The Experts below are selected from a list of 8322 Experts worldwide ranked by ideXlab platform
Devanand B Shinde - One of the best experts on this subject based on the ideXlab platform.
-
synthesis and Hypolipidemic activity of novel 2 4 2 substituted aminothiazole 4 yl phenoxy acetic acid derivatives
ChemInform, 2010Co-Authors: Santosh N Mokale, Priyanka T Sanap, Devanand B ShindeAbstract:All synthesized compounds (I) are evaluated for their Hypolipidemic activity by using high fat-diet induced hyperlipidemia in Sprague-Dawley rats.
-
synthesis and Hypolipidemic activity of novel 2 4 2 substituted aminothiazole 4 yl phenoxy acetic acid derivatives
European Journal of Medicinal Chemistry, 2010Co-Authors: Santosh N Mokale, Priyanka T Sanap, Devanand B ShindeAbstract:A novel series of aminotihazole compounds possessing phenoxy acetic acid moiety were synthesized. The synthesized compounds were evaluated for their Hypolipidemic activity by using high fat diet induced hyperlipidemia in Sprague-Dawley rats.
Santosh N Mokale - One of the best experts on this subject based on the ideXlab platform.
-
synthesis and Hypolipidemic activity of novel 2 4 2 substituted aminothiazole 4 yl phenoxy acetic acid derivatives
ChemInform, 2010Co-Authors: Santosh N Mokale, Priyanka T Sanap, Devanand B ShindeAbstract:All synthesized compounds (I) are evaluated for their Hypolipidemic activity by using high fat-diet induced hyperlipidemia in Sprague-Dawley rats.
-
synthesis and Hypolipidemic activity of novel 2 4 2 substituted aminothiazole 4 yl phenoxy acetic acid derivatives
European Journal of Medicinal Chemistry, 2010Co-Authors: Santosh N Mokale, Priyanka T Sanap, Devanand B ShindeAbstract:A novel series of aminotihazole compounds possessing phenoxy acetic acid moiety were synthesized. The synthesized compounds were evaluated for their Hypolipidemic activity by using high fat diet induced hyperlipidemia in Sprague-Dawley rats.
Priyanka T Sanap - One of the best experts on this subject based on the ideXlab platform.
-
synthesis and Hypolipidemic activity of novel 2 4 2 substituted aminothiazole 4 yl phenoxy acetic acid derivatives
ChemInform, 2010Co-Authors: Santosh N Mokale, Priyanka T Sanap, Devanand B ShindeAbstract:All synthesized compounds (I) are evaluated for their Hypolipidemic activity by using high fat-diet induced hyperlipidemia in Sprague-Dawley rats.
-
synthesis and Hypolipidemic activity of novel 2 4 2 substituted aminothiazole 4 yl phenoxy acetic acid derivatives
European Journal of Medicinal Chemistry, 2010Co-Authors: Santosh N Mokale, Priyanka T Sanap, Devanand B ShindeAbstract:A novel series of aminotihazole compounds possessing phenoxy acetic acid moiety were synthesized. The synthesized compounds were evaluated for their Hypolipidemic activity by using high fat diet induced hyperlipidemia in Sprague-Dawley rats.
Ramesh Chandra - One of the best experts on this subject based on the ideXlab platform.
-
Synthesis and pharmacological evaluation of substituted 5-[4-[2-(6,7-dimethyl-1,2,3,4-tetrahydro-2-oxo-4-quinoxalinyl)ethoxy]phenyl]methylene]thiazolidine-2,4-dione derivatives as potent euglycemic and Hypolipidemic agents.
Bioorganic & Medicinal Chemistry Letters, 2005Co-Authors: Dipti Gupta, Narendra N. Ghosh, Ramesh ChandraAbstract:A series of substituted 5-[4-[2-(6,7-dimethyl-1,2,3,4-tetrahydro-2-oxo-4-quinoxalinyl)ethoxy]phenyl]methylene]thiazolidine-2,4-diones were synthesized and their euglycemic and Hypolipidemic activities were investigated in Wistar male rats. Based on the in vivo data in rats, compound 4a was identified as a potent euglycemic and Hypolipidemic agent.
-
bis 3 4 substituted phenyl prop 2 ene disulfides as a new class of antihyperlipidemic compounds
Bioorganic & Medicinal Chemistry Letters, 2004Co-Authors: Meenakshi Sharma, Manisha Tiwari, Ramesh ChandraAbstract:A series of bis[3-(4'-substituted phenyl)prop-2-ene]disulfides were prepared and their Hypolipidemic activities were examined in hypercholesterolemic Wistar rats. Introduction of an electron withdrawing group to the phenyl ring in the parent compound led to the identification of compound 8 as a potent and efficacious Hypolipidemic agent.
Robert W Mahley - One of the best experts on this subject based on the ideXlab platform.
-
pathogenesis of type iii hyperlipoproteinemia dysbetalipoproteinemia questions quandaries and paradoxes
Journal of Lipid Research, 1999Co-Authors: Robert W Mahley, Yadong Huang, S C RallAbstract:Type III hyperlipoproteinemia (HLP) is a genetic disorder characterized by accumulation of remnant lipoproteins in the plasma and development of premature atherosclerosis. Although receptor binding-defective forms of apolipoprotein (apo) E are the common denominator in this disorder, a number of apparent paradoxes concerning its pathogenesis still exist. However, studies in transgenic animals are resolving the mechanisms underlying this disorder. Paradox I: Defective apoE (commonly apoE2) is essential but not sufficient to cause overt type III HLP. In fact, most apoE2 homozygotes are Hypolipidemic. Studies in apoE2 transgenic models have demonstrated the impact of other genes or hormones in converting the hypolipidemia to hyperlipidemia. Paradox II: Among apoE2 homozygotes, men are more susceptible than women to type III HLP. Transgenic studies have shown that estrogen affects both LDL receptor expression and lipolytic processing, explaining the resistance of women to this disorder until after menopause. Paradox III: ApoE deficiency is associated with hypercholesterolemia, whereas the type III HLP phenotype is characterized by both hypercholesterolemia and hypertriglyceridemia. The hypercholesterolemia is caused by impaired receptor-mediated clearance, whereas the hypertriglyceridemia is caused primarily by impaired lipolytic processing of remnants and increased VLDL production associated with increased levels of apoE. Paradox IV: ApoE2 is associated with recessive inheritance of this disorder, whereas other defective apoE variants are associated with dominant inheritance. Determinants of the mode of inheritance are the differential binding of apoE variants to the LDL receptor versus the HSPG/LRP complex and the preference of certain apoE variants for specific lipoproteins. Thus, the pathogenesis of this sometimes mysterious disorder has been clarified.—Mahley, R. W., Y. Huang, and S. C. Rall, Jr. Pathogenesis of type III hyperlipoproteinemia (dysbetalipoproteinemia): questions, quandaries, and paradoxes. J. Lipid Res. 1999. 40: 1933–1949.
-
genetic factors precipitating type iii hyperlipoproteinemia in Hypolipidemic transgenic mice expressing human apolipoprotein e2
Arteriosclerosis Thrombosis and Vascular Biology, 1997Co-Authors: Yadong Huang, S C Rall, Robert W MahleyAbstract:Several factors are hypothesized to precipitate or exacerbate type III hyperlipoproteinemia (HLP) in humans. Among such factors are those that directly overload remnant lipoprotein production or disrupt removal pathways, including an increased ratio of apolipoprotein (apo) E2 to normal apoE, overproduction of apoB-containing lipoproteins, and decreased LDL receptor activity. Hypolipidemic apoE2-transgenic mice bred onto an apoE-null background had dramatically higher plasma total cholesterol (192 +/- 26 mg/dL for males, 203 +/- 40 mg/dL for females) and triglyceride (295 +/- 51 mg/dL for males, 277 +/- 58 mg/dL for females) levels than apoE2 mice with endogenous mouse apoE. Thus, eliminating normal apoE in the presence of apoE2 (thereby increasing the relative abundance of the defective ligand) can convert a Hypolipidemic to a hyperlipidemic phenotype. Hypolipidemic apoE2 transgenic mice overexpressing human apoB had moderate remnant accumulation compared with apoE2-only or apoB-only transgenic mice, indicating that overproduction of apoB-containing lipoproteins in the presence of apoE2 can augment remnant production. Hypolipidemic apoE2 transgenic mice bred-onto an LDL receptor-null background had markedly higher plasma total cholesterol (288 +/- 51 mg/dL for males, 298 +/- 73 mg/dL for females) and triglyceride (356 +/- 72 mg/dL for males, 317 +/- 88 mg/dL for females) levels than apoE2-only mice, and remnant accumulation increased even in apoE2 mice with a heterozygous LDL receptor-knockout background (compared with apoE2-only mice), suggesting that reducing or eliminating a major receptor-mediated remnant-removal pathway in the presence of apoE2 can also precipitate a hyperlipidemic phenotype. In all cases where either lipoprotein remnant production or removal pathways were severely stressed, increased remnant accumulation was apparent. As judged by the chemical characteristics of the remnant lipoproteins, the lipoprotein phenotype was quite similar to that of human type III HLP, especially in the apoE2-expressing mice with no endogenous apoE or LDL receptors, and thus these mice represent improved models of the disorder.