Apoproteins
Apolipoproteins
Lipoproteins, HDL
Apoenzymes
Lipoproteins, VLDL
Apolipoproteins B
Lipoproteins
Lipoproteins, LDL
Apolipoproteins A
Chylomicrons
Apolipoprotein A-I
Enediynes
Electrophoresis, Polyacrylamide Gel
Apolipoproteins E
Heme
Tetrapyrroles
Cholesterol
Phycobilins
Phycocyanin
Flavodoxin
Retinaldehyde
Lipoproteins, HDL3
Cholesterol Esters
Apolipoproteins C
Spectrophotometry
Liver
Lipoproteins, HDL2
Pulmonary Surfactants
Urease
Ultracentrifugation
Abetalipoproteinemia
Amino Acid Sequence
Apolipoprotein A-II
Phospholipids
Light-Harvesting Protein Complexes
Chlorophyll
Pulmonary Surfactant-Associated Proteins
Helicobacter mustelae
Flavin-Adenine Dinucleotide
Immunoelectrophoresis
Molecular Sequence Data
Protein Conformation
Phosphatidylcholine-Sterol O-Acyltransferase
Amino Acids
Immunodiffusion
Cytochrome P-450 CYP2B1
Flavin Mononucleotide
Circular Dichroism
Lipids
Apolipoprotein B-100
Protein Binding
Apolipoprotein C-III
Chemistry
Chemical Phenomena
Hypolipoproteinemias
Hyperlipoproteinemia Type IV
Apolipoprotein B-48
Enterobacter aerogenes
Lipoprotein(a)
Cytochrome c Group
Metalloproteins
Hyperlipoproteinemias
Iron-Sulfur Proteins
Chromatography, Gel
Binding Sites
Spectrum Analysis
Phosphatidylcholines
Photosynthetic Reaction Center Complex Proteins
Chyle
Oxidation-Reduction
Bromotrichloromethane
Fats, Unsaturated
Dietary Fats
Escherichia coli
Biliverdine
Cytochrome P-450 Enzyme System
Proteolipids
Bile Pigments
Spectrophotometry, Ultraviolet
Carrier Proteins
Centrifugation, Density Gradient
Flavins
Iron
Leghemoglobin
Electron Spin Resonance Spectroscopy
Copper
Nickel
Microscopy, Electron
Receptors, LDL
Myoglobin
Phycoerythrin
Cytochromes
D-Aspartate Oxidase
Egg Yolk
Receptors, Lipoprotein
Lipoprotein Lipase
Allylisopropylacetamide
Immunoelectrophoresis, Two-Dimensional
Rats, Inbred Strains
Base Sequence
Oleic Acids
Diatomaceous Earth
Apolipoproteins D
Rod Opsins
Surface Tension
Trypsin
Bacteriorhodopsins
Plant Proteins
Models, Molecular
Chloroplasts
Electrophoresis, Agar Gel
Rhodopsin
Radioimmunoassay
Ethinyl Estradiol
Hemeproteins
Cloning, Molecular
Halobacterium
Rhodospirillales
Chromatography, Agarose
Ferredoxins
Rabbits
Magnetic Resonance Spectroscopy
Cattle
Mesentery
Protein Denaturation
Holoenzymes
Lyases
Hemin
Carotenoids
Zinc
Plastocyanin
Phytochrome A
Structure-Activity Relationship
RNA, Messenger
5-Aminolevulinate Synthetase
Cholesterol, HDL
Chromatography, Affinity
Chromatography, High Pressure Liquid
Apolipoprotein C-II
Hyperlipoproteinemia Type III
Isoelectric Focusing
Lecithin Acyltransferase Deficiency
Coenzymes
Photosystem II Protein Complex
Cobalt
Aryl Hydrocarbon Hydroxylases
Cholesterol, LDL
Schiff Bases
Macromolecular Substances
Oleic Acid
Mutation
Hydrogen-Ion Concentration
Molecular Structure
Temperature
Plants
Isotope Labeling
Biological Transport
Thioctic Acid
Arteriosclerosis
Hydroxylamine
Dithionitrobenzoic Acid
Pulmonary Alveolar Proteinosis
Photosystem I Protein Complex
Transducin
Cytochrome b Group
Thromboplastin
Antibiotics, Antineoplastic
Chickens
Cells, Cultured
Phenobarbital
Iodine Radioisotopes
Cycloheximide
Apoferritins
Peptides
The main symptom of abetalipoproteinemia is a complete absence of chylomicrons, which are small particles that carry triglycerides and other lipids in the bloodstream. This results in low levels of triglycerides and other lipids in the blood, as well as an impaired ability to absorb vitamins and other nutrients from food.
Abetalipoproteinemia is usually diagnosed during infancy or early childhood, when symptoms such as fatigue, weakness, and poor growth become apparent. The disorder can be identified through blood tests that measure lipid levels and genetic analysis.
Treatment for abetalipoproteinemia typically involves a combination of dietary changes and supplements to ensure adequate nutrition and prevent complications such as malnutrition and liver disease. In some cases, medications may be prescribed to lower triglyceride levels or improve the absorption of fat-soluble vitamins.
The prognosis for abetalipoproteinemia varies depending on the severity of the disorder and the presence of any complications. In general, early diagnosis and appropriate treatment can help to manage symptoms and prevent long-term health problems. However, some individuals with abetalipoproteinemia may experience ongoing health issues throughout their lives.
There are several types of hyperlipidemia, including:
1. High cholesterol: This is the most common type of hyperlipidemia and is characterized by elevated levels of low-density lipoprotein (LDL) cholesterol, also known as "bad" cholesterol.
2. High triglycerides: This type of hyperlipidemia is characterized by elevated levels of triglycerides in the blood. Triglycerides are a type of fat found in the blood that is used for energy.
3. Low high-density lipoprotein (HDL) cholesterol: HDL cholesterol is known as "good" cholesterol because it helps remove excess cholesterol from the bloodstream and transport it to the liver for excretion. Low levels of HDL cholesterol can contribute to hyperlipidemia.
Symptoms of hyperlipidemia may include xanthomas (fatty deposits on the skin), corneal arcus (a cloudy ring around the iris of the eye), and tendon xanthomas (tender lumps under the skin). However, many people with hyperlipidemia have no symptoms at all.
Hyperlipidemia can be diagnosed through a series of blood tests that measure the levels of different types of cholesterol and triglycerides in the blood. Treatment for hyperlipidemia typically involves dietary changes, such as reducing intake of saturated fats and cholesterol, and increasing physical activity. Medications such as statins, fibric acid derivatives, and bile acid sequestrants may also be prescribed to lower cholesterol levels.
In severe cases of hyperlipidemia, atherosclerosis (hardening of the arteries) can occur, which can lead to cardiovascular disease, including heart attacks and strokes. Therefore, it is important to diagnose and treat hyperlipidemia early on to prevent these complications.
The most common form of hypolipoproteinemia is familial hypobetalipoproteinemia (FHBL), which is caused by mutations in the gene encoding apoB, a protein component of low-density lipoproteins (LDL). People with FHBL have extremely low levels of LDL cholesterol and often develop symptoms such as fatty liver disease, liver cirrhosis, and cardiovascular disease.
Another form of hypolipoproteinemia is familial hypoalphalipoproteinemia (FHAL), which is caused by mutations in the gene encoding apoA-I, a protein component of high-density lipoproteins (HDL). People with FHAL have low levels of HDL cholesterol and often develop symptoms such as cardiovascular disease and premature coronary artery disease.
Hypolipoproteinemia can be diagnosed through a combination of clinical evaluation, laboratory tests, and genetic analysis. Treatment for the disorder typically involves managing associated symptoms and reducing lipid levels through diet, exercise, and medication. In some cases, liver transplantation may be necessary.
Prevention of hypolipoproteinemia is challenging, as it is often inherited in an autosomal recessive pattern, meaning that both parents must be carriers of the mutated gene to pass it on to their children. However, genetic counseling and testing can help identify carriers and allow for informed family planning.
Overall, hypolipoproteinemia is a rare and complex group of disorders that affect lipid metabolism and transport. While treatment and management options are available, prevention and early diagnosis are key to reducing the risk of complications associated with these disorders.
The condition is caused by mutations in genes that code for enzymes involved in lipid metabolism, such as ACY1 and APOB100. These mutations lead to a deficiency in the breakdown and transport of lipids in the body, resulting in the accumulation of chylomicrons and other lipoproteins in the blood.
Symptoms of hyperlipoproteinemia Type IV can include abdominal pain, fatigue, and joint pain, as well as an increased risk of pancreatitis and cardiovascular disease. Treatment typically involves a combination of dietary modifications, such as reducing intake of saturated fats and cholesterol, and medications to lower lipid levels. In severe cases, liver transplantation may be necessary.
Hyperlipoproteinemia Type IV is a rare disorder, and the prevalence is not well-defined. However, it is estimated to affect approximately 1 in 100,000 individuals worldwide. The condition can be diagnosed through a combination of clinical evaluation, laboratory tests, and genetic analysis.
In summary, hyperlipoproteinemia Type IV is a rare genetic disorder that affects the metabolism of lipids and lipoproteins in the body, leading to elevated levels of chylomicrons and other lipoproteins in the blood, as well as low levels of HDL. The condition can cause a range of symptoms and is typically treated with dietary modifications and medications.
There are several types of hyperlipoproteinemias, each with distinct clinical features and laboratory findings. The most common forms include:
1. Familial hypercholesterolemia (FH): This is the most common type of hyperlipoproteinemia, caused by mutations in the LDLR gene that codes for the low-density lipoprotein receptor. FH is characterized by extremely high levels of low-density lipoprotein (LDL) cholesterol in the blood, which can lead to premature cardiovascular disease, including heart attacks and strokes.
2. Familial hypobetalipoproteinemia (FHBL): This rare disorder is caused by mutations in the APOB100 gene that codes for a protein involved in lipid metabolism. FHBL is characterized by very low levels of low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol, as well as a deficiency of Apolipoprotein B-100, a protein that helps transport lipids in the blood.
3. Hypertriglyceridemia: This condition is caused by mutations in genes that regulate triglyceride metabolism, leading to extremely high levels of triglycerides in the blood. Hypertriglyceridemia can increase the risk of pancreatitis and other health problems.
4. Lipoprotein lipase deficiency: This rare disorder is caused by mutations in the LPL gene that codes for the enzyme lipoprotein lipase, which helps break down triglycerides in the blood. Lipoprotein lipase deficiency can lead to very high levels of triglycerides and cholesterol in the blood, increasing the risk of pancreatitis and other health problems.
5. Familial dyslipidemia: This is a group of rare inherited disorders that affect lipid metabolism and can cause extremely high or low levels of various types of cholesterol and triglycerides in the blood. Some forms of familial dyslipidemia are caused by mutations in genes that code for enzymes involved in lipid metabolism, while others may be caused by unknown factors.
6. Chylomicronemia: This rare disorder is characterized by extremely high levels of chylomicrons (type of triglyceride-rich lipoprotein) in the blood, which can increase the risk of pancreatitis and other health problems. The exact cause of chylomicronemia is not fully understood, but it may be related to genetic mutations or other factors that affect lipid metabolism.
7. Hyperchylomicronemia: This rare disorder is similar to chylomicronemia, but it is characterized by extremely high levels of chylomicrons in the blood, as well as very low levels of HDL (good) cholesterol. Hyperchylomicronemia can increase the risk of pancreatitis and other health problems.
8. Hypoalphalipoproteinemia: This rare disorder is characterized by extremely low levels of apolipoprotein A-I (ApoA-I), a protein that plays a key role in lipid metabolism and helps to regulate the levels of various types of cholesterol and triglycerides in the blood. Hypoalphalipoproteinemia can increase the risk of pancreatitis and other health problems.
9. Hypobetalipoproteinemia: This rare disorder is characterized by extremely low levels of apolipoprotein B (ApoB), a protein that helps to regulate the levels of various types of cholesterol and triglycerides in the blood. Hypobetalipoproteinemia can increase the risk of pancreatitis and other health problems.
10. Sitosterolemia: This rare genetic disorder is caused by mutations in the gene that codes for sterol-CoA-desmethylase (SCD), an enzyme involved in the metabolism of plant sterols. Sitosterolemia can cause elevated levels of plant sterols and sitosterol in the blood, which can increase the risk of pancreatitis and other health problems.
11. Familial hyperchylomicronemia type 1 (FHMC1): This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein C-II (APOC2), a protein that helps to regulate the levels of various types of cholesterol and triglycerides in the blood. FHMC1 can cause elevated levels of chylomicrons and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
12. Familial hyperchylomicronemia type 2 (FHMC2): This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein A-IV (APOA4), a protein that helps to regulate the levels of various types of cholesterol and triglycerides in the blood. FHMC2 can cause elevated levels of chylomicrons and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
13. Lipoprotein (a) deficiency: This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein (a), a protein that helps to regulate the levels of lipoproteins in the blood. Lipoprotein (a) deficiency can cause low levels of lipoprotein (a) and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
14. Chylomicron retention disease: This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein C-II (APOC2), a protein that helps to regulate the levels of chylomicrons in the blood. Chylomicron retention disease can cause elevated levels of chylomicrons and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
15. Hypertriglyceridemia-apolipoprotein C-II deficiency: This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein C-II (APOC2), a protein that helps to regulate the levels of triglycerides in the blood. Hypertriglyceridemia-apolipoprotein C-II deficiency can cause elevated levels of triglycerides and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
16. Familial partial lipodystrophy (FPLD): This rare genetic disorder is characterized by the loss of fat tissue in certain areas of the body, such as the arms, legs, and buttocks. FPLD can cause elevated levels of lipids in the blood, which can increase the risk of pancreatitis and other health problems.
17. Lipodystrophy: This rare genetic disorder is characterized by the loss of fat tissue in certain areas of the body, such as the face, arms, and legs. Lipodystrophy can cause elevated levels of lipids in the blood, which can increase the risk of pancreatitis and other health problems.
18. Abetalipoproteinemia: This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein B, a protein that helps to regulate the levels of lipids in the blood. Abetalipoproteinemia can cause elevated levels of triglycerides and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
19. Chylomicronemia: This rare genetic disorder is characterized by the presence of excessively large amounts of chylomicrons (type of lipid particles) in the blood. Chylomicronemia can cause elevated levels of triglycerides and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
20. Hyperlipidemia due to medications: Certain medications, such as corticosteroids and some anticonvulsants, can cause elevated levels of lipids in the blood.
It's important to note that many of these disorders are rare and may not be common causes of high triglycerides. Additionally, there may be other causes of high triglycerides that are not listed here. It's important to talk to a healthcare provider for proper evaluation and diagnosis if you have concerns about your triglyceride levels.
There are several types of blood protein disorders, including:
1. Hemophilia A: a deficiency of factor VIII, which is necessary for blood clotting.
2. Hemophilia B: a deficiency of factor IX, also involved in blood clotting.
3. Von Willebrand disease: a deficiency of von Willebrand factor, which helps to platelets stick together and form blood clots.
4. Protein C deficiency: a lack of protein C, an anticoagulant protein that helps to prevent blood clots.
5. Protein S deficiency: a lack of protein S, another anticoagulant protein that helps to prevent blood clots.
6. Antithrombin III deficiency: a lack of antithrombin III, a protein that prevents the formation of blood clots.
7. Fibrinogen deficiency: a lack of fibrinogen, a protein that is essential for blood clotting.
8. Dysproteinemia: an abnormal amount or type of proteins in the blood, which can lead to various symptoms and complications.
Symptoms of blood protein disorders can vary depending on the specific condition and the severity of the deficiency. Common symptoms include easy bruising or bleeding, frequent nosebleeds, prolonged bleeding after injuries or surgery, and joint pain or swelling.
Treatment for blood protein disorders typically involves replacing the missing protein or managing symptoms with medication or lifestyle changes. In some cases, gene therapy may be an option to correct the underlying genetic defect.
It's important for individuals with blood protein disorders to work closely with their healthcare provider to manage their condition and prevent complications such as joint damage, infections, and bleeding episodes.
The condition is caused by mutations in the genes that code for proteins involved in lipid metabolism, such as the LDL receptor gene or the apoB100 gene. These mutations lead to a deficiency of functional LDL receptors on the surface of liver cells, which results in reduced clearance of LDL cholesterol from the blood and increased levels of LDL-C.
The main symptom of hyperlipoproteinemia type III is very high levels of LDL-C (>500 mg/dL) and low levels of HDL-C (<20 mg/dL). Other signs and symptoms may include xanthomas (fatty deposits in the skin), corneal arcus (a cloudy ring around the cornea of the eye), and an increased risk of cardiovascular disease.
Treatment for hyperlipoproteinemia type III typically involves a combination of dietary changes, such as reducing intake of saturated fats and cholesterol, and medications, such as statins or other lipid-lowering drugs, to lower LDL-C levels. In severe cases, a liver transplant may be necessary.
Hyperlipoproteinemia type III is an autosomal dominant disorder, meaning that a single copy of the mutated gene is enough to cause the condition. It is important to identify and treat individuals with this condition early to prevent or delay the development of cardiovascular disease.
The primary symptom of LCAT deficiency is a high level of low-density lipoprotein (LDL) cholesterol, also known as "bad" cholesterol, in the blood. This can lead to the development of cholesterol deposits in the skin, eyes, and other tissues, which can cause a range of health problems including xanthomas (yellowish patches on the skin), corneal arcus (a cloudy ring around the cornea of the eye), and xanthelasma (yellowish patches on the eyelids).
Treatment for LCAT deficiency typically involves a combination of dietary changes, such as reducing intake of saturated fats and cholesterol, and medication to lower cholesterol levels. In some cases, liver transplantation may be necessary.
Prevention of LCAT deficiency is not possible, as it is a genetic disorder that is inherited in an autosomal recessive pattern. This means that a child must inherit two copies of the mutated LCAT gene, one from each parent, to develop the condition. However, early detection and treatment can help manage the symptoms and prevent complications.
The diagnosis of LCAT deficiency is based on a combination of clinical features, laboratory tests, and genetic analysis. Laboratory tests may include measurements of lipid levels in the blood, as well as assays for LCAT enzyme activity. Genetic testing can identify the presence of mutations in the LCAT gene that cause the condition.
Overall, LCAT deficiency is a rare and potentially serious genetic disorder that affects the body's ability to metabolize cholesterol and other fats. Early diagnosis and treatment can help manage the symptoms and prevent complications, but there is currently no cure for the condition.
Arteriosclerosis can affect any artery in the body, but it is most commonly seen in the arteries of the heart, brain, and legs. It is a common condition that affects millions of people worldwide and is often associated with aging and other factors such as high blood pressure, high cholesterol, diabetes, and smoking.
There are several types of arteriosclerosis, including:
1. Atherosclerosis: This is the most common type of arteriosclerosis and occurs when plaque builds up inside the arteries.
2. Arteriolosclerosis: This type affects the small arteries in the body and can cause decreased blood flow to organs such as the kidneys and brain.
3. Medial sclerosis: This type affects the middle layer of the artery wall and can cause stiffness and narrowing of the arteries.
4. Intimal sclerosis: This type occurs when plaque builds up inside the innermost layer of the artery wall, causing it to become thick and less flexible.
Symptoms of arteriosclerosis can include chest pain, shortness of breath, leg pain or cramping during exercise, and numbness or weakness in the limbs. Treatment for arteriosclerosis may include lifestyle changes such as a healthy diet and regular exercise, as well as medications to lower blood pressure and cholesterol levels. In severe cases, surgery may be necessary to open up or bypass blocked arteries.
The primary symptom of PAP is shortness of breath (dyspnea), which can range from mild to severe and may be accompanied by coughing, wheezing, and chest tightness. PAP can also lead to respiratory failure, which can be life-threatening if left untreated.
The diagnosis of PAP is based on a combination of clinical symptoms, physical examination findings, and diagnostic tests such as chest radiographs (X-rays), computed tomography (CT) scans, and lung biopsy. A lung biopsy is the most definitive test for PAP, allowing for the identification of characteristic pathological features such as the accumulation of lipoproteinaceous material within the air spaces of the lungs.
Treatment options for PAP include surgical lung biopsy to obtain a definitive diagnosis and monitor disease progression, chest radiation therapy to reduce symptoms and slow disease progression, and medications such as corticosteroids to modulate the immune system and reduce inflammation. In severe cases, lung transplantation may be necessary.
The prognosis for PAP varies depending on the severity of the disease and response to treatment. With appropriate therapy, many patients with PAP can achieve stabilization of their symptoms and improved lung function. However, some patients may experience recurrent episodes of disease exacerbation and may require long-term management and monitoring.
There are several types of hypercholesterolemia, including:
1. Familial hypercholesterolemia: This is an inherited condition that causes high levels of low-density lipoprotein (LDL) cholesterol, also known as "bad" cholesterol, in the blood.
2. Non-familial hypercholesterolemia: This type of hypercholesterolemia is not inherited and can be caused by a variety of factors, such as a high-fat diet, lack of exercise, obesity, and certain medical conditions, such as hypothyroidism or polycystic ovary syndrome (PCOS).
3. Mixed hypercholesterolemia: This type of hypercholesterolemia is characterized by high levels of both LDL and high-density lipoprotein (HDL) cholesterol in the blood.
The diagnosis of hypercholesterolemia is typically made based on a physical examination, medical history, and laboratory tests, such as a lipid profile, which measures the levels of different types of cholesterol and triglycerides in the blood. Treatment for hypercholesterolemia usually involves lifestyle changes, such as a healthy diet and regular exercise, and may also include medication, such as statins, to lower cholesterol levels.
The condition is caused by mutations in the genes that code for proteins involved in cholesterol transport and metabolism, such as the low-density lipoprotein receptor gene (LDLR) or the PCSK9 gene. These mutations lead to a decrease in the ability of the liver to remove excess cholesterol from the bloodstream, resulting in high levels of LDL cholesterol and low levels of HDL cholesterol.
Hyperlipoproteinemia type II is usually inherited in an autosomal dominant pattern, meaning that a single copy of the mutated gene is enough to cause the condition. However, some cases can be caused by spontaneous mutations or incomplete penetrance, where not all individuals with the mutated gene develop the condition.
Symptoms of hyperlipoproteinemia type II can include xanthomas (yellowish deposits of cholesterol in the skin), corneal arcus (a white, waxy deposit on the iris of the eye), and tendon xanthomas (small, soft deposits of cholesterol under the skin). Treatment typically involves a combination of dietary changes and medication to lower LDL cholesterol levels and increase HDL cholesterol levels. In severe cases, liver transplantation may be necessary.
Hyperlipoproteinemia type II is a serious condition that can lead to cardiovascular disease, including heart attacks, strokes, and peripheral artery disease. Early diagnosis and treatment are important to prevent or delay the progression of the disease and reduce the risk of complications.
Apoprotein
ApoA-1 Milano
Aequorin
Andre Francis Palmer
Vertebrate visual opsin
Free radical damage to DNA
Cytochrome c family
Surfactant protein A2
Aplysioviolin
Surfactant protein A1
Apolipoprotein
David J. Galton
CYP2A6
Genetic association
Candidate gene
Light-harvesting complex
Succinate dehydrogenase
Retinal
Drosophila melanogaster
Rhodopsin
Opsin
Transferrin
Serum amyloid A1
Holoprotein
Lipid-lowering agent
Brian Andrew Hills
Lipoprotein lipase deficiency
Chylomicron retention disease
Autumn leaf color
APOA5
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Lipoprotein4
- Valimaki M, Maass L, Harno K, Nikkila EA "Lipoprotein lipids and apoproteins during beta-blocker administration: comparison of penbutolol and atenolol. (drugs.com)
- Potential for increasing high-density lipoprotein cholesterol, subfractions HDL2-C and HDL3-C, and apoprotein AI among middle-age women. (uchicago.edu)
- Characteristics associated with apoprotein and lipoprotein lipid levels in middle-aged women. (uchicago.edu)
- In the first, high density lipoprotein apoproteins were radioiodinated in situ in the lipoprotein particle (endogenous apoprotein labeling) while in the second, individually labeled apolipoprotein A-I or A-II was incorporated into the particle by in vitro incubation (exogenous apoprotein labeling). (houstonmethodist.org)
Lipids1
- Lipids and apoproteins are analyzed on the Roche Diagnostics c501 automated chemistry analyzer. (wustl.edu)
Surfactant6
- A micropapillary pattern is predictive of a poor prognosis in lung adenocarcinoma, and reduced surfactant apoprotein A expression in the micropapillary pattern is an excellent indicator of a poor prognosis. (nih.gov)
- It was noteworthy that the disease-free interval in patients with high surfactant apoprotein A expression was significantly better than in patients with low surfactant apoprotein A expression (P=0.03), and no recurrence or death occurred in patients with high surfactant apoprotein A expression. (nih.gov)
- High MUC1 expression on the surface is an important characteristic of a micropapillary pattern, and reduced surfactant apoprotein A expression in the micropapillary pattern may be an excellent indicator for poor prognosis in small-size lung adenocarcinoma. (nih.gov)
- Surfactant is a complex lipoprotein (see the image below) composed of six phospholipids and four apoproteins. (medscape.com)
- Among the four surfactant apoproteins identified, surfactant protein B (SP-B) and SP-C are two small hydrophobic proteins that make up 2-4% of the surfactant mass and are present in commercially available surfactant preparations. (medscape.com)
- 19. Combined status of MUC1 mucin and surfactant apoprotein A expression can predict the outcome of patients with small-size lung adenocarcinoma. (nih.gov)
Proteins1
- Research findings of Dr. Fredrickson and colleagues have also included the discovery of several previously unknown apolipo-proteins, and new knowledge including descriptions concerning the structure and function of various apoproteins. (nih.gov)
Patients2
- Nov. 4, 2003 - Infusion of the Milano apoprotein A rapidly causes regression of atherosclerosis in patients with acute coronary syndromes (ACS), according to the results of a preliminary randomized trial published in the Nov. 5 issue of The Journal of the American Medical Association. (medscape.com)
- Nous avons réalisé un essai en double aveugle contre placebo sur 50 patients atteints de diabète de type 2 randomisés pour recevoir 2 g/jour d'acides gras oméga 3 purifiés ou un placebo pendant 10 semaines. (who.int)