No abstract

Dietary fat-mediated alterations in the rate of hepatic removal of postprandial TRLs, which carry cholesterol accepted from LDL+HDL via cholesteryl ester transfer protein in vivo, may contribute to the dietary fat-mediated change in endogenous lipoprotein cholesterol.

The alcohol-mediated increase in postprandial TRL flux and the hepatic removal of postprandial TRL after the acceptance of cholesterol from CRL and cell membranes contribute to increased HDL cholesterol and enhancement of reverse cholesterol transport in humans.

Reverse cholesterol transport (RCT), a process of transporting cholesterol from cell membranes to the liver for its excretion, occurs in the plasma compartment in vivo. Both lecithin:cholesterol acyltransferase (LCAT) and cholesteryl ester transfer proteins (CETPs) may play an important role in regulating the rate of RCT by influencing the rate at which cholesterol released from cell membranes into plasma is trapped in the core of HDL via esterification and the rate at which the trapped HDL-cholesteryl ester (CE) is then transferred to apolipoprotein B (apoB)-containing lipoproteins for delivery to the liver (1-3). CETP promotes the transfer of CE from HDL to various apoB-containing lipoproteins [LDL, VLDL, IDL, and chylomicrons (CMs)] in plasma (3-9), but the catabolic rate and fate of these various apoB-containing lipoproteins differ in vivo (10). Thus, the rate of RCT promoted by LCAT and CETP might then depend on the rate and extent of transfer of HDL-CE to various apoB-containing lipoproteins in plasma in vivo. Although the extent of in vivo transfer of CE from HDL to various apoB-containing lipoproteins is known to be influenced by the levels of individual apoB-containing lipoproteins in plasma (11), the rate and potencies of the various apoB-containing lipoproteins to accept CE from HDL in vivo have not yet been fully elucidated. An earlier study (12) examining the fate of [ 3 H]CE-labeled HDL injected into fasting humans showed that 3 H-labeled CE on HDL appeared more rapidly on VLDL than on LDL. In rabbits, 3 H-labeled CE on

Chlorine (Cl2) is a chemical used in both industry and society alike, despite it being a highly irritant and reactive gas. Acute exposure can result in symptoms of airway obstruction such as wheezing, shortness of breath, mouth/nose/chest pain, and bronchospasm. Currently, there is no known antidote for chlorine’s poisoning effects. Potential treatments include topical exposure of the airways to nebulized drugs such as local anesthetics which have been shown to improve the mobility of monitored animals after exposure to Cl2 gas. In this research project, we assess the effects of the nebulized local anesthetics lidocaine (1% and 4%), 3% 2‐Chloroprocaine following exposure to 100 or 400 ppm of chlorine gas on biochemical measurements of injury to airway. Wet‐to‐dry lung weight ratios, bronchoalveolar lavage (BAL) cell counts and total protein, and lung homogenate cytokine levels were determined 24 hours after Cl2 gas exposure and anesthetic treatment. In mice exposed to 400 ppm Cl2 gas, 1% lidocaine had the greatest decrease of wet‐to‐dry lung weight ratio in addition to lower live cell infiltration and lower protein concentrations in BAL fluids indicating a potential anti‐inflammatory affect. Cytokine levels from lung homogenates after exposure and treatments had a decreasing trend compared to untreated animals. Levels of IL‐10, IFNγ, MCP‐1 and IL‐13 were significantly lower in the 1% lidocaine animal group. Similar but not identical results were found following treatment with 100ppm Cl2. Treatment with 4% lidocaine and 3% 2‐chloroprocaine had potential toxic effects. This study indicates that nebulized 1% lidocaine is potentially a good treatment option after chlorine induced lung injury based on behavioral and biochemical data. Grant Funding Source: Supported by 1R21ES022876