Diaza derivative of cholesterol which acts as a hypocholesteremic agent by blocking delta-24-reductase, which causes the accumulation of desmosterol.
Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)
Necrosis or disintegration of skeletal muscle often followed by myoglobinuria.
An anticonvulsant used to control grand mal and psychomotor or focal seizures. Its mode of action is not fully understood, but some of its actions resemble those of PHENYTOIN; although there is little chemical resemblance between the two compounds, their three-dimensional structure is similar.
7-carbon saturated monocarboxylic acids.
A lipid-regulating agent that lowers elevated serum lipids primarily by decreasing serum triglycerides with a variable reduction in total cholesterol.
An anticonvulsant that is used to treat a wide variety of seizures. It is also an anti-arrhythmic and a muscle relaxant. The mechanism of therapeutic action is not clear, although several cellular actions have been described including effects on ion channels, active transport, and general membrane stabilization. The mechanism of its muscle relaxant effect appears to involve a reduction in the sensitivity of muscle spindles to stretch. Phenytoin has been proposed for several other therapeutic uses, but its use has been limited by its many adverse effects and interactions with other drugs.
Azoles of one NITROGEN and two double bonds that have aromatic chemical properties.
The outer layer of the adrenal gland. It is derived from MESODERM and comprised of three zones (outer ZONA GLOMERULOSA, middle ZONA FASCICULATA, and inner ZONA RETICULARIS) with each producing various steroids preferentially, such as ALDOSTERONE; HYDROCORTISONE; DEHYDROEPIANDROSTERONE; and ANDROSTENEDIONE. Adrenal cortex function is regulated by pituitary ADRENOCORTICOTROPIN.
Alkaloid isolated from seeds of Peganum harmala L., Zygophyllaceae. It is identical to banisterine, or telepathine, from Banisteria caapi and is one of the active ingredients of hallucinogenic drinks made in the western Amazon region from related plants. It has no therapeutic use, but (as banisterine) was hailed as a cure for postencephalitic Parkinson disease in the 1920's.
Spectroscopic method of measuring the magnetic moment of elementary particles such as atomic nuclei, protons or electrons. It is employed in clinical applications such as NMR Tomography (MAGNETIC RESONANCE IMAGING).
A hormone secreted by the ADRENAL CORTEX that regulates electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium.
The characteristic three-dimensional shape of a molecule.
An adrenocortical steroid that has modest but significant activities as a mineralocorticoid and a glucocorticoid. (From Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th ed, p1437)
INFLAMMATION of the UDDER in cows.
A board-certified specialty of VETERINARY MEDICINE, requiring at least four years of special education, training, and practice of veterinary surgery after graduation from veterinary school. In the written, oral, and practical examinations candidates may choose either large or small animal surgery. (From AVMA Directory, 43d ed, p278)
INFLAMMATION of the BREAST, or MAMMARY GLAND.
A group of broad-spectrum antibiotics first isolated from the Mediterranean fungus ACREMONIUM. They contain the beta-lactam moiety thia-azabicyclo-octenecarboxylic acid also called 7-aminocephalosporanic acid.
A state in south central Australia. Its capital is Adelaide. It was probably first visited by F. Thyssen in 1627. Later discoveries in 1802 and 1830 opened up the southern part. It became a British province in 1836 with this self-descriptive name and became a state in 1901. (From Webster's New Geographical Dictionary, 1988, p1135)
Substances that reduce the growth or reproduction of BACTERIA.
The controlling of access to health services, usually by primary care providers; often used in managed care settings to reduce utilization of expensive services and reduce referrals. (From BIOETHICS Thesaurus, 1999)
A potent and specific HIV protease inhibitor that appears to have good oral bioavailability.
Cell surface proteins that bind CALCITONIN GENE-RELATED PEPTIDE with high affinity and trigger intracellular changes which influence the behavior of cells. CGRP receptors are present in both the CENTRAL NERVOUS SYSTEM and the periphery. They are formed via the heterodimerization of the CALCITONIN RECEPTOR-LIKE PROTEIN and RECEPTOR ACTIVITY-MODIFYING PROTEIN 1.
A multienzyme complex responsible for the formation of ACETYL COENZYME A from pyruvate. The enzyme components are PYRUVATE DEHYDROGENASE (LIPOAMIDE); dihydrolipoamide acetyltransferase; and LIPOAMIDE DEHYDROGENASE. Pyruvate dehydrogenase complex is subject to three types of control: inhibited by acetyl-CoA and NADH; influenced by the energy state of the cell; and inhibited when a specific serine residue in the pyruvate decarboxylase is phosphorylated by ATP. PYRUVATE DEHYDROGENASE (LIPOAMIDE)-PHOSPHATASE catalyzes reactivation of the complex. (From Concise Encyclopedia Biochemistry and Molecular Biology, 3rd ed)
De novo fat synthesis in the body. This includes the synthetic processes of FATTY ACIDS and subsequent TRIGLYCERIDES in the LIVER and the ADIPOSE TISSUE. Lipogenesis is regulated by numerous factors, including nutritional, hormonal, and genetic elements.
The process of finding chemicals for potential therapeutic use.
Calcitonin gene-related peptide. A 37-amino acid peptide derived from the calcitonin gene. It occurs as a result of alternative processing of mRNA from the calcitonin gene. The neuropeptide is widely distributed in neural tissue of the brain, gut, perivascular nerves, and other tissue. The peptide produces multiple biological effects and has both circulatory and neurotransmitter modes of action. In particular, it is a potent endogenous vasodilator.
Exclusive legal rights or privileges applied to inventions, plants, etc.
A novel composition, device, or process, independently conceived de novo or derived from a pre-existing model.
A physiologically diverse phylum of acidophilic, gram-negative bacteria found in a wide variety of habitats, but particularly abundant in soils and sediments.
Polypeptide chains, consisting of 211 to 217 amino acid residues and having a molecular weight of approximately 22 kDa. There are two major types of light chains, kappa and lambda. Two Ig light chains and two Ig heavy chains (IMMUNOGLOBULIN HEAVY CHAINS) make one immunoglobulin molecule.
Small double-stranded, non-protein coding RNAs, 21-25 nucleotides in length generated from single-stranded microRNA gene transcripts by the same RIBONUCLEASE III, Dicer, that produces small interfering RNAs (RNA, SMALL INTERFERING). They become part of the RNA-INDUCED SILENCING COMPLEX and repress the translation (TRANSLATION, GENETIC) of target RNA by binding to homologous 3'UTR region as an imperfect match. The small temporal RNAs (stRNAs), let-7 and lin-4, from C. elegans, are the first 2 miRNAs discovered, and are from a class of miRNAs involved in developmental timing.
A transferase that catalyzes formation of PHOSPHOCREATINE from ATP + CREATINE. The reaction stores ATP energy as phosphocreatine. Three cytoplasmic ISOENZYMES have been identified in human tissues: the MM type from SKELETAL MUSCLE, the MB type from myocardial tissue and the BB type from nervous tissue as well as a mitochondrial isoenzyme. Macro-creatine kinase refers to creatine kinase complexed with other serum proteins.
An isoenzyme of creatine kinase found in the MUSCLE.

Alteration of cholesterol biosynthetic pathways in the skin of mice administered polycyclic aromatic hydrocarbons. (1/4)

When polycyclic aromatic hydrocarbons were applied solely or together with a tumor promoter (12-O-tetradecanoylphorbol-13-acetate) to the skin of mice, a marked decrease in the level of lathosterol was observed, reflecting a significant change in the metabolism of sterols. Yet the total amount of cholesterol was not changed. When diazacholesterol (a metabolic inhibitor) was administered to mice, both desmosterol and 5 alpha-cholesta-7,24-dien-3 beta-ol accumulated in the skin, whereas the level of lathosterol decreased. These results seem to suggest that a significant portion of lathosterol is formed via 5 alpha-cholesta-7,24-dien-3 beta-ol in addition to the pathway through methostenol. When polycyclic aromatic hydrocarbon was applied to the skin of the mouse treated with diazacholesterol, a significant increase of desmosterol and a marked drop of the level of 5 alpha-cholesta-7,24-dien-3 beta-ol were observed. These results strongly suggest that polycyclic aromatic hydrocarbons perturb the metabolism of sterol in the skin of mice while keeping the total amount of cholesterol unchanged. A similar metabolism also seems to be operating in tumor tissue itself.  (+info)

Metabolic interconversion of free sterols and steryl esters in Saccharomyces cerevisiae. (2/4)

The interconversion of free and esterified sterols was followed radioisotopically with [U-14C]acetate and [methyl-14C]methionine. In pulse-chase experiments, radioactivity first appeared mainly in unesterified sterols in exponential-phase cells. Within one generation time, the label equilibrated between the free and esterified sterol pools and subsequently accumulated in steryl esters in stationary-phase cells. When the sterol pools were prelabeled by growing cells aerobically to the stationary phase and the cells were diluted into unlabeled medium, the prelabeled steryl esters returned to the free sterol form under several conditions. (i) During aerobic growth, the prelabeled sterols decreased from 80% to 45% esters in the early exponential phase and then returned to 80% esters as the culture reached the stationary phase. (ii) Under anaerobic conditions, the percentage of prelabeled steryl esters declined continuously. When growth stopped, only 15% of the sterols remained esterified. (iii) In the presence of an inhibitor of sterol biosynthesis, which causes accumulation of a precursor to ergosterol, prelabeled sterols decreased to 40% steryl esters while the precursor was found preferentially in the esterified form. These results indicate that the bulk of the free sterol and steryl ester pools are freely interconvertible, with the steryl esters serving as a supply of free sterols. Furthermore, there is an active cellular control over what types of sterol are found in the free and esterified sterol pools.  (+info)

Effects of steroid blockers on LH-induced ovulation in the domestic fowl, Gallus domesticus. (3/4)

The spontaneous ovulation of hens was suppressed by daily injection of PMSG. The LH injected to overcome the block was accompanied by one of 4 compounds known to inhibit steroidogenesis at different sites in the biosynthetic pathway. A dose of 300 mg aminoglutethimide phosphate, which inhibits the conversion of cholesterol to 20 alpha-hydroxycholesterol, blocked the LH-induced ovulation and prevented the normal rise in plasma progesterone. Metyrapone, an inhibitor of 11 beta-hydroxylase, and SC 12937 and AY 9944, inhibitors of cholesterol synthesis, did not prevent ovulation or the progesterone rise induced by exogenous LH. Administration of progesterone overcame the inhibitory effect of aminoglutethimide, and it is suggested that progesterone is involved in the ovulatory process of the fowl.  (+info)

Effect of a chemical carcinogen and phorbol esters on sterol metabolism of mouse skin. (4/4)

The effect of 20-methylcholanthrene and phorbol esters on sterol metabolism of mouse skin was studied. When 4 beta-phorbol esters were administered to mice that were previously painted once with 20-methylcholanthrene, a depression of some sterols in skin occurred, of which that of lathosterol was most marked. This effect was not observed when the order of application was reversed. Using a metabolic inhibitor, diazacholesterol, it was shown that sterols which reduce in mouse skin by administration of carcinogen and promoters were similar to those which reduce by administration of carcinogen only and are the members of one of the two cholesterol-biosynthetic pathways, i.e., a pathway which proceeds through intermediates with a saturated side chain. The intensity of the lathosterol-depressing effect of phorbol esters depends on the order of application of 20-methylcholanthrene and promoters, the amount of promoters, molecular species of alcoholic moiety of esters, and configuration at C-4 of phorbol moiety. Of the phorbol esters tested, 4 beta-phorbol-12-myristate-13-acetate revealed the highest activity, which was followed by 4 beta-phorbol-12,13-didecanoate, 4 beta-phorbol-12,13-dibutyrate, 4 beta-phorbol-12,13-dibenzoate, 4 beta-phorbol-12,13-diacetate, 4 alpha-phorbol-12,13-didecanoate, and 4 alpha-phorbol. 4 alpha-Phorbol was practically inactive. When beta-naphthoflavone was substituted for 20-methylcholanthrene, little effect was observed except in TPA, which revealed a rather marked lathosterol-depressing activity. Phorbol esters themselves did show some activity of lathosterol depression without prior application of 20-methylcholanthrene, but the effects were much weaker. When anthralin was applied to mouse skin after the painting of 20-methylcholanthrene, a low but definite lathosterol-depressing effect was observed.  (+info)

During his 2 decades as a clinical and basic research scientist at the National Heart Institute, Don Fredrickson was part of a remarkable team that helped transform our understanding of the pathophysiology of cardiovascular disease. The work of this team was instrumental in creating the field of lipidology and establishing the foundation for present-day approaches to the management of lipid disorders. Don also trained a generation of international basic and clinical research scientists, fostering their careers in immeasurable ways. These investigators are now among the worlds preeminent lipidologists.. After his early work on sterol metabolism, Don studied the structure and metabolism of the plasma lipoproteins, their role in fat transport, and the genetic factors that regulate their metabolism and concentration in the blood (personal communication, NIH, July 23, 2002). He participated in research on apolipoproteins A, B, and C, including the separation of apolipoproteins A and C into their ...
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View details for the job vacancy Role of sterol metabolism in host response to virus posted by National Institute of Environmental Health Science on CareerAddict Jobs.
Easy to read patient leaflet for Deep Sea Nasal Spray. Includes indications, proper use, special instructions, precautions, and possible side effects.
The developers of triparanol jokingly referred to it as a "non-estrogenic estrogen". Azacosterol Desmosterolosis X-linked ...
Unlike late-stage cholesterol biosynthesis inhibitors like triparanol and azacosterol, no accumulation of sterols has been ...
24-Dehydrocholesterol reductase (24-DHCR) inhibitors such as azacosterol and triparanol inhibit the production of cholesterol ...
... azacosterol (INN) Azactam azacyclonol (INN) azaftozine (INN) Azahexal (Hexal Australia) [Au], also known as azathioprine. ...
... azacosterol MeSH D10.570.938.208.160 - cholestanol MeSH D10.570.938.208.222 - cholesterol, dietary MeSH D10.570.938.208.250 - ...
... azacosterol MeSH D04.808.247.808.197.135 - cholestanol MeSH D04.808.247.808.197.200 - cholesterol esters MeSH D04.808.247.808. ... azacosterol MeSH D04.808.247.222.284.200 - cholesterol esters MeSH D04.808.247.222.284.478 - hydroxycholesterols MeSH D04.808. ...
On December 2, 2006 Pfizer cut off torcetrapib's phase III trial because of "an imbalance of mortality and cardiovascular events" associated with its use.[16] This was a sudden and unexpected event and as late as November 30, 2006 Jeff Kindler, Pfizer's chief executive, was quoted, "This will be one of the most important compounds of our generation."[16] In the terminated trial, a 60% increase in deaths was observed among patients taking torcetrapib and atorvastatin versus taking atorvastatin alone.[17] Pfizer recommended that all patients stop taking the drug immediately.[18] Six studies were terminated early.[6] One of the completed studies found it raised systolic blood pressure and concluded "Torcetrapib showed no clinical benefit in this or other studies, and will not be developed further."[19] The drug cost $800m+ to bring into Phase III development.[20] ...
Interactions with clofibrate, fenofibrate, gemfibrozil, which are fibrates used in accessory therapy in many forms of hypercholesterolemia, usually in combination with statins, increase the risk of myopathy and rhabdomyolysis.[38][42][43] Co-administration of atorvastatin with one of CYP3A4 inhibitors such as itraconazole,[44] telithromycin, and voriconazole, may increase serum concentrations of atorvastatin, which may lead to adverse reactions. This is less likely to happen with other CYP3A4 inhibitors such as diltiazem, erythromycin, fluconazole, ketoconazole, clarithromycin, cyclosporine, protease inhibitors, or verapamil,[45] and only rarely with other CYP3A4 inhibitors, such as amiodarone and aprepitant.[32] Often, bosentan, fosphenytoin, and phenytoin, which are CYP3A4 inducers, can decrease the plasma concentrations of atorvastatin. Only rarely, though, barbiturates, carbamazepine, efavirenz, nevirapine, oxcarbazepine, rifampin, and rifamycin,[46] which are also CYP3A4 inducers, can ...
Biosynthesis of mevastatin is primarily accomplished via a type 1 PKS pathway it proceeds in the PKS pathway as seen in figure 1 until it reaches a hexaketide state where it undergoes a Diels-Alder cyclization. After cyclization it continues via the PKS pathway to a nonaketide after which it is released and undergoes oxidation and dehydration. It is presumed that the oxidations are preformed by a polypeptide that is similar to cytochrome p450 monooxygenase, which is encoded by mlcC within the mevastatin gene. Lastly the biosynthesis is completed by the PKS facilitating the addition of a diketide sidechain and a methylation by SAM.[7] Figure 1 shows mevastatin in its acid form but it can also be in the more commonly seen lactone form. This pathway was first observed in Penicillium cilrinum and was later discovered that another type of fungus, Penicillium brevicompaetum also produced mevastatin via a PKS pathway. ...
The role of cholesterol in the development of cardiovascular disease was elucidated in the second half of the 20th century.[138] This lipid hypothesis prompted attempts to reduce cardiovascular disease burden by lowering cholesterol. Treatment consisted mainly of dietary measures, such as a low-fat diet, and poorly tolerated medicines, such as clofibrate, cholestyramine, and nicotinic acid. Cholesterol researcher Daniel Steinberg writes that while the Coronary Primary Prevention Trial of 1984 demonstrated cholesterol lowering could significantly reduce the risk of heart attacks and angina, physicians, including cardiologists, remained largely unconvinced.[139] Scientists in academic settings and the pharmaceutical industry began trying to develop a drug to reduce cholesterol more effectively. There were several potential targets, with 30 steps in the synthesis of cholesterol from acetyl-coenzyme A.[140] In 1971, Akira Endo, a Japanese biochemist working for the pharmaceutical company Sankyo, ...
... (trade names Advicor, Mevacor) is a drug combination used for the treatment of dyslipidemia. It is a combination of the vitamin niacin and the statin drug lovastatin. The combination preparation is marketed by Abbott Laboratories. It was approved by the FDA on December 17, 2001. ...
Azacosterol molecule ball.png 2,023 × 1,000; 448 KB. *. Azacosterol molecule skeletal.png 2,366 × 1,000; 239 KB. ...
The developers of triparanol jokingly referred to it as a "non-estrogenic estrogen". Azacosterol Desmosterolosis X-linked ...
Unlike late-stage cholesterol biosynthesis inhibitors like triparanol and azacosterol, no accumulation of sterols has been ...
... azacosterol, azacyclonol, azaftozine, azalanstat, azalomycin, azaloxan, azamethonium bromide, azamulin, azanator, azanidazole, ... azacosterol, azacyclonol, azaftozine, azalanstat, azalomycin, azaloxan, azamethonium bromide, azamulin, azanator, azanidazole, ...
... azacosterol, azacyclonol, azaftozine, azaguanidine, azaloxan, azamethonium bromide, azamulin, azanator, azanidazole, azaperone ...
On December 2, 2006 Pfizer cut off torcetrapibs phase III trial because of "an imbalance of mortality and cardiovascular events" associated with its use.[16] This was a sudden and unexpected event and as late as November 30, 2006 Jeff Kindler, Pfizers chief executive, was quoted, "This will be one of the most important compounds of our generation."[16] In the terminated trial, a 60% increase in deaths was observed among patients taking torcetrapib and atorvastatin versus taking atorvastatin alone.[17] Pfizer recommended that all patients stop taking the drug immediately.[18] Six studies were terminated early.[6] One of the completed studies found it raised systolic blood pressure and concluded "Torcetrapib showed no clinical benefit in this or other studies, and will not be developed further."[19] The drug cost $800m+ to bring into Phase III development.[20] ...
Interactions with clofibrate, fenofibrate, gemfibrozil, which are fibrates used in accessory therapy in many forms of hypercholesterolemia, usually in combination with statins, increase the risk of myopathy and rhabdomyolysis.[38][42][43] Co-administration of atorvastatin with one of CYP3A4 inhibitors such as itraconazole,[44] telithromycin, and voriconazole, may increase serum concentrations of atorvastatin, which may lead to adverse reactions. This is less likely to happen with other CYP3A4 inhibitors such as diltiazem, erythromycin, fluconazole, ketoconazole, clarithromycin, cyclosporine, protease inhibitors, or verapamil,[45] and only rarely with other CYP3A4 inhibitors, such as amiodarone and aprepitant.[32] Often, bosentan, fosphenytoin, and phenytoin, which are CYP3A4 inducers, can decrease the plasma concentrations of atorvastatin. Only rarely, though, barbiturates, carbamazepine, efavirenz, nevirapine, oxcarbazepine, rifampin, and rifamycin,[46] which are also CYP3A4 inducers, can ...
Ascari, E., Marini, G., Invernizzi, R., Ippoliti, G., Casirola, G., Fontana, G. & Rizzo, S. C., Sep 1975, In : Haematologica. 60, 3, p. 300-307 8 p.. Research output: Contribution to journal › Article › peer-review ...
Azacosterol 11141-17-6. Azadirachtin. 95507-03-2. Azadirachtin B 68049-83-2. Azafenidin ...
Azacosterol dicholesteroyl diselenide DT01 compound EpiCeram ergosta-. 6,9,22-. triene-. 3,5,8-. triol ...
Cholesterol substituted in any position by a keto moiety. The 7-keto isomer inhibits 3-hydroxy-3-methylglutaryl-CoA reductase activity and inhibits cholesterol uptake in the coronary arteries and aorta in vitro ...
Azacosterol tumor, and tumor cells. The released exosomes are located in many natural fluids, such as for Azacosterol example ... The material indicate the metabolic position from the donor cells, and for that reason material Azacosterol of EVs used in ... For conversation via transfer Azacosterol of biomolecules, cells launch extracellular vesicles (EVs), such as for example ... A recently available study Azacosterol has examined the data offered for the Vesiclepedia site (http://www.microvesicle.org) ...
Azacosterol. Volicitin. Lead Sulfide. Thiophenol. Thiamiprine. Scoparius. 2,5-Di-tert-pentylhydroquinone. ...
Azacosterol. (S,S)-Chiraphos. Thonzonium Bromide. Glycine. Ethanethiol. Calcium Arsenite. Apiin. Dibenzyl Phosphite. Pellotine ...
Azacosterol Li, K. Lee, J.C. Canzoneri, A. Fajardo, M. Thomas, J.T. Piazza, E. Gurpinar, D. Otali, W. Grizzle. B. Zhu, A. ... Western blotting showed a greater reduction of PDE10 protein levels in the Azacosterol stable knockdown cells by shRNA (inset, ... during lung cancer development and essential for lung tumor cell growth in which inhibitors can selectively Azacosterol induce ...
Azacosterol D4.808.247.222.284.70 D4.210.500.247.222.284.70 D4.808.247.808.197.70 D4.210.500.247.808.197.70 Azaguanine D3.438. ...
0090] Non-limiting examples of miscellaneous antihyperlipoproteinemics include acifran, azacosterol, benfluorex, β- ...
8-tetrahydro-1-naphthalenecarboxamide 2-Azacarbazole 3-Azacarbazole Azaconazole Azacosterol Azacosterol hydrochloride 1-Aza-2- ...
Azacosterol. Thorium Oxide. Etomidate. Alvimopan. ©2016 DrugLead US FDA&EMEA. ...
In the mid-2000s, in a trial with 1613 patients, 10.2% patients stopped taking the medication in the combination drug group versus 22.2% under niacin monotherapy.[6] On April 28, 2008, the U.S. Food and Drug Administration (FDA) issued a "not approved" letter for Cordaptive.[7] Tredaptive was approved by the European Medicines Agency (EMA) on July 3, 2008.[8] On January 11, 2013, Merck & Co Inc. announced they were withdrawing the drug worldwide as a result of European regulators recommendations.[9] The Heart Protection Study 2-Treatment of HDL to Reduce the Incidence of Vascular Events (HPS2-THRIVE) involved more than 25,000 adults. The treatment group received 2 g of extended-release niacin and 40 mg of laropiprant daily. Study results, reported in July 2014, showed that the combination of niacin and laropiprant did not have any beneficial effects when compared with a placebo treatment and had an increase in adverse effects.[10] ...
In 2016 the United States Preventive Services Task Force recommended statins for those who have at least one risk factor for coronary heart disease, are between 40 and 75 years old, and have at least a 10% 10-year risk of heart disease.[14] The risk factors for coronary heart disease included abnormal lipid levels in the blood, diabetes mellitus, high blood pressure, and smoking.[14] The risk of heart disease is estimated using the ACC/AHA Pooled Cohort equation.[15] They recommended selective use of low-to-moderate doses statins in the same adults who have a calculated 10-year cardiovascular disease event risk of 7.5-10% or greater.[14] Most evidence suggests that statins are effective in preventing heart disease in those with high cholesterol, but no history of heart disease. A 2013 Cochrane review found a decrease in risk of death and other poor outcomes without any evidence of harm.[2] For every 138 people treated for 5 years one fewer dies and for every 49 treated one fewer has an episode ...
Azacosterol. Drotaverine. Lazurite. Methyl Ethyl Ketone. Turanose. DMMP. Azintamide. Probenecid. Sulfurous Acid. Rhodopsin. ...
The role of cholesterol in the development of cardiovascular disease was elucidated in the second half of the 20th century.[168] This lipid hypothesis prompted attempts to reduce cardiovascular disease burden by lowering cholesterol. Treatment consisted mainly of dietary measures, such as a low-fat diet, and poorly tolerated medicines, such as clofibrate, cholestyramine, and nicotinic acid. Cholesterol researcher Daniel Steinberg writes that while the Coronary Primary Prevention Trial of 1984 demonstrated cholesterol lowering could significantly reduce the risk of heart attacks and angina, physicians, including cardiologists, remained largely unconvinced.[169] Scientists in academic settings and the pharmaceutical industry began trying to develop a drug to reduce cholesterol more effectively. There were several potential targets, with 30 steps in the synthesis of cholesterol from acetyl-coenzyme A.[170] In 1971, Akira Endo, a Japanese biochemist working for the pharmaceutical company Sankyo, ...
20,25-Diazacholesterol use Azacosterol 21-Hydroxyprogesterone use Desoxycorticosterone 21st Century History use History. 21st ...
20,25-Diazacholesterol use Azacosterol 21-Hydroxyprogesterone use Desoxycorticosterone 21st Century History use History. 21st ...
20,25-Diazacholesterol use Azacosterol 21-Hydroxyprogesterone use Desoxycorticosterone 21st Century History use History. 21st ...
20,25-Diazacholesterol use Azacosterol 21-Hydroxyprogesterone use Desoxycorticosterone 21st Century History use History. 21st ...
20,25-Diazacholesterol use Azacosterol. 20-alpha-Dihydroprogesterone. 20-alpha-Hydroxysteroid Dehydrogenase ...

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