Assignment to chromosome 12 of the gene coding for the human cell surface antigen CD9(p24) using the monoclonal antibody ALB6

An analysis of 20 independent man-mouse and man-hamster hybrids has shown that the gene coding for the cell-surface protein CD9(p24), a differentiation antigen recognized by the monoclonal antibody ALB6, is located on chromosome 12. A positive correlation was shown between CD9(p24) and chromosome 12 and all other chromosomes were excluded. In addition a synteny was observed between CD9(p24) and LDH-B, a well known marker of chromosome 12 (out of 27 hybrids, 15 were LDH-B+ ALB6+ and 12 were LDH-B-ALB6-). Expression of the antigen in hybrid CH-35K issued from parental fibroblasts possessing a balanced reciprocal translocation 46,X,Y,t(X,12)(q23,q12) indicated that the gene for CD9(p24) is probably localized on 12q12----pter. Monoclonal antibodies ALB6, Ba2 and 602/29 recognize the same protein of molecular weight 21 to 24 KD controlled by a gene located on chromosome 12. It is known that Ba2 and 602/29 recognize two different epitopes but the existence of a third epitope recognized by ALB6 remains to be shown.     

Applied psychophysiology and biofeedback of event-related potentials (brain waves): historical perspective, review, future directions

This paper reviews the efforts of workers in the 1960s-1980s to demonstrate voluntary control of exogenously evoked (event-related) potentials in visual, somatic sensory, and auditory systems in rats, cats, and humans. The first part of the paper reviews the conceptual foundation and development of the work--it actually arose from traditional sensory coding and neural correlates of behavior studies. The second part summarizes recent applications of the method in the area of pain control. In reviewing these matters, the major effort is directed at revealing how the ideas unfolded in very human, day-to-day, anecdotal terms. There is not much of an attempt to formally review the literature, which is cited for consultation elsewhere. In the same spirit, many possible future experiments are suggested by way of elucidating the key remaining questions in the area.     

Sediment as a possible source of food for corals

Reef building corals are generally believed to require clear, nutrient-poor water. Yet, paradoxically, coral reefs are among the most productive marine ecosystems in the world. This paradox is commonly explained by the coral's ability to utilize a number of food resources, including zooplankton, phytoplankton, dissolved organic matter and photosynthetic products derived from their endosymbiotic algae, the zooxanthellae. Sedimentation is a known stressor for corals, inhibiting most feeding modes in various ways. However, evidence for enhanced sediment deposition on certain corals, induced by their morphologies, as well as for sediment ingestion by some corals, has led us to examine the use of sediment as a possible source of food for corals in addition to the other, known food sources. Our experiments with fluorescently labelled sediment show transfer of labelled organic matter from the sediment into the cells of the solitary coral Fungia horrida Dana 1846. The results provide the first direct evidence for the ability of a coral to digest the sediment's organic fraction. These results may indicate a positive role of sediment, which up until now was considered to have only deleterious effects on corals.     

Decrease in human lymphocyte surface glycoconjugates in leukemia as demonstrated by lectin binding

Qualitative variations in the glycoconjugates which make up the lectin receptor sites on the membranes of leukemic lymphocytes, compared with those of normal cells, have been studied by the use of three tritiated lectins: Robinia pseudoacacia lectin, Concanavalin A and Ricinus communis (var. Sanquineus) agglutinin (RCA 120). The binding specificity of these lectins has been demonstrated using specific determinants: alpha-methylmannoside and galactose for Concanavalin A and Ricinus communis agglutinin respectively. For the Robinia lectin this specificity was determined by saturation of the receptor sites with the unlabeled Robinia lectin before the addition of isotopically labeled Robinia lectin. The results show a decrease in the number of receptor sites on the leukemia cells, especially in chronic lymphoid leukemia, relative to that on normal cells. The apparent affinity constants of leukemic cells in all cases remain higher than those of normal cells.     

Neurotransmitter mediation of morphine hypothermia in rats.

Subcutaneous (sc) injections of morphine (10 mg/kg) caused transient falls in body temperature of rats. The hypothermic responses to morphine were inhibited by the prior intracerebroventricular (icv) administration of methysergide or phentolamine. Methysergide treatment also prevented hypothermic responses to icv 5-hydroxytryptamine (5-HT), but not responses to icv norepinephrine or dopamine. Phentolamine inhibited responses to icv norepinephrine and dopamine, but not to 5-HT. Haloperidol, which inhibited responses to icv dopamine, did not alter the hypothermia induced by sc or icv morphine. The results indicate that both 5-HT and norepinephrine participate as central mediators of morphine-induced hypothermia.