PubMed · 3638618
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
J Kennedy. Sobering thoughts.. https://pubmed.ncbi.nlm.nih.gov/3638618/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Although lipids are essential to brain function, almost nothing is known of lipid transfer proteins in the brain. Early reports indicates cross-reactivity of brain proteins with antisera against two native liver sterol transfer proteins, sterol carrier protein-2 (SCP-2) and the liver form of fatty acid-binding protein (L-FABP). Herein, polyclonal antibodies raised against the recombinant liver sterol transfer proteins SCP-2 and L-FABP were used to identify the lipid transfer proteins in the brains of alcohol-treated and control mice. L-FABP was not detectable in brain of either control or chronic ethanol-treated mice. In contrast, SCP-2 not only was present, but its level was significantly (p < 0.05) increased 23 and 50%, respectively, in brain homogenates and synaptosomes of mice exposed to alcohol. To determine whether antibodies against the recombinant liver SCP-2 reflected true levels of SCP-2 in brain, the cDNA sequence for brain SCP-2 was isolated from a brain cDNA library. The mouse brain SCP-2 sequence was 99.99% identical to the mouse liver SCP-2 sequence. The translated sequence differed by only one amino acid, and the replacement was conservative. Thus, unlike the fatty acid binding proteins, the SCP-2 moieties of brain and liver are essentially identical. Polyclonal antibodies against acyl-CoA binding protein, a lipid-binding protein that does not bind or transfer sterol, showed that increased levels of brain SCP-2 with chronic ethanol consumption did not represent a general increase in content of all lipid transfer proteins. Changes in the amount of SCP-2 may contribute to membrane tolerance to ethanol.
Explore the source record for details and available documents.
Nearly half of all trauma beds are occupied by patients who were injured while under the influence of alcohol. Alcoholism plays such a significant role in trauma that efforts to reduce injury recurrence are unlikely to be successful if it remains untreated. An injury requiring hospitalization creates a unique opportunity to intervene and to motivate patients to alter their drinking behavior, thereby making trauma centers ideal sites to implement an alcohol screening, intervention, and referral program. However, despite emphasis on injury control and prevention, little has been done to incorporate alcohol intervention programs into care of the injured patient. Effective means of intervention exist that are consistent with the time, financial, and staffing constraints of trauma centers, and they should be implemented.