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Biomedical subjects

M R Sanchez

Publications and source records attributed to M R Sanchez.

24 records · Page 2Linked to original sources

Reduced Langerhans' cell Ia antigen and ATPase activity in patients with the acquired immunodeficiency syndrome.

We investigated the possible role of a defect in antigen-presenting cells in the acquired immunodeficiency syndrome (AIDS), by enumeration of Langerhans' cells, the epidermal antigen-presenting cells. These cells were stained for the characteristic markers, surface Ia antigen and surface ATPase activity. A significant reduction was observed in the number of stained cells per square millimeter of body-surface area in 24 patients with AIDS and either opportunistic infections (Ia, 258 +/- 34, and ATPase, 274 +/- 46) or Kaposi's sarcoma (Ia, 378 +/- 100, and ATPase, 530 +/- 26), as compared with 38 appropriate controls (Ia, 721 +/- 13, and ATPase, 693 +/- 12). Examination of six patients with an "AIDS-related complex" revealed significantly reduced numbers of Langerhans' cells per square millimeter; this reduction was more pronounced in staining for Ia antigen (306 +/- 69) than in staining for ATPase activity (517 +/- 101). Given the known role of Ia expression in antigen presentation, we suggest that functional alterations in Langerhans' cells, and perhaps also in antigen-presenting cells in tissues other than skin, may be involved in the pathogenesis of AIDS.

Acquired Immunodeficiency Syndrome↗

Cholecystokinin and satiation with alcohol.

Release of the brain-gut peptide cholecystokinin (CCK) is stimulated by intragastric instillation of ethanol, and peripheral administration of CCK inhibits ethanol consumption. To assess the temporal specificity of the inhibitory effect of CCK on alcohol intake, water-deprived rats were given 5% ethanol at 20, 10 or 0 min after intraperitoneal injections of CCK octapeptide. Delaying access to ethanol for 20 min prevented a significant effect of CCK on intake. CCK's temporally constrained inhibitory action on alcohol consumption is consistent with an ethanol satiation effect. To test the motivational specificity of CCK's effect on fluid intake, rats were allowed a 2-bottle choice of 2% ethanol and water after CCK injections. Ethanol solution intake was suppressed by CCK, and total water intake was unaffected. The putative alcohol satiation action of CCK is appropriately specific to ethanol solution in free-choice tests. Hungry, but not fluid-deprived rats that were either ethanol experienced or naive received a 2-bottle choice of 4% ethanol or water after CCK or saline injections. CCK again specifically inhibited ethanol intake, but this effect required prior ethanol experience. Doses of CCK and naloxone, an opioid receptor blocker, combined to inhibit ethanol intake in an infra-dose-additive manner in water-deprived rats. CCK may act endogenously, in part on opioid receptor-mediated processes, as a preabsorptive satiety signal of ethanol. The full expression of this action appears to depend on prior conditioning of nutritive expectancy of the postingestive effects of alcohol.

Alcohol Drinking↗

Bombesin reduces alcohol choice in nutritive expectancy and limited-access procedures.

Bombesin is a bioactive tetradecapeptide found in nerves of the brain and gut and previously shown to inhibit intake of ethanol in forced-choice, one-bottle tests in water-deprived rats. In the present experiments, intraperitoneal bombesin (4-100 micrograms/kg) reduced selection of alcohol in two-bottle choice tests with water. In an application of the "nutritive expectancy" procedure, weight-reduced rats received access to 4% w/v ethanol and water. Bombesin injection suppressed the intake of ethanol, but not of water, in rats with prior ethanol experience. In an application of the "limited access" procedure, nondeprived rats received access to 6% w/v ethanol and water in nonhome cages during either the light or the dark phase of a 12:12 h lighting cycle. Bombesin injection lowered the intake of ethanol, but not of water, in both phases of the lighting cycle and in both sexes. Water deprivation is not necessary for bombesin to inhibit alcohol intake and this effect cannot be explained by hypodipsia, nonspecific debilitation, or conditioned aversion. Endogenous bombesin-like neuropeptides may specifically reduce choice of alcohol by signaling satiation with ethanol.

Alcohol Drinking↗