGOMYELIN CONSISTS OF EITHER A VERY LONG CHAIN (C24 - C34) POLYUNSATURATED FATTY ACIDS OR PHOSPHORYLCHOLINE AND CERAMIDE.
p.s. batsmeyts sa be-esh-shoo!jke..tong nabiruk kong sagot...d lng xure..
p.s. manen. oo nga
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Sphingomyelin is a phospholipid found in cell surface membranes (plasma membranes).
Glucosylcerebroside is a glycolipid found in the myelin sheath of nerve cells (neurones).
Both contain sphingosine.
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Jennifer M. Yule has written:
'Phosphatidylcholine and sphingomyelin signalling pathways in the control of proliferation and differentiation'
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Phospholipid bilayer (types of phospholipids are Sphingomyelin, Sphingoethanolamin, Sphingoserin, Phosphatidylcholine, Sphingocholine).
In between the phospholipds you also find cholesterol and intermembrane protein.
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In patients with Types A and B NPD, there is a build up of sphingomyelin in cells of the brain, liver, spleen, kidney and lung.
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Brian G. Schuster has written:
'Production of antibodies against phosphocholine, phosphatidylcholine, sphingomyelin, and lipid A by injection of liposomes containing lipid A'
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The four major phospholipids found in the plasma membrane of mammalian cells are phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, and sphingomyelin. Each of these phospholipids contributes to the structure and function of the plasma membrane, helping maintain its integrity and allowing for selective permeability.
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Ceramides are a family of waxy lipid molecules composed of sphingosine and a fatty acid. Ceramides are found in high concentration within the cell membrane of cells, they are one of the component lipids that make up sphingomyelin.
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The predominant lipids in the lipid bilayer are phospholipids. These include phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, and sphingomyelin. These lipids have a hydrophilic head and hydrophobic tail, allowing them to form the stable bilayer structure of cell membranes.
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The three most abundant lipids found in the brain in increasing order are cholesterol, sphingomyelin, and phosphatidylcholine. Cholesterol is an important component of cell membranes, sphingomyelin is a type of sphingolipid that plays a role in cell signaling, and phosphatidylcholine is a major component of cell membranes.
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a class of lipids and are a major component of all cell membranes. Most phospholipids contain a diglyceride, a phosphate group, and a simple organic molecule such as choline; one exception to this rule is sphingomyelin, which is derived from sphingosine instead of glycerol. They are a type of molecule. They form a lipid bilayer within a cell membrane.
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Marjatta Rahikainen is a Finnish author who has written books on various topics such as historical fiction, children's literature, and poetry. Some of her works include "The Red Mountain" and "The Glassbird."
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phospholipids, glycero phosphilipids, and sphingophospholipids
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Acid sphingomyelinase (ASM) is an enzyme involved in the metabolism of sphingolipids. Mutations in the gene encoding ASM lead to deficient enzyme activity, causing Niemann-Pick disease, a lysosomal storage disorder characterized by the accumulation of sphingomyelin in cells. Experimental treatments targeting ASM are being developed as potential therapies for this disease.
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Myelin is composed of about 80% lipid and about 20% protein. Some of the proteins that make up myelin are myelin basic protein (MBP),myelin oligodendrocyte glycoprotein (MOG), and proteolipid protein (PLP). Myelin is made up primarily of a glycolipid calledgalactocerebroside. The intertwining of the hydrocarbon chains of sphingomyelin serve to strengthen the myelin sheath.
There are quite a few disease (multiple sclerosis, optic neuritis, transverse myelitis..) involved in the destruction of the axon myelin sheath also known as myelin sheath.
http://en.wikipedia.org/wiki/Myelin
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The cell membrane is primarily made out of a double layer of phospholipid molecules with embedded proteins. These phospholipids have a hydrophilic (water-attracting) head and hydrophobic (water-repelling) tails that form the bilayer structure of the membrane. The proteins within the membrane serve various functions, including transport, communication, and structural support.
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There are four main types of lipids: triglycerides, phospholipids, sterols, and waxes. Each type serves different functions in the body, such as energy storage, cell membrane structure, hormone production, and waterproofing.
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The Golgi apparatus functions to modify, sort, and package proteins and lipids that are synthesized by the cell. It acts as a distribution center for these molecules, sending them to their correct destinations within the cell or for secretion outside of the cell.
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Much of the choline Americans consume comes from lecithin (phosphytidylcholine). Lecithin is most often added to foods as an emulsifier (a substance that helps keeps food components blended together). Most of the lecithin in the U.S. food supply comes from soybeans. Food sources of choline include soybeans and soybean products, potatoes, collards, brewer's yeast, chard, cauliflower, peas, corn, spinach, asparagus, peanuts and peanut butter, crimini mushrooms, grapefruit, oats, broccoli, Brussels sprouts, green beans, miso, and tomatoes. Many of these foods contain not only choline itself, but also other forms of the vitamin including lecithin (phosphatidylcholine) and sphingomyelin.
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Phospholipids are a class of lipids and are a major component of all cell membranes as they can form lipid bilayer.
The further classification if a s follows:
Most phospholipids contain a diglyceride,a phosphate group,and a simple organic molecule such as choline.
- Diacylglyceride structures
- phosphatidic acid (phosphatidate) (PA)
- phosphatidylethanolamine (cephalin) (PE)
- phosphatidylecholine (lecithin) (PC)
- phosphatidylserine(PS)
- Phosphoinositides:
- Phosphatidylinositol(PI)
- Phosphatidylinositol phosphate(PIP)
- Phosphatidylinositol bisphosphate(PIP2)
- phosphatidylinositol triphosphate(PIP3)
- Phosphosphingolipids
- Ceramide phosphorylcholine(sphingomylin)
- Ceramide phosphorylethanolamene
- Ceramide phosphorylglycerol
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A phospholipid molecule is formed when two fatty acids combine with a phosphate group. This structure is a major component of cell membranes, with the fatty acid tails providing a hydrophobic barrier and the phosphate head group being hydrophilic.
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The polar end of a phospholipid contains a phosphate group and a small, hydrophilic molecule like choline, serine, or ethanolamine. This polar head interacts with water, while the nonpolar tails interact with each other to form a cell membrane bilayer.
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Niemann-Pick disease refers to a group of diseases passed down through families (inherited) in which fatty substances called lipids collect in the cells of the spleen, liver, and brain.
There are four most commonly recognized forms of the disease: Types A, B, C, and D. Types A and B are also called Type I. Types C and D are also known as Type II.
Each type involves different organs and may or may not involve the central nervous system or respiratory system. Each one can cause different symptoms and may occur at different times throughout life, from infancy to adulthood.
Alternative NamesSphingomyelinase deficiency
Causes, incidence, and risk factorsNiemann-Pick disease Type A and B occur when cells in the body lack an enzymecalled acid sphingomyelinase (ASM). ASM helps break down (metabolize) a fatty substance called sphingomyelin, which is found in every cell of the body. If ASM is missing or does not work properly, sphingomyelin builds up inside cells. This leads to cell death and makes it hard for organs to work properly. Type A occurs in all races and ethnicities, but higher rates are seen in the Ashkenazi (Eastern European) Jew population.
Niemann-Pick Type C occurs when the body can not properly break down cholesterol and other lipids (fats). This leads to too much cholesterol in the liver and spleen and excessive amounts of other lipids in the brain. There may be reduced ASM activity in some cells. Type C Niemann-Pick disease has been reported in all ethnic groups but it is most common among Puerto Ricans of Spanish descent.
Type D Niemann-Pick involves a defect that interferes with the movement of cholesterol between brain cells. It is now thought to be a variant of type C. This type of Niemann-Pick disease has only been found in the French Canadian population of Yarmouth County, Nova Scotia.
An adult-onset form of Niemann-Pick disease has been suggested. It is sometimes referred to as Type E disease.
SymptomsType A usually begins in the first few months of life. Symptoms may include:
- Abdominal (belly area) swelling within 3 - 6 months
- Cherry red spot in the eye
- Feeding difficulties
- Loss of early motor skills (gets worse over time)
Type B symptoms are usually milder and occur in late childhood or adolescence. Abdominal swelling may be seen in early childhood, but there is almost no neurological involvement, such as loss of motor skills. Some patients may have repeated respiratory infections.
Type C usually affects school-aged children, but the disease may occur any time between early infancy to adulthood. Symptoms may include:
- Difficulty in posturing of limbs (dystonia)
- Enlarged spleen
- Enlarged liver
- Jaundice at (or shortly after) birth
- Learning difficulties and progressive intellectual decline (dementia)
- Seizures
- Slurred, irregular speech
- Sudden loss of muscle tone which may lead to falls (cataplexy)
- Tremors
- Trouble moving the eyes up and down (vertical supranuclear gaze palsy)
- Unsteady gait, clumsiness, walking problems (ataxia)
Symptoms of Type D are similar to Type C.
Type E occurs in adults. Symptoms include swelling of the spleen and neurological problems. Little is known about this rare type of Niemann-Pick disease.
Symptoms and disease progression of all forms of Niemann-Pick vary from person to person. No single symptom should be used to include or exclude Niemann-Pick as a diagnosis. Other, more common, diseases may cause symptoms similar to Niemann-Pick.
A person in the early stages of the disease may show only a few symptoms. Not every symptom will be seen in the later stages of the disease.
Signs and testsType A and B are diagnosed by measuring the amount of ASM in white blood cells. The test can be done using a blood or bone marrow sample. Such testing can tell who has the disease, but does not reveal who may be carriers. DNA tests can be done to diagnose carriers of Type A and B.
A skin biopsy is usually used to diagnose Type C and Type D Niemann-Pick. Laboratory scientists will watch how the skin cells grow and study how they move and store cholesterol. DNA tests may also be done to look for the two genes that cause Niemann-Pick disease Type C.
Additional tests might include:
- Slit-lamp eye exam
- Liver biopsy or bone marrow aspiration
- Liver biopsy (usually not necessary)
- Sphingomyelinase assays
At this time, there is no effective treatment for Type A.
Bone marrow transplantation has been performed on a few patients with Type B with encouraging results. Researchers continue to study possible treatments, including enzyme replacement therapy and gene therapy.
There is no specific treatment for Type C and D. A healthy, low-cholesterol diet is recommended, although research into low-cholesterol diets and cholesterol-lowering drugs does not show that these methods stop the disease from getting worse or change how cells break down cholesterol. However, medicines are available to control or relieve many symptoms, such as cataplexy and seizures.
Support GroupsFor more information, visit the National Niemann-Pick Disease Foundation website: www.nnpdf.org
Expectations (prognosis)Type A Niemann-Pick is a severe disease, which generally leads to death by age 2 or 3.
Those with Type B may live into late childhood or adulthood.
A child who shows signs of Type C before age 1 may not live to school age. Those who show show symptoms after entering school may live into their mid-to-late teens, with a few surviving into the 20s.
Complications- Brain damage with varying degrees of mental retardation and delayed development of physical skills
- Blindness
- Deafness
- Death
Make an appointment with your health care provider if you have a family history of Niemann-Pick disease and you plan to have children. Genetic counseling and screening is recommended for such individuals.
Call your health care provider if your child has symptoms of this disease, including
- Feeding problems
- Developmental problems
- Inadequate weight gain
All types of Niemann-Pick are autosomal recessive. This means that both parents are carriers -- they each carry one copy of the abnormal gene without having any signs of the disease themselves.
When both parents are carriers, there is a 25% chance that their child will have the disease and a 50% chance that a child will be a carrier.
Carrier detection testing is only possible if the specific genetic defect is identified. The defects involved in Types A and B have been extensively studied, and DNA tests for these forms of Niemann-Pick are available.
Genetic defects have been identified in the DNA of many patients with Type C, so it may be possible to diagnose those who carry the abnormal gene.
A few centers offer tests to diagnose a baby still in the womb.
ReferencesStanley CA, Bennett MJ. Defects of metabolism in lipids. In: Kliegman RM, Behrman RE, Jenson HB, Stanton BF, eds. Nelson Textbook of Pediatrics. 18th ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 86.
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