Dérivés Monotritylés du D-xylose

Monotritylation of O-acetyl derivatives of D-xylopyranose and D-xylofuranose with trityl chloride in acetonitrile-pyridine gave the tri-O-acetyl derivatives of 1-,2-, 3-, and 5-O-trityl-D-xylofuranose and of 1-, 2-, 3-, and 4-O-trityl-D-xylopyranose which were required for the identification of the various monotrityl derivatives obtained in the tritylation at 50° of D-xylose with trityl chloride in pyridine or hexamethylphosphoric triamide-silver acetate.     

Control of the Ca2+-triggered bioluminescence of Veretillum cynomorium lumisomes

Calcium ions can trigger an emission of light from Veretillum cynomorium lumisomes (bioluminescent vesicles) under conditions where they are not lysed. This process does not require a metabolically-linked source of energy, but is dependent upon the nature of the ions present inside and outside the vesicles. The Ca²⁺-triggered bioluminescence is stimulated by an asymmetrical distribution of cations or anions. Either high internal sodium or high external chloride is required for the maximal effect. When sodium is present outside the structure and potassium inside, the slow inward diffusion of calcium is decreased. Unbalanced diffusion of internal cations also stimulates the bioluminescence, suggesting control of the calcium influx by an electrochemical gradient. It is assumed that rapid outward diffusion of sodium or inward diffusion of chloride generates an electrical potential difference (inside negative) which drives the Ca²⁺-influx. With purified lumisomes it has been shown that Ca²⁺-triggered bioluminescence and calcium uptake (presumably net uptake) were correlated. In two instances uptake of the lipophilic cation dibenzyldimethylammonium has given direct evidence for the existence of a potential difference. With NaCl-loaded vesicles, it has not been possible to demonstrate an uptake of lipophilic cations but experiments with ²²Na and ⁴²K indicated a higher rate of sodium efflux, in accord with the proposed hypothesis.     

Effects of lesions in the pontine tegmentum on the sleep stages in the rat]

1. Limited coagulations of the locus coeruleus and subcoeruleus nuclei have been performed in rats and the sleep-waking cycle was continuously monitored during 9 days. The cortical and diencephalic noradrenaline content was mesured at the termination of the experiment, on the 10th post lesion day. 2. The bilateral destruction of the locus coeruleus is followed by the appearance of a uro-genital syndrome consisting of hema turia, bladder distension and penile erection. The states of sleep are disturbed during the first two days (increase of slow-wave sleep and decrease of paradoxical sleep times) and thereafter return to normal. Additionally, an hyperthermia appears during the third experimental day. The cortical and diencephalic noradrenaline content decrease to 70%. 3. The simultaneous lesion of both locus coeruleus and subcoeruleus nuclei is followed by the appearance of an aphagia adipsia syndrome in addition to the uro-genital syndrome. After these lesions, it is no long possible to find paradoxical sleep episodes in polygraphic recordings while the amount of slow wave sleep is normal. Cortical and diencephalic noradrenaline content decrease more than 50%. 4. In normal rats direct injection of 6 hydroxydopamine directly in both locus coeruleus and nuclei subcoeruleus had no discernable effects either on the behaviour or on the states of sleep. The cortical noradrenaline content decreased 30% below control values. 5. These results are consistent with but do not prove the hypothesis that part of the pontine tegmentum might play an important role in triggering paradoxical sleep episodes. The role of these regions in the regulation of internal temperature, food consumption and bladder motricity is also discussed.     

Studies on the electrogenic action of acetylcholine with Torpedo marmorata electric organ: V. Qualitative correlation between pharmacological effects and equilibration processes of the cholinergic receptor protein as revealed by the structural probe quinacrine

When the differential fluorescence emission at 515 nm of receptor-rich membrane fragments from Torpedo marmorata labelled with quinacrine is followed by energy transfer, addition of a high concentration of an agonist such as 0.4 mm-carbamylcholine or 0.4 mm-phenyltrimethylammonium causes a fast (unresolved) increase of fluorescence intensity followed by a slow (minute range) decrease, which leads to a final stable level. On the other hand, a stepwise addition of agonist at low concentrations gives only a slow fluorescence increase. Antagonists, such as flaxedil and d-tubocurarine, at all the concentrations tested, bring about exclusively slow fluorescence increases. Decamethonium at 0.4 mm gives no slow reaction but only a fast (unresolved) increase without transient overshoot.Addition of a local anaesthetic reduces the amplitude of the fluorescence response to carbamylcholine. The α-toxin from Naja nigricollis does not cause any change of fluorescence intensity but blocks the effect of the cholinergic agonists and antagonists.Dissolution of the membrane fragments by a non-ionic detergent abolishes the fast transient reaction triggered by the agonists but preserves the slow ones observed in the presence of agonists or antagonists. The data are interpreted in terms of a three-state model, a revised version of the model of Katz & Thesleff (1957): the fast transient reaction brought about by the agonists being assigned to the “activation” of the receptor-ionophore complex and the slow one to its “desensitization”.     

Spatiotemporal analysis of mycolactone distribution in vivo reveals partial diffusion in the central nervous system

Mycobacterium ulcerans, the causative agent of Buruli ulcer (BU) disease, is unique amongst human pathogens in its capacity to produce a lipid toxin called mycolactone. While previous studies have demonstrated that bacterially-released mycolactone diffuses beyond infection foci, the spatiotemporal distribution of mycolactone remained largely unknown. Here, we used the zebrafish model to provide the first global kinetic analysis of mycolactone’s diffusion in vivo, and multicellular co-culture systems to address the critical question of the toxin’s access to the brain.Zebrafish larvae were injected with a fluorescent-derivative of mycolactone to visualize the in vivo diffusion of the toxin from the peripheral circulation. A rapid, body-wide distribution of mycolactone was observed, with selective accumulation in tissues near the injection site and brain, together with an important excretion through the gastro-intestinal tract. Our conclusion that mycolactone reached the central nervous system was reinforced by an in cellulo model of human blood brain barrier and a mouse model of M. ulcerans-infection.Here we show that mycolactone has a broad but heterogenous profile of distribution in vivo. Our investigations in vitro and in vivo support the view that a fraction of bacterially-produced mycolactone gains access to the central nervous system. The relative persistence of mycolactone in the bloodstream suggests that assays of circulating mycolactone are relevant for BU disease monitoring and treatment optimization.     

Potential adaptive divergence between subspecies and populations of snapdragon plants inferred from QST–FST comparisons

Phenotypic divergence among natural populations can be explained by natural selection or by neutral processes such as drift. Many examples in the literature compare putatively neutral (F_ST) and quantitative genetic (Q_ST) differentiation in multiple populations to assess their evolutionary signature and identify candidate traits involved with local adaptation. Investigating these signatures in closely related or recently diversified species has the potential to shed light on the divergence processes acting at the interspecific level. Here, we conducted this comparison in two subspecies of snapdragon plants (eight populations of Antirrhinum majus pseudomajus and five populations of A. m. striatum) in a common garden experiment. We also tested whether altitude was involved with population phenotypic divergence. Our results identified candidate phenological and morphological traits involved with local adaptation. Most of these traits were identified in one subspecies but not the other. Phenotypic divergence increased with altitude for a few biomass‐related traits, but only in A. m. striatum. These traits therefore potentially reflect A. m. striatum adaptation to altitude. Our findings imply that adaptive processes potentially differ at the scale of A. majus subspecies.     

Association of CAT polymorphisms with catalase activity and exposure to environmental oxidative stimuli

We tested the hypotheses that catalase activity is modified by CAT single nucleotide polymorphisms (SNPs) (-262;-844), and by their interactions with oxidant exposures (coal dusts, smoking), lymphotoxin alpha (LTA, NcoI) and tumor necrosis factor (TNF, -308) in 196 miners. Erythrocyte catalase, superoxide dismutase, and glutathione peroxidase activities were measured. The CAT -262 SNP was related to lower catalase activity (104, 87 and 72 k/g hemoglobin for CC, CT and TT, respectively, p < 0.0001). Regardless of CAT SNPs, the LTA NcoI but not the TNF-308 SNP was associated with catalase activity (p = 0.04 and p = 0.8). CAT -262 T carriers were less frequent in highly exposed miners (OR = 0.39 [0.20–0.78], p = 0.007). In CAT -262 T carriers only, catalase activity decreased with high dust exposure (p = 0.01). Haplotype analyses (combined CAT SNPs) confirm these results. Results show that CAT -262 and LTA NcoI SNPs, and interaction with coal dust exposure, influenced catalase activity.     

2-Substituted-3H-indol-3-one-1-oxides: Preparation and Radical Trapping Properties

A series of 2-alkyl and 2-aryl substituted-3H-indol-3-one-1-oxides was prepared and evaluated for its radical trapping properties. Spin trapping and electron paramagnetic resonance experiments demonstrate the ability of these indolone-1-oxides to trap hetero- and carbon-centered radicals. The most stable spin adducts (lifetime of several hours) are obtained with 2-alkyl substituted nitrones, the 2-ethyl-5,6-dioxolo-3H-indolone-1-oxide, 5e and the 2-secbutyl-3H-indolone-1-oxide, 5f. These two nitrones are also sensitive to redox reactions in solution. Therefore this indolone-1-oxide series lacking a β-hydrogen atom gives rise to highly stable adducts with free radicals.