The physiologically active form of vitamin D. It is formed primarily in the kidney by enzymatic hydroxylation of 25-hydroxycholecalciferol (CALCIFEDIOL). Its production is stimulated by low blood calcium levels and parathyroid hormone. Calcitriol increases intestinal absorption of calcium and phosphorus, and in concert with parathyroid hormone increases bone resorption.
Proteins, usually found in the cytoplasm, that specifically bind calcitriol, migrate to the nucleus, and regulate transcription of specific segments of DNA with the participation of D receptor interacting proteins (called DRIP). Vitamin D is converted in the liver and kidney to calcitriol and ultimately acts through these receptors.
Agents that increase calcium influx into calcium channels of excitable tissues. This causes vasoconstriction in VASCULAR SMOOTH MUSCLE and/or CARDIAC MUSCLE cells as well as stimulation of insulin release from pancreatic islets. Therefore, tissue-selective calcium agonists have the potential to combat cardiac failure and endocrinological disorders. They have been used primarily in experimental studies in cell and tissue culture.
Abnormally elevated PARATHYROID HORMONE secretion as a response to HYPOCALCEMIA. It is caused by chronic KIDNEY FAILURE or other abnormalities in the controls of bone and mineral metabolism, leading to various BONE DISEASES, such as RENAL OSTEODYSTROPHY.
A polypeptide hormone (84 amino acid residues) secreted by the PARATHYROID GLANDS which performs the essential role of maintaining intracellular CALCIUM levels in the body. Parathyroid hormone increases intracellular calcium by promoting the release of CALCIUM from BONE, increases the intestinal absorption of calcium, increases the renal tubular reabsorption of calcium, and increases the renal excretion of phosphates.
Derivatives of ERGOSTEROL formed by ULTRAVIOLET RAYS breaking of the C9-C10 bond. They differ from CHOLECALCIFEROL in having a double bond between C22 and C23 and a methyl group at C24.
Organic substances that are required in small amounts for maintenance and growth, but which cannot be manufactured by the human body.
Two pairs of small oval-shaped glands located in the front and the base of the NECK and adjacent to the two lobes of THYROID GLAND. They secrete PARATHYROID HORMONE that regulates the balance of CALCIUM; PHOSPHORUS; and MAGNESIUM in the body.
Abnormally high level of calcium in the blood.
A non-metal element that has the atomic symbol P, atomic number 15, and atomic weight 31. It is an essential element that takes part in a broad variety of biochemical reactions.
A vitamin that includes both CHOLECALCIFEROLS and ERGOCALCIFEROLS, which have the common effect of preventing or curing RICKETS in animals. It can also be viewed as a hormone since it can be formed in SKIN by action of ULTRAVIOLET RAYS upon the precursors, 7-dehydrocholesterol and ERGOSTEROL, and acts on VITAMIN D RECEPTORS to regulate CALCIUM in opposition to PARATHYROID HORMONE.
Reduction of the blood calcium below normal. Manifestations include hyperactive deep tendon reflexes, Chvostek's sign, muscle and abdominal cramps, and carpopedal spasm. (Dorland, 27th ed)
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
Decalcification of bone or abnormal bone development due to chronic KIDNEY DISEASES, in which 1,25-DIHYDROXYVITAMIN D3 synthesis by the kidneys is impaired, leading to reduced negative feedback on PARATHYROID HORMONE. The resulting SECONDARY HYPERPARATHYROIDISM eventually leads to bone disorders.
A clinical syndrome associated with the retention of renal waste products or uremic toxins in the blood. It is usually the result of RENAL INSUFFICIENCY. Most uremic toxins are end products of protein or nitrogen CATABOLISM, such as UREA or CREATININE. Severe uremia can lead to multiple organ dysfunctions with a constellation of symptoms.
A mitochondrial cytochrome P450 enzyme that catalyzes the 1-alpha-hydroxylation of 25-hydroxyvitamin D3 (also known as 25-hydroxycholecalciferol) in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP27B1 gene, converts 25-hydroxyvitamin D3 to 1-alpha,25-dihydroxyvitamin D3 which is the active form of VITAMIN D in regulating bone growth and calcium metabolism. This enzyme is also active on plant 25-hydroxyvitamin D2 (ergocalciferol).
A condition of abnormally elevated output of PARATHYROID HORMONE (or PTH) triggering responses that increase blood CALCIUM. It is characterized by HYPERCALCEMIA and BONE RESORPTION, eventually leading to bone diseases. PRIMARY HYPERPARATHYROIDISM is caused by parathyroid HYPERPLASIA or PARATHYROID NEOPLASMS. SECONDARY HYPERPARATHYROIDISM is increased PTH secretion in response to HYPOCALCEMIA, usually caused by chronic KIDNEY DISEASES.
Cytochrome P-450 monooxygenases (MIXED FUNCTION OXYGENASES) that are important in steroid biosynthesis and metabolism.
The major circulating metabolite of VITAMIN D3. It is produced in the LIVER and is the best indicator of the body's vitamin D stores. It is effective in the treatment of RICKETS and OSTEOMALACIA, both in azotemic and non-azotemic patients. Calcifediol also has mineralizing properties.
The geographic designation for states bordering on or located in the Pacific Ocean. The states so designated are Alaska, California, Hawaii, Oregon, and Washington. (U.S. Geologic Survey telephone communication)
A DNA sequence that is found in the promoter region of vitamin D regulated genes. Vitamin D receptor (RECEPTOR, CALCITRIOL) binds to and regulates the activity of genes containing this element.
Inorganic salts of phosphoric acid.
Derivative of 7-dehydroxycholesterol formed by ULTRAVIOLET RAYS breaking of the C9-C10 bond. It differs from ERGOCALCIFEROL in having a single bond between C22 and C23 and lacking a methyl group at C24.
A condition caused by a deficiency of PARATHYROID HORMONE (or PTH). It is characterized by HYPOCALCEMIA and hyperphosphatemia. Hypocalcemia leads to TETANY. The acquired form is due to removal or injuries to the PARATHYROID GLANDS. The congenital form is due to mutations of genes, such as TBX1; (see DIGEORGE SYNDROME); CASR encoding CALCIUM-SENSING RECEPTOR; or PTH encoding parathyroid hormone.
Disorder caused by an interruption of the mineralization of organic bone matrix leading to bone softening, bone pain, and weakness. It is the adult form of rickets resulting from disruption of VITAMIN D; PHOSPHORUS; or CALCIUM homeostasis.
Therapy for the insufficient cleansing of the BLOOD by the kidneys based on dialysis and including hemodialysis, PERITONEAL DIALYSIS, and HEMODIAFILTRATION.
Excision of one or more of the parathyroid glands.
Phosphorus used in foods or obtained from food. This element is a major intracellular component which plays an important role in many biochemical pathways relating to normal physiological functions. High concentrations of dietary phosphorus can cause nephrocalcinosis which is associated with impaired kidney function. Low concentrations of dietary phosphorus cause an increase in calcitriol in the blood and osteoporosis.
Agents that inhibit BONE RESORPTION and/or favor BONE MINERALIZATION and BONE REGENERATION. They are used to heal BONE FRACTURES and to treat METABOLIC BONE DISEASES such as OSTEOPOROSIS.
Disorders caused by interruption of BONE MINERALIZATION manifesting as OSTEOMALACIA in adults and characteristic deformities in infancy and childhood due to disturbances in normal BONE FORMATION. The mineralization process may be interrupted by disruption of VITAMIN D; PHOSPHORUS; or CALCIUM homeostasis, resulting from dietary deficiencies, or acquired, or inherited metabolic, or hormonal disturbances.
An inherited condition of abnormally low serum levels of PHOSPHATES (below 1 mg/liter) which can occur in a number of genetic diseases with defective reabsorption of inorganic phosphorus by the PROXIMAL RENAL TUBULES. This leads to phosphaturia, HYPOPHOSPHATEMIA, and disturbances of cellular and organ functions such as those in X-LINKED HYPOPHOSPHATEMIC RICKETS; OSTEOMALACIA; and FANCONI SYNDROME.
A condition of an abnormally low level of PHOSPHATES in the blood.
Carbonic acid calcium salt (CaCO3). An odorless, tasteless powder or crystal that occurs in nature. It is used therapeutically as a phosphate buffer in hemodialysis patients and as a calcium supplement.
A specialized CONNECTIVE TISSUE that is the main constituent of the SKELETON. The principle cellular component of bone is comprised of OSTEOBLASTS; OSTEOCYTES; and OSTEOCLASTS, while FIBRILLAR COLLAGENS and hydroxyapatite crystals form the BONE MATRIX.
Antihistamine drug now withdrawn from the market in many countries because of rare but potentially fatal side effects.
A sulfanilamide that is used as an anti-infective agent.
Vitamin K-dependent calcium-binding protein synthesized by OSTEOBLASTS and found primarily in BONES. Serum osteocalcin measurements provide a noninvasive specific marker of bone metabolism. The protein contains three residues of the amino acid gamma-carboxyglutamic acid (Gla), which, in the presence of CALCIUM, promotes binding to HYDROXYAPATITE and subsequent accumulation in BONE MATRIX.
An enzyme that catalyzes the conversion of an orthophosphoric monoester and water to an alcohol and orthophosphate. EC 3.1.3.1.
A hereditary disorder characterized by HYPOPHOSPHATEMIA; RICKETS; OSTEOMALACIA; renal defects in phosphate reabsorption and vitamin D metabolism; and growth retardation. Autosomal and X-linked dominant and recessive variants have been reported.
The giving of drugs, chemicals, or other substances by mouth.
The end-stage of CHRONIC RENAL INSUFFICIENCY. It is characterized by the severe irreversible kidney damage (as measured by the level of PROTEINURIA) and the reduction in GLOMERULAR FILTRATION RATE to less than 15 ml per min (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002). These patients generally require HEMODIALYSIS or KIDNEY TRANSPLANTATION.
A calbindin protein found in many mammalian tissues, including the UTERUS, PLACENTA, BONE, PITUITARY GLAND, and KIDNEYS. In intestinal ENTEROCYTES it mediates intracellular calcium transport from apical to basolateral membranes via calcium binding at two EF-HAND MOTIFS. Expression is regulated in some tissues by VITAMIN D.
An NAPH-dependent cytochrome P450 enzyme that catalyzes the oxidation of the side chain of sterol intermediates such as the 27-hydroxylation of 5-beta-cholestane-3-alpha,7-alpha,12-alpha-triol.
A class of G-protein-coupled receptors that react to varying extracellular CALCIUM levels. Calcium-sensing receptors in the PARATHYROID GLANDS play an important role in the maintenance of calcium HOMEOSTASIS by regulating the release of PARATHYROID HORMONE. They differ from INTRACELLULAR CALCIUM-SENSING PROTEINS which sense intracellular calcium levels.
I'm sorry for any confusion, but "Idaho" is a U.S. state located in the Pacific Northwest and it doesn't have a medical definition. If you have any medical questions or terms you would like me to define, I'd be happy to help!
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)
Catalyzes reversibly the oxidation of hydroxyl groups of prostaglandins.
9,10-Secoergosta-5,7,10(19),22-tetraene-3,25-diol. Biologically active metabolite of vitamin D2 which is more active in curing rickets than its parent. The compound is believed to attach to the same receptor as vitamin D2 and 25-hydroxyvitamin D3.
Hydroxy analogs of vitamin D 3; (CHOLECALCIFEROL); including CALCIFEDIOL; CALCITRIOL; and 24,25-DIHYDROXYVITAMIN D 3.
Cholecalciferols substituted with two hydroxy groups in any position.
Administration of high doses of pharmaceuticals over short periods of time.
Tumors or cancer of the PROSTATE.
The relationship between the dose of an administered drug and the response of the organism to the drug.
A family of small polypeptide growth factors that share several common features including a strong affinity for HEPARIN, and a central barrel-shaped core region of 140 amino acids that is highly homologous between family members. Although originally studied as proteins that stimulate the growth of fibroblasts this distinction is no longer a requirement for membership in the fibroblast growth factor family.
The calcium salt of gluconic acid. The compound has a variety of uses, including its use as a calcium replenisher in hypocalcemic states.
Disorders in the processing of phosphorus in the body: its absorption, transport, storage, and utilization.
Calcium-binding proteins that are found in DISTAL KIDNEY TUBULES, INTESTINES, BRAIN, and other tissues where they bind, buffer and transport cytoplasmic calcium. Calbindins possess a variable number of EF-HAND MOTIFS which contain calcium-binding sites. Some isoforms are regulated by VITAMIN D.
A diphosphonate which affects calcium metabolism. It inhibits ectopic calcification and slows down bone resorption and bone turnover.
Devices which can substitute for normally functioning KIDNEYS in removing components from the blood by DIALYSIS that are normally eliminated in the URINE.
Injections made into a vein for therapeutic or experimental purposes.
Protein of the annexin family with a probable role in exocytotic and endocytotic membrane events.
Calcium compounds used as food supplements or in food to supply the body with calcium. Dietary calcium is needed during growth for bone development and for maintenance of skeletal integrity later in life to prevent osteoporosis.
Bone loss due to osteoclastic activity.
Excision of kidney.
A carrier or inert medium used as a solvent (or diluent) in which the medicinally active agent is formulated and or administered. (Dictionary of Pharmacy, 1986)
The action of a drug in promoting or enhancing the effectiveness of another drug.
Injections introduced directly into localized lesions.
An anti-inflammatory 9-fluoro-glucocorticoid.
A nonhormonal medication for the treatment of postmenopausal osteoporosis in women. This drug builds healthy bone, restoring some of the bone loss as a result of osteoporosis.
Conditions in which the KIDNEYS perform below the normal level for more than three months. Chronic kidney insufficiency is classified by five stages according to the decline in GLOMERULAR FILTRATION RATE and the degree of kidney damage (as measured by the level of PROTEINURIA). The most severe form is the end-stage renal disease (CHRONIC KIDNEY FAILURE). (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002)
Small organic molecules that act as allosteric activators of the calcium sensing receptor (CaSR) in the PARATHYROID GLANDS and other tissues. They lower the threshold for CaSR activation by extracellular calcium ions and diminish PARATHYROID HORMONE (PTH) release from parathyroid cells.

Vitamin D regulates human ectocervical epithelial cell proliferation and insulin-like growth factor-binding protein-3 level. (1/2474)

The differentiation status of the cervical epithelial cell has an important influence on responsiveness to estrogens and progestins. Several agents, including glucocorticoids and retinoids, are known to influence cervical cell differentiation. However, the effects of vitamin D have not been examined. Vitamin D is known to regulate cell proliferation and gene expression in a variety of epithelial cells. In the present study we investigated the ability of 1alpha25-dihydroxyvitamin D3 (D3) to regulate cell proliferation and expression of insulin-like growth factor-binding protein-3 (IGFBP-3) in human ectocervical epithelial cells. ECE16-1, a non-tumorigenic cervical cell line, was growth inhibited by D3 with maximal inhibition at 1000 nM. IGFBP-3 levels increased in parallel with the growth inhibition. IGFBP-3 levels were half-maximally increased at approximately 10-100 nM and maximally increased (10- to 30-fold) at 1000 nM D3. These studies show that vitamin D regulates cervical epithelial cell gene regulation and cell proliferation and that IGFBP-3 may be an in vivo marker of vitamin D action in the cervix.  (+info)

22-oxacalcitriol suppresses secondary hyperparathyroidism without inducing low bone turnover in dogs with renal failure. (2/2474)

BACKGROUND: Calcitriol therapy suppresses serum levels of parathyroid hormone (PTH) in patients with renal failure but has several drawbacks, including hypercalcemia and/or marked suppression of bone turnover, which may lead to adynamic bone disease. A new vitamin D analogue, 22-oxacalcitriol (OCT), has been shown to have promising characteristics. This study was undertaken to determine the effects of OCT on serum PTH levels and bone turnover in states of normal or impaired renal function. METHODS: Sixty dogs were either nephrectomized (Nx, N = 38) or sham-operated (Sham, N = 22). The animals received supplemental phosphate to enhance PTH secretion. Fourteen weeks after the start of phosphate supplementation, half of the Nx and Sham dogs received doses of OCT (three times per week); the other half were given vehicle for 60 weeks. Thereafter, the treatment modalities for a subset of animals were crossed over for an additional eight months. Biochemical and hormonal indices of calcium and bone metabolism were measured throughout the study, and bone biopsies were done at baseline, 60 weeks after OCT or vehicle treatment, and at the end of the crossover period. RESULTS: In Nx dogs, OCT significantly decreased serum PTH levels soon after the induction of renal insufficiency. In long-standing secondary hyperparathyroidism, OCT (0.03 microg/kg) stabilized serum PTH levels during the first months. Serum PTH levels rose thereafter, but the rise was less pronounced compared with baseline than the rise seen in Nx control. These effects were accompanied by episodes of hypercalcemia and hyperphosphatemia. In animals with normal renal function, OCT induced a transient decrease in serum PTH levels at a dose of 0.1 microg/kg, which was not sustained with lowering of the doses. In Nx dogs, OCT reversed abnormal bone formation, such as woven osteoid and fibrosis, but did not significantly alter the level of bone turnover. In addition, OCT improved mineralization lag time, (that is, the rate at which osteoid mineralizes) in both Nx and Sham dogs. CONCLUSIONS: These results indicate that even though OCT does not completely prevent the occurrence of hypercalcemia in experimental dogs with renal insufficiency, it may be of use in the management of secondary hyperparathyroidism because it does not induce low bone turnover and, therefore, does not increase the risk of adynamic bone disease.  (+info)

Serum levels of 1,25-dihydroxyvitamin D, 24,25-dihydroxyvitamin D, and 25-hydroxyvitamin D in nondialyzed patients with chronic renal failure. (3/2474)

BACKGROUND: In patients with chronic renal failure (CRF), abnormalities in vitamin D metabolism are known to be present, and several factors could contribute to the abnormalities. METHODS: We measured serum levels of three vitamin D metabolites, 1,25(OH)2D, 24, 25(OH)2D and 25(OH)D, and analyzed factors affecting their levels in 76 nondialyzed patients with CRF (serum creatinine> 1.6 and < 9.0 mg/dl), 37 of whom had diabetes mellitus (DM-CRF) and 39 of whom were nondiabetic (nonDM-CRF). RESULTS: Serum levels of 1,25(OH)2D were positively correlated with estimated creatinine clearance (CCr; r = 0.429; P < 0.0001), and levels of 24,25(OH)2D were weakly correlated with CCr (r = 0.252, P < 0.05); no correlation was noted for 25(OH)D. Serum levels of all three vitamin D metabolites were significantly and positively correlated with serum albumin. Although there were no significant differences in age, sex, estimated CCr, calcium and phosphate between DM-CRF and nonDM-CRF, all three vitamin D metabolites were significantly lower in DM-CRF than in nonDM-CRF. To analyze factors influencing vitamin D metabolite levels, we performed multiple regression analyses. Serum 25(OH)D levels were significantly and independently associated with serum albumin, presence of DM and serum phosphate (R2 = 0.599; P < 0.0001). 24,25(OH)2D levels were significantly and strongly associated with 25(OH)D (beta = 0.772; R2 = 0.446; P < 0.0001). Serum 1,25(OH)2D levels were significantly associated only with estimated CCr (R2 = 0. 409; P < 0.0001). CONCLUSIONS: These results suggest that hypoalbuminemia and the presence of DM independently affect serum 25(OH)D levels, probably via diabetic nephropathy and poor nutritional status associated with diabetes, and that 25(OH)D is actively catalyzed to 24,25(OH)2D in CRF, probably largely via extrarenal 24-hydroxylase. Serum levels of 1,25(OH)2D were significantly affected by the degree of renal failure. Thus, this study indicates that patients with CRF, particularly those with DM, should receive supplements containing the active form of vitamin D prior to dialysis.  (+info)

1,25-Dihydroxyvitamin D3 enhances the susceptibility of breast cancer cells to doxorubicin-induced oxidative damage. (4/2474)

1,25-Dihydroxyvitamin D3 (1,25(OH)2D3), the hormonal form of vitamin D, has anticancer activity in vivo and in vitro. Doxorubicin exerts its cytotoxic effect on tumor cells mainly by two mechanisms: (a) generation of reactive oxygen species (ROS); and (b) inhibition of topoisomerase II. We studied the combined cytotoxic action of 1,25(OH)2D3 and doxorubicin on MCF-7 breast cancer cells. Pretreatement with 1,25(OH)2D3 resulted in enhanced cytotoxicity of doxorubicin. The average enhancing effect after a 72-h pretreatment with 1,25(OH)2D3 (10 nM) followed by a 24-h treatment with 1 microg/ml doxorubicin was 74+/-9% (mean +/- SE). Under these experimental conditions, 1,25(OH)2D3 on its own did not affect cell number or viability. 1,25(OH)2D3 also enhanced the cytotoxic activity of another ROS generating quinone, menadione, but did not affect cytotoxicity induced by the topoisomerase inhibitor etoposide. The antioxidant N-acetylcysteine slightly reduced the cytotoxic activity of doxorubicin but had a marked protective effect against the combined action of 1,25(OH)2D3 and doxorubicin. These results indicate that ROS are involved in the interaction between 1,25(OH)2D3 and doxorubicin. 1,25(OH)2D3 also increased doxorubicin cytotoxicity in primary cultures of rat cardiomyocytes. Treatment of MCF-7 cells with 1,25(OH)2D3 alone markedly reduced the activity, protein, and mRNA levels of the cytoplasmic antioxidant enzyme Cu/Zn superoxide dismutase, which indicated that the hormone inhibits its biosynthesis. This reduction in the antioxidant capacity of the cells could account for the synergistic interaction between 1,25(OH)2D3 and doxorubicin and may also suggest increased efficacy of 1,25(OH)2D3 or its analogues in combination with other ROS-generating anticancer therapeutic modalities.  (+info)

Convergence of transforming growth factor-beta and vitamin D signaling pathways on SMAD transcriptional coactivators. (5/2474)

Cell proliferation and differentiation are regulated by growth regulatory factors such as transforming growth factor-beta (TGF-beta) and the liphophilic hormone vitamin D. TGF-beta causes activation of SMAD proteins acting as coactivators or transcription factors in the nucleus. Vitamin D controls transcription of target genes through the vitamin D receptor (VDR). Smad3, one of the SMAD proteins downstream in the TGF-beta signaling pathway, was found in mammalian cells to act as a coactivator specific for ligand-induced transactivation of VDR by forming a complex with a member of the steroid receptor coactivator-1 protein family in the nucleus. Thus, Smad3 may mediate cross-talk between vitamin D and TGF-beta signaling pathways.  (+info)

Regulation of PiT-1, a sodium-dependent phosphate co-transporter in rat parathyroid glands. (6/2474)

A cDNA encoding an Na+-Pi co-transporter, termed rat PiT-1, has now been isolated from rat parathyroid. Expression of rat PiT-1 in Xenopus oocytes revealed that it possesses Na+-dependent Pi co-transport activity. The amount of PiT-1 mRNA in the parathyroid of vitamin D-deficient rats was reduced compared with that in normal animals, and increased markedly after administration of 1,25-dihydroxyvitamin D3. Furthermore, the abundance of PiT-1 mRNA in the parathyroid was much greater in rats fed a low-Pi diet than in those fed a high-Pi diet. Thus, rat PiT-1 may contribute to the effects of Pi and vitamin D on parathyroid function.  (+info)

Regulation of vitamin D action. (7/2474)

The control of gene transcription by vitamin D compounds is initiated by binding to the VDR, which enhances the receptor's ability to heterodimerize to RXR, interact with response elements in target genes and attract components of the transcriptional initiation complex. A number of factors are capable of influencing this process, including (i) the rate of uptake and catabolism of the ligand, (ii) the nature of the conformational change induced by a specific ligand, (iii) the cellular content of the VDR, (iv) post-translational modifications of the VDR and (v) the availability of other transcriptional components. Vitamin D analogues may affect these factors differently to 1,25(OH)2D3 to produce unique biological profiles that can be exploited for therapeutic use.  (+info)

Topical psoriasis therapy. (8/2474)

Psoriasis is a common dermatosis, affecting from 1 to 3 percent of the population. Until recently, the mainstays of topical therapy have been corticosteroids, tars, anthralins and keratolytics. Recently, however, vitamin D analogs, a new anthralin preparation and topical retinoids have expanded physicians' therapeutic armamentarium. These new topical therapies offer increased hope and convenience to the large patient population with psoriasis.  (+info)

Calcitriol is the active form of vitamin D, also known as 1,25-dihydroxyvitamin D. It is a steroid hormone that plays a crucial role in regulating calcium and phosphate levels in the body to maintain healthy bones. Calcitriol is produced in the kidneys from its precursor, calcidiol (25-hydroxyvitamin D), which is derived from dietary sources or synthesized in the skin upon exposure to sunlight.

Calcitriol promotes calcium absorption in the intestines, helps regulate calcium and phosphate levels in the kidneys, and stimulates bone cells (osteoblasts) to form new bone tissue while inhibiting the activity of osteoclasts, which resorb bone. This hormone is essential for normal bone mineralization and growth, as well as for preventing hypocalcemia (low calcium levels).

In addition to its role in bone health, calcitriol has various other physiological functions, including modulating immune responses, cell proliferation, differentiation, and apoptosis. Calcitriol deficiency or resistance can lead to conditions such as rickets in children and osteomalacia or osteoporosis in adults.

Calcitriol receptors, also known as Vitamin D receptors (VDR), are nuclear receptor proteins that bind to calcitriol (1,25-dihydroxyvitamin D3), the active form of vitamin D. These receptors are found in various tissues and cells throughout the body, including the small intestine, bone, kidney, and parathyroid gland.

When calcitriol binds to its receptor, it forms a complex that regulates the expression of genes involved in calcium and phosphate homeostasis, cell growth, differentiation, and immune function. Calcitriol receptors play a critical role in maintaining normal levels of calcium and phosphate in the blood by increasing the absorption of these minerals from the gut, promoting bone mineralization, and regulating the production of parathyroid hormone (PTH).

Calcitriol receptors have also been implicated in various disease processes, including cancer, autoimmune disorders, and infectious diseases. Modulation of calcitriol receptor activity has emerged as a potential therapeutic strategy for the treatment of these conditions.

Calcium channel agonists are substances that increase the activity or function of calcium channels. Calcium channels are specialized proteins in cell membranes that regulate the flow of calcium ions into and out of cells. They play a crucial role in various physiological processes, including muscle contraction, hormone secretion, and nerve impulse transmission.

Calcium channel agonists can enhance the opening of these channels, leading to an increased influx of calcium ions into the cells. This can result in various pharmacological effects, depending on the type of cell and tissue involved. For example, calcium channel agonists may be used to treat conditions such as hypotension (low blood pressure) or heart block by increasing cardiac contractility and heart rate. However, these agents should be used with caution due to their potential to cause adverse effects, including increased heart rate, hypertension, and arrhythmias.

Examples of calcium channel agonists include drugs such as Bay K 8644, FPL 64176, and A23187. It's important to note that some substances can act as both calcium channel agonists and antagonists, depending on the dose, concentration, or duration of exposure.

Secondary hyperparathyroidism is a condition characterized by an overproduction of parathyroid hormone (PTH) from the parathyroid glands due to hypocalcemia (low levels of calcium in the blood). This condition is usually a result of chronic kidney disease, where the kidneys fail to convert vitamin D into its active form, leading to decreased absorption of calcium in the intestines. The body responds by increasing PTH production to maintain normal calcium levels, but over time, this results in high PTH levels and associated complications such as bone disease, kidney stones, and cardiovascular calcification.

Parathyroid hormone (PTH) is a polypeptide hormone that plays a crucial role in the regulation of calcium and phosphate levels in the body. It is produced and secreted by the parathyroid glands, which are four small endocrine glands located on the back surface of the thyroid gland.

The primary function of PTH is to maintain normal calcium levels in the blood by increasing calcium absorption from the gut, mobilizing calcium from bones, and decreasing calcium excretion by the kidneys. PTH also increases phosphate excretion by the kidneys, which helps to lower serum phosphate levels.

In addition to its role in calcium and phosphate homeostasis, PTH has been shown to have anabolic effects on bone tissue, stimulating bone formation and preventing bone loss. However, chronic elevations in PTH levels can lead to excessive bone resorption and osteoporosis.

Overall, Parathyroid Hormone is a critical hormone that helps maintain mineral homeostasis and supports healthy bone metabolism.

Ergocalciferols are a form of vitamin D, specifically vitamin D2, that is found in some plants. They are not produced by the human body and must be obtained through diet or supplementation. Ergocalciferols can be converted into an active form of vitamin D in the body, which is important for maintaining healthy bones and calcium levels. However, vitamin D3 (cholecalciferol), which is produced by the body in response to sunlight exposure, is generally considered to be more effective at raising and maintaining vitamin D levels in the body than ergocalciferols.

Vitamins are organic substances that are essential in small quantities for the normal growth, development, and maintenance of life in humans. They are required for various biochemical functions in the body such as energy production, blood clotting, immune function, and making DNA.

Unlike macronutrients (carbohydrates, proteins, and fats), vitamins do not provide energy but they play a crucial role in energy metabolism. Humans require 13 essential vitamins, which can be divided into two categories: fat-soluble and water-soluble.

Fat-soluble vitamins (A, D, E, and K) are stored in the body's fat tissues and liver, and can stay in the body for a longer period of time. Water-soluble vitamins (B-complex vitamins and vitamin C) are not stored in the body and need to be replenished regularly through diet or supplementation.

Deficiency of vitamins can lead to various health problems, while excessive intake of certain fat-soluble vitamins can also be harmful due to toxicity. Therefore, it is important to maintain a balanced diet that provides all the essential vitamins in adequate amounts.

The parathyroid glands are four small endocrine glands located in the neck, usually near or behind the thyroid gland. They secrete parathyroid hormone (PTH), which plays a critical role in regulating calcium and phosphate levels in the blood and bones. PTH helps maintain the balance of these minerals by increasing the absorption of calcium from food in the intestines, promoting reabsorption of calcium in the kidneys, and stimulating the release of calcium from bones when needed. Additionally, PTH decreases the excretion of calcium through urine and reduces phosphate reabsorption in the kidneys, leading to increased phosphate excretion. Disorders of the parathyroid glands can result in conditions such as hyperparathyroidism (overactive glands) or hypoparathyroidism (underactive glands), which can have significant impacts on calcium and phosphate homeostasis and overall health.

Hypercalcemia is a medical condition characterized by an excess of calcium ( Ca2+ ) in the blood. While the normal range for serum calcium levels is typically between 8.5 to 10.2 mg/dL (milligrams per deciliter) or 2.14 to 2.55 mmol/L (millimoles per liter), hypercalcemia is generally defined as a serum calcium level greater than 10.5 mg/dL or 2.6 mmol/L.

Hypercalcemia can result from various underlying medical disorders, including primary hyperparathyroidism, malignancy (cancer), certain medications, granulomatous diseases, and excessive vitamin D intake or production. Symptoms of hypercalcemia may include fatigue, weakness, confusion, memory loss, depression, constipation, nausea, vomiting, increased thirst, frequent urination, bone pain, and kidney stones. Severe or prolonged hypercalcemia can lead to serious complications such as kidney failure, cardiac arrhythmias, and calcification of soft tissues. Treatment depends on the underlying cause and severity of the condition.

Phosphorus is an essential mineral that is required by every cell in the body for normal functioning. It is a key component of several important biomolecules, including adenosine triphosphate (ATP), which is the primary source of energy for cells, and deoxyribonucleic acid (DNA) and ribonucleic acid (RNA), which are the genetic materials in cells.

Phosphorus is also a major constituent of bones and teeth, where it combines with calcium to provide strength and structure. In addition, phosphorus plays a critical role in various metabolic processes, including energy production, nerve impulse transmission, and pH regulation.

The medical definition of phosphorus refers to the chemical element with the atomic number 15 and the symbol P. It is a highly reactive non-metal that exists in several forms, including white phosphorus, red phosphorus, and black phosphorus. In the body, phosphorus is primarily found in the form of organic compounds, such as phospholipids, phosphoproteins, and nucleic acids.

Abnormal levels of phosphorus in the body can lead to various health problems. For example, high levels of phosphorus (hyperphosphatemia) can occur in patients with kidney disease or those who consume large amounts of phosphorus-rich foods, and can contribute to the development of calcification of soft tissues and cardiovascular disease. On the other hand, low levels of phosphorus (hypophosphatemia) can occur in patients with malnutrition, vitamin D deficiency, or alcoholism, and can lead to muscle weakness, bone pain, and an increased risk of infection.

Vitamin D is a fat-soluble secosteroid that is crucial for the regulation of calcium and phosphate levels in the body, which are essential for maintaining healthy bones and teeth. It can be synthesized by the human body when skin is exposed to ultraviolet-B (UVB) rays from sunlight, or it can be obtained through dietary sources such as fatty fish, fortified dairy products, and supplements. There are two major forms of vitamin D: vitamin D2 (ergocalciferol), which is found in some plants and fungi, and vitamin D3 (cholecalciferol), which is produced in the skin or obtained from animal-derived foods. Both forms need to undergo two hydroxylations in the body to become biologically active as calcitriol (1,25-dihydroxyvitamin D3), the hormonally active form of vitamin D. This activated form exerts its effects by binding to the vitamin D receptor (VDR) found in various tissues, including the small intestine, bone, kidney, and immune cells, thereby influencing numerous physiological processes such as calcium homeostasis, bone metabolism, cell growth, and immune function.

Hypocalcemia is a medical condition characterized by an abnormally low level of calcium in the blood. Calcium is a vital mineral that plays a crucial role in various bodily functions, including muscle contraction, nerve impulse transmission, and bone formation. Normal calcium levels in the blood usually range from 8.5 to 10.2 milligrams per deciliter (mg/dL). Hypocalcemia is typically defined as a serum calcium level below 8.5 mg/dL or, when adjusted for albumin (a protein that binds to calcium), below 8.4 mg/dL (ionized calcium).

Hypocalcemia can result from several factors, such as vitamin D deficiency, hypoparathyroidism (underactive parathyroid glands), kidney dysfunction, certain medications, and severe magnesium deficiency. Symptoms of hypocalcemia may include numbness or tingling in the fingers, toes, or lips; muscle cramps or spasms; seizures; and, in severe cases, cognitive impairment or cardiac arrhythmias. Treatment typically involves correcting the underlying cause and administering calcium and vitamin D supplements to restore normal calcium levels in the blood.

Calcium is an essential mineral that is vital for various physiological processes in the human body. The medical definition of calcium is as follows:

Calcium (Ca2+) is a crucial cation and the most abundant mineral in the human body, with approximately 99% of it found in bones and teeth. It plays a vital role in maintaining structural integrity, nerve impulse transmission, muscle contraction, hormonal secretion, blood coagulation, and enzyme activation.

Calcium homeostasis is tightly regulated through the interplay of several hormones, including parathyroid hormone (PTH), calcitonin, and vitamin D. Dietary calcium intake, absorption, and excretion are also critical factors in maintaining optimal calcium levels in the body.

Hypocalcemia refers to low serum calcium levels, while hypercalcemia indicates high serum calcium levels. Both conditions can have detrimental effects on various organ systems and require medical intervention to correct.

Renal osteodystrophy is a bone disease that occurs in individuals with chronic kidney disease (CKD). It is characterized by abnormalities in the bones' structure and mineral composition due to disturbances in the metabolism of calcium, phosphorus, and vitamin D. These metabolic disturbances result from the kidneys' decreased ability to maintain balance in the levels of these minerals and hormones.

Renal osteodystrophy can manifest as several bone disorders, including:

1. Osteitis fibrosa cystica: Increased bone turnover due to excessive parathyroid hormone (PTH) production, leading to high levels of alkaline phosphatase and increased resorption of bones.
2. Adynamic bone disease: Decreased bone turnover due to reduced PTH levels, resulting in low bone formation rates and increased fracture risk.
3. Mixed uremic osteodystrophy: A combination of high and low bone turnover, with varying degrees of mineralization defects.
4. Osteomalacia: Defective mineralization of bones due to vitamin D deficiency or resistance, leading to soft and weak bones.

Symptoms of renal osteodystrophy may include bone pain, muscle weakness, fractures, deformities, and growth retardation in children. Diagnosis typically involves laboratory tests, imaging studies, and sometimes bone biopsies. Treatment focuses on correcting the metabolic imbalances through dietary modifications, medications (such as phosphate binders, vitamin D analogs, and calcimimetics), and addressing any secondary hyperparathyroidism if present.

Uremia is not a disease itself, but rather it's a condition that results from the buildup of waste products in the blood due to kidney failure. The term "uremia" comes from the word "urea," which is one of the waste products that accumulate when the kidneys are not functioning properly.

In uremia, the kidneys are unable to effectively filter waste and excess fluids from the blood, leading to a variety of symptoms such as nausea, vomiting, fatigue, itching, mental confusion, and ultimately, if left untreated, can lead to coma and death. It is a serious condition that requires immediate medical attention, often involving dialysis or a kidney transplant to manage the underlying kidney dysfunction.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase is an enzyme that is responsible for converting 25-hydroxyvitamin D3 (a precursor form of vitamin D) to its active form, 1,25-dihydroxyvitamin D3. This activation process occurs primarily in the kidneys and is tightly regulated by various factors such as calcium levels, parathyroid hormone, and vitamin D status.

The activated form of vitamin D, 1,25-dihydroxyvitamin D3, plays a crucial role in maintaining calcium homeostasis by increasing the absorption of calcium from the gut and promoting bone health. It also has various other functions, including modulation of immune function, cell growth regulation, and protection against cancer.

Deficiencies in 25-Hydroxyvitamin D3 1-alpha-Hydroxylase can lead to vitamin D deficiency and its associated symptoms, such as osteomalacia (softening of the bones) and osteoporosis (brittle bones). Conversely, overactivity of this enzyme can result in hypercalcemia (elevated levels of calcium in the blood), which can cause a range of symptoms including kidney stones, abdominal pain, nausea, and vomiting.

Hyperparathyroidism is a condition in which the parathyroid glands produce excessive amounts of parathyroid hormone (PTH). There are four small parathyroid glands located in the neck, near or within the thyroid gland. They release PTH into the bloodstream to help regulate the levels of calcium and phosphorus in the body.

In hyperparathyroidism, overproduction of PTH can lead to an imbalance in these minerals, causing high blood calcium levels (hypercalcemia) and low phosphate levels (hypophosphatemia). This can result in various symptoms such as fatigue, weakness, bone pain, kidney stones, and cognitive issues.

There are two types of hyperparathyroidism: primary and secondary. Primary hyperparathyroidism occurs when there is a problem with one or more of the parathyroid glands, causing them to become overactive and produce too much PTH. Secondary hyperparathyroidism develops as a response to low calcium levels in the body due to conditions like vitamin D deficiency, chronic kidney disease, or malabsorption syndromes.

Treatment for hyperparathyroidism depends on the underlying cause and severity of symptoms. In primary hyperparathyroidism, surgery to remove the overactive parathyroid gland(s) is often recommended. For secondary hyperparathyroidism, treating the underlying condition and managing calcium levels with medications or dietary changes may be sufficient.

Steroid hydroxylases are enzymes that catalyze the addition of a hydroxyl group (-OH) to a steroid molecule. These enzymes are located in the endoplasmic reticulum and play a crucial role in the biosynthesis of various steroid hormones, such as cortisol, aldosterone, and sex hormones. The hydroxylation reaction catalyzed by these enzymes increases the polarity and solubility of steroids, allowing them to be further metabolized and excreted from the body.

The most well-known steroid hydroxylases are part of the cytochrome P450 family, specifically CYP11A1, CYP11B1, CYP11B2, CYP17A1, CYP19A1, and CYP21A2. Each enzyme has a specific function in steroid biosynthesis, such as converting cholesterol to pregnenolone (CYP11A1), hydroxylating the 11-beta position of steroids (CYP11B1 and CYP11B2), or performing multiple hydroxylation reactions in the synthesis of sex hormones (CYP17A1, CYP19A1, and CYP21A2).

Defects in these enzymes can lead to various genetic disorders, such as congenital adrenal hyperplasia, which is characterized by impaired steroid hormone biosynthesis.

Calcifediol is the medical term for 25-hydroxyvitamin D, which is a form of vitamin D that is produced in the liver when it processes vitamin D from sunlight or from dietary sources. It is an important precursor to the active form of vitamin D, calcitriol, and is often used as a supplement for people who have low levels of vitamin D. Calcifediol is converted to calcitriol in the kidneys, where it plays a role in regulating calcium and phosphate levels in the body, which are important for maintaining healthy bones and teeth.

I'm sorry for any confusion, but there seems to be a mistake in your question. "Pacific States" is not a recognized medical term or concept. The term "Pacific" usually refers to the Pacific Ocean or regions near it, and "states" typically refers to political divisions like countries or states within a country. If you're referring to a specific medical term that includes these words, could you please provide more context or clarify your question? I'm here to help!

A Vitamin D Response Element (VDRE) is a specific sequence in the DNA to which the vitamin D receptor (VDR) binds, upon activation by its ligand, vitamin D or one of its metabolites. This binding results in the regulation of gene transcription and subsequent protein synthesis. VDREs are typically located in the promoter region of genes that are involved in calcium homeostasis, cell growth and differentiation, immune function, and other processes. The interaction between VDR and VDRE plays a crucial role in the genomic actions of vitamin D.

Phosphates, in a medical context, refer to the salts or esters of phosphoric acid. Phosphates play crucial roles in various biological processes within the human body. They are essential components of bones and teeth, where they combine with calcium to form hydroxyapatite crystals. Phosphates also participate in energy transfer reactions as phosphate groups attached to adenosine diphosphate (ADP) and adenosine triphosphate (ATP). Additionally, they contribute to buffer systems that help maintain normal pH levels in the body.

Abnormal levels of phosphates in the blood can indicate certain medical conditions. High phosphate levels (hyperphosphatemia) may be associated with kidney dysfunction, hyperparathyroidism, or excessive intake of phosphate-containing products. Low phosphate levels (hypophosphatemia) might result from malnutrition, vitamin D deficiency, or certain diseases affecting the small intestine or kidneys. Both hypophosphatemia and hyperphosphatemia can have significant impacts on various organ systems and may require medical intervention.

Cholecalciferol is the chemical name for Vitamin D3. It is a fat-soluble vitamin that is essential for the regulation of calcium and phosphate levels in the body, which helps to maintain healthy bones and teeth. Cholecalciferol can be synthesized by the skin upon exposure to sunlight or obtained through dietary sources such as fatty fish, liver, and fortified foods. It is also available as a dietary supplement.

Hypoparathyroidism is a medical condition characterized by decreased levels or insufficient function of parathyroid hormone (PTH), which is produced and released by the parathyroid glands. These glands are located in the neck, near the thyroid gland, and play a crucial role in regulating calcium and phosphorus levels in the body.

In hypoparathyroidism, low PTH levels result in decreased absorption of calcium from the gut, increased excretion of calcium through the kidneys, and impaired regulation of bone metabolism. This leads to low serum calcium levels (hypocalcemia) and high serum phosphorus levels (hyperphosphatemia).

Symptoms of hypoparathyroidism can include muscle cramps, spasms, or tetany (involuntary muscle contractions), numbness or tingling sensations in the fingers, toes, and around the mouth, fatigue, weakness, anxiety, cognitive impairment, and in severe cases, seizures. Hypoparathyroidism can be caused by various factors, including surgical removal or damage to the parathyroid glands, autoimmune disorders, radiation therapy, genetic defects, or low magnesium levels. Treatment typically involves calcium and vitamin D supplementation to maintain normal serum calcium levels and alleviate symptoms. In some cases, recombinant PTH (Natpara) may be prescribed as well.

Osteomalacia is a medical condition characterized by the softening of bones due to defective bone mineralization, resulting from inadequate vitamin D, phosphate, or calcium. It mainly affects adults and is different from rickets, which occurs in children. The primary symptom is bone pain, but muscle weakness can also occur. Prolonged osteomalacia may lead to skeletal deformities and an increased risk of fractures. Treatment typically involves supplementation with vitamin D, calcium, and sometimes phosphate.

Renal dialysis is a medical procedure that is used to artificially remove waste products, toxins, and excess fluids from the blood when the kidneys are no longer able to perform these functions effectively. This process is also known as hemodialysis.

During renal dialysis, the patient's blood is circulated through a special machine called a dialyzer or an artificial kidney, which contains a semi-permeable membrane that filters out waste products and excess fluids from the blood. The cleaned blood is then returned to the patient's body.

Renal dialysis is typically recommended for patients with advanced kidney disease or kidney failure, such as those with end-stage renal disease (ESRD). It is a life-sustaining treatment that helps to maintain the balance of fluids and electrolytes in the body, prevent the buildup of waste products and toxins, and control blood pressure.

There are two main types of renal dialysis: hemodialysis and peritoneal dialysis. Hemodialysis is the most common type and involves using a dialyzer to filter the blood outside the body. Peritoneal dialysis, on the other hand, involves placing a catheter in the abdomen and using the lining of the abdomen (peritoneum) as a natural filter to remove waste products and excess fluids from the body.

Overall, renal dialysis is an essential treatment option for patients with kidney failure, helping them to maintain their quality of life and prolong their survival.

Parathyroidectomy is a surgical procedure for the removal of one or more of the parathyroid glands. These glands are located in the neck and are responsible for producing parathyroid hormone (PTH), which helps regulate the levels of calcium and phosphorus in the body.

Parathyroidectomy is typically performed to treat conditions such as hyperparathyroidism, where one or more of the parathyroid glands become overactive and produce too much PTH. This can lead to high levels of calcium in the blood, which can cause symptoms such as weakness, fatigue, bone pain, kidney stones, and mental confusion.

There are different types of parathyroidectomy procedures, including:

* Partial parathyroidectomy: removal of one or more, but not all, of the parathyroid glands.
* Total parathyroidectomy: removal of all four parathyroid glands.
* Subtotal parathyroidectomy: removal of three and a half of the four parathyroid glands, leaving a small portion of one gland to prevent hypoparathyroidism (a condition where the body produces too little PTH).

The choice of procedure depends on the underlying condition and its severity. After the surgery, patients may need to have their calcium levels monitored and may require calcium and vitamin D supplements to maintain normal calcium levels in the blood.

Dietary Phosphorus is a mineral that is an essential nutrient for human health. It is required for the growth, maintenance, and repair of body tissues, including bones and teeth. Phosphorus is also necessary for the production of energy, the formation of DNA and RNA, and the regulation of various physiological processes.

In the diet, phosphorus is primarily found in protein-containing foods such as meat, poultry, fish, dairy products, legumes, and nuts. It can also be found in processed foods that contain additives such as phosphoric acid, which is used to enhance flavor or as a preservative.

The recommended daily intake of phosphorus for adults is 700 milligrams (mg) per day. However, it's important to note that excessive intake of phosphorus, particularly from supplements and fortified foods, can lead to health problems such as kidney damage and calcification of soft tissues. Therefore, it's recommended to obtain phosphorus primarily from whole foods rather than supplements.

Bone density conservation agents, also known as anti-resorptive agents or bone-sparing drugs, are a class of medications that help to prevent the loss of bone mass and reduce the risk of fractures. They work by inhibiting the activity of osteoclasts, the cells responsible for breaking down and reabsorbing bone tissue during the natural remodeling process.

Examples of bone density conservation agents include:

1. Bisphosphonates (e.g., alendronate, risedronate, ibandronate, zoledronic acid) - These are the most commonly prescribed class of bone density conservation agents. They bind to hydroxyapatite crystals in bone tissue and inhibit osteoclast activity, thereby reducing bone resorption.
2. Denosumab (Prolia) - This is a monoclonal antibody that targets RANKL (Receptor Activator of Nuclear Factor-κB Ligand), a key signaling molecule involved in osteoclast differentiation and activation. By inhibiting RANKL, denosumab reduces osteoclast activity and bone resorption.
3. Selective estrogen receptor modulators (SERMs) (e.g., raloxifene) - These medications act as estrogen agonists or antagonists in different tissues. In bone tissue, SERMs mimic the bone-preserving effects of estrogen by inhibiting osteoclast activity and reducing bone resorption.
4. Hormone replacement therapy (HRT) - Estrogen hormone replacement therapy has been shown to preserve bone density in postmenopausal women; however, its use is limited due to increased risks of breast cancer, cardiovascular disease, and thromboembolic events.
5. Calcitonin - This hormone, secreted by the thyroid gland, inhibits osteoclast activity and reduces bone resorption. However, it has largely been replaced by other more effective bone density conservation agents.

These medications are often prescribed for individuals at high risk of fractures due to conditions such as osteoporosis or metabolic disorders that affect bone health. It is essential to follow the recommended dosage and administration guidelines to maximize their benefits while minimizing potential side effects. Regular monitoring of bone density, blood calcium levels, and other relevant parameters is also necessary during treatment with these medications.

Rickets is a medical condition characterized by the softening and weakening of bones in children, primarily caused by deficiency of vitamin D, calcium, or phosphate. It leads to skeletal deformities, bone pain, and growth retardation. Prolonged lack of sunlight exposure, inadequate intake of vitamin D-rich foods, or impaired absorption or utilization of vitamin D can contribute to the development of rickets.

Familial Hypophosphatemia is a genetic disorder characterized by low levels of phosphate in the blood (hypophosphatemia) due to impaired absorption of phosphates in the gut. This condition results from mutations in the SLC34A3 gene, which provides instructions for making a protein called NaPi-IIc, responsible for reabsorbing phosphates from the filtrate in the kidney tubules back into the bloodstream.

In familial hypophosphatemia, the impaired function of NaPi-IIc leads to excessive loss of phosphate through urine, resulting in hypophosphatemia. This condition can cause rickets (a softening and weakening of bones) in children and osteomalacia (softening of bones) in adults. Symptoms may include bowed legs, bone pain, muscle weakness, and short stature.

Familial Hypophosphatemia is inherited as an autosomal recessive trait, meaning that an individual must inherit two copies of the mutated gene (one from each parent) to develop the condition.

Hypophosphatemia is a medical condition characterized by abnormally low levels of phosphate (phosphorus) in the blood, specifically below 2.5 mg/dL. Phosphate is an essential electrolyte that plays a crucial role in various bodily functions such as energy production, bone formation, and maintaining acid-base balance.

Hypophosphatemia can result from several factors, including malnutrition, vitamin D deficiency, alcoholism, hormonal imbalances, and certain medications. Symptoms of hypophosphatemia may include muscle weakness, fatigue, bone pain, confusion, and respiratory failure in severe cases. Treatment typically involves correcting the underlying cause and administering phosphate supplements to restore normal levels.

Calcium carbonate is a chemical compound with the formula CaCO3. It is a common substance found in rocks and in the shells of many marine animals. As a mineral, it is known as calcite or aragonite.

In the medical field, calcium carbonate is often used as a dietary supplement to prevent or treat calcium deficiency. It is also commonly used as an antacid to neutralize stomach acid and relieve symptoms of heartburn, acid reflux, and indigestion.

Calcium carbonate works by reacting with hydrochloric acid in the stomach to form water, carbon dioxide, and calcium chloride. This reaction helps to raise the pH level in the stomach and neutralize excess acid.

It is important to note that excessive use of calcium carbonate can lead to hypercalcemia, a condition characterized by high levels of calcium in the blood, which can cause symptoms such as nausea, vomiting, constipation, confusion, and muscle weakness. Therefore, it is recommended to consult with a healthcare provider before starting any new supplement regimen.

"Bone" is the hard, dense connective tissue that makes up the skeleton of vertebrate animals. It provides support and protection for the body's internal organs, and serves as a attachment site for muscles, tendons, and ligaments. Bone is composed of cells called osteoblasts and osteoclasts, which are responsible for bone formation and resorption, respectively, and an extracellular matrix made up of collagen fibers and mineral crystals.

Bones can be classified into two main types: compact bone and spongy bone. Compact bone is dense and hard, and makes up the outer layer of all bones and the shafts of long bones. Spongy bone is less dense and contains large spaces, and makes up the ends of long bones and the interior of flat and irregular bones.

The human body has 206 bones in total. They can be further classified into five categories based on their shape: long bones, short bones, flat bones, irregular bones, and sesamoid bones.

Astemizole is a second-generation antihistamine that was previously used to treat symptoms associated with allergies, such as hay fever, hives, and other allergic skin reactions. It works by blocking the action of histamine, a substance in the body that causes allergic symptoms. However, astemizole has been withdrawn from the market in many countries due to rare but serious side effects on the heart.

Sulfadimethoxine is an antimicrobial agent, specifically a sulfonamide. It is defined as a synthetic antibacterial drug that contains the sulfanilamide nucleus and is used to treat various bacterial infections in both humans and animals. In human medicine, it is used to treat urinary tract infections, bronchitis, and traveler's diarrhea. In veterinary medicine, it is commonly used to treat coccidiosis in animals such as poultry, cattle, and pets.

The drug works by inhibiting the bacterial synthesis of folic acid, which is essential for bacterial growth. It is usually administered orally and is available in various forms, including tablets, capsules, and powder for suspension. As with any medication, it should be used under the guidance of a healthcare professional to ensure its safe and effective use.

Osteocalcin is a protein that is produced by osteoblasts, which are the cells responsible for bone formation. It is one of the most abundant non-collagenous proteins found in bones and plays a crucial role in the regulation of bone metabolism. Osteocalcin contains a high affinity for calcium ions, making it essential for the mineralization of the bone matrix.

Once synthesized, osteocalcin is secreted into the extracellular matrix, where it binds to hydroxyapatite crystals, helping to regulate their growth and contributing to the overall strength and integrity of the bones. Osteocalcin also has been found to play a role in other physiological processes outside of bone metabolism, such as modulating insulin sensitivity, energy metabolism, and male fertility.

In summary, osteocalcin is a protein produced by osteoblasts that plays a critical role in bone formation, mineralization, and turnover, and has been implicated in various other physiological processes.

Alkaline phosphatase (ALP) is an enzyme found in various body tissues, including the liver, bile ducts, digestive system, bones, and kidneys. It plays a role in breaking down proteins and minerals, such as phosphate, in the body.

The medical definition of alkaline phosphatase refers to its function as a hydrolase enzyme that removes phosphate groups from molecules at an alkaline pH level. In clinical settings, ALP is often measured through blood tests as a biomarker for various health conditions.

Elevated levels of ALP in the blood may indicate liver or bone diseases, such as hepatitis, cirrhosis, bone fractures, or cancer. Therefore, physicians may order an alkaline phosphatase test to help diagnose and monitor these conditions. However, it is essential to interpret ALP results in conjunction with other diagnostic tests and clinical findings for accurate diagnosis and treatment.

Familial Hypophosphatemic Rickets (FHR) is a genetic disorder characterized by impaired reabsorption of phosphate in the kidneys, leading to low levels of phosphate in the blood (hypophosphatemia). This condition results in defective mineralization of bones and teeth, causing rickets in children and osteomalacia in adults.

FHR is typically caused by mutations in the PHEX gene, which encodes a protein that helps regulate phosphate levels in the body. In FHR, the mutation leads to an overproduction of a hormone called fibroblast growth factor 23 (FGF23), which increases phosphate excretion in the urine and decreases the activation of vitamin D, further contributing to hypophosphatemia.

Symptoms of FHR may include bowing of the legs, bone pain, muscle weakness, short stature, dental abnormalities, and skeletal deformities. Treatment typically involves oral phosphate supplements and active forms of vitamin D to correct the hypophosphatemia and improve bone mineralization. Regular monitoring of blood phosphate levels, kidney function, and bone health is essential for effective management of this condition.

Oral administration is a route of giving medications or other substances by mouth. This can be in the form of tablets, capsules, liquids, pastes, or other forms that can be swallowed. Once ingested, the substance is absorbed through the gastrointestinal tract and enters the bloodstream to reach its intended target site in the body. Oral administration is a common and convenient route of medication delivery, but it may not be appropriate for all substances or in certain situations, such as when rapid onset of action is required or when the patient has difficulty swallowing.

Chronic kidney failure, also known as chronic kidney disease (CKD) stage 5 or end-stage renal disease (ESRD), is a permanent loss of kidney function that occurs gradually over a period of months to years. It is defined as a glomerular filtration rate (GFR) of less than 15 ml/min, which means the kidneys are filtering waste and excess fluids at less than 15% of their normal capacity.

CKD can be caused by various underlying conditions such as diabetes, hypertension, glomerulonephritis, polycystic kidney disease, and recurrent kidney infections. Over time, the damage to the kidneys can lead to a buildup of waste products and fluids in the body, which can cause a range of symptoms including fatigue, weakness, shortness of breath, nausea, vomiting, and confusion.

Treatment for chronic kidney failure typically involves managing the underlying condition, making lifestyle changes such as following a healthy diet, and receiving supportive care such as dialysis or a kidney transplant to replace lost kidney function.

S100 calcium binding protein G, also known as calgranulin A or S100A8, is a member of the S100 family of proteins. These proteins are characterized by their ability to bind calcium ions and play a role in intracellular signaling and regulation of various cellular processes.

S100 calcium binding protein G forms a heterodimer with S100 calcium binding protein B (S100A9) and is involved in the inflammatory response, immune function, and tumor growth and progression. The S100A8/A9 heterocomplex has been shown to play a role in neutrophil activation and recruitment, as well as the regulation of cytokine production and cell proliferation.

Elevated levels of S100 calcium binding protein G have been found in various inflammatory conditions, such as rheumatoid arthritis, Crohn's disease, and psoriasis, as well as in several types of cancer, including breast, lung, and colon cancer. Therefore, it has been suggested that S100 calcium binding protein G may be a useful biomarker for the diagnosis and prognosis of these conditions.

Cholestanetriol 26-monooxygenase is an enzyme that is involved in the metabolism of bile acids and steroids in the body. This enzyme is responsible for adding a hydroxyl group (-OH) to the cholestanetriol molecule at position 26, which is a critical step in the conversion of cholestanetriol to bile acids.

The gene that encodes this enzyme is called CYP3A4, which is located on chromosome 7 in humans. Mutations in this gene can lead to various metabolic disorders, including impaired bile acid synthesis and altered steroid hormone metabolism.

Deficiency or dysfunction of cholestanetriol 26-monooxygenase has been associated with several diseases, such as liver disease, cerebrotendinous xanthomatosis, and some forms of cancer. Therefore, understanding the function and regulation of this enzyme is essential for developing new therapies and treatments for these conditions.

Calcium-sensing receptors (CaSR) are a type of G protein-coupled receptor that play a crucial role in the regulation of extracellular calcium homeostasis. They are widely expressed in various tissues, including the parathyroid gland, kidney, and bone.

The primary function of CaSR is to detect changes in extracellular calcium concentrations and transmit signals to regulate the release of parathyroid hormone (PTH) from the parathyroid gland. When the concentration of extracellular calcium increases, CaSR is activated, which leads to a decrease in PTH secretion, thereby preventing further elevation of calcium levels. Conversely, when calcium levels decrease, CaSR is inhibited, leading to an increase in PTH release and restoration of normal calcium levels.

In addition to regulating calcium homeostasis, CaSR also plays a role in other physiological processes, including cell proliferation, differentiation, and apoptosis. Dysregulation of CaSR has been implicated in various diseases, such as hyperparathyroidism, hypoparathyroidism, and cancer. Therefore, understanding the function and regulation of CaSR is essential for developing new therapeutic strategies to treat these conditions.

I am not aware of any medical definition for the term "Idaho." It is primarily used as the name of a state in the United States. If you have any specific medical context or terminology that you would like me to help define, please let me know and I will be happy to assist you.

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.

Hydroxyprostaglandin Dehydrogenases (HPGDs) are a group of enzymes that catalyze the oxidation of prostaglandins, which are hormone-like lipid compounds with various physiological effects in the body. The oxidation reaction catalyzed by HPGDs involves the removal of hydrogen atoms from the prostaglandin molecule and the addition of a ketone group in its place.

The HPGD family includes several isoforms, each with distinct tissue distributions and substrate specificities. The most well-known isoform is 15-hydroxyprostaglandin dehydrogenase (15-PGDH), which preferentially oxidizes PGE2 and PGF2α at the 15-hydroxyl position, thereby inactivating these prostaglandins.

The regulation of HPGD activity is critical for maintaining prostaglandin homeostasis, as imbalances in prostaglandin levels have been linked to various pathological conditions, including inflammation, cancer, and cardiovascular disease. For example, decreased 15-PGDH expression has been observed in several types of cancer, leading to increased PGE2 levels and promoting tumor growth and progression.

Overall, Hydroxyprostaglandin Dehydrogenases play a crucial role in regulating prostaglandin signaling and have important implications for human health and disease.

25-Hydroxyvitamin D 2 (25(OH)D2) is a form of vitamin D that is produced in the body as a result of the metabolism of ergocalciferol, also known as vitamin D2. Vitamin D2 is found in some plant-based foods and is sometimes used as a dietary supplement.

When vitamin D2 is ingested or absorbed through the skin after exposure to sunlight, it is converted in the liver to 25(OH)D2. This form of vitamin D is then further metabolized in the kidneys to the active form of vitamin D, calcitriol (1,25-dihydroxyvitamin D).

Like other forms of vitamin D, 25(OH)D2 is important for maintaining healthy bones and muscles by regulating the absorption of calcium and phosphorus from the diet. It may also have other health benefits, such as reducing the risk of certain cancers and autoimmune disorders.

It's worth noting that 25-Hydroxyvitamin D2 is not usually measured in clinical settings, as it is converted to 25-Hydroxyvitamin D3 (25(OH)D3) in the body, and total 25(OH)D (which includes both 25(OH)D2 and 25(OH)D3) is typically measured to assess vitamin D status.

Hydroxycholecalciferols are metabolites of vitamin D that are formed in the liver and kidneys. They are important for maintaining calcium homeostasis in the body by promoting the absorption of calcium from the gut and reabsorption of calcium from the kidneys.

The two main forms of hydroxycholecalciferols are 25-hydroxyvitamin D (25(OH)D) and 1,25-dihydroxyvitamin D (1,25(OH)2D). 25-hydroxyvitamin D is the major circulating form of vitamin D in the body and is used as a clinical measure of vitamin D status. It is converted to 1,25-dihydroxyvitamin D in the kidneys by the enzyme 1α-hydroxylase, which is activated in response to low serum calcium or high phosphate levels.

1,25-dihydroxyvitamin D is the biologically active form of vitamin D and plays a critical role in regulating calcium homeostasis by increasing intestinal calcium absorption and promoting bone health. Deficiency in hydroxycholecalciferols can lead to rickets in children and osteomalacia or osteoporosis in adults, characterized by weakened bones and increased risk of fractures.

Dihydroxycholecalciferols are a form of calcifediol, which is a type of secosteroid hormone that is produced in the body as a result of the exposure to sunlight and the dietary intake of vitamin D. The term "dihydroxycholecalciferols" specifically refers to the compounds 1,25-dihydroxycholecalciferol (calcitriol) and 24,25-dihydroxycholecalciferol. These compounds are produced in the body through a series of chemical reactions involving enzymes that convert vitamin D into its active forms.

Calcitriol is the biologically active form of vitamin D and plays an important role in regulating the levels of calcium and phosphorus in the blood, as well as promoting the absorption of these minerals from the gut. It also has other functions, such as modulating cell growth and immune function.

24,25-dihydroxycholecalciferol is a less active form of vitamin D that is produced in larger quantities than calcitriol. Its exact role in the body is not well understood, but it is thought to have some effects on calcium metabolism and may play a role in regulating the levels of other hormones in the body.

Dihydroxycholecalciferols are typically measured in the blood as part of an evaluation for vitamin D deficiency or to monitor treatment with vitamin D supplements. Low levels of these compounds can indicate a deficiency, while high levels may indicate excessive intake or impaired metabolism.

Pulse therapy, in the context of drug treatment, refers to a therapeutic regimen where a medication is administered in large doses for a short period of time, followed by a break or "drug-free" interval before the next dose. This cycle is then repeated at regular intervals. The goal of pulse therapy is to achieve high concentrations of the drug in the body to maximize its therapeutic effect while minimizing overall exposure and potential side effects.

This approach is often used for drugs that have a long half-life or slow clearance, as it allows for periodic "washing out" of the drug from the body. Pulse therapy can also help reduce the risk of developing drug resistance in certain conditions like rheumatoid arthritis and tuberculosis. Common examples include pulse methotrexate for rheumatoid arthritis and intermittent preventive treatment with anti-malarial drugs.

It is important to note that the use of pulse therapy should be based on a thorough understanding of the drug's pharmacokinetics, therapeutic index, and potential adverse effects. Close monitoring of patients undergoing pulse therapy is essential to ensure safety and efficacy.

Prostatic neoplasms refer to abnormal growths in the prostate gland, which can be benign or malignant. The term "neoplasm" simply means new or abnormal tissue growth. When it comes to the prostate, neoplasms are often referred to as tumors.

Benign prostatic neoplasms, such as prostate adenomas, are non-cancerous overgrowths of prostate tissue. They usually grow slowly and do not spread to other parts of the body. While they can cause uncomfortable symptoms like difficulty urinating, they are generally not life-threatening.

Malignant prostatic neoplasms, on the other hand, are cancerous growths. The most common type of prostate cancer is adenocarcinoma, which arises from the glandular cells in the prostate. Prostate cancer often grows slowly and may not cause any symptoms for many years. However, some types of prostate cancer can be aggressive and spread quickly to other parts of the body, such as the bones or lymph nodes.

It's important to note that while prostate neoplasms can be concerning, early detection and treatment can significantly improve outcomes for many men. Regular check-ups with a healthcare provider are key to monitoring prostate health and catching any potential issues early on.

A dose-response relationship in the context of drugs refers to the changes in the effects or symptoms that occur as the dose of a drug is increased or decreased. Generally, as the dose of a drug is increased, the severity or intensity of its effects also increases. Conversely, as the dose is decreased, the effects of the drug become less severe or may disappear altogether.

The dose-response relationship is an important concept in pharmacology and toxicology because it helps to establish the safe and effective dosage range for a drug. By understanding how changes in the dose of a drug affect its therapeutic and adverse effects, healthcare providers can optimize treatment plans for their patients while minimizing the risk of harm.

The dose-response relationship is typically depicted as a curve that shows the relationship between the dose of a drug and its effect. The shape of the curve may vary depending on the drug and the specific effect being measured. Some drugs may have a steep dose-response curve, meaning that small changes in the dose can result in large differences in the effect. Other drugs may have a more gradual dose-response curve, where larger changes in the dose are needed to produce significant effects.

In addition to helping establish safe and effective dosages, the dose-response relationship is also used to evaluate the potential therapeutic benefits and risks of new drugs during clinical trials. By systematically testing different doses of a drug in controlled studies, researchers can identify the optimal dosage range for the drug and assess its safety and efficacy.

Fibroblast Growth Factors (FGFs) are a family of growth factors that play crucial roles in various biological processes, including cell survival, proliferation, migration, and differentiation. They bind to specific tyrosine kinase receptors (FGFRs) on the cell surface, leading to intracellular signaling cascades that regulate gene expression and downstream cellular responses. FGFs are involved in embryonic development, tissue repair, and angiogenesis (the formation of new blood vessels). There are at least 22 distinct FGFs identified in humans, each with unique functions and patterns of expression. Some FGFs, like FGF1 and FGF2, have mitogenic effects on fibroblasts and other cell types, while others, such as FGF7 and FGF10, are essential for epithelial-mesenchymal interactions during organ development. Dysregulation of FGF signaling has been implicated in various pathological conditions, including cancer, fibrosis, and developmental disorders.

Calcium gluconate is a medical compound that is used primarily as a medication to treat conditions related to low calcium levels in the body (hypocalcemia) or to prevent calcium deficiency. It is also used as an antidote for treating poisoning from certain chemicals, such as beta-blockers and fluoride.

Calcium gluconate is a form of calcium salt, which is combined with gluconic acid, a natural organic acid found in various fruits and honey. This compound has a high concentration of calcium, making it an effective supplement for increasing calcium levels in the body.

In medical settings, calcium gluconate can be administered orally as a tablet or liquid solution, or it can be given intravenously (directly into a vein) by a healthcare professional. The intravenous route is typically used in emergency situations to quickly raise calcium levels and treat symptoms of hypocalcemia, such as muscle cramps, spasms, or seizures.

It's important to note that while calcium gluconate can be beneficial for treating low calcium levels, it should only be used under the guidance of a healthcare provider, as improper use or overdose can lead to serious side effects, including kidney damage and heart problems.

Phosphorus metabolism disorders refer to a group of conditions that affect the body's ability to properly regulate the levels and utilization of phosphorus. Phosphorus is an essential mineral that plays a critical role in many biological processes, including energy production, bone formation, and nerve function.

Disorders of phosphorus metabolism can result from genetic defects, kidney dysfunction, vitamin D deficiency, or other medical conditions. These disorders can lead to abnormal levels of phosphorus in the blood, which can cause a range of symptoms, including muscle weakness, bone pain, seizures, and respiratory failure.

Examples of phosphorus metabolism disorders include:

1. Hypophosphatemia: This is a condition characterized by low levels of phosphorus in the blood. It can be caused by various factors, such as malnutrition, vitamin D deficiency, and kidney dysfunction.
2. Hyperphosphatemia: This is a condition characterized by high levels of phosphorus in the blood. It can be caused by kidney failure, tumor lysis syndrome, and certain medications.
3. Hereditary hypophosphatemic rickets: This is a genetic disorder that affects the body's ability to regulate vitamin D and phosphorus metabolism. It can lead to weakened bones and skeletal deformities.
4. Oncogenic osteomalacia: This is a rare condition that occurs when tumors produce substances that interfere with phosphorus metabolism, leading to bone pain and weakness.

Treatment for phosphorus metabolism disorders depends on the underlying cause of the disorder and may include dietary changes, supplements, medications, or surgery.

Calbindins are a family of calcium-binding proteins that are widely distributed in various tissues, including the gastrointestinal tract, brain, and kidney. They play important roles in regulating intracellular calcium levels and modulating calcium-dependent signaling pathways. Calbindin D28k, one of the major isoforms, is particularly abundant in the central nervous system and has been implicated in neuroprotection, neuronal plasticity, and regulation of neurotransmitter release. Deficiencies or alterations in calbindins have been associated with various pathological conditions, including neurological disorders and cancer.

Etidronic acid is a type of medication known as a bisphosphonate. It is used to treat conditions such as Paget's disease, osteoporosis, and certain types of cancer that have spread to the bones.

Etidronic acid works by inhibiting the activity of cells called osteoclasts, which are responsible for breaking down bone tissue. This helps to slow down the process of bone loss and can increase bone density, making bones stronger and less likely to break.

The medication is available in the form of a solution that is given intravenously (through a vein) in a hospital or clinic setting. It may be given as a single dose or as multiple doses over a period of time, depending on the condition being treated and the individual patient's needs.

As with any medication, etidronic acid can have side effects, including nausea, vomiting, diarrhea, and bone pain. It is important for patients to discuss the potential risks and benefits of this medication with their healthcare provider before starting treatment.

Artificial kidney, also known as a renal replacement therapy or dialysis, is a device that performs the essential functions of the human kidney when the natural kidneys are unable to do so. The main function of an artificial kidney is to filter and remove waste, excess water, and toxic substances from the blood, helping to maintain the body's chemical balance and regulate blood pressure.

There are two primary types of artificial kidney treatments: hemodialysis and peritoneal dialysis. Hemodialysis involves circulating the patient's blood through an external filter (dialyzer) that contains a semi-permeable membrane, which separates waste products and excess fluids from the blood. The cleaned blood is then returned to the body. This process typically takes place in a clinical setting, such as a hospital or dialysis center, for about 3-5 hours, several times a week.

Peritoneal dialysis, on the other hand, uses the patient's own peritoneum (a membrane lining the abdominal cavity) as a natural filter. A special solution called dialysate is introduced into the peritoneal cavity via a catheter, and waste products and excess fluids pass from the blood vessels in the peritoneum into the dialysate. After a dwell time of several hours, the used dialysate is drained out and replaced with fresh solution. This process can be performed manually (continuous ambulatory peritoneal dialysis) or using a machine (automated peritoneal dialysis), typically at home and during sleep.

Artificial kidneys are life-saving treatments for patients with end-stage renal disease, helping them maintain their quality of life and extend their lifespan until a kidney transplant becomes available.

Intravenous injections are a type of medical procedure where medication or fluids are administered directly into a vein using a needle and syringe. This route of administration is also known as an IV injection. The solution injected enters the patient's bloodstream immediately, allowing for rapid absorption and onset of action. Intravenous injections are commonly used to provide quick relief from symptoms, deliver medications that are not easily absorbed by other routes, or administer fluids and electrolytes in cases of dehydration or severe illness. It is important that intravenous injections are performed using aseptic technique to minimize the risk of infection.

Annexin A6 is a protein that belongs to the annexin family, which are calcium-dependent phospholipid-binding proteins. Annexin A6 is involved in various cellular processes such as exocytosis, endocytosis, and membrane trafficking. It has been shown to play a role in regulating ion channels, modulating the actin cytoskeleton, and interacting with other proteins to form multimolecular complexes. Annexin A6 is expressed in various tissues, including the heart, lung, kidney, and pancreas. Mutations in the ANXA6 gene have been associated with certain diseases, such as kidney stones and cataracts.

Dietary calcium is a type of calcium that is obtained through food sources. Calcium is an essential mineral that is necessary for many bodily functions, including bone formation and maintenance, muscle contraction, nerve impulse transmission, and blood clotting.

The recommended daily intake of dietary calcium varies depending on age, sex, and other factors. For example, the recommended daily intake for adults aged 19-50 is 1000 mg, while women over 50 and men over 70 require 1200 mg per day.

Good dietary sources of calcium include dairy products such as milk, cheese, and yogurt; leafy green vegetables like broccoli and kale; fortified cereals and juices; and certain types of fish, such as salmon and sardines. It is important to note that some foods can inhibit the absorption of calcium, including oxalates found in spinach and rhubarb, and phytates found in whole grains and legumes.

If a person is unable to get enough calcium through their diet, they may need to take calcium supplements. However, it is important to talk to a healthcare provider before starting any new supplement regimen, as excessive intake of calcium can lead to negative health effects.

Bone resorption is the process by which bone tissue is broken down and absorbed into the body. It is a normal part of bone remodeling, in which old or damaged bone tissue is removed and new tissue is formed. However, excessive bone resorption can lead to conditions such as osteoporosis, in which bones become weak and fragile due to a loss of density. This process is carried out by cells called osteoclasts, which break down the bone tissue and release minerals such as calcium into the bloodstream.

Nephrectomy is a surgical procedure in which all or part of a kidney is removed. It may be performed due to various reasons such as severe kidney damage, kidney cancer, or living donor transplantation. The type of nephrectomy depends on the reason for the surgery - a simple nephrectomy involves removing only the affected portion of the kidney, while a radical nephrectomy includes removal of the whole kidney along with its surrounding tissues like the adrenal gland and lymph nodes.

"Pharmaceutical vehicles" is not a standard term in medical or pharmaceutical sciences. However, I can provide some context based on the phrase's possible meaning. If by "pharmaceutical vehicles," you mean the carriers or delivery systems for drugs or medications, then the definition would be:

Pharmaceutical vehicles refer to various formulations, preparations, or technologies that facilitate and control the administration of a drug or therapeutic agent to its target site in the body. These can include different types of drug delivery systems such as tablets, capsules, liposomes, nanoparticles, transdermal patches, inhalers, injectables, and other innovative drug carrier technologies.

These pharmaceutical vehicles ensure that the active ingredients are safely and effectively transported to their intended site of action within the body, enhancing therapeutic efficacy while minimizing potential side effects.

Drug synergism is a pharmacological concept that refers to the interaction between two or more drugs, where the combined effect of the drugs is greater than the sum of their individual effects. This means that when these drugs are administered together, they produce an enhanced therapeutic response compared to when they are given separately.

Drug synergism can occur through various mechanisms, such as:

1. Pharmacodynamic synergism - When two or more drugs interact with the same target site in the body and enhance each other's effects.
2. Pharmacokinetic synergism - When one drug affects the metabolism, absorption, distribution, or excretion of another drug, leading to an increased concentration of the second drug in the body and enhanced therapeutic effect.
3. Physiochemical synergism - When two drugs interact physically, such as when one drug enhances the solubility or permeability of another drug, leading to improved absorption and bioavailability.

It is important to note that while drug synergism can result in enhanced therapeutic effects, it can also increase the risk of adverse reactions and toxicity. Therefore, healthcare providers must carefully consider the potential benefits and risks when prescribing combinations of drugs with known or potential synergistic effects.

"Intralesional injection" is a medical term that refers to the administration of a medication directly into a lesion or skin abnormality, such as a tumor, cyst, or blister. This technique is used to deliver the medication directly to the site of action, allowing for higher local concentrations and potentially reducing systemic side effects. Common examples include the injection of corticosteroids into inflamed tissues to reduce swelling and pain, or the injection of chemotherapeutic agents directly into tumors to shrink them.

Dexamethasone is a type of corticosteroid medication, which is a synthetic version of a natural hormone produced by the adrenal glands. It is often used to reduce inflammation and suppress the immune system in a variety of medical conditions, including allergies, asthma, rheumatoid arthritis, and certain skin conditions.

Dexamethasone works by binding to specific receptors in cells, which triggers a range of anti-inflammatory effects. These include reducing the production of chemicals that cause inflammation, suppressing the activity of immune cells, and stabilizing cell membranes.

In addition to its anti-inflammatory effects, dexamethasone can also be used to treat other medical conditions, such as certain types of cancer, brain swelling, and adrenal insufficiency. It is available in a variety of forms, including tablets, liquids, creams, and injectable solutions.

Like all medications, dexamethasone can have side effects, particularly if used for long periods of time or at high doses. These may include mood changes, increased appetite, weight gain, acne, thinning skin, easy bruising, and an increased risk of infections. It is important to follow the instructions of a healthcare provider when taking dexamethasone to minimize the risk of side effects.

Alendronate is a medication that falls under the class of bisphosphonates. It is commonly used in the treatment and prevention of osteoporosis in postmenopausal women and men, as well as in the management of glucocorticoid-induced osteoporosis and Paget's disease of bone.

Alendronate works by inhibiting the activity of osteoclasts, which are cells responsible for breaking down and reabsorbing bone tissue. By reducing the activity of osteoclasts, alendronate helps to slow down bone loss and increase bone density, thereby reducing the risk of fractures.

The medication is available in several forms, including tablets and oral solutions, and is typically taken once a week for osteoporosis prevention and treatment. It is important to follow the dosing instructions carefully, as improper administration can reduce the drug's effectiveness or increase the risk of side effects. Common side effects of alendronate include gastrointestinal symptoms such as heartburn, stomach pain, and nausea.

Chronic Renal Insufficiency (CRI) is a medical condition characterized by a gradual and progressive loss of kidney function over a period of months or years. It is also known as Chronic Kidney Disease (CKD). The main function of the kidneys is to filter waste products and excess fluids from the blood, which are then excreted in the urine. When the kidneys become insufficient, these waste products and fluids accumulate in the body, leading to various complications.

CRI is defined as a glomerular filtration rate (GFR) of less than 60 ml/min/1.73m2 for three months or more, regardless of cause. GFR is a measure of kidney function that estimates how well the kidneys are filtering waste products from the blood. The condition is classified into five stages based on the severity of the disease and the GFR value.

Stage 1: GFR greater than or equal to 90 ml/min/1.73m2
Stage 2: GFR between 60-89 ml/min/1.73m2
Stage 3: GFR between 30-59 ml/min/1.73m2
Stage 4: GFR between 15-29 ml/min/1.73m2
Stage 5: GFR less than 15 ml/min/1.73m2 or dialysis

CRI can be caused by various underlying conditions such as diabetes, hypertension, glomerulonephritis, polycystic kidney disease, and other genetic or acquired disorders. Symptoms of CRI may include fatigue, weakness, loss of appetite, swelling in the legs and ankles, shortness of breath, and changes in urination patterns. Treatment for CRI focuses on slowing down the progression of the disease, managing symptoms, and preventing complications. This may involve lifestyle modifications, medication, dialysis, or kidney transplantation.

Calcimimetic agents are a type of medication that mimic the action of calcium on the calcium-sensing receptor (CaSR) in the parathyroid gland. These agents enhance the sensitivity of the CaSR to extracellular calcium, which leads to a decrease in parathyroid hormone (PTH) secretion.

Calcimimetics are primarily used in the treatment of secondary hyperparathyroidism in patients with chronic kidney disease (CKD) on dialysis. By decreasing PTH levels, calcimimetics can help to prevent the development of bone disease, reduce the risk of cardiovascular calcification, and improve overall clinical outcomes in these patients.

The most commonly prescribed calcimimetic agent is cinacalcet (Sensipar/Mimpara), which has been shown to effectively lower PTH levels, as well as serum calcium and phosphorus levels, in patients with CKD on dialysis. Other calcimimetic agents include etelcalcetide (Parsabiv) and evocalcet (Rocaltrol).

It is important to note that calcimimetics should be used with caution in patients with hypocalcemia, as they can further lower serum calcium levels. Close monitoring of calcium, phosphorus, and PTH levels is necessary during treatment with these agents.

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Carrillo-López N, Fernández-Martín JL, Cannata-Andía JB (2009-04-01). "[The role of calcium, calcitriol and their receptors in ... calcitriol), which is released into the circulation. This latter form of vitamin D is the active hormone which stimulates ... Calcitriol Increase in serum phosphate. Fibroblast growth factor-23 (FGF23) is produced in osteoblasts (from bone) in response ...
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... (INN) is an analog of calcitriol. It has a higher potency both in vivo and in vitro systems, and longer duration ...
Caniggia A, Nuti R, Lore F, Martini G, Turchetti V, Righi G (April 1990). "Long-term treatment with calcitriol in ...
Caniggia A, Nuti R, Lore F, Martini G, Turchetti V, Righi G (April 1990). "Long-term treatment with calcitriol in ...
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Calcitriol (vitamin D) significantly inhibits the expression of the COX-2 gene. Caution should be exercised in combining low ...
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It has been suggested, based on animal research, that calcitriol, the active metabolite of vitamin D, can provide significant ... Cass WA, Smith MP, Peters LE (2006). "Calcitriol protects against the dopamine- and serotonin-depleting effects of neurotoxic ...
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Atkins KB, Troen BR (July 1995). "Regulation of cathepsin D gene expression in HL-60 cells by retinoic acid and calcitriol". ...
ESRD occurs when the kidneys fail to produce calcitriol, a form of vitamin D, which assists in the absorption of calcium into ... When calcitriol levels decrease, parathyroid hormone levels increase, halting the storage of calcium, and instead triggering ... Medical management of OFC consists of vitamin D treatment, generally alfacalcidol or calcitriol, delivered intravenously. ...
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Calcitriol Topical: learn about side effects, dosage, special precautions, and more on MedlinePlus ... Apply calcitriol ointment to the areas of skin affected by plaque psoriasis. Do not apply calcitriol ointment to healthy skin ... Before using calcitriol topical,. *tell your doctor and pharmacist if you are allergic to calcitriol, any other medications, or ... If you become pregnant while using calcitriol topcial, call your doctor. If you are breastfeeding while using calcitriol ...
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Tag: Rocaltrol, Calcitriol. Exploring the Uses and Interactions of Rocaltrol - Key Medications in General Health and Ongoing ...
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Calcitriol in the sample or standard competes with a fixed amount of biotin-labeled Calcitriol for sites on a pre-coated ... The concentration of Calcitriol in the samples is then determined by comparing the O.D. of the samples to the standard curve. ... Chicken Calcitriol ELISA Kit, Chicken 1,25-dihydroxycholecalciferol ELISA Kit, Chicken 1,25-dihydroxyvitamin D3 ELISA Kit, ... The microtiter plate provided in this kit has been pre-coated with an antibody specific to Calcitriol, During the reaction, ...
Calcitriol Calcitriol is a synthetic vitamin D analog, prescribed for hypocalcemia in patients undergoing chronic renal ...
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... also known as calcitriol, is a medication prescribed to treat various conditions related to calcium metabolism ... This hormone stimulates the production of an active form of vitamin D called calcitriol, mainly in the kidneys. Calcitriol ... Calcitriol, commonly known as Rocaltrol, is a medication that plays a vital role in managing calcium levels in the body. It is ... Calcitriol is the active form of vitamin D, which is naturally produced in the human body upon exposure to sunlight. ...
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Calcitriol. Calcitriol also binds to a vitamin D receptor (VDR), a nuclei of target cells found in such organs as the brain, ... The calcidiol is then converted into calcitriol. Once this synthesized process takes place, the calcitriol behaves like a ... When the synthesized calcitriol reaches the kidneys, it circulates as a hormone and is transported to certain organs with ... The vitamin d-binding protein (VDBP), which is a protein found in the plasma, binds itself to the calcitriol, acting as a ...
Vitamin D and its analogs may be used-including calcitriol and analogs of calcitriol such as calcifediol, paricalcitol, ... Calcitriol is started at 0.5 mcg twice daily and increased as required. Patients in whom total parathyroidectomy and ... A constant calcium infusion is often required, and oral calcium and calcitriol requirements can be quite high. The target ... calcitriol), which increases intestinal absorption of calcium. Thus, overproduction of parathyroid hormone results in elevated ...
Indeed, we found that small doses of active vitamin D, 1α,25-dihydroxyvitamin D3 (1,25D3) (calcitriol), into the third ...
Calcitriol Oral Solution March 17, 2024. Calcium Acetate Oral Capsules and Tablets January 30, 2023. ...
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Vitamin D is very similar to calcitriol. Do not use medications containing calcitriol while using vitamin D. ... such as calcitriol); or if you have any other allergies. This product may contain inactive ingredients (such as peanut/soy), ...
calcitriol. *carbamazepine. *cholestyramine (with oral methylprednisolone only). *cobicistat. *colesevelam. *colestipol (with ...
Active Vitamin D (Calcitriol) as a Falls Intervention Gallagher, et al. (2007) ...
CEE (0.625 mg/d + MPA [2.5 mg/d] plus calcitriol [0.25 μg twice daily]) (n = 122). Calcitriol (0.25 μg twice daily) (n = 123). ... Combination treatment with estrogen and calcitriol in the prevention of age-related bone loss. J Clin Endocrinol Metab. 2001;86 ...
Effects of Calcitriol and Paricalcitol on Renal Fibrosis in CKD. Nephrol Dial Transplant (2021) 36:793-803. doi: 10.1093/ndt/ ... Bonakdaran S, Hami M, Hatefi A. The Effects of Calcitriol on Albuminuria in Patients With Type-2 Diabetes Mellitus. Saudi J ... Inhibition of T Lymphocyte Mitogenesis by 1, 25-Dihydroxy Vitamin D3 (Calcitriol). J Clin Invest (1984) 74:1451-5. doi: 10.1172 ... However, several non-calcemic actions of its bioactive form (calcitriol) are well documented (1-3). These actions are possible ...
Transformation to calcitriol takes place in the kidney; thus, in case of severe renal impairment (creatinine clearance of less ... Bone: calcitriol enhances bone formation by increasing levels of calcium and phosphate and stimulates action of osteoblasts. ... Kidney: calcitriol enhances tubular reabsorption of calcium.. Parathyroid glands: vitamin D inhibits the secretion of ... The conversion of calcifediol monohydrate to calcitriol is catalysed by the 1-alpha-hydroxylase enzyme, CYP27B1 which is ...
Mosieniak, G.; Sliwinska, M.; Piwocka, K.; Sikora, E. Curcumin abolishes apoptosis resistance of calcitriol-differentiated HL- ...
1?OHD3), calcitriol (1?,25OH2D3), low phosphate diet (no milk). 42. IV calcium*Symptomatic patients ...
CALCITRIOL 0.25 MCG CAPSULE [Rocaltrol] 3. Preferred Brand. 20%. 20%. P CALCITRIOL 0.5 MCG CAPSULE [Rocaltrol] 3. Preferred ... CALCITRIOL 1 MCG/ML SOLUTION ORAL 4. Non-Preferred Drug. 40%. 40%. P ...
The efficacy of calcitriol therapy in the management of bone loss and fractures: a qualitative review.﻽. Peppone LJ, Hebl S, ...
Fibroblast growth factor-23 mitigates hyperphosphatemia but accentuates calcitriol deficiency in chronic kidney disease. J Am ... Fibroblast growth factor-23 mitigates hyperphosphatemia but accentuates calcitriol deficiency in chronic kidney disease. J Am ...
  • This research was part of a PhD thesis for Dr. Cheered on how much does rocaltrol cost per pill by faculty members, calcitriol rocaltrol 0.25 mcg capsule Dr. (artpol-uk.com)
  • In someone with hypercalcaemia and high calcitriol levels, low intact parathyroid hormone levels are usually present. (wikipedia.org)
  • Calcitriol acts in concert with parathyroid hormone (PTH) in all three of these roles. (wikipedia.org)
  • Options for chronic treatment of hypoparathyroidism include calcitriol, recombinant human parathyroid hormone, and high-dose vitamin D (D 2 ). (medscape.com)
  • [ 4 ] Currently available treatments for hypoparathyroidism include high-dose vitamin D (ergocalciferol, D 2 and cholecalciferol, D 3 ), the active metabolite 1,25-dihydroxvitamin D (calcitriol), recombinant human parathyroid hormone, in addition to calcium supplements. (medscape.com)
  • Calcitriol is the drug used most commonly in the United States for chronic hypoparathyroidism now, with only ~6% treated with D 2 [ 3 ] and increasing numbers of patients on human recombinant parathyroid hormone. (medscape.com)
  • The main effects of parathyroid hormone are to increase the concentration of plasma calcium by increasing the release of calcium and phosphate from bone matrix, increasing calcium reabsorption by the kidney, and increasing renal production of 1,25-dihydroxyvitamin D-3 (calcitriol), which increases intestinal absorption of calcium. (medscape.com)
  • For instance, the unbound inactive form of the calcitriol receptor in intestinal epithelial cells resides in the cytoplasm. (wikipedia.org)
  • apalutamide will decrease the level or effect of calcitriol by affecting hepatic/intestinal enzyme CYP3A4 metabolism. (medscape.com)
  • clarithromycin will increase the level or effect of calcitriol by affecting hepatic/intestinal enzyme CYP3A4 metabolism. (medscape.com)
  • enzalutamide will decrease the level or effect of calcitriol by affecting hepatic/intestinal enzyme CYP3A4 metabolism. (medscape.com)
  • idelalisib will increase the level or effect of calcitriol by affecting hepatic/intestinal enzyme CYP3A4 metabolism. (medscape.com)
  • indinavir will increase the level or effect of calcitriol by affecting hepatic/intestinal enzyme CYP3A4 metabolism. (medscape.com)
  • Compared to other vitamin D compounds in clinical use (cholecalciferol, ergocalciferol), calcitriol has a higher risk of inducing hypercalcemia. (wikipedia.org)
  • The best evidence is for vitamin D. The sunshine vitamin is manufactured in the skin by ultraviolet (UV) light (primarily UV-B). This reaction produces vitamin D3 (also called cholecalciferol), which is converted to a biologically active form (called calcitriol) in the kidneys and immune cells. (msology.ca)
  • Many of the effects of calcitriol are mediated by its interaction with the calcitriol receptor, also called the vitamin D receptor or VDR. (wikipedia.org)
  • Calcitriol is the active form of vitamin D, normally made in the kidney. (wikipedia.org)
  • Calcitriol was identified as the active form of vitamin D in 1971 and the drug was approved for medical use in the United States in 1978. (wikipedia.org)
  • Calcitriol is prescribed for: Treatment of hypocalcaemia - hypoparathyroidism, osteomalacia (adults), rickets (infants, children), renal osteodystrophy, chronic kidney disease Treatment of osteoporosis Prevention of corticosteroid-induced osteoporosis Calcitriol has been used in an ointment for the treatment of psoriasis, although the vitamin D analogue calcipotriol (calcipotriene) is more commonly used. (wikipedia.org)
  • Calcitriol is in a class of medications called vitamin D analogs. (medlineplus.gov)
  • Active Vitamin D (Calcitriol) as a Falls Intervention Gallagher, et al. (cdc.gov)
  • Compare renal function, hypercalcemia, and hypocalcemia in patients with hypoparathyroidism treated chronically with either D 2 (D2 group) or calcitriol. (medscape.com)
  • However, we are aware of no reports comparing treatment outcome with D 2 vs calcitriol for hypoparathyroidism. (medscape.com)
  • In this retrospective study, our goal was to compare renal function and incidents of hypercalcemia and hypocalcemia requiring medical treatment in patients with hypoparathyroidism treated chronically with D 2 (D2 group) vs calcitriol. (medscape.com)
  • Calcitriol increases blood calcium (Ca2+) mainly by increasing the uptake of calcium from the intestines. (wikipedia.org)
  • Calcitriol increases blood calcium levels ([Ca2+ ]) by: Promoting absorption of dietary calcium from the gastrointestinal tract. (wikipedia.org)
  • Calcitriol comes as an ointment to apply to the skin. (medlineplus.gov)
  • Apply calcitriol ointment at around the same times every day. (medlineplus.gov)
  • Apply calcitriol ointment exactly as directed. (medlineplus.gov)
  • In children 2 to 6 years of age, do not use more than one tube (100 gm) of calcitriol ointment per week. (medlineplus.gov)
  • In adults and children 7 years of age and older, do not use more than two tubes (200 gm) of calcitriol ointment per week. (medlineplus.gov)
  • Apply calcitriol ointment to the areas of skin affected by plaque psoriasis. (medlineplus.gov)
  • Do not apply calcitriol ointment to healthy skin or anywhere on your face, eyes, lips, or vagina. (medlineplus.gov)
  • Do not cover the skin where you applied calcitriol ointment with a bandage or dressing unless your doctor tells you that you should. (medlineplus.gov)
  • Wash your hands well with soap and water after you apply calcitriol ointment. (medlineplus.gov)
  • There were no differences between D2 and calcitriol groups in hospitalizations or ED visits for hypercalcemia, serum creatinine or calcium, or kidney stones. (medscape.com)
  • We found less morbidity from hypocalcemia in hypoparathyroid patients treated chronically with D 2 compared with calcitriol and found no difference in renal function or morbidity from hypercalcemia. (medscape.com)
  • Calcitriol topical is used to treat mild to moderate plaque psoriasis (a skin disease in which red, scaly patches form on some areas of the body) in adults and children 2 years of age and older. (medlineplus.gov)
  • High calcitriol levels may also be seen in human disease states in patients not on supplementation. (wikipedia.org)
  • The major conditions with hypercalcaemia due to elevated calcitriol levels are lymphoma, tuberculosis and sarcoidosis where excess production occurs due to ectopic 25(OH)D-1-hydroxylase (CYP27B1) expressed in macrophages. (wikipedia.org)
  • Indeed, it is in anticipation to such requirements that maternal calcitriol levels increase during pregnancy. (who.int)
  • While the total calcitriol levels double in the first trimester, free calcitriol levels do not increase until the third trimester, and remain so into lactation [2, 4] . (who.int)
  • The changes in calcitriol levels led to the description of pregnancy as a state of absorptive hypercalciuria [1 , 2 ]. (who.int)
  • Calcitriol topical may cause side effects. (medlineplus.gov)
  • Calcitriol protects against the dopamine- and serotonin-depleting effects of neurotoxic doses of methanphetamine. (bvsalud.org)
  • Research on the noncalcemic actions of calcitriol and other VDR-ligand analogs and their possible therapeutic applications has been reviewed. (wikipedia.org)
  • If you are breastfeeding while using calcitriol topical, do not apply it directly to the nipple and areola (the colored area around each nipple). (medlineplus.gov)
  • Calcitriol may also directly facilitate calcification. (medscape.com)
  • PTH also stimulates the production of calcitriol (see below). (wikipedia.org)