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1

Ang, Justin K., and Charles W. Bamforth. "Foam inhibitors from specialty malts." Journal of the Institute of Brewing 120, no. 3 (2014): 193–200. http://dx.doi.org/10.1002/jib.141.

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2

Zhang, Xun, Jing Yang, Pengfei Xie, Hao Liu, Qiang Deng, and Fengwei Dai. "Experimental study on controlled-release inhibitor foam for restraining spontaneous combustion of coal." Energy Exploration & Exploitation 38, no. 4 (2020): 1159–77. http://dx.doi.org/10.1177/0144598720910266.

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A new method is proposed based on temperature-controlled self-reaction to generate and release inhibitors in the form of foam at a specific temperature, which can overcome the disadvantages of short effective time and low efficiency in the inhibition of the spontaneous combustion of coal when inhibitors are released in advance, and greatly increase the action range of inhibitor through foam diffusion. The proposed temperature-controlled foaming system was prepared with hollow spheres as solution carriers, NaHCO3 and acetic acid as basic reactants, reaction-generated CO2 as foaming gas, sodium
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3

Tang, Chao-Ke, Guo-Hua Tang, Guang-Hui Yi, et al. "Effect of Apolipoprotein A-I on ATP Binding Cassette Transporter A1 Degradation and Cholesterol Efflux in THP-1 Macrophage-derived Foam Cells." Acta Biochimica et Biophysica Sinica 36, no. 3 (2004): 218–26. http://dx.doi.org/10.1093/abbs/36.3.218.

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Abstract Cholesterol-loaded macrophage foam cells are a central component of atherosclerotic lesions. ATP binding cassette transporter A1 (ABCA1), the defective molecule in Tangier disease, mediates the efflux of phospholipid and cholesterol from cells to apolipoprotein A-I (apoA-I), reversing foam cell formation. This study investigated the effect of apoA-I on ABCA1 degradation and cholesterol efflux in THP-1 macrophage-derived foam cells. After exposure of the cultured THP-1 macrophage-derived foam cells to apoA-I for different time, cholesterol efflux, ABCA1 mRNA and protein levels were det
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4

Ritchie, Helen, Alec Jamieson, and Nuala A. Booth. "Regulation, Location and Activity of Plasminogen Activator Inhibitor 2 (PAI-2) in Peripheral Blood Monocytes, Macrophages and Foam Cells." Thrombosis and Haemostasis 77, no. 06 (1997): 1168–73. http://dx.doi.org/10.1055/s-0038-1656132.

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SummaryMonocytes, macrophages and foam cells are central to atherogenesis. We have examined the potential ability of monocytes, macrophages and foam cells to affect the stability of deposited fibrin, characteristic of the atherosclerotic plaque, by their production of plasminogen activators and their inhibitors. Monocytes respond to thrombin and LPS by up-regulation of PAI-2 synthesis, and PAI-2 is their major product among the plasminogen activators/inhibitors. In contrast, macrophages and foam cells, while they did produce PAI-2, did not respond to thrombin and LPS by an increase in its synt
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5

Lantz, Sean, Jack Zakarian, Scott Deskin, and Ashlie Martini. "Filtration Effects on Foam Inhibitors and Optically Detected Oil Cleanliness." Tribology Transactions 60, no. 6 (2017): 1159–64. http://dx.doi.org/10.1080/10402004.2017.1285089.

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6

Hejna, Aleksander. "Clays as Inhibitors of Polyurethane Foams’ Flammability." Materials 14, no. 17 (2021): 4826. http://dx.doi.org/10.3390/ma14174826.

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Polyurethanes are a very important group of polymers with an extensive range of applications in different branches of industry. In the form of foams, they are mainly used in bedding, furniture, building, construction, and automotive sectors. Due to human safety reasons, these applications require an appropriate level of flame retardance, often required by various law regulations. Nevertheless, without the proper modifications, polyurethane foams are easily ignitable, highly flammable, and generate an enormous amount of smoke during combustion. Therefore, proper modifications or additives shoul
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7

Terasaki, Michishige, Hironori Yashima, Yusaku Mori, et al. "A Dipeptidyl Peptidase-4 Inhibitor Inhibits Foam Cell Formation of Macrophages in Type 1 Diabetes via Suppression of CD36 and ACAT-1 Expression." International Journal of Molecular Sciences 21, no. 13 (2020): 4811. http://dx.doi.org/10.3390/ijms21134811.

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Dipeptidyl peptidase-4 (DPP-4) inhibitors have been reported to play a protective role against atherosclerosis in both animal models and patients with type 2 diabetes (T2D). However, since T2D is associated with dyslipidemia, hypertension and insulin resistance, part of which are ameliorated by DPP-4 inhibitors, it remains unclear whether DPP-4 inhibitors could have anti-atherosclerotic properties directly by attenuating the harmful effects of hyperglycemia. Therefore, we examined whether a DPP-4 inhibitor, teneligliptin, could suppress oxidized low-density lipoprotein (ox-LDL) uptake, foam ce
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8

Keewan, Mohammad, Fawzi Banat, Priyabrata Pal, Jerina Zain, and Emad Alhseinat. "Foaming of industrial lean methyldiethanolamine solution in the presence of hydrocarbon and fatty acid based corrosion inhibitors." Oil & Gas Science and Technology – Revue d’IFP Energies nouvelles 73 (2018): 76. http://dx.doi.org/10.2516/ogst/2018073.

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In natural gas sweetening alkanolamine processes one of the regularly used chemical is the corrosion inhibitor. For better operation of the plant it is essential to understand the effect of their presence on foaming of industrial lean Methyldiethanolamine (MDEA) used as solvents at different temperatures. This study aimed at investigating the effect of HydroCarbon Based (HCB) and fatty acid based corrosion inhibitor having chemical name Bis(2-Hydroxyethyl)Cocoalkylamine (BHCL) on the foaming tendency of industrial real lean MDEA solutions. Experiments were conducted with different operating pa
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9

Plotkin, Jesse D., Michael G. Elias, Anthony L. Dellinger та Christopher L. Kepley. "NF-κB inhibitors that prevent foam cell formation and atherosclerotic plaque accumulation". Nanomedicine: Nanotechnology, Biology and Medicine 13, № 6 (2017): 2037–48. http://dx.doi.org/10.1016/j.nano.2017.04.013.

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10

Terasaki, Michishige, Munenori Hiromura, Yusaku Mori, et al. "A Dipeptidyl Peptidase-4 Inhibitor Suppresses Macrophage Foam Cell Formation in Diabetic db/db Mice and Type 2 Diabetes Patients." International Journal of Endocrinology 2018 (December 9, 2018): 1–9. http://dx.doi.org/10.1155/2018/8458304.

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Dipeptidyl peptidase-4 (DPP-4) inhibitors could have antiatherosclerotic action, in addition to antihyperglycemic roles. Because macrophage foam cells are key components of atherosclerosis, we investigated the effect of the DPP-4 inhibitor teneligliptin on foam cell formation and its related gene expression levels in macrophages extracted from diabetic db/db (C57BLKS/J Iar -+Leprdb/+Leprdb) mice and type 2 diabetes (T2D) patients ex vivo. We incubated mouse peritoneal macrophages and human monocyte-derived macrophages differentiated by 7-day culture with oxidized low-density lipoprotein in the
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11

Bradshaw, Emily L., Xiang-An Li, Theresa Guerin, et al. "Nucleoside reverse transcriptase inhibitors prevent HIV protease inhibitor-induced atherosclerosis by ubiquitination and degradation of protein kinase C." American Journal of Physiology-Cell Physiology 291, no. 6 (2006): C1271—C1278. http://dx.doi.org/10.1152/ajpcell.00211.2006.

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HIV protease inhibitors are important pharmacological agents used in the treatment of HIV-infected patients. One of the major disadvantages of HIV protease inhibitors is that they increase several cardiovascular risk factors, including the expression of CD36 in macrophages. The expression of CD36 in macrophages promotes the accumulation of cholesterol, the development of foam cells, and ultimately atherosclerosis. Recent studies have suggested that α-tocopherol can prevent HIV protease inhibitor-induced increases in macrophage CD36 levels. Because of the potential clinical utility of using α-t
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12

Yu, Zemou, Qing Peng, Songyue Li, et al. "Myriocin and d-PDMP ameliorate atherosclerosis in ApoE−/− mice via reducing lipid uptake and vascular inflammation." Clinical Science 134, no. 5 (2020): 439–58. http://dx.doi.org/10.1042/cs20191028.

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Abstract Sphingolipids have been implicated in the etiology of atherosclerosis. The commonly used sphingolipid inhibitors, myriocin (a ceramide inhibitor) and d-PDMP (d-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol, a glycosphingolipid inhibitor), have shown therapeutic potential but their efficacy and their underlying mechanisms remain unclear. Here, apolipoprotein E-deficient (apoE−/−) mice were fed a high-fat diet (HFD) and treated with a control, myriocin, d-PDMP, or atorvastatin for 12 weeks. We analyzed the effects of these drugs on the size and detailed composition of atheroscl
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13

Smith, D. A., M. L. Metz, and S. L. Cuppett. "High-temperature Short-time Thermal Processing of Bean Flour to Remove Raw Bean Flavor." HortScience 32, no. 3 (1997): 490B—490. http://dx.doi.org/10.21273/hortsci.32.3.490b.

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Dry edible beans (Phaseolis vulgaris) represent an inexpensive way to incorporate protein into the diet as a food ingredient, but beans contain unpleasant flavors and several anti-nutritional factors that limit their use without first processing with long heat treatments. `Great Northern' bean flour was processed using either static or specially designed dynamic (continuous) processing methods. The dynamic process treated flour slurries at temperatures up to 124°for 20 sec. The slurries were quick-frozen and freeze-dried after frozen storage periods of 0, 8, 24, 120, or 504 hr. The flours were
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14

Terasaki, Michishige, Munenori Hiromura, Yusaku Mori, et al. "Combination Therapy with a Sodium-Glucose Cotransporter 2 Inhibitor and a Dipeptidyl Peptidase-4 Inhibitor Additively Suppresses Macrophage Foam Cell Formation and Atherosclerosis in Diabetic Mice." International Journal of Endocrinology 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/1365209.

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Dipeptidyl peptidase-4 inhibitors (DPP-4is), in addition to their antihyperglycemic roles, have antiatherosclerotic effects. We reported that sodium-glucose cotransporter 2 inhibitors (SGLT2is) suppress atherosclerosis in a glucose-dependent manner in diabetic mice. Here, we investigated the effects of combination therapy with SGLT2i and DPP-4i on atherosclerosis in diabetic mice. SGLT2i (ipragliflozin, 1.0 mg/kg/day) and DPP-4i (alogliptin, 8.0 mg/kg/day), either alone or in combination, were administered to db/db mice or streptozotocin-induced diabetic apolipoprotein E-null (Apoe−/−) mice. I
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15

Voloshyna, Iryna, Lora J. Kasselman, Steven E. Carsons, et al. "COX-2-dependent and independent effects of COX-2 inhibitors and NSAIDs on proatherogenic changes in human monocytes/macrophages." Journal of Investigative Medicine 65, no. 3 (2016): 694–704. http://dx.doi.org/10.1136/jim-2016-000259.

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It is the second decade of controversy regarding the cardiovascular effects of cyclo-oxygenase-2 (COX-2) inhibitors. At this time, celecoxib is the only available COX-2-specific inhibitor for treatment of pain and inflammation. Therefore, the present study was designed primarily to determine the impact of celecoxib on cholesterol handling (uptake via scavenger receptors and efflux from the cells) and foam cell formation in human THP-1 macrophages, followed by comparison to rofecoxib and other non-steroidal anti-inflammatory drugs (NSAIDs). THP-1 human macrophages and peripheral blood mononucle
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16

Hill, James R., Xia Shao, Jay S. Wright, et al. "Synthesis and Evaluation of 11C- and 18F-Labeled SOAT1 Inhibitors as Macrophage Foam Cell Imaging Agents." ACS Medicinal Chemistry Letters 11, no. 6 (2020): 1299–304. http://dx.doi.org/10.1021/acsmedchemlett.0c00127.

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17

Dai, Yao, Xianwei Wang, Zufeng Ding, Dongsheng Dai, and Jawahar L. Mehta. "DPP-4 inhibitors repress foam cell formation by inhibiting scavenger receptors through protein kinase C pathway." Acta Diabetologica 51, no. 3 (2013): 471–78. http://dx.doi.org/10.1007/s00592-013-0541-3.

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18

NAMATAME, Ichiji, Hiroshi TOMODA, Daisuke MATSUDA, Noriko TABATA, Susumu KOBAYASHI, and Satoshi OMURA. "K97-0239A and B, new inhibitors of macrophage foam cell formation, produced by Streptomyces sp. K97-0239." Proceedings of the Japan Academy. Ser. B: Physical and Biological Sciences 78, no. 3 (2002): 45–50. http://dx.doi.org/10.2183/pjab.78.45.

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19

Wiciński, Michał, Karol Górski, Eryk Wódkiewicz, Maciej Walczak, Magdalena Nowaczewska, and Bartosz Malinowski. "Vasculoprotective Effects of Vildagliptin. Focus on Atherogenesis." International Journal of Molecular Sciences 21, no. 7 (2020): 2275. http://dx.doi.org/10.3390/ijms21072275.

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Vildagliptin is a representative of Dipeptidyl Peptidase-4 (DPP-4) inhibitors, antihyperglycemic drugs, approved for use as monotherapy and combination therapy in type 2 diabetes mellitus. By inhibiting enzymatic decomposition, DPP-4 inhibitors increase the half-life of incretins such as GLP-1 (Glucagon-like peptide-1) and GIP (Gastric inhibitors polypeptide) and prolong their action. Some studies present results suggesting the anti-sclerotic and vasculoprotective effects of vildagliptin reaching beyond glycemic control. Vildagliptin is able to limit inflammation by suppression of the NF-κB (n
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20

Fleming, Rachel I., Cameron D. Mackenzie, Alan Cooper, and Malcolm W. Kennedy. "Foam nest components of the túngara frog: a cocktail of proteins conferring physical and biological resilience." Proceedings of the Royal Society B: Biological Sciences 276, no. 1663 (2009): 1787–95. http://dx.doi.org/10.1098/rspb.2008.1939.

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The foam nests of the túngara frog ( Engystomops pustulosus ) form a biocompatible incubation medium for eggs and sperm while resisting considerable environmental and microbiological assault. We have shown that much of this behaviour can be attributed to a cocktail of six proteins, designated ranaspumins (Rsn-1 to Rsn-6), which predominate in the foam. These fall into two discernable classes based on sequence analysis and biophysical properties. Rsn-2, with an amphiphilic amino acid sequence unlike any hitherto reported, exhibits substantial detergent-like surfactant activity necessary for pro
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21

Yao, Dai, Dai Dongsheng, and Mehta Jawahar L. "GW25-e0440 DPP-4 Inhibitors Repress Foam Cell Formation by Inhibiting Scavenger Receptors through Protein Kinase C Pathway." Journal of the American College of Cardiology 64, no. 16 (2014): C35. http://dx.doi.org/10.1016/j.jacc.2014.06.165.

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22

Argmann, Carmen A., Jane Y. Edwards, Cynthia G. Sawyez, et al. "Regulation of Macrophage Cholesterol Efflux through Hydroxymethylglutaryl-CoA Reductase Inhibition." Journal of Biological Chemistry 280, no. 23 (2005): 22212–21. http://dx.doi.org/10.1074/jbc.m502761200.

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The cholesterol biosynthetic pathway produces numerous signaling molecules. Oxysterols through liver X receptor (LXR) activation regulate cholesterol efflux, whereas the non-sterol mevalonate metabolite, geranylgeranyl pyrophosphate (GGPP), was recently demonstrated to inhibit ABCA1 expression directly, through antagonism of LXR and indirectly through enhanced RhoA geranylgeranylation. We used HMG-CoA reductase inhibitors (statins) to test the hypothesis that reduced synthesis of mevalonate metabolites would enhance cholesterol efflux and attenuate foam cell formation. Preincubation of THP-1 m
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23

Zhou, Lichun, Dezhi Yang, Dong Fang Wu, Zhong Mao Guo, Emmanuel Okoro, and Hong Yang. "Inhibition of Endoplasmic Reticulum Stress and Atherosclerosis by 2-Aminopurine in Apolipoprotein E-Deficient Mice." ISRN Pharmacology 2013 (July 31, 2013): 1–8. http://dx.doi.org/10.1155/2013/847310.

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We previously reported that the apolipoprotein (apo) B48-carrying lipoproteins obtained from apoE knockout (apoE−/−) mice, so called E−/B48 lipoproteins, transformed mouse macrophages into foam cells and enhanced the phosphorylation of eukaryotic translation initiation factor 2α (eIF-2α). Furthermore, the eIF-2α phosphorylation inhibitor, 2-aminopurine (2-AP), attenuated E−/B48 lipoprotein-induced foam cell formation. The present report studied the effect of 2-AP on atherosclerosis in apoE−/− mice. Our results showed that the level of food intake, bodyweight, plasma cholesterol, and triglyceri
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24

Gu, Jian-Qiu, Di-Fei Wang, Xiao-Guang Yan, et al. "A Toll-like receptor 9-mediated pathway stimulates perilipin 3 (TIP47) expression and induces lipid accumulation in macrophages." American Journal of Physiology-Endocrinology and Metabolism 299, no. 4 (2010): E593—E600. http://dx.doi.org/10.1152/ajpendo.00159.2010.

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Excessive accumulation of lipids in macrophages results in formation of foam cells and is a hallmark of atherosclerosis. The PAT family of proteins has been implicated in this process, but details of their involvement in foam cell formation have not been fully elucidated. One of dominant members of the PAT proteins, perilipin 3 (TIP47), is likely to be involved in such a regulatory mechanism. In this study, we demonstrated that the Toll-like receptor 9 (TLR9)-mediated pathway stimulates perilipin 3 expression and accumulation of lipids, especially triglycerides, in macrophages. Oligodeoxynucle
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25

Hongo, Shigeki, Takuya Watanabe, Shigeko Arita, et al. "Leptin modulates ACAT1 expression and cholesterol efflux from human macrophages." American Journal of Physiology-Endocrinology and Metabolism 297, no. 2 (2009): E474—E482. http://dx.doi.org/10.1152/ajpendo.90369.2008.

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Leptin is an adipose tissue-derived hormone implicated in atherosclerosis and macrophage foam cell formation. The current study was conducted to examine the effect of leptin on cholesteryl ester accumulation in human monocytes/macrophages. Exogenously added leptin at 5 nM during differentiation of monocytes into macrophages for 7 days accelerated acetylated LDL (acetyl-LDL)-induced cholesteryl ester accumulation by 30–50%. Leptin did not affect endocytic uptake of acetyl-LDL; however, it increased ACAT activity 1.8-fold and ACAT-1 protein expression 1.9-fold. Among the four ACAT-1 mRNA transcr
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26

Yuan, Yang, Lei Zhao, Yaxi Chen, et al. "Advanced glycation end products (AGEs) increase human mesangial foam cell formation by increasing Golgi SCAP glycosylation in vitro." American Journal of Physiology-Renal Physiology 301, no. 1 (2011): F236—F243. http://dx.doi.org/10.1152/ajprenal.00646.2010.

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Advanced glycation end products (AGEs) is one of the causative factors of diabetic nephropathy, which is associated with lipid accumulation in glomeruli. This study was designed to investigate whether Nε-(carboxymethyl) lysine (CML; a member of the AGEs family) increases lipid accumulation by impairing the function of sterol-regulatory element binding protein (SREBP) cleavage-activating protein (SCAP) in human mesangial cells (HMCs). Intracellular cholesterol content was assessed by Oil Red O staining and quantitative assay. The expression of molecules controlling cholesterol homeostasis was e
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27

Umezawa, Koji, and Isao Kii. "Druggable Transient Pockets in Protein Kinases." Molecules 26, no. 3 (2021): 651. http://dx.doi.org/10.3390/molecules26030651.

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Drug discovery using small molecule inhibitors is reaching a stalemate due to low selectivity, adverse off-target effects and inevitable failures in clinical trials. Conventional chemical screening methods may miss potent small molecules because of their use of simple but outdated kits composed of recombinant enzyme proteins. Non-canonical inhibitors targeting a hidden pocket in a protein have received considerable research attention. Kii and colleagues identified an inhibitor targeting a transient pocket in the kinase DYRK1A during its folding process and termed it FINDY. FINDY exhibits a uni
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28

MacRitchie, Neil, and Pasquale Maffia. "‘Blow my mind(in)’ – mindin neutralization for the prevention of atherosclerosis?" Clinical Science 132, no. 14 (2018): 1509–12. http://dx.doi.org/10.1042/cs20180358.

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The hallmark features of atherosclerosis include accumulation of low-density lipoprotein (LDL) carrying cholesterol in the vessel wall, formation of lipid-laden foam cells, and the creation of a pro-inflammatory microenvironment. To date, no effective treatments are clinically available for increasing cholesterol efflux from vascular macrophages and inducing reverse cholesterol transport (RCT). In an article published recently in Clinical Science (vol 132, issue 6, 1199-1213), Zhang and colleagues identified the extracellular matrix protein mindin/spondin 2 as a positive regulator of atheroscl
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29

SUŁEK, Marian Włodzimierz, Jacek PRZEPIÓRKA, Andrzej KULCZYCKI, and Wiesław HRECZUCH. "THE EFFECT OF SURFACTANTS WITH STERIC HINDRANCE ON THE PHYSICOCHEMICAL AND TRIBOLOGICAL PROPERTIES OF METALWORKING FLUIDS." Tribologia 290, no. 2 (2020): 75–84. http://dx.doi.org/10.5604/01.3001.0014.3742.

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In earlier studies, it has been postulated that solutions of surfactants should be used as an original solution for formulation of Metal Working Fluids (MWF) compositions. The negative feature of some of the fluids was their excessive foamability whose reduction, by introducing hydrophobic foam inhibitors, was limited. Therefore, a synthesis of new oxyalkylated derivatives of 2-ethylhexyl alcohol and sulfosuccinate obtained from this alcohol was planned. Due to steric hindrance, these compounds exhibit low foamability. Aqueous solutions of these surfactants were subjected to physicochemical an
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30

Shi, Qizhen, Erin L. Kuether, Jocelyn A. Schroeder, Crystal L. Perry, Scot A. Fahs, and Robert R. Montgomery. "Factor VIII Inhibitors: Von Willebrand Factor Makes A Difference In Vitro and In Vivo." Blood 116, no. 21 (2010): 709. http://dx.doi.org/10.1182/blood.v116.21.709.709.

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Abstract Abstract 709 The important association between von Willebrand factor (VWF) and factor VIII (FVIII) has been investigated for decades, but the effect of VWF on FVIII inhibitors is still controversial. Studies have demonstrated that some anti-FVIII inhibitory antibodies inhibit VWF-FVIII interaction, while others rely on the presence of VWF to inhibit FVIII activities. The influence of VWF on the Bethesda assay, which is routinely used in the clinic to determine the titer of FVIII-neutralizing inhibitors, is still uncertain because the plasma from hemophilia A patients with inhibitors c
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Kasselman, LJ, I. Voloshyna, MJ Littlefield, et al. "1: COMPARATIVE EFFECT OF SELECTIVE AND NON-SELECTIVE COX-2 INHIBITORS ON LIPID ACCUMULATION IN HUMAN MACROPHAGES." Journal of Investigative Medicine 64, no. 3 (2016): 800.1–800. http://dx.doi.org/10.1136/jim-2016-000080.1.

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Purpose of StudyIt is the second decade of controversy regarding the cardiovascular (CV) effects of cycloxygenase-2 (COX-2) inhibitors. COX-2 inhibitors possess anti-inflammatory and analgesic effects comparable with conventional non-steroidal anti-inflammatory drugs, but produce fewer gastrointestinal adverse effects. Here we demonstrate that only selective COX-2 inhibitors cause disruption of the delicate balance between cholesterol efflux and influx that leads to lipid overload and macrophage foam cell formation (FCF).Methods UsedTHP-1 human macrophages were incubated with: celecoxib (10 µM
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Kurihara, Hideyuki, and Kazuki Kujira. "Phlorotannins Derived From the Brown Alga Colpomenia bullosa as Tyrosinase Inhibitors." Natural Product Communications 16, no. 7 (2021): 1934578X2110213. http://dx.doi.org/10.1177/1934578x211021317.

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Tyrosinase catalyzes hydroxylation of L-tyrosine and dehydrogenation of L-DOPA in the melanin biosynthesis pathway. Tyrosinase inhibitors have potential use as cosmetic whitening agents and for preventing seafood deterioration. In this report, tyrosinase inhibitors extracted from brown alga Colpomenia bullosa (Scytosiphonaceae, Scytosiphonales) were investigated. Inhibitory principles were isolated from the extract and identified as phlorotannins, phloroglucinol (1), diphlorethol (2), triphlorethol C (3), which have not been isolated in a free form previously, and fucophlorethol C (4). Compoun
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33

Magaeva, S. V., A. A. Kubatiev, E. A. Shirokov, and V. B. Simonenko. "Regression of atherosclecrotic lesions: medicinal and alimentary factors." Clinical Medicine (Russian Journal) 94, no. 9 (2016): 668–71. http://dx.doi.org/10.18821/0023-2149-2016-94-9-668-671.

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The article reports results of clinical studies aimed to elucidate the influence of medicines on the size and density of atherosclerotic plaques in the walls of coronary and cerebral arteries. The phenomenon of regression of atherosclerotic lesions in the survivors of Leningrad siege during a long period of starvation is analyzed. The influence of inhibitors of angiotensinconverting enzyme on apoptosis of smooth muscle and foam cells of atherosclerotic plaques in the sanological mechanisms of atherosclerosis is discussed. The concept of natural regression of atherosclerosis is formulated and t
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Yuan, Xinrui, Yineng Xia, Peng Lu, Lijuan Zhu, Yuejiao Zhong, and Yubin Wang. "Synthesis and evaluation of 1H-pyrrole-2,5-dione derivatives as cholesterol absorption inhibitors for suppressing the formation of foam cells and inflammatory response." Bioorganic & Medicinal Chemistry 26, no. 8 (2018): 1435–47. http://dx.doi.org/10.1016/j.bmc.2017.08.046.

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35

Gao, Shoucui, Xiaojing Wang, Daxing Cheng, et al. "Overexpression of Cholesteryl Ester Transfer Protein Increases Macrophage-Derived Foam Cell Accumulation in Atherosclerotic Lesions of Transgenic Rabbits." Mediators of Inflammation 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/3824276.

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High levels of plasma high-density lipoprotein-cholesterol (HDL-C) are inversely associated with the risk of atherosclerosis and other cardiovascular diseases; thus, pharmacological inhibition of cholesteryl ester transfer protein (CETP) is considered to be a therapeutic method of raising HDL-C levels. However, many CETP inhibitors have failed to achieve a clinical benefit despite raising HDL-C. In the study, we generated transgenic (Tg) rabbits that overexpressed the human CETP gene to examine the influence of CETP on the development of atherosclerosis. Both Tg rabbits and their non-Tg litter
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36

Mintzer, Robert J., Kenneth C. Appell, Andrew Cole, et al. "A Novel High-Throughput Screening Format to Identify Inhibitors of Secreted Acid Sphingomyelinase." Journal of Biomolecular Screening 10, no. 3 (2005): 225–34. http://dx.doi.org/10.1177/1087057104272546.

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Secreted extracellular acid sphingomyelinase (sASM) activity has been suggested to promote atherosclerosis by enhancing subendothelial aggregation and retention of low-density lipoprotein (LDL) with resultant foam cell formation. Compounds that inhibit sASM activity, at neutral pH, may prevent lipid retention and thus would be expected to be anti-atherosclerotic. With the goal of identifying novel compounds that inhibit sASM at pH 7.4, a high-throughput screen was performed. Initial screening was run using a modification of a proven system that measures the hydrolysis of radiolabeled sphingomy
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37

Zozulya, N. I., V. M. Chernov, I. S. Tarasova, and A. G. Rumyantsev. "Unsolved issues of providing medical care to patients with hemophilia with inhibitors in Russia." Russian Journal of Pediatric Hematology and Oncology 6, no. 2 (2019): 48–53. http://dx.doi.org/10.21682/2311-1267-2019-6-2-48-53.

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The implementation of the state program “7 highcost nosologies” and the active work of Russian hematologists have significantly improved the specialized care for children and adults with Hemophilia. Russian hemophilia patient registry as of 10.25.2018 contained information about 7433 patients, of whom with hemophilia A – 6525 people. About 400 people were diagnosed with hemophilia with inhibitors. The inhibitor predominantly appeared at child and young age (up to 20 years). There is a high supply of coagulation factors concentrates for the treatment of hemophilia in the Russian Federation – 8.
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38

KUMAR, Priyadarsini, and Donal A. WALSH. "A dual-specificity isoform of the protein kinase inhibitor PKI produced by alternate gene splicing." Biochemical Journal 362, no. 3 (2002): 533–37. http://dx.doi.org/10.1042/bj3620533.

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We have previously shown that the protein kinase inhibitor β (PKIβ) form of the cAMP-dependent protein kinase inhibitor exists in multiple isoforms, some of which are specific inhibitors of the cAMP-dependent protein kinase, whereas others also inhibit the cGMP-dependent enzyme [Kumar, Van Patten and Walsh (1997), J. Biol. Chem. 272, 20011–20020]. We have now demonstrated that the switch from a cAMP-dependent protein kinase (PKA)-specific inhibitor to one with dual specificity arises as a consequence of alternate gene splicing. We have confirmed using bacterially produced pure protein that a s
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39

Zhou, Ming-Sheng, Kiranmai Chadipiralla, Armando J. Mendez, et al. "Nicotine potentiates proatherogenic effects of oxLDL by stimulating and upregulating macrophage CD36 signaling." American Journal of Physiology-Heart and Circulatory Physiology 305, no. 4 (2013): H563—H574. http://dx.doi.org/10.1152/ajpheart.00042.2013.

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Cigarette smoking is a major risk factor for atherosclerosis and cardiovascular disease. CD36 mediates oxidized LDL (oxLDL) uptake and contributes to macrophage foam cell formation. We investigated a role for the CD36 pathway in nicotine-induced activation of macrophages and foam cell formation in vitro and in vivo. Nicotine in the same plasma concentration range found in smokers increased the CD36+/CD14+ cell population in human peripheral blood mononuclear cells, increased CD36 expression of human THP1 macrophages, and increased macrophage production of reactive oxygen species, PKCδ phosphor
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40

Mihelič, Marko, and Dušan Turk. "Two decades of thyroglobulin type-1 domain research." Biological Chemistry 388, no. 11 (2007): 1123–30. http://dx.doi.org/10.1515/bc.2007.155.

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Abstract Thyroglobulin type-1 repeats are primarily found in thyroglobulin and several other functionally unrelated proteins. Because a few of them exhibit inhibitory activity against cysteine proteases they were named thyropins (thyroglobulin type-1 domain protease inhibitors). In contrast to cystatins, the best-characterized group of papain-like protease inhibitors, they exhibit greater selectivity in their interactions with target proteases. Interestingly, a few members inhibit aspartic protease cathepsin D and metalloproteases. In contrast to the inhibitory fragment of the major histocompa
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41

Hou, Yi-Chou, Wen-Chih Liu, Cai-Mei Zheng, Jing-Quan Zheng, Tzung-Hai Yen, and Kuo-Cheng Lu. "Role of Vitamin D in Uremic Vascular Calcification." BioMed Research International 2017 (2017): 1–13. http://dx.doi.org/10.1155/2017/2803579.

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The risk of cardiovascular death is 10 times higher in patients with CKD (chronic kidney disease) than in those without CKD. Vascular calcification, common in patients with CKD, is a predictor of cardiovascular mortality. Vitamin D deficiency, another complication of CKD, is associated with vascular calcification in patients with CKD. GFR decline, proteinuria, tubulointerstitial injury, and the therapeutic dose of active form vitamin D aggravate vitamin D deficiency and reduce its pleiotropic effect on the cardiovascular system. Vitamin D supplement for CKD patients provides a protective role
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42

Zhou, Huiping, Emily C. Gurley, Sirikalaya Jarujaron, et al. "HIV protease inhibitors activate the unfolded protein response and disrupt lipid metabolism in primary hepatocytes." American Journal of Physiology-Gastrointestinal and Liver Physiology 291, no. 6 (2006): G1071—G1080. http://dx.doi.org/10.1152/ajpgi.00182.2006.

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Treatment of human immunodeficiency virus (HIV)-infected patients with HIV protease inhibitors (PIs) has been associated with serious lipid disturbances. However, the incidence and degree of impaired lipid metabolism observed in the clinic vary considerably between individual HIV PIs. Our previous studies demonstrated that HIV PIs differ in their ability to increase the levels of transcriptionally active sterol regulatory element-binding proteins (SREBPs), activate the unfolded protein response (UPR), induce apoptosis, and promote foam cell formation in macrophages. In the present study, we ex
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43

Hai, Qimin, and Jonathan D. Smith. "Acyl-Coenzyme A: Cholesterol Acyltransferase (ACAT) in Cholesterol Metabolism: From Its Discovery to Clinical Trials and the Genomics Era." Metabolites 11, no. 8 (2021): 543. http://dx.doi.org/10.3390/metabo11080543.

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The purification and cloning of the acyl-coenzyme A: cholesterol acyltransferase (ACAT) enzymes and the sterol O-acyltransferase (SOAT) genes has opened new areas of interest in cholesterol metabolism given their profound effects on foam cell biology and intestinal lipid absorption. The generation of mouse models deficient in Soat1 or Soat2 confirmed the importance of their gene products on cholesterol esterification and lipoprotein physiology. Although these studies supported clinical trials which used non-selective ACAT inhibitors, these trials did not report benefits, and one showed an incr
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44

Conners, Rebecca, Alexander V. Konarev, Jane Forsyth, et al. "An Unusual Helix-Turn-Helix Protease Inhibitory Motif in a Novel Trypsin Inhibitor from Seeds of Veronica (Veronica hederifolia L.)." Journal of Biological Chemistry 282, no. 38 (2007): 27760–68. http://dx.doi.org/10.1074/jbc.m703871200.

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The storage tissues of many plants contain protease inhibitors that are believed to play an important role in defending the plant from invasion by pests and pathogens. These proteinaceous inhibitor molecules belong to a number of structurally distinct families. We describe here the isolation, purification, initial inhibitory properties, and three-dimensional structure of a novel trypsin inhibitor from seeds of Veronica hederifolia (VhTI). The VhTI peptide inhibits trypsin with a submicromolar apparent Ki and is expected to be specific for trypsin-like serine proteases. VhTI differs dramaticall
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45

Naito, Y., and J. M. Lowenstein. "5′-Nucleotidase from rat heart membranes. Inhibition by adenine nucleotides and related compounds." Biochemical Journal 226, no. 3 (1985): 645–51. http://dx.doi.org/10.1042/bj2260645.

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ADP and ATP and their analogues were evaluated as inhibitors of 5′-nucleotidase purified from heart plasma membrane. ADP analogues are more powerful inhibitors than the corresponding ATP analogues. The most powerful inhibitor found is adenosine 5′-[alpha beta-methylene]diphosphate (AOPCP) for which the enzyme shows a Ki of 5 nM at pH 7.2. Measurements of pKi values for ADP and AOPCP as a function of pH indicate that the major inhibitory species of both nucleotides is the dianion. In the physiological range of pH values, AOPCP is a more powerful inhibitor than ADP principally because a higher p
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Cai, Qiangjun, Linda Lanting, and Rama Natarajan. "Growth factors induce monocyte binding to vascular smooth muscle cells: implications for monocyte retention in atherosclerosis." American Journal of Physiology-Cell Physiology 287, no. 3 (2004): C707—C714. http://dx.doi.org/10.1152/ajpcell.00170.2004.

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Adhesive interactions between monocytes and vascular smooth muscle cells (VSMC) may contribute to subendothelial monocyte-macrophage retention in atherosclerosis. We investigated the effects of angiotensin II (ANG II) and platelet-derived growth factor (PDGF)-BB on VSMC-monocyte interactions. Treatment of human aortic VSMC (HVSMC) with ANG II or PDGF-BB significantly increased binding to human monocytic THP-1 cells and to peripheral blood monocytes. This was inhibited by antibodies to monocyte β1- and β2-integrins. The binding was also attenuated by blocking VSMC arachidonic acid (AA) metaboli
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47

GRØN, Hanne, Ida B. THØGERSEN, Jan J. ENGHILD та Salvatore V. PIZZO. "Structural and functional analysis of the spontaneous re-formation of the thiol ester bond in human α2-macroglobulin, rat α1-inhibitor-3 and chemically modified derivatives". Biochemical Journal 318, № 2 (1996): 539–45. http://dx.doi.org/10.1042/bj3180539.

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The α-macroglobulins are proteinase inhibitors that form part of a superfamily along with components of the complement system. Internal β-cysteinyl–γ-glutamyl thiol ester bonds are an important structural feature of most α-macroglobulins and several complement components. We have studied the reversibility of thiol ester cleavage caused by NH3 or CH3NH2 in tetrameric human α2-macroglobulin (α2M) and monomeric rat α1-inhibitor-3 (α1 I3). When employing NH3 as the nucleophile, the thiol ester in α1I3 re-formed spontaneously at room temperature after gel filtration to remove excess nucleophile, an
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48

RYAN, Ciara A., Henning R. STENNICKE, Victor E. NAVA, Jennifer B. BURCH, J. Marie HARDWICK, and Guy S. SALVESEN. "Inhibitor specificity of recombinant and endogenous caspase-9." Biochemical Journal 366, no. 2 (2002): 595–601. http://dx.doi.org/10.1042/bj20020863.

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Apoptosis triggered through the intrinsic pathway by radiation and anti-neoplastic drugs is initiated by the activation of caspase-9. To elucidate control mechanisms in this pathway we used a range of synthetic and natural reagents. The inhibitory potency of acetyl-Asp-Glu-Val-Asp-aldehyde ('Ac-DEVD-CHO'), benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone ('Z-VAD-FMK') and the endogenous caspase inhibitor X-chromosome-linked inhibitor of apoptosis protein ('XIAP') against recombinant caspase-9 were predictive of the efficacy of these compounds in a cell-free system. However, the viral proteins
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49

Kos, Jiri, Violetta Kozik, Dominika Pindjakova, et al. "Synthesis and Hybrid SAR Property Modeling of Novel Cholinesterase Inhibitors." International Journal of Molecular Sciences 22, no. 7 (2021): 3444. http://dx.doi.org/10.3390/ijms22073444.

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A library of novel 4-{[(benzyloxy)carbonyl]amino}-2-hydroxybenzoic acid amides was designed and synthesized in order to provide potential acetyl- and butyrylcholinesterase (AChE/BChE) inhibitors; the in vitro inhibitory profile and selectivity index were specified. Benzyl(3-hydroxy-4-{[2-(trifluoromethoxy)phenyl]carbamoyl}phenyl)carbamate was the best AChE inhibitor with the inhibitory concentration of IC50 = 36.05 µM in the series, while benzyl{3-hydroxy-4-[(2-methoxyphenyl)carbamoyl]phenyl}-carbamate was the most potent BChE inhibitor (IC50 = 22.23 µM) with the highest selectivity for BChE (
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50

Donato, Nicholas J., Ji Wu, William Bornmann, and Moshe Talpaz. "Activity of ABL Kinase Inhibitors in Two Distinct Models of Imatinib Resistance." Blood 108, no. 11 (2006): 4819. http://dx.doi.org/10.1182/blood.v108.11.4819.4819.

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Abstract The tyrosine kinase inhibitor imatinib mesylate (Gleevec) is effective in controlling BCR-ABL expressing leukemias but resistance occurs in a small subset of early stage patients and is very common in advanced stage patients. Resistance is associated with overexpression and/or mutations in the BCR-ABL gene but patients are also increasingly reported to fail imatinib therapy while retaining wild-type BCR-ABL expression. To circumvent or overcome resistance novel kinase inhibitors have been synthesized and tested clinically. However, while investigators have designed models to measure a
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