Decouverte du genre Iowaphyllum (Tetracoralliaire) dans un biostrome eodevonien du Cotentin

After a few remarks on the coral fauna in deposits near La Roquelle in Cotentin, the genus Iowaphyllum is identifiedfor the first time in France. One species (I. bohemicum) is described here; it brings new paleogeographic and stratigraphic data.     

Isozyme differentiation of aldolase and pyruvate kinase in fetal,regenerating, preneoplastic,and malignant rat hepatocytes during culture

Summary Aldolase and pyruvate kinase isozymes were investigated in cultured hepatocytes from fetal, regenerating, and 2-acetyl-aminofluorene-fed rat liver as well as in some epithelial liver cell lines. Our results show that: (a) cell proliferation and prolonged expression of specific isozymes were found only in cultured hepatocytes from 17-day old fetuses; (b) the fetal type of pyruvate kinase expressed in regenerating and carcinogen-treated liver was temporarily lost only in cultured hepatocytes from regenerating liver; (c) the adult type of aldolase and pyruvate kinase was absent in one epithelial cell line derived from a carcinogen-treated liver and in the hepatoma tissue cell (HTC) line but was found in the Faza clone of the Reuber H₃₅ cell line during the 50 first passages in vitro; and (d) the isozyme pattern of pyruvate kinase was always more strongly shifted than that of aldolase. The observations suggest that: (a) hepatocytes from carcinogen-treated liver exhibit the same lack of ability to proliferate in primary culture as normal adult hepatocytes; (b) adult hepatocytes can produce fetal isozymes without prior cell division; (c) pyruvate kinase is a stronger marker of dedifferentiation (retrodifferentiation) than aldolase; and (d) regulatory processes of isozyme expression are different during ontogenesis, regeneration, and hepatocarcinogenesis. This work was supported by the “Institut National de la Santé et de la Recherche Médicale” and the “Fondation pour la Recherche Medicale Fran?aise”     

Site-specific mutagenesis of an essential histidine residue in pancreatic cholesterol esterase

The histidine residue essential for the catalytic activity of pancreatic cholesterol esterase (carboxylester lipase) has been identified in this study using sequence comparison and site-specific mutagenesis techniques. In the first approach, comparison of the primary structure of rat pancreatic cholesterol esterase with that of acetylcholinesterase and cholinesterase revealed two conserved histidine residues located at positions 420 and 435. The sequence in the region around histidine 420 is quite different between the three enzymes. However, histidine 435 is located in a 22-amino acid domain that is 47% homologous with other serine esterases. Based on this sequence homology, it was hypothesized that histidine 435 is the histidine residue essential for catalytic activity of cholesterol esterase. The role of His435 in the catalytic activity of pancreatic cholesterol esterase was then studied by the site-specific mutagenesis technique. Substitution of the histidine in position 435 with glutamine, arginine, alanine, serine, or aspartic acid abolished the ability of cholesterol esterase to hydrolyze p-nitrophenyl butyrate and cholesterol [14C]oleate. In contrast, mutagenesis of the histidine residue at position 420 to glutamine had no effect on cholesterol esterase enzyme activity. The results of this study strongly suggested that histidine 435 may be a component of the catalytic triad of pancreatic cholesterol esterase.     

The regulatory effect of histamine on the immune response: characterization of the cells involved

Any immunological response is the end result of the equilibrium between many positive and negative regulatory factors. It has been recently demonstrated that histamine receptor-bearing T lymphocytes could play a role in this regulation. This work aims to study the effects of different cell populations after incubation with histamine on the proliferative response of normal lymphocytes. The histamine-incubated peripheral blood lymphocytes (PBL) lower the proliferative response of normal cells toward mitogens (phytohemagglutinin, concanavalin A) and antigens (mixed lymphocyte culture). In order to precise the cell subpopulations involved in this suppression, PBL have been depleted of adherent cells and B and T lymphocytes have been purified by a standard rosette technique. The enriched B cells do not suppress the normal response but the suppressor activity of T cells, as well as adherent cell-depleted PBL, are significantly reduced compared to the one of PBL. The initial suppressor activity is restored by addition of 1% adherent cells (and not 5 or 10%) to adherent cell-depleted lymphocytes and 10% adherent cells (not 1 or 5%) to T-enriched population. These observations suggest a role for adherent cells in this regulation.     

Alteration of secretin-stimulated cardiac adenylate cyclase activity in rats with portacaval shunt

Wistar rats were submitted to portacaval anastomosis (PCA). Control rats were sham-operated and pair-fed (SOPF). After 3 weeks, PCA led to the hypertrophy of right atrium (+50%), left atrium (+67%) and both ventricles (+26%). The response of adenylate cyclase activity to secretin was specifically and markedly decreased in membranes from atria (-51 to 59%) and ventricles (-68 to 69%). These data suggest a decrease in the number of functional secretin receptors in heart considering that: the half-maximal stimulatory secretin concentration was unchanged; glucagon stimulations were unaltered and D,L-isoproterenol stimulations were hardly affected; the Gpp(NH)p-, NaF-, and forskolin-stimulated adenylate cyclase activities were moderately decreased (in ventricles, by 14-28%) or unchanged (in atria).     

Effect of cultural conditions on the protein and lipopolysaccharide profiles of Haemophilus ducreyi analysed by SDS-PAGE

Abstract A comparative study of the protein and lipopolysaccharide (LPS) profiles of 8 strains of Haemophilus ducreyi revealed that protein patterns remained unaffected by changes in medium composition, atmospheric conditions and temperature. In contrast, the LPS patterns exhibited marked variations under the different cultural conditions.     

Rotavirus VP4 and VP7-Derived Synthetic Peptides as Potential Substrates of Protein Disulfide Isomerase Lead to Inhibition of Rotavirus Infection

Rotavirus infection of MA104 cells has been shown to be inhibited by cell membrane-impermeant thiol/disulfide exchange inhibitors and anti-PDI antibodies. To characterise the amino acid sequences of rotavirus structural proteins potentially mediating cell surface PDI?Csubstrate interactions, rotavirus-derived peptides from VP4 and VP7 (RRV) and VP7 (Wa), and their modified versions containing serine instead of cysteine were synthesized. Cysteine-containing VP7 peptides corresponding to residues 189?C210 or 243?C263 caused an infectivity inhibitory effect of about 64 and 85?%, respectively, when added to cells. Changing cysteine to serine significantly decreased the inhibitory effect. A cysteine-containing peptide corresponding to VP4 residues 200?C219 and its scrambled version reduced infectivity by 92 and 80?%, respectively. A cysteine to serine change in the original VP4 200?C219 peptide did not affect its inhibitory effect. Non-rotavirus related sequences containing cysteine residues efficiently inhibited rotavirus infectivity. Antibodies against VP7 residues 189?C210 or 243?C263 significantly inhibited rotavirus infectivity only after virus attachment to cells had occurred, whereas those against VP4 200?C219 peptide inhibited infectivity irrespective of whether virus or cell-attached virus was antibody-treated. A direct PDI?Cpeptide interaction was shown by ELISA for cysteine-containing VP7 and VP4 peptides. Virus?Ccell attachment was unaffected by the peptides inhibiting virus infectivity. The results showed that even though cysteine residues in the peptides tested are important in both virus infectivity inhibition and in vitro PDI?Cpeptide interaction, the accompanying amino acid sequence also plays some role. As a whole, our findings further support our hypothesis that cell surface PDI from MA104 cells might be contributing to rotavirus entry at a post-attachment step.