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| enlist, breaking news, plump thighs , omega3, insulin, cross, canada, fat black girls , doctor, noble feeder, bulk, nhs, nutritional, tainted blood, drugs, journalsentinel, hepatitus, tocopherol concentrations, fatty fat fat , plump asian , state, immunizations, 24 7 fat girls , | We are currently studying the effect of plump girls galleries tissue specific deletion of ABCA1 on HDL formation and catabolism, and on atherosclerosis development. [See publication listed below] [See Press Release]. In the second plump girls galleries project, which is funded by an R01 grant from NHLBI of the NIH, we are investigating the molecular mechanisms by which LCAT expression influences atherosclerosis development. LCAT is an enzyme plump girls galleries that makes cholesterol esters in plasma; cholesterol esters are the lipid that accumulates in arteries during atherosclerosis, leading to lumen stenosis. We have found in previous studies that elimination of LCAT activity in plasma by gene targeting increases arterial cholesterol ester deposition in a mouse model of atherosclerosis, which is a paradox since LCAT makes cholesterol esters. |
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| the first project, which is part of a tocopherol concentrations Program Project Grant from the National Heart, Lung, and Blood Institute (NHLBI) of the NIH, we seek to understand the role of tissue specific expression tocopherol concentrations of ATP binding cassette transporter A1 (ABCA1) in high density lipoprotein (HDL) metabolism and atherosclerosis development. HDLs are referred to as the “good cholesterol” and are protective against the development of atherosclerosis. HDLs are formed tocopherol concentrations by the interaction of apoA-I, the major protein on HDL particles, with a lipid transporter on cell surfaces known as ABCA1. Individuals with a genetic deficiency of ABCA1 have Tangier disease, which is characterized by plasma HDL concentrations that are <5% of normal and accumulation of cholesterol in peripheral tissues. Using gene targeting techniques, we have developed tissue specific deletions of ABCA1 protein. |
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