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Biomedical subjects

L Feinman

Publications and source records attributed to L Feinman.

11 recordsLinked to original sources
PubMed1988

Biphasic control of polymorphonuclear cell migration by Kupffer cells. Effect of exposure to metabolic products of ethanol.

In order to investigate the role of the Kupffer cells in the regulation of the inflammatory reaction seen in alcoholic hepatitis, rat liver Kupffer cells were cultured and exposed to products of ethanol metabolism. The resultant supernatants were tested to study their ability to stimulate or inhibit polymorphonuclear cell chemotaxis. Kupffer cells produced increased chemokinetic activity for human polymorphonuclear leukocytes (84 +/- 6 vs. 61 +/- 4 randomly migrating cells per 5 high power fields; p less than 0.01); when incubated with soluble products of microsomal peroxidation, the Kupffer cells engendered more chemokinetic activity than that produced by untreated Kupffer cells (106 +/- 6 vs. 84 +/- 6 cells per 5 high power fields; p less than 0.05). When Kupffer cells were incubated with acetaldehyde, the chemokinetic activity that appeared in the supernatant did not differ from control (51 +/- 3 vs. 61 +/- 4 randomly migrating cells per 5 high power fields; p = NS). Chemotaxis of polymorphonuclear cells was not observed when the Kupffer cell supernatants were tested by checkerboard analysis. Kupffer cells released a factor which, at different concentrations, inhibited the response of polymorphonuclear cells to the synthetic polypeptide chemotactic factor f-met-leu-phe by 47% (p less than 0.001). This effect was unchanged when the cells were exposed to acetaldehyde or to soluble products of microsomal peroxidation. Our results demonstrate that Kupffer cells are capable of stimulating or inhibiting polymorphonuclear cell chemotaxis and that some of these effects may be influenced by the products of ethanol metabolism, suggesting that Kupffer cells may play an important role in the regulation of the inflammatory reaction seen in alcoholic hepatitis.

Acetaldehyde↗
PubMed1988

Prediction of variceal hemorrhage: a prospective study.

Prophylactic therapy to prevent the first variceal hemorrhage ceased being recommended for any cirrhotic because risks outweighed benefits. In this study, we identified cirrhotics that have never bled who are most prone to hemorrhage from varices. We developed a numerical grading system which combined size with other endoscopic characteristics, so varices would get an aggregate grade of 1 to 10. Varices were classified as either high grade (scored greater than or equal to 8) or low grade (scored less than or equal to 7). The grading system had a predictive value for bleeding when studied prospectively for a mean duration of 26 months in 52 patients subjected to placebo (15 patients) or various treatments (37 patients) in a randomized trial. High grade varices had a significantly higher association with bleeding than did low grade varices; 73% versus 7% (p less than 0.001) analyzing all 52 patients (of which 21% bled), and 83% versus 11% (p less than 0.05) analyzing the 15 placebo-treated patients (of which 40% bled). An esophagram positive for varices proved to be a sensitive screen for high grade varices, picking up 91% of them. However, it was a poor predictor of bleeding (one-third bled), since only 45% of radiologically evident varices were high grade. Since almost all cirrhotics with high grade varices can be expected to bleed within 2 yr, this group should be the focus of controlled trials to determine whether low risk prophylactic therapies reduce the incidence of first variceal hemorrhage.

Combined Modality Therapy↗
PubMed1985

Balloon cytology in screening of asymptomatic alcoholics for esophageal cancer, Part I.

We assessed the feasibility of using balloon cytology to screen an asymptomatic group of alcoholics at increased risk for esophageal cancer. The results indicate that this group can be studied with minimal morbidity and that useful material can be obtained in 85% of subjects. Keratinization was present in 68% of specimens and fungus was noted in 9%. Individuals with moderate to large amounts of keratinization consumed significantly more alcohol than those without cytologic evidence of keratin. We speculate that keratinization and fungus may represent markers of enhanced malignant potential in this population.

Adult↗
PubMed1975

High blood acetaldehyde levels after ethanol administration. Difference between alcoholic and nonalcoholic subjects.

Blood actaldehyde and ethanol levels were measured in 11 subjects, six with chronic alcholoism and five nonalcholic controls, after alcohol had been given intravenously. Despite a progressive fall in blood ethanol over a range of 54 to 33 mM/acetaldehyde did not decrease in any of the 11 subjects. The mean acetaldehyde plateau level was significantly (p less than 0.001) higher in alcoholic (42.7 plus or minus 1.2 mum) than in nonalcoholic (26.5 plus or minus 1.5 mum) subjects. When the mean blood ethanol concentration reached 24 mM,the acetaldehyde plateau ended abruptly in each subject. The ethanol concentration at which this fall of blood acetaldehyde occurred suggests desaturation of an ethanol oxidizing system other than alcohol dehydrogenase and indicates that at high ethanol blood levels, such a system contributes to ethanol oxidation. The highet acetaldehyde levels in alcholism may result from both greater activity of this system and mitochondrial damage, and could contribut to the neurologic, hepatic and cardiac complications of alcoholism.

Acetaldehyde↗
PubMed1975

Effect of chronic alcohol consumption on ethanol and acetaldehyde metabolism.

Hepatic metabolism of ethanol to acetaldehyde by the alcohol dehydrogenase (ADH) pathway is associated with the generation of reducing equivalents as NADH. Conversely, reducing equivalents are consumed when ethanol oxidation is catalyzed by the NADPH dependent microsomal ethanol oxidizing system (MEOS). Since the major fraction of ethanol metabolism proceeds via ADH and since the oxidation of acetaldehyde also generates NADH, an excess of reducing equivalents is produced. This explains a variety of effects following acute ethanol administration, including hyperlactacidemia, hyperuricemia, enhanced lipogenesis and depressed lipid oxidation. To the extent that ethanol is oxidized by the alternate MEOS pathway, it slows the metabolism of other microsomal substrates. Following chronic ethanol consumption, adaptive microsomal changes prevail, which include enhanced ethanol and drug metabolism, and increased lipoprotein production. Eventually, injury develops with alterations of the rough endoplasmic reticulum and structural and functional abnormalities of the mitochondria.

Acetaldehyde↗
PubMed1972

Hepatic collagen metabolism: effect of alcohol consumption in rats and baboons.

Long-term ethanol feeding causes collagen accumulation in livers of rats and baboons. Activity of collagen proline hydroxylase in the liver is also stimulated, and incorporation of proline into collagen hydroxyproline in rat liver slices is significantly enhanced, a result indicating that increased synthesis is responsible, in part, for the collagen accumulation.

Animals↗