A tomato enzyme catalyzing the phosphorylation of 3,4-dihydroxy-2-butanone

A riboflavin biosynthesis ribB mutant of Escherichia coli deficient of 3,4-dihydroxy-2-butanone 4-phosphate synthase was complemented with a cDNA library from Lycopersicon esculentum. The complementing gene was isolated and expressed in E. coli. The resulting protein was shown to specify a 62 kDa protein which phosphorylates dihydroxyacetone, both enantiomers of 3,4-dihydroxy-2-butanone, and several other aldoses and ketoses. Sequence analysis revealed homology to dihydroacetone kinases (dak) genes from plants, animals, fungi and some eubacteria. Genes with similarity to the 5' part of the dak gene from tomato were found in many other eubacteria. The physiological role of the dak gene is still incompletely known.     

Stereochemistry of strictic acid and related furano-diterpenes from conyza japonica and grangea maderaspatana

Extraction of Conyza japonica gave strictic acid, ent-2β-hydroxy-15,16-epoxy-3,13(16),14-clerodatrien-18-oic acid and 5,7-dihydroxy-3,8,4′-trimethoxyflavone. Extraction of Grangea maderaspatana gave (-)-hardwickiic acid, ent-15,16-epoxy-1,3,13(16),14-clerodatetraen-18-oic acid and 3-hydroxy-8-acetoxypentadeca-1,9,14-trien-4,6-diyne. The structure of ent-2β-hydroxy-15,16-epoxy-3,13(16),14-cleroclatrien-18-oic acid was deduced by spectroscopic methods and by partial synthesis from (-)-hardwickiic acid and the stereochemistries of strictic acid and (ent-15,16-epoxy-1,3,13(16),14-clerodatraen-18-oic acid were established by correlation with ent-2β-hydroxy-15,16-epoxy-3,13(16),14-clerodatrien-18-oic acid.     

Shifting the phase of the circadian rhythm in bioluminescence in gonyaulax with vanillic Acid

Exposure for 4 hours to vanillic acid (4-hydroxy 3-methoxy benzoic acid) caused large delay phase shifts (5 to 6 hours) in the circadian rhythm of bioluminescence in Gonyaulax polyedra, when assayed at either 10 to 14 circadian time or 22 to 02 circadian time in constant light and temperature, provided that the pH of the medium was 7.1 or lower. Corresponding changes in the pH with acetic acid did not shift phase. Vanillic acid caused detectable depolarization of the membranes of Gonyaulax, as demonstrated with the cyanine dye fluorescence technique.     

β-Endorphin-like immunoreactivity in plasma,pituitaries and hypothalamus of rats following treatment with opiates

β-Endorphin was measured using a radioimmunoassay (RIA) in plasma, pituitary lobes and hypothalamus of rats following treatment with the opiate agonist morphine and the antagonist naloxone. β-Endorphine-like immunoreactivity (β-ELI) in plasma was found to be increased after high doses of morphine (50 mg/kg i.p.). A high increase of β-ELI in plasma was further observed in morphine tolerant/dependent rats after precipitated withdrawal by naloxone. This release of β-ELI into plasma was accompanied by a significant reduction of β-ELI content in the anterior lobe of the pituitary and the hypothalamus but not in the intermediate/posterior lobe of pituitary. Chronic treatment of the rats by the s.c. implantation of morphine pellets (each containing 75 mg morphine; 6 within 10 days) did not alter β-ELI levels in plasma and in the pituitary lobes. A long term administration of morphine (21 pellets within 1 month), however, causes a significant reduction of the β-ELI content of anterior lobe and intermediate/posterior lobe of pituitary without changing the β-ELI levels in plasma.     

Characteristics of a monoclonal beta-endorphin antibody recognizing the N-terminus of opioid peptides

The properties of a mouse monoclonal antibody to beta-endorphin secreted by a clone of hybrid myelomas (3-E7) are described. The antibody displays virtually complete cross-reactivity to met-enkephalin and leu-enkephalin, but no cross-reactivity to beta-lipotropin, alpha-N-acetyl-beta-endorphin and des-Tyr1-beta-endorphin. Substantial cross-reactivity is seen with some other naturally occurring opioid peptides bearing the enkephalin sequence, such as dynorphin, alpha-neo-endorphin and BAM 22, but cross-reactivity is lacking in the case of certain synthetic enkephalin derivatives possessing a D-amino acid in position 2. The data indicate that for the binding of an antigen to the antibody the N-terminal tyrosine moiety is essential. The antibody recognizes, thus, a site which is of functional significance for the interaction of many naturally occurring opioid peptides with the opiate receptor.     

Xanthones from Calophyllum teysmannii var. inophylloide

Further study of the wood of Calophyllum teysmannii Miq. var. inophylloide yielded xanthones 7-hydroxy-1,2,8-trimethoxyxanthone, 6-hydroxy-1,2,5-trimethoxyxanthone, and 2-carbomethoxy-6-methoxyxanthone in addition to 3,8-dihydroxy-1,2,4-trimethoxyxanthone, 3-hydroxy-2,4-dimethoxyxanthone, 1,7-dihydroxy-3-methoxyanthone (gentisin) and 2-hydroxyxanthone.     

Ent-norlabdane triols from Austroeupatorium inulaefolium

Two new ent-norlabdane triols were isolated from the above-ground parts of Austroeupatorium inulaefolium.     

Blocking IL-15 prevents the induction of allergen-specific T cells and allergic inflammation in vivo

IL-15 has been shown to accelerate and boost allergic sensitization in mice. Using a murine model of allergic sensitization to OVA, we present evidence that blocking endogenous IL-15 during the sensitization phase using a soluble IL-15Ralpha (sIL-15Ralpha) suppresses the induction of Ag-specific, Th2-differentiated T cells. This significantly reduces the production of OVA-specific IgE and IgG and prevents the induction of a pulmonary inflammation. Release of proinflammatory TNF-alpha, IL-1beta, IL-6, and IL-12 as well as that of Th2 cytokines IL-4, IL-5, and IL-13 into the bronchi are significantly reduced, resulting in suppressed recruitment of eosinophils and lymphocytes after allergen challenge. It is of clinical relevance that the airway hyper-responsiveness, a major symptom of human asthma bronchiale, is significantly reduced by sIL-15Ralpha treatment. Ex vivo analysis of the draining lymph nodes revealed reduced numbers of CD8, but not CD4, memory cells and the inability of T cells of sIL-15Ralpha-treated mice to proliferate and to produce Th2 cytokines after in vitro OVA restimulation. This phenomenon is not mediated by enhanced numbers of CD4(+)/CD25(+) T cells. These results show that IL-15 is important for the induction of allergen-specific, Th2-differentiated T cells and induction of allergic inflammation in vivo.