Topical anti-inflammatory activity of some Mediterranean marine species.
Explore the source record for details and available documents.
Administration, Topical↗
Biomedical subjects
R Blasco
Publications and source records attributed to R Blasco.
Effect of fatty acid anilides on immune responses of Swiss mice.
The possible relationship between fatty acid anilides and the toxic oil syndrome (TOS) which appeared in Spain in 1981 has been debated during recent years. These anilides have been detected as anomalous compound in toxic oils analysed. After treatment with one daily dose of 50 mg/kg of oleilanilide (88.86% pure) for 5 days, animals showed a tendency towards progressive loss of body weight and a significant increase in serum concentration of immunoglobulins. The percentage of suppressor T cells in spleen diminished significantly compared with the control group. Consequently, an increase in the helper T cells/suppressor T cells was also observed. The production of IgM and IgG in culture was significantly higher than in controls and no differences were seen in IgA synthesis. The functional studies of generation of specific IgM, IgA and IgG suppressor cells at variable doses of concanavalin A (Con A) showed paradoxical behaviour of suppressor T cells generated by low doses of Con A. A similar change occurred at higher doses of Con A. These results suggest that low-dose treatment with oleilanilides induces an alteration in the immune response in Swiss mice.
Anilides↗
Selective inhibition of calcium entry induced by benzylisoquinolines in rat smooth muscle.
The mechanism of relaxant activity of six benzylisoquinolines was examined in order to determine the minimal structural requirements that enable these compounds to have either a non-specific action like papaverine or an inhibitory activity on calcium entry via potential-operated channels. All the alkaloids tested totally or partially relaxed KCl-depolarized rat uterus and inhibited oxytocin-induced rhythmic contractions. Only glaucine and laudanosine inhibited K(+)-induced uterine contractions more than oxytocin-induced uterine contractions. In Ca(+)-free medium, sustained contractions induced by oxytocin or vanadate were relaxed by the alkaloids tested except for glaucine and laudanosine indicating no inhibitory effect on intracellular calcium release. Those alkaloids containing an unsaturated heterocyclic ring (papaverine, papaverinol, papaveraldine, N-methylpapaverine and dehydropapaverine) exhibited a more specific activity than those with a tetrahydroisoquinoline ring.
Alkaloids↗
Light-dependent degradation of nitrophenols by the phototrophic bacterium Rhodobacter capsulatus E1F1.
Rhodobacter capsulatus E1F1, a phototrophic purple nonsulfur bacterium capable of photoassimilating nitrate or nitrite, grew phototrophically in the presence of mono- and dinitrophenols with acetate as a carbon source, the highest growth levels being obtained under microaerobic conditions. Utilization of 2,4-dinitrophenol was strictly light dependent, was inhibited by O2 and by ammonium, and took place with the simultaneous and stoichiometric production of 2-amino-4-nitrophenol, which accumulated in the medium and was poorly used for further growth in anaerobiosis. Metabolism of mononitrophenols was also light dependent but was activated by O2 and by ammonium. Metabolism of nitrophenols seemed to depend on inducible systems which were repressed in nitrogen-starved cells. Induction of the in vivo 2,4-dinitrophenol reducing system was strongly inhibited by chloramphenicol.
2,4-Dinitrophenol↗
Role of cell-associated enveloped vaccinia virus in cell-to-cell spread.
The roles of intracellular naked (INV), cell-associated enveloped (CEV), and extracellular enveloped (EEV) forms of vaccinia virus in cell-to-cell and longer-range spread were investigated by using two closely related strains of vaccinia virus, WR and IHD-J. We confirmed previous results that WR and IHD-J produced similar amounts of INV and formed similar-size primary plaques but that IHD-J produced 10 to 40 times more EEV and spread to distant cells much more efficiently than did WR. Nevertheless, cells infected with WR and IHD-J had similar amounts of CEV, indicating that wrapping and transport of WR virions were unimpaired. A WR mutant with a deletion in VP37, the major outer envelope protein, formed normal amounts of INV; however, the generation of CEV was blocked and plaque formation was inhibited. These results suggested that CEV is the form of virus that mediates cell-to-cell spread. Marker rescue experiments indicated that the differences in EEV production by WR and IHD-J were not due to sequence differences in VP37. The low amount of WR EEV could be attributed to retention of CEV on the cell membrane. In support of this hypothesis, mild treatment with trypsin released as much or more infectious virus from cells infected with WR as it did with cells infected with IHD-J. Most of the virus released by trypsin sedimented with the buoyant density of EEV. Also, addition of trypsin to cells following inoculation with WR led to a comet-shaped distribution of secondary plaques characteristic of IHD-J. These results demonstrated that the release of CEV from the cell surface was limiting for extracellular virus formation and affirmed the role of EEV in long-range spread.
Base Sequence↗
[Familial recurrent paralysis of the brachial plexus. Tomaculous neuropathy].
Familial recurrent plexopathy related to tomacular neuropathy is only the localized expression, with a familial predisposition, of a more diffuse disease. Such are the conclusions we drew from a study of 3 cases, in 2 families, of recurrent tomacular brachial plexopathy. In all 3 cases the condition was transmitted by the mother as an autosomal dominant trait. Biopsy of a sensory nerve was performed in 2 cases and showed, in one, typical images of myelinic degeneration at various stages, corresponding to the formation of tomacular tickenings. Tomacular brachial plexopathy must be distinguished from hereditary amyotrophic neuralgia.
Adolescent↗
Escherichia coli thymidine kinase: nucleotide sequence of the gene and relationships to other thymidine kinases.
The thymidine kinase (TK)-encoding gene (tdk) of Escherichia coli is located at min 27 of the E. coli genetic map. Sequence analysis of this region revealed an open reading frame of 205 codons. Identification of this region as the E. coli tdk gene was confirmed by its similarity to other TK-encoding genes. The E. coli amino acid (aa) sequence showed significant similarity to the corresponding TK polypeptides of vertebrates and large DNA viruses, but showed no similarity to known herpes virus TK enzymes. Mapping of highly conserved positions among all sequences indicates the importance of these residues for catalytic activity and may facilitate further functional studies. Using a distance matrix method, the evolutionary relationships among the TK aa sequence of poxviruses, eukaryotes and prokaryotes were analyzed and a potential phylogenetic tree was established.
Amino Acid Sequence↗
Inhibition of calcium entry induced by cularines and isocrasifoline in uterine smooth muscle.
The effects of nifedipine, papaverine and four benzylisoquinoline alkaloids (cularine, cularidine, celtisine and isocrasifoline) were studied in isolated rat uterus in order to clarify the mechanism of their relaxant action. All the compounds tested completely relaxed KCl-induced contractions and totally or partially inhibited oxytocin-induced rhythmic contractions. Only papaverine acted intracellularly, promoting relaxation of contractile responses induced by oxytocin or vanadate in a Ca(2+)-free medium. In spite of the structural relationship between papaverine and the other alkaloids, the mechanism of their relaxant action is not the same. The activities of cularine derivatives and of isocrasifoline were similar to that of nifedipine.
Alkaloids↗
Extracellular vaccinia virus formation and cell-to-cell virus transmission are prevented by deletion of the gene encoding the 37,000-Dalton outer envelope protein.
There are two types of infectious vaccinia virus particles: intracellular naked virions and extracellular enveloped virions (EEV). To determine the biological role of the enveloped form of vaccinia virus, we produced and characterized a mutant that is defective in EEV formation. The strategy involved replacement by homologous recombination of the gene F13L, encoding a 37,000-Da protein (VP37) that is specific for the outer envelope of EEV, with a selectable antibiotic resistance marker, the Escherichia coli gpt gene. Initial experiments, however, suggested that such a mutation was lethal or prevented plaque formation. By employing a protocol consisting of high-multiplicity passages of intracellular virus from the transfected cells and then limiting dilution cloning, we succeeded in isolating the desired mutant, which was defective in production of plaques and extracellular virus but made normal amounts of intracellular naked virions. Electron microscopic examination indicated that the mutant virus particles, unlike wild type, were neither wrapped with Golgi-derived membranes nor associated with the cell surface. The absence of VP37 did not prevent the transport of the viral hemagglutinin to the plasma membrane but nevertheless abrogated both low-pH- and antibody-mediated cell fusion. These results indicate that VP37 is required for EEV formation and also plays a critical role in the local cell-to-cell transmission of vaccinia virus, perhaps via enveloped virions attached to or released from the cell membrane. By contrast, a mutated virus with a deletion of the K4L open reading frame, which is a homolog of the VP37 gene, was not defective in formation of plaques or EEV.
Animals↗
Sequence analysis, expression, and deletion of a vaccinia virus gene encoding a homolog of profilin, a eukaryotic actin-binding protein.
A 4,500-bp BamHI fragment, located within the HindIII A segment of the vaccinia virus genome, was found to contain eight potential coding regions for polypeptides of 78 to 346 amino acids. The open reading frames with 133, 346, and 125 codons were homologous to profilin (an actin-binding protein), 3-beta-hydroxysteroid dehydrogenase, and Cu-Zn superoxide dismutase, respectively. Sequence alignments indicated that the vaccinia virus and mammalian profilins were more closely related to each other than to known profilins of other eukaryotes. The expression and possible role of the profilin homolog in the virus replicative cycle were therefore investigated. Antibody raised to Escherichia coli expressed vaccinia virus profilin was used to demonstrate the synthesis of the 15-kDa polypeptide at late times after vaccinia virus infection of mammalian cells. The protein accumulated in the cytoplasm, but only trace amounts remained associated with highly purified virions. The isolation of vaccinia virus mutants (in strains WR and IHD-J), with nearly the entire profilin gene replaced by the E. coli gpt gene, indicated that the protein is not essential for infectivity. The characteristic vaccinia virus-induced changes in actin fibers, seen by fluorescence microscopy, occurred in cells infected with the mutant. Moreover, the virus-encoded profilin homolog was not required for actin-associated events, including intracellular virus movement to the periphery of the cell, formation of specialized microvilli, or release of mature virions, as shown by electron microscopy and yields of infectious intra- and extracellular virus.
3-Hydroxysteroid Dehydrogenases↗
[Neuroimaging of Jakob-Creutzfeldt disease: bilateral hyperintensity of basal ganglia in magnetic resonance].
Explore the source record for details and available documents.
Basal Ganglia↗
Analysis of naturally occurring deletion variants of African swine fever virus: multigene family 110 is not essential for infectivity or virulence in pigs.
A comparison of uncloned African swine fever virus isolates with their cloned counterparts revealed the presence of genetic variants in three out of seven uncloned field virus populations tested. Five different virus clones were isolated from the uncloned KIR69 virus stock by limit dilution. Structural analysis of the variants showed that they differed by single deletions of 10-16 kilobases in the region located between 6.8 and 27 kilobases from the left DNA terminus. There was no homology between DNA sequences immediately to the left and right of the deletions indicating that the mechanism generating deletion variants was not homologous recombination. The alignment of the restriction maps of the variants with those of other virus isolates indicated that two of the variants lacked the whole multigene family 110. This was confirmed by hybridization of the viral DNA with a degenerate oligonucleotide probe. Each virus variant replicated to high titer and was virulent in domestic pigs. Therefore, the multigene family 110 was not required for viral replication or virulence in domestic pigs. The virus variants were stable upon repeated passage in swine macrophages, indicating that the generation of variants is not a frequent genetic event in vitro.
African Swine Fever↗
Genetic variation and multigene families in African swine fever virus.
The genome of a virulent strain (LIS57) of African swine fever virus differs from that of the Vero-cell-adapted strain (BA71V) in several deletions located in the variable regions. The region which contains the most differences is located 8-20 kb from the left end. The DNA sequence of this region was obtained from LIS57 virus DNA and compared with the overlapping sequences of BA71V virus. This comparison revealed that the changes in the variable regions result in differences in the number of genes which belong to the multigene families 360 and 110. Virus isolate LIS57 contains at least 8 genes of the multigene family 360 and 12 genes of the multigene family 110, instead of the 6 and 5 genes, respectively, found in BA71V virus strain. The position of the deletions indicates that new combinations of multigene family members in African swine fever virus DNA may arise by in-frame recombination between homologous genes. These data indicate that the evolution of the multigene families 360 and 110 in African swine fever virus DNA has involved different processes, including gene duplication, divergence of duplicated genes, and gene deletion.
African Swine Fever Virus↗
Sequence and evolutionary relationships of African swine fever virus thymidine kinase.
The thymidine kinase gene of African swine fever virus was mapped in a 1.4-kb EcoRI-PstI fragment located in the left half of the Eco RI K fragment of African swine fever virus DNA by using degenerate oligonucleotide probes derived from regions of the thymidine kinase sequence conserved in several poxviruses, man, mouse, and chicken. The nucleotide sequence of this region revealed an open reading frame of 196 codons, whose translated amino acid sequence showed significant similarity to the thymidine kinases of vaccinia virus, variola virus, monkeypox virus, shope fibroma virus, fowlpox virus, capripox virus, man, mouse, and chicken. The similarity scores obtained after comparison of known thymidine kinase sequences indicated that the African swine fever virus thymidine kinase is more distantly related than the poxvirus thymidine kinases to their cellular homologs. The evolutionary implications of these findings are discussed.
African Swine Fever Virus↗
Multigene families in African swine fever virus: family 110.
The genome of African swine fever virus was screened for the existence of repetitive sequences by hybridization between different cloned restriction fragments covering the viral DNA. Several sets of repeated sequences were detected in fragments located close to the DNA ends. One of these groups of repetitions involved fragments located at both ends of the genome. The remaining groups involved fragments that were located exclusively at the left end. The sequence of a 3.2-kilobase segment spanning from 7.5 to 11 kilobases from the left DNA end, which showed a complex pattern of cross-hybridizations, was determined. Two short and three long blocks of direct repeated sequences were found in this DNA region, which accounted for the hybridization results. The repeated sequences formed a family of five homologous genes with an average length of 116 codons (multigene family 110), one of which had a dimeric structure. Transcripts of the five members of the family were detected both in RNA synthesized in vitro by purified African swine fever virions and in RNA isolated at early times after infection. Comparison of the predicted protein sequences revealed a striking conservation of a cysteine-rich domain in the central part of the proteins. In addition, a highly hydrophobic NH2-terminal sequence present in all the proteins suggests that these proteins are processed through the endoplasmic reticulum.
African Swine Fever Virus↗
Multigene families in African swine fever virus: family 360.
A group of cross-hybridizing DNA segments contained within the restriction fragments RK', RL, RJ, and RD' of African swine fever virus DNA were mapped and sequenced. Analysis of these sequences revealed the presence of a family of homologous open reading frames in regions close to the DNA ends. The whole family is composed of six open reading frames with an average length of 360 coding triplets (multigene family 360), four of which are located in the left part of the genome and two of which are in the right terminal EcoRI fragment. In close proximity to the right terminal inverted repeat, we found an additional small open reading frame which was homologous to the 5'-terminal portion of the other open reading frames, suggesting that most of that open reading frame has been deleted. These repeated sequences account for the previously described inverted internal repetitions (J.M. Sogo, J.M. Almendral, A. Talavera, and E. Viñuela, Virology 133:271-275, 1984). Most of the genes of multigene family 360 are transcribed in African swine fever virus-infected cells. A comparison of the predicted protein sequences of family 360 indicated that several residues are conserved, suggesting that an overall structure is maintained for every member of the family. The transcription direction of each open reading frame, as well as the evolutionary relationships among the genes, suggests that the family originated by gene duplication and translocation of sequences between the DNA ends.
Amino Acid Sequence↗
Study of delayed neurotoxicity caused by fatty acid anilides in hens.
We have observed that the oral administration of a single dose of a mixture of oleyl and linoleylanilides (80 mg/kg) in adult hens determines the apparition of delayed muscular neuropathy, which we have compared to that induced by metamidophos as a model of organophosphate-induced delayed neuropathy (OPIDN). We have compared the modifications produced by each of the 2 treatments on the enzymatic activity of neuropathy target esterase (NTE) measured in nervous tissue homogenates of brain, medulla and sciatic nerve. In addition we determined total esterases (TE), acetylcholine esterase (AchE) and serum creatine phosphate kinase (CPK). The organophosphate compound (OP) induced an initial reduction in the activity of NTE, TE and AchE which was reestablished 48 h later, except for brain TE which increased slowly during the latency period. This behaviour was accompanied by a permanent increase in the activity of serum CPK. Anilides induced a strong activation of AchE, NTE and TE (except brain TE) in the first 24-36 h. Normal levels were relatively quickly reestablished in brain (by 48 h) and slowly in medulla and sciatic nerve. But the AchE activity remained high throughout the whole period of latency. This activity level coincided with the AchE level observed at the onset of signs in animals dosed with OPs. CPK was also increased in sciatic nerve at 15 d but was depressed in serum throughout the whole latency period. Substances with chemical characteristics very different from OPs can induce a delayed neuropathy with modification of the activity of NTE.
Acetylcholinesterase↗