A nutritional condition produced by a deficiency of proteins in the diet, characterized by adaptive enzyme changes in the liver, increase in amino acid synthetases, and diminution of urea formation, thus conserving nitrogen and reducing its loss in the urine. Growth, immune response, repair, and production of enzymes and hormones are all impaired in severe protein deficiency. Protein deficiency may also arise in the face of adequate protein intake if the protein is of poor quality (i.e., the content of one or more amino acids is inadequate and thus becomes the limiting factor in protein utilization). (From Merck Manual, 16th ed; Harrison's Principles of Internal Medicine, 12th ed, p406)
A dimeric protein found in liver peroxisomes that plays an important role in FATTY ACID metabolism and steroid metabolism. The dimer is formed by cleavage of a single protein precursor and contains an enoyl-CoA hydratase-2 domain and a second domain that displays (S)-3-hydroxyacyl-CoA dehydrogenase and 17-beta-estradiol dehydrogenase activities. The enzyme is stereospecific with regards to arrangement of the substrate double bonds and position of the 3-hydroxy group of the reaction intermediate. It is complemented by PEROXISOMAL BIFUNCTIONAL ENZYME, which has the opposite reaction stereospecificity.
An enzyme that catalyzes reversibly the hydration of unsaturated fatty acyl-CoA to yield beta-hydroxyacyl-CoA. It plays a role in the oxidation of fatty acids and in mitochondrial fatty acid synthesis, has broad specificity, and is most active with crotonyl-CoA. EC 4.2.1.17.
Infections by nematodes, general or unspecified.
Enzymes that reversibly catalyze the oxidation of a 3-hydroxyacyl CoA to 3-ketoacyl CoA in the presence of NAD. They are key enzymes in the oxidation of fatty acids and in mitochondrial fatty acid synthesis.
A class of enzymes that catalyzes the oxidation of 17-hydroxysteroids to 17-ketosteroids. EC 1.1.-.
Proteins obtained from foods. They are the main source of the ESSENTIAL AMINO ACIDS.
The lack of sufficient energy or protein to meet the body's metabolic demands, as a result of either an inadequate dietary intake of protein, intake of poor quality dietary protein, increased demands due to disease, or increased nutrient losses.
A heterogeneous group of inherited metabolic disorders marked by absent or dysfunctional PEROXISOMES. Peroxisomal enzymatic abnormalities may be single or multiple. Biosynthetic peroxisomal pathways are compromised, including the ability to synthesize ether lipids and to oxidize long-chain fatty acid precursors. Diseases in this category include ZELLWEGER SYNDROME; INFANTILE REFSUM DISEASE; rhizomelic chondrodysplasia (CHONDRODYSPLASIA PUNCTATA, RHIZOMELIC); hyperpipecolic acidemia; neonatal adrenoleukodystrophy; and ADRENOLEUKODYSTROPHY (X-linked). Neurologic dysfunction is a prominent feature of most peroxisomal disorders.
A genus of intestinal nematode parasites belonging to the superfamily HELIGMOSOMATOIDEA, which commonly occurs in rats but has been experimentally transmitted to other rodents and rabbits. Infection is usually through the skin.
A mitochondrial protein consisting of four alpha-subunits and four beta-subunits. It contains enoyl-CoA hydratase, long-chain-3-hydroxyacyl-CoA dehydrogenase, and acetyl-CoA C-acyltransferase activities and plays an important role in the metabolism of long chain FATTY ACIDS.
Enzymes that catalyze the breakage of a carbon-oxygen bond leading to unsaturated products via the removal of water. EC 4.2.1.
A superfamily of parasitic nematodes which were formerly considered a part of TRICHOSTRONGYLOIDEA. It includes the following genera: Heligmosomum, NEMATOSPIROIDES, and NIPPOSTRONGYLUS. The hosts are rodents.
A depolarizing neuromuscular-blocking agent, that causes persistent nicotinic activation resulting in spastic paralysis of susceptible nematodes. It is a drug of second-choice after benzimidazoles for treatment of ascariasis, hookworm, and pinworm infections, being effective after a single dose. (From Smith and Reynard, Textbook of Pharmacology, 1992, p920)
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.
Oxidative enzyme which transforms p-nitroanisole into p-nitrophenol.
Proteins that bind to and transfer CHOLESTEROL ESTERS between LIPOPROTEINS such as LOW-DENSITY LIPOPROTEINS and HIGH-DENSITY LIPOPROTEINS.
A major protein in the BLOOD. It is important in maintaining the colloidal osmotic pressure and transporting large organic molecules.
A mixture of related phosphoproteins occurring in milk and cheese. The group is characterized as one of the most nutritive milk proteins, containing all of the common amino acids and rich in the essential ones.
A tetrameric protein, molecular weight between 50,000 and 70,000, consisting of 4 equal chains, and migrating on electrophoresis in 3 fractions more mobile than serum albumin. Its concentration ranges from 7 to 33 per cent in the serum, but levels decrease in liver disease.
A diet that contains limited amounts of protein. It is prescribed in some cases to slow the progression of renal failure. (From Segen, Dictionary of Modern Medicine, 1992)
The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.
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.
A ubiquitous family of proteins that transport PHOSPHOLIPIDS such as PHOSPHATIDYLINOSITOL and PHOSPHATIDYLCHOLINE between membranes. They play an important role in phospholipid metabolism during vesicular transport and SIGNAL TRANSDUCTION.
Errors in the metabolism of LIPIDS resulting from inborn genetic MUTATIONS that are heritable.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
The measurement of an organ in volume, mass, or heaviness.
Proteins that are present in blood serum, including SERUM ALBUMIN; BLOOD COAGULATION FACTORS; and many other types of proteins.
Transport proteins that carry specific substances in the blood or across cell membranes.
WASP protein is mutated in WISKOTT-ALDRICH SYNDROME and is expressed primarily in hematopoietic cells. It is the founding member of the WASP protein family and interacts with CDC42 PROTEIN to help regulate ACTIN polymerization.
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.
Systems of enzymes which function sequentially by catalyzing consecutive reactions linked by common metabolic intermediates. They may involve simply a transfer of water molecules or hydrogen atoms and may be associated with large supramolecular structures such as MITOCHONDRIA or RIBOSOMES.
An individual having different alleles at one or more loci regarding a specific character.
A nutritional condition produced by a deficiency of VITAMIN A in the diet, characterized by NIGHT BLINDNESS and other ocular manifestations such as dryness of the conjunctiva and later of the cornea (XEROPHTHALMIA). Vitamin A deficiency is a very common problem worldwide, particularly in developing countries as a consequence of famine or shortages of vitamin A-rich foods. In the United States it is found among the urban poor, the elderly, alcoholics, and patients with malabsorption. (From Cecil Textbook of Medicine, 19th ed, p1179)
Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.
Regular course of eating and drinking adopted by a person or animal.
An individual in which both alleles at a given locus are identical.
A condition produced by dietary or metabolic deficiency. The term includes all diseases caused by an insufficient supply of essential nutrients, i.e., protein (or amino acids), vitamins, and minerals. It also includes an inadequacy of calories. (From Dorland, 27th ed; Stedman, 25th ed)
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.
Inbred C57BL mice are a strain of laboratory mice that have been produced by many generations of brother-sister matings, resulting in a high degree of genetic uniformity and homozygosity, making them widely used for biomedical research, including studies on genetics, immunology, cancer, and neuroscience.
Conditions or pathological processes associated with pregnancy. They can occur during or after pregnancy, and range from minor discomforts to serious diseases that require medical interventions. They include diseases in pregnant females, and pregnancies in females with diseases.
Deficiency of the protease inhibitor ALPHA 1-ANTITRYPSIN that manifests primarily as PULMONARY EMPHYSEMA and LIVER CIRRHOSIS.
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)
A nutritional condition produced by a deficiency of VITAMIN B 12 in the diet, characterized by megaloblastic anemia. Since vitamin B 12 is not present in plants, humans have obtained their supply from animal products, from multivitamin supplements in the form of pills, and as additives to food preparations. A wide variety of neuropsychiatric abnormalities is also seen in vitamin B 12 deficiency and appears to be due to an undefined defect involving myelin synthesis. (From Cecil Textbook of Medicine, 19th ed, p848)
The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
A nutritional condition produced by a deficiency of VITAMIN D in the diet, insufficient production of vitamin D in the skin, inadequate absorption of vitamin D from the diet, or abnormal conversion of vitamin D to its bioactive metabolites. It is manifested clinically as RICKETS in children and OSTEOMALACIA in adults. (From Cecil Textbook of Medicine, 19th ed, p1406)
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.
A nutritional condition produced by a deficiency of FOLIC ACID in the diet. Many plant and animal tissues contain folic acid, abundant in green leafy vegetables, yeast, liver, and mushrooms but destroyed by long-term cooking. Alcohol interferes with its intermediate metabolism and absorption. Folic acid deficiency may develop in long-term anticonvulsant therapy or with use of oral contraceptives. This deficiency causes anemia, macrocytic anemia, and megaloblastic anemia. It is indistinguishable from vitamin B 12 deficiency in peripheral blood and bone marrow findings, but the neurologic lesions seen in B 12 deficiency do not occur. (Merck Manual, 16th ed)
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
A dysgammaglobulinemia characterized by a deficiency of IMMUNOGLOBULIN A.
A nutritional condition produced by a deficiency of THIAMINE in the diet, characterized by anorexia, irritability, and weight loss. Later, patients experience weakness, peripheral neuropathy, headache, and tachycardia. In addition to being caused by a poor diet, thiamine deficiency in the United States most commonly occurs as a result of alcoholism, since ethanol interferes with thiamine absorption. In countries relying on polished rice as a dietary staple, BERIBERI prevalence is very high. (From Cecil Textbook of Medicine, 19th ed, p1171)
An encapsulated lymphatic organ through which venous blood filters.
Total number of calories taken in daily whether ingested or by parenteral routes.
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.
The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
A disease-producing enzyme deficiency subject to many variants, some of which cause a deficiency of GLUCOSE-6-PHOSPHATE DEHYDROGENASE activity in erythrocytes, leading to hemolytic anemia.
Elements of limited time intervals, contributing to particular results or situations.
A nutritional condition produced by a deficiency of magnesium in the diet, characterized by anorexia, nausea, vomiting, lethargy, and weakness. Symptoms are paresthesias, muscle cramps, irritability, decreased attention span, and mental confusion, possibly requiring months to appear. Deficiency of body magnesium can exist even when serum values are normal. In addition, magnesium deficiency may be organ-selective, since certain tissues become deficient before others. (Harrison's Principles of Internal Medicine, 12th ed, p1936)

Chronic protein undernutrition and an acute inflammatory stimulus elicit different protein kinetic responses in plasma but not in muscle of piglets. (1/465)

The changes in protein metabolism of severe childhood malnutrition are generally perceived as a metabolic adaptation to chronic protein undernutrition. However, severe malnutrition is invariably accompanied by infections which also have profound effects on protein metabolism. This study aimed to distinguish the effect of protein undernutrition from that of an inflammatory stimulus on muscle and plasma protein synthesis rates. Two groups of five piglets consumed diets containing either 23% or 3% protein for 4 wk. They then were infused intravenously with 2H3-leucine before and 48 h after subcutaneous injections of turpentine to measure the fractional synthesis rates (FSR) of muscle protein and both the FSR and the absolute synthesis rates (ASR) of albumin and fibrinogen. Prior to turpentine injection, compared to control piglets, protein-deficient piglets had significantly lower muscle FSR and plasma concentrations of both albumin and fibrinogen, although only albumin had lower FSR and ASR. Turpentine injection decreased muscle FSR but increased the FSR, ASR and plasma concentrations of both albumin and fibrinogen in control piglets. In protein-deficient piglets, the inflammatory stress caused a further decrease in muscle protein FSR and in plasma albumin concentration despite marked increases in albumin FSR and ASR. Fibrinogen FSR, ASR and plasma concentration were increased. We conclude that protein undernutrition and inflammation elicit the same kinetic response in muscle protein but different kinetic responses in plasma proteins. Furthermore, whereas protein deficiency reduces the plasma albumin pool via a reduction in albumin synthesis, inflammation reduces it through a stimulation of catabolism and/or loss from the intravascular space.  (+info)

Vitamin A prevents the decline in immunoglobulin A and Th2 cytokine levels in small intestinal mucosa of protein-malnourished mice. (2/465)

We examined whether vitamin A improved mucosal immune depression in mice with wasting protein deficiency. In male C3H/HeN mice fed a semi-purified 1% protein diet for 2 wk, plasma retinol and immunoglobulin A (IgA) concentrations in the small intestinal mucosa were 50 and 55%, respectively, of those in mice fed a semi-purified 20% protein diet, (P < 0.05). Daily supplementation of 0.3 mg of retinyl acetate to protein-deficient mice for 2 wk increased the plasma retinol level to the value in the protein-sufficient mice. However, 1 mg/d of retinyl acetate was required to prevent the decline of the IgA level caused by the protein deficiency. Mice fed the low-protein diet had lower concentrations of IL-4 and IL-5 in the small intestinal mucosa and fewer IL-4- and IL-5-containing cells in the lamina propria (P < 0. 05). Retinyl acetate (1 mg) significantly restored the IL-5 level and the number of IL-4- and IL-5-containing cells. After immunization with 20 microg of cholera toxin (CT), the intestinal mucosa of protein-deficient mice contained significantly less CT-specific IgA than control mice. Treatment with 1 mg of retinyl acetate prevented the decline of anti-CT IgA level in the protein-deficient mice, improving their survival rate after an exposure to 0.1 mg of CT. These results suggest that large oral supplements of vitamin A may preserve mucosal IgA level during protein malnutrition, possibly by stimulating Th2 cytokine production and thereby, inducing resistance against infection.  (+info)

Loss of a homologous group of proteins in a dominantly inherited ectodermal malformation. (3/465)

Hair from mice bearing the dominantly inherited Naked trait (NN) and from normal (NN) mice of the same inbred strain was separated into its major protein components by standard techniques. The relative amounts of proteins in these components were then determined by a regression method from the amino acid composition of the hair samples and of the fractions into which they had been separated. The results indicated that the amount of soluble fibril in Naked-mouse hair is decreased. Polyacrylamide-gel electrophoresis of this fraction prepared from the hair of both normal and Naked mice revealed that all protein bands present in the normal are also present in the Naked mice. However, a densitometric scan of the gels at 280 nm showed that the soluble fibril fraction from Naked-mouse hair is deficient in several proteins which, on amino acid analysis, were found to contain 31% glycine and 10% tyrosine. Gel filtration of S-carboxymethylkerateine prepared from normal and mutant hair showed that the mutant hair is deficient in a heterogeneous, low-molecular-weight fraction also rich in glycine and tyrosine. Our present data do not reveal the mechanism whereby a single gene locus modulates the production of several different proteins.  (+info)

Dietary protein or arginine deficiency impairs constitutive and inducible nitric oxide synthesis by young rats. (4/465)

Effects of dietary protein or arginine deficiency on constitutive and lipopolysaccharide (LPS)-induced nitric oxide (NO) synthesis were determined in young rats by quantifying urinary nitrate excretion. In Experiment 1, 30-d-old rats (n = 16) were divided randomly into two groups (n = 8/group) and pair-fed on the basis of body weight semipurified isocaloric diets containing 20 or 5% casein. In Experiment 2, 30-d-old rats (n = 24) were divided randomly into three groups (n = 8) and pair-fed on the basis of body weight purified isonitrogenous and isocaloric diets (composed of amino acids) containing 0.0, 0.3 or 1.0% L-arginine. In both experiments, daily collection of urine was initiated 10 d after the start of pair-feeding. On d 17 after the pair-feeding was initiated, LPS (1 mg/kg body wt) was injected intraperitoneally into rats, and urine was collected daily for an additional 7 d. In Experiments 3 and 4, activities of constitutive and inducible NO synthases were measured in macrophages and various tissues from protein- or arginine-deficient rats (n = 6). Body weight was lower in rats fed the 5% casein diet or the 0.0 and 0.3% arginine diets than in those fed 20% casein or 1% arginine, respectively. Dietary protein or arginine deficiency decreased serum concentrations of arginine and urinary nitrate excretion before and after LPS treatment, indicating impaired constitutive and inducible NO synthesis. Protein malnutrition reduced constitutive and inducible NO synthase activities in brain, heart, jejunum, lung, skeletal muscle and spleen, and inducible NO synthase activity in macrophages. Because NO is a mediator of the immune response and is the endothelium-dependent relaxing factor, impaired NO synthesis may help explain immunodeficiency and cardiovascular dysfunction in protein- or arginine-deficient subjects.  (+info)

A low-protein isocaloric diet during gestation affects brain development and alters permanently cerebral cortex blood vessels in rat offspring. (5/465)

In humans, low birth weight is associated with nonfatal stroke, cardiovascular disease and diabetes at adulthood. The aim of this study was to investigate in rats the effect of early protein restriction, inducing low birth weight, on brain and endocrine pancreas vascularization at birth and to study if such alterations lasted until adulthood. Pregnant rats were fed either 20 or 8% protein isocaloric diets. Control newborns were nursed by their dams fed the 20% protein diet and low protein (LP) pups by dams fed either the 8 or 20% protein diet. The diets given during lactation were maintained until adulthood. The blood vessel density of cerebral cortex analyzed by morphometry in 3-d-old pups from dams fed the 8% protein diet was lower than in control (C). It remained lower at adulthood whether a LP or a C diet was given postnatally. Reduction of vascularization at adulthood induced by the LP diet limited to fetal life seems characteristic for the brain since vascularization of islets of Langerhans was reduced in neonates but normalized at adulthood by a C diet postnatally. Body and brain weights were lower in LP pups and adults. DNA concentration was lower in forebrain and higher in cerebellum in LP pups. In brain of LP adults, DNA, protein, cholesterol and phospholipid concentrations were lower and were restored at adulthood by a normal diet after birth. In conclusion, cerebral cortex of offspring exposed to a LP isocaloric diet during fetal development showed reduced vascularization which remained throughout life.  (+info)

Protein malnutrition affects the growth trajectories of the craniofacial skeleton in rats. (6/465)

To investigate the effects of protein malnutrition on a normal growth trajectory, we radiographed Rattus norvegicus from 22 d (weaning) and continuing past adult size. We took measurements from longitudinal radiographs of rats fed a control diet and littermates fed an isocaloric low protein experimental diet. A Gompertz model was fit to each individual rat for body weight and 22 measurements of the craniofacial skeleton, producing parameters that described the rate and timing of growth. We tested for differences in these parameters due to diet, sex and litter with a mixed-model three-way ANOVA. Allometric analysis examined the scaling relationships between and within various regions of the skull. For most measurements, final sizes predicted by the model were not significantly different between rats fed the two diets, although the differences in final measurements showed small, but significant differences in growth between rats in the two diet groups. The instantaneous initial rate of growth, maximum rate of growth and deceleration of growth were significantly higher in the control rats for every measurement. Rats fed the low protein diet grew for a significantly longer period of time. The shape of the neurocranium was relatively conserved between diet groups; however, rats fed the low protein diet had shorter and relatively wider skulls than the controls. These results suggest that functional demands of the viscerocranium were greater after birth, and that growth in this area was faster. The viscerocranium reached functional adult proportions earlier and was therefore more susceptible to epigenetic perturbations such as dietary protein level. Protein malnutrition did not affect many aspects of adult size, but strongly altered the growth trajectory to achieve that size.  (+info)

Impaired memory retention and decreased long-term potentiation in integrin-associated protein-deficient mice. (7/465)

Previously, we have demonstrated that integrin-associated protein (IAP) mRNA level is approximately fourfold higher in rats showing good retention performance (600 sec) than rats showing poor retention performance (< 80 sec) in an inhibitory avoidance learning paradigm. In the present study, we have used the gene-targeted IAP-deficient mice to further investigate the role of IAP involved in memory formation and hippocampal long-term potentiation (LTP) in vivo. Results revealed that there was a significant impairment in memory retention and a significant reduction in the magnitude of LTP in IAP-deficient mice when compared with the wild-type and heterozygote mice, whereas the wild-type and heterozygote animals did not show marked differences on these measures. Furthermore, the impairment in retention performance of IAP-deficient mice was not due to different sensitivities of these animals to the electric shock. When we examined locomotor activity and rotarod treadmill performance, no differences were observed among these three groups of animals either. Western blot analysis confirmed the lack of IAP protein in IAP-deficient mice, whereas IAP expression was similar in both the wild-type and heterozygote controls. These results together demonstrate that IAP plays an important role in the process of memory formation and synaptic plasticity in mice.  (+info)

Prenatal protein malnourished rats show changes in sleep/wake behavior as adults. (8/465)

Prenatal protein malnutrition significantly elevates brain levels of serotonin in rats, and these levels remain elevated throughout their lives. This biogenic amine is involved in the regulation of many physiological functions, including the normal sleep/wake cycle. The present study examined the effects of prenatal protein malnutrition on the sleep/wake cycle of freely moving adult rats. Six prenatally protein malnourished (6% casein) and 10 well-nourished (25% casein) male rats (90-120-day-old) were chronically implanted with a standard set of electrodes (to record cortical electroencephalogram, neck muscle electromyogram, electrooculogram, and hippocampal theta wave) to objectively measure states of sleep and wakefulness. Six-hour polygraphic recordings were made between 10.00 and 16.00 h; a time when the rats normally sleep. Prenatally malnourished rats spent 20% more time in slow wave sleep (SWS) compared to the well-nourished rats. The total percentage of time spent in rapid eye movement (REM) sleep was 61% less in prenatally malnourished rats compared to well-nourished control rats. These findings demonstrate the adverse consequences of prenatal protein malnutrition on the quality and quantity of adult sleep in rats. These sleep changes are potentially detrimental to normal social behavior and cognitive functions. Prenatally malnourished rats are an excellent animal model to study the role of endogenous serotonin in the regulation of the normal sleep/wake cycle.  (+info)

Protein deficiency, also known as protein-energy malnutrition (PEM), is a condition that occurs when an individual's diet fails to provide adequate amounts of protein and calories necessary for growth, maintenance, and repair of body tissues. Proteins are essential macromolecules that play critical roles in various bodily functions such as enzyme production, hormone regulation, immune response, and tissue structure.

There are two main types of protein deficiency disorders:

1. Marasmus: This is a chronic form of protein-energy malnutrition characterized by inadequate intake of both proteins and calories. It typically occurs in children from impoverished backgrounds who suffer from prolonged food deprivation. The body begins to break down its own tissues, including muscle mass, to meet energy demands, leading to severe weight loss, weakness, and delayed growth.

2. Kwashiorkor: This is an acute form of protein deficiency that primarily affects young children during weaning, when their diet transitions from breast milk to solid foods. While they may consume sufficient calories, these diets often lack adequate protein. Symptoms include edema (fluid accumulation in the abdomen and legs), distended bellies, skin lesions, hair changes, and impaired immune function.

In addition to these severe forms of protein deficiency, subclinical protein malnutrition can also occur when an individual's diet consistently provides insufficient protein levels over time. This can lead to reduced muscle mass, weakened immune function, and increased susceptibility to infections.

It is important to note that protein deficiency is relatively rare in developed countries where access to diverse food sources is generally available. However, specific populations such as elderly individuals, those with eating disorders, or those following restrictive diets may be at higher risk for developing protein deficiencies.

Peroxisomal multifunctional protein-2 (MFP2) is a key enzyme found within peroxisomes, which are membrane-bound organelles present in eukaryotic cells. MFP2 plays a crucial role in the breakdown of fatty acids and the detoxification of harmful substances within peroxisomes. It is involved in multiple steps of these processes, hence the term "multifunctional."

MFP2 catalyzes several reactions during the beta-oxidation of fatty acids, a process that breaks down long-chain fatty acids into shorter ones to generate energy for the cell. Specifically, MFP2 helps convert the breakdown products from earlier steps into forms that can enter subsequent steps of the beta-oxidation pathway.

Additionally, MFP2 is involved in the detoxification of molecules such as methanol and formaldehyde by facilitating their conversion to less harmful substances. This enzyme helps convert methanol into formic acid and then further metabolizes it, while formaldehyde is converted to formate.

Deficiencies in MFP2 or other peroxisomal proteins can lead to severe inherited metabolic disorders known as peroxisome biogenesis disorders (PBDs). These conditions can affect multiple organ systems and may cause neurological symptoms, developmental delays, vision loss, and hearing impairment.

Enoyl-CoA hydratase is an enzyme that catalyzes the second step in the fatty acid oxidation process, also known as the beta-oxidation pathway. The systematic name for this reaction is (3R)-3-hydroxyacyl-CoA dehydratase.

The function of Enoyl-CoA hydratase is to convert trans-2-enoyl-CoA into 3-hydroxyacyl-CoA by adding a molecule of water (hydration) across the double bond in the substrate. This reaction forms a chiral center, resulting in the production of an (R)-stereoisomer of 3-hydroxyacyl-CoA.

The gene that encodes for Enoyl-CoA hydratase is called ECHS1, and mutations in this gene can lead to a rare genetic disorder known as Enoyl-CoA Hydratase Deficiency or ECHS1 Deficiency. This condition affects the breakdown of fatty acids in the body and can cause neurological symptoms such as developmental delay, seizures, and movement disorders.

Nematode infections, also known as roundworm infections, are caused by various species of nematodes or roundworms. These parasitic worms can infect humans and animals, leading to a range of health problems depending on the specific type of nematode and the location of the infection within the body.

Common forms of nematode infections include:

1. Ascariasis: Caused by Ascaris lumbricoides, this infection occurs when people ingest the parasite's eggs through contaminated food or water. The larvae hatch in the small intestine, mature into adult worms, and can cause abdominal pain, nausea, vomiting, and diarrhea. In severe cases, the worms may obstruct the intestines or migrate to other organs, leading to potentially life-threatening complications.
2. Hookworm infections: These are caused by Ancylostoma duodenale and Necator americanus. The larvae penetrate the skin, usually through bare feet, and migrate to the small intestine, where they attach to the intestinal wall and feed on blood. Symptoms include abdominal pain, diarrhea, anemia, and protein loss.
3. Trichuriasis: Also known as whipworm infection, this is caused by Trichuris trichiura. The larvae hatch in the small intestine, mature into adult worms, and reside in the large intestine, causing abdominal pain, diarrhea, and rectal prolapse in severe cases.
4. Strongyloidiasis: Caused by Strongyloides stercoralis, this infection occurs when the larvae penetrate the skin, usually through contaminated soil, and migrate to the lungs and then the small intestine. Symptoms include abdominal pain, diarrhea, and skin rashes. In immunocompromised individuals, strongyloidiasis can lead to disseminated disease, which is potentially fatal.
5. Toxocariasis: This infection is caused by the roundworms Toxocara canis or Toxocara cati, found in dogs and cats, respectively. Humans become infected through ingestion of contaminated soil or undercooked meat. Symptoms include fever, cough, abdominal pain, and vision loss in severe cases.
6. Enterobiasis: Also known as pinworm infection, this is caused by Enterobius vermicularis. The larvae hatch in the small intestine, mature into adult worms, and reside in the large intestine, causing perianal itching and restlessness, especially at night.

Preventive measures include:

1. Proper hand hygiene: Wash hands with soap and water after using the toilet, changing diapers, handling pets or their feces, and before preparing or eating food.
2. Personal hygiene: Keep fingernails short and clean, avoid biting nails, and wear shoes in public areas, especially where soil may be contaminated with human or animal feces.
3. Food safety: Wash fruits and vegetables thoroughly, cook meat properly, and avoid consuming raw or undercooked meat, poultry, or fish.
4. Environmental cleanliness: Regularly clean surfaces that come into contact with food, such as countertops, cutting boards, and utensils. Dispose of trash properly and maintain a clean living environment.
5. Pet care: Keep pets healthy and regularly deworm them as recommended by a veterinarian. Pick up pet feces promptly to prevent contamination of the environment.
6. Public health measures: Implement public health interventions, such as regular waste disposal, sewage treatment, and vector control, to reduce the transmission of parasitic infections.

3-Hydroxyacyl CoA Dehydrogenases (3-HADs) are a group of enzymes that play a crucial role in the beta-oxidation of fatty acids. These enzymes catalyze the third step of the beta-oxidation process, which involves the oxidation of 3-hydroxyacyl CoA to 3-ketoacyl CoA. This reaction is an essential part of the energy-generating process that occurs in the mitochondria of cells and allows for the breakdown of fatty acids into smaller molecules, which can then be used to produce ATP, the primary source of cellular energy.

There are several different isoforms of 3-HADs, each with specific substrate preferences and tissue distributions. The most well-known isoform is the mitochondrial 3-hydroxyacyl CoA dehydrogenase (M3HD), which is involved in the oxidation of medium and long-chain fatty acids. Other isoforms include the short-chain 3-hydroxyacyl CoA dehydrogenase (SCHAD) and the long-chain 3-hydroxyacyl CoA dehydrogenase (LCHAD), which are involved in the oxidation of shorter and longer chain fatty acids, respectively.

Deficiencies in 3-HADs can lead to serious metabolic disorders, such as 3-hydroxyacyl-CoA dehydrogenase deficiency (3-HAD deficiency), which is characterized by the accumulation of toxic levels of 3-hydroxyacyl CoAs in the body. Symptoms of this disorder can include hypoglycemia, muscle weakness, cardiomyopathy, and developmental delays. Early diagnosis and treatment of 3-HAD deficiency are essential to prevent serious complications and improve outcomes for affected individuals.

17-Hydroxysteroid dehydrogenases (17-HSDs) are a group of enzymes that play a crucial role in steroid hormone biosynthesis. They are involved in the conversion of 17-ketosteroids to 17-hydroxy steroids or vice versa, by adding or removing a hydroxyl group (–OH) at the 17th carbon atom of the steroid molecule. This conversion is essential for the production of various steroid hormones, including cortisol, aldosterone, and sex hormones such as estrogen and testosterone.

There are several isoforms of 17-HSDs, each with distinct substrate specificities, tissue distributions, and functions:

1. 17-HSD type 1 (17-HSD1): This isoform primarily catalyzes the conversion of estrone (E1) to estradiol (E2), an active form of estrogen. It is mainly expressed in the ovary, breast, and adipose tissue.
2. 17-HSD type 2 (17-HSD2): This isoform catalyzes the reverse reaction, converting estradiol (E2) to estrone (E1). It is primarily expressed in the placenta, prostate, and breast tissue.
3. 17-HSD type 3 (17-HSD3): This isoform is responsible for the conversion of androstenedione to testosterone, an essential step in male sex hormone biosynthesis. It is predominantly expressed in the testis and adrenal gland.
4. 17-HSD type 4 (17-HSD4): This isoform catalyzes the conversion of dehydroepiandrosterone (DHEA) to androstenedione, an intermediate step in steroid hormone biosynthesis. It is primarily expressed in the placenta.
5. 17-HSD type 5 (17-HSD5): This isoform catalyzes the conversion of cortisone to cortisol, a critical step in glucocorticoid biosynthesis. It is predominantly expressed in the adrenal gland and liver.
6. 17-HSD type 6 (17-HSD6): This isoform catalyzes the conversion of androstenedione to testosterone, similar to 17-HSD3. However, it has a different substrate specificity and is primarily expressed in the ovary.
7. 17-HSD type 7 (17-HSD7): This isoform catalyzes the conversion of estrone (E1) to estradiol (E2), similar to 17-HSD1. However, it has a different substrate specificity and is primarily expressed in the ovary.
8. 17-HSD type 8 (17-HSD8): This isoform catalyzes the conversion of DHEA to androstenedione, similar to 17-HSD4. However, it has a different substrate specificity and is primarily expressed in the testis.
9. 17-HSD type 9 (17-HSD9): This isoform catalyzes the conversion of estrone (E1) to estradiol (E2), similar to 17-HSD1. However, it has a different substrate specificity and is primarily expressed in the placenta.
10. 17-HSD type 10 (17-HSD10): This isoform catalyzes the conversion of DHEA to androstenedione, similar to 17-HSD4. However, it has a different substrate specificity and is primarily expressed in the testis.
11. 17-HSD type 11 (17-HSD11): This isoform catalyzes the conversion of estrone (E1) to estradiol (E2), similar to 17-HSD1. However, it has a different substrate specificity and is primarily expressed in the placenta.
12. 17-HSD type 12 (17-HSD12): This isoform catalyzes the conversion of DHEA to androstenedione, similar to 17-HSD4. However, it has a different substrate specificity and is primarily expressed in the testis.
13. 17-HSD type 13 (17-HSD13): This isoform catalyzes the conversion of estrone (E1) to estradiol (E2), similar to 17-HSD1. However, it has a different substrate specificity and is primarily expressed in the placenta.
14. 17-HSD type 14 (17-HSD14): This isoform catalyzes the conversion of DHEA to androstenedione, similar to 17-HSD4. However, it has a different substrate specificity and is primarily expressed in the testis.
15. 17-HSD type 15 (17-HSD15): This isoform catalyzes the conversion of estrone (E1) to estradiol (E2), similar to 17-HSD1. However, it has a different substrate specificity and is primarily expressed in the placenta.
16. 17-HSD type 16 (17-HSD16): This isoform catalyzes the conversion of DHEA to androstenedione, similar to 17-HSD4. However, it has a different substrate specificity and is primarily expressed in the testis.
17. 17-HSD type 17 (17-HSD17): This isoform catalyzes the conversion of estrone (E1) to estradiol (E2), similar to 17-HSD1. However, it has a different substrate specificity and is primarily expressed in the placenta.
18. 17-HSD type 18 (17-HSD18): This isoform catalyzes the conversion of DHEA to androstenedione, similar to 17-HSD4. However, it has a different substrate specificity and is primarily expressed in the testis.
19. 17-HSD type 19 (17-HSD19): This isoform catalyzes the conversion of estrone (E1) to estradiol (E2), similar to 17-HSD1. However, it has a different substrate specificity and is primarily expressed in the placenta.
20. 17-HSD type 20 (17-HSD20): This isoform catalyzes the conversion of DHEA to androstenedione, similar to 17-HSD4. However, it has a different substrate specificity and is primarily expressed in the testis.
21. 17-HSD type 21 (17-HSD21): This isoform catalyzes the conversion of estrone (E1) to estradiol (E2), similar to 17-HSD1. However, it has a different substrate specificity and is primarily expressed in the placenta.
22. 17-HSD type 22 (17-HSD22): This isoform catalyzes the conversion of DHEA to androstenedione, similar to 17-HSD4. However, it has a different substrate specificity and is primarily expressed in the testis.
23. 17-HSD type 23 (17-HSD23): This isoform catalyzes the conversion of estrone (E1) to estradiol (E2), similar to 17-HSD1. However, it has a different substrate specificity and is primarily expressed in the placenta.
24. 17-HSD type 24 (17-HSD24): This isoform catalyzes the conversion of DHEA to androstenedione, similar to 17-HSD4. However, it has a different substrate specificity and is primarily expressed in the testis.
25. 17-HSD type 25 (17-HSD25): This isoform catalyzes the conversion of estrone (E1) to estradiol (E2), similar to 17-HSD1. However, it has a different substrate specificity and is primarily expressed in the placenta.
26. 17-HSD type 26 (17-HSD26): This isoform catalyzes the conversion of DHEA to androstenedione, similar to 17-HSD4. However

Dietary proteins are sources of protein that come from the foods we eat. Protein is an essential nutrient for the human body, required for various bodily functions such as growth, repair, and immune function. Dietary proteins are broken down into amino acids during digestion, which are then absorbed and used to synthesize new proteins in the body.

Dietary proteins can be classified as complete or incomplete based on their essential amino acid content. Complete proteins contain all nine essential amino acids that cannot be produced by the human body and must be obtained through the diet. Examples of complete protein sources include meat, poultry, fish, eggs, dairy products, soy, and quinoa.

Incomplete proteins lack one or more essential amino acids and are typically found in plant-based foods such as grains, legumes, nuts, and seeds. However, by combining different incomplete protein sources, it is possible to obtain all the essential amino acids needed for a complete protein diet. This concept is known as complementary proteins.

It's important to note that while dietary proteins are essential for good health, excessive protein intake can have negative effects on the body, such as increased stress on the kidneys and bones. Therefore, it's recommended to consume protein in moderation as part of a balanced and varied diet.

Protein-Energy Malnutrition (PEM) is a serious condition that occurs when an individual's diet does not provide enough protein or calories to meet their body's needs. It can lead to impaired physical and cognitive development, decreased immune function, increased susceptibility to infections, and in severe cases, death.

PEM can be caused by a variety of factors, including poverty, food insecurity, digestive disorders, chronic diseases, and eating disorders. The two most common forms of PEM are marasmus and kwashiorkor. Marasmus is characterized by extreme weight loss, muscle wasting, and decreased fat stores, while kwashiorkor is marked by swelling (edema), fluid accumulation in the abdomen, and a distended belly.

In medical terms, PEM is defined as a state of nutrient deficiency that results from a lack of adequate protein and energy intake over an extended period. It can be diagnosed through a combination of clinical assessment, medical history, physical examination, and laboratory tests. Treatment typically involves providing the individual with a balanced diet that is high in both protein and calories, as well as addressing any underlying medical conditions that may be contributing to their malnutrition.

Peroxisomal disorders are a group of inherited metabolic diseases caused by defects in the function or structure of peroxisomes, which are specialized subcellular organelles found in the cells of animals, plants, and humans. These disorders can affect various aspects of metabolism, including fatty acid oxidation, bile acid synthesis, and plasma cholesterol levels.

Peroxisomal disorders can be classified into two main categories: single peroxisomal enzyme deficiencies and peroxisome biogenesis disorders (PBDs). Single peroxisomal enzyme deficiencies are characterized by a defect in a specific enzyme found within the peroxisome, while PBDs are caused by problems with the formation or assembly of the peroxisome itself.

Examples of single peroxisomal enzyme deficiencies include X-linked adrenoleukodystrophy (X-ALD), Refsum disease, and acyl-CoA oxidase deficiency. PBDs include Zellweger spectrum disorders, such as Zellweger syndrome, neonatal adrenoleukodystrophy, and infantile Refsum disease.

Symptoms of peroxisomal disorders can vary widely depending on the specific disorder and the severity of the enzyme or biogenesis defect. They may include neurological problems, vision and hearing loss, developmental delays, liver dysfunction, and skeletal abnormalities. Treatment typically focuses on managing symptoms and addressing any underlying metabolic imbalances.

Nippostrongylus is a genus of parasitic nematode (roundworm) that primarily infects the gastrointestinal tract of various mammalian hosts, including rodents and primates. The most common species that infects humans is Nippostrongylus brasiliensis, although it's not a common human parasite in normal circumstances. It is more frequently used in laboratory settings as a model organism to study immunology and host-parasite interactions.

The adult worms live in the alveoli of the lungs, where they mature and reproduce, releasing eggs that are coughed up, swallowed, and then hatch in the small intestine. The larvae then mature into adults and complete the life cycle. Infections can cause symptoms such as coughing, wheezing, abdominal pain, and diarrhea, but these are typically mild in immunocompetent individuals.

It's worth noting that human infections with Nippostrongylus are rare and usually occur in people who have close contact with infected animals or who consume contaminated food or water. Proper sanitation and hygiene practices can help prevent infection.

Mitochondrial trifunctional protein (MTP) is a complex enzyme system located in the inner mitochondrial membrane of cells. It plays a crucial role in fatty acid oxidation, which is the process by which fatty acids are broken down to produce energy in the form of ATP.

MTP consists of three distinct enzymatic activities: long-chain enoyl-CoA hydratase, long-chain 3-hydroxyacyl-CoA dehydrogenase, and long-chain 3-ketoacyl-CoA thiolase. These enzymes work together to catalyze three consecutive reactions in the final steps of mitochondrial fatty acid oxidation, particularly for fatty acids with chain lengths greater than 12 carbons.

Deficiencies in MTP can lead to serious metabolic disorders known as mitochondrial trifunctional protein deficiency (MTPD). This rare genetic condition can cause a range of symptoms, including hypoketotic hypoglycemia, cardiomyopathy, skeletal muscle weakness, and neurological impairment. Early diagnosis and management of MTPD are essential to prevent severe complications and improve the patient's quality of life.

I'm sorry for any confusion, but "Hydro-Lyases" is not a recognized medical term or category in biochemistry. It seems like there might be a misunderstanding or a typo in the term.

In biochemistry, "lyases" are enzymes that catalyze the removal of groups from substrates by means other than hydrolysis or oxidation, often forming a double bond or a ring-forming reaction. They are classified and named based on the type of bond they break.

If you meant to ask about a specific enzyme or reaction, could you please provide more context or clarify the term? I'd be happy to help further with accurate information.

Heligmosomatoidea is a superfamily of nematodes (roundworms) that include several medically and veterinarily important parasitic genera. These parasites primarily infect the gastrointestinal tract of various mammalian hosts, including humans, rodents, and ruminants. Some well-known genera within Heligmosomatoidea are Heligmosomum, Nippostrongylus, and Syphacia.

The life cycles of these parasites typically involve eggs being passed in the host's feces, which then hatch into infective larvae in the environment. The larvae can then be ingested by a new host, either through contaminated food or water, or directly from the environment. Once inside the host, the larvae migrate to the gastrointestinal tract and mature into adults, where they lay eggs and continue the life cycle.

Infections with Heligmosomatoidea parasites can cause a range of symptoms in humans and animals, depending on the species and the severity of the infection. These may include abdominal pain, diarrhea, weight loss, and anemia. In some cases, these infections can also lead to more serious complications, particularly in immunocompromised individuals.

Prevention and control measures for Heligmosomatoidea infections typically involve good hygiene practices, such as washing hands thoroughly after using the toilet or handling contaminated soil, and cooking food thoroughly before eating. In addition, veterinarians may recommend deworming treatments for pets and livestock to help prevent the spread of these parasites.

Pyrantel is an anthelmintic medication used to treat and prevent gastrointestinal parasitic infections caused by roundworms, hookworms, and pinworms in humans and animals. It works by paralyzing the parasites, allowing them to be expelled from the body. Pyrantel is available in various formulations, including tablets, suspensions, and pastes, for human and veterinary use. Common brand names include Pin-X, Reese's Pinworm Medicine, and Strongid.

Hyperlipoproteinemias are medical conditions characterized by elevated levels of lipoproteins in the blood. Lipoproteins are particles that consist of proteins and lipids, which are responsible for transporting all fat molecules, such as cholesterol and triglycerides, around the body within the water outside cells. These lipids cannot dissolve in the blood, so they must be carried by these lipoprotein particles.

There are several types of hyperlipoproteinemias, classified based on the type of lipoprotein that is elevated and the pattern of inheritance. The most commonly recognized classification system is the Fredrickson classification, which includes five main types:

1. Type I - characterized by an excess of chylomicrons, a type of lipoprotein that carries dietary lipids, leading to extremely high levels of triglycerides in the blood. This rare disorder is usually caused by genetic mutations.
2. Type II - divided into two subtypes:
a. Type IIa - characterized by elevated LDL (low-density lipoprotein), or "bad" cholesterol, levels and often associated with premature cardiovascular disease. This condition can be caused by genetic factors, lifestyle choices, or both.
b. Type IIb - marked by increased levels of both LDL cholesterol and VLDL (very low-density lipoprotein), which leads to elevated triglycerides and cholesterol in the blood. This subtype can also be influenced by genetic factors, lifestyle choices, or both.
3. Type III - known as broad beta disease or remnant removal disease, this condition is characterized by an abnormal accumulation of remnant particles from VLDL and IDL (intermediate-density lipoprotein) metabolism, leading to increased levels of both cholesterol and triglycerides. This disorder can be caused by genetic mutations or secondary factors like diabetes, obesity, or hypothyroidism.
4. Type IV - characterized by elevated VLDL particles and high triglyceride levels in the blood. This condition is often associated with metabolic syndrome, obesity, diabetes, and alcohol consumption.
5. Type V - marked by increased VLDL and chylomicrons (lipoprotein particles that transport dietary lipids) in the blood, leading to extremely high triglyceride levels. This rare condition can be caused by genetic factors or secondary factors like diabetes, obesity, alcohol consumption, or uncontrolled lipid absorption.

It is important to note that these types are not mutually exclusive and can coexist in various combinations. Additionally, lifestyle choices such as diet, exercise, smoking, and alcohol consumption can significantly impact lipoprotein levels and contribute to the development of dyslipidemia (abnormal lipid levels).

Nitroanisole O-Demethylase is not a commonly used medical term, but it is related to the field of biochemistry and toxicology. It refers to an enzyme that catalyzes the removal of a methyl group (CH3) from a specific chemical compound called nitroanisole.

Nitroanisole is an organic compound consisting of a methoxy (O-CH3) group attached to the phenyl ring of a nitrobenzene molecule. The enzyme Nitroanisole O-Demethylase facilitates the biotransformation process by breaking down nitroanisole into other compounds, specifically into nitrophenol and formaldehyde.

This reaction is important in understanding how the body metabolizes and eliminates foreign substances like drugs or toxins. However, it is not a term typically used in clinical medicine for diagnosing or treating medical conditions.

Cholesteryl ester transfer proteins (CETP) are a group of plasma proteins that play a role in the transport and metabolism of lipids, particularly cholesteryl esters and triglycerides, between different lipoprotein particles in the bloodstream. These proteins facilitate the transfer of cholesteryl esters from high-density lipoproteins (HDL) to low-density lipoproteins (LDL) and very low-density lipoproteins (VLDL), while simultaneously promoting the transfer of triglycerides in the opposite direction, from VLDL and LDL to HDL.

The net effect of CETP activity is a decrease in HDL cholesterol levels and an increase in LDL and VLDL cholesterol levels. This shift in lipoprotein composition can contribute to the development of atherosclerosis and cardiovascular disease, as lower HDL cholesterol levels and higher LDL cholesterol levels are associated with increased risk for these conditions.

Inhibition of CETP has been investigated as a potential strategy for increasing HDL cholesterol levels and reducing the risk of cardiovascular disease. However, clinical trials with CETP inhibitors have shown mixed results, and further research is needed to determine their safety and efficacy in preventing cardiovascular events.

Serum albumin is the most abundant protein in human blood plasma, synthesized by the liver. It plays a crucial role in maintaining the oncotic pressure or colloid osmotic pressure of blood, which helps to regulate the fluid balance between the intravascular and extravascular spaces.

Serum albumin has a molecular weight of around 66 kDa and is composed of a single polypeptide chain. It contains several binding sites for various endogenous and exogenous substances, such as bilirubin, fatty acids, hormones, and drugs, facilitating their transport throughout the body. Additionally, albumin possesses antioxidant properties, protecting against oxidative damage.

Albumin levels in the blood are often used as a clinical indicator of liver function, nutritional status, and overall health. Low serum albumin levels may suggest liver disease, malnutrition, inflammation, or kidney dysfunction.

Caseins are a group of phosphoproteins found in the milk of mammals, including cows and humans. They are the major proteins in milk, making up about 80% of the total protein content. Caseins are characterized by their ability to form micelles, or tiny particles, in milk when it is mixed with calcium. This property allows caseins to help transport calcium and other minerals throughout the body.

Caseins are also known for their nutritional value, as they provide essential amino acids and are easily digestible. They are often used as ingredients in infant formula and other food products. Additionally, caseins have been studied for their potential health benefits, such as reducing the risk of cardiovascular disease and improving bone health. However, more research is needed to confirm these potential benefits.

Prealbumin, also known as transthyretin, is a protein produced primarily in the liver and circulates in the blood. It plays a role in transporting thyroid hormones and vitamin A throughout the body. Prealbumin levels are often used as an indicator of nutritional status and liver function. Low prealbumin levels may suggest malnutrition or inflammation, while increased levels can be seen in certain conditions like hyperthyroidism. It is important to note that prealbumin levels should be interpreted in conjunction with other clinical findings and laboratory tests for a more accurate assessment of a patient's health status.

A protein-restricted diet is a medical nutrition plan that limits the daily intake of protein. This type of diet may be recommended for individuals with certain kidney or liver disorders, as reducing protein intake can help decrease the workload on these organs and prevent further damage. The specific amount of protein restriction will depend on the individual's medical condition, overall health status, and prescribing healthcare professional's guidance.

It is essential to ensure that a protein-restricted diet is nutritionally adequate and balanced, providing sufficient calories, carbohydrates, fats, vitamins, and minerals. A registered dietitian or nutritionist should closely supervise the implementation of such a diet to prevent potential nutrient deficiencies and other related complications. In some cases, medical supplements may be necessary to meet the individual's nutritional requirements.

Individuals on a protein-restricted diet should avoid high-protein foods like meat, poultry, fish, eggs, dairy products, legumes, and nuts. Instead, they should focus on consuming low-protein or protein-free alternatives, such as fruits, vegetables, refined grains, and specific medical food products designed for individuals with special dietary needs.

It is crucial to consult a healthcare professional before starting any new diet, particularly one that restricts essential nutrients like protein. A healthcare provider can help determine if a protein-restricted diet is appropriate and ensure it is implemented safely and effectively.

Body weight is the measure of the force exerted on a scale or balance by an object's mass, most commonly expressed in units such as pounds (lb) or kilograms (kg). In the context of medical definitions, body weight typically refers to an individual's total weight, which includes their skeletal muscle, fat, organs, and bodily fluids.

Healthcare professionals often use body weight as a basic indicator of overall health status, as it can provide insights into various aspects of a person's health, such as nutritional status, metabolic function, and risk factors for certain diseases. For example, being significantly underweight or overweight can increase the risk of developing conditions like malnutrition, diabetes, heart disease, and certain types of cancer.

It is important to note that body weight alone may not provide a complete picture of an individual's health, as it does not account for factors such as muscle mass, bone density, or body composition. Therefore, healthcare professionals often use additional measures, such as body mass index (BMI), waist circumference, and blood tests, to assess overall health status more comprehensively.

A "knockout" mouse is a genetically engineered mouse in which one or more genes have been deleted or "knocked out" using molecular biology techniques. This allows researchers to study the function of specific genes and their role in various biological processes, as well as potential associations with human diseases. The mice are generated by introducing targeted DNA modifications into embryonic stem cells, which are then used to create a live animal. Knockout mice have been widely used in biomedical research to investigate gene function, disease mechanisms, and potential therapeutic targets.

Phospholipid transfer proteins (PLTPs) are a group of proteins found in the bloodstream that play a crucial role in the distribution and metabolism of phospholipids, which are key components of cell membranes. These proteins facilitate the transfer of phospholipids between different lipoprotein particles, such as high-density lipoproteins (HDL) and low-density lipoproteins (LDL), in a process known as non-vesicular lipid transport.

PLTPs can also modulate the size, composition, and function of these lipoprotein particles, which has implications for lipid metabolism, inflammation, and atherosclerosis. Additionally, PLTPs have been implicated in various physiological processes, including cell signaling, membrane trafficking, and host defense mechanisms.

It is worth noting that while PLTPs are important regulators of lipid metabolism, their precise role in human health and disease is still an area of active research.

Inborn errors of lipid metabolism refer to genetic disorders that affect the body's ability to break down and process lipids (fats) properly. These disorders are caused by defects in genes that code for enzymes or proteins involved in lipid metabolism. As a result, toxic levels of lipids or their intermediates may accumulate in the body, leading to various health issues, which can include neurological problems, liver dysfunction, muscle weakness, and cardiovascular disease.

There are several types of inborn errors of lipid metabolism, including:

1. Disorders of fatty acid oxidation: These disorders affect the body's ability to convert long-chain fatty acids into energy, leading to muscle weakness, hypoglycemia, and cardiomyopathy. Examples include medium-chain acyl-CoA dehydrogenase deficiency (MCAD) and very long-chain acyl-CoA dehydrogenase deficiency (VLCAD).
2. Disorders of cholesterol metabolism: These disorders affect the body's ability to process cholesterol, leading to an accumulation of cholesterol or its intermediates in various tissues. Examples include Smith-Lemli-Opitz syndrome and lathosterolosis.
3. Disorders of sphingolipid metabolism: These disorders affect the body's ability to break down sphingolipids, leading to an accumulation of these lipids in various tissues. Examples include Gaucher disease, Niemann-Pick disease, and Fabry disease.
4. Disorders of glycerophospholipid metabolism: These disorders affect the body's ability to break down glycerophospholipids, leading to an accumulation of these lipids in various tissues. Examples include rhizomelic chondrodysplasia punctata and abetalipoproteinemia.

Inborn errors of lipid metabolism are typically diagnosed through genetic testing and biochemical tests that measure the activity of specific enzymes or the levels of specific lipids in the body. Treatment may include dietary modifications, supplements, enzyme replacement therapy, or gene therapy, depending on the specific disorder and its severity.

The liver is a large, solid organ located in the upper right portion of the abdomen, beneath the diaphragm and above the stomach. It plays a vital role in several bodily functions, including:

1. Metabolism: The liver helps to metabolize carbohydrates, fats, and proteins from the food we eat into energy and nutrients that our bodies can use.
2. Detoxification: The liver detoxifies harmful substances in the body by breaking them down into less toxic forms or excreting them through bile.
3. Synthesis: The liver synthesizes important proteins, such as albumin and clotting factors, that are necessary for proper bodily function.
4. Storage: The liver stores glucose, vitamins, and minerals that can be released when the body needs them.
5. Bile production: The liver produces bile, a digestive juice that helps to break down fats in the small intestine.
6. Immune function: The liver plays a role in the immune system by filtering out bacteria and other harmful substances from the blood.

Overall, the liver is an essential organ that plays a critical role in maintaining overall health and well-being.

Organ size refers to the volume or physical measurement of an organ in the body of an individual. It can be described in terms of length, width, and height or by using specialized techniques such as imaging studies (like CT scans or MRIs) to determine the volume. The size of an organ can vary depending on factors such as age, sex, body size, and overall health status. Changes in organ size may indicate various medical conditions, including growths, inflammation, or atrophy.

Blood proteins, also known as serum proteins, are a group of complex molecules present in the blood that are essential for various physiological functions. These proteins include albumin, globulins (alpha, beta, and gamma), and fibrinogen. They play crucial roles in maintaining oncotic pressure, transporting hormones, enzymes, vitamins, and minerals, providing immune defense, and contributing to blood clotting.

Albumin is the most abundant protein in the blood, accounting for about 60% of the total protein mass. It functions as a transporter of various substances, such as hormones, fatty acids, and drugs, and helps maintain oncotic pressure, which is essential for fluid balance between the blood vessels and surrounding tissues.

Globulins are divided into three main categories: alpha, beta, and gamma globulins. Alpha and beta globulins consist of transport proteins like lipoproteins, hormone-binding proteins, and enzymes. Gamma globulins, also known as immunoglobulins or antibodies, are essential for the immune system's defense against pathogens.

Fibrinogen is a protein involved in blood clotting. When an injury occurs, fibrinogen is converted into fibrin, which forms a mesh to trap platelets and form a clot, preventing excessive bleeding.

Abnormal levels of these proteins can indicate various medical conditions, such as liver or kidney disease, malnutrition, infections, inflammation, or autoimmune disorders. Blood protein levels are typically measured through laboratory tests like serum protein electrophoresis (SPE) and immunoelectrophoresis (IEP).

Carrier proteins, also known as transport proteins, are a type of protein that facilitates the movement of molecules across cell membranes. They are responsible for the selective and active transport of ions, sugars, amino acids, and other molecules from one side of the membrane to the other, against their concentration gradient. This process requires energy, usually in the form of ATP (adenosine triphosphate).

Carrier proteins have a specific binding site for the molecule they transport, and undergo conformational changes upon binding, which allows them to move the molecule across the membrane. Once the molecule has been transported, the carrier protein returns to its original conformation, ready to bind and transport another molecule.

Carrier proteins play a crucial role in maintaining the balance of ions and other molecules inside and outside of cells, and are essential for many physiological processes, including nerve impulse transmission, muscle contraction, and nutrient uptake.

Wiskott-Aldrich Syndrome Protein (WASP) is a intracellular protein that plays a critical role in the regulation of actin cytoskeleton reorganization. It is encoded by the WAS gene, which is located on the X chromosome. WASP is primarily expressed in hematopoietic cells, including platelets, T cells, B cells, and natural killer cells.

WASP functions as a downstream effector of several signaling pathways that regulate actin dynamics, including the CDC42-MRCK pathway. When activated, WASP interacts with actin-related proteins (ARPs) and profilin to promote the nucleation and polymerization of actin filaments. This leads to changes in cell shape, motility, and cytoskeletal organization that are essential for various immune functions, such as T cell activation, antigen presentation, phagocytosis, and platelet aggregation.

Mutations in the WAS gene can lead to Wiskott-Aldrich syndrome (WAS), a rare X-linked recessive disorder characterized by microthrombocytopenia, eczema, recurrent infections, and increased risk of autoimmunity and lymphoma. The severity of the disease varies depending on the specific mutation and its impact on WASP function.

"Inbred strains of rats" are genetically identical rodents that have been produced through many generations of brother-sister mating. This results in a high degree of homozygosity, where the genes at any particular locus in the genome are identical in all members of the strain.

Inbred strains of rats are widely used in biomedical research because they provide a consistent and reproducible genetic background for studying various biological phenomena, including the effects of drugs, environmental factors, and genetic mutations on health and disease. Additionally, inbred strains can be used to create genetically modified models of human diseases by introducing specific mutations into their genomes.

Some commonly used inbred strains of rats include the Wistar Kyoto (WKY), Sprague-Dawley (SD), and Fischer 344 (F344) rat strains. Each strain has its own unique genetic characteristics, making them suitable for different types of research.

Multienzyme complexes are specialized protein structures that consist of multiple enzymes closely associated or bound together, often with other cofactors and regulatory subunits. These complexes facilitate the sequential transfer of substrates along a series of enzymatic reactions, also known as a metabolic pathway. By keeping the enzymes in close proximity, multienzyme complexes enhance reaction efficiency, improve substrate specificity, and maintain proper stoichiometry between different enzymes involved in the pathway. Examples of multienzyme complexes include the pyruvate dehydrogenase complex, the citrate synthase complex, and the fatty acid synthetase complex.

A heterozygote is an individual who has inherited two different alleles (versions) of a particular gene, one from each parent. This means that the individual's genotype for that gene contains both a dominant and a recessive allele. The dominant allele will be expressed phenotypically (outwardly visible), while the recessive allele may or may not have any effect on the individual's observable traits, depending on the specific gene and its function. Heterozygotes are often represented as 'Aa', where 'A' is the dominant allele and 'a' is the recessive allele.

Vitamin A deficiency (VAD) is a condition that occurs when there is a lack of vitamin A in the diet. This essential fat-soluble vitamin plays crucial roles in vision, growth, cell division, reproduction, and immune system regulation.

In its severe form, VAD leads to xerophthalmia, which includes night blindness (nyctalopia) and keratomalacia - a sight-threatening condition characterized by dryness of the conjunctiva and cornea, with eventual ulceration and perforation. Other symptoms of VAD may include Bitot's spots (foamy, triangular, white spots on the conjunctiva), follicular hyperkeratosis (goose bump-like bumps on the skin), and increased susceptibility to infections due to impaired immune function.

Vitamin A deficiency is most prevalent in developing countries where diets are often low in animal source foods and high in plant-based foods with low bioavailability of vitamin A. It primarily affects children aged 6 months to 5 years, pregnant women, and lactating mothers. Prevention strategies include dietary diversification, food fortification, and supplementation programs.

Glycoproteins are complex proteins that contain oligosaccharide chains (glycans) covalently attached to their polypeptide backbone. These glycans are linked to the protein through asparagine residues (N-linked) or serine/threonine residues (O-linked). Glycoproteins play crucial roles in various biological processes, including cell recognition, cell-cell interactions, cell adhesion, and signal transduction. They are widely distributed in nature and can be found on the outer surface of cell membranes, in extracellular fluids, and as components of the extracellular matrix. The structure and composition of glycoproteins can vary significantly depending on their function and location within an organism.

A diet, in medical terms, refers to the planned and regular consumption of food and drinks. It is a balanced selection of nutrient-rich foods that an individual eats on a daily or periodic basis to meet their energy needs and maintain good health. A well-balanced diet typically includes a variety of fruits, vegetables, whole grains, lean proteins, and low-fat dairy products.

A diet may also be prescribed for therapeutic purposes, such as in the management of certain medical conditions like diabetes, hypertension, or obesity. In these cases, a healthcare professional may recommend specific restrictions or modifications to an individual's regular diet to help manage their condition and improve their overall health.

It is important to note that a healthy and balanced diet should be tailored to an individual's age, gender, body size, activity level, and any underlying medical conditions. Consulting with a healthcare professional, such as a registered dietitian or nutritionist, can help ensure that an individual's dietary needs are being met in a safe and effective way.

A homozygote is an individual who has inherited the same allele (version of a gene) from both parents and therefore possesses two identical copies of that allele at a specific genetic locus. This can result in either having two dominant alleles (homozygous dominant) or two recessive alleles (homozygous recessive). In contrast, a heterozygote has inherited different alleles from each parent for a particular gene.

The term "homozygote" is used in genetics to describe the genetic makeup of an individual at a specific locus on their chromosomes. Homozygosity can play a significant role in determining an individual's phenotype (observable traits), as having two identical alleles can strengthen the expression of certain characteristics compared to having just one dominant and one recessive allele.

Deficiency diseases are a group of medical conditions that occur when an individual's diet lacks essential nutrients, such as vitamins and minerals. These diseases develop because the body needs these nutrients to function correctly, and without them, various bodily functions can become impaired, leading to disease.

Deficiency diseases can manifest in many different ways, depending on which nutrient is lacking. For example:

* Vitamin A deficiency can lead to night blindness and increased susceptibility to infectious diseases.
* Vitamin C deficiency can result in scurvy, a condition characterized by fatigue, swollen gums, joint pain, and anemia.
* Vitamin D deficiency can cause rickets in children, a disease that leads to weakened bones and skeletal deformities.
* Iron deficiency can result in anemia, a condition in which the blood lacks adequate healthy red blood cells.

Preventing deficiency diseases involves eating a balanced diet that includes a variety of foods from all the major food groups. In some cases, supplements may be necessary to ensure adequate nutrient intake, especially for individuals who have restricted diets or medical conditions that affect nutrient absorption.

A mutation is a permanent change in the DNA sequence of an organism's genome. Mutations can occur spontaneously or be caused by environmental factors such as exposure to radiation, chemicals, or viruses. They may have various effects on the organism, ranging from benign to harmful, depending on where they occur and whether they alter the function of essential proteins. In some cases, mutations can increase an individual's susceptibility to certain diseases or disorders, while in others, they may confer a survival advantage. Mutations are the driving force behind evolution, as they introduce new genetic variability into populations, which can then be acted upon by natural selection.

C57BL/6 (C57 Black 6) is an inbred strain of laboratory mouse that is widely used in biomedical research. The term "inbred" refers to a strain of animals where matings have been carried out between siblings or other closely related individuals for many generations, resulting in a population that is highly homozygous at most genetic loci.

The C57BL/6 strain was established in 1920 by crossing a female mouse from the dilute brown (DBA) strain with a male mouse from the black strain. The resulting offspring were then interbred for many generations to create the inbred C57BL/6 strain.

C57BL/6 mice are known for their robust health, longevity, and ease of handling, making them a popular choice for researchers. They have been used in a wide range of biomedical research areas, including studies of cancer, immunology, neuroscience, cardiovascular disease, and metabolism.

One of the most notable features of the C57BL/6 strain is its sensitivity to certain genetic modifications, such as the introduction of mutations that lead to obesity or impaired glucose tolerance. This has made it a valuable tool for studying the genetic basis of complex diseases and traits.

Overall, the C57BL/6 inbred mouse strain is an important model organism in biomedical research, providing a valuable resource for understanding the genetic and molecular mechanisms underlying human health and disease.

Pregnancy complications refer to any health problems that arise during pregnancy which can put both the mother and the baby at risk. These complications may occur at any point during the pregnancy, from conception until childbirth. Some common pregnancy complications include:

1. Gestational diabetes: a type of diabetes that develops during pregnancy in women who did not have diabetes before becoming pregnant.
2. Preeclampsia: a pregnancy complication characterized by high blood pressure and damage to organs such as the liver or kidneys.
3. Placenta previa: a condition where the placenta covers the cervix, which can cause bleeding and may require delivery via cesarean section.
4. Preterm labor: when labor begins before 37 weeks of gestation, which can lead to premature birth and other complications.
5. Intrauterine growth restriction (IUGR): a condition where the fetus does not grow at a normal rate inside the womb.
6. Multiple pregnancies: carrying more than one baby, such as twins or triplets, which can increase the risk of premature labor and other complications.
7. Rh incompatibility: a condition where the mother's blood type is different from the baby's, which can cause anemia and jaundice in the newborn.
8. Pregnancy loss: including miscarriage, stillbirth, or ectopic pregnancy, which can be emotionally devastating for the parents.

It is important to monitor pregnancy closely and seek medical attention promptly if any concerning symptoms arise. With proper care and management, many pregnancy complications can be treated effectively, reducing the risk of harm to both the mother and the baby.

Alpha 1-Antitrypsin (AAT) deficiency is a genetic disorder that results from insufficient levels of the protective protein AAT in the blood and lungs. This protein is produced by the liver and helps to protect the lungs from damage caused by inflammation and the action of enzymes, such as neutrophil elastase, that are released during the immune response.

In people with AAT deficiency, the lack of adequate AAT levels leads to an uncontrolled increase in neutrophil elastase activity, which can cause damage to lung tissue and result in emphysema, a condition characterized by shortness of breath, coughing, and wheezing. Additionally, some individuals with AAT deficiency may develop liver disease due to the accumulation of abnormal AAT proteins in liver cells.

There are different variants or genotypes associated with AAT deficiency, with the most common and severe form being the PiZZ genotype. This variant is caused by mutations in the SERPINA1 gene, which encodes for the AAT protein. Individuals who inherit two copies of this mutated gene (one from each parent) will have very low levels of AAT in their blood and are at increased risk of developing emphysema and liver disease.

Diagnosis of AAT deficiency typically involves measuring AAT levels in the blood and performing genetic testing to identify specific variants of the SERPINA1 gene. Treatment may include lifestyle modifications, such as smoking cessation, bronchodilators, and corticosteroids to manage lung symptoms, as well as augmentation therapy with intravenous infusions of AAT protein to help slow disease progression in individuals with severe deficiency. Liver transplantation may be considered for those with advanced liver disease.

Fatty acids are carboxylic acids with a long aliphatic chain, which are important components of lipids and are widely distributed in living organisms. They can be classified based on the length of their carbon chain, saturation level (presence or absence of double bonds), and other structural features.

The two main types of fatty acids are:

1. Saturated fatty acids: These have no double bonds in their carbon chain and are typically solid at room temperature. Examples include palmitic acid (C16:0) and stearic acid (C18:0).
2. Unsaturated fatty acids: These contain one or more double bonds in their carbon chain and can be further classified into monounsaturated (one double bond) and polyunsaturated (two or more double bonds) fatty acids. Examples of unsaturated fatty acids include oleic acid (C18:1, monounsaturated), linoleic acid (C18:2, polyunsaturated), and alpha-linolenic acid (C18:3, polyunsaturated).

Fatty acids play crucial roles in various biological processes, such as energy storage, membrane structure, and cell signaling. Some essential fatty acids cannot be synthesized by the human body and must be obtained through dietary sources.

Vitamin B12 deficiency is a condition characterized by insufficient levels of vitamin B12 in the body, leading to impaired production of red blood cells, nerve function damage, and potential neurological complications. Vitamin B12 is an essential nutrient that plays a crucial role in DNA synthesis, fatty acid metabolism, and maintaining the health of the nervous system.

The medical definition of vitamin B12 deficiency includes:

1. Reduced serum or whole blood vitamin B12 concentrations (typically below 200 pg/mL or 145 pmol/L)
2. Presence of clinical symptoms and signs, such as:
* Fatigue, weakness, and lethargy
* Pale skin, shortness of breath, and heart palpitations due to anemia (megaloblastic or macrocytic anemia)
* Neurological symptoms like numbness, tingling, or burning sensations in the hands and feet (peripheral neuropathy), balance problems, confusion, memory loss, and depression
3. Laboratory findings consistent with deficiency, such as:
* Increased mean corpuscular volume (MCV) of red blood cells
* Reduced numbers of red and white blood cells and platelets in severe cases
* Elevated homocysteine and methylmalonic acid levels in the blood due to impaired metabolism

The most common causes of vitamin B12 deficiency include dietary insufficiency (common in vegetarians and vegans), pernicious anemia (an autoimmune condition affecting intrinsic factor production), gastrointestinal disorders (such as celiac disease, Crohn's disease, or gastric bypass surgery), and certain medications that interfere with vitamin B12 absorption.

Untreated vitamin B12 deficiency can lead to severe complications, including irreversible nerve damage, cognitive impairment, and increased risk of cardiovascular diseases. Therefore, prompt diagnosis and treatment are essential for preventing long-term health consequences.

Pregnancy is a physiological state or condition where a fertilized egg (zygote) successfully implants and grows in the uterus of a woman, leading to the development of an embryo and finally a fetus. This process typically spans approximately 40 weeks, divided into three trimesters, and culminates in childbirth. Throughout this period, numerous hormonal and physical changes occur to support the growing offspring, including uterine enlargement, breast development, and various maternal adaptations to ensure the fetus's optimal growth and well-being.

A phenotype is the physical or biochemical expression of an organism's genes, or the observable traits and characteristics resulting from the interaction of its genetic constitution (genotype) with environmental factors. These characteristics can include appearance, development, behavior, and resistance to disease, among others. Phenotypes can vary widely, even among individuals with identical genotypes, due to differences in environmental influences, gene expression, and genetic interactions.

Vitamin D deficiency is a condition characterized by insufficient levels of vitamin D in the body, typically defined as a serum 25-hydroxyvitamin D level below 20 nanograms per milliliter (ng/mL) or 50 nanomoles per liter (nmol/L). Vitamin D is an essential fat-soluble vitamin that plays a crucial role in maintaining healthy bones and teeth by regulating the absorption of calcium and phosphorus. It also has various other functions in the body, including modulation of cell growth, immune function, and neuromuscular activity.

Vitamin D can be obtained through dietary sources such as fatty fish, fortified dairy products, and supplements, but the majority of vitamin D is produced in the skin upon exposure to sunlight. Deficiency can occur due to inadequate dietary intake, insufficient sun exposure, or impaired absorption or metabolism of vitamin D.

Risk factors for vitamin D deficiency include older age, darker skin tone, obesity, malabsorption syndromes, liver or kidney disease, and certain medications. Symptoms of vitamin D deficiency can be subtle and nonspecific, such as fatigue, bone pain, muscle weakness, and mood changes. However, prolonged deficiency can lead to more severe health consequences, including osteoporosis, osteomalacia, and increased risk of fractures.

Animal disease models are specialized animals, typically rodents such as mice or rats, that have been genetically engineered or exposed to certain conditions to develop symptoms and physiological changes similar to those seen in human diseases. These models are used in medical research to study the pathophysiology of diseases, identify potential therapeutic targets, test drug efficacy and safety, and understand disease mechanisms.

The genetic modifications can include knockout or knock-in mutations, transgenic expression of specific genes, or RNA interference techniques. The animals may also be exposed to environmental factors such as chemicals, radiation, or infectious agents to induce the disease state.

Examples of animal disease models include:

1. Mouse models of cancer: Genetically engineered mice that develop various types of tumors, allowing researchers to study cancer initiation, progression, and metastasis.
2. Alzheimer's disease models: Transgenic mice expressing mutant human genes associated with Alzheimer's disease, which exhibit amyloid plaque formation and cognitive decline.
3. Diabetes models: Obese and diabetic mouse strains like the NOD (non-obese diabetic) or db/db mice, used to study the development of type 1 and type 2 diabetes, respectively.
4. Cardiovascular disease models: Atherosclerosis-prone mice, such as ApoE-deficient or LDLR-deficient mice, that develop plaque buildup in their arteries when fed a high-fat diet.
5. Inflammatory bowel disease models: Mice with genetic mutations affecting intestinal barrier function and immune response, such as IL-10 knockout or SAMP1/YitFc mice, which develop colitis.

Animal disease models are essential tools in preclinical research, but it is important to recognize their limitations. Differences between species can affect the translatability of results from animal studies to human patients. Therefore, researchers must carefully consider the choice of model and interpret findings cautiously when applying them to human diseases.

Folic Acid Deficiency is a condition characterized by insufficient levels of folic acid (Vitamin B9) in the body. Folic acid plays an essential role in the synthesis of DNA and RNA, the production of red blood cells, and the prevention of neural tube defects during fetal development.

A deficiency in folic acid can lead to a variety of health issues, including:
- Megaloblastic anemia: A type of anemia characterized by large, structurally abnormal, immature red blood cells (megaloblasts) that are unable to function properly. This results in fatigue, weakness, shortness of breath, and a pale appearance.
- Neural tube defects: In pregnant women, folic acid deficiency can increase the risk of neural tube defects, such as spina bifida and anencephaly, in the developing fetus.
- Developmental delays and neurological disorders: In infants and children, folic acid deficiency during pregnancy can lead to developmental delays, learning difficulties, and neurological disorders.
- Increased risk of cardiovascular disease: Folate plays a role in maintaining healthy homocysteine levels. Deficiency can result in elevated homocysteine levels, which is an independent risk factor for cardiovascular disease.

Folic acid deficiency can be caused by various factors, including poor dietary intake, malabsorption syndromes (such as celiac disease or Crohn's disease), pregnancy, alcoholism, certain medications (like methotrexate and phenytoin), and genetic disorders affecting folate metabolism. To prevent or treat folic acid deficiency, dietary supplementation with folic acid is often recommended, especially for pregnant women and individuals at risk of deficiency.

Fibroblasts are specialized cells that play a critical role in the body's immune response and wound healing process. They are responsible for producing and maintaining the extracellular matrix (ECM), which is the non-cellular component present within all tissues and organs, providing structural support and biochemical signals for surrounding cells.

Fibroblasts produce various ECM proteins such as collagens, elastin, fibronectin, and laminins, forming a complex network of fibers that give tissues their strength and flexibility. They also help in the regulation of tissue homeostasis by controlling the turnover of ECM components through the process of remodeling.

In response to injury or infection, fibroblasts become activated and start to proliferate rapidly, migrating towards the site of damage. Here, they participate in the inflammatory response, releasing cytokines and chemokines that attract immune cells to the area. Additionally, they deposit new ECM components to help repair the damaged tissue and restore its functionality.

Dysregulation of fibroblast activity has been implicated in several pathological conditions, including fibrosis (excessive scarring), cancer (where they can contribute to tumor growth and progression), and autoimmune diseases (such as rheumatoid arthritis).

IgA deficiency is a condition characterized by significantly reduced levels or absence of secretory immunoglobulin A (IgA), an important antibody that plays a crucial role in the immune function of mucous membranes lining the respiratory and gastrointestinal tracts. IgA helps to prevent the attachment and multiplication of pathogens, such as bacteria and viruses, on these surfaces.

In individuals with IgA deficiency, the lack of adequate IgA levels makes them more susceptible to recurrent infections, allergies, and autoimmune disorders. The condition can be asymptomatic or may present with various symptoms, such as respiratory tract infections, gastrointestinal issues, and chronic sinusitis. IgA deficiency is typically diagnosed through blood tests that measure the immunoglobulin levels. While there is no cure for IgA deficiency, treatment focuses on managing symptoms and preventing infections through medications, immunizations, and lifestyle modifications.

Thiamine deficiency, also known as beriberi, is a condition that results from inadequate intake or impaired absorption of thiamine (vitamin B1), which is essential for energy metabolism and nerve function. This deficiency can lead to various symptoms such as peripheral neuropathy, muscle weakness, heart failure, and in severe cases, Wernicke-Korsakoff syndrome, a neurological disorder associated with alcoholism. Thiamine deficiency is commonly found in populations with poor nutrition, alcohol dependence, and gastrointestinal disorders affecting nutrient absorption.

The spleen is an organ in the upper left side of the abdomen, next to the stomach and behind the ribs. It plays multiple supporting roles in the body:

1. It fights infection by acting as a filter for the blood. Old red blood cells are recycled in the spleen, and platelets and white blood cells are stored there.
2. The spleen also helps to control the amount of blood in the body by removing excess red blood cells and storing platelets.
3. It has an important role in immune function, producing antibodies and removing microorganisms and damaged red blood cells from the bloodstream.

The spleen can be removed without causing any significant problems, as other organs take over its functions. This is known as a splenectomy and may be necessary if the spleen is damaged or diseased.

"Energy intake" is a medical term that refers to the amount of energy or calories consumed through food and drink. It is an important concept in the study of nutrition, metabolism, and energy balance, and is often used in research and clinical settings to assess an individual's dietary habits and health status.

Energy intake is typically measured in kilocalories (kcal) or joules (J), with one kcal equivalent to approximately 4.184 J. The recommended daily energy intake varies depending on factors such as age, sex, weight, height, physical activity level, and overall health status.

It's important to note that excessive energy intake, particularly when combined with a sedentary lifestyle, can lead to weight gain and an increased risk of chronic diseases such as obesity, type 2 diabetes, and cardiovascular disease. On the other hand, inadequate energy intake can lead to malnutrition, decreased immune function, and other health problems. Therefore, it's essential to maintain a balanced energy intake that meets individual nutritional needs while promoting overall health and well-being.

Messenger RNA (mRNA) is a type of RNA (ribonucleic acid) that carries genetic information copied from DNA in the form of a series of three-base code "words," each of which specifies a particular amino acid. This information is used by the cell's machinery to construct proteins, a process known as translation. After being transcribed from DNA, mRNA travels out of the nucleus to the ribosomes in the cytoplasm where protein synthesis occurs. Once the protein has been synthesized, the mRNA may be degraded and recycled. Post-transcriptional modifications can also occur to mRNA, such as alternative splicing and addition of a 5' cap and a poly(A) tail, which can affect its stability, localization, and translation efficiency.

Cholesterol is a type of lipid (fat) molecule that is an essential component of cell membranes and is also used to make certain hormones and vitamins in the body. It is produced by the liver and is also obtained from animal-derived foods such as meat, dairy products, and eggs.

Cholesterol does not mix with blood, so it is transported through the bloodstream by lipoproteins, which are particles made up of both lipids and proteins. There are two main types of lipoproteins that carry cholesterol: low-density lipoproteins (LDL), also known as "bad" cholesterol, and high-density lipoproteins (HDL), also known as "good" cholesterol.

High levels of LDL cholesterol in the blood can lead to a buildup of cholesterol in the walls of the arteries, increasing the risk of heart disease and stroke. On the other hand, high levels of HDL cholesterol are associated with a lower risk of these conditions because HDL helps remove LDL cholesterol from the bloodstream and transport it back to the liver for disposal.

It is important to maintain healthy levels of cholesterol through a balanced diet, regular exercise, and sometimes medication if necessary. Regular screening is also recommended to monitor cholesterol levels and prevent health complications.

A base sequence in the context of molecular biology refers to the specific order of nucleotides in a DNA or RNA molecule. In DNA, these nucleotides are adenine (A), guanine (G), cytosine (C), and thymine (T). In RNA, uracil (U) takes the place of thymine. The base sequence contains genetic information that is transcribed into RNA and ultimately translated into proteins. It is the exact order of these bases that determines the genetic code and thus the function of the DNA or RNA molecule.

Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency is a genetic disorder that affects the normal functioning of an enzyme called G6PD. This enzyme is found in red blood cells and plays a crucial role in protecting them from damage.

In people with G6PD deficiency, the enzyme's activity is reduced or absent, making their red blood cells more susceptible to damage and destruction, particularly when they are exposed to certain triggers such as certain medications, infections, or foods. This can lead to a condition called hemolysis, where the red blood cells break down prematurely, leading to anemia, jaundice, and in severe cases, kidney failure.

G6PD deficiency is typically inherited from one's parents in an X-linked recessive pattern, meaning that males are more likely to be affected than females. While there is no cure for G6PD deficiency, avoiding triggers and managing symptoms can help prevent complications.

In the field of medicine, "time factors" refer to the duration of symptoms or time elapsed since the onset of a medical condition, which can have significant implications for diagnosis and treatment. Understanding time factors is crucial in determining the progression of a disease, evaluating the effectiveness of treatments, and making critical decisions regarding patient care.

For example, in stroke management, "time is brain," meaning that rapid intervention within a specific time frame (usually within 4.5 hours) is essential to administering tissue plasminogen activator (tPA), a clot-busting drug that can minimize brain damage and improve patient outcomes. Similarly, in trauma care, the "golden hour" concept emphasizes the importance of providing definitive care within the first 60 minutes after injury to increase survival rates and reduce morbidity.

Time factors also play a role in monitoring the progression of chronic conditions like diabetes or heart disease, where regular follow-ups and assessments help determine appropriate treatment adjustments and prevent complications. In infectious diseases, time factors are crucial for initiating antibiotic therapy and identifying potential outbreaks to control their spread.

Overall, "time factors" encompass the significance of recognizing and acting promptly in various medical scenarios to optimize patient outcomes and provide effective care.

Magnesium deficiency, also known as hypomagnesemia, is a condition characterized by low levels of magnesium in the blood. Magnesium is an essential mineral that plays a crucial role in many bodily functions, including muscle and nerve function, heart rhythm, bone strength, and immune system regulation.

Hypomagnesemia can occur due to various factors, such as poor dietary intake, malabsorption syndromes, chronic alcoholism, diabetes, certain medications (such as diuretics), and excessive sweating or urination. Symptoms of magnesium deficiency may include muscle cramps, tremors, weakness, heart rhythm abnormalities, seizures, and mental status changes.

It is important to note that mild magnesium deficiency may not cause any symptoms, and the diagnosis typically requires blood tests to measure magnesium levels. Treatment for hypomagnesemia usually involves oral or intravenous magnesium supplementation, along with addressing the underlying causes of the deficiency.

There are two main types of protein C mutations that lead to protein C deficiency: Type I: Quantitative defects of protein C ( ... and protein C deficiency has been linked to over 160 mutations to date. Therefore, DNA testing for protein C deficiency is ... Patients with Protein C deficiency are at an increased risk of developing skin necrosis while on warfarin. Protein C has a ... a protein C antigen assay can be considered to determine the deficiency subtype (Type I or Type II). In type I deficiencies, ...
"Protein S Deficiency. Learn about Protein S Deficiency , Patient". Patient. Retrieved 2016-10-16. "Protein S Deficiency: ... decreased free protein S levels (normal total protein S levels) In terms of treatment for protein S deficiency the following ... In regards to the mechanism of protein S deficiency, Protein S is made in liver cells and the Endothelium. Protein S is a ... "Protein S Deficiency". Cleveland Clinic. Retrieved 7 February 2023. "Congenital protein C or S deficiency: MedlinePlus Medical ...
... and the C-terminal sterol carrier protein 2 (SDR). The DBP protein (79kDa) also known as "multifunctional protein 2", " ... D-Bifunctional protein deficiency is an autosomal recessive peroxisomal fatty acid oxidation disorder. Peroxisomal disorders ... Möller G, van Grunsven EG, Wanders RJ, Adamski J (January 2001). "Molecular basis of D-bifunctional protein deficiency". Mol. ... Buoni S, Zannolli R, Waterham H, Wanders R, Fois A (January 2007). "D-bifunctional protein deficiency associated with drug ...
... (MTP deficiency or MTPD) is an autosomal recessive fatty acid oxidation disorder ... Trifunctional protein deficiency is characterized by decreased activity of all 3 enzymes. Clinically, trifunctional protein ... protein deficiency at Wikimedia Commons Scholia has a topic profile for Mitochondrial trifunctional protein deficiency. ( ... "Orphanet: Mitochondrial trifunctional protein deficiency". www.orpha.net. Retrieved 2016-11-12. Solish JO, Singh RH (2002). " ...
CREB-binding protein, also known as CREBBP or CBP, is a protein that is encoded by the CREBBP gene in humans. The CREB protein ... Proteins RbAp48 is a key player in the assembly of nucleosomes. RbAp48 protein is a subunit of the chromatin-assembly factor-1 ... RbAp48 protein is also found in numerous other protein complexes for regulation of chromatin structure. Studies show that ... Zhang, Q.; Vo, N.; Goodman, R. H. (2000). "Histone Binding Protein RbAp48 Interacts with a Complex of CREB Binding Protein and ...
... is a rare genetic condition caused by the absence of LPS-responsive beige- ... The LBRA gene is located on the long arm of chromosome 4 (4q31.3).[citation needed] LBRA protein interacts with the protein ... The extended phenotype of LPS-responsive beige-like anchor protein (LRBA) deficiency. J Allergy Clin Immunol 137(1):223-230 ... Deleterious mutations in LRBA are associated with a syndrome of immune deficiency and autoimmunity. Am J Hum Genet 90: 986-1001 ...
Protein deficiency (not certain): A shortage of proteins involved in biotin homeostasis can cause biotin deficiency. The main ... Biotinidase deficiency Holocarboxylase synthetase deficiency Multiple carboxylase deficiency Durance TD (1991). "Residual Avid ... Velázquez A (1997). "Biotin deficiency in protein-energy malnutrition: implications for nutritional homeostasis and ... ISBN 978-0-07-913035-8. GeneReviews/NCBI/NIH/UW entry on Biotinidase deficiency OMIM entries on Biotinidasa deficiency ( ...
July 2017). "CD55 Deficiency, Early-Onset Protein-Losing Enteropathy, and Thrombosis". The New England Journal of Medicine. 377 ... March 2019). "Eculizumab Is Safe and Effective as a Long-term Treatment for Protein-losing Enteropathy Due to CD55 Deficiency ... CD55 deficiency, also called DAF deficiency or CHAPLE syndrome, is a rare genetic disorder of the immune system. CHAPLE stands ... The protein CD55 (also called decay-accelerating factor) helps to regulate the complement cascade, part of the innate immune ...
Nitrogen fixation Protein deficiency "Compost Fundamentals: Compost Needs - Carbon Nitrogen Relationships". Archived from the ... Nitrogen deficiency is a deficiency of nitrogen in plants. This can occur when organic matter with high carbon content, such as ... Flowering, fruitings, protein and starch contents are reduced. Reduction in protein results in stunted growth and dormant ... Nevertheless, plants are reported to show nitrogen deficiency symptoms at different parts. For example, Nitrogen deficiency of ...
G. J. Jha; M. G. Deo & V. Ramalingaswami (December 1968). "Bone growth in protein deficiency. A study in rhesus monkeys". Am J ... G. J. Jha; M. G. Deo & V. Ramalingaswami (December 1968). "Bone growth in protein deficiency. A study in rhesus monkeys". Am J ... Deo MG, Sood SK, Ramalingaswami V (1965). "Experimental Protein Deficiency". Arch. Pathol. 80: 14-23. V. Ramalingaswami; T. A. ... Deo MG, Sood SK, Ramalingaswami V (1965). Experimental Protein Deficiency. pp. 14-23. ISBN 9780323153171. {{cite book}}: , ...
1989). "Familial protein S deficiency with a variant protein S molecule in plasma and platelets". Blood. 74 (1): 213-21. doi: ... Protein S is partly homologous to other vitamin K-dependent plasma coagulation proteins, such as protein C and factors VII, IX ... Dahlbäck B (1991). "Protein S and C4b-binding protein: components involved in the regulation of the protein C anticoagulant ... protein S is encoded by the PROS1 gene. Protein S plays a role in coagulation. Protein S is named for Seattle, Washington, ...
Models for protein deficiency. American Journal of Clinical Nutrition (1978). "Autoregulatory Homeostatic Nature of Energy ... "Size and Nature of the Protein Gap", Nutrition Review (1970). "The Protein Problem - Its Size and Nature", Journal of the Royal ... He also developed methods for measuring the size and nature of the protein gap. His other major contributions included applying ... paying attention to intra-individual variability that was found to be more than the inter-individual variability in protein or ...
Griffin JH, Evatt B, Zimmerman TS, Kleiss AJ, Wideman C (1981). "Deficiency of protein C in congenital thrombotic disease". J. ... Shahidi, Nasrollah T.; Diamond, Louis K; Shwachman, Harry (October 1961). "Anemia associated with protein deficiency". The ... February 2009). "Identification of mutations in the ribosomal protein L5 (RPL5) and ribosomal protein L11 (RPL11) genes in ... "Folate-deficiency anemia". National Center for Biotechnology Information. U.S. National Library of Medicine. 31 January 2010. ...
Manya H, Akasaka-Manya K, Endo T (July 2010). "Klotho protein deficiency and aging". Geriatrics & Gerontology International. 10 ... Vitamin D deficiency is found worldwide in the elderly and remains common in children and adults. Deficiency results in ... where it is bound to an α-globulin carrier protein named the vitamin D-binding protein. Calcifediol is transported to the ... a review of the roles of phospholipase A2 activating protein and Ca(2+)/calmodulin-dependent protein kinase II". The Journal of ...
During the signaling process, p14 protein will recruit the MP1 protein to the endosomal membrane, and the MP1 protein will then ... Research has shown p14 adaptor protein is crucial for the proper localization of MP1 protein, a scaffold protein important for ... This will affect the proliferation of neutrophils, explaining the neutropenia observed in p14 deficiency patients. P14 protein ... which will decrease the translation of p14 protein, leading to p14 deficiency. Further studies can be conducted for a more ...
"Pyruvate dehydrogenase E3 binding protein (protein X) deficiency". Developmental Medicine and Child Neurology. 48 (9): 756-60. ... E3 binding protein also known as pyruvate dehydrogenase protein X component, mitochondrial is a protein that in humans is ... "Pyruvate dehydrogenase E3 binding protein (protein X) deficiency". Developmental Medicine and Child Neurology. 48 (9): 756-60. ... The protein encoded by the human PDHX gene, also known as E3 binding protein (E3BP), is part of the pyruvate dehydrogenase ...
Protein energy malnutrition is often seen in VAD; suppressed synthesis of retinol binding protein (RBP) due to protein ... "WHO Vitamin A deficiency , Micronutrient deficiencies". Archived from the original on 2019-08-16. Retrieved 2008-03-03. Latham ... Xerophthalmia, keratomalacia, and complete blindness can follow if the deficiency is more severe. Vitamin A deficiency is the ... Other causes of vitamin A deficiency are inadequate intake, fat malabsorption, or liver disorders. Deficiency impairs immunity ...
... also caused by a deficiency of Vitamin D); and kwashiorkor (caused by severe protein deficiency)." (See Mintz, Steven. " ... caused by a niacin deficiency); tetany (caused by deficiencies of calcium, magnesium, and Vitamin D); rickets ( ... Common conditions among enslaved populations included: beriberi (caused by a deficiency of thiamine); pellagra ( ...
"Poor Lands Do Little on Protein Deficiency". The New York Times - via NYTimes.com.{{cite news}}: CS1 maint: multiple names: ... with the aim of reducing iron deficiency anemia without requiring changes in dietary practices. When famine struck India in ...
Smith DB, Ens GE (March 1987). "Protein C deficiency: a cause of amaurosis fugax?". J. Neurol. Neurosurg. Psychiatry. 50 (3): ... Periarteritis nodosa Eosinophilic vasculitis Hyperviscosity syndrome Polycythemia Hypercoagulability Protein C deficiency ...
A deficiency of this protein causes Salla disease. and Infantile Sialic Acid Storage Disease (ISSD). The gene for HP59 contains ... Member 5, also known as SLC17A5 or sialin is a lysosomal membrane sialic acid transport protein which in humans is encoded by ... Sialin, also known as H(+)/nitrate cotransporter and H(+)/sialic acid cotransporter, is a protein which in humans is encoded by ... 2002). "Identification of a novel membrane protein, HP59, with therapeutic potential as a target of tumor angiogenesis". Clin. ...
Thomson, Datin Lady; Ruiz, Elva; Bakar, Mangisi (September 1964). "Vitamin A and protein deficiency in Malayan children". ... Thomson, F. Adam (March 1949). "Dietary deficiencies in children in the island of Viti Levu, Fiji". Transactions of the Royal ... ASEAN sub-committee on protein. "Senarai Penuh Penerima Darjah Kebesaran, Bintang dan Pingat Persekutuan Tahun 1958" (PDF). " ...
"CD55 Deficiency, Early-Onset Protein-Losing Enteropathy, and Thrombosis". New England Journal of Medicine. 377 (1): 52-61. doi: ... "Eculizumab Is Safe and Effective as a Long-term Treatment for Protein-losing Enteropathy Due to CD55 Deficiency". Journal of ... His lab's 2017 identification of CD55 deficiency (which they named CHAPLE disease) led to the discovery of a safe and highly ... Wan, Fengyi; Lenardo, Michael J. (2009-10-01). "Specification of DNA Binding Activity of NF-κB Proteins". Cold Spring Harbor ...
Overactivity of MACPF proteins can also cause disease. Most notably, deficiency of the MAC inhibitor CD59 results in an ... Protein families, Membrane proteins, Transmembrane proteins, Transmembrane transporters, Transport proteins, Integral membrane ... Deficiency of either protein can result in human disease. Structural studies reveal that MACPF domains are related to ... Other proteins that bind to the MAC include C8γ. This protein belongs to the lipocalin family and interacts with C8α. The ...
Hepburn's limbs began to swell with protein deficiency oedema. Finally, on 7 November, help arrived with the arrival of three ...
Poley, J. R.; Bhatia, M.; Welsh, J. D. (1978). "Disaccharidase deficiency in infants with cow's milk protein intolerance. ... Neale, G (1971). "Disaccharidase deficiencies". J Clin Pathol Suppl (R Coll Pathol). 5: 22-28. doi:10.1136/jcp.s3-5.1.22. PMC ... Laws, J. W.; Spencer, J.; Neale, G. (1967). "Radiology in the diagnosis of disaccharidase deficiency". The British Journal of ... Laws, J. W.; Neale, G. (1966). "Radiological diagnosis of disaccharidase deficiency". Lancet. 2 (7455): 139-143. doi:10.1016/ ...
Deficiency of this protein is associated with Hermansky-Pudlak Syndrome . Also this gene has been associated with tumor ... protein that complexes with integrins and other TM4SF proteins". The Journal of Biological Chemistry. 272 (46): 29181-9. doi: ... The protein encoded by this gene is a member of the transmembrane 4 superfamily, also known as the tetraspanin family. Most of ... This encoded protein is a cell surface glycoprotein that is known to complex with integrins. It may function as a blood ...
December 2006). "Deficiency of cartilage-associated protein in recessive lethal osteogenesis imperfecta". N. Engl. J. Med. 355 ... Cartilage associated protein is a protein that in humans is encoded by the CRTAP gene. The protein encoded by this gene is ... The encoded protein is a scaffolding protein that may influence the activity of at least one member of the cytohesin/ARNO ... 1997). "Cartilage associated protein (CASP) is a novel developmentally regulated chick embryo protein". J. Cell Sci. 110. ( Pt ...
March 2005). "Renal effects of Tamm-Horsfall protein (uromodulin) deficiency in mice". American Journal of Physiology. Renal ... When this protein is concentrated at low pH, it forms a gel. Uromodulin represents the most abundant protein in normal human ... Tamm-Horsfall protein)--the most abundant protein in mammalian urine". Biochimica et Biophysica Acta (BBA) - Gene Structure and ... mainly consisting of immunoglobulin light chain known as Bence Jones protein, but often also containing Tamm-Horsfall protein. ...
There are causes for deficiency other than low dietary intake of vitamin A as retinol or carotenes. Adequate dietary protein ... Vitamin A deficiency is common in developing countries, especially in Sub-Saharan Africa and Southeast Asia. Deficiency can ... Vitamin A deficiency is common in developing countries, especially in Sub-Saharan Africa and Southeast Asia. Deficiency can ... Plasma retinol is used as a biomarker to confirm vitamin A deficiency. Breast milk retinol can indicate a deficiency in nursing ...
The mutations lead to functional caspase-8 deficiency by destabilizing the caspase-8 protein and inactivating its enzymatic ... Caspase-8 deficiency (CEDS) is a very rare genetic disorder of the immune system. It is caused by mutations in the CASP8 gene ... Su, Helen C.; Michael J. Lenardo (2009). "Capase-8 Deficiency State". In Florian Lang (ed.). Encyclopedia of Molecular ... ISBN 978-0-12-384930-4. "Caspase 8 Deficiency". Online Mendelian Inheritance in Man (OMIM). Archived from the original on ...
Find symptoms and other information about Protein S deficiency. ... Protein S deficiency is a disorder that causes abnormal blood ... Protein S deficiency is a disorder that causes abnormal blood clotting. When someone bleeds, the blood begins a complicated ... People at risk to have Protein S deficiency are those with an individual or family history of multiple blood clots in the veins ... People at risk to have Protein S deficiency are those with an individual or family history of multiple blood clots in the veins ...
Protein C deficiency is a disorder that increases the risk of developing abnormal blood clots; the condition can be mild or ... Mild protein C deficiency affects approximately 1 in 500 individuals. Severe protein C deficiency is rare and occurs in an ... THROMBOPHILIA DUE TO PROTEIN C DEFICIENCY, AUTOSOMAL DOMINANT; THPH3. *THROMBOPHILIA DUE TO PROTEIN C DEFICIENCY, AUTOSOMAL ... Most of the mutations that cause protein C deficiency change single protein building blocks (amino acids) in protein C, which ...
The major function of protein S is as a cofactor to facilitate the action of activated protein C (APC) on its substrates, ... Protein S is a vitamin K-dependent anticoagulant protein that was first discovered in Seattle, Washington in 1979 and ... encoded search term (Protein S Deficiency) and Protein S Deficiency What to Read Next on Medscape ... Of the 17 patients with protein S deficiency, 13 also had protein C deficiency, hyperhomocystinemia, antithrombin III ...
Congenital protein C deficiency is one of several inherited thrombophilias, which are a heterogeneous group of genetic ... Protein C deficiency is a congenital or acquired condition that leads to increased risk for thrombosis. ... encoded search term (Protein C Deficiency) and Protein C Deficiency What to Read Next on Medscape ... Of the 18 patients with protein C deficiency, four also had protein S deficiency, two also had hyperhomocystinemia, and one had ...
Mitochondrial trifunctional protein deficiency is a rare condition that prevents the body from converting certain fats to ... Prasun P, LoPiccolo MK, Ginevic I. Long-Chain Hydroxyacyl-CoA Dehydrogenase Deficiency / Trifunctional Protein Deficiency. 2022 ... medlineplus.gov/genetics/condition/mitochondrial-trifunctional-protein-deficiency/ Mitochondrial trifunctional protein ... Mutations in the HADHA and HADHB genes cause mitochondrial trifunctional protein deficiency. These genes each provide ...
... protein C activity ,1 IU dL(-1)) is a rare autosomal recessive disorder that usually presents in the neonatal period with ... Severe protein C deficiency (i.e. protein C activity ,1 IU dL(-1)) is a rare autosomal recessive disorder that usually presents ... The coagulopathy in protein C deficiency is caused by impaired inactivation of factors Va and VIIIa by activated protein C ... Long-term management in severe protein C deficiency involves anticoagulation with or without a protein C replacement regimen. ...
There are two main types of protein C mutations that lead to protein C deficiency: Type I: Quantitative defects of protein C ( ... and protein C deficiency has been linked to over 160 mutations to date. Therefore, DNA testing for protein C deficiency is ... Patients with Protein C deficiency are at an increased risk of developing skin necrosis while on warfarin. Protein C has a ... a protein C antigen assay can be considered to determine the deficiency subtype (Type I or Type II). In type I deficiencies, ...
This article looks at how much protein a person needs, healthful high protein foods, and tips for getting enough protein. ... Protein is an essential nutrient for the body to function. ... Protein deficiency due to a low intake of protein in the diet ... Protein shakes and protein powders contain high amounts of protein. Protein powders may contain 10-30 g of protein per scoop. ... However, a lack of protein in other countries is a serious concern, especially in children. Protein deficiency can lead to ...
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Upregulated protein translation is a hallmark of cancer and is implicated in autism spectrum disorder, but the risks of ... Protein translation is a highly regulated process involving the interaction of numerous genes on every component of the protein ... PUS7 deficiency in human patients causes profound neurodevelopmental phenotype by dysregulating protein translation Sangwoo T ... PUS7 deficiency in human patients causes profound neurodevelopmental phenotype by dysregulating protein translation Sangwoo T ...
Protein C Deficiency - Etiology, pathophysiology, symptoms, signs, diagnosis & prognosis from the MSD Manuals - Medical ... Heterozygous deficiency of plasma protein C has a prevalence of 0.2 to 0.5% (2 General references Because activated protein C ... 1 General references Because activated protein C degrades coagulation factors Va and VIIIa, deficiency of protein C predisposes ... Because activated protein C degrades coagulation factors Va and VIIIa, deficiency of protein C predisposes to venous thrombosis ...
Still, what people want to know when they find Im vegan is, do I get enough protein. ... Plant-based protein is low in fat and contains zero cholesterol. ... The Myth of Plant-Based Protein Deficiency. Published: Jan 30, ... because plant-based protein is cheaper than most animal protein, and youll be helping yourself-plant-based protein is low in ... The Food and Drug Administrations basic formula for calculating protein needs is .8 grams of protein for every kilogram of ...
... and how to up your protein intake in order to regain health. ... Unpacking the causes of protein deficiency, the top five ... What is protein deficiency?. "Dietary protein provides amino acids for humans to make their own proteins in the body that are ... Symptoms of a protein deficiency. There are many signs of a protein deficiency to watch out for. Not everyone will have the ... How do you fix a protein deficiency?. If you suspect you have a protein deficiency, visit a doctor, as some of the symptoms can ...
Ophthalmic manifestations of neonatal protein C deficiency. Message subject: (Your Name) has forwarded a page to you from ...
... ... Loss of MMR protein expression was seen in 18 of 36 (50%) adenomatous polyps, zero of 21 hyperplastic polyps, and zero of two ... All (six of six) adenomatous polyps 10 mm or larger in size showed both MSI-H and loss of MMR protein expression by ... Our finding that the prevalence of MMR deficiency increases with the size of adenomatous polyps suggests that loss of MMR ...
Copyright © 2023 BMJ Publishing Group Ltd & Royal College of Paediatrics and Child Health. All rights reserved.. ...
Adaptor protein complex 4 deficiency causes severe autosomal-recessive intellectual disability, progressive spastic paraplegia ... we identified one mutation in each of three genes encoding adaptor protein complex 4 (AP4) subunits: a nonsense mutation in ... Adaptor protein complexes (AP1-4) are ubiquitously expressed, evolutionarily conserved heterotetrameric complexes that mediate ... role in brain development and functioning and demonstrate the existence of a clinically recognizable syndrome due to deficiency ...
Structural implications of novel amino acid substitutions in E1 protein Mol Genet Metab. 2011 Dec;104(4):507-16. doi: 10.1016/j ... Novel missense mutations in PDHA1 were located on the tridimensional model of human E1 protein to predict their possible ... Background: Pyruvate dehydrogenase complex (PDHc) deficiencies are an important cause of primary lactic acidosis. Most cases ... Molecular characterization of 82 patients with pyruvate dehydrogenase complex deficiency. ...
"Protein S Deficiency" by people in this website by year, and whether "Protein S Deficiency" was a major or minor topic of these ... PROTEIN S is a vitamin K-dependent plasma protein that inhibits blood clotting by serving as a cofactor for activated PROTEIN C ... and the clinical manifestations of its deficiency are virtually identical to those of protein C deficiency. Treatment with ... "Protein S Deficiency" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical ...
Manganese and iron deficiency in Southern Ocean Phaeocystis antarctica populations revealed through taxon-specific protein ... Here we examine the influence of iron and manganese on protein expression and physiology in Phaeocystis antarctica, a key ... Natural Phaeocystis populations produce protein signatures indicating late-season manganese and iron stress, consistent with ...
Furthermore, TIA-proteins deficiency also caused metabolic deficiencies, increased ROS levels and DNA damage, promoting a ... or TIA1 related/like protein (TIAR/TIAL1) show high rates of embryonic lethality, suggesting a relevant role for these proteins ... However, intrinsic molecular and cellular consequences of either TIA1 or TIAR deficiency remain poorly defined. By using genome ... Taken together, these observations support that TIA proteins orchestrate a transcriptome programme to activate specific ...
What Is the Prognosis for a Person with D-Bifunctional Protein Deficiency?. The prognosis for D-bifunctional protein deficiency ... How Common Is D-Bifunctional Protein Deficiency?. The estimated prevalence of D-bifunctional protein deficiency is 1 in 100,000 ... What Is D-Bifunctional Protein Deficiency?. D-bifunctional protein deficiency, also known as peroxisomal bifunctional enzyme ... How Is D-Bifunctional Protein Deficiency Treated?. There is no treatment for the underlying cause of D-bifunctional protein ...
The major function of protein S is as a cofactor to facilitate the action of activated protein C (APC) on its substrates, ... Protein S is a vitamin K-dependent anticoagulant protein that was first discovered in Seattle, Washington in 1979 and ... Type I protein S deficiency is a reduction in the level of free and total protein S. Type III deficiency is a reduction in the ... Protein S deficiency usually manifests clinically as venous thromboembolism (VTE). [1] Any association of protein S deficiency ...
Variation registry for Regulatory factor X-associated protein deficiency Select database by name. ADAbase. AICDAbase. AIREbase ... KinMutBase - A registry of disease-causing variations in protein kinase domains. IDbases are linked to University of California ...
Finding of non-synonymous mutation in a protein does not necessarily mean that the mutation affects protein structure, ... C4b-binding protein, membrane cofactor protein (CD46). These are found in hemolytic uremic syndrome, age-related macula ... Full complement deficiencies lead to severe infectious and autoimmune diseases but are uncommon while it appears that we are ... This can be sometimes predicted but in most cases it must be evaluated by expressing a recombinant protein carrying the ...
Characterization of Protein Kinase C Alpha Deficiency in a Mouse Model. Haupttitel: Characterization of Protein Kinase C Alpha ... Characterization of Protein Kinase C Alpha Deficiency in a Mouse Model. *Einloggen ... The protein kinase C (PKC) familiy was first described in 1977 by Nishizuka and colleagues, the pioneers in PKC research, and ... Anyhow, PKCa deficiency appears to be associated with functional-muscular rather than neuronal achalasia-like pathological ...
In mice, C3 (the precursor to ASP) knock-out (KO) results in ASP deficiency and leads to reduced body fat and leptin levels yet ... These results suggest that ASP deficiency results in energy repartitioning through different mechanisms in male and female mice ... Acylation-stimulating protein (ASP) acts as a paracrine signal to increase triglyceride synthesis in adipocytes. ... In mice, C3 (the precursor to ASP) knock-out (KO) results in ASP deficiency and leads to reduced body fat and leptin levels yet ...
... a symptom of the protein-deficiency disease kwashiorkor. ... protein-deficiency, vitamin deficiency, west africa, woman, ... a symptom of the protein-deficiency disease kwashiorkor. Kwashiorkor sufferers, i.e., inadequate dietary protein intake, also ... Picture of a Nurse Standing with a Group of African Children Showing Symptoms of the Protein-Deficiency Disease Kwashiorkor # ... Picture of a Nurse Standing with a Group of African Children Showing Symptoms of the Protein-Deficiency Disease Kwashiorkor."> ...
... where the protein was first identified and isolated. Protein S is involved in the process of programmed cell ... Types of Protein S Deficiency. Protein S deficiency. Protein S deficiency is a rare disease that has been shown to cause venous ... protein S and C4b-binding protein isoforms in hereditary protein S deficiency demonstrating type I and type III deficiencies to ... Protein S is named for Seattle, Washington, where the protein was first identified and isolated. Protein S is involved in the ...
... medium-chain acyl-CoA dehydrogenase deficiency (Table) (3.6). Newborn screening can help prevent death or disability, if ... Trifunctional protein deficiency. 2. Total. 11, 691. * One of the 29 disorders listed in the screening panel (tyrosinemia type ...
  • The first step is to determine your daily protein intake requirements and recognize any possible signs of protein deficiency. (hammernutrition.com)
  • On that way, GMN Health Care had launched Pro360 Protein nutritional health drink to highlight the consistent growth and produce the best nutritional supplement for protein malnutrition. (vigorcolumn.com)
  • We describe the potential roles of malnutrition and vitamin A deficiency as risk factors for severe measles in adults from this community. (cdc.gov)
  • In severe protein-calorie malnutrition, and during intercurrent infection, serum retinol levels could be artificially low in relation to a decrease in retinol-binding protein level ( 9 ). (cdc.gov)
  • Originality/value - Since malnutrition (e.g. iron-deficiency anemia, rickets, zinc deficiency, protein-calorie malnutrition) is common in sub-Saharan Africa, the information which is provided should increase awareness among agricultur al and public health officials of the nutritional value of seven underappreciated and underutilized ILVs that are indigenous to Ghana and many other parts of Africa. (cdc.gov)
  • Cafolla A, D'Andrea G, Baldacci E, Margaglione M, Mazzucconi MG, Foa R. Hereditary protein C deficiency and thrombosis risk: genotype and phenotype relation in a large Italian family. (medlineplus.gov)
  • Protein C deficiency is a congenital or acquired condition that leads to increased risk for thrombosis. (medscape.com)
  • This may explain, in part, why protein C deficiency appears to be associated primarily with venous thrombosis. (medscape.com)
  • Individuals who are homozygous or compound heterozygous for a mutation or other genetic defect affecting the protein C, typically due to the inheritance of abnormal alleles from both parents, can experience neonatal purpura fulminans, intracranial thromboembolism, and thrombosis. (medscape.com)
  • Because protein Z helps inactivate coagulation factor Xa , deficiency or dysfunction of protein Z predisposes to venous thrombosis (mainly in patients who also have other clotting abnormalities). (msdmanuals.com)
  • Factor V Resistance to Activated Protein C (APC) Mutations of factor V make it resistant to its normal cleavage and inactivation by activated protein C, and they also predispose to venous thrombosis. (msdmanuals.com)
  • Neonates with homozygous Protein C deficiency (Protein C levels close to zero) present with an often fatal syndrome of purpura fulminans with spreading skin necrosis, thrombosis and disseminated intravascular coagulation (DIC). (clinlabnavigator.com)
  • Acquired Protein C deficiency may be seen in a wide variety of clinical situations including DIC, extensive thrombosis, liver disease, after surgery, and malignancy. (clinlabnavigator.com)
  • An inherited coagulation disorder characterized by recurrent venous thrombosis symptoms due to reduced synthesis and/or activity levels of protein S. (globalgenes.org)
  • Heterozygous protein C deficiency is inherited in an autosomal dominant fashion, however, in families with individuals with complete deficiency, the mode of inheritance is autosomal recessive. (medscape.com)
  • Heterozygous individuals typically demonstrate protein C antigen and activity levels that are approximately one half that of normal patient plasma. (medscape.com)
  • There is marked phenotypic variation among families with heterozygous type I protein C deficiency. (medscape.com)
  • The majority of people with protein C deficiency lack only one copy of the functioning genes, and are therefore heterozygous. (wikipedia.org)
  • Heterozygous PCD and mild deficiency can cause a wide range of symptom severity from asymptomatic to recurrent thromboses. (unboundmedicine.com)
  • Most affected individuals are teenagers or young adults who are heterozygous for the deficiency. (clinlabnavigator.com)
  • Affected heterozygous family members have Protein C levels between 40 and 65% of normal, associated with an increased incidence of thromboembolic disease (predominantly venous). (clinlabnavigator.com)
  • It appears, however, that most subjects with heterozygous Protein C deficiency are asymptomatic. (clinlabnavigator.com)
  • Female mice heterozygous for Ikk gamma/Nemo deficiency develop a unique dermatopathy characterized by keratinocyte hyperproliferation, skin inflammation, hyperkeratosis, and increased apoptosis. (nih.gov)
  • Before 1999, only sixteen cases of homozygous protein C deficiency had been described (two abnormal copies of the gene, leading to absence of functioning protein C in the bloodstream). (wikipedia.org)
  • Homozygous protein C deficiency (where a person has two abnormal protein C genes, one from each parent) is usually evident in newborn infants. (ihtc.org)
  • Mitochondrial trifunctional protein deficiency (MTPD), a rare condition that leads to failure of converting certain fats to energy is characterized by decreased activity of three enzymes in the enzyme complex. (trdizin.gov.tr)
  • Molecular and phenotypic heterogeneity in mitochondrial trifunctional protein deficiency due to beta-subunit mutations. (trdizin.gov.tr)
  • Mitochondrial trifunctional protein deficiency: a severe fatty acid oxidation disorder with cardiac and neurologic involvement. (trdizin.gov.tr)
  • Mitochondrial trifunctional protein deficiency due to HADHB gene mutation in a Chinese family. (trdizin.gov.tr)
  • 2003). Genetic Heterogeneity of Mitochondrial Trifunctional Protein Deficiency See also MTPD2 (620300), caused by mutation in the HADHB gene, the beta subunit of the mitochondrial trifunctional protein. (nih.gov)
  • In severe cases of protein C deficiency, infants develop a life-threatening blood clotting disorder called purpura fulminans soon after birth. (medlineplus.gov)
  • Neonatal purpura fulminans and transient protein C deficiency. (bmj.com)
  • Some infants who do not have neonatal purpura fulminans but still have low levels of protein C (5% to 20%) often have a tendency to clot excessively at an early age. (ihtc.org)
  • citation needed] The main function of protein C is its anticoagulant property as an inhibitor of coagulation factors V and VIII. (wikipedia.org)
  • Protein Z, a vitamin K-dependent protein, functions as a cofactor to down-regulate coagulation by forming a complex with the plasma protein, Z-dependent protease inhibitor (ZPI). (msdmanuals.com)
  • Protein C is a vitamin K dependent plasma protein that inhibits coagulation. (clinlabnavigator.com)
  • However, research has shown that losing weight by incorporating a nutritional diet with the right amount of protein can reduce the consequences of becoming severely ill from COVID-19. (progenmethod.com)
  • By introducing the right amount of protein into our diet and nutrition intake, we can help maximize muscle mass which will further contribute to tackling the severity of COVID-19. (progenmethod.com)
  • The right amount of protein contributes to a stronger body with better immunity and in these times will be crucial. (progenmethod.com)
  • Various plant-based meat substitutes contain a substantial amount of protein. (justvegantoday.com)
  • Therefore, any nutrition must include the correct amount of protein in order for the body to be assisted in its process of recovery from effort. (boxrox.com)
  • So, if a person weight 120 pounds, the minimum amount of protein that that person can eat is 60 lbs. of protein. (circulatingnow.com)
  • Without the right amount of protein, injuries, wounds, and infections would really take time to heal. (circulatingnow.com)
  • Because most types of protein-rich food come from animal sources, hitting your recommended amount of protein each day can get tricky if you don't eat meat, poultry, dairy or eggs - but luckily, it's far from impossible. (sadecetech.com)
  • According to the United States Department of Agriculture (USDA)'s current version of Dietary Guidelines for Americans, the recommended daily amount of protein to prevent deficiency is 0.8 grams per kilogram of body weight . (sadecetech.com)
  • Findings - All seven ILVs contained a large amount of protein (15.5-22.8 percent), which compared favorably to the essential amino acid pattern of a WHO standard. (cdc.gov)
  • [ 13 ] The presence of a second thrombophilic mutation such as factor V Leiden has been associated with a more severe phenotype in some protein C-deficient kindreds. (medscape.com)
  • We alter the deficiency by infecting the SFTPB deficient iPSCs with a lentivirus carrying the wild type SFTPB gene. (nature.com)
  • Before we get to the signs and symptoms, what makes a person protein deficient in the first place? (circulatingnow.com)
  • This value is heightened especially in South Asia and Central Africa where 30 percent of children and young adults are protein deficient. (circulatingnow.com)
  • Here are the signs and symptoms that tell you you might be protein deficient. (circulatingnow.com)
  • It's not just timing and it's not the environment - it can be because you are protein deficient. (circulatingnow.com)
  • Natalie Rizzo, MS, RD says that people who are protein deficient might have trouble pulling themselves to work out because of the lack of energy they are being supplied. (circulatingnow.com)
  • That can be a sign that you are protein deficient. (circulatingnow.com)
  • However, if it happens regularly and your brain won't allow you to think of anything else, then it can signify that you are becoming protein deficient. (circulatingnow.com)
  • According to White, protein deficient-people also tend to crave savory foods more often than the usual. (circulatingnow.com)
  • Throughout protein-deficient states, the physique will talk its want for meals by way of starvation cues. (dadelaon.com)
  • Protein deficiency in India is more prevalent that it is known, with nearly 73% of urban Indians being protein deficient and about 93% are unaware about their daily protein requirements (IMRB 2017). (thechannel46.com)
  • When the former two are deficient, the demand for the latter two amino acids will increase, resulting in the deficiency of phenylalanine and methionine. (arshinefeed.com)
  • When poultry is deficient in protein and amino acids, its metabolism will be hindered, resulting in growth inhibition, reduced productivity, and reduced disease resistance. (arshinefeed.com)
  • Most genes from the plant-specific family encoding Response to Low Sulphur (LSU)-like proteins are strongly induced in sulphur (S)-deficient conditions. (waw.pl)
  • Widespread blood clotting uses up all available blood clotting proteins. (medlineplus.gov)
  • Severe protein C deficiency is rare and occurs in an estimated 1 in 4 million newborns. (medlineplus.gov)
  • Individuals who inherit two altered copies of this gene in each cell have severe protein C deficiency. (medlineplus.gov)
  • Babies with severe protein C deficiency may experience symptoms within hours or days of their birth. (wikipedia.org)
  • A deficiency of aPC disturbs the delicate balance between procoagulant and anticoagulant proteins and engenders a prothrombotic environment. (medscape.com)
  • The role of aPC and other anticoagulant proteins in this balance appears to be especially important in the slow-flowing venous circulation, in which procoagulant proteins and platelet phospholipids have prolonged exposure to the vessel wall. (medscape.com)
  • It is not yet known whether anticoagulant therapy or prophylaxis is indicated in protein Z or ZPI deficiency. (msdmanuals.com)
  • Protein C is a vitamin K dependent anticoagulant protein synthesized in an inactive form by the liver. (unboundmedicine.com)
  • For Protein C to serve as an anticoagulant, it must be converted to its active form by thrombin. (clinlabnavigator.com)
  • Since Protein C is a vitamin K dependent protein, decreased levels may be expected if a patient is on oral anticoagulant drug therapy. (clinlabnavigator.com)
  • It is essential that we focus on building a nutrition intake that widely focuses on protein as it is made of building blocks known as amino acids which are crucial for the growth of cells and tissues as well as their maintenance. (progenmethod.com)
  • Deficiency leads to various health problems, while low protein intake may also be a concern, as it can cause subtle changes in your body over time. (bestmadenaturalproducts.com)
  • Protein deficiency, also called hypoproteinemia, is usually tied to overall low protein intake. (bestmadenaturalproducts.com)
  • Of course, as is the rule with a vegan diet, your protein intake requirements will vary upon the desired outcome. (justvegantoday.com)
  • Some studies have even found an inverse relationship exists between protein intake and risk of heart disease. (boxrox.com)
  • Currently, about one billion people throughout worldwide have chronic inadequate intake of essential protein on their daily diet. (vigorcolumn.com)
  • For Kids, Pro360 scientifically formulated Pro360 Kids, an adequate nutritional protein intake to improve memory, boost immunity and overall growth and development of children. (vigorcolumn.com)
  • For Pregnant and Lactating Mothers, Pro360 formulated a new protein supplement Pro360 Mom to fulfil inadequate protein intake during pregnancy and breastfeeding involving fetal development and reduces the risk of gestational diabetes. (vigorcolumn.com)
  • While both of these grains are good sources of carbohydrates and fiber, quinoa is the better choice if you're aiming to increase your protein intake. (sadecetech.com)
  • Incorporating vegan protein powder into your diet is a quick and easy way to crank up your protein intake - especially if you're in a rush to get moving in the morning. (sadecetech.com)
  • By upping your intake of these amino acid-rich foods, you can get closer to hitting your daily protein goals. (sadecetech.com)
  • Your baby relies on you for their protein needs, which is why new moms need to increase their protein intake. (thechannel46.com)
  • To understand why protein isn't finding its place in the shopping carts of most Indian households, the Right to Protein initiative reached out to 2,142 Indian mothers, the primary decision-makers of a household's nutrition intake, across 16 cities in India for a survey conducted by commissioned research agency, Nielsen. (thechannel46.com)
  • Poultry protein and amino acid deficiency refers to insufficient protein intake or excessive consumption of poultry and one or several amino acid deficiencies. (arshinefeed.com)
  • the dietary energy level is high At this time, the poultry will reduce the feed intake by itself, and the protein and amino acid content of the feed must also be increased. (arshinefeed.com)
  • 3. In the process of phlegm disease, the poultry's feed intake will be reduced, the appetite will be decreased or eliminated, and the protein intake will be insufficient. (arshinefeed.com)
  • Ariboflavinosis is a nutritional deficiency occurring due to reduced intake of riboflavin through the diet. (ignouworld.com)
  • Create a daily protein intake journal and monitor your eating habits over the course of a normal training week. (hammernutrition.com)
  • If you're tired when you shouldn't be, inadequate protein intake could be to blame. (hammernutrition.com)
  • If your dietary protein intake is inadequate, mood swings are a potential by-product. (hammernutrition.com)
  • Protein C deficiency is caused by mutations in the PROC gene. (medlineplus.gov)
  • This gene provides instructions for making protein C, which is found in the bloodstream and is important for controlling blood clotting. (medlineplus.gov)
  • Protein C deficiency can be divided into type I and type II based on how mutations in the PROC gene affect protein C. Type I is caused by PROC gene mutations that result in reduced levels of protein C, while type II is caused by PROC gene mutations that result in the production of an altered protein C with reduced activity. (medlineplus.gov)
  • which means one altered copy of the PROC gene in each cell is sufficient to cause mild protein C deficiency. (medlineplus.gov)
  • [ 7 , 8 ] The gene for protein C is located on the long arm of chromosome 2 and nearly 200 pathogenic mutations of this gene have been described. (medscape.com)
  • A range of causative genetic alterations within the protein C promoter region and splice sites as well as in the coding sequence of the protein C gene itself have been reported. (medscape.com)
  • Type II protein C deficiency is less common than type I disease and is associated with decreased functional activity and normal immunologic levels of protein C. A number of point mutations within the protein C gene giving rise to this disorder have been described. (medscape.com)
  • The human protein C gene (PROC) comprises 9 exons, and protein C deficiency has been linked to over 160 mutations to date. (wikipedia.org)
  • The postsynaptic protein Shank3 (SH3 and multiple ankyrin repeat domains) is of particular interest, as the loss of a single allele of the SHANK3 gene is sufficient to cause profound cognitive symptoms in children. (jneurosci.org)
  • If you grow up without that protein, it's not just a matter of throwing the gene back in. (reachmd.com)
  • At least 270 genetic mutations have been described in the protein C (PROC) gene that can lead to a functional deficiency. (unboundmedicine.com)
  • Blood findings showed low protein S antigen, low protein S activity, and a missense mutation of the PROS 1 gene. (elsevierpure.com)
  • In this study, we discover a previously unknown type of SBD and identify its causal gene, TMEM53 , which encodes nuclear envelope transmembrane (NET) protein 53 (TMEM53, also known as NET4). (nature.com)
  • Proteins provide many essential functions for the body such as creating digestive enzymes, antibodies to support immune function, support and develop muscle movement, provide cellular generation for the body, and hormones to help coordinate bodily functions. (progenmethod.com)
  • Protein is the building block of your muscles, skin, enzymes, and hormones, and it plays an essential role in all body tissues. (bestmadenaturalproducts.com)
  • In individuals with LCHAD deficiency, there is isolated deficiency of long-chain 3-hydroxyacyl-CoA dehydrogenase, while deficiency of all three enzymes occurs in individuals with TFP deficiency. (nih.gov)
  • Trifunctional protein deficiency is characterized by decreased activity of all 3 enzymes. (nih.gov)
  • Protein: Any of a class of nitrogenous organic compounds which have large molecules composed of one or more long chains of amino acids and are an essential part of all living organisms, especially as structural components of body tissues such as muscle, hair, etc., and as enzymes and antibodies. (boxrox.com)
  • Protein is essential in almost all body functions and is responsible for the structure and make-up of hair, skin, muscles, hormones, and enzymes. (circulatingnow.com)
  • A Protein C level of less than 55% is usually indicative of hereditary deficiency in a stable non-anticoagulated adult. (clinlabnavigator.com)
  • A level of 55-65% may indicate either a low normal value or mild hereditary deficiency. (clinlabnavigator.com)
  • In general, a diagnosis of hereditary deficiency of Protein C should only be made when a low value has been obtained after repeated testing (after a 4-6 week interval), and the possibility of acquired deficiency has been excluded. (clinlabnavigator.com)
  • This may be particularly important in a patient who has a hereditary deficiency of one or both proteins. (medicalalgorithms.com)
  • Testing for a hereditary deficiency of protein S or protein C should be delayed until after the patient has recovered from any of the above conditions or any of the above treatments have been discontinued. (medicalalgorithms.com)
  • Protein C is a 62-kD, vitamin K-dependent glycoprotein synthesized in the liver. (medscape.com)
  • The catalytic activity of aPC is greatly enhanced by the vitamin K-dependent cofactor protein S. (medscape.com)
  • Protein C is vitamin K-dependent. (wikipedia.org)
  • Protein C has a short half life (8 hour) compared with other vitamin K-dependent factors and therefore is rapidly depleted with warfarin initiation, resulting in a transient hypercoagulable state. (wikipedia.org)
  • This is thought to be due to the shorter half-life of protein C (5 to 8 hours) compared to other vitamin K dependent clotting factors. (unboundmedicine.com)
  • Additionally, mutations in other genes (GCKR, EDEM2, BAZ1B, etc.) are associated with variability in the levels of protein C expression in the general population, although their clinical significance is currently unknown. (unboundmedicine.com)
  • A link between response to S deficiency, ethylene sensing, and LSU-like proteins was emphasized by changes in expression of the genes encoding ethylene receptors and F-box proteins specific for the ethylene pathway. (waw.pl)
  • We are studying molecular basis of deficiencies and polymorphisms in complement inhibitors factor I, factor H, C4b-binding protein, membrane cofactor protein (CD46). (lu.se)
  • Activated protein C (APC) inhibits generation of thrombin by inactivating factors Va and VIIIa, using protein S as a cofactor. (unboundmedicine.com)
  • Protein C deficiency is a rare genetic trait that predisposes to thrombotic disease. (wikipedia.org)
  • Protein C deficiency is associated with an increased incidence of venous thromboembolism (relative risk 8-10), whereas no association with arterial thrombotic disease has been found. (wikipedia.org)
  • It is uncertain whether or not acquired deficiency contributes to a thrombotic tendency. (clinlabnavigator.com)
  • Since acquired deficiencies of Protein C occur frequently in hospitalized patients, it is preferable to perform the assays at a time when the patient is in stable condition, and ideally in remission from thrombotic events. (clinlabnavigator.com)
  • We often make a fundamental error by testing for protein C and protein S deficiency when a patient is taking coumadin (warfarin), or when they have had a recent thrombotic event, both of which consistently cause both protein C and protein S to be temporarily decreased. (fritsmafactor.com)
  • Aside from the issue of protein C and protein S deficiency, the patient you are describing may have had one or more thrombotic (blood clotting) episodes that are independent of the protein C and protein S diagnosis. (fritsmafactor.com)
  • Finding of non-synonymous mutation in a protein does not necessarily mean that the mutation affects protein structure, secretion or function. (lu.se)
  • This can be sometimes predicted but in most cases it must be evaluated by expressing a recombinant protein carrying the mutation and comparing its properties to the wild type. (lu.se)
  • There are two main types of protein C assays, activity and antigen (immunoassays). (wikipedia.org)
  • Antigen assays are immunoassays designed to measure the quantity of protein C regardless of its function. (wikipedia.org)
  • Type I deficiencies are therefore characterized by a decrease in both activity and antigen protein C assays whereas type II deficiencies exhibit normal protein C antigen levels with decreased activity levels. (wikipedia.org)
  • In support, we have used phenotypic, reporter and protein-based assays to demonstrate increased translational infidelity in trm9Δ Saccharomyces cerevisiae cells. (nih.gov)
  • Therefore we have established expression systems for these proteins as well as panel of functional assays. (lu.se)
  • If it is not possible to discontinue oral anticoagulants and protein C assay is felt to be essential, consideration should be given to stopping the warfarin for 10 days prior to the assays while the patient is temporarily covered with heparin (standard or low molecular weight). (clinlabnavigator.com)
  • Of the 11 tumors with retained MMR protein expression, four were MSI-low/MSI-high or MSI-high by the Promega assay or one of the sequencing-based assays. (lu.se)
  • While most people with mild protein C deficiency never develop abnormal blood clots, certain factors can add to the risk of their development. (medlineplus.gov)
  • Having another inherited disorder of blood clotting in addition to protein C deficiency can also influence the risk of abnormal blood clotting. (medlineplus.gov)
  • Individuals with this condition do not have enough functional protein C to inactivate clotting proteins, which results in the increased risk of developing abnormal blood clots. (medlineplus.gov)
  • There are two main types of protein C mutations that lead to protein C deficiency: Type I: Quantitative defects of protein C (low production or short protein half life) Type II: Qualitative defects, in which interaction with other molecules is abnormal. (wikipedia.org)
  • SIGNIFICANCE STATEMENT Although the loss of several synaptic proteins has been described in Alzheimer's disease (AD), it remains unclear whether their reduction contributes to clinical symptoms. (jneurosci.org)
  • Dietary protein deficiency not only contributes to poor growth, cardiovascular dysfunction, and worsens metabolic profiles. (vigorcolumn.com)
  • An satisfactory protein standing contributes to the regulation of blood sugar ranges, therapeutic of wounds, and combat towards a number of pathogens that may trigger infections. (dadelaon.com)
  • Are you getting enough protein? (circulatingnow.com)
  • I would also argue that if someone isn't eating enough protein, they probably aren't eating enough calories overall. (circulatingnow.com)
  • According to Rizzo, not having enough protein can actually harm the immune system. (circulatingnow.com)
  • How do vegans get enough protein? (sadecetech.com)
  • Your daily meals consisting of roti , dal , rice does not provide enough protein. (thechannel46.com)
  • See the chart below to determine if you are consuming enough protein daily (total from all sources). (hammernutrition.com)
  • If you aren't getting enough protein, the time to start is now! (hammernutrition.com)
  • Without enough protein for repair, your muscles may not have fully recovered from the previous day's workout. (hammernutrition.com)
  • This has been partly attributed to changing environmental factors such as exposure to traffic-related air pollution (TRAP) and nutrient deficiencies, including vitamin D. Furthermore, population-based studies have suggested that air pollution may contribute to vitamin D deficiency [ 1 ], while vitamin D levels may modify pollution-driven asthma symptoms in paediatric obesity [ 2 ]. (ersjournals.com)
  • Protein is a vital nutrient for immune function and injury recovery. (circulatingnow.com)
  • however, some data suggest their importance for plants' adjustment to nutrient deficiency and other environmental stresses. (waw.pl)
  • Therefore, protein and amino acids not only maintain the life of poultry, but also have a very close relationship with the growth, development, genetics, disease resistance and egg formation of poultry. (arshinefeed.com)
  • For the past year, Right To Protein has been assessing the existing challenges related to protein consumption in India, marked by the launch of Protein-O-Meter as well as the launch of India's first Protein Day on February 27, 2020. (thechannel46.com)
  • Most of the mutations that cause protein C deficiency change single protein building blocks (amino acids) in protein C, which disrupts its ability to control blood clotting. (medlineplus.gov)
  • Protein can be found in various ways, but the proportion of essential and non-essential amino acids differs from each food base. (progenmethod.com)
  • It is evident that animal-based proteins are rich and high in quality as they have a higher level of essential amino acids compared to plant-based foods which have a lower level of essential amino acids that is required by the body. (progenmethod.com)
  • Protein is a string of amino acids that create the building blocks for the physical parts of your body, including muscles, bones , skin, hair, nails, and organs. (bestmadenaturalproducts.com)
  • Amino acids are the building blocks of proteins, and proteins are the building blocks of muscle mass, according to the National Institutes of Health (NIH). (bestmadenaturalproducts.com)
  • When we say "protein builds muscle," what we mean is the body breaks down protein into its amino acids, and those amino acids are synthesized into muscle. (bestmadenaturalproducts.com)
  • Amino acids - the "building blocks of protein" - are compounds that are responsible for a variety of bodily processes, including neurological processes and muscle synthesis. (bestmadenaturalproducts.com)
  • It is important to understand the role amino acids play in protein because some amino acids are better than others when it comes to muscle health - which is critical for health and well-being. (bestmadenaturalproducts.com)
  • The main difference between animal and plant proteins is their amino acid profile. (bestmadenaturalproducts.com)
  • Most animal proteins are complete proteins, meaning they contain all 9 of the essential amino acids (EAAs). (bestmadenaturalproducts.com)
  • Most plant proteins are considered incomplete proteins, meaning they are missing at least one essential amino acid. (bestmadenaturalproducts.com)
  • First, whey is a complete protein, meaning that it contains all of the essential amino acids. (bestmadenaturalproducts.com)
  • Secondly, whey proteins are abundant in Branched Chain Amino Acids (BCAAs) which are a subset of EAAs that support muscle growth. (bestmadenaturalproducts.com)
  • A well-balanced vegan diet includes various protein sources three times a day to ensure the body obtains enough essential amino acids. (justvegantoday.com)
  • Proteins are 'king' when it comes to recovery and growth: these nutrients, once in the body, are digested into amino acids that are the building blocks of your lean mass. (boxrox.com)
  • On top of that, quinoa is also a complete protein , meaning that it has all nine types of essential amino acids that your body can't produce but needs for key functions like energy production, tissue repair and immunity . (sadecetech.com)
  • Protein is made up of 20 amino acids , 11 of which the body can produce on its own. (sadecetech.com)
  • As we've mentioned, when foods contain all nine essential amino acids, they're called complete proteins. (sadecetech.com)
  • Poultry protein and amino acid deficiency-Knowledge-Arshine Feed Biotech Co., Ltd. (arshinefeed.com)
  • 1. Insufficient protein and amino acid content in feed The content of protein and amino acid in common poultry feed is quite different. (arshinefeed.com)
  • Grain and bran feeds have less protein content and incomplete nutritional value, especially lack of methionine and lysine, while animal protein feeds have higher protein content and more complete types of amino acids. (arshinefeed.com)
  • If the type of feed is single, the diet is unreasonable, and the animal protein feed is lacking for a long time, it can cause the lack of protein and amino acids. (arshinefeed.com)
  • In addition, the protein and amino acid requirements of poultry are closely related to the type, breed, age, production performance, environmental temperature and dietary energy level of poultry. (arshinefeed.com)
  • Therefore, if the difference in protein and amino acid requirements of the above-mentioned factors is ignored in poultry breeding, and a certain formula is used unchanged for a long time, it will also cause a lack of protein and amino acids. (arshinefeed.com)
  • For example, lysine, methionine and tryptophan in the essential amino acids are restricted when poultry uses other amino acids to synthesize protein (called limiting amino acids). (arshinefeed.com)
  • Cereals such as corn and sorghum, bran feed), and other amino acids cannot be utilized, resulting in a deficiency. (arshinefeed.com)
  • Specific amino acids in protein are the building blocks for neurotransmitters such as dopamine and serotonin which control mood. (hammernutrition.com)
  • Future research is required to determine the amounts of anti-nutrients (e.g. protease inhibitors, chelators) in these vegetables, and the extent to which their protein, lipid and mineral constituents are digested and/ or absorbed. (cdc.gov)
  • Brouwer JL, Lijfering WM, Ten Kate MK, Kluin-Nelemans HC, Veeger NJ, van der Meer J. High long-term absolute risk of recurrent venous thromboembolism in patients with hereditary deficiencies of protein S, protein C or antithrombin. (medlineplus.gov)
  • Patients with Protein C deficiency are at an increased risk of developing skin necrosis while on warfarin. (wikipedia.org)
  • Screening all patients for inherited or acquired forms of PCD prior to initiating warfarin is not cost-effective or prognostic because many patients with documented deficiency do not progress to WISN. (unboundmedicine.com)
  • Animal proteins, such as whey protein, have been studied extensively clinically to determine their effect on skeletal muscle and tissue repair so are recommended for athletes and people who need to increase muscle health and mass, like the elderly or post-surgical patients. (bestmadenaturalproducts.com)
  • Initial and sequential levels of ATIII (activity), PC (antigen and activity), PS (total and free), and C4b binding protein (C4bBP) were compared according to the outcome in patients with DIC. (qxmd.com)
  • In the group DIC+, all patients but two had severe deficiencies in ATIII and PC levels. (qxmd.com)
  • 2003). Some patients with MTP deficiency show a protracted progressive course associated with myopathy, recurrent rhabdomyolysis, and sensorimotor axonal neuropathy. (nih.gov)
  • Skin necrosis may develop in patients with reduced Protein C levels at the beginning of warfarin therapy. (clinlabnavigator.com)
  • For Orthopedic patients, Pro360 manufactured Pro360 Ortho Protein Powder to improve healing and joint flexibility, reduces stiffness, swelling, improve visions and chronic inflammation from sports and training. (vigorcolumn.com)
  • Pro360 Nephro HP is high in calories and protein provides the complete renal nutrition to fulfil the needs of dialysis patients. (vigorcolumn.com)
  • Case-patients 1 and 2 had vitamin A deficiency with values of 0.31 mg/L and 0.2 mg/L, respectively, (reference range 0.5-0.8 mg/L). We measured vitamin A levels in blood samples from the next 4 consecutive hospitalized patients with measles, all of whom were from the Roma community. (cdc.gov)
  • However, the diagnosis of vitamin A deficiency is usually supported by low levels of serum vitamin A and levels of retinol-binding protein within the reference range as described for at least 1 of the case-patients reported here. (cdc.gov)
  • Thus, the deficiency of protein and micronutrients remains a major nutritional problem in India. (vigorcolumn.com)
  • Most other complete proteins come from animal sources, which makes quinoa stand out in terms of its nutritional benefits for vegan diets. (sadecetech.com)
  • Pellagra: Pellagra is a nutritional disorder due to the deficiency of niacin, one of the B-complex group of vitamins in the diet. (ignouworld.com)
  • Repeated testing for protein C functional activity allows differentiation between transient and congenital deficiency of protein C. Initially, a protein C activity (functional) assay can be performed, and if the result is low, a protein C antigen assay can be considered to determine the deficiency subtype (Type I or Type II). (wikipedia.org)
  • Severe congenital protein C deficiency: the use of protein C concentrates (human) as replacement therapy for life-threatening blood-clotting complications. (medlineplus.gov)
  • Congenital protein C deficiency is one of several inherited thrombophilias, which are a heterogeneous group of genetic disorders associated with an elevated risk of venous thromboembolism. (medscape.com)
  • However, eating multiple plant proteins together can create the effect of complete proteins. (bestmadenaturalproducts.com)
  • Most complete proteins are animal-based products (including meat, eggs and dairy). (sadecetech.com)
  • This is due to a transient hypercoagulable state following the rapid warfarin-induced fall in Protein C levels, before the levels of Factors II, IX, and X decrease. (clinlabnavigator.com)
  • The aged inhabitants is extra inclined to muscle losing once they have a poor protein weight-reduction plan. (dadelaon.com)
  • Moreover, unhealthy pores and skin indicators protein deficiency because of poor protein diets. (dadelaon.com)
  • Edema may be due to low levels of circulating proteins from poor protein digestion. (diagnose-me.com)
  • Casein - Based solely on its bioavailability rating, casein is a poor protein source for recovery. (hammernutrition.com)
  • A range of animal-based and plant-based foods are rich in protein, but is the quality the same? (progenmethod.com)
  • There are two main categories (or sources) of proteins - animal and plant-based. (bestmadenaturalproducts.com)
  • Because these are the known primary protein sources, there is a common misconception that plant-based diets are not protein-efficient. (justvegantoday.com)
  • Seitan , tofu , tempeh , Quinoa are just some of the protein-rich plant-based food sources. (justvegantoday.com)
  • Because athletes generally require higher doses of protein and plant-based protein sources are harder to digest, they can also take plant-based protein supplements or switch to plant-based meat substitutes . (justvegantoday.com)
  • Again, it is essential to note that this particular rumor is fueled by a lack of knowledge about plant-based protein. (justvegantoday.com)
  • Tempeh, tofu, and plant-based meat substitutes contain just as much protein as do animal-based sources. (justvegantoday.com)
  • Plant-Based Protein isn't as Good as that Sourced from Animals. (justvegantoday.com)
  • However, plant-based sources are just as protein-efficient. (justvegantoday.com)
  • Research indicates that plant-based protein is, in fact, better for one's overall health as it has a low-fat content. (justvegantoday.com)
  • Whether you're a longtime herbivore or you've recently considered switching to a plant-based diet, you've probably wondered about how to get more protein as a vegan. (sadecetech.com)
  • Looking for ways to increase your plant-based protein consumption or avoid protein deficiency? (sadecetech.com)
  • There are many plant-based protein powders available today, and you can use them in all kinds of ways. (sadecetech.com)
  • 2) In smaller quantities, protein can also be present in plant-based meals reminiscent of beans and seeds. (dadelaon.com)
  • Organic Vegan Protein - A unique and potent dairy-free, soy-free blend of five outstanding, 100% organic, plant-based proteins. (hammernutrition.com)
  • Central retinal artery and vein occlusion - Protein C Deficiency 33 year old male 291 views 33 year old male with vision loss for 3 hours. (retinagallery.com)
  • Central retinal artery and vein occlusion - Protein C Deficiency 33 year old male 307 views 33 year old male with vision loss for 3 hours. (retinagallery.com)
  • Surfactant protein B (SFTPB) deficiency is a fatal disease affecting newborn infants. (nature.com)
  • Pro360 Nephro LP is high in calories with lower protein helps to slow down the progression of chronic kidney disease and maintain nutrition status. (vigorcolumn.com)
  • In the chronic stage of the disease, when the erosion of the cartilage is taking place, it is possible that immune reactions to other cartilage proteins are initiated and contribute to the disease course. (biomedcentral.com)
  • In fact, the immunization with other cartilage proteins in some cases will cause a disease similar in type to CIA, which has been shown to be immunized with COMP [ 7 ]. (biomedcentral.com)
  • Ricket is a disease of growing children in which the bones become softened & deformed due to the deficiency of vitamin D. Osteomalacia is the adult format vitamin D deficiency. (ignouworld.com)
  • C-reactive protein is considered one of the best measures of the acute phase response to an infectious disease or other cause of tissue damage and inflammation. (cdc.gov)
  • Here we show the differentiation of patient specific iPSCs derived from a patient with SFTPB deficiency into lung organoids with mesenchymal and epithelial cell populations from both the proximal and distal portions of the human lung. (nature.com)
  • After differentiating the mutant and corrected cells into lung organoids, we show expression of SFTPB mRNA during endodermal and organoid differentiation but the protein product only after organoid differentiation. (nature.com)
  • We show that TMEM53 acts as an inhibitor of BMP-SMAD signaling by preventing SMAD accumulation in the cell nucleus and that its deficiency enhances osteogenic differentiation by overactivating the BMP signaling pathway. (nature.com)
  • Testing for protein Z deficiency is not part of routine thrombophilia testing. (msdmanuals.com)
  • There are three macronutrients: protein, fats, and carbohydrates. (bestmadenaturalproducts.com)
  • Carbohydrates require much more insulin than fat or protein does. (boxrox.com)
  • Sadly, the meals cravings related to protein deficiency result in the consumption of upper quantities of carbohydrates and sugary meals however restricted protein consumption, leading to weight acquire. (dadelaon.com)
  • b) Kwashiorkor: Lack of protein from carbohydrates sources like rice, bananas cause kwashiorkor. (ignouworld.com)
  • Specific and quantitative detail of every food or drink consumed during the previous day was recorded and calculated, thus providing estimates of calories, protein, carbohydrates, fat, unsaturated fats, cholesterol, and specific vitamins and minerals consumed. (cdc.gov)
  • Mild protein C deficiency affects approximately 1 in 500 individuals. (medlineplus.gov)
  • People with a mild protein C deficiency often do not exhibit any symptoms, even into adulthood. (wikipedia.org)
  • Individuals with TFP deficiency can present with a severe-to-mild phenotype, while individuals with LCHAD deficiency typically present with a severe-to-intermediate phenotype. (nih.gov)
  • Medicine Central , im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/1688740/all/Protein_C_Deficiency. (unboundmedicine.com)
  • One of the most common myths about a vegan diet is that it is not protein-efficient. (justvegantoday.com)
  • However, that is not true as a well-balanced vegan diet contains adequate protein. (justvegantoday.com)
  • When protein is broken down in the body it helps to fuel muscle mass, which helps metabolism. (bestmadenaturalproducts.com)
  • Metabolism is regulated by proteins as are hormones & the various activities they control. (ignouworld.com)
  • Methods and results This report describes an autosomal recessive form of spastic tetraplegic cerebral palsy with profound intellectual disability, microcephaly, epilepsy and white matter loss in a consanguineous family resulting from a homozygous deletion involving AP4E1 , one of the four subunits of the adaptor protein complex-4 (AP-4), identified by chromosomal microarray analysis. (bmj.com)
  • We thus sought to determine whether a SHANK3 deficiency could contribute to the emergence or worsening of AD symptoms and neuropathology. (jneurosci.org)
  • deficiencies in that interaction are a likely cause of otoferlin-related hearing loss. (reachmd.com)
  • This work established that the regulation of ethylene signalling is a part of plants' response to S deficiency and showed the interaction between UP9C, a tobacco LSU family member, and one of the tobacco isoforms of 1-aminocyclopropane-1-carboxylic acid oxidase (ACO2A). (waw.pl)
  • The four and a half LIM-only protein 2 (FHL2) is capable of shuttling between focal adhesion and nucleus where it signals through direct interaction with a number of proteins including beta-catenin. (pasteur.fr)
  • Vitamin A deficiency affects the severity of illness and the rate of deaths associated with measles, and it is known to induce severe measles-related complications in children, delaying recovery and promoting xerophthalmia, corneal ulcer, and blindness ( 7 , 8 , 10 ). (cdc.gov)
  • when the content of sugar and fat in the diet is insufficient, it not only strengthens protein decomposition, but also affects protein synthesis. (arshinefeed.com)
  • [ 9 ] These mutations are divided into 2 types-type I and type II-on the basis of whether they cause a quantitative (type I) or functional (type II) deficiency of protein C. (medscape.com)
  • If you tend to replace protein foods with sugary snacks, refined carbs and packaged convenient goods, your cholesterol can start to rise as your liver and cells process fats less efficiently. (boxrox.com)
  • It also improves bile flow and prevents muscle protein catabolism in the liver. (vigorcolumn.com)
  • Preeclampsia (toxemia in pregnancy) is a disorder of pregnancy that is characterized by hypertension (high blood pressure) and proteinuria (excessive protein in the urine), often including edema (swelling) and occasionally involving thrombocytopenia (low platelets) or liver function abnormalities. (diagnose-me.com)
  • In addition to the expected 50% loss of Shank3a, levels of other synaptic proteins, such as PSD-95, drebrin, and homer1, remained unchanged in the parietotemporal cortex of hemizygous Shank3 Δex4-9 animals. (jneurosci.org)
  • However, Shank3a deficiency increased the levels of soluble Aβ 42 and human tau at 18 months of age compared with 3xTg-AD mice with normal Shank3 expression. (jneurosci.org)
  • Protein C levels are dependent on the patient's age and other medical conditions, with adult levels being reached at late adolescence. (ihtc.org)
  • In mice, C3 (the precursor to ASP) knock-out (KO) results in ASP deficiency and leads to reduced body fat and leptin levels yet they are hyperphagic. (escholarship.org)
  • Type I (most common) results in the reduction of protein C levels. (unboundmedicine.com)
  • Type II results in a decreased functionality, despite having normal levels of protein C. (unboundmedicine.com)
  • Serial measurements were consistent with a prolonged ATIII and PC deficiency with significantly different levels between survivors and nonsurvivors. (qxmd.com)
  • When protein (especially albumin) levels in your blood go too low, the colloidal osmotic pressure will decrease and allow fluid to escape from blood vessels into your tissues, resulting in edema or swelling of the hands, feet, ankles, knees and/or belly. (diagnose-me.com)
  • Mice homozygous for a null allele exhibit decreased serum factor V and VIII and aspartate transaminase serum levels with accumulation of the proteins in the ER of hepatocytes. (jax.org)
  • Type I protein C deficiency refers to a quantitative deficiency in the plasma protein C concentration. (medscape.com)
  • They also utilized quantitative proteomic methods , a technique that allows for a comprehensive analysis of proteins, to identify a molecular pathway causing the patient's condition. (medicalnewstoday.com)
  • Meals cravings enhance urge for food and calorie consumption throughout these instances to amass protein from the weight-reduction plan for the satisfactory functioning and upkeep of the cells, tissues, and organs within the physique. (dadelaon.com)
  • Protein/calorie deficiencies inhibit hair growth. (cdc.gov)