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Journal articles on the topic 'Blood cholesterol'

Author: Grafiati

Published: 4 June 2021

Last updated: 30 July 2024

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1

Feoktistova, N. A., M. A. Shtarberg, E. V. Egorshina, G. K. Doroshenko, L. Ya Etmanova, and L. G. Tertychnaya. "VEGETABLE PROTEIN DECREASES BLOOD CHOLESTEROL." Amur Medical Journal, no. 4 (2017): 31–32. http://dx.doi.org/10.22448/amj.2017.3.31-32.

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2

DR. USMAN M.S, DR USMAN M. S., and DR B. A. THOBANI DR. B.A.THOBANI. "Correlation of Fitness, Fatness, Blood Cholesterol and Blood Sugar." International Journal of Scientific Research 2, no. 9 (June 1, 2012): 383–85. http://dx.doi.org/10.15373/22778179/sep2013/134.

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3

Levin, Susan, Cameron Wells, and Neal Barnard. "Dietary Cholesterol and Blood Cholesterol Concentrations." JAMA 314, no. 19 (November 17, 2015): 2083. http://dx.doi.org/10.1001/jama.2015.12595.

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4

Stellaard, Frans. "From Dietary Cholesterol to Blood Cholesterol." Nutrients 15, no. 14 (July 10, 2023): 3086. http://dx.doi.org/10.3390/nu15143086.

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5

LaRosa, Judith H., Diane M. Becker, and Sheila Fitzgerald. "Elevated Blood Cholesterol." AAOHN Journal 38, no. 5 (May 1990): 211–15. http://dx.doi.org/10.1177/216507999003800502.

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6

POLZIEN, GLADYS. "Blood Cholesterol Levels." Home Healthcare Nurse: The Journal for the Home Care and Hospice Professional 25, no. 2 (February 2007): 136–39. http://dx.doi.org/10.1097/00004045-200702000-00016.

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7

Craig, Steven R., Rupal V. Amin, Daniel W. Russell, and Norman F. Paradise. "Blood cholesterol screening." Journal of General Internal Medicine 15, no. 6 (June 2000): 395–99. http://dx.doi.org/10.1046/j.1525-1497.2000.03509.x.

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8

Siscovick, David S. "Lowering blood cholesterol." Journal of General Internal Medicine 1, no. 3 (May 1986): 196–97. http://dx.doi.org/10.1007/bf02602337.

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9

Hussain, Shabbir, Safdar Amir, and Naureen Naeem. "Nature and Effects of Cholesterol; Its Origin, Metabolism and Characterization." Lahore Garrison University Journal of Life Sciences 3, no. 4 (April 22, 2020): 196–203. http://dx.doi.org/10.54692/lgujls.2019.030465.

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Cholesterol ((3β)-cholest-5-en-3-ol) is basically a fatty component present in blood, plasma and tissues. It belongs to the class of lipids namely steroids and is formed from squalene via lanosterol. It is present as a combination of cholesterol and cholesteryl esters in almost all types of foodstuffs. There is the direct relation between the risk of cardiovascular sicknesses and the total cholesterol amount in human blood. The bad- and good-cholesterol are types of lipoproteins. Good-cholesterol basically eliminates cholesterol from bloodstream while bad-cholesterol releases cholesterol into the blood and various part of body. Cholesterol amount can be reduced by physical activity or by use of proper diet. Cholesterol can be characterized by the SIM-selected ion monitoring, HPLC, UHPLC, GLC, GC-MS, LC-MS.

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10

Stanley, John. "Dietary cholesterol, blood cholesterol and cardiovascular disease." Lipid Technology 22, no. 5 (May 2010): 110–12. http://dx.doi.org/10.1002/lite.201000024.

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11

Mozaffarian, Dariush, and David S. Ludwig. "Dietary Cholesterol and Blood Cholesterol Concentrations—Reply." JAMA 314, no. 19 (November 17, 2015): 2084. http://dx.doi.org/10.1001/jama.2015.12604.

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12

Nuari, Nian Afrian, Efa Nur Aini, and Dhina Widayati. "Blood cholesterol and its related factors among Indonesian blood donors." International Journal of Public Health Science (IJPHS) 12, no. 1 (March 1, 2023): 371. http://dx.doi.org/10.11591/ijphs.v12i1.21816.

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Blood donation nowadays were considered to improve health status of the donors by declining human’s cholesterol level. The high level of cholesterol inside the blood bags influenced the blood quality. However, there was limited data about cholesterol level and its influencing factor on the blood donors. This cross-sectional study aimed to analyse the associated factors of cholesterol levels in blood donors. This study involved 120 respondents using the purposive sampling as sampling method. Data was collected using questionnaires and blood cholesterol examination. The obtained data was analysed using univariate and bivariate statistic tests with significance level α=0.05. This study found that the majority of respondents aged 35-45 years (60.8%) and male (60.8%). More than half respondents were routine to donate their blood. Although they consumed cholesterol foods, their cholesterol level remained normal (88.3%). This study also found that blood donation had an association with cholesterol level p=0.000, while the other variables did not show any relationship. The normal cholesterol level among blood donors was influenced by frequent blood donation. Further study needs to be explored about the activities and the foods type to identify the cholesterol level among blood donors.

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13

Hallfrisch, J. "Fructose and blood cholesterol." American Journal of Clinical Nutrition 57, no. 1 (January 1, 1993): 89. http://dx.doi.org/10.1093/ajcn/57.1.89.

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14

McNUTT, KRISTEN. "AMA Blood Cholesterol Campaign." Nutrition Today 24, no. 3 (May 1989): 30???34. http://dx.doi.org/10.1097/00017285-198905000-00008.

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15

McNUTT, KRISTEN. "AMA Blood Cholesterol Campaign." Nutrition Today 24, no. 3 (May 1989): 30–34. http://dx.doi.org/10.1097/00017285-198905000-00009.

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16

Retterstøl, K. "Too low blood cholesterol?" Scandinavian Journal of Clinical and Laboratory Investigation 65, no. 1 (February 2005): 1–2. http://dx.doi.org/10.1080/00365510510013488.

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17

Alenghat, Francis J., and Andrew M. Davis. "Management of Blood Cholesterol." JAMA 321, no. 8 (February 26, 2019): 800. http://dx.doi.org/10.1001/jama.2019.0015.

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18

Perona, Javier S., Julio Cañizares, Emilio Montero, José M. Sánchez-Domínguez, and Valentina Ruiz-Gutierrez. "Plasma lipid modifications in elderly people after administration of two virgin olive oils of the same variety (Olea europaeavar.hojiblanca) with different triacylglycerol composition." British Journal of Nutrition 89, no. 6 (June 2003): 819–26. http://dx.doi.org/10.1079/bjn2003852.

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In the present study we examined whether two virgin olive oils (VOO1 and VOO2), of the same variety (Olea europaeavar.hojiblanca) and with a similar composition of minor components but differing in the content of triacylglycerol molecular species, had different effects on blood pressure and plasma lipid levels in a healthy elderly population. Thirty-one participants, aged 84·9 (SD 6·4) years, were asked to participate in the study. No differences were found with regard to blood pressure after both experimental periods (VOO1 and VOO2). However, plasma total cholesterol and LDL-cholesterol were reduced only after VOO1 (P<0·01). The reduction of plasma cholesterol concentrations was related to the incorporation of oleic acid into plasma cholesteryl esters and phospholipids, which was higher after VOO1 (P<0·01). Indeed, the oleic acid concentration in cholesteryl esters and phospholipids strongly correlated with plasma total cholesterol and LDL-cholesterol levels in all experimental periods studied (r2>0·418,P<0·07), except for phospholipids in VOO1 (P=0·130 for total cholesterol andP=0·360 for LDL-cholesterol). These results have demonstrated that blood pressure and plasma lipids can be modified by the consumption of VOO in elderly people, but that the extent of such modification depends on the composition and amount of active minor components and triacylglycerol molecular species.

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19

Ohkawa, Ryunosuke, Hann Low, Nigora Mukhamedova, Ying Fu, Shao-Jui Lai, Mai Sasaoka, Ayuko Hara, et al. "Cholesterol transport between red blood cells and lipoproteins contributes to cholesterol metabolism in blood." Journal of Lipid Research 61, no. 12 (September 9, 2020): 1577–88. http://dx.doi.org/10.1194/jlr.ra120000635.

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Lipoproteins play a key role in transport of cholesterol to and from tissues. Recent studies have also demonstrated that red blood cells (RBCs), which carry large quantities of free cholesterol in their membrane, play an important role in reverse cholesterol transport. However, the exact role of RBCs in systemic cholesterol metabolism is poorly understood. RBCs were incubated with autologous plasma or isolated lipoproteins resulting in a significant net amount of cholesterol moved from RBCs to HDL, while cholesterol from LDL moved in the opposite direction. Furthermore, the bi-directional cholesterol transport between RBCs and plasma lipoproteins was saturable and temperature-, energy-, and time-dependent, consistent with an active process. We did not find LDLR, ABCG1, or scavenger receptor class B type 1 in RBCs but found a substantial amount of ABCA1 mRNA and protein. However, specific cholesterol efflux from RBCs to isolated apoA-I was negligible, and ABCA1 silencing with siRNA or inhibition with vanadate and Probucol did not inhibit the efflux to apoA-I, HDL, or plasma. Cholesterol efflux from and cholesterol uptake by RBCs from Abca1+/+ and Abca1−/− mice were similar, arguing against the role of ABCA1 in cholesterol flux between RBCs and lipoproteins. Bioinformatics analysis identified ABCA7, ABCG5, lipoprotein lipase, and mitochondrial translocator protein as possible candidates that may mediate the cholesterol flux. Together, these results suggest that RBCs actively participate in cholesterol transport in the blood, but the role of cholesterol transporters in RBCs remains uncertain.

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20

Mindham, M. A., and P. A. Mayes. "Application of simultaneous spleen and liver perfusion to the study of reverse cholesterol transport." Biochemical Journal 302, no. 1 (August 15, 1994): 207–13. http://dx.doi.org/10.1042/bj3020207.

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1. A new method to isolate and perfuse the rat spleen and liver simultaneously with a common blood perfusate at high haematocrit was developed. The spleen was pre-labelled with [3H]cholesterol, enabling reverse cholesterol transport from an extrahepatic tissue to the blood and thence to the liver and bile to be studied in a single preparation in vitro. 2. The presence of the liver significantly increased the release of [3H]cholesterol from the spleen by 15%, compared with experiments where the spleen was perfused alone. 3. There was a substantial release of [3H]cholesterol and cholesterol mass from the spleen to serum lipoproteins, the majority (80%) to high-density lipoprotein (HDL), in which cholesteryl ester accumulated. 4. The HDL subfractions HDL2 and HDL3 (d 1.085-1.250) were most important for removal of cholesterol from the spleen, whereas HDL1 and HDL2 (d 1.050-1.125) were important for delivery of cholesterol to the liver, a net uptake of cholesteryl ester occurring only from these fractions. 5. Approximately half of the [3H]cholesterol released by the spleen was recovered in erythrocytes. Also, in experiments utilizing a lipoprotein-free perfusate containing erythrocytes, a substantial quantity of [3H]cholesterol was transported and/or exchanged into the liver and bile, indicating that erythrocytes play an important role in the equilibration of unesterified cholesterol between the tissues.

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21

Hartoyo, Bambang, Ning Iriyanti, and Efka Aris Rimbawanto. "The Use of “Fermeherbafit” (Mixed Herbs) in Broiler Chicken Feed on Performance and Cholesterol profile." ANIMAL PRODUCTION 20, no. 3 (September 26, 2019): 139. http://dx.doi.org/10.20884/1.jap.2018.20.3.709.

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This research was aimed to imporve of broiler chiken performance and reduce the blood, meat and liver cholesterol levels. This research used 100 female broilers MB 200 Platinum DOC which were reared for 5 weeks at battery-postal cages. The treatments were R0= control/ 0% fermeherbafit; R1= used 2% fermeherbafit; R2= used 4% fermeherbafit; R3= used 6% fermeherbafit. The experimental design was carried out using a complete randomized design. Data were analyzed by analysis of variance (ANOVA). The results showed that the use fermeherbafit did not showed any significant differences (P>0.05) in feed consumption, absolute growth, relative growth and carcas percentage. However, it showed significant differences (P<0.05) in blood and breast meat cholesterols. The average for Performance (feed consumption by 3268.775±293.421 g/bird; absolute growth by 1684.92±126.12; relative growth by 0.3682±0.0019; carcas percentage by 74.61± 1.12%). Blood cholesterol 89.20+12.76 mg/dl (R3) up to 111.80+17.02 mg/dl (R0); Breast meat cholesterol 150.03+11.64 mg/g (R3) up to 174.88+8.53 mg/g (R0); Leg meat cholesterol 173.00+7.21 (R1) up to 152.15+17.83 mg/g (R3); Liver cholesterol 83.37+31.01 mg/g (R0) up to 102.75+1.68 mg/g (R3). Conclusion of this research was that the Fermeherbafit could be used in broiler feed up to 6% which could reduce blood and breast meat cholesterols.

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22

Weissfeld, Joel L., and James J. Holloway. "Precision of blood cholesterol measurement and high blood cholesterol case-finding and treatment." Journal of Clinical Epidemiology 45, no. 9 (September 1992): 971–84. http://dx.doi.org/10.1016/0895-4356(92)90113-2.

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23

Stellaard, Frans. "From Dietary Cholesterol to Blood Cholesterol, Physiological Lipid Fluxes, and Cholesterol Homeostasis." Nutrients 14, no. 8 (April 14, 2022): 1643. http://dx.doi.org/10.3390/nu14081643.

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Dietary cholesterol (C) is a major contributor to the endogenous C pool, and it affects the serum concentration of total C, particularly the low-density lipoprotein cholesterol (LDL-C). A high serum concentration of LDL-C is associated with an increased risk for atherosclerosis and cardiovascular diseases. This concentration is dependent on hepatic C metabolism creating a balance between C input (absorption and synthesis) and C elimination (conversion to bile acids and fecal excretion). The daily C absorption rate is determined by dietary C intake, biliary C secretion, direct trans-intestinal C excretion (TICE), and the fractional C absorption rate. Hepatic C metabolism coordinates C fluxes entering the liver via chylomicron remnants (CMR), LDL, high-density lipoproteins (HDL), hepatic C synthesis, and those leaving the liver via very low-density lipoproteins (VLDL), biliary secretion, and bile acid synthesis. The knowns and the unknowns of this C homeostasis are discussed.

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24

Rink, Jonathan, Shuo Yang, Osman Cen, Reem Karmali, Colby Shad Thaxton, and Leo I. Gordon. "Inhibition of Pro-Survival Pathways in DLBCL Cells By Functional Lipoprotein-like Nanoparticles." Blood 132, Supplement 1 (November 29, 2018): 1668. http://dx.doi.org/10.1182/blood-2018-99-119122.

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Abstract Introduction: Diffuse large B cell lymphoma (DLBCL) cells have an increased demand for cholesterol and cholesteryl esters to maintain membrane-anchored pro-survival signaling pathways, such as B cell receptor (BCR) signaling. In addition to BCR-mediated stimulation of de novo cholesterol synthesis, another mechanism employed by lymphoma cells to maintain cholesterol and cholesteryl ester homeostasis is by binding cholesterol-rich HDLs via the high-affinity receptor, scavenger receptor type B-1 (SCARB1). We previously reported that, unlike normal B cells, DLBCL cells highly express SCARB1, and that synthetic, cholesterol-poor high-density lipoprotein (HDL)-like nanoparticles (HDL NPs) exquisitely target SCARB1, deplete cellular cholesterol, and induce lymphoma cell death in vitro and in vivo. Given the critical role of cholesterol in maintaining proper membrane organization for BCR-mediated intracellular signaling, we hypothesized that HDL NP binding to SCARB1 and subsequent cellular cholesterol depletion modulates the organization of the cell membrane, reduces intracellular signaling downstream of membrane-anchored pathways like the BCR, and modulates the expression of genes relevant to cholesterol synthesis. Collectively, these mechanisms potently induce lymphoma cell death. Methods: We focused on germinal center (GC) DLBCL and Burkitt's Lymphoma (BL), due to the previously reported sensitivity of the SUDHL4 (GC DLBCL) and Ramos (BL) cell lines to HDL NP-induced cell death. In addition to SUDHL4 and Ramos, we tested the GC DLBCL cell line SUDHL6 and the BL cell lines Raji, Daudi and Namalwa. HDL NPs were synthesized, purified and characterized using standard protocols. Cell viability was quantified using the MTS assay, and total cholesterol levels were measured using the Amplex Red cholesterol assay. A blocking antibody against SCARB1 was used to inhibit binding of HDL NPs to the receptor. Confocal microscopy was used to visualize changes in membrane organization of SUDHL4 and Ramos cells following HDL NP treatment. Changes in the phosphorylation of signaling kinases (e.g. AKT, ERK1/2) following HDL NP treatment was measured using phospho-kinase arrays, phos-flow analysis, and western blot assays. RNA was harvested from cells treated with the HDL NPs for 48 hours and analyzed using Illumina's HT-12 microarray and RT-qPCR. Protein expression changes were measured using western blot assays. Results: HDL NPs potently induced cell death in all of the GC DBLCL and BL cell lines, all of which expressed SCARB1, with HDL NP IC50 values between 1 ~ 5 nM. As expected, HDL NP-induced cell death correlated with reduced total cellular cholesterol levels. Inhibition of HDL NP binding to SCARB1 by antibody blockade protected cells from HDL NP-induced cell death. HDL NP treatment induced a reorganization of the plasma membrane in SUDHL4 and Ramos cells, resulting in clustering of SCARB1, a phenomenon not seen in cholesterol-rich human HDL or saline controls. HDL NP treatment led to a decrease in the phosphorylation of a number of kinases downstream of BCR signaling, including AKT, ERK1/2, LCK and LYN over time. HDL NPs demonstrated synergy with small molecule inhibitors of various signaling kinases, such as ATK (inhibitor = GDC-0068) and SYK (inhibitor = R406), in Ramos and SUDHL4 cells. By microarray analysis and RT-qPCR, HDL NPs up-regulated a number of cholesterol biosynthesis genes, as well as the cell cycle inhibitor p21 and the pro-apoptotic protein APOPT1. Conclusions: These data demonstrate that HDL NPs bind SCARB1, altering the organization of the plasma membrane and reducing cellular cholesterol levels. Collectively, this results in decreased membrane-anchored pro-survival signaling, changes in gene expression pathways, and, ultimately, lymphoma cell death. Enhancing cholesterol depletion strategies, such as the combination of the targeted cholesterol depletion agent HDL NP with small molecule inhibitors of signaling kinases (e.g. AKT and SYK inhibitors), represents a novel and targeted therapeutic strategy for DLBCL and may be broadly applicable to other malignancies dependent on cholesterol homeostasis and membrane-anchored signaling pathways. Disclosures Karmali: Gilead: Speakers Bureau; AstraZeneca: Speakers Bureau. Thaxton:AuraSense: Other: Co-founder of the biotech company AuraSense.

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25

Roseveare, K., D. Southard, J. Walberg, and R. Humphrey. "EFFECTIVENESS OF CHOLESTEROL FEEDBACK IN REDUCING BLOOD CHOLESTEROL LEVELS." Journal of Cardiopulmonary Rehabilitation 10, no. 10 (October 1990): 356. http://dx.doi.org/10.1097/00008483-199010200-00010.

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26

Bowers, G. N. "Accuracy and blood cholesterol measurements." Clinical Chemistry 34, no. 1 (January 1, 1988): 192. http://dx.doi.org/10.1093/clinchem/34.1.192.

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27

Grundy, S. M., and G. L. Vega. "Causes of high blood cholesterol." Circulation 81, no. 2 (February 1990): 412–27. http://dx.doi.org/10.1161/01.cir.81.2.412.

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28

Buchwald, Henry, James R. Boen, Stanley E. Williams, Phuong A. Nguyen, and John P. Matts. "Blood pressure, weight, and cholesterol." Journal of the American College of Cardiology 41, no. 6 (March 2003): 320. http://dx.doi.org/10.1016/s0735-1097(03)82493-2.

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29

Davidson, Dennis M., Beverly J. Bradley, Sandra M. Landry, Cynthia A. Iftner, and Susan N. Bramblett. "School-based blood Cholesterol screening." Journal of Pediatric Health Care 3, no. 1 (January 1989): 3–8. http://dx.doi.org/10.1016/0891-5245(89)90043-6.

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30

Schucker, Beth, and Reagan H. Bradford. "Screening for High Blood Cholesterol." Clinics in Laboratory Medicine 9, no. 1 (March 1989): 29–36. http://dx.doi.org/10.1016/s0272-2712(18)30640-1.

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31

Rahkovsky, Ilya, and Christian A. Gregory. "Food prices and blood cholesterol." Economics & Human Biology 11, no. 1 (January 2013): 95–107. http://dx.doi.org/10.1016/j.ehb.2012.01.004.

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32

Brendolan, Andrea, and Vincenzo Russo. "Targeting cholesterol homeostasis in hematopoietic malignancies." Blood 139, no. 2 (January 13, 2022): 165–76. http://dx.doi.org/10.1182/blood.2021012788.

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Abstract Cholesterol is a vital lipid for cellular functions. It is necessary for membrane biogenesis, cell proliferation, and differentiation. In addition to maintaining cell integrity and permeability, increasing evidence indicates a strict link between cholesterol homeostasis, inflammation, and hematological tumors. This makes cholesterol homeostasis an optimal therapeutic target for hematopoietic malignancies. Manipulating cholesterol homeostasis by either interfering with its synthesis or activating the reverse cholesterol transport via the engagement of liver X receptors affects the integrity of tumor cells both in vitro and in vivo. Cholesterol homeostasis has also been manipulated to restore antitumor immune responses in preclinical models. These observations have prompted clinical trials involving acute myeloid leukemia to test the combination of chemotherapy with drugs interfering with cholesterol synthesis (ie, statins). We review the role of cholesterol homeostasis in hematopoietic malignancies as well as in cells of the tumor microenvironment and discuss the potential use of lipid modulators for therapeutic purposes.

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33

Kuypers, Frans A., Sandra Larkin, Jenifer Beckstead, Michael Oda, Kazumitsu Ueda, and Robert O. Ryan. "Red Blood Cells Facilitate Reverse Cholesterol Transport." Blood 104, no. 11 (November 16, 2004): 1589. http://dx.doi.org/10.1182/blood.v104.11.1589.1589.

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Abstract Lecithin:cholesterol acyl transferase (LCAT)-dependent conversion of cholesterol (CH) to cholesteryl ester (CE), a key component of the reverse cholesterol transport (RCT) pathway, is essential for cholesterol processing. We hypothesized that red blood cells (RBCs) function in this pathway by facilitating phosphatidylcholine (PC) re-generation from LCAT-derived lysophosphatidylcholine (LPC). Addition of 14C-oleate to fresh RBCs resulted in an ATP-dependent incorporation of radiolabel into PC via the Lands pathway. Prior depletion of red cell LPC content reduced the incorporation of 14C-oleate into PC, which was restored by the addition of LPC. Reconstituted PC/cholesterol/apolipoprotein A-I (apoA-I) high-density lipoprotein (rHDL) was used as substrate for LCAT dependent conversion of CH to CE. Addition of LPC to this reaction mix inhibited CE production. The inhibition was overcome, however, by inclusion of RBCs, suggesting rHDL-generated LPC migration to RBCs. RBCs depleted of LPC increased their ability to generate 14C-PC from 14C-oleate in the presence of rHDL with LCAT, indicating that LCAT-derived LPC can be utilized as a substrate for PC production in RBCs. Radio-labeled CH associated with RBCs was recovered as CE only when rHDL substrate and LCAT were present, indicating RBC-associated CH migration to rHDL. When RBCs containing 14C-PC were incubated with rHDL and LCAT, PC transferred from RBCs to the rHDL particles. The interaction of apoA-I with the membrane lipid transporter ATP-Binding Cassette A1 protein (ABCA1) in cell membranes has been shown to play an essential role in the formation of HDL and facilitates RCT. Using monoclonal antibodies, we were able to show that RBCs contain ABCA7, closely related to ABCA1. Our data show that fluorescently labeled apoA-I binds to RBCs, suggesting that the interaction between ABCA7 and apoA-I may be important for HDL/RBC interaction. Together, our data supports an active role for RBCs, the major cell type in blood, in LCAT-mediated lipoprotein remodeling. Thus, RBCs represent a hitherto underappreciated component of the RCT pathway.

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34

Neary, Richard H., Mark D. Kilby, Padma Kumpatula, Francis L. Game, Deepak Bhatnagar, Paul N. Durrington, and P. M. Shaughn O'Brien. "Fetal and Maternal Lipoprotein Metabolism in Human Pregnancy." Clinical Science 88, no. 3 (March 1, 1995): 311–18. http://dx.doi.org/10.1042/cs0880311.

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1. Lipid, apolipoprotein concentration and composition were determined in maternal venous and umbilical arterial and venous blood at delivery by elective Caesarean section in 13 full-term pregnancies and in 25 healthy non-pregnant females. The indications of Caesarean section were a previous Caesarean section or breech presentation. None of the women was in labour and there were no other complications of pregnancy or fetal distress. 2. The objectives of the study were to establish whether the placenta has a role in feto-maternal cholesterol metabolism through either synthesis or transplacental cholesterol flux. The potential for free cholesterol diffusion between mother and fetus and rates of cholesterol esterification and transfer between lipoproteins were determined and related to the differences in composition between fetal and maternal lipoproteins. 3. Pregnant women had raised levels of all lipid and lipoprotein fractions compared with control subjects. The greatest increases were in free cholesterol and triacylglycerol (P < 0.0001). Lipoprotein (a) levels were significantly greater in the pregnant women [112(12.2) mg/l] than in the control women [50 (10.0) mg/l]. 4. The only significant correlation between maternal and fetal lipoprotein concentrations was in lipoprotein (a) levels (r = 0.791, P = 0.002). In both umbilical venous and arterial blood, concentrations of very-low- and low-density lipoproteins, particularly apolipoprotein B, cholesteryl ester and triacylglycerol, were lower than in maternal blood (P < 0.0001), but high-density lipoprotein levels were similar. 5. There was no umbilical arteriovenous differences in lipoprotein concentration or composition. This suggests that cholesterol synthesis or free cholesterol diffusion does not occur in the placenta. The relative concentrations of free cholesterol to phospholipid in maternal and fetal lipoproteins do not indicate the existence of a concentration gradient favouring free cholesterol diffusion across the placenta. 6. The esterification of free cholesterol was significantly reduced in maternal [17.7 (2.4) μmol h−1 l−1, P < 0.001] and fetal [6.7 (3.5) μmol h−1 l−1, P < 0.0001] compared with control [40.9 (13.2) μmol h−1 l−1] blood. 7. In fetal compared with maternal high-density lipoproteins the ratios cholesteryl ester/apoliproprotein A-I [0.84 (0.35) versus 0.40 (0.05), P < 0.01] and phospholipid/apolipoprotein A-I [1.66 (0.14) versus 0.58 (0.10), P < 0.0001] indicated lipid enrichment of these particles in the fetus. 8. Lipid enrichment of high-density lipoprotein is due in part to a marked reduction in transfer of cholesteryl ester in the fetus [1.0 (0.6) μmol h−1 l−1] compared with maternal [6.15 (1.3) μmol h−1 l−1, P = 0.004] and control [17.3 (7.2) μmol h−1 l−1, P < 0.0001] blood. 9. In conclusion, there was no evidence for involvement of the placenta in cholesterol metabolism during pregnancy. In fetal life high-density lipoproteins are lipid rich, partly because of a reduction in transfer of esterified cholesterol to other particles. Maternal and fetal lipoprotein levels are not correlated, although the results suggested that lipoprotein (a) levels may be related.

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35

Mindham, M. A., and P. A. Mayes. "Reverse cholesterol transport in the rat. Studies using the isolated perfused spleen in conjunction with the perfused liver." Biochemical Journal 279, no. 2 (October 15, 1991): 503–8. http://dx.doi.org/10.1042/bj2790503.

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1. A new method combining the use of an isolated perfused extrahepatic tissue with a perfused liver was developed as a model system for the study of reverse cholesterol transport. Rat spleens, initially labelled in vivo with [3H]cholesterol, were perfused for 3 h with whole blood. The spleen was then replaced with an isolated rat liver, whose uptake of cholesterol from the spleen-derived blood and excretion of cholesterol into bile constituents were determined. 2. During spleen perfusion, a net release of cholesterol mass and radioactivity to lipoproteins was observed. 3. During liver perfusion, there was also a rapid exchange or transport of unesterified cholesterol between high-density lipoprotein (HDL) and the liver, in particular with HDL2 (d = 1.085-1.125). 4. The liver showed an increased uptake of cholesteryl ester from serum that had previously been used in spleen perfusion. 5. Approximately half of the [3H]cholesterol released by the spleen was recovered in erythrocytes. During subsequent liver perfusion there was a substantial uptake of radioactivity from the erythrocytes, although less than that recorded from serum lipoproteins. 6. In all experiments there was significant excretion of [3H]cholesterol into bile; most (85%) was in bile acids. Thus the complete process of reverse cholesterol transport is observed in this dual-perfusion system.

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Syokumawena, Syokumawena, and Marta Pastari. "Pengobatan Alternatif Bekam Kering terhadap Kadar Kolesterol Darah." Jurnal Keperawatan Silampari 5, no. 1 (August 23, 2021): 11–19. http://dx.doi.org/10.31539/jks.v5i1.2109.

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This study aimed to determine the effectiveness of dry cupping alternative treatment on blood cholesterol levels. The research method in this study used a pre-experimental design with a two-group pre-and post-test design. The results showed that most of the blood cholesterol levels before cupping were nine people (30.0%) with worrying blood cholesterol levels (200-239). Most of the blood cholesterol levels before 13-point cupping were 11 people (36.7%) with High Blood Cholesterol Levels (>240), then after 13-point cupping, 11 people (36.7%) had Worrying Blood Cholesterol Levels (200-239). In conclusion, groups 9 and 13 cupping points affect reducing blood cholesterol levels. Keywords: Cupping, Cholesterol, Alternative Medicine

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37

Shen, Yajie, Jingqi Zhou, Kui Nie, Shuhua Cheng, Zhengming Chen, Wenhan Wang, Weiqing Wei, et al. "Oncogenic role of the SOX9-DHCR24-cholesterol biosynthesis axis in IGH-BCL2+ diffuse large B-cell lymphomas." Blood 139, no. 1 (January 6, 2022): 73–86. http://dx.doi.org/10.1182/blood.2021012327.

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Abstract Although oncogenicity of the stem cell regulator SOX9 has been implicated in many solid tumors, its role in lymphomagenesis remains largely unknown. In this study, SOX9 was overexpressed preferentially in a subset of diffuse large B-cell lymphomas (DLBCLs) that harbor IGH-BCL2 translocations. SOX9 positivity in DLBCL correlated with an advanced stage of disease. Silencing of SOX9 decreased cell proliferation, induced G1/S arrest, and increased apoptosis of DLBCL cells, both in vitro and in vivo. Whole-transcriptome analysis and chromatin immunoprecipitation–sequencing assays identified DHCR24, a terminal enzyme in cholesterol biosynthesis, as a direct target of SOX9, which promotes cholesterol synthesis by increasing DHCR24 expression. Enforced expression of DHCR24 was capable of rescuing the phenotypes associated with SOX9 knockdown in DLBCL cells. In models of DLBCL cell line xenografts, SOX9 knockdown resulted in a lower DHCR24 level, reduced cholesterol content, and decreased tumor load. Pharmacological inhibition of cholesterol synthesis also inhibited DLBCL xenograft tumorigenesis, the reduction of which is more pronounced in DLBCL cell lines with higher SOX9 expression, suggesting that it may be addicted to cholesterol. In summary, our study demonstrated that SOX9 can drive lymphomagenesis through DHCR24 and the cholesterol biosynthesis pathway. This SOX9-DHCR24-cholesterol biosynthesis axis may serve as a novel treatment target for DLBCLs.

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38

Youn, Ham, Yoon, Choi, Lee, Cho, and Kim. "Cynanchum wilfordii Etanolic Extract Controls Blood Cholesterol: A Double-blind, Randomized, Placebo-Controlled, Parallel Trial." Nutrients 11, no. 4 (April 12, 2019): 836. http://dx.doi.org/10.3390/nu11040836.

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We evaluated the effects of Cynanchum wilfordii (CW) ethanolic extract on blood cholesterol levels in adults with high low-density lipoprotein cholesterol (LDL-C) levels. In a double-blind, randomized, placebo-controlled, parallel trial, 84 subjects were recruited. Participants were randomly divided into two groups with a low-dose (300 mg/d) or high-dose (600 mg/d) of CW. Levels of very low-density lipoprotein (p = 0.022) and triglycerides (p = 0.022) were significantly lower in the low-dose CW group than in the placebo group after 8 weeks. In a subgroup of participants with LDL-C≥ 150 mg/dL (n = 33), there was a significant decrease in total cholesterol (low-dose, p = 0.012; high-dose, p = 0.021), apolipoprotein B (low-dose, p = 0.022; high-dose, p = 0.016), and cholesteryl ester transfer protein (low-dose, p = 0.037; high-dose, p = 0.016) after 8 weeks of CW. The correlation between changes in total cholesterol and baseline LDL-C levels was significant in the groups that received both doses of CW (low-dose, p = 0.010; high-dose, p = 0.015). These results show that the CW ethanolic extract can regulate blood cholesterol in subjects with LDL-C≥ 150 mg/dL.

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39

Ager, E., H. I. Møck, T. Brendstrup, H. Hollnagel, M. Schroll, and F. Gyntelberg. "Cholesterol, High Density Lipoprotein-Cholesterol (HDL) and Cholesterol/HDL-ratio Versus Arterial Blood Pressure." Acta Medica Scandinavica 209, S646 (April 24, 2009): 25–30. http://dx.doi.org/10.1111/j.0954-6820.1981.tb02616.x.

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40

Mindham, M. A., P. A. Mayes, and N. E. Miller. "Reverse cholesterol transport in the isolated perfused rat spleen." Biochemical Journal 268, no. 2 (June 1, 1990): 499–505. http://dx.doi.org/10.1042/bj2680499.

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1. A method has been developed which enables the rat spleen to be loaded in vivo with [3H]cholesterol to a high specific radioactivity using cholesterol-labelled erythrocytes. The erythrocytes were shown to be rapidly degraded by the spleen and not released intact during subsequent perfusion. 2. When labelled spleens were perfused with whole blood or serum, lipoproteins in the high-density lipoprotein (HDL) range were shown to be the principal lipoprotein vehicles for the removal of cholesterol, the specific radioactivity of cholesterol being much greater in the HDL fractions than in other lipoproteins, particularly in the d 1.175-1.210 fraction. 3. The formation of [3H]cholesteryl ester was restricted to the major HDL fractions. 4. Experiments utilizing individual HDL fractions added to a basal perfusate indicated that HDL1 (d 1.050-1.085) was of less importance in the removal of cholesterol from the spleen than HDL subfractions of higher density. Also, a decrease in density of the lipoproteins was observed during perfusion, concurrent with uptake of cholesterol, especially in the d 1.085-1.125 subfraction. 5. When [3H]cholesterol-labelled spleens were perfused with whole blood, about half of the radioactivity released was detected in erythrocytes, indicating a rapid exchange or transport of cholesterol. Thus erythrocytes could play an important role in the transfer of unesterified cholesterol when the chemical potential gradient is favourable.

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41

Bergman, R., Y. Kasif, M. Aviram, I. Maor, Y. Ullman, M. Gdal-On, and R. Friedman-Birnbaum. "Normolipidemic xanthelasma palpebrarum: lipid composition, cholesterol metabolism in monocyte-derived macrophages, and plasma lipid peroxidation." Acta Dermato-Venereologica 76, no. 2 (March 1, 1996): 107–10. http://dx.doi.org/10.2340/0001555576107110.

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The lipid compositions of 8 normolipidemic xanthelasma palpebrarum (XP) lesions were analyzed using thin-layer chromatography, with the adjacent uninvolved skin used as control. The lesions were found to be composed predominantly of cholesterol, mostly cholesteryl ester, whereas in the control specimens phospholipids predominated. The degradation rates of 125I-low-density lipoprotein (LDL), oxidized LDL, and acetyl LDL, and the rates of intracellular cholesterol synthesis from 1,2-(14)C-acetate, in blood monocyte-derived macrophages (MDM) from 3 normolipidemic patients, were similar to those of MDM from 3 normal control subjects. The mean levels of lipid peroxides and conjugated dienes under basal conditions, as well as following the addition of a free radical-generating compound (2,2-azobis-2-amidinopropane hydrochloride) to the plasma of 14 normolipidemic XP patients were significantly higher than those of 14 age- and sex-matched normal controls. We conclude that the predominant lipid accumulated in normolipidemic XP lesions is cholesteryl ester, but there is no evidence for intrinsic cellular cholesterol metabolism derangement in blood MDM from patients which could account for this. Since macrophage cholesterol accumulation can also result from enhanced uptake of increased levels of oxidized LDL, the increased plasma lipid peroxidation (derived from oxidized LDL) might lead to accumulation of cholesterol in macrophages and formation of foam cells via this mechanism.

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42

Hernell, O., L. Beckman, and T. Olivecrona. "ABO blood groups, serum cholesteryl esters and plasma lecithin: cholesterol acyltransferase activity." Clinical Genetics 3, no. 3 (April 23, 2008): 183–87. http://dx.doi.org/10.1111/j.1399-0004.1972.tb01457.x.

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43

Rink, Jonathan, Adam Yuh Lin, Shuo Yang, Amir Behdad, Reem Karmali, Colby Shad Thaxton, and Leo I. Gordon. "Bio-Inspired Functional Lipoprotein-like Nanoparticles (Flip-NPs) Cause Cholesterol Starvation and Ferroptosis in B-Cell Lymphomas: Studies in Cell Lines, Xenograft Models and Primary Patient Samples." Blood 134, Supplement_1 (November 13, 2019): 2857. http://dx.doi.org/10.1182/blood-2019-127805.

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Introduction: Hematologic malignancies, including B cell lymphomas such as diffuse large B cell lymphoma (DLBCL) and follicular lymphoma (FL), have increased demands for cholesterol and cholesteryl esters to maintain membrane anchored pro-proliferative and pro-survival signaling pathways, including B cell receptor signaling. Recent evidence suggests that certain cancer cell lines, including several anaplastic large T cell lymphoma (ALCL) cell lines, are auxotrophic for cholesterol and are sensitive to cholesterol reduction-induced ferroptosis (Garcia-Bermudez, Nature 2019), an iron dependent form of programmed cell death characterized by accumulation of lipid peroxides. We have developed a cholesterol depleting functional lipoprotein-like nanoparticle (Flip-NP) that specifically targets the high-affinity HDL receptor, scavenger receptor type B1 (SCARB1), which maintains cellular and cell membrane cholesterol homeostasis. Our prior data demonstrated that Flip-NPs induce B cell lymphoma cell death in vitro and in in vivo xenograft models. Accordingly, we hypothesized that the mechanism of cell death by Flip-NPs in B cell lymphomas is ferroptosis, and that Flip-NPs would be potent therapy for an expanded number of cholesterol-addicted malignancies, including ALCL. Methods: After informed consent, primary B cell lymphoma cells were isolated from excisional biopsies from patients with FL or DLBCL. The SUDHL4 [germinal center (GC) DLBCL], Ramos [Burkitt's lymphoma], SUDHL1 [ALCL] and SR-786 [ALCL] cell lines were used for in vitro experiments. SCARB1 expression was quantified using flow cytometry and western blot analysis. Cell viability was quantified using the MTS assay and flow cytometry. Ferroptosis was measured using the lipophilic antioxidant ferrostatin-1 or the iron chelator deferoxamine. Gene expression changes were quantified using RT-qPCR. Lipid peroxidation was measured using C11-BODIPY and flow cytometry. SUDHL1 and SUDHL4 flank tumor xenografts were initiated in SCID-beige mice, with Flip-NPs administered 3 times per week IV. Results: Primary B cell lymphoma cells were isolated from patients with FL (n=4) or DLBCL (n=2), and all samples expressed some level of SCARB1 by flow cytometry. Flip-NPs increased cell death in 3 of the 4 FL samples and 1 of 2 DLBCL samples. In Ramos and SUDHL4 cells, RT-qPCR data showed that Flip-NP-mediated cholesterol reduction led to up-regulation of cholesterol biosynthesis genes and down-regulation of glutathione peroxidase-4 (GPX4), a critical protein responsible for degradation of lipid peroxides. Correspondingly, as shown with C11-BODIPY, Flip-NP treatment increased lipid peroxide accumulation in Ramos and SUDHL4 cells. Addition of ferrostatin-1 or deferoxamine reduced Flip-NP induced cell death, demonstrating that the mechanism-of-action of Flip-NPs involves, at least in part, ferroptosis. Given the sensitivity of cholesterol auxotrophic cell lines to cholesterol reduction-induced ferroptosis, we tested the efficacy of the Flip-NPs against cholesterol auxotrophic ALK+ ALCL cell lines SUDHL1 and SR-786. SCARB1 was expressed in both cell lines. Flip-NPs potently induced cell death in both SUDHL1 and SR-786 cells in vitro. In vivo, systemic administration of Flip-NPs reduced tumor volumes in both SUDHL4 and SUDHL1 tumor xenograft models. Conclusions: Our data show that Flip-NPs reduce GPX4 expression and increase lipid peroxide accumulation in B cell lymphoma cell lines, resulting in ferroptosis. Expanding on these results, Flip-NP efficacy was also demonstrated in cholesterol auxotrophic ALK+ ALCL cell lines and primary patient-derived B cell lymphoma cells. These in vitro results translated to in vivo murine models, as systemic administration of Flip-NPs potently reduced DLBCL and ALK+ ALCL tumor xenograft burden. Flip-NPs are a molecularly targeted, first-in-class therapy that may be effective for malignancies reliant upon cellular cholesterol. Disclosures Behdad: Pfizer: Other: Speaker; Thermo Fisher: Membership on an entity's Board of Directors or advisory committees; Loxo-Bayer: Membership on an entity's Board of Directors or advisory committees. Karmali:Astrazeneca: Speakers Bureau; Takeda, BMS: Other: Research Funding to Institution; Gilead/Kite; Juno/Celgene: Consultancy, Speakers Bureau. Thaxton:Zylem: Other: Co-founder of the biotech company Zylem. Gordon:Juno/Celgene: Other: Advisory Board, Research Funding; Gilead: Other: Advisory Board; Bayer: Other: Advisory Board; Zylem LLC: Other: co-founder; research in nanoparticles in cancer.

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Kristal-Boneh, Estela, Gil Harari, and Manfred S. Green. "Circannual Variations in Blood Cholesterol Levels." Chronobiology International 10, no. 1 (January 1993): 37–42. http://dx.doi.org/10.3109/07420529309064480.

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45

&NA;. "Lower Blood Cholesterol in Elderly Men." Emergency Medicine News 23, no. 3 (April 2001): 50. http://dx.doi.org/10.1097/00132981-200104000-00025.

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46

Smith, George Davey. "Blood cholesterol and non-coronary mortality." Coronary Artery Disease 4, no. 10 (October 1993): 860–66. http://dx.doi.org/10.1097/00019501-199310000-00004.

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47

Otter, Arthur, and Gareth Hateley. "Blood cholesterol concentrations in dairy calves." Veterinary Record 180, no. 2 (January 12, 2017): 52. http://dx.doi.org/10.1136/vr.j122.

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48

Ferrara, L. "Serum cholesterol affects blood pressure regulation." American Journal of Hypertension 14, no. 11 (November 2001): A50. http://dx.doi.org/10.1016/s0895-7061(01)02095-7.

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49

Amarenco, Pierre, Philippa Lavallée, and Pierre-Jean Touboul. "Stroke prevention, blood cholesterol, and statins." Lancet Neurology 3, no. 5 (May 2004): 271–78. http://dx.doi.org/10.1016/s1474-4422(04)00734-3.

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50

Keys, Ancel. "SERUM CHOLESTEROL, BLOOD PRESSURE, AND MORTALITY." Lancet 329, no. 8529 (February 1987): 382. http://dx.doi.org/10.1016/s0140-6736(87)91751-x.

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