Large granular lymphocytes,Leu 7 reactivity and natural killer cell function in peripheral blood of patients with Hodgkin's disease

Summary The percentage and absolute number of lymphocytes and Leu 7⁺ cells were significantly lower in HD even in active stages. There was no significant difference in the percentage of LGL between the three groups (control, active HD, inactive HD), however, because of differences in counts of lymphocytes the absolute number of LGL was significantly lower in HD even in the active group than that in healthy controls. The absolute count of LGL and Leu 7⁺ cells in patients in remission was significantly higher than that in active HD. Natural cytotoxicity against K-562 cells was also significantly lower in active patients in comparison with controls, while the percentage of cytotoxicity was slightly but not significantly higher in patients in remission than that in the active group. A positive correlation was observed between all the three examined parameters both in controls and in patients with active and inactive HD.     

The gene coding for the α1 subunit of the skeletal dihydropyridine receptor (Cchl1a3=mdg) maps to mouse Chromosome 1 and human 1q32

Using both chromosomal in situ hybridization and molecular techniques, we report the genetic localization of the gene coding for the alpha 1 subunit of the skeletal slow Ca²⁺ current channel/DHP receptor gene (Cchl1a3) on human Chromosome (Chr) 1 (1q31–1q32 region) and on mouse Chr 1 region (F-G). On the basis of single-strand conformation polymorphism (SSCP-PCR) analysis in an interspecific backcross, we have determined that the Cchl1a3=mdg (muscular dysgenesis) locus is very closely linked to the myogenin (Myog) locus.     

Trypsin complexed with α1-proteinase inhibitor has an increased structural flexibility

Mutant rat trypsin Asp¹⁸⁹Ser was prepared and complexed with highly purified human α₁-proteinase inhibitor. The complex formed was purified to homogeneity and studied by N-terminal amino acid sequence analysis and limited proteolysis with bovine trypsin. As compared to uncomplexed mutant trypsin, the mutant enzyme complexed with α₁-proteinase inhibitor showed a highly increased susceptibility to enzymatic digestion. The peptide bond selectively attacked by bovine trypsin was identified as the Arg¹¹⁷-Val¹¹⁸ one of trypsin. The structural and mechanistic relevance of this observation to serine proteinase-substrate and serine proteinase-serpin reactions are discussed.     

Inhibitory effect of high oxygen pressure on potassiuminduced activation of pyruvate dehydrogenase and glucose metabolism in rat brain slices

The effects of high oxygen pressure on pyruvate dehydrogenase (pyruvate: lipoate oxidoreductase (decarboxylating and acceptor-acylating), EC 1.2.4.1) activity, tissue concentration of ATP, and CO₂ production from glucose were studied in rat brain cortical slices. The increase in pyruvate dehydrogenase activity and the lowering of cellular ATP, occurring during potassium-induced depolarization at 1 atm of oxygen, were reversed by increasing the oxygen pressure to 5 atm. When brain slices were incubated at 1 atm oxygen with [U-¹⁴C]glucose, a high potassium medium approximately doubled the production of ¹⁴CO₂. Oxygen at 5 atm abolished this potassium-dependent increase in ¹⁴CO₂ production with no significant effect on glucose oxidation in normal Krebs-Ringer phosphate medium. Adding 4 atm helium to 1 atm oxygen did not interfere with the ability of potassium ions to activate pyruvate dehydrogenase, lower ATP, or increase glucose oxidation. The results show that toxic effects of hyperbaric oxygen, not manifest in “resting” tissue, may be revealed during stress such as potassium depolarization. The site of the toxic effects of oxygen is probably the cell membrane where excess oxygen appears to interfere with the action of the sodium pump, calcium transport or other processes stimulated by increased concentrations of extracellular potassium.     

On the non-existence of eloxanthin

Abandonment of the name eloxanthin is proposed. The principal carotenoids in various species of Elodea were (3R, 3′R, 6′R)-lutein (β,ε-carotene-3, 3′-diol) and β, β-carotene. The minor pigments were neoxanthin-X (5′, 6′-epoxy-6, 7-didehydro-5, 6, 5′, 6′-tetrahydro-β, β-carotene-3, 5, 3′-triol), 9′-cis-neoxanthin- X, 9- and 13-cis-violaxanthin (5, 6, 5′, 6′-diepoxy-5, 6, 5′, 6′-tetrahydro-β, β-carotene-3, 3′-diol), antheraxanthin (5, 6-epoxy-5, 6-dihydro-β, β-carotene-3, 3′-diol), neolutein A (13- or 13′-cis-lutein) and neolutein B (9- or 9′-cis-lutein). All attempts to isolate eloxanthin failed.     

Adaptor Identity Modulates Adaptation Effects in Familiar Face Identification and Their Neural Correlates

Adaptation-related aftereffects (AEs) show how face perception can be altered by recent perceptual experiences. Along with contrastive behavioural biases, modulations of the early event-related potentials (ERPs) were typically reported on categorical levels. Nevertheless, the role of the adaptor stimulus per se for face identity-specific AEs is not completely understood and was therefore investigated in the present study. Participants were adapted to faces (S1s) varying systematically on a morphing continuum between pairs of famous identities (identities A and B), or to Fourier phase-randomized faces, and had to match the subsequently presented ambiguous faces (S2s; 50/50% identity A/B) to one of the respective original faces. We found that S1s identical with or near to the original identities led to strong contrastive biases with more identity B responses following A adaptation and vice versa. In addition, the closer S1s were to the 50/50% S2 on the morphing continuum, the smaller the magnitude of the AE was. The relation between S1s and AE was, however, not linear. Additionally, stronger AEs were accompanied by faster reaction times. Analyses of the simultaneously recorded ERPs revealed categorical adaptation effects starting at 100 ms post-stimulus onset, that were most pronounced at around 125–240 ms for occipito-temporal sites over both hemispheres. S1-specific amplitude modulations were found at around 300–400 ms. Response-specific analyses of ERPs showed reduced voltages starting at around 125 ms when the S1 biased perception in a contrastive way as compared to when it did not. Our results suggest that face identity AEs do not only depend on physical differences between S1 and S2, but also on perceptual factors, such as the ambiguity of S1. Furthermore, short-term plasticity of face identity processing might work in parallel to object-category processing, and is reflected in the first 400 ms of the ERP.     

Ghrelin amplifies the nicotine-induced dopamine release in the rat striatum

The orexigenic peptide ghrelin plays a prominent role in the regulation of energy balance and in the mediation of reward mechanisms and reinforcement for addictive drugs, such as nicotine. Nicotine is the principal psychoactive component in tobacco, which is responsible for addiction and relapse of smokers. Nicotine activates the mesencephalic dopaminergic neurons via nicotinic acetylcholine receptors (nAchR). Ghrelin stimulates the dopaminergic neurons via growth hormone secretagogue receptors (GHS-R1A) in the ventral tegmental area and the substantia nigra pars compacta resulting in the release of dopamine in the ventral and dorsal striatum, respectively. In the present study an in vitro superfusion of rat striatal slices was performed, in order to investigate the direct action of ghrelin on the striatal dopamine release and the interaction of ghrelin with nicotine through this neurotransmitter release. Ghrelin increased significantly the dopamine release from the rat striatum following electrical stimulation. This stimulatory effect was reversed by both the selective nAchR antagonist mecamylamine and the selective GHS-R1A antagonist GHRP-6. Nicotine also increased significantly the dopamine release under the same conditions. This stimulatory effect was antagonized by mecamylamine, but not by GHRP-6. Ghrelin further stimulated the nicotine-induced dopamine release and this effect was abolished by mecamylamine and was partially inhibited by GHRP-6. The present results demonstrate that ghrelin stimulates directly the dopamine release and amplifies the nicotine-induced dopamine release in the rat striatum. We presume that striatal cholinergic interneurons also express GHS-R1A, through which ghrelin can amplify the nicotine-induced dopamine release in the striatum. This study provides further evidence of the impact of ghrelin on the mesolimbic and nigrostriatal dopaminergic pathways. It also suggests that ghrelin signaling may serve as a novel pharmacological target for treatment of addictive and neurodegenerative disorders.