Relevant bibliographies by topics / Cholesterol control

Academic literature on the topic 'Cholesterol control'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Journal articles on the topic "Cholesterol control":

1

Kiberstis, P. A. "Idolizing Cholesterol Control." Science Signaling 2, no. 78 (July 7, 2009): ec232-ec232. http://dx.doi.org/10.1126/scisignal.278ec232.

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Fletcher, Gerald F. "Fat and Cholesterol Control." Journal of Cardiopulmonary Rehabilitation 12, no. 3 (May 1992): 162–63. http://dx.doi.org/10.1097/00008483-199205000-00002.

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Marecic, Maryfrances, and Robin Bagby. "Take Control of Cholesterol." Nutrition Today 23, no. 5 (September 1988): 47. http://dx.doi.org/10.1097/00017285-198809000-00011.

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Belavic, Jennifer. "Drugs to control cholesterol." Nursing 42, no. 3 (March 2012): 68. http://dx.doi.org/10.1097/01.nurse.0000398753.52565.6a.

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Haug, Anna, Arne T. Høstmark, Øystein Spydevold, and Einar Eilertsen. "Hypercholesterolaemia, hypotriacylglycerolaemia and increased lipoprotein lipase activity following orchidectomy in rats." Acta Endocrinologica 113, no. 1 (September 1986): 133–39. http://dx.doi.org/10.1530/acta.0.1130133.

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Abstract. Plasma lipoproteins, faecal cholesterol excretion, and activities of lecithin: cholesterol acyltransferase (LCAT) hepatic lipase (HL), and lipoprotein lipase (LPL) were determined in castrated rats, in rats treated with testosterone propionate after castration, and in sham-operated controls. Compared to control rats, whole-plasma total cholesterol (TC) rose, and triacylglycerols (TG) fell in castrated rats, but were normalized by androgen substitution. VLDL components tended to be reduced, whereas HDL2 components rose following castration. In general, testosterone substitution normalized the alterations induced by castration. Adipose tissue LPL was higher in castrated rats than in control rats, whereas activities of HL and LCAT were not significantly affected by the treatments. Hepatic cholesterol concentration, and faecal excretion of cholesterol and bile acids were not significantly altered by the treatments. Considering all 3 groups together, there was a significant positive correlation between the concentration of plasma cholesterol and cholesterol in liver, between plasma HDL2-cholesteryl esters and hepatic cholesterol, and also between HL and faecal cholesterol excretion. The results suggest that short term castration of rats causes increased levels of lipoprotein lipase and thereby brings about a lowering of VLDL and an increased concentration of LDL and HDL2. These effects are reflected in hypotriacylglycerolaemia and hypercholesterolaemia.
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Khan, B., H. G. Wilcox, and M. Heimberg. "Cholesterol is required for secretion of very-low-density lipoprotein by rat liver." Biochemical Journal 258, no. 3 (March 15, 1989): 807–16. http://dx.doi.org/10.1042/bj2580807.

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To study potential effects of hepatic cholesterol concentration on secretion of very-low-density lipoprotein (VLDL) by the liver, male rats were fed on unsupplemented chow, chow with lovastatin (0.1%), or chow with lovastatin (0.1%) and cholesterol (0.1%) for 1 week. Livers were isolated from these animals and perfused in vitro, with a medium containing [2-14C]acetate, bovine serum albumin and glucose in Krebs-Henseleit buffer, and with an oleate-albumin complex. With lovastatin feeding, the hepatic concentrations of cholesteryl esters and triacylglycerols before perfusion were decreased, although free cholesterol was unchanged. However, hepatic secretion of all the VLDL lipids was decreased dramatically by treatment with lovastatin. Although total secretion of VLDL triacylglycerol, phospholipid, cholesterol and cholesteryl esters was decreased, the decrease in triacylglycerol was greater than that in free cholesterol or cholesteryl esters, resulting in secretion of a VLDL particle enriched in sterols relative to triacylglycerol. In separate studies, the uptake of VLDL by livers from control animals or animals treated with lovastatin was measured. Uptake of VLDL was estimated by disappearance of VLDL labelled with [1-14C]oleate in the triacylglycerol moiety, and was observed to be similar in both groups. During perfusion, triacylglycerol accumulated to a greater extent in livers from lovastatin-fed rats than in control animals. The depressed output of VLDL triacylglycerols and the increase in triacylglycerol in the livers from lovastatin-treated animals was indicative of a limitation in the rate of VLDL secretion. Addition of cholesterol (either free cholesterol or human low-density lipoprotein) to the medium perfusing livers from lovastatin-fed rats, or addition of cholesterol to the diet of lovastatin-fed rats, increased the hepatic concentration of cholesteryl esters and the output of VLDL lipids. The concentration of cholesteryl esters in the liver was correlated with the secretion of VLDL by the liver. These data suggest that cholesterol is an obligate component of the VLDL required for its secretion. It is additionally suggested that cholesteryl esters are in rapid equilibrium with a small pool of free cholesterol which comprises a putative metabolic pool available and necessary for the formation and secretion of the VLDL. Furthermore, the specific radioactivity (d.p.m./mumol) of the secreted VLDL free cholesterol was much greater than that of hepatic free cholesterol, suggesting that the putative hepatic metabolic pool is only a minor fraction of total hepatic free cholesterol.
7

Anonymous. "Steps Overlooked in Cholesterol Control." Journal of Gerontological Nursing 20, no. 12 (December 1994): 47. http://dx.doi.org/10.3928/0098-9134-19941201-13.

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Florez, Hermes, Kelly J. Hunt, and Willy Marcos Valencia. "Reducing Disparities in Cholesterol Control." JAMA 328, no. 8 (August 23, 2022): 714. http://dx.doi.org/10.1001/jama.2022.13284.

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Björkhem, Ingemar. "Do oxysterols control cholesterol homeostasis?" Journal of Clinical Investigation 110, no. 6 (September 15, 2002): 725–30. http://dx.doi.org/10.1172/jci0216388.

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Kiberstis, P. A. "MiR-33 in Cholesterol Control." Science Signaling 3, no. 127 (June 22, 2010): ec189-ec189. http://dx.doi.org/10.1126/scisignal.3127ec189.

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You might also be interested in the extended bibliographies on the topic 'Cholesterol control' for particular source types:
Journal articles Dissertations / Theses Books

Dissertations / Theses on the topic "Cholesterol control":

1

Al-Seeni, Madeha N. "Control of hepatic cholesterol esterification." Thesis, University of Nottingham, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293154.

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Sampson, William James. "The intracellular control of cholesterol metabolism." Thesis, University of Edinburgh, 1988. http://hdl.handle.net/1842/26913.

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The liver has a major role in the metabolism of cholesterol, being the main site of lipoprotein assembly and degradation and the only tissue where the metabolism of cholesterol to bile acids occurs. This provides the major pathway for the removal of cholesterol from the body. The results described in this thesis concern the use of specific enzyme inhibitors (58-035, Azacholesterol, Mevinolin) to determine the intracellular use of different sources of cholesterol in monolayers of rat hepatocytes. In particular, the fates of newly synthesized cholesterol from mevalonic acid and cholesterol derived from HDL2 were investigated. Incubation of hepatocyte monolayers with 58-035 resulted in the inhibition of esterification. In the presence of mevalonic acid as a cholesterol source, 58-035 stimulated bile acid synthesis. Azacholesterol inhibited bile acid synthesis, had no effect on cholesterol synthesis, and in the presence of mevalonic acid, stimulated secretion of cholesterol by the hepatocytes; it had no effect on cholesterol esterification. Mevinolin inhibited cholesterol synthesis and as a result inhibited esterification. HDL2, in the presence of mevinolin, was used as a cholesterol source. It stimulated bile acid synthesis and cholesterol esterification. Addition of 58-035 to the system resulted in the inhibition of both esterification and bile acid synthesis. Overall, the results indicated that different intracllular pools of free cholesterol exist and that the inter-relationships of these pools give a complex pattern of flux of intracellular cholesterol between various pathways in the rat hepatocyte.
3

Veen, Jelske Nynke van der. "Nuclear receptors in control of cholesterol transport." [S.l. : Groningen : s.n. ; University Library Groningen] [Host], 2007. http://irs.ub.rug.nl/ppn/304675490.

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Dunn, Stuart Antony. "Hormone-sensitive lipase and the control of lipid metabolism in the human macrophage foam cell." Thesis, University of Newcastle Upon Tyne, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311114.

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Sims, Helen M. "Transcriptional control of microsomal triglyceride transfer protein gene expression in the hamster." Thesis, University of Nottingham, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366470.

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Martinic, Goran (Gary), of Western Sydney Hawkesbury University, of Science Technology and Environment College, and School of Environment and Agriculture. "Cyclodextrins as potential human anti-atherosclerotic agents." THESIS_CSTE_EAG_Martinic_G.xml, 2001. http://handle.uws.edu.au:8081/1959.7/129.

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Cyclodextrins (CDs) are naturally occurring cyclic oligosaccharides. Since it is believed that OxC blocks the removal of normal cholesterol from cells in the artery wall, it is possible that selective removal of OxC in the vessel wall in-vivo may prevent or reverse atherosclerosis.As a prelude to major studies, this research project was designed to answer two critical questions; 1/. What is the best route for delivery of CD. 2/. How do animals (apoE-/- mice) tolerate it. Pilot studies were established and results noted. These studies have provided valuable information in the apoE-/- mouse for subsequent studies to prevent or reverse atherosclerosis in this animal model.
Master of Science (Hons)
7

Witsken, Colleen. "The Effect of Parental Control Over Child-Feeding on Compliance to Dietary Recommendations to Lower Blood Cholesterol." University of Cincinnati / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1179758468.

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Dun, Alison. "Spatial and temporal control of regulated exocytosis by protein and lipid interactions." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/8087.

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Cellular communication requires the transport of chemical messengers between intracellular compartments and from cell to cell. The regulated exocytosis of a secretory vesicle at the plasma membrane involves the merger of two bilayers, with markedly different lipid composition, within a millisecond time scale. The spatial and temporal control of the protein and lipid complement at these fusion sites is essential. A highly conserved family of proteins are known to drive this fusion event; SNAP-25 and syntaxin-1 (t-SNAREs) associate at the plasma membrane in a 1:1 stoichiometry to provide a binding site for the vesicle-membrane protein synaptobrevin (v-SNARE). The formation of this complex and subsequent fusion requires accessory proteins for efficient calcium-triggered exocytosis; which of these proteins facilitate the initial attachment of vesicle to the plasma membrane prior to fusion is still under debate. Specific sites for vesicle fusion have been proposed and the organisation of lipids and proteins at these fusion sites has been extensively investigated with limited spatial and temporal resolution; however the presence of raft-forming lipids at these sites as well as the arrangement of SNARE proteins at the molecular level is still under contention. The data presented within this thesis aims to elucidate the protein and lipid environment at the fusion site using super-resolution microscopy and advanced vesicle tracking. Under diffraction-limited microscopy the t-SNAREs are visualised as 200 nm homogenous clusters; however I have used single molecule localisation microscopy to reveal a more complex heterogeneous molecular arrangement. Quantification of lipid order exclusively at the plasma membrane provided insight into the influence of cholesterol-induced lipid arrangement on SNAP-25 localisation. In addition the t-SNARE interaction was investigated using TCSPC-FLIM identifying two lipid-order-dependent conformations in distinct clusters at the plasma membrane. Extensive vesicle tracking at optimum sampling rates demonstrated the ‘sampling’ behaviour of LDCVs and allowed characterisation of vesicle fusion sites. In summary I find that vesicles exhibit preference for residence and probably fusion at regions of plasma membrane with a low t-SNARE density; these proteins appear to exert control over exocytosis by adopting alternative conformations that are under cholesterol-induced regulation.
9

Kangas-Kontio, T. (Tiia). "Genetic background of HDL-cholesterol and atherosclerosis:linkage and case-control studies in the Northern Finnish population." Doctoral thesis, Oulun yliopisto, 2011. http://urn.fi/urn:isbn:9789514295812.

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Abstract Coronary heart disease (CHD), a manifestation of atherosclerosis, is the leading single cause of death in Finland. CHD is affected by numerous genetic and environmental factors, their combined effects and interactions between them. Low HDL-cholesterol (HDL-C) is an independent risk factor for atherosclerosis and the most common dyslipidemia associated with early onset CHD, but the mechanisms regulating HDL-C levels and protecting from atherosclerosis are still not completely understood. Adiponectin is a hormone that is secreted by adipose tissue and has several anti-atherosclerotic effects. There is multiple evidence suggesting that adiponectin could protect against CHD via positive effects on HDL metabolism. Vascular endothelial growth factor (VEGF) is a potent angiogenic growth factor that has a potentially conflicting role in atherosclerosis; it may have protecting or predisposing effects. The objective of this thesis was to study the genetic background of HDL-C regulation and atherosclerosis. Three studies were executed using extended families with CHD or case-control setting, with samples collected from Northern Finland. In the first study, seven chromosomal regions showing suggestive evidence of linkage were identified for HDL-C regulation, using genome-wide linkage approach. In the second study, we found a strong correlation between HDL-C and adiponectin, but failed to show evidence of a shared genetic background. However, a genetic correlation between adiponectin and low-density lipoprotein-cholesterol was revealed. We also studied the genetic regulation of adiponectin, and for the first time its most active form, high-molecular weight adiponectin, and found suggestive evidence of linkage to three chromosomal regions. In the third study, it was discovered that the studied VEGF gene polymorphisms did not have a major effect on atherosclerosis quantified as carotid intima-media thickness or the risk of acute myocardial infarction (AMI). This thesis presents potential regions for the genetic regulation of HDL-C and adiponectin and gives new information about their relationship and the effect of VEGF polymorphisms in atherosclerosis. The strong correlation between adiponectin and HDL-C was further strengthened, but we failed to show a shared genetic background between them
Tiivistelmä Sepelvaltimotauti, eräs valtimonkovettumataudin ilmentymä, on yleisin yksittäinen kuolinsyy maassamme. Taudin syntyyn vaikuttavat lukuisat geneettiset ja ympäristötekijät sekä niiden väliset yhteis- ja vuorovaikutukset. Pieni HDL-kolesterolipitoisuus on valtimonkovettumataudin itsenäinen riskitekijä ja yleisin kolesterolipoikkeavuus, joka liittyy varhain ilmenevään sepelvaltimotautiin. HDL-kolesterolin vaihtelun syitä ja tämän "hyvän kolesterolin" sepelvaltimotaudilta suojaavia vaikutusmekanismeja ei kuitenkaan pystytä täysin selittämään. Adiponektiini on rasvakudoksen tuottama hormoni, jonka sepelvaltimotaudilta suojaavan ominaisuuden on ehdotettu johtuvan siitä, että se vaikuttaisi HDL-kolesterolin aineenvaihduntaan. VEGF (vascular endothelial growth factor) on verisuonten sisäseinämissä vaikuttava kasvutekijä, jolla saattaa olla joko sepelvaltimotaudilta suojaavia tai sille altistavia vaikutuksia. Väitöskirjatyön tavoitteena oli tutkia HDL-kolesterolin ja valtimonkovettumataudin geneettistä taustaa. Kolmessa osatyössä tutkittiin suuria pohjoissuomalaisia sepelvaltimotautisukuja; lisäksi käytettiin väestö- ja potilasaineistoja. Ensimmäisessä tutkimuksessa löydettiin koko genomin kytkentäkartoitusmenetelmällä seitsemän kromosomialuetta, jotka saattavat vaikuttaa HDL-kolesterolin säätelyyn. Toisessa tutkimuksessa selvitettiin adiponektiinin, ja ensimmäistä kertaa myös sen aktiivisimman muodon, HMW-adiponektiinin geneettistä taustaa. Kytkentäanalyysissä saatiin viitteitä kolmesta adiponektiineja mahdollisesti säätelevästä kromosomialueesta. Havaittiin myös, että HDL-kolesterolin ja adiponektiinin pitoisuudet korreloivat vahvasti keskenään, mutta yhteistä geneettistä säätelytekijää ei pystytty osoittamaan. LDL-kolesterolin ja adiponektiinin välillä kuitenkin havaittiin geneettinen korrelaatio. Kolmannessa tutkimuksessa todettiin, ettei tutkituilla VEGF-geenin nukleotidimuutoksilla todennäköisesti ole merkittävää syy-yhteyttä valtimonkovettumatautiin kaulavaltimoiden sisäseinämän paksuudella tai sydäninfarktiriskillä mitattuna. Tämä tutkimus tuo uutta tietoa HDL-kolesterolin ja adiponektiinin geneettisestä säätelystä ja niiden suhteesta sekä VEGF-geenin nukleotidimuutosten osuudesta valtimonkovettumataudissa. Tutkimus vahvistaa edelleen HDL-kolesterolin ja adiponektiinin yhteyden, muttei pysty osoittamaan niille yhteistä geneettistä tekijää
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Kranz, Eylath. "Dietary habits and life style in the etiology of cholesterol gallstone disease a matched case control study /." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=968492649.

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Books on the topic "Cholesterol control":

1

Turner, Roger Newman. Diets to help control cholesterol. London: Thorsons, 1993.

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Roth, Harriet. Harriet Roth's cholesterol-control cookbook. New York: New American Library, 1989.

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Roth, Harriet. Harriet Roth's cholesterol control cookbook. 2nd ed. New York: Plume, 2008.

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Roth, Harriet. Harriet Roth"s Cholesterol Control Cookbook. New York: A Plume Book, 1991.

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Thompson, G. R. The cholesterol controversy. London: Royal Society of Medicine Press, 2008.

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B, Parsons William. Cholesterol control without diet!: The niacin solution. Scottdale, Ariz: Lilac Press, 1998.

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Bergasa, Ana María Lajusticia. Colesterol, triglicéridos y su control. Madrid: EDAF, 2002.

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Horovitz, Emmanuel. Cholesterol control made easy: How to lower your cholesterol for a healthier heart. Los Angeles, Calif: Health Trend Pub., 1990.

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Horovitz, Emmanuel. Cholesterol control made easy: How to lower your cholesterol for a healthier heart. Los Angeles: Health Trend Pub., 1990.

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Ulene, Art. Count out cholesterol. Berkeley, CA: Ulysses Press, 1994.

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Book chapters on the topic "Cholesterol control":

1

Rittershaus, Charles W. "Inducing Autoreactivity to Control Cholesterol Metabolism." In Vascular Endothelium, 273. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4899-0133-0_35.

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Bosisio, E. "Dietary and Pharmacological Control of Cholesterol 7α-Hydroxylase." In Drugs Affecting Lipid Metabolism, 21–28. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71702-4_4.

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Luskey, K. L. "The Control of Cholesterol Homeostasis: Regulation of HMG CoA Reductase." In Receptor-Mediated Uptake in the Liver, 80–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-70956-2_15.

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Henrion, André. "In- and off-laboratory sources of uncertainty in the use of a serum standard reference material as a means of accuracy control in cholesterol determination." In Measurement Uncertainty in Chemical Analysis, 248–51. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-662-05173-3_44.

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Teramoto, Akio, Kazuto Yoshiba, Shigeru Matsushima, and Naotake Nakamura. "Helical Conformations of Conjugating Polymers and Their Control of Cholesteric Order." In ACS Symposium Series, 47–62. Washington, DC: American Chemical Society, 2005. http://dx.doi.org/10.1021/bk-2005-0916.ch005.

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Johnson, Heather M., and Patrick E. McBride. "Chapter 12High Blood Cholesterol." In Chronic Disease Epidemiology and Control. American Public Health Association, 2010. http://dx.doi.org/10.2105/9780875531922ch12.

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"Program on the Surgical Control of the Hyperlipidemias (POSCH) Trial: A Pivotal 25-Year Study." In Cholesterol-Lowering Therapy, 135–90. CRC Press, 1999. http://dx.doi.org/10.1201/b15444-7.

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Kubica, Krystian, and Joanna Balbus. "Mathematical modeling of cholesterol homeostasis." In Control Theory in Biomedical Engineering, 43–61. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-821350-6.00002-0.

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Purcell, John. "Cholesterol Oxidase for the Control of Boll Weevil." In Advances In Insect Control. CRC Press, 1997. http://dx.doi.org/10.1201/9780203211731.ch6.

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"Statins: Fermentation Products for Cholesterol Control in Humans." In Chemistry and Pharmacology of Naturally Occurring Bioactive Compounds, 457–66. CRC Press, 2013. http://dx.doi.org/10.1201/b13867-21.

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Conference papers on the topic "Cholesterol control":

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Pescador, R., R. Porta, R. Niada, M. Mantovani, and G. Prino. "DEFIBROTIDE DECREASES CHOLESTEROL CONTENT IN HYPERCHOLESTEROLEMIC RABBIT AORTA, WITH NO MODIFICATION OF PLASMA OR LIPOPROTEIN CHOLESTEROL." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643153.

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Defibrotide was shown to stimulate the production of endogenous PGI2 from rat and hamster aortic tissue, as well as the production of PGi2 frcm the coronary vascular bed in the platelet perfused heart model. This effect was only seen in presence of platelets. Durirg the infusion period with Defibrotide thromboxane release remained unaffected while platelet cAMP rised. Defibrotide, was also able to reduce the secretion of ATP from platelets as well as to deaggregate platelet cluTps. It has been postulated that long-term administration of stable PGI^ metabolites or analogues could be a more useful means of enhancing cholesterol and cholesteryl ester mobilization out of the arterial “ foam” cell during early stages of cardiovascular disease. These observations prompted us to administer Defibrotide i.v. to cholesterol fed rabbits to verify if it could cause a decrease in cholesterol content of aortas. Aorta cholesterol was evaluated by gas chromatography. Plasma or lipoprotein lipids were assayed by enzymatic kits from Boehringer Biochemia. Plasma lipoproteins were separated by density gradient ultracentrifugation. Platelet aggregation was carried out with ADP using an optical aggregometer to find out the effective aggregatory concentration fifty (EC). Histology of the rabbit hearts was performed by optical microscopy on heart sections coloured with hematoxylin-eosine. Defibrotide caused a decrease (-49%, P < 0.05, vs. cholesterol fed rabbits treated with placebo) in cholesterol content of aortas with no modification of total plasma cholesterol, triglyceride and phospholipid. The cholesterol, triglyceride, phospholipid and protein of plasma lipoproteins were not affected too. The EC of rabbits treated with Defibrotide was 50 normalized (-9%, N.S. vs. control animals fed the normal diet and treated with placebo; cholesterol fed animals treated with placebo: -32%, P< 0.05 vs. control animals fed the normal diet). Vascular lesions in the hearts of animals treated with Defibrotide had a lower rate (33%) in comparison to that (87%) of animals fed with cholesterol and treated with placebo. It is concluded that the ability of Defibrotide to stimulate vascular PGI2 formation and to reduce platelet sensitivity could be helpful in reducing the amount of cholesterol in the cardiovascular system in atherosclerotic prone situations.
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Verbeuren, T. J., M. J. Van Diest, and A. G. Herman. "CONTRACTIONS TO PLATELETS IN AORTAS OF CONTROL AND CHOLESTEROL-FED RABBITS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643799.

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Atherosclerotic aortas obtained from cholesterol-fed rabbits show a decreased responsiveness to noradrenaline, an increased responsiveness to low concentrations of serotoninand an unaltered responsiveness to prostaglandins. In vitro contractions induced by aggregating platelets are largely due to serotonin liberated during the aggregation. The present study was designed to compare the contractile responses to aggregating platelets inaortas obtained from control and cholesterol-fed rabbits.Male New Zealand rabbits were fed either a control or a 0.3% cholesterol diet during 16 weeks. Macroscopic and microscopic examination of the luminal surface of the aortas obtained from these animals revealed a substantial amount of fatty streaks in the tissuesobtained from the cholesterol-fed rabbits. Segments of the aortic arch of the rabbits were then mounted in organ chambers for isometric tension recording.In both the control and the atherosclerotic aortas increasing concentrations of platelets evoked contractions; the contractions obtained with the lower concentrations of platelets were significantly greater in the atherosclerotic tissues. The maximal responses and the ED50-values were comparable in both groups of blood vessels. No significant differences were observed when platelets obtained from control or hypercholesterolemic rabbits were compared. In the control and the atherosclerotic aortas the thromboxane receptorantagonist BM13505 at 2 x 10-5M did not significantly affect the contractionsto platelets obtained from either control or cholesterol-fed rabbits. The serotonin receptor antagonist ketanserin at 5 x 10-8M nearly abolished the responses to platelets in bothgroups of aortas.These experiments illustrate that (1) thecontractions induced by rabbit platelets in control and atherosclerotic aortas are mediated by serotonin and (2) the responses to platelets, as those to serotonin, are augmented in the atherosclerotic preparations.
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Purwanti, Nunik, Rahmadiar Aditya Putri, and Siti Nurjanah. "Effectiveness of Sembung Tree Honey on Decreasing Cholesterol Level in Hypercolesterolemia." In The 7th International Conference on Public Health 2020. Masters Program in Public Health, Universitas Sebelas Maret, 2020. http://dx.doi.org/10.26911/the7thicph.05.22.

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ABSTRACT Background: Lifestyle changes, causing an increase in cholesterol. Honey has done a lot of research. The content of flavonoids can lower cholesterol. Many people consume Sembung tree honey, but not much research has been done, including its effectiveness in reducing cholesterol. This study aimed to analyze the effectiveness of sembung tree honey to reduce cholesterol levels in hypercholesterolemia. Subjects and Method: This was a quasi-experiment with pretest and posttest control group. A sample of 20 hypercholesterolemia sufferers in Kedensari Village was selected by purposive sampling. The dependent variable was hypercholesterolemia. The independent variable was sembung tree honey. The data was analyzed by Wilcoxon. Results: Cholesterol level after intervention (<240 mg / dL), lower before intervention (> 240 mg / dl), significant value p = 0.000. The mean coverage of cholesterol levels after the intervention (Mean = 185.50; SD = 6.05) was lower than that before the intervention (Mean = 247.20; SD = 6.96), it was statistically significant (p <0.001). Conclusion: Sembung tree honey is effective in reducing cholesterol levels. Keywords: Sembung tree honey, Hypercholesterolemia Correspondence: Nunik Purwanti. Faculty of Nursing and Midwifery, Universitas Nahdatul Ulama, Surabaya. Jl SMEA No 57 Surabaya. Email: noniek@unusa.ac.id. Mobile: 082141511655 DOI: https://doi.org/10.26911/the7thicph.05.22
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Gunduz, Canan, Ozen K. Basoglu, Jan Hedner, Maria R. Bonsignore, Holger Hein, Richard Staats, Izoldi Bouloukaki, et al. "Hyperlipidemia Prevalence and Cholesterol Control in OSA: Data from European Sleep Apnea Database (ESADA)." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.oa3274.

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Badimon, J., L. Bodimon, and V. Fuster. "HIGH AND VERY HIGH DENSITY LIPOPROTEINS ADMINISTRATION INHIBITS PROGRESSION OF EXPERIMENTAL ATHEROSCLEROSIS IN THE RABBIT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643748.

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Epidemiologic studies have shown an inverse relationship between HDL and coronary artery disease. We have previously demonstrated that in vivo administration of HDL-VHDL inhibits thedevelopment of atherosclerosis in cholesterol (cho)-fed rabbits. In the present study we have analyzed whether high levels of the physiological cholesterol acceptor, homologous HDL-VHDL,could inhibit the progression of established atherosclerotic lesions. Atherosclerosis was induced by feeding rabbits a 0.5% cho-rich diet for 2 months (140g/day). At that moment, a subgroup of animal (N=4) was sacrificed and their aortas showed 30 ± 8% of aortic atherosclerotic involvement. The remaining animals, kept on the same atherogenic diet, were randomly divided in two identical groups (N=7): a control and a treated group administered with 50 mg of HDL-VHDL a week for 4 weeks. HDL-VHDL fraction wasisolated from normal rabbit plasma byultracentrifugation at a density range of 1.063-1.25g/ml. The amount of HDL-VHDL administered was determined byits protein content according to Lowry"s technique. The 50mg of HDL-VHDL, measured as protein, contained1.4mg of total cholesterol, 1.43mg oftriglycerides and 0.6mg of phospholipids. At sacrifice, the treated group showed a marked decrease on the extent of aortic by fatty streaks (20 ± 6%X ± 1SE) as compared to(36% + 6) inthe control group (p < 0.05). Similar results were obtained in aortic wall lipid accumulation (See table, results expressed as X±1SEM; rag/gr dry aorta.)In conclusion, administration of HDL-VHDL induced a marked inhibition on the progression of atherosclerosis in cholesterol-fed rabbits.
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Tamaoki, Nobuyuki, Yasuyuki Aoki, Masaya Moriyama, and Masatoshi Kidowaki. "Photochemical control of helical pitch of glass-forming dimeric cholesteric liquid crystals by isomerization of embedded di-mesogenic compounds with both cholesterol and azobenzene groups." In International Symposium on Optical Science and Technology, edited by Iam-Choon Khoo. SPIE, 2002. http://dx.doi.org/10.1117/12.453260.

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Wanner, C., M. Cooper, S. Inzucchi, B. Zinman, I. Zwiener, M. Eynatten, and A. Koitka-Weber. "Empagliflozin Improves Kidney Outcomes Irrespective of Control of Blood Pressure, Low-Density Lipoprotein Cholesterol and HbA1c." In Diabetes Kongress 2019 – 54. Jahrestagung der DDG. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1688342.

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Fitchett, D., J. Lee, JT George, HJ Woerle, and SE Inzucchi. "Empagliflozin reduces heart failure irrespective of control of blood pressure, low density lipoprotein cholesterol and HbA1c." In Diabetes Kongress 2018 – 53. Jahrestagung der DDG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641913.

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Fazil, Qurratu'Aini Aishah Ahmad, and Ummu Kulthum Jamaludin. "Investigation on the relationship between cholesterol and blood glucose levels using decision tree method in healthy subjects." In 2017 IEEE 2nd International Conference on Automatic Control and Intelligent Systems (I2CACIS). IEEE, 2017. http://dx.doi.org/10.1109/i2cacis.2017.8239051.

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Lobel, P., M. Palmer, and K. Schor. "CHRONIC ORAL DEFIBROTIDE STIMULATES VASCULAR PGI2 AND INHIBITS ATHEROSCLEROTIC PLAQUE FORMATION IN CHOLESTEROL-FED RABBITS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643150.

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Defibrotide (DEF) is a polydeoxyribonucleotide fraction from bovine lung, possessing profibrinolytic and PGI2 stimulating properties. Male rabbits were fed for 4 months a standard laboratory diet (150 g/day) without (A) or with (B) DEF or a cholesterol (1%) supplemented diet without (C) or with (D) DEF (60 mg/kg x day) was administered orally (drinking water) and withdrawn 24-36 h prior to the acute experiments.DEF did not change the elevated serum cholesterol: 18 ± 2 (C) vs. 26 ± 5 (D) mM but significantly reduced the plaque formation in the aorta from 4.5 ± 0.3 (C) to 3.3 ± 0.2 (D) (subjective score). Collagen induced (0.6 pg/ml) thromboxane formation and ATP release was significantly reduced by DEF: 55+2 (C) vs. 42 ± 2 (D) ng/ml TXB2; 152 ± 11 (C) vs. 74±5 (D) AU ATP (platelet rTch plasma). DEF significantly increased the basal and bradykinin (Bk, 30 nM) stimulated PGI2 release from rabbit aorta preparations in Krebs buffer, while the PGI2 forming capacity (arachidonic acid, AA, 30 pg/ml) was unchanged Furthermore, the iloprost (30 nM) stimulated cAMP was significantly elevated by DEF in both control: 115 ± 10 (A) vs. 155 ± 18 (B) pmoles/1 and cholesterol-fed rabbits: 120 ± 14 (C) vs. 172 ± 9 (D). DEF, directly added to the platelets in vitro did not inhibit platelet activation up to 100 pg/ml.The data demonstrate a 2-3-fold stimulation of basal and hormone (Bk) induced PGI2 formation of control and sclerotic rabbit aorta after 4 months DEF treatment while the atherosclerosis per se does not significantly change these parameters. DEF treatment also significantly reduces platelet hyperreactivity at unchanged serum ch() lesterol. Both properties might be useful to prevent complication’s of atherosclerosis, such as myocardial infarction and stroke.

Reports on the topic "Cholesterol control":

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Gao, Hui, Chen Gong, Shi-chun Shen, Jia-ying Zhao, Dou-dou Xu, Fang-biao Tao, Yang Wang, and Xiao-chen Fan. A systematic review on the associations between prenatal phthalate exposure and childhood glycolipid metabolism and blood pressure: evidence from epidemiological studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0111.

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Review question / Objective: The present systematic review was performed to obtain a summary of epidemiological evidence on the relationships of in utero exposure to phthalates with childhood glycolipid metabolism and blood pressure. Condition being studied: Childhood cardiovascular risk factors including blood pressure, lipid profile (e.g., triglycerides, total cholesterol, HDL−C, LDL−C) and glucose metabolism (e.g., insulin, insulin resistance, insulin sensitivity, glucose) were the interested outcomes. Eligibility criteria: In brief, epidemiological studies including cohort study, case-control study and cross-sectional survey were screened. Studies regarding relationships between human exposure to organophosphate esters and neurotoxicity were possible eligible for the present systematic review. The adverse neurodevelopmental outcomes included development of cognition, behavior, motor, brain change, emotion, etc. Studies that did not meet the above criteria were not included in this systematic review.
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Chen, Jiankun, Yingming Gu, Lihong Yin, Minyi He, Na Liu, Yue Lu, Changcai Xie, Jiqiang Li, and Yu Chen. Network meta-analysis of curative efficacy of different acupuncture methods on obesity combined with insulin resistance. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2022. http://dx.doi.org/10.37766/inplasy2022.8.0075.

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Review question / Objective: Population：Patients diagnosed as obesity with insulin resistance. Obesity reference: Consensus of experts on the Prevention and treatment of adult obesity in China in 2011 and Consensus of Chinese experts on medical nutrition therapy for overweight/obesity in 2016 were developed by the Obesity Group of Chinese Society of Endocrinology(CSE); BMI≥28. IR reference: According to the Expert opinions on insulin resistance evaluation published by Chinese Diabetes Society, HOMA-IR≥2.68 is regarded as the standard for the diagnosis of IR. Regardless of age, gender and course of disease. Patients diagnosed as obesity with insulin resistance. Intervention：Any kind of acupuncture, moxibustion, acupuncture+moxibustion, warm acupuncture, electropuncture, auricular point, acupoint application and acupoint catgut embedding. Comparison：Other acupuncture treatments, Drug therapy or blank control. Outcome：Primary outcomes: ①Fasting blood-glucose (FBG); ②Fasting serum insulin (FINS); ③Homeostasis model assessment-IR (HOMA-IR); ④Body Mass Index (BMI). Secondary outcomes: ①Waistline; ②Waist-hip ratio;③Triglyceride (TG); ④Total cholesterol (TC); ⑤High-density lipoprotein (HDL); ⑥Low-density lipoprotein (LDL). Study: Randomized controlled trials (RCTs) of different acupuncture methods in the treatment on obesity with insulin resistance, blind method and language are not limited. Randomized controlled trials (RCTs).

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