Apolipoprotein b 100. Medical search

Major structural proteins of triacylglycerol-rich LIPOPROTEINS. There are two forms, apolipoprotein B-100 and apolipoprotein B-48, both derived from a single gene. ApoB-100 expressed in the liver is found in low-density lipoproteins (LIPOPROTEINS, LDL; LIPOPROTEINS, VLDL). ApoB-48 expressed in the intestine is found in CHYLOMICRONS. They are important in the biosynthesis, transport, and metabolism of triacylglycerol-rich lipoproteins. Plasma Apo-B levels are high in atherosclerotic patients but non-detectable in ABETALIPOPROTEINEMIA.

The most abundant protein component of HIGH DENSITY LIPOPROTEINS or HDL. This protein serves as an acceptor for CHOLESTEROL released from cells thus promoting efflux of cholesterol to HDL then to the LIVER for excretion from the body (reverse cholesterol transport). It also acts as a cofactor for LECITHIN CHOLESTEROL ACYLTRANSFERASE that forms CHOLESTEROL ESTERS on the HDL particles. Mutations of this gene APOA1 cause HDL deficiency, such as in FAMILIAL ALPHA LIPOPROTEIN DEFICIENCY DISEASE and in some patients with TANGIER DISEASE.

A 513-kDa protein synthesized in the LIVER. It serves as the major structural protein of low-density lipoproteins (LIPOPROTEINS, LDL; LIPOPROTEINS, VLDL). It is the ligand for the LDL receptor (RECEPTORS, LDL) that promotes cellular binding and internalization of LDL particles.

A 241-kDa protein synthesized only in the INTESTINES. It serves as a structural protein of CHYLOMICRONS. Its exclusive association with chylomicron particles provides an indicator of intestinally derived lipoproteins in circulation. Apo B-48 is a shortened form of apo B-100 and lacks the LDL-receptor region.

A class of protein components which can be found in several lipoproteins including HIGH-DENSITY LIPOPROTEINS; VERY-LOW-DENSITY LIPOPROTEINS; and CHYLOMICRONS. Synthesized in most organs, Apo E is important in the global transport of lipids and cholesterol throughout the body. Apo E is also a ligand for LDL receptors (RECEPTORS, LDL) that mediates the binding, internalization, and catabolism of lipoprotein particles in cells. There are several allelic isoforms (such as E2, E3, and E4). Deficiency or defects in Apo E are causes of HYPERLIPOPROTEINEMIA TYPE III.

Protein components on the surface of LIPOPROTEINS. They form a layer surrounding the hydrophobic lipid core. There are several classes of apolipoproteins with each playing a different role in lipid transport and LIPID METABOLISM. These proteins are synthesized mainly in the LIVER and the INTESTINES.

A 9-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS and CHYLOMICRON REMNANTS. Apo C-III, synthesized in the liver, is an inhibitor of LIPOPROTEIN LIPASE. Apo C-III modulates the binding of chylomicron remnants and VLDL to receptors (RECEPTORS, LDL) thus decreases the uptake of triglyceride-rich particles by the liver cells and subsequent degradation. The normal Apo C-III is glycosylated. There are several polymorphic forms with varying amounts of SIALIC ACID (Apo C-III-0, Apo C-III-1, and Apo C-III-2).

Structural proteins of the alpha-lipoproteins (HIGH DENSITY LIPOPROTEINS), including APOLIPOPROTEIN A-I and APOLIPOPROTEIN A-II. They can modulate the activity of LECITHIN CHOLESTEROL ACYLTRANSFERASE. These apolipoproteins are low in atherosclerotic patients. They are either absent or present in extremely low plasma concentration in TANGIER DISEASE.

A major and the second most common isoform of apolipoprotein E. In humans, Apo E4 differs from APOLIPOPROTEIN E3 at only one residue 112 (cysteine is replaced by arginine), and exhibits a lower resistance to denaturation and greater propensity to form folded intermediates. Apo E4 is a risk factor for ALZHEIMER DISEASE and CARDIOVASCULAR DISEASES.

A 34-kDa glycosylated protein. A major and most common isoform of apolipoprotein E. Therefore, it is also known as apolipoprotein E (ApoE). In human, Apo E3 is a 299-amino acid protein with a cysteine at the 112 and an arginine at the 158 position. It is involved with the transport of TRIGLYCERIDES; PHOSPHOLIPIDS; CHOLESTEROL; and CHOLESTERYL ESTERS in and out of the cells.

A class of lipoproteins of very light (0.93-1.006 g/ml) large size (30-80 nm) particles with a core composed mainly of TRIGLYCERIDES and a surface monolayer of PHOSPHOLIPIDS and CHOLESTEROL into which are imbedded the apolipoproteins B, E, and C. VLDL facilitates the transport of endogenously made triglycerides to extrahepatic tissues. As triglycerides and Apo C are removed, VLDL is converted to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LOW-DENSITY LIPOPROTEINS from which cholesterol is delivered to the extrahepatic tissues.

The second most abundant protein component of HIGH DENSITY LIPOPROTEINS or HDL. It has a high lipid affinity and is known to displace APOLIPOPROTEIN A-I from HDL particles and generates a stable HDL complex. ApoA-II can modulate the activation of LECITHIN CHOLESTEROL ACYLTRANSFERASE in the presence of APOLIPOPROTEIN A-I, thus affecting HDL metabolism.

Lipid-protein complexes involved in the transportation and metabolism of lipids in the body. They are spherical particles consisting of a hydrophobic core of TRIGLYCERIDES and CHOLESTEROL ESTERS surrounded by a layer of hydrophilic free CHOLESTEROL; PHOSPHOLIPIDS; and APOLIPOPROTEINS. Lipoproteins are classified by their varying buoyant density and sizes.

A 9-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS. It contains a cofactor for LIPOPROTEIN LIPASE and activates several triacylglycerol lipases. The association of Apo C-II with plasma CHYLOMICRONS; VLDL, and HIGH-DENSITY LIPOPROTEINS is reversible and changes rapidly as a function of triglyceride metabolism. Clinically, Apo C-II deficiency is similar to lipoprotein lipase deficiency (HYPERLIPOPROTEINEMIA TYPE I) and is therefore called hyperlipoproteinemia type IB.

A class of lipoproteins of small size (18-25 nm) and light (1.019-1.063 g/ml) particles with a core composed mainly of CHOLESTEROL ESTERS and smaller amounts of TRIGLYCERIDES. The surface monolayer consists mostly of PHOSPHOLIPIDS, a single copy of APOLIPOPROTEIN B-100, and free cholesterol molecules. The main LDL function is to transport cholesterol and cholesterol esters to extrahepatic tissues.

The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.

One of three major isoforms of apolipoprotein E. In humans, Apo E2 differs from APOLIPOPROTEIN E3 at one residue 158 where arginine is replaced by cysteine (R158--C). In contrast to Apo E3, Apo E2 displays extremely low binding affinity for LDL receptors (RECEPTORS, LDL) which mediate the internalization and catabolism of lipoprotein particles in liver cells. ApoE2 allelic homozygosity is associated with HYPERLIPOPROTEINEMIA TYPE III.

A 6.6-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS; INTERMEDIATE-DENSITY LIPOPROTEINS; and HIGH-DENSITY LIPOPROTEINS. Apo C-I displaces APO E from lipoproteins, modulate their binding to receptors (RECEPTORS, LDL), and thereby decrease their clearance from plasma. Elevated Apo C-I levels are associated with HYPERLIPOPROTEINEMIA and ATHEROSCLEROSIS.

A group of apolipoproteins that can readily exchange among the various classes of lipoproteins (HDL; VLDL; CHYLOMICRONS). After lipolysis of TRIGLYCERIDES on VLDL and chylomicrons, Apo-C proteins are normally transferred to HDL. The subtypes can modulate remnant binding to receptors, LECITHIN CHOLESTEROL ACYLTRANSFERASE, or LIPOPROTEIN LIPASE.

A class of lipoproteins of small size (4-13 nm) and dense (greater than 1.063 g/ml) particles. HDL lipoproteins, synthesized in the liver without a lipid core, accumulate cholesterol esters from peripheral tissues and transport them to the liver for re-utilization or elimination from the body (the reverse cholesterol transport). Their major protein component is APOLIPOPROTEIN A-I. HDL also shuttle APOLIPOPROTEINS C and APOLIPOPROTEINS E to and from triglyceride-rich lipoproteins during their catabolism. HDL plasma level has been inversely correlated with the risk of cardiovascular diseases.

A generic term for fats and lipoids, the alcohol-ether-soluble constituents of protoplasm, which are insoluble in water. They comprise the fats, fatty oils, essential oils, waxes, phospholipids, glycolipids, sulfolipids, aminolipids, chromolipids (lipochromes), and fatty acids. (Grant & Hackh's Chemical Dictionary, 5th ed)

Conditions with abnormally low levels of BETA-LIPOPROTEINS (low density lipoproteins or LDL) in the blood. It is defined as LDL values equal to or less than the 5th percentile for the population. They include the autosomal dominant form involving mutation of the APOLIPOPROTEINS B gene, and the autosomal recessive form involving mutation of the microsomal triglyceride transfer protein. All are characterized by low LDL and dietary fat malabsorption.

A large and highly glycosylated protein constituent of LIPOPROTEIN (A). It has very little affinity for lipids but forms disulfide-linkage to APOLIPOPROTEIN B-100. Apoprotein(a) has SERINE PROTEINASE activity and can be of varying sizes from 400- to 800-kDa. It is homologous to PLASMINOGEN and is known to modulate THROMBOSIS and FIBRINOLYSIS.

Cholesterol which is contained in or bound to low density lipoproteins (LDL), including CHOLESTEROL ESTERS and free cholesterol.

A lipoprotein that resembles the LOW-DENSITY LIPOPROTEINS but with an extra protein moiety, APOPROTEIN (A) also known as APOLIPOPROTEIN (A), linked to APOLIPOPROTEIN B-100 on the LDL by one or two disulfide bonds. High plasma level of lipoprotein (a) is associated with increased risk of atherosclerotic cardiovascular disease.

An enzyme that catalyzes the deamination of cytidine, forming uridine. EC 3.5.4.5.

Receptors on the plasma membrane of nonhepatic cells that specifically bind LDL. The receptors are localized in specialized regions called coated pits. Hypercholesteremia is caused by an allelic genetic defect of three types: 1, receptors do not bind to LDL; 2, there is reduced binding of LDL; and 3, there is normal binding but no internalization of LDL. In consequence, entry of cholesterol esters into the cell is impaired and the intracellular feedback by cholesterol on 3-hydroxy-3-methylglutaryl CoA reductase is lacking.

A process that changes the nucleotide sequence of mRNA from that of the DNA template encoding it. Some major classes of RNA editing are as follows: 1, the conversion of cytosine to uracil in mRNA; 2, the addition of variable number of guanines at pre-determined sites; and 3, the addition and deletion of uracils, templated by guide-RNAs (RNA, GUIDE).

Cholesterol which is contained in or bound to high-density lipoproteins (HDL), including CHOLESTEROL ESTERS and free cholesterol.

A mixture of very-low-density lipoproteins (VLDL), particularly the triglyceride-poor VLDL, with slow diffuse electrophoretic mobilities in the beta and alpha2 regions which are similar to that of beta-lipoproteins (LDL) or alpha-lipoproteins (HDL). They can be intermediate (remnant) lipoproteins in the de-lipidation process, or remnants of mutant CHYLOMICRONS and VERY-LOW-DENSITY LIPOPROTEINS which cannot be metabolized completely as seen in FAMILIAL DYSBETALIPOPROTEINEMIA.

A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.

A type of familial lipid metabolism disorder characterized by a variable pattern of elevated plasma CHOLESTEROL and/or TRIGLYCERIDES. Multiple genes on different chromosomes may be involved, such as the major late transcription factor (UPSTREAM STIMULATORY FACTORS) on CHROMOSOME 1.

A group of familial disorders characterized by elevated circulating cholesterol contained in either LOW-DENSITY LIPOPROTEINS alone or also in VERY-LOW-DENSITY LIPOPROTEINS (pre-beta lipoproteins).

Conditions with excess LIPIDS in the blood.

An autosomal dominant disorder of lipid metabolism. It is caused by mutations of APOLIPOPROTEINS B, main components of CHYLOMICRONS and BETA-LIPOPROTEINS (low density lipoproteins or LDL). Features include abnormally low LDL, normal triglyceride level, and dietary fat malabsorption.

Conditions with abnormally low levels of LIPOPROTEINS in the blood. This may involve any of the lipoprotein subclasses, including ALPHA-LIPOPROTEINS (high-density lipoproteins); BETA-LIPOPROTEINS (low-density lipoproteins); and PREBETA-LIPOPROTEINS (very-low-density lipoproteins).

A class of lipoproteins that carry dietary CHOLESTEROL and TRIGLYCERIDES from the SMALL INTESTINE to the tissues. Their density (0.93-1.006 g/ml) is the same as that of VERY-LOW-DENSITY LIPOPROTEINS.

Thickening and loss of elasticity of the walls of ARTERIES of all sizes. There are many forms classified by the types of lesions and arteries involved, such as ATHEROSCLEROSIS with fatty lesions in the ARTERIAL INTIMA of medium and large muscular arteries.

Physiological processes in biosynthesis (anabolism) and degradation (catabolism) of LIPIDS.

A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.

Conditions with abnormally elevated levels of LIPOPROTEINS in the blood. They may be inherited, acquired, primary, or secondary. Hyperlipoproteinemias are classified according to the pattern of lipoproteins on electrophoresis or ultracentrifugation.

A glycoprotein component of HIGH-DENSITY LIPOPROTEINS that transports small hydrophobic ligands including CHOLESTEROL and STEROLS. It occurs in the macromolecular complex with LECITHIN CHOLESTEROL ACYLTRANSFERASE. Apo D is expressed in and secreted from a variety of tissues such as liver, placenta, brain tissue and others.

A condition with abnormally high levels of CHOLESTEROL in the blood. It is defined as a cholesterol value exceeding the 95th percentile for the population.

An unsaturated fatty acid that is the most widely distributed and abundant fatty acid in nature. It is used commercially in the preparation of oleates and lotions, and as a pharmaceutical solvent. (Stedman, 26th ed)

An autosomal recessive disorder of lipid metabolism. It is caused by mutation of the microsomal triglyceride transfer protein that catalyzes the transport of lipids (TRIGLYCERIDES; CHOLESTEROL ESTERS; PHOSPHOLIPIDS) and is required in the secretion of BETA-LIPOPROTEINS (low density lipoproteins or LDL). Features include defective intestinal lipid absorption, very low serum cholesterol level, and near absent LDL.

Fatty acid esters of cholesterol which constitute about two-thirds of the cholesterol in the plasma. The accumulation of cholesterol esters in the arterial intima is a characteristic feature of atherosclerosis.

Cholesterol which is contained in or bound to very low density lipoproteins (VLDL). High circulating levels of VLDL cholesterol are found in HYPERLIPOPROTEINEMIA TYPE IIB. The cholesterol on the VLDL is eventually delivered by LOW-DENSITY LIPOPROTEINS to the tissues after the catabolism of VLDL to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LDL.

RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.

Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.

The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.

A hypertriglyceridemia disorder, often with autosomal dominant inheritance. It is characterized by the persistent elevations of plasma TRIGLYCERIDES, endogenously synthesized and contained predominantly in VERY-LOW-DENSITY LIPOPROTEINS (pre-beta lipoproteins). In contrast, the plasma CHOLESTEROL and PHOSPHOLIPIDS usually remain within normal limits.

A condition of elevated levels of TRIGLYCERIDES in the blood.

An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. The enzyme hydrolyzes triacylglycerols in chylomicrons, very-low-density lipoproteins, low-density lipoproteins, and diacylglycerols. It occurs on capillary endothelial surfaces, especially in mammary, muscle, and adipose tissue. Genetic deficiency of the enzyme causes familial hyperlipoproteinemia Type I. (Dorland, 27th ed) EC 3.1.1.34.

Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.

Variant forms of the same gene, occupying the same locus on homologous CHROMOSOMES, and governing the variants in production of the same gene product.

Cell surface proteins that bind lipoproteins with high affinity. Lipoprotein receptors in the liver and peripheral tissues mediate the regulation of plasma and cellular cholesterol metabolism and concentration. The receptors generally recognize the apolipoproteins of the lipoprotein complex, and binding is often a trigger for endocytosis.

An enzyme secreted from the liver into the plasma of many mammalian species. It catalyzes the esterification of the hydroxyl group of lipoprotein cholesterol by the transfer of a fatty acid from the C-2 position of lecithin. In familial lecithin:cholesterol acyltransferase deficiency disease, the absence of the enzyme results in an excess of unesterified cholesterol in plasma. EC 2.3.1.43.

An autosomal recessively inherited disorder characterized by the accumulation of intermediate-density lipoprotein (IDL or broad-beta-lipoprotein). IDL has a CHOLESTEROL to TRIGLYCERIDES ratio greater than that of VERY-LOW-DENSITY LIPOPROTEINS. This disorder is due to mutation of APOLIPOPROTEINS E, a receptor-binding component of VLDL and CHYLOMICRONS, resulting in their reduced clearance and high plasma levels of both cholesterol and triglycerides.

The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.

Fats present in food, especially in animal products such as meat, meat products, butter, ghee. They are present in lower amounts in nuts, seeds, and avocados.

Substances used to lower plasma CHOLESTEROL levels.

The regular and simultaneous occurrence in a single interbreeding population of two or more discontinuous genotypes. The concept includes differences in genotypes ranging in size from a single nucleotide site (POLYMORPHISM, SINGLE NUCLEOTIDE) to large nucleotide sequences visible at a chromosomal level.

An individual having different alleles at one or more loci regarding a specific character.

Transport proteins that carry specific substances in the blood or across cell membranes.

Chemical analysis based on the phenomenon whereby light, passing through a medium with dispersed particles of a different refractive index from that of the medium, is attenuated in intensity by scattering. In turbidimetry, the intensity of light transmitted through the medium, the unscattered light, is measured. In nephelometry, the intensity of the scattered light is measured, usually, but not necessarily, at right angles to the incident light beam.

Proteins that bind to and transfer CHOLESTEROL ESTERS between LIPOPROTEINS such as LOW-DENSITY LIPOPROTEINS and HIGH-DENSITY LIPOPROTEINS.

The section of the alimentary canal from the STOMACH to the ANAL CANAL. It includes the LARGE INTESTINE and SMALL INTESTINE.

The rate dynamics in chemical or physical systems.

A quinazoline derivative with hypnotic and sedative properties. It has been withdrawn from the market in many countries because of problems with abuse. (From Martindale, The Extra Pharmacopoeia, 30th ed, p604)

Cholesterol present in food, especially in animal products.

Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.

Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides see GLYCEROPHOSPHOLIPIDS) or sphingosine (SPHINGOLIPIDS). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system.

A superfamily of large integral ATP-binding cassette membrane proteins whose expression pattern is consistent with a role in lipid (cholesterol) efflux. It is implicated in TANGIER DISEASE characterized by accumulation of cholesteryl ester in various tissues.

Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.

Centrifugation with a centrifuge that develops centrifugal fields of more than 100,000 times gravity. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)

The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.

The main trunk of the systemic arteries.

An individual in which both alleles at a given locus are identical.

An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. It is produced by glands on the tongue and by the pancreas and initiates the digestion of dietary fats. (From Dorland, 27th ed) EC 3.1.1.3.

Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.

The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.

Relating to the size of solids.

Established cell cultures that have the potential to propagate indefinitely.

(Z)-9-Octadecenoic acid 1,2,3-propanetriyl ester.

Abnormalities in the serum levels of LIPIDS, including overproduction or deficiency. Abnormal serum lipid profiles may include high total CHOLESTEROL, high TRIGLYCERIDES, low HIGH DENSITY LIPOPROTEIN CHOLESTEROL, and elevated LOW DENSITY LIPOPROTEIN CHOLESTEROL.

Compounds that inhibit HMG-CoA reductases. They have been shown to directly lower cholesterol synthesis.

The range or frequency distribution of a measurement in a population (of organisms, organs or things) that has not been selected for the presence of disease or abnormality.

An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.

7-carbon saturated monocarboxylic acids.

A system of cisternae in the CYTOPLASM of many cells. In places the endoplasmic reticulum is continuous with the plasma membrane (CELL MEMBRANE) or outer membrane of the nuclear envelope. If the outer surfaces of the endoplasmic reticulum membranes are coated with ribosomes, the endoplasmic reticulum is said to be rough-surfaced (ENDOPLASMIC RETICULUM, ROUGH); otherwise it is said to be smooth-surfaced (ENDOPLASMIC RETICULUM, SMOOTH). (King & Stansfield, A Dictionary of Genetics, 4th ed)

Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.

A group of fatty acids that contain 18 carbon atoms and a double bond at the omega 9 carbon.

An imbalance between myocardial functional requirements and the capacity of the CORONARY VESSELS to supply sufficient blood flow. It is a form of MYOCARDIAL ISCHEMIA (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels.

An enzyme that catalyzes the formation of cholesterol esters by the direct transfer of the fatty acid group from a fatty acyl CoA derivative. This enzyme has been found in the adrenal gland, gonads, liver, intestinal mucosa, and aorta of many mammalian species. EC 2.3.1.26.

A diet that contributes to the development and acceleration of ATHEROGENESIS.

The main structural component of the LIVER. They are specialized EPITHELIAL CELLS that are organized into interconnected plates called lobules.

The time frame after a meal or FOOD INTAKE.

The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.

A highly conserved heterodimeric glycoprotein that is differentially expressed during many severe physiological disturbance states such as CANCER; APOPTOSIS; and various NEUROLOGICAL DISORDERS. Clusterin is ubiquitously expressed and appears to function as a secreted MOLECULAR CHAPERONE.

A pyrimidine nucleoside that is composed of the base CYTOSINE linked to the five-carbon sugar D-RIBOSE.

The record of descent or ancestry, particularly of a particular condition or trait, indicating individual family members, their relationships, and their status with respect to the trait or condition.

A group of acylated oligopeptides produced by Actinomycetes that function as protease inhibitors. They have been known to inhibit to varying degrees trypsin, plasmin, KALLIKREINS, papain and the cathepsins.

The movement of materials (including biochemical substances and drugs) through a biological system at the cellular level. The transport can be across cell membranes and epithelial layers. It also can occur within intracellular compartments and extracellular compartments.

A degenerative disease of the BRAIN characterized by the insidious onset of DEMENTIA. Impairment of MEMORY, judgment, attention span, and problem solving skills are followed by severe APRAXIAS and a global loss of cognitive abilities. The condition primarily occurs after age 60, and is marked pathologically by severe cortical atrophy and the triad of SENILE PLAQUES; NEUROFIBRILLARY TANGLES; and NEUROPIL THREADS. (From Adams et al., Principles of Neurology, 6th ed, pp1049-57)

Elements of limited time intervals, contributing to particular results or situations.

Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.

Highly crosslinked and insoluble basic anion exchange resin used as anticholesteremic. It may also may reduce triglyceride levels.

Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.

Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.

A technique using antibodies for identifying or quantifying a substance. Usually the substance being studied serves as antigen both in antibody production and in measurement of antibody by the test substance.

Triple-looped protein domains linked by disulfide bonds. These common structural domains, so-named for their resemblance to Danish pastries known as kringlers, play a role in binding membranes, proteins, and phospholipids as well as in regulating proteolysis. Kringles are also present in coagulation-related and fibrinolytic proteins and other plasma proteinases.

The proportion of one particular in the total of all ALLELES for one genetic locus in a breeding POPULATION.

Classic quantitative assay for detection of antigen-antibody reactions using a radioactively labeled substance (radioligand) either directly or indirectly to measure the binding of the unlabeled substance to a specific antibody or other receptor system. Non-immunogenic substances (e.g., haptens) can be measured if coupled to larger carrier proteins (e.g., bovine gamma-globulin or human serum albumin) capable of inducing antibody formation.

The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)

Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.

Abstaining from all food.

Proteins found in eggs which are consumed as a food.

A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine).

Variation occurring within a species in the presence or length of DNA fragment generated by a specific endonuclease at a specific site in the genome. Such variations are generated by mutations that create or abolish recognition sites for these enzymes or change the length of the fragment.

Proteolytic enzymes that are involved in the conversion of protein precursors such as peptide prohormones into PEPTIDE HORMONES. Some are ENDOPEPTIDASES, some are EXOPEPTIDASES.

The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.

Organic, monobasic acids derived from hydrocarbons by the equivalent of oxidation of a methyl group to an alcohol, aldehyde, and then acid. Fatty acids are saturated and unsaturated (FATTY ACIDS, UNSATURATED). (Grant & Hackh's Chemical Dictionary, 5th ed)

An autosomal recessively inherited disorder caused by mutation of ATP-BINDING CASSETTE TRANSPORTERS involved in cellular cholesterol removal (reverse-cholesterol transport). It is characterized by near absence of ALPHA-LIPOPROTEINS (high-density lipoproteins) in blood. The massive tissue deposition of cholesterol esters results in HEPATOMEGALY; SPLENOMEGALY; RETINITIS PIGMENTOSA; large orange tonsils; and often sensory POLYNEUROPATHY. The disorder was first found among inhabitants of Tangier Island in the Chesapeake Bay, MD.

Compounds with three contiguous nitrogen atoms in linear format, H2N-N=NH, and hydrocarbyl derivatives.

Unstable isotopes of sulfur that decay or disintegrate spontaneously emitting radiation. S 29-31, 35, 37, and 38 are radioactive sulfur isotopes.

A primary malignant neoplasm of epithelial liver cells. It ranges from a well-differentiated tumor with EPITHELIAL CELLS indistinguishable from normal HEPATOCYTES to a poorly differentiated neoplasm. The cells may be uniform or markedly pleomorphic, or form GIANT CELLS. Several classification schemes have been suggested.

Proteins prepared by recombinant DNA technology.

Derivatives of phosphatidic acids in which the phosphoric acid is bound in ester linkage to a choline moiety. Complete hydrolysis yields 1 mole of glycerol, phosphoric acid and choline and 2 moles of fatty acids.

A colorless liquid made by oxidation of aliphatic hydrocarbons that is used as a solvent and chemical intermediate.

Electrophoresis in which agar or agarose gel is used as the diffusion medium.

The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.

Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.

The interstitial fluid that is in the LYMPHATIC SYSTEM.

In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.

Azoles of one NITROGEN and two double bonds that have aromatic chemical properties.

Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.

Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.

A fungal metabolite isolated from cultures of Aspergillus terreus. The compound is a potent anticholesteremic agent. It inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It also stimulates the production of low-density lipoprotein receptors in the liver.

The metabolic process of breaking down LIPIDS to release FREE FATTY ACIDS, the major oxidative fuel for the body. Lipolysis may involve dietary lipids in the DIGESTIVE TRACT, circulating lipids in the BLOOD, and stored lipids in the ADIPOSE TISSUE or the LIVER. A number of enzymes are involved in such lipid hydrolysis, such as LIPASE and LIPOPROTEIN LIPASE from various tissues.

A family of MEMBRANE TRANSPORT PROTEINS that require ATP hydrolysis for the transport of substrates across membranes. The protein family derives its name from the ATP-binding domain found on the protein.

Short sequences (generally about 10 base pairs) of DNA that are complementary to sequences of messenger RNA and allow reverse transcriptases to start copying the adjacent sequences of mRNA. Primers are used extensively in genetic and molecular biology techniques.

A highly dense subclass of the high-density lipoproteins, with particle sizes below 7 nm. They are also known as nascent HDL, composed of a few APOLIPOPROTEIN A-I molecules which are complexed with PHOSPHOLIPIDS. The lipid-poor pre-beta-HDL particles serve as progenitors of HDL3 and then HDL2 after absorption of free cholesterol from cell membranes, cholesterol esterification, and acquisition of apolipoproteins A-II, Cs, and E. Pre-beta-HDL initiate the reverse cholesterol transport process from cells to liver.

Antibodies produced by a single clone of cells.

A synthetic phospholipid used in liposomes and lipid bilayers for the study of biological membranes.

A derivative of LOVASTATIN and potent competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It may also interfere with steroid hormone production. Due to the induction of hepatic LDL RECEPTORS, it increases breakdown of LDL CHOLESTEROL.

An antilipemic agent which reduces both CHOLESTEROL and TRIGLYCERIDES in the blood.

Post-transcriptional biological modification of messenger, transfer, or ribosomal RNAs or their precursors. It includes cleavage, methylation, thiolation, isopentenylation, pseudouridine formation, conformational changes, and association with ribosomal protein.

A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471).

Fatty acids which are unsaturated in only one position.

The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.

Techniques for removal by adsorption and subsequent elution of a specific antibody or antigen using an immunosorbent containing the homologous antigen or antibody.

Work-related situations in which the employees as a group refuse to work until certain conditions of employment are granted by the employer.

Studies comparing two or more treatments or interventions in which the subjects or patients, upon completion of the course of one treatment, are switched to another. In the case of two treatments, A and B, half the subjects are randomly allocated to receive these in the order A, B and half to receive them in the order B, A. A criticism of this design is that effects of the first treatment may carry over into the period when the second is given. (Last, A Dictionary of Epidemiology, 2d ed)

Metabolic products of chylomicron particles in which TRIGLYCERIDES have been selectively removed by the LIPOPROTEIN LIPASE. These remnants carry dietary lipids in the blood and are cholesterol-rich. Their interactions with MACROPHAGES; ENDOTHELIAL CELLS; and SMOOTH MUSCLE CELLS in the artery wall can lead to ATHEROSCLEROSIS.

Pathological processes involving any part of the AORTA.

Technique involving the diffusion of antigen or antibody through a semisolid medium, usually agar or agarose gel, with the result being a precipitin reaction.

Intermediate-density subclass of the high-density lipoproteins, with particle sizes between 7 to 8 nm. As the larger lighter HDL2 lipoprotein, HDL3 lipoprotein is lipid-rich.

Enzymes that catalyze the reversible reduction of alpha-carboxyl group of 3-hydroxy-3-methylglutaryl-coenzyme A to yield MEVALONIC ACID.

Microscopy using an electron beam, instead of light, to visualize the sample, thereby allowing much greater magnification. The interactions of ELECTRONS with specimens are used to provide information about the fine structure of that specimen. In TRANSMISSION ELECTRON MICROSCOPY the reactions of the electrons that are transmitted through the specimen are imaged. In SCANNING ELECTRON MICROSCOPY an electron beam falls at a non-normal angle on the specimen and the image is derived from the reactions occurring above the plane of the specimen.

The interaction of two or more substrates or ligands with the same binding site. The displacement of one by the other is used in quantitative and selective affinity measurements.

Pathological conditions involving the CARDIOVASCULAR SYSTEM including the HEART; the BLOOD VESSELS; or the PERICARDIUM.

Electrophoresis in which a pH gradient is established in a gel medium and proteins migrate until they reach the site (or focus) at which the pH is equal to their isoelectric point.

Genotypic differences observed among individuals in a population.

The portion of the GASTROINTESTINAL TRACT between the PYLORUS of the STOMACH and the ILEOCECAL VALVE of the LARGE INTESTINE. It is divisible into three portions: the DUODENUM, the JEJUNUM, and the ILEUM.

The formation of a solid in a solution as a result of a chemical reaction or the aggregation of soluble substances into complexes large enough to fall out of solution.

Sites on an antigen that interact with specific antibodies.

A LDL-receptor related protein involved in clearance of chylomicron remnants and of activated ALPHA-MACROGLOBULINS from plasma.

Lipid-laden macrophages originating from monocytes or from smooth muscle cells.

Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.

Regular course of eating and drinking adopted by a person or animal.

The sum of the weight of all the atoms in a molecule.

A water-soluble vitamin of the B complex occurring in various animal and plant tissues. It is required by the body for the formation of coenzymes NAD and NADP. It has PELLAGRA-curative, vasodilating, and antilipemic properties.

Artifactual vesicles formed from the endoplasmic reticulum when cells are disrupted. They are isolated by differential centrifugation and are composed of three structural features: rough vesicles, smooth vesicles, and ribosomes. Numerous enzyme activities are associated with the microsomal fraction. (Glick, Glossary of Biochemistry and Molecular Biology, 1990; from Rieger et al., Glossary of Genetics: Classical and Molecular, 5th ed)

The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. PROTEIN STRUCTURE, QUATERNARY describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain).

Method for assessing flow through a system by injection of a known quantity of radionuclide into the system and monitoring its concentration over time at a specific point in the system. (From Dorland, 28th ed)

Tumors or cancer of the LIVER.

Use of restriction endonucleases to analyze and generate a physical map of genomes, genes, or other segments of DNA.

Pathological processes of CORONARY ARTERIES that may derive from a congenital abnormality, atherosclerotic, or non-atherosclerotic cause.

An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed.

A diet that contains limited amounts of fat with less than 30% of calories from all fats and less than 10% from saturated fat. Such a diet is used in control of HYPERLIPIDEMIAS. (From Bondy et al, Metabolic Control and Disease, 8th ed, pp468-70; Dorland, 27th ed)

Individuals whose ancestral origins are in the continents of the Americas.

A family of proteins that share sequence similarity with the low density lipoprotein receptor (RECEPTORS, LDL).

Unstable isotopes of iodine that decay or disintegrate emitting radiation. I atoms with atomic weights 117-139, except I 127, are radioactive iodine isotopes.

The insertion of recombinant DNA molecules from prokaryotic and/or eukaryotic sources into a replicating vehicle, such as a plasmid or virus vector, and the introduction of the resultant hybrid molecules into recipient cells without altering the viability of those cells.

Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group.

A subclass of DIABETES MELLITUS that is not INSULIN-responsive or dependent (NIDDM). It is characterized initially by INSULIN RESISTANCE and HYPERINSULINEMIA; and eventually by GLUCOSE INTOLERANCE; HYPERGLYCEMIA; and overt diabetes. Type II diabetes mellitus is no longer considered a disease exclusively found in adults. Patients seldom develop KETOSIS but often exhibit OBESITY.

A change from planar to elliptic polarization when an initially plane-polarized light wave traverses an optically active medium. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)

A latent susceptibility to disease at the genetic level, which may be activated under certain conditions.

Immunologic method used for detecting or quantifying immunoreactive substances. The substance is identified by first immobilizing it by blotting onto a membrane and then tagging it with labeled antibodies.

The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.

A stack of flattened vesicles that functions in posttranslational processing and sorting of proteins, receiving them from the rough ENDOPLASMIC RETICULUM and directing them to secretory vesicles, LYSOSOMES, or the CELL MEMBRANE. The movement of proteins takes place by transfer vesicles that bud off from the rough endoplasmic reticulum or Golgi apparatus and fuse with the Golgi, lysosomes or cell membrane. (From Glick, Glossary of Biochemistry and Molecular Biology, 1990)

A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1).

A sulfur-containing essential L-amino acid that is important in many body functions.

Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.

Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.

The parts of a macromolecule that directly participate in its specific combination with another molecule.

Diseases in which there is a familial pattern of AMYLOIDOSIS.

A category of nucleic acid sequences that function as units of heredity and which code for the basic instructions for the development, reproduction, and maintenance of organisms.

Dietary fish oils inhibit early events in the assembly of very low density lipoproteins and target apoB for degradation within the rough endoplasmic reticulum of hamster hepatocytes. (1/731)

Dietary fish oils inhibited secretion and stimulated intracellular degradation of apolipoprotein (apo)B in hamster hepatocytes, while dietary sunflower oils stimulated secretion and had no effect on degradation of apoB. To investigate the intracellular site at which fish oils act, we have made use of our previous observations that inhibition of degradation by N-acetyl-leucyl-leucyl-norleucinal (ALLN) results in accumulation of apoB in the trans -Golgi membrane and does not stimulate secretion, while inhibition of degradation by o-phenanthroline results in accumulation of apoB in the rough endoplasmic reticulum membrane and stimulates secretion. Thus, ALLN protects apoB which has been diverted from secretion and o -phenanthroline protects apoB which is targetted for secretion. Addition of o -phenantholine to the incubation medium of hepatocytes from fish oil-fed hamsters inhibited degradation of apoB and stimulated its secretion in particles of the density of VLDL, while addition of ALLN had no effect. These observations suggest that dietary fish oils reversibly inhibit early steps in the assembly of very low density lipoprotein precursors and target apoB for degradation in the rough endoplasmic reticulum. (+info)

Role of cholesterol ester mass in regulation of secretion of ApoB100 lipoprotein particles by hamster hepatocytes and effects of statins on that relationship. (2/731)

Our understanding of the factors that regulate the secretion of apoB100 lipoproteins remains incomplete with considerable debate as to the role, if any, for cholesterol ester in this process. This study examines this issue in primary cultures of hamster hepatocytes, a species in which both cholesterol and apoB100 metabolism are very similar to man. Addition of oleate to medium increased the mass of triglyceride and cholesterol ester within the hepatocyte and also increased the secretion of triglycerides, cholesterol ester, and apoB100 into the medium. Next, the responses of hamster hepatocytes to addition of either an HMG-CoA reductase inhibitor (lovastatin) or an acyl-CoA cholesterol acyltransferase inhibitor (58-035) to the medium, with or without added oleate, were determined. Effects of either agent were only evident in the oleate-supplemented medium in which cholesterol ester mass had been increased above basal. If oleate was not added to the medium, neither agent reduced apoB100 secretion; equally important, over the 24-hour incubation, neither agent, at the concentration used, produced any detectable change in intracellular cholesterol ester mass. However, in contrast to the estimates of mass, which were unchanged, under the same conditions radioisotopic estimates of cholesterol ester synthesis were markedly reduced. Any conclusion as to the relation of cholesterol ester mass to apoB100 secretion would therefore depend on which of the 2 methods was used. Overall, the data indicate a close correlation between the mass of cholesterol ester within the hepatocyte and apoB100 secretion from it and they go far to explain previous apparently contradictory data as to this relation. More importantly, though, taken with other available data, they indicate that the primary response of the liver to increased delivery of lipid is increased secretion rather than decreased uptake. These results point, therefore, to a hierarchy of hepatic responses to increased flux of fatty acids and increased synthesis of cholesterol that in turn suggests a more dynamic model of cholesterol homeostasis in the liver than has been appreciated in the past. (+info)

Characterization of a new form of inherited hypercholesterolemia: familial recessive hypercholesterolemia. (3/731)

We previously described a Sardinian family in which the probands had a severe form of hypercholesterolemia, suggestive of familial hypercholesterolemia (FH). However, low density lipoprotein (LDL) receptor activity in fibroblasts from these subjects and LDL binding ability were normal. The characteristics of the pedigree were consistent with an autosomal recessive trait. Sitosterolemia and pseudohomozygous hyperlipidemia were ruled out. A second Sardinian kindred with similar characteristics was identified. Probands showed severe hypercholesterolemia, whereas their parents and grandparents were normolipidemic. FH, familial defective apoprotein (apo) B, sitosterolemia, and cholesteryl ester storage disease were excluded by in vitro studies. We addressed the metabolic basis of this inherited disorder by studying the in vivo metabolism of LDL in 3 probands from these 2 families. 125I-LDL turnover studies disclosed a marked reduction in the fractional catabolic rate (0.19+/-0.01 versus 0.36+/-0.03 pools per day, respectively; P<0.001) and a significant increase in the production rate [20.7+/-4.4 versus 14. 0+/-2.4 mg. kg-1. d-1, respectively; P<0.01] of LDL apoB in the probands compared with normolipidemic controls. We then studied the in vivo biodistribution and tissue uptake of 99mtechnetium-labeled LDL in the probands and compared them with those in normal controls and 1 FH homozygote. The probands showed a significant reduction in hepatic LDL uptake, similar to that observed in the FH homozygote. A reduced uptake of LDL by the kidney and spleen was also observed in all patients. Our findings suggest that this recessive form of hypercholesterolemia is due to a marked reduction of in vivo LDL catabolism. This appears to be caused by a selective reduction in hepatic LDL uptake. We propose that in this new lipid disorder, a recessive defect causes a selective impairment of LDL receptor function in the liver. (+info)

Selective modification of apoB-100 in the oxidation of low density lipoproteins by myeloperoxidase in vitro. (4/731)

Oxidative modification of LDL may be important in the initiation and/or progression of atherosclerosis, but the precise mechanisms through which low density lipoprotein (LDL) is oxidized are unknown. Recently, evidence for the existence of HOCl-oxidized LDL in human atherosclerotic lesions has been reported, and myeloperoxidase (MPO), which is thought to act through production of HOCl, has been identified in human atherosclerotic lesions. In the present report we describe the formation of 2,4-dinitrophenylhydrazine (DNPH)-reactive modifications in the apolipoprotein (apo) by exposure of LDL to myeloperoxidase in vitro. In contrast with the complex mixture of peptides from oxidation of LDL with reagent HOCl, oxidation with MPO in vitro produced a major tryptic peptide showing absorbance at 365 nm. This peptide was isolated and characterized as VELEVPQL(*C)SFILK..., corresponding to amino acid residues 53-66...on apoB-100. Mass spectrometric analyses of two tryptic peptides from oxidation of LDL by HOCl indicated formation of the corresponding methionine sulfoxide (M=O), cysteinyl azo (*C), RS -N= N-DNP, derivatives of EEL(*C)T(M=O)FIR and LNDLNS VLV(M=O)PTFHVPFTDLQVPS(*C)K, which suggest oxidation to the corresponding sulfinic acids (RSO2H) by HOCl. The present results demonstrate that DNPH-reactive modifications other than aldehydes and ketones can be formed in the oxidation of proteins and illustrate how characterization of specific products of protein oxidation can be useful in assessing the relative contributions of different and unexpected mechanisms to the oxidation of LDL and other target substrates. The data also suggest a direct interaction of the LDL particle with the active site on myeloperoxidase and indicate that effects of the protein microenvironment can greatly influence product formation and stability. (+info)

ApoB100 secretion from HepG2 cells is decreased by the ACAT inhibitor CI-1011: an effect associated with enhanced intracellular degradation of ApoB. (5/731)

The concept that hepatic cholesteryl ester (CE) mass and the rate of cholesterol esterification regulate hepatocyte assembly and secretion of apoB-containing lipoproteins remains controversial. The present study was carried out in HepG2 cells to correlate the rate of cholesterol esterification and CE mass with apoB secretion by CI-1011, an acyl CoA:cholesterol acyltransferase (ACAT) inhibitor that is known to decrease apoB secretion, in vivo, in miniature pigs. HepG2 cells were incubated with CI-1011 (10 nmol/L, 1 micromol/L, and 10 micromol/L) for 24 hours. ApoB secretion into media was decreased by 25%, 27%, and 43%, respectively (P<0.0012). CI-1011 (10 micromol/L) inhibited HepG2 cell ACAT activity by 79% (P<0.002) and cellular CE mass by 32% (P<0.05). In contrast, another ACAT inhibitor, DuP 128 (10 micromol/L), decreased cellular ACAT activity and CE mass by 85% (P<0.002) and 42% (P=0.01), respectively, but had no effect on apoB secretion into media. To characterize the reduction in apoB secretion by CI-1011, pulse-chase experiments were performed and analyzed by multicompartmental modelling using SAAM II. CI-1011 did not affect the synthesis of apoB or albumin. However, apoB secretion into the media was decreased by 42% (P=0.019). Intracellular apoB degradation increased proportionately (P=0.019). The secretion of albumin and cellular reuptake of labeled lipoproteins were unchanged. CI-1011 and DuP 128 did not affect apoB mRNA concentrations. These results show that CI-1011 decreases apoB secretion by a mechanism that involves an enhanced intracellular degradation of apoB. This study demonstrates that ACAT inhibitors can exert differential effects on apoB secretion from HepG2 cells that do not reflect their efficacy in inhibiting cholesterol esterification. (+info)

Secondary radicals derived from chloramines of apolipoprotein B-100 contribute to HOCl-induced lipid peroxidation of low-density lipoproteins. (6/731)

Oxidation of low-density lipoproteins (LDL) is thought to contribute to atherogenesis. Although there is increasing evidence for a role of myeloperoxidase-derived oxidants such as hypochlorite (HOCl), the mechanism by which HOCl modifies LDL remains controversial. Some studies report the protein component to be the major site of attack, whereas others describe extensive lipid peroxidation. The present study addresses this controversy. The results obtained are consistent with the hypothesis that radical-induced oxidation of LDL's lipids by HOCl is a secondary reaction, with most HOCl consumed via rapid, non-radical reaction with apolipoprotein B-100. Subsequent incubation of HOCl-treated LDL gives rise to lipid peroxidation and antioxidant consumption in a time-dependent manner. Similarly, with myeloperoxidase/H2O2/Cl- (the source of HOCl in vivo), protein oxidation is rapid and followed by an extended period of lipid peroxidation during which further protein oxidation does not occur. The secondary lipid peroxidation process involves EPR-detectable radicals, is attenuated by a radical trap or treatment of HOCl-oxidized LDL with methionine, and occurs less rapidly when the lipoprotein was depleted of alpha-tocopherol. The initial reaction of low concentrations of HOCl (400-fold or 800-fold molar excess) with LDL therefore seems to occur primarily by two-electron reactions with side-chain sites on apolipoprotein B-100. Some of the initial reaction products, identified as lysine-residue-derived chloramines, subsequently undergo homolytic (one-electron) reactions to give radicals that initiate antioxidant consumption and lipid oxidation via tocopherol-mediated peroxidation. The identification of these chloramines, and the radicals derived from them, as initiating agents in LDL lipid peroxidation offers potential new targets for antioxidative therapy in atherogenesis. (+info)

Molecular bases of low production rates of apolipoprotein B-100 and truncated apoB-82 in a mutant HepG2 cell line generated by targeted modification of the apolipoprotein B gene. (7/731)

In subjects with familial hypobetalipoproteinemia heterozygous for truncated forms of apolipoprotein B, both apoB-100 and the truncated forms are produced at lower than expected rates. We studied the mechanism of low levels of apoB in a cell model produced by targeted modification of the apob gene of HepG2 cells. One of the three alleles of apob was found to be targeted. The targeted cells expressed apoB-100 and B-82. The media of mutant cells contained 56% of the levels of apoB-100 present in the media of wild-type (WT) HepG2 cells. ApoB-82 was present at 11% of the apoB-100 levels in mutant cell media. An 85-kD protein (apoB-15) representing the N-terminal fragment of apoB was also secreted, but only in the mutant cell media. We examined the mechanism of low levels of apoB-82. Cellular apoB-82 mRNA was 11% of apoB-100 mRNA, lower than the 33% expected, but consistent with relative levels of apoB-82 in the media. ApoB mRNA transcription in WT and the mutant cells did not differ, while the levels of apoB-82 mRNA in nuclei and polysomes were 46% and 12% of the levels of apoB-100 mRNA, respectively, suggesting that the lower levels of apoB-82 mRNA were due to altered message stability. In a pulse/chase experiment with [35S] methionine, at zero time of chase, the amounts of apoB-100 in mutant cells was 66% that of WT levels, consistent with the modification of one allele. The fractions of newly synthesized apoB-100 secreted into the media at 2 h were 10% in the mutant cells and 19% in the WT cells, suggesting greater presecretory degradation of apoB-100 in the mutant cells. Thus, low levels of mutant apoB-82 mRNA gave rise to the low levels of apoB-82, while low levels of apoB-100 were due to low rates of secretion. (+info)

Truncated apo B-70.5-containing lipoproteins bind to megalin but not the LDL receptor. (8/731)

Apo B-100 of LDL can bind to both the LDL receptor and megalin, but the molecular interactions of apo B-100 with these 2 receptors are not completely understood. Naturally occurring mutant forms of apo B may be a source of valuable information on these interactions. Apo B-70.5 is uniquely useful because it contains the NH2-terminal portion of apo B-100, that includes only one of the two putative LDL receptor-binding sites (site A). The lipoprotein containing apo B-70. 5 (Lp B-70.5) was purified from apo B-100/apo B-70.5 heterozygotes by sequential ultracentrifugation combined with immunoaffinity chromatography. Cell culture experiments, ligand blot analysis, and in vivo studies all consistently showed that Lp B-70.5 is not recognized by the LDL receptor. The kidney was identified as a major organ in catabolism of Lp B-70.5 in New Zealand white rabbits. Autoradiographic analysis revealed that renal proximal tubular cells selectively removed Lp B-70.5. On ligand blotting of renal cortical membranes, Lp B-70.5 bound only to megalin. The ability of megalin to mediate cellular endocytosis of Lp B-70.5 was confirmed using retinoic acid/dibutyryl cAMP-treated F9 cells. This study suggests that the putative LDL receptor-binding site A on apo B-100 might not by itself be a functional binding domain and that the apo B-binding sites recognized by the LDL receptor and by megalin may be different. Moreover, megalin may play an important role in renal catabolism of apo B truncations, including apo B-70.5. (+info)

The symptoms of hypobetalipoproteinemia usually become apparent during childhood or adolescence and can include:

* Poor growth and development
* Delayed puberty
* Abnormal fat distribution (e.g., accumulation of fat in the face, neck, and abdomen)
* Elevated levels of HDL cholesterol
* Low levels of LDL cholesterol
* Increased risk of bleeding due to low levels of clotting factors
* Abnormal liver function tests

Hypobetalipoproteinemia is caused by mutations in the genes that code for apolipoprotein B-100 or other proteins involved in lipid metabolism. These mutations can be inherited from one or both parents, or they can occur spontaneously.

The diagnosis of hypobetalipoproteinemia is based on a combination of clinical findings, laboratory tests, and genetic analysis. Laboratory tests may include measurements of lipids and lipoproteins, as well as genetic testing to identify mutations in the apolipoprotein B-100 gene or other genes involved in lipid metabolism.

Treatment for hypobetalipoproteinemia typically involves a combination of dietary changes and medication. Dietary changes may include increasing the intake of healthy fats, such as nuts and avocados, while avoiding foods high in saturated and trans fats. Medications may be used to raise HDL cholesterol levels or lower LDL cholesterol levels. In some cases, liver transplantation may be necessary if the condition is caused by a genetic mutation that leads to liver dysfunction.

The prognosis for hypobetalipoproteinemia varies depending on the underlying cause of the condition and the severity of the symptoms. In general, early diagnosis and treatment can improve outcomes and reduce the risk of complications such as cardiovascular disease. However, some individuals with severe forms of the condition may have a poor prognosis if left untreated.

In conclusion, hypobetalipoproteinemia is a rare genetic disorder characterized by very low levels of apolipoprotein B-100 and other lipid abnormalities. The diagnosis is based on laboratory tests and genetic analysis, and treatment typically involves a combination of dietary changes and medication. Early diagnosis and treatment can improve outcomes and reduce the risk of complications such as cardiovascular disease.

The condition is caused by mutations in genes that code for proteins involved in lipid metabolism, such as the low-density lipoprotein receptor gene (LDLR), apolipoprotein A-1 gene (APOA1), and proprotein convertase subtilisin/kexin type 9 (PCSK9) genes. These mutations can lead to the overproduction or underexpression of certain lipids, leading to the characteristic lipid abnormalities seen in HeFH.

HeFH is usually inherited in an autosomal dominant manner, meaning that a single copy of the mutated gene is enough to cause the condition. However, some cases may be caused by recessive inheritance or de novo mutations. The condition can affect both children and adults, and it is important for individuals with HeFH to be monitored closely by a healthcare provider to manage their lipid levels and reduce the risk of cardiovascular disease.

Treatment for HeFH typically involves a combination of dietary modifications, such as reducing saturated fat intake and increasing fiber and omega-3 fatty acid intake, and medications, such as statins, to lower cholesterol levels. In some cases, apheresis or liver transplantation may be necessary to reduce lipid levels. Early detection and management of HeFH can help prevent or delay the development of cardiovascular disease, which is the leading cause of death worldwide.

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.

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.

People with FH have a high risk of developing cardiovascular disease, including heart attacks, strokes, and peripheral artery disease, due to the abnormally low levels of LDL cholesterol in their blood. This is because LDL cholesterol is essential for the proper functioning of the body's cell membranes and is also involved in the transportation of cholesterol from the liver to other parts of the body. Without enough LDL cholesterol, cells become dysfunctional and cannot properly regulate their cholesterol levels, leading to a range of health problems.

FH is typically inherited in an autosomal dominant pattern, meaning that a single copy of the mutated gene is enough to cause the condition. However, some cases may be caused by spontaneous mutations or other factors. Symptoms of FH can vary in severity and may include high levels of triglycerides, low levels of HDL or "good" cholesterol, and a range of cardiovascular problems.

There is no cure for FH, but treatment typically involves a combination of dietary modifications, such as limiting intake of saturated and trans fats, and medications to lower LDL cholesterol levels. In some cases, patients may also require regular monitoring and management of cardiovascular risk factors, such as high blood pressure or diabetes.

In summary, hypobetalipoproteinemia, familial, apolipoprotein B (FH) is a rare genetic disorder that affects the metabolism of lipids and causes low levels of LDL cholesterol and triglycerides in the blood. While there is no cure for the condition, treatment can help manage symptoms and reduce the risk of cardiovascular 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.

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 disease begins with endothelial dysfunction, which allows lipid accumulation in the artery wall. Macrophages take up oxidized lipids and become foam cells, which die and release their contents, including inflammatory cytokines, leading to further inflammation and recruitment of more immune cells.

The atherosclerotic plaque can rupture or ulcerate, leading to the formation of a thrombus that can occlude the blood vessel, causing ischemia or infarction of downstream tissues. This can lead to various cardiovascular diseases such as myocardial infarction (heart attack), stroke, and peripheral artery disease.

Atherosclerosis is a multifactorial disease that is influenced by genetic and environmental factors such as smoking, hypertension, diabetes, high cholesterol levels, and obesity. It is diagnosed by imaging techniques such as angiography, ultrasound, or computed tomography (CT) scans.

Treatment options for atherosclerosis include lifestyle modifications such as smoking cessation, dietary changes, and exercise, as well as medications such as statins, beta blockers, and angiotensin-converting enzyme (ACE) inhibitors. In severe cases, surgical interventions such as bypass surgery or angioplasty may be necessary.

In conclusion, atherosclerosis is a complex and multifactorial disease that affects the arteries and can lead to various cardiovascular diseases. Early detection and treatment can help prevent or slow down its progression, reducing the risk of complications and improving patient outcomes.

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 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 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.

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 causes of hypertriglyceridemia, including:

* Genetics: Some people may inherit a tendency to have high triglyceride levels due to genetic mutations that affect the genes involved in triglyceride metabolism.
* Obesity: Excess body weight is associated with higher triglyceride levels, as there is more fat available for energy.
* Diabetes: Both type 1 and type 2 diabetes can lead to high triglyceride levels due to insulin resistance and altered glucose metabolism.
* High-carbohydrate diet: Consuming high amounts of carbohydrates, particularly refined or simple carbohydrates, can cause a spike in blood triglycerides.
* Alcohol consumption: Drinking too much alcohol can increase triglyceride levels in the blood.
* Certain medications: Some drugs, such as anabolic steroids and some antidepressants, can raise triglyceride levels.
* Underlying medical conditions: Certain medical conditions, such as hypothyroidism, kidney disease, and polycystic ovary syndrome (PCOS), can also contribute to high triglyceride levels.

Hypertriglyceridemia is typically diagnosed with a blood test that measures the level of triglycerides in the blood. Treatment options for hypertriglyceridemia depend on the underlying cause of the condition, but may include lifestyle modifications such as weight loss, dietary changes, and medications to lower triglyceride levels.

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.

There are several types of dyslipidemias, including:

1. Hyperlipidemia: Elevated levels of lipids and lipoproteins in the blood, which can increase the risk of CVD.
2. Hypolipidemia: Low levels of lipids and lipoproteins in the blood, which can also increase the risk of CVD.
3. Mixed dyslipidemia: A combination of hyperlipidemia and hypolipidemia.
4. Familial dyslipidemia: An inherited condition that affects the levels of lipids and lipoproteins in the blood.
5. Acquired dyslipidemia: A condition caused by other factors, such as poor diet or medication side effects.

Dyslipidemias can be diagnosed through a variety of tests, including fasting blood sugar (FBS), lipid profile, and apolipoprotein testing. Treatment for dyslipidemias often involves lifestyle changes, such as dietary modifications and increased physical activity, as well as medications to lower cholesterol and triglycerides.

In conclusion, dyslipidemias are abnormalities in the levels or composition of lipids and lipoproteins in the blood that can increase the risk of CVD. They can be caused by a variety of factors and diagnosed through several tests. Treatment often involves lifestyle changes and medications to lower cholesterol and triglycerides.

Coronary disease is often caused by a combination of genetic and lifestyle factors, such as high blood pressure, high cholesterol levels, smoking, obesity, and a lack of physical activity. It can also be triggered by other medical conditions, such as diabetes and kidney disease.

The symptoms of coronary disease can vary depending on the severity of the condition, but may include:

* Chest pain or discomfort (angina)
* Shortness of breath
* Fatigue
* Swelling of the legs and feet
* Pain in the arms and back

Coronary disease is typically diagnosed through a combination of physical examination, medical history, and diagnostic tests such as electrocardiograms (ECGs), stress tests, and cardiac imaging. Treatment for coronary disease may include lifestyle changes, medications to control symptoms, and surgical procedures such as angioplasty or bypass surgery to improve blood flow to the heart.

Preventative measures for coronary disease include:

* Maintaining a healthy diet and exercise routine
* Quitting smoking and limiting alcohol consumption
* Managing high blood pressure, high cholesterol levels, and other underlying medical conditions
* Reducing stress through relaxation techniques or therapy.

The symptoms of Alzheimer's disease can vary from person to person and may progress slowly over time. Early symptoms may include memory loss, confusion, and difficulty with problem-solving. As the disease progresses, individuals may experience language difficulties, visual hallucinations, and changes in mood and behavior.

There is currently no cure for Alzheimer's disease, but there are several medications and therapies that can help manage its symptoms and slow its progression. These include cholinesterase inhibitors, memantine, and non-pharmacological interventions such as cognitive training and behavioral therapy.

Alzheimer's disease is a significant public health concern, affecting an estimated 5.8 million Americans in 2020. It is the sixth leading cause of death in the United States, and its prevalence is expected to continue to increase as the population ages.

There is ongoing research into the causes and potential treatments for Alzheimer's disease, including studies into the role of inflammation, oxidative stress, and the immune system. Other areas of research include the development of biomarkers for early detection and the use of advanced imaging techniques to monitor progression of the disease.

Overall, Alzheimer's disease is a complex and multifactorial disorder that poses significant challenges for individuals, families, and healthcare systems. However, with ongoing research and advances in medical technology, there is hope for improving diagnosis and treatment options in the future.

People with Tangier disease often have extremely high levels of low-density lipoprotein (LDL) cholesterol, which can lead to the development of cardiovascular disease at an early age. The disorder is caused by mutations in the gene that codes for a protein called ATP-binding cassette transporter 1 (ABC1), which plays a critical role in the transport of cholesterol and other lipids in the body.

The symptoms of Tangier disease can vary depending on the severity of the disorder, but may include:

* High levels of LDL cholesterol
* Low levels of HDL cholesterol
* Abnormal liver function tests
* Yellowing of the skin and eyes (jaundice)
* Fatigue
* Weakness
* Muscle cramps
* Heart disease
* Stroke

Tangier disease is usually diagnosed through a combination of clinical evaluation, laboratory tests, and genetic analysis. Treatment for the disorder typically involves a combination of dietary modifications, medications, and lipid-lowering therapy to reduce the levels of LDL cholesterol and increase the levels of HDL cholesterol. In some cases, a liver transplant may be necessary to treat the liver damage that can occur as a result of the disorder.

There are several risk factors for developing HCC, including:

* Cirrhosis, which can be caused by heavy alcohol consumption, viral hepatitis (such as hepatitis B and C), or fatty liver disease
* Family history of liver disease
* Chronic obstructive pulmonary disease (COPD)
* Diabetes
* Obesity

HCC can be challenging to diagnose, as the symptoms are non-specific and can be similar to those of other conditions. However, some common symptoms of HCC include:

* Yellowing of the skin and eyes (jaundice)
* Fatigue
* Loss of appetite
* Abdominal pain or discomfort
* Weight loss

If HCC is suspected, a doctor may perform several tests to confirm the diagnosis, including:

* Imaging tests, such as ultrasound, CT scan, or MRI, to look for tumors in the liver
* Blood tests to check for liver function and detect certain substances that are produced by the liver
* Biopsy, which involves removing a small sample of tissue from the liver to examine under a microscope

Once HCC is diagnosed, treatment options will depend on several factors, including the stage and location of the cancer, the patient's overall health, and their personal preferences. Treatment options may include:

* Surgery to remove the tumor or parts of the liver
* Ablation, which involves destroying the cancer cells using heat or cold
* Chemoembolization, which involves injecting chemotherapy drugs into the hepatic artery to reach the cancer cells
* Targeted therapy, which uses drugs or other substances to target specific molecules that are involved in the growth and spread of the cancer

Overall, the prognosis for HCC is poor, with a 5-year survival rate of approximately 20%. However, early detection and treatment can improve outcomes. It is important for individuals at high risk for HCC to be monitored regularly by a healthcare provider, and to seek medical attention if they experience any symptoms.

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

1. Aneurysms: A bulge or ballooning in the wall of the aorta that can lead to rupture and life-threatening bleeding.
2. Atherosclerosis: The buildup of plaque in the inner lining of the aorta, which can narrow the artery and restrict blood flow.
3. Dissections: A tear in the inner layer of the aortic wall that can cause bleeding and lead to an aneurysm.
4. Thoracic aortic disease: Conditions that affect the thoracic portion of the aorta, such as atherosclerosis or dissections.
5. Abdominal aortic aneurysms: Enlargement of the abdominal aorta that can lead to rupture and life-threatening bleeding.
6. Aortic stenosis: Narrowing of the aortic valve, which can impede blood flow from the heart into the aorta.
7. Aortic regurgitation: Backflow of blood from the aorta into the heart due to a faulty aortic valve.
8. Marfan syndrome: A genetic disorder that affects the body's connective tissue, including the aorta.
9. Ehlers-Danlos syndrome: A group of genetic disorders that affect the body's connective tissue, including the aorta.
10. Turner syndrome: A genetic disorder that affects females and can cause aortic diseases.

Aortic diseases can be diagnosed through imaging tests such as ultrasound, CT scan, or MRI. Treatment options vary depending on the specific condition and may include medication, surgery, or endovascular procedures.

1. Coronary artery disease: The narrowing or blockage of the coronary arteries, which supply blood to the heart.
2. Heart failure: A condition in which the heart is unable to pump enough blood to meet the body's needs.
3. Arrhythmias: Abnormal heart rhythms that can be too fast, too slow, or irregular.
4. Heart valve disease: Problems with the heart valves that control blood flow through the heart.
5. Heart muscle disease (cardiomyopathy): Disease of the heart muscle that can lead to heart failure.
6. Congenital heart disease: Defects in the heart's structure and function that are present at birth.
7. Peripheral artery disease: The narrowing or blockage of blood vessels that supply oxygen and nutrients to the arms, legs, and other organs.
8. Deep vein thrombosis (DVT): A blood clot that forms in a deep vein, usually in the leg.
9. Pulmonary embolism: A blockage in one of the arteries in the lungs, which can be caused by a blood clot or other debris.
10. Stroke: A condition in which there is a lack of oxygen to the brain due to a blockage or rupture of blood vessels.

Liver neoplasms, also known as liver tumors or hepatic tumors, are abnormal growths of tissue in the liver. These growths can be benign (non-cancerous) or malignant (cancerous). Malignant liver tumors can be primary, meaning they originate in the liver, or metastatic, meaning they spread to the liver from another part of the body.

There are several types of liver neoplasms, including:

1. Hepatocellular carcinoma (HCC): This is the most common type of primary liver cancer and arises from the main cells of the liver (hepatocytes). HCC is often associated with cirrhosis and can be caused by viral hepatitis or alcohol abuse.
2. Cholangiocarcinoma: This type of cancer arises from the cells lining the bile ducts within the liver (cholangiocytes). Cholangiocarcinoma is rare and often diagnosed at an advanced stage.
3. Hemangiosarcoma: This is a rare type of cancer that originates in the blood vessels of the liver. It is most commonly seen in dogs but can also occur in humans.
4. Fibromas: These are benign tumors that arise from the connective tissue of the liver (fibrocytes). Fibromas are usually small and do not spread to other parts of the body.
5. Adenomas: These are benign tumors that arise from the glandular cells of the liver (hepatocytes). Adenomas are usually small and do not spread to other parts of the body.

The symptoms of liver neoplasms vary depending on their size, location, and whether they are benign or malignant. Common symptoms include abdominal pain, fatigue, weight loss, and jaundice (yellowing of the skin and eyes). Diagnosis is typically made through a combination of imaging tests such as CT scans, MRI scans, and ultrasound, and a biopsy to confirm the presence of cancer cells.

Treatment options for liver neoplasms depend on the type, size, location, and stage of the tumor, as well as the patient's overall health. Surgery may be an option for some patients with small, localized tumors, while others may require chemotherapy or radiation therapy to shrink the tumor before surgery can be performed. In some cases, liver transplantation may be necessary.

Prognosis for liver neoplasms varies depending on the type and stage of the cancer. In general, early detection and treatment improve the prognosis, while advanced-stage disease is associated with a poorer prognosis.

The buildup of plaque in the coronary arteries is often caused by high levels of low-density lipoprotein (LDL) cholesterol, smoking, high blood pressure, diabetes, and a family history of heart disease. The plaque can also rupture, causing a blood clot to form, which can completely block the flow of blood to the heart muscle, leading to a heart attack.

CAD is the most common type of heart disease and is often asymptomatic until a serious event occurs. Risk factors for CAD include:

* Age (men over 45 and women over 55)
* Gender (men are at greater risk than women, but women are more likely to die from CAD)
* Family history of heart disease
* High blood pressure
* High cholesterol
* Diabetes
* Smoking
* Obesity
* Lack of exercise

Diagnosis of CAD typically involves a physical exam, medical history, and results of diagnostic tests such as:

* Electrocardiogram (ECG or EKG)
* Stress test
* Echocardiogram
* Coronary angiography

Treatment for CAD may include lifestyle changes such as a healthy diet, regular exercise, stress management, and quitting smoking. Medications such as beta blockers, ACE inhibitors, and statins may also be prescribed to manage symptoms and slow the progression of the disease. In severe cases, surgical intervention such as coronary artery bypass grafting (CABG) or percutaneous coronary intervention (PCI) may be necessary.

Prevention of CAD includes managing risk factors such as high blood pressure, high cholesterol, and diabetes, quitting smoking, maintaining a healthy weight, and getting regular exercise. Early detection and treatment of CAD can help to reduce the risk of complications and improve quality of life for those affected by the disease.

Type 2 diabetes can be managed through a combination of diet, exercise, and medication. In some cases, lifestyle changes may be enough to control blood sugar levels, while in other cases, medication or insulin therapy may be necessary. Regular monitoring of blood sugar levels and follow-up with a healthcare provider are important for managing the condition and preventing complications.

Common symptoms of type 2 diabetes include:

* Increased thirst and urination
* Fatigue
* Blurred vision
* Cuts or bruises that are slow to heal
* Tingling or numbness in the hands and feet
* Recurring skin, gum, or bladder infections

If left untreated, type 2 diabetes can lead to a range of complications, including:

* Heart disease and stroke
* Kidney damage and failure
* Nerve damage and pain
* Eye damage and blindness
* Foot damage and amputation

The exact cause of type 2 diabetes is not known, but it is believed to be linked to a combination of genetic and lifestyle factors, such as:

* Obesity and excess body weight
* Lack of physical activity
* Poor diet and nutrition
* Age and family history
* Certain ethnicities (e.g., African American, Hispanic/Latino, Native American)
* History of gestational diabetes or delivering a baby over 9 lbs.

There is no cure for type 2 diabetes, but it can be managed and controlled through a combination of lifestyle changes and medication. With proper treatment and self-care, people with type 2 diabetes can lead long, healthy lives.

Explanation: Genetic predisposition to disease is influenced by multiple factors, including the presence of inherited genetic mutations or variations, environmental factors, and lifestyle choices. The likelihood of developing a particular disease can be increased by inherited genetic mutations that affect the functioning of specific genes or biological pathways. For example, inherited mutations in the BRCA1 and BRCA2 genes increase the risk of developing breast and ovarian cancer.

The expression of genetic predisposition to disease can vary widely, and not all individuals with a genetic predisposition will develop the disease. Additionally, many factors can influence the likelihood of developing a particular disease, such as environmental exposures, lifestyle choices, and other health conditions.

Inheritance patterns: Genetic predisposition to disease can be inherited in an autosomal dominant, autosomal recessive, or multifactorial pattern, depending on the specific disease and the genetic mutations involved. Autosomal dominant inheritance means that a single copy of the mutated gene is enough to cause the disease, while autosomal recessive inheritance requires two copies of the mutated gene. Multifactorial inheritance involves multiple genes and environmental factors contributing to the development of the disease.

Examples of diseases with a known genetic predisposition:

1. Huntington's disease: An autosomal dominant disorder caused by an expansion of a CAG repeat in the Huntingtin gene, leading to progressive neurodegeneration and cognitive decline.
2. Cystic fibrosis: An autosomal recessive disorder caused by mutations in the CFTR gene, leading to respiratory and digestive problems.
3. BRCA1/2-related breast and ovarian cancer: An inherited increased risk of developing breast and ovarian cancer due to mutations in the BRCA1 or BRCA2 genes.
4. Sickle cell anemia: An autosomal recessive disorder caused by a point mutation in the HBB gene, leading to defective hemoglobin production and red blood cell sickling.
5. Type 1 diabetes: An autoimmune disease caused by a combination of genetic and environmental factors, including multiple genes in the HLA complex.

Understanding the genetic basis of disease can help with early detection, prevention, and treatment. For example, genetic testing can identify individuals who are at risk for certain diseases, allowing for earlier intervention and preventive measures. Additionally, understanding the genetic basis of a disease can inform the development of targeted therapies and personalized medicine."

The different types of familial amyloidosis include:

1. Familial amyloid polyneuropathy (FAP): This is the most common type of familial amyloidosis and is characterized by the accumulation of amyloid fibers in the nerves, leading to progressive nerve damage and loss of sensation.
2. Familial amyloid cardiomyopathy (FAC): This type of amyloidosis affects the heart and is characterized by the accumulation of amyloid fibers in the heart muscle, leading to progressive heart failure.
3. Familial amyloidotic polyneuropathy (FAP): This type of amyloidosis affects the nerves and is characterized by the accumulation of amyloid fibers in the nerves, leading to progressive nerve damage and loss of sensation.
4. Primary amyloidosis (AL): This is a type of amyloidosis that is not inherited and is characterized by the accumulation of amyloid fibers in various organs and tissues throughout the body.

The symptoms of familial amyloidosis can vary depending on the specific type and the organs affected. Common symptoms include:

* Nerve damage and loss of sensation
* Heart failure
* Weakness and fatigue
* Pain
* Nausea and vomiting
* Diarrhea
* Constipation
* Weight loss

The diagnosis of familial amyloidosis is based on a combination of clinical findings, laboratory tests, and genetic analysis. Laboratory tests may include:

* Blood tests to measure the level of amyloid fibers in the blood
* Urine tests to measure the level of amyloid fibers in the urine
* Imaging studies such as X-rays, CT scans, or MRI scans to visualize the accumulation of amyloid fibers in the organs and tissues.

Treatment for familial amyloidosis is aimed at managing the symptoms and slowing the progression of the disease. Treatment options may include:

* Medications to manage pain, nausea, and vomiting
* Physical therapy to maintain muscle strength and mobility
* Dietary modifications to manage weight loss and malnutrition
* Heart failure medications to manage heart failure
* Kidney dialysis or transplantation to manage kidney failure
* Stem cell transplantation to slow the progression of the disease.

The prognosis for familial amyloidosis is generally poor, and the disease can be fatal within a few years after diagnosis. However, with early diagnosis and appropriate treatment, some people with familial amyloidosis may experience a better quality of life and longer survival time. It is important to note that there is currently no cure for familial amyloidosis, and research is ongoing to develop new and more effective treatments for the disease.

Body weight is an important health indicator, as it can affect an individual's risk for certain medical conditions, such as obesity, diabetes, and cardiovascular disease. Maintaining a healthy body weight is essential for overall health and well-being, and there are many ways to do so, including a balanced diet, regular exercise, and other lifestyle changes.

There are several ways to measure body weight, including:

1. Scale: This is the most common method of measuring body weight, and it involves standing on a scale that displays the individual's weight in kg or lb.
2. Body fat calipers: These are used to measure body fat percentage by pinching the skin at specific points on the body.
3. Skinfold measurements: This method involves measuring the thickness of the skin folds at specific points on the body to estimate body fat percentage.
4. Bioelectrical impedance analysis (BIA): This is a non-invasive method that uses electrical impulses to measure body fat percentage.
5. Dual-energy X-ray absorptiometry (DXA): This is a more accurate method of measuring body composition, including bone density and body fat percentage.

It's important to note that body weight can fluctuate throughout the day due to factors such as water retention, so it's best to measure body weight at the same time each day for the most accurate results. Additionally, it's important to use a reliable scale or measuring tool to ensure accurate measurements.

Examples of experimental liver neoplasms include:

1. Hepatocellular carcinoma (HCC): This is the most common type of primary liver cancer and can be induced experimentally by injecting carcinogens such as diethylnitrosamine (DEN) or dimethylbenz(a)anthracene (DMBA) into the liver tissue of animals.
2. Cholangiocarcinoma: This type of cancer originates in the bile ducts within the liver and can be induced experimentally by injecting chemical carcinogens such as DEN or DMBA into the bile ducts of animals.
3. Hepatoblastoma: This is a rare type of liver cancer that primarily affects children and can be induced experimentally by administering chemotherapy drugs to newborn mice or rats.
4. Metastatic tumors: These are tumors that originate in other parts of the body and spread to the liver through the bloodstream or lymphatic system. Experimental models of metastatic tumors can be studied by injecting cancer cells into the liver tissue of animals.

The study of experimental liver neoplasms is important for understanding the underlying mechanisms of liver cancer development and progression, as well as identifying potential therapeutic targets for the treatment of this disease. Animal models can be used to test the efficacy of new drugs or therapies before they are tested in humans, which can help to accelerate the development of new treatments for liver cancer.

There are several factors that can contribute to the development of insulin resistance, including:

1. Genetics: Insulin resistance can be inherited, and some people may be more prone to developing the condition based on their genetic makeup.
2. Obesity: Excess body fat, particularly around the abdominal area, can contribute to insulin resistance.
3. Physical inactivity: A sedentary lifestyle can lead to insulin resistance.
4. Poor diet: Consuming a diet high in refined carbohydrates and sugar can contribute to insulin resistance.
5. Other medical conditions: Certain medical conditions, such as polycystic ovary syndrome (PCOS) and Cushing's syndrome, can increase the risk of developing insulin resistance.
6. Medications: Certain medications, such as steroids and some antipsychotic drugs, can increase insulin resistance.
7. Hormonal imbalances: Hormonal changes during pregnancy or menopause can lead to insulin resistance.
8. Sleep apnea: Sleep apnea can contribute to insulin resistance.
9. Chronic stress: Chronic stress can lead to insulin resistance.
10. Aging: Insulin resistance tends to increase with age, particularly after the age of 45.

There are several ways to diagnose insulin resistance, including:

1. Fasting blood sugar test: This test measures the level of glucose in the blood after an overnight fast.
2. Glucose tolerance test: This test measures the body's ability to regulate blood sugar levels after consuming a sugary drink.
3. Insulin sensitivity test: This test measures the body's ability to respond to insulin.
4. Homeostatic model assessment (HOMA): This is a mathematical formula that uses the results of a fasting glucose and insulin test to estimate insulin resistance.
5. Adiponectin test: This test measures the level of adiponectin, a protein produced by fat cells that helps regulate blood sugar levels. Low levels of adiponectin are associated with insulin resistance.

There is no cure for insulin resistance, but it can be managed through lifestyle changes and medication. Lifestyle changes include:

1. Diet: A healthy diet that is low in processed carbohydrates and added sugars can help improve insulin sensitivity.
2. Exercise: Regular physical activity, such as aerobic exercise and strength training, can improve insulin sensitivity.
3. Weight loss: Losing weight, particularly around the abdominal area, can improve insulin sensitivity.
4. Stress management: Strategies to manage stress, such as meditation or yoga, can help improve insulin sensitivity.
5. Sleep: Getting adequate sleep is important for maintaining healthy insulin levels.

Medications that may be used to treat insulin resistance include:

1. Metformin: This is a commonly used medication to treat type 2 diabetes and improve insulin sensitivity.
2. Thiazolidinediones (TZDs): These medications, such as pioglitazone, improve insulin sensitivity by increasing the body's ability to use insulin.
3. Sulfonylureas: These medications stimulate the release of insulin from the pancreas, which can help improve insulin sensitivity.
4. DPP-4 inhibitors: These medications, such as sitagliptin, work by reducing the breakdown of the hormone incretin, which helps to increase insulin secretion and improve insulin sensitivity.
5. GLP-1 receptor agonists: These medications, such as exenatide, mimic the action of the hormone GLP-1 and help to improve insulin sensitivity.

It is important to note that these medications may have side effects, so it is important to discuss the potential benefits and risks with your healthcare provider before starting treatment. Additionally, lifestyle modifications such as diet and exercise can also be effective in improving insulin sensitivity and managing blood sugar levels.

People with hyperlipoproteinemia type V often have a history of low birth weight and growth retardation, and may experience a range of health problems including fatigue, muscle weakness, and liver disease. The disorder is usually inherited in an autosomal recessive pattern, meaning that a person must inherit two copies of the mutated gene - one from each parent - to develop the condition.

Treatment for hyperlipoproteinemia type V typically involves a combination of dietary changes and medication. Dietary recommendations may include avoiding foods high in saturated fats and cholesterol, and increasing intake of unsaturated fats, such as those found in nuts and vegetable oils. Medications may include drugs that raise HDL levels or lower LDL levels, such as niacin or statins. In severe cases, liver transplantation may be necessary.

In summary, hyperlipoproteinemia type V is a rare genetic disorder that affects the metabolism of lipids and lipoproteins in the body, leading to extremely low levels of LDL cholesterol and high levels of HDL cholesterol. Treatment typically involves a combination of dietary changes and medication, and may include liver transplantation in severe cases.

Early detection and management of atherosclerosis through regular health check-ups, healthy lifestyle choices, and medications can help prevent or delay the progression of the disease and reduce the risk of complications.

The most common carotid artery disease is atherosclerosis, which is the buildup of plaque in the inner lining of the arteries. This buildup can lead to a narrowing or blockage of the arteries, reducing blood flow to the brain and increasing the risk of stroke. Other conditions that can affect the carotid arteries include:

1. Carotid artery stenosis: A narrowing of the carotid arteries caused by atherosclerosis or other factors.
2. Carotid artery dissection: A tear in the inner lining of the arteries that can cause bleeding and blockage.
3. Carotid artery aneurysm: A bulge in the wall of the arteries that can lead to rupture and stroke.
4. Temporal bone fracture: A break in the bones of the skull that can cause damage to the carotid arteries and result in stroke or other complications.

Carotid artery diseases are typically diagnosed using imaging tests such as ultrasound, computed tomography (CT) angiography, or magnetic resonance angiography (MRA). Treatment options for carotid artery diseases depend on the underlying condition and its severity, but may include lifestyle changes, medications, surgery, or endovascular procedures.

Prevention of carotid artery diseases is key to reducing the risk of stroke and other complications. This includes managing risk factors such as high blood pressure, high cholesterol, smoking, and diabetes, as well as maintaining a healthy lifestyle and getting regular check-ups with your doctor.

There are several different types of obesity, including:

1. Central obesity: This type of obesity is characterized by excess fat around the waistline, which can increase the risk of health problems such as type 2 diabetes and cardiovascular disease.
2. Peripheral obesity: This type of obesity is characterized by excess fat in the hips, thighs, and arms.
3. Visceral obesity: This type of obesity is characterized by excess fat around the internal organs in the abdominal cavity.
4. Mixed obesity: This type of obesity is characterized by both central and peripheral obesity.

Obesity can be caused by a variety of factors, including genetics, lack of physical activity, poor diet, sleep deprivation, and certain medications. Treatment for obesity typically involves a combination of lifestyle changes, such as increased physical activity and a healthy diet, and in some cases, medication or surgery may be necessary to achieve weight loss.

Preventing obesity is important for overall health and well-being, and can be achieved through a variety of strategies, including:

1. Eating a healthy, balanced diet that is low in added sugars, saturated fats, and refined carbohydrates.
2. Engaging in regular physical activity, such as walking, jogging, or swimming.
3. Getting enough sleep each night.
4. Managing stress levels through relaxation techniques, such as meditation or deep breathing.
5. Avoiding excessive alcohol consumption and quitting smoking.
6. Monitoring weight and body mass index (BMI) on a regular basis to identify any changes or potential health risks.
7. Seeking professional help from a healthcare provider or registered dietitian for personalized guidance on weight management and healthy lifestyle choices.

There are two main types of fatty liver disease:

1. Alcoholic fatty liver disease (AFLD): This type of fatty liver disease is caused by excessive alcohol consumption and is the most common cause of fatty liver disease in the United States.
2. Non-alcoholic fatty liver disease (NAFLD): This type of fatty liver disease is not caused by alcohol consumption and is the most common cause of fatty liver disease worldwide. It is often associated with obesity, diabetes, and high cholesterol.

There are several risk factors for developing fatty liver disease, including:

* Obesity
* Physical inactivity
* High calorie intake
* Alcohol consumption
* Diabetes
* High cholesterol
* High triglycerides
* History of liver disease

Symptoms of fatty liver disease can include:

* Fatigue
* Abdominal discomfort
* Loss of appetite
* Nausea and vomiting
* Abnormal liver function tests

Diagnosis of fatty liver disease is typically made through a combination of physical examination, medical history, and diagnostic tests such as:

* Liver biopsy
* Imaging studies (ultrasound, CT or MRI scans)
* Blood tests (lipid profile, glucose, insulin, and liver function tests)

Treatment of fatty liver disease depends on the underlying cause and severity of the condition. Lifestyle modifications such as weight loss, exercise, and a healthy diet can help improve the condition. In severe cases, medications such as antioxidants, fibric acids, and anti-inflammatory drugs may be prescribed. In some cases, surgery or other procedures may be necessary.

Prevention of fatty liver disease includes:

* Maintaining a healthy weight
* Eating a balanced diet low in sugar and saturated fats
* Engaging in regular physical activity
* Limiting alcohol consumption
* Managing underlying medical conditions such as diabetes and high cholesterol.

Disease progression can be classified into several types based on the pattern of worsening:

1. Chronic progressive disease: In this type, the disease worsens steadily over time, with a gradual increase in symptoms and decline in function. Examples include rheumatoid arthritis, osteoarthritis, and Parkinson's disease.
2. Acute progressive disease: This type of disease worsens rapidly over a short period, often followed by periods of stability. Examples include sepsis, acute myocardial infarction (heart attack), and stroke.
3. Cyclical disease: In this type, the disease follows a cycle of worsening and improvement, with periodic exacerbations and remissions. Examples include multiple sclerosis, lupus, and rheumatoid arthritis.
4. Recurrent disease: This type is characterized by episodes of worsening followed by periods of recovery. Examples include migraine headaches, asthma, and appendicitis.
5. Catastrophic disease: In this type, the disease progresses rapidly and unpredictably, with a poor prognosis. Examples include cancer, AIDS, and organ failure.

Disease progression can be influenced by various factors, including:

1. Genetics: Some diseases are inherited and may have a predetermined course of progression.
2. Lifestyle: Factors such as smoking, lack of exercise, and poor diet can contribute to disease progression.
3. Environmental factors: Exposure to toxins, allergens, and other environmental stressors can influence disease progression.
4. Medical treatment: The effectiveness of medical treatment can impact disease progression, either by slowing or halting the disease process or by causing unintended side effects.
5. Co-morbidities: The presence of multiple diseases or conditions can interact and affect each other's progression.

Understanding the type and factors influencing disease progression is essential for developing effective treatment plans and improving patient outcomes.

There are several key features of inflammation:

1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.

Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.

There are several types of inflammation, including:

1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.

There are several ways to reduce inflammation, including:

1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.

It's important to note that chronic inflammation can lead to a range of health problems, including:

1. Arthritis
2. Diabetes
3. Heart disease
4. Cancer
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.

Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.

There are several types of inborn errors of lipid metabolism, each with its own unique set of symptoms and characteristics. Some of the most common include:

* Familial hypercholesterolemia: A condition that causes high levels of low-density lipoprotein (LDL) cholesterol in the blood, which can lead to heart disease and other health problems.
* Fabry disease: A rare genetic disorder that affects the body's ability to break down certain fats, leading to a buildup of toxic substances in the body.
* Gaucher disease: Another rare genetic disorder that affects the body's ability to break down certain lipids, leading to a buildup of toxic substances in the body.
* Lipoid cerebral degeneration: A condition that causes fatty deposits to accumulate in the brain, leading to cognitive decline and other neurological problems.
* Tangier disease: A rare genetic disorder that affects the body's ability to break down certain lipids, leading to a buildup of toxic substances in the body.

Inborn errors of lipid metabolism can be diagnosed through a variety of tests, including blood tests and genetic analysis. Treatment options vary depending on the specific disorder and its severity, but may include dietary changes, medication, and other therapies. With proper treatment and management, many individuals with inborn errors of lipid metabolism can lead active and fulfilling lives.

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.

The condition is caused by mutations in the genes that code for proteins involved in cholesterol transport and metabolism, particularly the low-density lipoprotein receptor gene. This leads to a deficiency of functional LDL receptors on the surface of liver cells, resulting in excessive accumulation of LDL cholesterol in the bloodstream.

Symptoms of hyperlipoproteinemia Type I can include xanthomas (yellowish deposits of cholesterol in the skin), corneal arcus (a white deposit on the edge of the cornea), and early-onset cardiovascular disease, such as heart attacks or strokes.

Treatment for hyperlipoproteinemia Type I typically involves a combination of dietary changes, such as reducing intake of saturated and trans fats and cholesterol, and medications, such as statins, to lower LDL cholesterol levels. In some cases, medical procedures such as liver transplantation or gene therapy may be necessary to treat the condition.

1. Abdominal obesity (excess fat around the waistline)
2. High blood pressure (hypertension)
3. Elevated fasting glucose (high blood sugar)
4. High serum triglycerides (elevated levels of triglycerides in the blood)
5. Low HDL cholesterol (low levels of "good" cholesterol)

Having three or more of these conditions is considered a diagnosis of metabolic syndrome X. It is estimated that approximately 34% of adults in the United States have this syndrome, and it is more common in women than men. Risk factors for developing metabolic syndrome include obesity, lack of physical activity, poor diet, and a family history of type 2 diabetes or CVD.

The term "metabolic syndrome" was first introduced in the medical literature in the late 1980s, and since then, it has been the subject of extensive research. The exact causes of metabolic syndrome are not yet fully understood, but it is believed to be related to insulin resistance, inflammation, and changes in body fat distribution.

Treatment for metabolic syndrome typically involves lifestyle modifications such as weight loss, regular physical activity, and a healthy diet. Medications such as blood pressure-lowering drugs, cholesterol-lowering drugs, and anti-diabetic medications may also be prescribed if necessary. It is important to note that not everyone with metabolic syndrome will develop type 2 diabetes or CVD, but the risk is increased. Therefore, early detection and treatment are crucial in preventing these complications.

There are several types of diabetic angiopathies, including:

1. Peripheral artery disease (PAD): This occurs when the blood vessels in the legs and arms become narrowed or blocked, leading to reduced blood flow and oxygen supply to the limbs.
2. Peripheral neuropathy: This is damage to the nerves in the hands and feet, which can cause pain, numbness, and weakness.
3. Retinopathy: This is damage to the blood vessels in the retina, which can lead to vision loss and blindness.
4. Nephropathy: This is damage to the kidneys, which can lead to kidney failure and the need for dialysis.
5. Cardiovascular disease: This includes heart attack, stroke, and other conditions that affect the heart and blood vessels.

The risk of developing diabetic angiopathies increases with the duration of diabetes and the level of blood sugar control. Other factors that can increase the risk include high blood pressure, high cholesterol, smoking, and a family history of diabetes-related complications.

Symptoms of diabetic angiopathies can vary depending on the specific type of complication and the location of the affected blood vessels or nerves. Common symptoms include:

* Pain or discomfort in the arms, legs, hands, or feet
* Numbness or tingling sensations in the hands and feet
* Weakness or fatigue in the limbs
* Difficulty healing wounds or cuts
* Vision changes or blindness
* Kidney problems or failure
* Heart attack or stroke

Diagnosis of diabetic angiopathies typically involves a combination of physical examination, medical history, and diagnostic tests such as ultrasound, MRI, or CT scans. Treatment options vary depending on the specific type of complication and may include:

* Medications to control blood sugar levels, high blood pressure, and high cholesterol
* Lifestyle changes such as a healthy diet and regular exercise
* Surgery to repair or bypass affected blood vessels or nerves
* Dialysis for kidney failure
* In some cases, amputation of the affected limb

Preventing diabetic angiopathies involves managing diabetes effectively through a combination of medication, lifestyle changes, and regular medical check-ups. Early detection and treatment can help prevent or delay the progression of complications.

The term "cerebral" refers to the brain, "amyloid" refers to the abnormal protein deposits, and "angiopathy" refers to the damage caused to the blood vessels. CAA is often associated with other conditions such as Alzheimer's disease, Down syndrome, and other forms of dementia.

CAA is a type of small vessel ischemic disease (SVID), which affects the smaller blood vessels in the brain. The exact cause of CAA is not yet fully understood, but it is thought to be related to a combination of genetic and environmental factors. There is currently no cure for CAA, but researchers are working to develop new treatments to slow its progression and manage its symptoms.

Some common symptoms of CAA include:

* Cognitive decline
* Seizures
* Stroke-like episodes
* Memory loss
* Confusion
* Difficulty with coordination and balance

If you suspect you or a loved one may be experiencing symptoms of CAA, it is important to speak with a healthcare professional for proper diagnosis and treatment. A thorough medical history and physical examination, along with imaging tests such as MRI or CT scans, can help confirm the presence of CAA.

While there is no cure for CAA, there are several treatment options available to manage its symptoms and slow its progression. These may include medications to control seizures, improve cognitive function, and reduce inflammation. In some cases, surgery or endovascular procedures may be necessary to repair or remove damaged blood vessels.

It is important to note that CAA is a complex condition, and its management requires a multidisciplinary approach involving neurologists, geriatricians, radiologists, and other healthcare professionals. With proper diagnosis and treatment, however, many individuals with CAA are able to lead active and fulfilling lives.

There are several types of diabetes mellitus, including:

1. Type 1 DM: This is an autoimmune condition in which the body's immune system attacks and destroys the cells in the pancreas that produce insulin, resulting in a complete deficiency of insulin production. It typically develops in childhood or adolescence, and patients with this condition require lifelong insulin therapy.
2. Type 2 DM: This is the most common form of diabetes, accounting for around 90% of all cases. It is caused by a combination of insulin resistance (where the body's cells do not respond properly to insulin) and impaired insulin secretion. It is often associated with obesity, physical inactivity, and a diet high in sugar and unhealthy fats.
3. Gestational DM: This type of diabetes develops during pregnancy, usually in the second or third trimester. Hormonal changes and insulin resistance can cause blood sugar levels to rise, putting both the mother and baby at risk.
4. LADA (Latent Autoimmune Diabetes in Adults): This is a form of type 1 DM that develops in adults, typically after the age of 30. It shares features with both type 1 and type 2 DM.
5. MODY (Maturity-Onset Diabetes of the Young): This is a rare form of diabetes caused by genetic mutations that affect insulin production. It typically develops in young adulthood and can be managed with lifestyle changes and/or medication.

The symptoms of diabetes mellitus can vary depending on the severity of the condition, but may include:

1. Increased thirst and urination
2. Fatigue
3. Blurred vision
4. Cuts or bruises that are slow to heal
5. Tingling or numbness in hands and feet
6. Recurring skin, gum, or bladder infections
7. Flu-like symptoms such as weakness, dizziness, and stomach pain
8. Dark, velvety skin patches (acanthosis nigricans)
9. Yellowish color of the skin and eyes (jaundice)
10. Delayed healing of cuts and wounds

If left untreated, diabetes mellitus can lead to a range of complications, including:

1. Heart disease and stroke
2. Kidney damage and failure
3. Nerve damage (neuropathy)
4. Eye damage (retinopathy)
5. Foot damage (neuropathic ulcers)
6. Cognitive impairment and dementia
7. Increased risk of infections and other diseases, such as pneumonia, gum disease, and urinary tract infections.

It is important to note that not all individuals with diabetes will experience these complications, and that proper management of the condition can greatly reduce the risk of developing these complications.

There are several types of amyloidosis, each with different causes and symptoms. The most common types include:

1. Primary amyloidosis: This type is caused by the production of abnormal proteins in the bone marrow. It mainly affects older adults and can lead to symptoms such as fatigue, weight loss, and numbness or tingling in the hands and feet.
2. Secondary amyloidosis: This type is caused by other conditions, such as rheumatoid arthritis, tuberculosis, or inflammatory bowel disease. It can also be caused by long-term use of certain medications, such as antibiotics or chemotherapy.
3. Familial amyloid polyneuropathy: This type is inherited and affects the nerves in the body, leading to symptoms such as muscle weakness, numbness, and pain.
4. Localized amyloidosis: This type affects a specific area of the body, such as the tongue or the skin.

The symptoms of amyloidosis can vary depending on the organs affected and the severity of the condition. Some common symptoms include:

1. Fatigue
2. Weakness
3. Pain
4. Numbness or tingling in the hands and feet
5. Swelling in the legs, ankles, and feet
6. Difficulty with speech or swallowing
7. Seizures
8. Heart problems
9. Kidney failure
10. Liver failure

The diagnosis of amyloidosis is based on a combination of physical examination, medical history, laboratory tests, and imaging studies. Laboratory tests may include blood tests to measure the levels of certain proteins in the body, as well as biopsies to examine tissue samples under a microscope. Imaging studies, such as X-rays, CT scans, and MRI scans, may be used to evaluate the organs affected by the condition.

There is no cure for amyloidosis, but treatment can help manage the symptoms and slow the progression of the disease. Treatment options may include:

1. Medications to control symptoms such as pain, swelling, and heart problems
2. Chemotherapy to reduce the production of abnormal proteins
3. Autologous stem cell transplantation to replace damaged cells with healthy ones
4. Dialysis to remove excess fluids and waste products from the body
5. Nutritional support to ensure adequate nutrition and hydration
6. Physical therapy to maintain muscle strength and mobility
7. Supportive care to manage pain, improve quality of life, and reduce stress on the family.

In conclusion, amyloidosis is a complex and rare group of diseases that can affect multiple organs and systems in the body. Early diagnosis and treatment are essential to managing the symptoms and slowing the progression of the disease. It is important for patients with suspected amyloidosis to seek medical attention from a specialist, such as a hematologist or nephrologist, for proper evaluation and treatment.

Types of Experimental Diabetes Mellitus include:

1. Streptozotocin-induced diabetes: This type of EDM is caused by administration of streptozotocin, a chemical that damages the insulin-producing beta cells in the pancreas, leading to high blood sugar levels.
2. Alloxan-induced diabetes: This type of EDM is caused by administration of alloxan, a chemical that also damages the insulin-producing beta cells in the pancreas.
3. Pancreatectomy-induced diabetes: In this type of EDM, the pancreas is surgically removed or damaged, leading to loss of insulin production and high blood sugar levels.

Experimental Diabetes Mellitus has several applications in research, including:

1. Testing new drugs and therapies for diabetes treatment: EDM allows researchers to evaluate the effectiveness of new treatments on blood sugar control and other physiological processes.
2. Studying the pathophysiology of diabetes: By inducing EDM in animals, researchers can study the progression of diabetes and its effects on various organs and tissues.
3. Investigating the role of genetics in diabetes: Researchers can use EDM to study the effects of genetic mutations on diabetes development and progression.
4. Evaluating the efficacy of new diagnostic techniques: EDM allows researchers to test new methods for diagnosing diabetes and monitoring blood sugar levels.
5. Investigating the complications of diabetes: By inducing EDM in animals, researchers can study the development of complications such as retinopathy, nephropathy, and cardiovascular disease.

In conclusion, Experimental Diabetes Mellitus is a valuable tool for researchers studying diabetes and its complications. The technique allows for precise control over blood sugar levels and has numerous applications in testing new treatments, studying the pathophysiology of diabetes, investigating the role of genetics, evaluating new diagnostic techniques, and investigating complications.

The most common form of xanthomatosis is called familial hypercholesterolemia, which is caused by a deficiency of low-density lipoprotein (LDL) receptors in the body. This results in high levels of LDL cholesterol in the blood, which can lead to the accumulation of cholesterol and other lipids in the skin, eyes, and other tissues.

Other forms of xanthomatosis include:

* Familial apo A-1 deficiency: This is a rare disorder caused by a deficiency of apolipoprotein A-1 (apoA-1), a protein that plays a critical role in the transportation of triglycerides and cholesterol in the blood.
* familial hyperlipidemia: This is a group of rare genetic disorders that are characterized by high levels of lipids in the blood, including cholesterol and triglycerides.
* Chylomicronemia: This is a rare disorder caused by a deficiency of lipoprotein lipase, an enzyme that breaks down triglycerides in the blood.

The symptoms of xanthomatosis vary depending on the specific form of the condition and the organs affected. They may include:

* Yellowish deposits (xanthomas) on the skin, particularly on the elbows, knees, and buttocks
* Deposits in the eyes (corneal arcus)
* Fatty liver disease
* High levels of cholesterol and triglycerides in the blood
* Abdominal pain
* Weight loss

Treatment for xanthomatosis typically involves managing the underlying genetic disorder, which may involve dietary changes, medication, or other therapies. In some cases, surgery may be necessary to remove affected tissue.

In summary, xanthomatosis is a group of rare genetic disorders that are characterized by deposits of lipids in the skin and other organs. The symptoms and treatment vary depending on the specific form of the condition.

The term "amyloid" refers specifically to the type of protein aggregate that forms these plaques, and is derived from the Greek word for "flour-like." Amyloidosis is the general term used to describe the condition of having amyloid deposits in the body, while Alzheimer's disease is a specific type of amyloidosis that is characterized by the accumulation of beta-amyloid peptides in the brain.

Plaques, amyloid play a central role in the pathogenesis of many neurodegenerative diseases, and understanding their formation and clearance is an area of ongoing research. In addition to their role in Alzheimer's disease, amyloid plaques have been implicated in other conditions such as cerebral amyloid angiopathy, primary lateral sclerosis, and progressive supranuclear palsy.

Plaques, amyloid are composed of a variety of proteins, including beta-amyloid peptides, tau protein, and apolipoprotein E (apoE). The composition and structure of these plaques can vary depending on the underlying disease, and their presence is often associated with inflammation and oxidative stress.

In addition to their role in neurodegeneration, amyloid plaques have been implicated in other diseases such as type 2 diabetes and cardiovascular disease. The accumulation of amyloid fibrils in these tissues can contribute to the development of insulin resistance and atherosclerosis, respectively.

Overall, plaques, amyloid are a complex and multifaceted area of research, with many open questions remaining about their formation, function, and clinical implications. Ongoing studies in this field may provide valuable insights into the pathogenesis of various diseases and ultimately lead to the development of novel therapeutic strategies for these conditions.

In conclusion, plaques, amyloid are a hallmark of several neurodegenerative diseases, including Alzheimer's disease, and have been associated with inflammation, oxidative stress, and neurodegeneration. The composition and structure of these plaques can vary depending on the underlying disease, and their presence is often linked to the progression of the condition. Furthermore, amyloid plaques have been implicated in other diseases such as type 2 diabetes and cardiovascular disease, highlighting their potential clinical significance beyond neurodegeneration. Ongoing research into the mechanisms of amyloid plaque formation and clearance may lead to the development of novel therapeutic strategies for these conditions.

Types of Cognition Disorders: There are several types of cognitive disorders that affect different aspects of cognitive functioning. Some common types include:

1. Attention Deficit Hyperactivity Disorder (ADHD): Characterized by symptoms of inattention, hyperactivity, and impulsivity.
2. Traumatic Brain Injury (TBI): Caused by a blow or jolt to the head that disrupts brain function, resulting in cognitive, emotional, and behavioral changes.
3. Alzheimer's Disease: A progressive neurodegenerative disorder characterized by memory loss, confusion, and difficulty with communication.
4. Stroke: A condition where blood flow to the brain is interrupted, leading to cognitive impairment and other symptoms.
5. Parkinson's Disease: A neurodegenerative disorder that affects movement, balance, and cognition.
6. Huntington's Disease: An inherited disorder that causes progressive damage to the brain, leading to cognitive decline and other symptoms.
7. Frontotemporal Dementia (FTD): A group of neurodegenerative disorders characterized by changes in personality, behavior, and language.
8. Post-Traumatic Stress Disorder (PTSD): A condition that develops after a traumatic event, characterized by symptoms such as anxiety, avoidance, and hypervigilance.
9. Mild Cognitive Impairment (MCI): A condition characterized by memory loss and other cognitive symptoms that are more severe than normal age-related changes but not severe enough to interfere with daily life.

Causes and Risk Factors: The causes of cognition disorders can vary depending on the specific disorder, but some common risk factors include:

1. Genetics: Many cognitive disorders have a genetic component, such as Alzheimer's disease, Parkinson's disease, and Huntington's disease.
2. Age: As people age, their risk of developing cognitive disorders increases, such as Alzheimer's disease, vascular dementia, and frontotemporal dementia.
3. Lifestyle factors: Factors such as physical inactivity, smoking, and poor diet can increase the risk of cognitive decline and dementia.
4. Traumatic brain injury: A severe blow to the head or a traumatic brain injury can increase the risk of developing cognitive disorders, such as chronic traumatic encephalopathy (CTE).
5. Infections: Certain infections, such as meningitis and encephalitis, can cause cognitive disorders if they damage the brain tissue.
6. Stroke or other cardiovascular conditions: A stroke or other cardiovascular conditions can cause cognitive disorders by damaging the blood vessels in the brain.
7. Chronic substance abuse: Long-term use of drugs or alcohol can damage the brain and increase the risk of cognitive disorders, such as dementia.
8. Sleep disorders: Sleep disorders, such as sleep apnea, can increase the risk of cognitive disorders, such as dementia.
9. Depression and anxiety: Mental health conditions, such as depression and anxiety, can increase the risk of cognitive decline and dementia.
10. Environmental factors: Exposure to certain environmental toxins, such as pesticides and heavy metals, has been linked to an increased risk of cognitive disorders.

It's important to note that not everyone with these risk factors will develop a cognitive disorder, and some people without any known risk factors can still develop a cognitive disorder. If you have concerns about your cognitive health, it's important to speak with a healthcare professional for proper evaluation and diagnosis.

There are several types of dementia, each with its own set of symptoms and characteristics. Some common types of dementia include:

* Alzheimer's disease: This is the most common form of dementia, accounting for 50-70% of all cases. It is a progressive disease that causes the death of brain cells, leading to memory loss and cognitive decline.
* Vascular dementia: This type of dementia is caused by problems with blood flow to the brain, often as a result of a stroke or small vessel disease. It can cause difficulty with communication, language, and visual-spatial skills.
* Lewy body dementia: This type of dementia is characterized by the presence of abnormal protein deposits called Lewy bodies in the brain. It can cause a range of symptoms, including memory loss, confusion, hallucinations, and difficulty with movement.
* Frontotemporal dementia: This is a group of diseases that affect the front and temporal lobes of the brain, leading to changes in personality, behavior, and language.

The symptoms of dementia can vary depending on the underlying cause, but common symptoms include:

* Memory loss: Difficulty remembering recent events or learning new information.
* Communication and language difficulties: Struggling to find the right words or understand what others are saying.
* Disorientation: Getting lost in familiar places or having difficulty understanding the time and date.
* Difficulty with problem-solving: Trouble with planning, organizing, and decision-making.
* Mood changes: Depression, anxiety, agitation, or aggression.
* Personality changes: Becoming passive, suspicious, or withdrawn.
* Difficulty with movement: Trouble with coordination, balance, or using utensils.
* Hallucinations: Seeing or hearing things that are not there.
* Sleep disturbances: Having trouble falling asleep or staying asleep.

The symptoms of dementia can be subtle at first and may progress slowly over time. In the early stages, they may be barely noticeable, but as the disease progresses, they can become more pronounced and interfere with daily life. It is important to seek medical advice if you or a loved one is experiencing any of these symptoms, as early diagnosis and treatment can help improve outcomes.

There are different types of myocardial infarctions, including:

1. ST-segment elevation myocardial infarction (STEMI): This is the most severe type of heart attack, where a large area of the heart muscle is damaged. It is characterized by a specific pattern on an electrocardiogram (ECG) called the ST segment.
2. Non-ST-segment elevation myocardial infarction (NSTEMI): This type of heart attack is less severe than STEMI, and the damage to the heart muscle may not be as extensive. It is characterized by a smaller area of damage or a different pattern on an ECG.
3. Incomplete myocardial infarction: This type of heart attack is when there is some damage to the heart muscle but not a complete blockage of blood flow.
4. Collateral circulation myocardial infarction: This type of heart attack occurs when there are existing collateral vessels that bypass the blocked coronary artery, which reduces the amount of damage to the heart muscle.

Symptoms of a myocardial infarction can include chest pain or discomfort, shortness of breath, lightheadedness, and fatigue. These symptoms may be accompanied by anxiety, fear, and a sense of impending doom. In some cases, there may be no noticeable symptoms at all.

Diagnosis of myocardial infarction is typically made based on a combination of physical examination findings, medical history, and diagnostic tests such as an electrocardiogram (ECG), cardiac enzyme tests, and imaging studies like echocardiography or cardiac magnetic resonance imaging.

Treatment of myocardial infarction usually involves medications to relieve pain, reduce the amount of work the heart has to do, and prevent further damage to the heart muscle. These may include aspirin, beta blockers, ACE inhibitors or angiotensin receptor blockers, and statins. In some cases, a procedure such as angioplasty or coronary artery bypass surgery may be necessary to restore blood flow to the affected area.

Prevention of myocardial infarction involves managing risk factors such as high blood pressure, high cholesterol, smoking, diabetes, and obesity. This can include lifestyle changes such as a healthy diet, regular exercise, and stress reduction, as well as medications to control these conditions. Early detection and treatment of heart disease can help prevent myocardial infarction from occurring in the first place.

The gene, APOE, is mapped to chromosome 19 in a cluster with apolipoprotein C1 (APOC1) and the apolipoprotein C2 (APOC2). The ... "Genetic studies of human apolipoproteins. X. The effect of the apolipoprotein E polymorphism on quantitative levels of ... Apolipoprotein E (APOE) is a protein involved in the metabolism of fats in the body of mammals. A subtype is implicated in ... Apolipoprotein E enhances proteolytic break-down of this peptide, both within and between cells. The isoform APOE-ε4 is not as ...

https://en.wikipedia.org/wiki/Apolipoprotein_E

Myklebost O, Rogne S (August 1986). "The gene for human apolipoprotein CI is located 4.3 kilobases away from the apolipoprotein ... "Two copies of the human apolipoprotein C-I gene are linked closely to the apolipoprotein E gene". The Journal of Biological ... Apolipoprotein C-I is a protein component of lipoproteins that in humans is encoded by the APOC1 gene. The protein encoded by ... "Entrez Gene: APOC1 apolipoprotein C-I". Puppione DL, Ryan CM, Bassilian S, Souda P, Xiao X, Ryder OA, Whitelegge JP (March 2010 ...

https://en.wikipedia.org/wiki/Apolipoprotein_C-I

... (ApoA-I) is a protein that in humans is encoded by the APOA1 gene. As the major component of HDL particles, ... The encoded apolipoprotein A-I, is a 28.1 kDa protein composed of 243 amino acids; 21 peptides have been observed through mass ... Apolipoprotein AI has also been isolated as a prostacyclin (PGI2) stabilizing factor, and thus may have an anticlotting effect ... Apolipoprotein AI is the major protein component of high density lipoprotein (HDL) particles in plasma. Chylomicrons secreted ...

https://en.wikipedia.org/wiki/Apolipoprotein_AI

... (ApoB) is a protein that in humans is encoded by the APOB gene. Apolipoprotein B is the primary apolipoprotein ... Su Q, Tsai J, Xu E, Qiu W, Bereczki E, Santha M, Adeli K (2009). "Apolipoprotein B100 acts as a molecular link between lipid- ... MedlinePlus Encyclopedia: Apolipoprotein B100 Cromwell WC, Otvos JD, Keyes MJ, Pencina MJ, Sullivan L, Vasan RS, Wilson PW, ... Overproduction of apolipoprotein B can result in lipid-induced endoplasmic reticulum stress and insulin resistance in the liver ...

https://en.wikipedia.org/wiki/Apolipoprotein_B

Identification of apolipoprotein D, apolipoprotein A-IV, apolipoprotein E, and apolipoprotein A-I". The Journal of Biological ... Apolipoprotein D (ApoD) is a component of HDL that has no marked similarity to other apolipoprotein sequences. It has a high ... "Entrez Gene: APOD apolipoprotein D". Muffat J, Walker DW (January 2010). "Apolipoprotein D: an overview of its role in aging ... Apolipoproteins+D at the US National Library of Medicine Medical Subject Headings (MeSH) Applied Research on Apolipoproteins ...

https://en.wikipedia.org/wiki/Apolipoprotein_D

Olofsson SO, Borèn J (November 2005). "Apolipoprotein B: a clinically important apolipoprotein which assembles atherogenic ... Apolipoprotein B can exist in two forms: B-100 and B-48. Apolipoprotein B-100 is present on several lipoproteins, including ... Apolipoprotein B-100 has been linked to the development of atherosclerosis. ApoB is ancestrally universal to all animals, as ... Huebbe P, Rimbach G (August 2017). "Evolution of human apolipoprotein E (APOE) isoforms: Gene structure, protein function and ...

https://en.wikipedia.org/wiki/Vitellogenin

... is an autosomal dominant disorder resulting from a missense mutation which reduces the affinity of ... apoB-100 for the low-density lipoprotein receptor (LDL Receptor). This causes impairments in LDL catabolism, resulting in ...

https://en.wikipedia.org/wiki/Apolipoprotein_B_deficiency

April 1987). "Association of an apolipoprotein CII allele with familial dementia of the Alzheimer type". Journal of ... 23 (1): 100-13. doi:10.1006/geno.1994.1464. hdl:2027.42/31345. PMID 7829057. Schellenberg GD, Deeb SS, Boehnke M, et al. ( ...

https://en.wikipedia.org/wiki/George_M._Martin

Cholesterol is imported into the neuron by apolipoprotein E (apoE) via LRP1 receptors on the cell surface. It has been ... Low density lipoprotein receptor-related protein 1 (LRP1), also known as alpha-2-macroglobulin receptor (A2MR), apolipoprotein ... "Apolipoprotein E isoform-specific effects on lipoprotein receptor processing". Neuromolecular Medicine. 16 (4): 686-696. doi: ... "Interaction of cytosolic adaptor proteins with neuronal apolipoprotein E receptors and the amyloid precursor protein". The ...

https://en.wikipedia.org/wiki/LRP1

... D Apolipoprotein E Apolipoprotein F Apolipoprotein H - a misnomer Apolipoprotein L Apolipoprotein M ... Apolipoprotein F (apoF) is one of the minor apolipoprotein in blood plasma and it is a lipid transfer inhibit protein to ... Apolipoprotein synthesis in the intestine is regulated principally by the fat content of the diet. Apolipoprotein synthesis in ... Apolipoprotein A (Apo-AI, Apo-A2, Apo-A4, and Apo-A5) Apolipoprotein B (Apo-B48 and Apo B-100) Apolipoprotein C (ApoC-I, apo ...

https://en.wikipedia.org/wiki/Apolipoprotein

... binds to the messenger RNA coding for apolipoprotein B-100 (ApoB-100), a protein that is the main component of low- ... It accumulates in the liver,[citation needed] which is convenient since apolipoprotein B predominantly acts there. Protein ... a second-generation antisense oligonucleotide inhibitor of apolipoprotein B". Clinical Pharmacokinetics. 54 (2): 133-146. doi: ... and ApoB-100 is not translated. After subcutaneous injection, mipomersen reaches highest blood levels after 3 to 4 hours. ...

https://en.wikipedia.org/wiki/Mipomersen

"Reduced hippocampal insulin-degrading enzyme in late-onset Alzheimer's disease is associated with the apolipoprotein E-epsilon4 ... 100 (7): 4162-7. Bibcode:2003PNAS..100.4162F. doi:10.1073/pnas.0230450100. PMC 153065. PMID 12634421. Cook DG, Leverenz JB, ...

https://en.wikipedia.org/wiki/Insulin-degrading_enzyme

"Covalent attachment of apolipoprotein AI and apolipoprotein B-100 to albumin nanoparticles enables drug transport into the ... Certain apolipoproteins, such as Apo E, ApoA1, and ApoB-100, could potentially functionalize nanoparticles to target the ...

https://en.wikipedia.org/wiki/Protein_corona

One form is thought to be caused by mutated apolipoprotein B. Another form is associated with microsomal triglyceride transfer ... Hypobetalipoproteinemia is a disorder consisting of low levels of LDL cholesterol or apolipoprotein B, below the 5th percentile ... June 1989). "Familial hypobetalipoproteinemia associated with a mutant species of apolipoprotein B (B-46)". N. Engl. J. Med. ... Notably, in people who do not have the genetic disorder hypobetalipoproteinemia, a very low cholesterol level (less than 100 mg ...

https://en.wikipedia.org/wiki/Hypobetalipoproteinemia

He and his associates were the first to achieve complete synthesis of a plasma apolipoprotein (apo C-I); they also determined ... the complete cDNA and amino acid sequence of apo B-100, one of the largest proteins ever sequenced and a key protein in ...

https://en.wikipedia.org/wiki/Antonio_Gotto

The receptor also recognizes apolipoprotein E (ApoE) which is found in chylomicron remnants and IDL. In humans, the LDL ... It is a cell-surface receptor that recognizes apolipoprotein B100 (ApoB100), which is embedded in the outer phospholipid layer ... namely lipoprotein lipase and apolipoprotein C-III. Combined, these observations suggest that, as well as LDL cholesterol, ... novel insights from recent kinetic studies of apolipoprotein B-100 metabolism". Atherosclerosis. Supplements. 2 (3): 1-4. doi: ...

https://en.wikipedia.org/wiki/LDL_receptor

Nascent VLDL released from the liver contains apolipoprotein B100, apolipoprotein C1 (apoC1), apolipoprotein E (apoE), ... As it circulates in blood, it picks up apolipoprotein C-II (apoC-II) and additional apoE donated from high-density lipoprotein ... VLDL is assembled in the liver from triglycerides, cholesterol, and apolipoproteins. VLDL is converted in the bloodstream to ... and apolipoprotein E receptor-2". Biochim Biophys Acta. 1529 (1-3): 287-298. doi:10.1016/S1388-1981(00)00155-4. PMID 11111096. ...

https://en.wikipedia.org/wiki/Very_low-density_lipoprotein

HDL particles donate apolipoprotein C-II and apolipoprotein E to the nascent VLDL particle. Once loaded with apolipoproteins C- ... and apolipoproteins. Plasma lipoproteins are divided into seven classes based on size, lipid composition, and apolipoproteins. ... resulting in HDL donation of apolipoprotein C-II and apolipoprotein E to the nascent chylomicron. The chylomicron at this stage ... LDL contains apolipoprotein B (apoB), which allows LDL to bind to different tissues, such as the artery wall if the glycocalyx ...

https://en.wikipedia.org/wiki/Lipoprotein

Kynamro targets the mRNA product of the APOB gene, which codes for the Apolipoprotein B-100 protein, a component of low-density ... lipoprotein (LDL). The binding of mipomersen to the APOB mRNA effectively blocks the translation of ApoB-100, and the gapmer- ...

https://en.wikipedia.org/wiki/Gapmer

Advanced the 4955 into drug development, which is a compound that targets Apolipoprotein B and could decrease and manage high ... Received the Red Herring Top 100 Europe Award. 2011: Obtained license from Mass General Hospital for intellectual property ...

https://en.wikipedia.org/wiki/Santaris_Pharma

... enzymatic activity induces hydrolytic modification of apolipoprotein B-100-containing lipoproteins, including LDL, ...

https://en.wikipedia.org/wiki/Cathepsin_D

... the apolipoprotein A1 remnant ratio (Apo A1/ [VLDL₃+IDL]). Lipids Health Dis. 2013 Apr 26;12:55. (Use dmy dates from July 2021 ... The ADA-ACC consensus statement establishes measurement and treatment guidelines for Apolipoprotein B,apoB in addition to LDL ... Also, estimated LDL-C is falsely low when directly measured LDL-C is < 100 mg/dL or when triglycerides are elevated. The VAP ...

https://en.wikipedia.org/wiki/Vertical_auto_profile

Mice deficient in apolipoprotein B are more susceptible to invasive bacterial infection. LDL can be grouped based on its size: ... Each particle contains a single apolipoprotein B-100 molecule (Apo B-100, a protein that has 4536 amino acid residues and a ... The mechanism of antagonism entails binding apolipoprotein B to a S. aureus autoinducer pheromone, preventing signaling through ... organized by a single apolipoprotein B for LDL and the larger particles). A single LDL particle is about 220-275 angstroms in ...

https://en.wikipedia.org/wiki/Low-density_lipoprotein

Apolipoprotein E4 allele in a population based study of early onset Alzheimer's disease. Nat Genet. 1994;7:74-9. Hendriks L, et ... Atherosclerosis, apolipoprotein and prevalence of dementia and Alzheimer's disease. The Rotterdam Study. Lancet. 1997;349:151-4 ... 1988;318:1093-100. Hofman A, Hazebroek A, Valkenburg HA. A randomized trial of sodium intake and blood pressure in newborn ...

https://en.wikipedia.org/wiki/Albert_Hofman

Familial defective apolipoprotein B-100 Familial dysbetalipoproteinemia (broad beta disease, remnant removal disease) Familial ... 100 (1): 111S-115S. doi:10.1038/jid.1993.33. PMID 8423379. Lynch, Peter J (1994). Dermatology. Williams & Wilkins. ISBN 978-0- ...

https://en.wikipedia.org/wiki/List_of_skin_conditions

Apolipoprotein B, in its ApoB100 form, is the main apolipoprotein, or protein part of the lipoprotein particle. Its gene is ... Class III: LDLR does not properly bind LDL on the cell surface because of a defect in either apolipoprotein B100 (R3500Q) or in ... In January 2013, The US FDA also approved mipomersen, which inhibits the action of the gene apolipoprotein B, for the treatment ... LDL cholesterol normally circulates in the body for 2.5 days, and subsequently the apolipoprotein B portion of LDL cholesterol ...

https://en.wikipedia.org/wiki/Familial_hypercholesterolemia

... although nonglycosylated and immature forms of apolipoprotein[a] are competent to associate with apolipoprotein B-100 in vitro ... The structure of apolipoprotein(a) is similar to plasminogen and tPA (tissue plasminogen activator) and it competes with ... Lipoprotein(a) [Lp(a)] consists of an LDL-like particle and the specific apolipoprotein(a), which is bound covalently to the ... 50 mg/dL (>125 nmol/L) Lp(a) appears with different isoforms (per kringle repeats) of apolipoprotein; 40% of the variation in ...

https://en.wikipedia.org/wiki/Lipoprotein(a)

... sickness Deep vein thrombosis Dabbing Syndrome Defect in synthesis of adenosylcobalamin Defective apolipoprotein B-100 ...

https://en.wikipedia.org/wiki/List_of_diseases_(D)

In 1979, researchers discovered that people in Limone possess a mutant form of apolipoprotein (called ApoA-1 Milano) in their ... "Cardiovascular status of carriers of the apolipoprotein A-I(Milano) mutant: the Limone sul Garda study" (PDF). Circulation. 103 ... a dozen of those living here are over the age of 100 (for c. 1,000 total inhabitants).[citation needed] The origin of the ...

https://en.wikipedia.org/wiki/Limone_sul_Garda

These molecules contain apolipoprotein B100 and apolipoprotein E in their shells, and can be degraded by lipoprotein lipase on ... Chylomicrons, the least dense cholesterol transport molecules, contain apolipoprotein B-48, apolipoprotein C, and ... adjusted for apolipoprotein A-I and apolipoprotein B) and increased risk of cardiovascular disease, casting doubt on the ... Upon binding of apolipoprotein B100, many LDL receptors concentrate in clathrin-coated pits. Both LDL and its receptor form ...

https://en.wikipedia.org/wiki/Cholesterol

Berge G, Sando SB, Rongve A, Aarsland D, White LR (November 2014). "Apolipoprotein E ε2 genotype delays onset of dementia with ... Goedert M, Spillantini MG, Del Tredici K, Braak H (January 2013). "100 years of Lewy pathology". Nat Rev Neurol (Practice ... 88-100. doi:10.1212/WNL.0000000000004058. PMC 5496518. PMID 28592453. McKeith IG, Dickson DW, Lowe J, et al. (December 2005). " ...

https://en.wikipedia.org/wiki/Dementia_with_Lewy_bodies

2009). "Gene-centric association signals for lipids and apolipoproteins identified via the HumanCVD BeadChip". Am. J. Hum. ... The complete sequences of 100 new cDNA clones from brain which code for large proteins in vitro". DNA Res. 7 (4): 273-81. doi: ...

https://en.wikipedia.org/wiki/WNK3

... apolipoprotein - apoptosis - aquaporin - archaea - arginine - argipressin - aromatic amine - aromatic compound - arrestin - ... nerve tissue protein S 100 - nervous system - neurobiology - neurofilament protein - neurokinin A - neurokinin K - neurokinin-1 ...

https://en.wikipedia.org/wiki/Index_of_biochemistry_articles

... of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins ... Use of B100 (100% biodiesel) is possible only in temperate climates, as the gel point is approximately 10 °C (50 °F). The oil ... Half of the saturated fat content of coconut oil is lauric acid (41.8 grams per 100 grams of total composition), while other ... "Fats and fatty acids contents per 100 g (click for "more details"). Example: Avocado oil (user can search for other oils)". ...

https://en.wikipedia.org/wiki/Coconut_oil

... mediates the efflux of cholesterol and phospholipids to lipid-poor apolipoproteins (apoA1 and apoE) (reverse cholesterol ... Oram JF, Vaughan AM (June 2000). "ABCA1-mediated transport of cellular cholesterol and phospholipids to HDL apolipoproteins". ... October 1999). "The Tangier disease gene product ABC1 controls the cellular apolipoprotein-mediated lipid removal pathway". The ... 100: 153953. doi:10.1016/j.metabol.2019.153953. PMID 31377319. S2CID 203413137. Mauerer R, Ebert S, Langmann T (February 2009 ...

https://en.wikipedia.org/wiki/ABCA1

... encoding protein Apolipoprotein M (6p21.33) ATXN1: encoding protein Ataxin 1 (6p16.3-p16.76) TSBP1: encoding protein TSBP1 ( ... It contains the major histocompatibility complex, which contains over 100 genes related to the immune response, and plays a ...

https://en.wikipedia.org/wiki/Chromosome_6

... and Apolipoproteins". Journal of Clinical Endocrinology & Metabolism. 68 (1): 17-21. doi:10.1210/jcem-68-1-17. PMID 2491859. ... She has authored or co-authored more than 100 scientific studies, research papers and policy reports. Her most recent research ...

https://en.wikipedia.org/wiki/Miriam_E._Nelson

... and apolipoproteins A and B. It was first reported to exacerbate hepatic porphyria in 1975. In 1981, it was shown that ... However, the patient reported by Kappy and Buckley would have had a serum level of 44.4 mg/100 mL instead of 8.5 mg/100 mL if ... The patient reported by Morley and Wynne would have had serum barbiturate levels of 50 mg/100 mL, which would have been fatal. ... Work done twelve years later found that the serum phenobarbital 0.111 mg/100 mL for every mg/kg of primidone ingested. Authors ...

https://en.wikipedia.org/wiki/Primidone

Low density lipoproteins are made up of cholesterol, TG, phospholipids, and apolipoproteins. LDL-C molecules bind to the ... In combined hyperlipidemia, there is an overproduction of apoB-100 in the liver. This causes high amounts of LDL and VLDL ...

https://en.wikipedia.org/wiki/Dyslipidemia

Its most abundant apolipoproteins are apo A-I and apo A-II. A rare genetic variant, ApoA-1 Milano, has been documented to be ... In the stress response, serum amyloid A, which is one of the acute-phase proteins and an apolipoprotein, is under the ... Sacks FM, Zheng C, Cohn JS (2011). "Complexities of plasma apolipoprotein C-III metabolism". Journal of Lipid Research. 52 (6 ... HDL lipoprotein particles that bear apolipoprotein C3 are associated with increased, rather than decreased, risk for coronary ...

https://en.wikipedia.org/wiki/High-density_lipoprotein

"Effect of Replacing Race With Apolipoprotein L1 Genotype in Calculation of Kidney Donor Risk Index". American Journal of ... leading to over 100 deaths. This experimentation went hand in hand with a legacy of colonialism. Colonies served as ample ...

https://en.wikipedia.org/wiki/Race_adjustment

MeSH D12.776.070.400.200.100 - apolipoprotein A1 MeSH D12.776.070.400.200.150 - apolipoprotein A2 See List of MeSH codes ( ... proto-oncogene proteins c-ets MeSH D12.776.624.664.700.175.100 - proto-oncogene protein c-ets-1 MeSH D12.776.624.664.700.175. ... fibrillar collagens MeSH D12.776.860.300.250.300.100 - Type I collagen MeSH D12.776.860.300.250.300.200 - Type II collagen MeSH ... non-fibrillar collagens MeSH D12.776.860.300.250.400.100 - Type IV collagen MeSH D12.776.860.300.250.400.200 - Type VI collagen ...

https://en.wikipedia.org/wiki/List_of_MeSH_codes_(D12.776)

apolipoprotein B deficiency, a related condition, is associated with deficiencies of apolipoprotein B.) The MTTP gene provides ... It is caused by a mutation in microsomal triglyceride transfer protein resulting in deficiencies in the apolipoproteins B-48 ... Low levels of plasma chylomicron are also characteristic.[citation needed] There is an absence of apolipoprotein B. On ... The disease is extremely rare with approximately 100 reported cases worldwide since it was first identified by doctors Bassen ...

https://en.wikipedia.org/wiki/Abetalipoproteinemia

"Derepression of microRNA-mediated protein translation inhibition by apolipoprotein B mRNA-editing enzyme catalytic polypeptide- ... 100 (7): 1234-42. doi:10.1111/j.1349-7006.2009.01164.x. PMID 19486339. Kan T, Sato F, Ito T, Matsumura N, David S, Cheng Y, ...

https://en.wikipedia.org/wiki/Mir-25_microRNA_precursor_family

Apolipoprotein E (ApoE) has been shown to be an important and common factor in CNS responses. ApoE controls the redistribution ... For particles with charge Z>10, an addition PEL requirement limits the physical dose (mGy) for 1 year and the career to 100 and ... 100 rad)) have not been a major consideration. However, the heavy ion component of space radiation presents distinct ...

https://en.wikipedia.org/wiki/Central_nervous_system_effects_from_radiation_exposure_during_spaceflight

Katan MB (March 1986). "Apolipoprotein E isoforms, serum cholesterol, and cancer". Lancet. 1 (8479): 507-8. doi:10.1016/s0140- ... If the likelihood is 100%, then x is instead called sufficient. A contributory cause may also be necessary. A causal diagram is ...

https://en.wikipedia.org/wiki/Causal_model

With oral estradiol, there are increases in circulating triglycerides, HDL cholesterol, apolipoprotein A1, and apolipoprotein ... 100 (1): 91-6. doi:10.1210/endo-100-1-91. PMID 830547. Clark JH, Hardin JW, McCormack SA (1979). "Mechanism of action of ... For birth control pills, VTE risk with high doses of ethinylestradiol (>50 μg, e.g., 100 to 150 μg) has been reported to be ... 100 (11): 4012-20. doi:10.1210/jc.2015-2237. PMID 26544651. Gregory Y. H. Lip; John E. Hall (28 June 2007). Comprehensive ...

https://en.wikipedia.org/wiki/Estrogen_(medication)

Angiotensin converting enzyme Antithrombin-III Lipoprotein lipase Apolipoproteins Growth factors Chemokines The enzymes and ... irregularly shaped layer extending approximately 50-100 nm into the lumen of a blood vessel. Another study used osmium ...

https://en.wikipedia.org/wiki/Glycocalyx

... lanosterol cyclase inhibits very low-density lipoprotein apolipoprotein B100 (apoB100) production and enhances low-density ... 100 (26): 15352-7. Bibcode:2003PNAS..10015352P. doi:10.1073/pnas.2536559100. PMC 307571. PMID 14660793. Brocks JJ, Logan GA, ...

https://en.wikipedia.org/wiki/Lanosterol_synthase

The apolipoprotein E (ApoE), that allows the transport and metabolism of triglycerides and cholesterol, has an interaction with ... "Epidermal expression of apolipoprotein E gene during fin and scale development and fin regeneration in zebrafish". ... Reflection through silvering is widespread or dominant in fish of the open sea, especially those that live in the top 100 ... of between 5 and 10 crystals of guanine spaced about ¼ of a wavelength apart to interfere constructively and achieve nearly 100 ...

https://en.wikipedia.org/wiki/Fish_scale

... of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins ... 100% fruit juice is high in calories. The ideal amount of milk and calcium is not known today. Pay attention to salt intake ... doi:10.5518/100/52. Retrieved 27 October 2020. "Heathlthy and Balanced Diet for Dogs". RSPCA. 2017. Retrieved 8 December 2017. ... Avoid bread, rice, and the like as well as pastries, sugared sodas, 100% fruit juice, artificially sweetened drinks, and other ...

https://en.wikipedia.org/wiki/Healthy_diet

Basu SK, Goldstein JL, Brown MS (Feb 1983). "Independent pathways for secretion of cholesterol and apolipoprotein E by ... 100 (4): 391-8. doi:10.1016/S0092-8674(00)80675-3. PMID 10693756. S2CID 12194770. Nohturfft A, Yabe D, Goldstein JL, Brown MS, ...

https://en.wikipedia.org/wiki/Michael_Stuart_Brown

... a number of key technical barriers in delivering the mRNA molecule into the host cell as distributed through apolipoprotein E ( ... which may be 100 nm in size. LNP delivery mechanisms have become an increasing source of encasing nucleic acids and may include ...

https://en.wikipedia.org/wiki/RNA_interference

Apolipoprotein (B). [PDF - 100 KB] March 2008. Aspergillus fumigatus in dust. [PDF - 347 KB] February 2014. ...

https://wwwn.cdc.gov/nchs/nhanes/ContinuousNhanes/labmethods.aspx?BeginYear=2005

The MVZ Dr. Eberhard & Partner Dortmund is specialised in the areas of laboratory medicine, microbiology, human genetics and endocrinology, both in a diagn...

https://www.medizin-zentrum-dortmund.de/en/laboratory-medicine/analyzes-directory/analysis/1068/

N2 - Apolipoprotein B-100, produced primarily in the human liver, is the sole protein component of low-density lipoprotein and ... AB - Apolipoprotein B-100, produced primarily in the human liver, is the sole protein component of low-density lipoprotein and ... Apolipoprotein B-100, produced primarily in the human liver, is the sole protein component of low-density lipoprotein and ... abstract = "Apolipoprotein B-100, produced primarily in the human liver, is the sole protein component of low-density ...

https://experts.unthsc.edu/en/publications/transcriptional-regulation-of-the-apolipoprotein-b-100-gene-ident

Mouse Monoclonal Apolipoprotein B antibody [F2C13]. Validated in ICC/IF, IP, ELISA, RIA. Tested in Human. ... There are currently no reviews for Apolipoprotein B antibody [F2C13] (GTX15663). Be the first to share your experience with ... This gene product is the main apolipoprotein of chylomicrons and low density lipoproteins. It occurs in plasma as two main ... ICC/IF analysis of HepG2 cells using GTX15663 Apolipoprotein B antibody [F2C13]. Panel e is a no primary antibody control. ...

https://www.genetex.com/Product/Detail/Apolipoprotein-B-antibody-F2C13/GTX15663

Regression of coronary artery disease as a result of intensive lipid-lowering therapy in men with high levels of apolipoprotein ... Extreme-risk patients: Goals: LDL , 55 mg/dL, non-HDL , 80 mg/dL, apolipoprotein B (apoB) , 70 mg/dL ... Physicians are no longer asked to treat patients with cardiovascular disease to below 100 mg/dL or the optional goal of below ... In high-risk patients, a serum low-density lipoprotein (LDL) cholesterol level of less than 100 mg/dL is the goal. ...

https://www.medscape.com/answers/150215-69357/what-are-the-esc-guidelines-class-iia-recommendations-for-medical-management-of-angina-pectoris

Name: apolipoprotein B. Synonyms: apob-100, apob-48. Type: Gene. Species: Mus musculus (mouse) ...

https://www.mmrrc.org/catalog/sds.php?mmrrc_id=44201

Apolipoprotein L1 gene variants in deceased organ donors are associated with renal allograft failure. Am J Transplant. 2015;15: ... Apolipoprotein L1 gene variants associate with hypertension-attributed nephropathy and the rate of kidney function decline in ... in African Americans has changed with discovery of the apolipoprotein L1 nephropathy gene (APOL1)88,89. Many non-diabetic ... 2016;100:194-202.. 97. Grams ME, Rebholz CM, Chen Y, et al. Race, APOL1 Risk, and eGFR Decline in the General Population. J Am ...

https://www.nhlbi.nih.gov/events/2015/working-group-research-needs-improve-hypertension-treatment-and-control-african

Evidence for two separate gene defects: one associated with an abnormal apolipoprotein B species, apolipoprotein B-37; and a ... The liver dysfunction causes accumulation of an abnormal, apolipoprotein A-II-deficient lipoprotein in plasma. Red cells are ... The alteration in plasma lipids in autosomal recessive abetalipoproteinemia caused by the absence of beta-apolipoprotein is ... Plasma phospholipid levels are very low, while plasma apolipoprotein B, chylomicrons, very-low-density lipoproteins (VLDLs), ...

https://emedicine.medscape.com/article/954356-overview

Mipomersen, an apolipoprotein B synthesis inhibitor, for lowering of LDL cholesterol concentrations in patients with homozygous ... Mipomersen, an apolipoprotein B synthesis inhibitor, reduces atherogenic lipoproteins in patients with severe ...

https://www.ncbi.nlm.nih.gov/pubmed/31741187

... apolipoprotein-B100 [-7.6 mg/dl (CI95% -13.6 to -1.6); p=0.013] and apolipoprotein-A1 [-6.0 mg/dl (CI95% -10.5 a -1.5); p=0.523 ...

https://pubmed.ncbi.nlm.nih.gov/23430574/

MeSH Terms: Aged; Aged, 80 and over; Apolipoprotein A-I/blood; Apolipoprotein B-100/blood; DDT/adverse effects*; ... p,p-DDE was furthermore associated with apolipoprotein B, but not apolipoprotein A1. CONCLUSIONS: The positive associations ...

https://tools.niehs.nih.gov/portfolio/index.cfm?do=portfolio.publicationDetail&id=4026220

Characterization of Apolipoprotein A-I Pathways in Idiopathic Pulmonary Fibrosis. Completed Study; data analyses ongoing. 18- ... 2-100 Years. NHLBI. 20-H-0141. Long-term Follow-up of Subjects With Sickle Cell Disease Treated With Ex Vivo Gene Therapy Using ... 5-100 Years. NHLBI. 08-H-0186. Safety and the Anti- Tumor Effects of Escalating Doses of Adoptively Infused Ex Vivo Expanded ... 1-100 Years. NHLBI. 10-H-0083. A Phase I Trial of Safety and Immunogenicity of Gardasil Vaccination Post Stem Cell ...

https://clinicalstudies.info.nih.gov/htmlSearchedFile.aspx?Query=&status=&gender=Select+One&Inst=NHLBI&age=&healthyVolunteer=0&page=prot_inst

099 Inhalational 5A Apolipoprotein A-I Mimetic Peptide for the Treatment of Asthma (SBIR-TT).. 100 MRI Myocardial Needle ...

https://grants.nih.gov/grants/guide/notice-files/NOT-OD-16-123.html

Apolipoprotein B-100, or ApoB for short, may…. *. Ask Leyla: Im diabetic; whats the best way to shed stubborn weight? ...

https://drhoffman.com/article/is-weight-gain-inevitable-as-you-grow-older/

KYNAMRO® is an oligonucleotide inhibitor of apolipoprotein B-100 synthesis indicated as an adjunct to lipid-lowering ... ApoB is the principal apolipoprotein of LDL and its metabolic precursor, very low density lipoprotein (VLDL). Mipomersen ... apolipoprotein B (apo B), total cholesterol (TC), and non-high density lipoprotein-cholesterol (non-HDL-C) in patients with ... the principal apolipoprotein of LDL and its metabolic precursor, VLDL. Mipomersen is complementary to the coding region of the ...

http://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=34de65be-f110-4000-a0f1-cb00ec98658f

... apolipoprotein B, and apolipoprotein E, and a lower level of apolipoprotein A. The median LDL level was 3.5 (3.2, 4.1) mmol/L ... Apolipoprotein B, g/L. 1.1 (1.0, 1.2). 1.0 (0.9, 1.1). ,0.001. Apolipoprotein E, mg/L. 42.3 (35.1, 53.2). 40.0 (33.2, 49.3). ... Apolipoprotein A. 5.8 (−3.2, 18.1). 4.4 (−5.9, 11.7). 0.079. Apolipoprotein B. −64.0 (−74.3, −49.8). −36.0 (−44.8, −26.0). , ... In comparison to the baseline, the level of LDL-C, cholesterol, triglyceride, apolipoprotein B, and apolipoprotein E at 1 month ...

https://journals.lww.com/cardioplus/Fulltext/2023/01000/Effect_of_in_hospital_evolocumab_therapy_on.7.aspx

... a short version called apolipoprotein B-48 and a longer version known as apolipoprotein B-100. Learn about this gene and ... The APOB gene provides instructions for making two versions of the apolipoprotein B protein, ... The normal-length apolipoprotein B-48 can form chylomicrons normally, but the abnormally short apolipoprotein B-100 produced in ... Other mutations result in a protein that is shorter than both apolipoprotein B-48 and apolipoprotein B-100. In these cases, no ...

https://medlineplus.gov/genetics/gene/apob/

apolipoprotein B (including Ag(x) antigen). Description. APOB, a secreted glycoprotein, is the main apolipoprotein of ... Apo B-100 functions as a recognition signal for the cellular binding and internalization of LDL particles by the apoB/E ... The shorter apoB-48 protein is produced after RNA editing of the apoB-100 transcript at residue 2180 (CAA-,UAA), resulting in ... apo B-100). It occurs in plasma as two main isoforms, apoB-48 and apoB-100: the former is synthesized exclusively in the gut ...

https://edrn.nci.nih.gov/data-and-resources/biomarkers/apob/

Increased vascular biosynthesis of tetrahydrobiopterin in apolipoprotein E-deficient mice. Livius V. DUscio, Zvonimir S. ... Dive into the research topics of Increased vascular biosynthesis of tetrahydrobiopterin in apolipoprotein E-deficient mice. ...

https://mayoclinic.pure.elsevier.com/en/publications/increased-vascular-biosynthesis-of-tetrahydrobiopterin-in-apolipo/fingerprints/

3. The I4399M variant of apolipoprotein(a) is associated with increased oxidized phospholipids on apolipoprotein B-100 ... Oxidized phospholipids on apolipoprotein B-100 versus plasminogen and risk of coronary heart disease in the PROCARDIS study. ... Effect of therapeutic interventions on oxidized phospholipids on apolipoprotein B100 and lipoprotein(a).. Yeang C; Hung MY; ... High-dose atorvastatin reduces total plasma levels of oxidized phospholipids and immune complexes present on apolipoprotein B- ...

https://pubmedhh.nlm.nih.gov/biomarkers/search.php?id=27831500&mod=related&page=1&outid=&proj=

Apolipoproteins [D12.776.070.400] * Apolipoproteins B [D12.776.070.400.300] * Apolipoprotein B-48 [D12.776.070.400.300.240] ... Apolipoproteins [D12.776.521.120] * Apolipoproteins B [D12.776.521.120.300] * Apolipoprotein B-48 [D12.776.521.120.300.240] ... Apolipoproteins [D10.532.091] * Apolipoproteins B [D10.532.091.300] * Apolipoprotein B-48 [D10.532.091.300.240] ... Apolipoproteins B (1983-2006). Public MeSH Note. 2007; APOLIPOPROTEIN B-100 was indexed under APOLIPOPROTEINS B (1983-2006). ...

https://meshb.nlm.nih.gov/record/ui?ui=D053299

Two ligands on LDL bind to the receptor, apolipoprotein B-100 (apoB-100) and apoE. The LDL receptor also binds another ligand, ... Disorders of the biogenesis and secretion of lipoproteins containing the B apolipoproteins. Scriver CR, Beaudet AL, Sly WS, ... LDL receptor analysis can be used to identify the specific LDL receptor defect, and LDL receptor or apoB-100 studies can help ... Tendon xanthomas may occur with other conditions such as familial defective apoB-100 and type III hyperlipoproteinemia. These ...

https://reference.medscape.com/article/121298-overview

Development and partial characterisation of an antiserum against apolipoprotein B of the short-finned eel, Anguilla australis. ... Development and partial characterisation of an antiserum against apolipoprotein B of the short-finned eel, Anguilla australis」の ...

https://keio.pure.elsevier.com/ja/publications/development-and-partial-characterisation-of-an-antiserum-against-/fingerprints/

Antibodies for proteins involved in lipoprotein biosynthetic process pathways, according to their Panther/Gene Ontology Classification

https://www.thermofisher.com/antibody/primary/panther/lipoprotein%20biosynthetic%20process

Apolipoprotein D (ApoD) is a lipocalin involved in several processes including lipid transport, but its modulation during human ... Identification of apolipoprotein D, apolipoprotein A-IV, apolipoprotein E, and apolipoprotein A-I. J Biol Chem. 1990, 265: ... Do Carmo S, Séguin D, Milne R, Rassart E: Modulation of apolipoprotein D and apolipoprotein E mRNA expression by growth arrest ... Terrisse L, Séguin D, Bertrand P, Poirier J, Milne R, Rassart E: Modulation of apolipoprotein D and apolipoprotein E expression ...

https://rbej.biomedcentral.com/articles/10.1186/1477-7827-7-92

The associations were examined using Cox proportional hazards models, adjusting for sex, education, and apolipoprotein E ε4, ... The associations were examined using Cox proportional hazards models, adjusting for sex, education, and apolipoprotein E ε4, ... The associations were examined using Cox proportional hazards models, adjusting for sex, education, and apolipoprotein E ε4, ... The associations were examined using Cox proportional hazards models, adjusting for sex, education, and apolipoprotein E ε4, ...

https://asu.pure.elsevier.com/en/publications/medical-doctors-and-dementia-a-longitudinal-study

Tissue and/or cellular expressions of interleukin-1 alpha (IL-1α), apolipoprotein E (ApoE), amyloid β (Aβ) precursor protein ( ... Aboud, O., Mrak, R.E., Boop, F. et al. Apolipoprotein epsilon 3 alleles are associated with indicators of neuronal resilience. ... Apolipoprotein epsilon 3 alleles are associated with indicators of neuronal resilience. *Orwa Aboud1,3, ... Liu L, Aboud O, Jones RA, Mrak RE, Griffin ST, Barger SW: Apolipoprotein E expression is elevated by interleukin 1 and other ...

https://bmcmedicine.biomedcentral.com/articles/10.1186/1741-7015-10-35

While apolipoprotein ε4, an allele of the apolipoprotein ε gene that increases the risk for Alzheimers disease, was associated ... Apolipoprotein ε4 was not associated with worse memory performance.. Memory and brain volume in non-demented elders have been ... score for amyloid accumulation becomes sharply higher around age 65 and occurs at younger ages in those with an apolipoprotein ... and 100 was "abnormal" (described as the 95th percentile for amyloid PET accumulation in those with moderately severe ...

https://www.ipa-online.org/news-and-issues/better-memory-and-greater-brain-volume-in-aging-female-brain

Albumin, Alkaline Phosphatase, ALT/SGPT, Ammonia, Amylase, Apolipoprotein A-1, Apolipoprotein B, AST/SGOT, Beta-Hydroxybutyrate ... 2022-2026 Iceland Clinical Chemistry Market Database--Supplier Shares, Volume and Sales Segment Forecasts for 100 Abused Drug, ... Volume and Sales Segment Forecasts for 100 Abused Drug, Cancer, Chemistry, Endocrine, Immunoprotein and TDM Tests ... the 2021-2026 volume and sales forecasts for 100 clinical chemistry, TDM, endocrine, cancer, immunoprotein and abused drug ...

https://www.aarkstore.com/healthcare/1871736/2022-2026-iceland-clinical-chemistry-market-databasetests

This gene product is the main apolipoprotein of chylomicrons and low density lipoproteins. (genetex.com)
APOB, a secreted glycoprotein, is the main apolipoprotein of chylomicrons (apo B-48), LDL (apo B-100) and VLDL (apo B-100). (nih.gov)

Methods Neuroimaging features of CAA, apolipoprotein (APOE), and cerebrospinal fluid amyloid β (Aβ) 40 levels were studied in subjects with Down syndrome (DS, n = 117), autosomal-dominant AD (ADAD, n = 29), sporadic EOAD (n = 42), and healthy controls (n = 68). (uab.cat)
The researchers found a correlation between 16 proteins found in blood and the ε2 form of the apolipoprotein E ( APOE ) gene. (nih.gov)

Plasma phospholipid levels are very low, while plasma apolipoprotein B, chylomicrons, very-low-density lipoproteins (VLDLs), and low-density lipoproteins (LDLs) are absent. (medscape.com)
The normal-length apolipoprotein B-48 can form chylomicrons normally, but the abnormally short apolipoprotein B-100 produced in the liver is less able to produce lipoproteins. (medlineplus.gov)

Apolipoprotein B-100, produced primarily in the human liver, is the sole protein component of low-density lipoprotein and serves as a ligand for the LDL receptor. (unthsc.edu)
In high-risk patients, a serum low-density lipoprotein (LDL) cholesterol level of less than 100 mg/dL is the goal. (medscape.com)
KYNAMRO ® is an oligonucleotide inhibitor of apolipoprotein B-100 synthesis indicated as an adjunct to lipid-lowering medications and diet to reduce low density lipoprotein-cholesterol (LDL-C), apolipoprotein B (apo B), total cholesterol (TC), and non-high density lipoprotein-cholesterol (non HDL-C) in patients with homozygous familial hypercholesterolemia (HoFH) ( 1 ). (nih.gov)
Apolipoprotein B-48 is produced in the intestine, where it is a building block of a type of lipoprotein called a chylomicron. (medlineplus.gov)
10. Effect of therapeutic interventions on oxidized phospholipids on apolipoprotein B100 and lipoprotein(a). (nih.gov)
13. Antisense oligonucleotide directed to human apolipoprotein B-100 reduces lipoprotein(a) levels and oxidized phospholipids on human apolipoprotein B-100 particles in lipoprotein(a) transgenic mice. (nih.gov)
16. Lipoprotein Apheresis for Lipoprotein(a)-Associated Cardiovascular Disease: Prospective 5 Years of Follow-Up and Apolipoprotein(a) Characterization. (nih.gov)
Plasma lipid metabolism is regulated in part by the specific apolipoprotein constituents of the various lipoprotein classes. (biomedcentral.com)
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)

To compare across groups, the authors created a scaled score in which zero was "normal" (i.e., based on participants ages 30-49) and 100 was "abnormal" (described as the 95th percentile for amyloid PET accumulation in those with moderately severe symptomatic Alzheimer's disease). (ipa-online.org)
The scaled score for amyloid accumulation becomes sharply higher around age 65 and occurs at younger ages in those with an apolipoprotein ε4 allele than those without. (ipa-online.org)

It occurs in plasma as two main isoforms, apoB-48 and apoB-100: the former is synthesized exclusively in the gut and the latter in the liver. (genetex.com)
The shorter apoB-48 protein is produced after RNA editing of the apoB-100 transcript at residue 2180 (CAA->UAA), resulting in the creation of a stop codon, and early translation termination. (genetex.com)
LDL receptor analysis can be used to identify the specific LDL receptor defect, and LDL receptor or apoB-100 studies can help distinguish heterozygous FH from the similar syndrome of familial defective apoB-100. (medscape.com)

More than 100 mutations in the APOB gene are known to cause familial hypercholesterolemia. (medlineplus.gov)

It is considered an atypical apolipoprotein as both its structure and major sites of synthesis differ from the other apolipoproteins. (biomedcentral.com)
He and his associates were the first to achieve the complete synthesis of a significant plasma apolipoprotein (apoC-I), and they also determined the complete cDNA and amino acid sequence of apo B-100, one of the largest proteins ever sequenced and a key protein in atherosclerosis and cardiovascular disease. (nyp.org)

Therefore these two cis-acting elements mediate hepatic-cell specific expression of the apolipoprotein gene by interacting with trans-acting protein factors. (unthsc.edu)
The APOB gene provides instructions for making two versions of the apolipoprotein B protein, a short version called apolipoprotein B-48 and a longer version known as apolipoprotein B-100. (medlineplus.gov)
Most APOB gene mutations that cause FHBL lead to the production of apolipoprotein B that is abnormally short. (medlineplus.gov)
The severity of the condition largely depends on the length of the abnormal apolipoprotein B. Some mutations in the APOB gene lead to the production of a protein that is shorter than apolipoprotein B-100, but longer than apolipoprotein B-48. (medlineplus.gov)
While apolipoprotein ε4, an allele of the apolipoprotein ε gene that increases the risk for Alzheimer's disease, was associated with lower brain volume, the benefit of female over male existed in both the carriers and non carriers. (ipa-online.org)
In studying genes regulated by this interaction, we identified apolipoprotein D (APOD) as one gene that is downregulated in mural cells by coculture with endothelial cells. (utmb.edu)

For moderately high-risk persons (2+ risk factors), the recommended LDL cholesterol level is less than 130 mg/dL, but an LDL cholesterol level of 100 mg/dL is a therapeutic option. (medscape.com)
All of these protein changes lead to a reduction of functional apolipoprotein B. As a result, the transportation of dietary fats and cholesterol is decreased or absent. (medlineplus.gov)
Among his contributions since he became Dean and Professor of Medicine at the Medical College in 1997, are his continuing insights into the salutary benefits of the cholesterol-lowering statin drugs for cardiovascular health in even healthy adults, and the potential predictive value of certain apolipoproteins that are major components of LDL and HDL, the so-called "bad" and "good" cholesterols, respectively. (nyp.org)
His latest published article, for example, in the journal Circulation , detailing results from the landmark Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS), contends that the apolipoproteins apoB and apoAI may be better predictors than the more widely used LDL cholesterol of risk for a first acute major coronary event. (nyp.org)

Apolipoprotein B-100, which is produced in the liver, is a component of several other types of lipoproteins. (medlineplus.gov)

Apolipoprotein D (ApoD) is a lipocalin involved in several processes including lipid transport, but its modulation during human pregnancy was never examined. (biomedcentral.com)
Apolipoprotein D (ApoD) is a secreted lipocalin assigned with many putative functions including lipid transport. (biomedcentral.com)

Physicians are no longer asked to treat patients with cardiovascular disease to below 100 mg/dL or the optional goal of below 70 mg/dL. (medscape.com)

In these cases, no normal-length apolipoprotein B protein is produced. (medlineplus.gov)

Apo B-100 functions as a recognition signal for the cellular binding and internalization of LDL particles by the apoB/E receptor. (nih.gov)

Description: This is Double-antibody Sandwich Enzyme-linked immunosorbent assay for detection of Human Apolipoprotein L (APOL1) in serum, plasma, tissue homogenates, cell lysates, cell culture supernates and other biological fluids. (jemsec.com)
Description: Enzyme-linked immunosorbent assay based on the Double-antibody Sandwich method for detection of Human Apolipoprotein L (APOL1) in samples from serum, plasma, tissue homogenates, cell lysates, cell culture supernates and other biological fluids with no significant corss-reactivity with analogues from other species. (jemsec.com)
In this manuscript, we also demonstrate the application of these methods for the detection of LPS in serum from pediatric patients with invasive Salmonella Typhimurium bacteremia (n = 7) and those with Staphylococcal bacteremia (n = 7) with 100% correlation with confirmatory culture. (nature.com)

15. High-dose atorvastatin reduces total plasma levels of oxidized phospholipids and immune complexes present on apolipoprotein B-100 in patients with acute coronary syndromes in the MIRACL trial. (nih.gov)
However, following acute phase stimulation, the CRP levels may increase 100- or even 500-fold ( 10 ). (spandidos-publications.com)

Two methods are compared for measuring the kinetic parameters of apolipoprotein A-I and A-II metabolism in human plasma. (houstonmethodist.org)

The ε2 form, which is much rarer than ε4, is more commonly detected among those over 100 years old and their children than in the general population. (nih.gov)

Each mutation that causes this condition changes a single protein building block (amino acid) in a critical region of apolipoprotein B-100. (medlineplus.gov)

The pregnancy induced hyperlipidemia is accompanied by a rise in the plasma levels of some apolipoproteins, namely ApoA-1, ApoB, ApoC-II and ApoC-III. (biomedcentral.com)
The fractional plasma clearance rates of endogenous apolipoproteins A-I and A-II were the same. (houstonmethodist.org)

The catabolic clearance rate of exogenously labeled apolipoprotein A-I was consistently faster than that of endogenous apolipoprotein A-I. Conversely, endogenously and exogenously labeled apolipoprotein A-II were catabolized at identical rates. (houstonmethodist.org)

Apolipoprotein B-100 allows LDLs to attach to specific receptors on the surface of cells, particularly in the liver. (medlineplus.gov)

ICC/IF analysis of HepG2 cells using GTX15663 Apolipoprotein B antibody [F2C13]. (genetex.com)

2. Relationship of oxidized phospholipids on apolipoprotein B-100 particles to race/ethnicity, apolipoprotein(a) isoform size, and cardiovascular risk factors: results from the Dallas Heart Study. (nih.gov)

12. Relationship of oxidized phospholipids on apolipoprotein B-100 to cardiovascular outcomes in patients treated with intensive versus moderate atorvastatin therapy: the TNT trial. (nih.gov)

In these cases, normal apolipoprotein B-48 is still made in the intestine. (medlineplus.gov)
With Cornell's President Hunter Rawlings, Dr. Gotto was largely responsible for the single largest gift ever made to Cornell University-a $100 million contribution in support of the Medical College's Strategic Plan by Joan and Sanford Weill. (nyp.org)

Anatomy18

Organisms8

Diseases31

Chemicals and Drugs111

Analytical, Diagnostic and Therapeutic Techniques and Equipment39

Psychiatry and Psychology2

Phenomena and Processes52

Technology, Industry, Agriculture5

Information Science3

Named Groups1

Health Care7

Dietary fish oils inhibit early events in the assembly of very low density lipoproteins and target apoB for degradation within the rough endoplasmic reticulum of hamster hepatocytes. (1/731)

Role of cholesterol ester mass in regulation of secretion of ApoB100 lipoprotein particles by hamster hepatocytes and effects of statins on that relationship. (2/731)

Characterization of a new form of inherited hypercholesterolemia: familial recessive hypercholesterolemia. (3/731)

Selective modification of apoB-100 in the oxidation of low density lipoproteins by myeloperoxidase in vitro. (4/731)

ApoB100 secretion from HepG2 cells is decreased by the ACAT inhibitor CI-1011: an effect associated with enhanced intracellular degradation of ApoB. (5/731)

Secondary radicals derived from chloramines of apolipoprotein B-100 contribute to HOCl-induced lipid peroxidation of low-density lipoproteins. (6/731)

Molecular bases of low production rates of apolipoprotein B-100 and truncated apoB-82 in a mutant HepG2 cell line generated by targeted modification of the apolipoprotein B gene. (7/731)

Truncated apo B-70.5-containing lipoproteins bind to megalin but not the LDL receptor. (8/731)

Apolipoproteins B

Apolipoprotein A-I

Apolipoprotein B-100

Apolipoprotein B-48

Apolipoproteins E

Apolipoproteins

Apolipoprotein C-III

Apolipoproteins A

Apolipoprotein E4

Apolipoprotein E3

Lipoproteins, VLDL

Apolipoprotein A-II

Lipoproteins

Apolipoprotein C-II

Lipoproteins, LDL

Triglycerides

Cholesterol

Apolipoprotein E2

Apolipoprotein C-I

Apolipoproteins C

Lipoproteins, HDL

Lipids

Hypobetalipoproteinemias

Apoprotein(a)

Cholesterol, LDL

Lipoprotein(a)

Cytidine Deaminase

Receptors, LDL

RNA Editing

Cholesterol, HDL

Lipoproteins, IDL

Liver

Hyperlipidemia, Familial Combined

Hyperlipoproteinemia Type II

Hyperlipidemias

Hypobetalipoproteinemia, Familial, Apolipoprotein B

Hypolipoproteinemias

Chylomicrons

Arteriosclerosis

Lipid Metabolism

Atherosclerosis

Hyperlipoproteinemias

Apolipoproteins D

Hypercholesterolemia

Oleic Acid

Abetalipoproteinemia

Cholesterol Esters

Cholesterol, VLDL

RNA, Messenger

Molecular Sequence Data

Base Sequence

Hyperlipoproteinemia Type IV

Hypertriglyceridemia

Lipoprotein Lipase

Mice, Knockout

Alleles

Receptors, Lipoprotein

Phosphatidylcholine-Sterol O-Acyltransferase

Hyperlipoproteinemia Type III

Genotype

Mice, Inbred C57BL

Dietary Fats

Anticholesteremic Agents

Polymorphism, Genetic

Heterozygote

Carrier Proteins

Nephelometry and Turbidimetry

Cholesterol Ester Transfer Proteins

Intestines

Kinetics

Methaqualone

Cholesterol, Dietary

Electrophoresis, Polyacrylamide Gel

Phospholipids

ATP Binding Cassette Transporter 1

Mice, Transgenic

Ultracentrifugation

Amino Acid Sequence

Aorta

Homozygote