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Biomedical subjects

C Roche

Publications and source records attributed to C Roche.

At least 55 records · Page 3Linked to original sources
PubMed1996

A selenium-containing phospholipid-hydroperoxide glutathione peroxidase in Schistosoma mansoni.

The 100000Xg supernatant parasite platyhelminth Schistosoma mansoni exhibits a glutathione peroxidase activity with the substrate phosphatidylcholine hydroperoxide. Purification yielded a protein of 20 kDa molecular mass both on gel filtration column chromatography and SDS/PAGE, thus suggesting that S. mansoni expresses a protein similar to the mammalian selenoenzynic phospholipid-hydroperoxide glutathione peroxidase. Kinetic analysis and substrate specificity corroborated this assumption, the second-order rate constants for the oxidation of the ground-state enzyme (k+1) being higher with phosphatidylcholine hydroperoxide than with other peroxide substrates, such as cumene liydroperoxide or H2O2, and quantitatively similar to those of mammalian phospholipid-hydroperoxide glutathione peroxidase. Partial sequencing of the protein and selenium measurement by neutron activation analysis established that the purified peroxidase corresponded to the product of the S. mansoni gene previously reported and supposed to encode a selenium-containing glutathione peroxidase [Roche, C., Williams, D. L., Khalife, J., LePresle, T., Capron, A. & Pierce, R. J. (1994) Cloning and characterization of gene encoding Schistosoma mansoni glutathione peroxidase, Gene 138, 149 - 152]. S. mansoni thus contains a scienoperoxidase sharing molecular mass, catalytic efficiency and substrate specificity with phospholipid-hydroperoxide glutathione peroxidase, dismantling the concept that those enzymes are unique to vertebrate organisms.

Amino Acid Sequence↗
PubMed1996

Tissue localization and stage-specific expression of the phospholipid hydroperoxide glutathione peroxidase of Schistosoma mansoni.

The tissue localization and the stage-specific expression of the phospholipid hydroperoxide glutathione peroxidase of Schistosoma mansoni (SmPHGSHpx) have been determined. An antiserum raised against the C-terminal region of the predicted protein sequence was used for immunocytochemical investigations. The native protein is expressed only in female and egg vitelline cells and is practically absent from male worm tissue. Western blot data confirmed these results and showed the complete absence of SmPHGSHpx from cercariae. However, Northern blotting indicated the presence of the corresponding mRNA at all life-cycle stages investigated. The sequence determination of the 5' flanking region of the SmPHGSHpx gene revealed the presence of an extended TATA box (5'-TAAATA-3') at -32, a possible CAAT box at -75 and a putative monomeric estrogen response element 5'-GGTCAA-3' at position -486. In addition, direct and inverted repeat elements are present.

Amino Acid Sequence↗
PubMed1996

[Do corticotherapy and hemodilution decrease postoperative inflammation after maxillofacial surgery?].

OBJECTIVE: To assess the efficiency of corticosteroids and preoperative acute normovolaemic haemodilution (PANHD) in reducing postoperative inflammation after maxillofacial surgery. STUDY DESIGN: Randomized clinical trial. PATIENTS: Thirty-two patients scheduled to undergo maxillary osteotomy for facial dysmorphia were randomized into four groups of eight (PANHD or not; corticosteroids or not). METHODS: PANHD decreased haematocrit to 30%. In the corticosteroid groups, methylprednisolone 1.5 mg.kg-1 was given intravenously at the beginning of surgery (after PANHD in haemodiluted group), and after surgery, 1.5 mg.kg-1 iv daily for three days. Postoperative inflammation was assessed with an X-Ray technique (radiotelemetry) providing data on tissue thickness (extent of facial oedema), and by measurement of plasma concentrations of four acute phase proteins during the first postoperative week. RESULTS: No change in facial oedema and in acute phase proteins occurred with PANHD. Corticosteroids decreased postoperative oedema and acute phase proteins. CONCLUSION: Corticosteroids decrease postoperative inflammation after maxillofacial surgery but not PANHD.

Acute-Phase Proteins↗
PubMed1996

Multicentre evaluation of dengue IgM dot enzyme immunoassay.

BACKGROUND: The traditional methods used in the diagnosis of dengue infection do not lend themselves to field application. As such, clinical specimens have to be sent to a central laboratory for processing which invariably leads to delay. This affects patient management and disease control. The development of the dengue IgM dot enzyme immunoassay has opened up the possibility of carrying out the test in peripheral health settings. OBJECTIVES: This multicentre study was conducted to evaluate a new, commercial nitrocellulose membrane based IgM capture enzyme immunoassay. STUDY DESIGN: The sensitivity and specificity of the test were compared with in-house dengue IgM enzyme-linked immunoassays routinely performed by each of the selected centres. Known positive and negative dengue specimens, as well as specimens from non-dengue cases, were included in the evaluation. RESULTS: Based on 402 specimens tested by the six centres, the sensitivity was 92.1% and specificity 88.1%, with an overall agreement of 92.8% when compared with IgM EIA assays performed on microplates. CONCLUSIONS: The results suggest that this commercial kit has a role to play in the diagnosis of dengue infection, especially in peripheral health settings.

Antibodies, Viral↗
PubMed1996

Regulation of intestinal cholecystokinin gene expression by glucocorticoids.

The effect of glucocorticoids on the expression of intestinal cholecystokinin (CCK) was investigated both in vivo and in cell culture systems. In vivo, 2-day administration of methylprednisolone to adult male rats induced a decrease in CCK-like immunoreactivity (CCK-L1) and CCK mRNA levels in mucosal extracts. In two CCK-producing cell lines, RIN 1056E and STC-1 of pancreatic and intestinal origin respectively, dexamethasone induced dose-dependent decreases in both CCK-L1 and steady-state CCK mRNA levels. The decrease in CCK mRNA was totally prevented by incubation of cells with an excess of RU 38486, a competitive inhibitor for the binding of glucocorticoids to their receptor. Actinomycin D, used to prevent RNA synthesis, did not modify CCK mRNA stability in dexamethasone-pretreated cells as compared with cells not exposed to dexamethasone. When cells were first incubated with actinomycin D, subsequent addition of dexamethasone left the steady-state CCK mRNA levels unaltered in both cell lines. Nuclear run-on assays performed in RIN 1056E cells showed that glucocorticoids decreased the rate of transcription of the CCK gene. In addition, cycloheximide, used to prevent protein synthesis, abolished the inhibitory effects of dexamethasone on steady-state CCK mRNA levels. These results demonstrate that glucocorticoids down-regulate CCK gene expression in the rat intestinal mucosa and in two CCK-producing cell lines. The effect is blocked by a glucocorticoid receptor antagonist. Inhibition of CCK gene expression may result from a decrease in the transcription rate, and probably involves one or several steps that depend on protein synthesis.

Animals↗
PubMed1996

[Neurogenic muscle hypertrophy: 3 cases].

Three cases of neurogenic muscular hypertrophy are reported. First case presented a hypertrophy of one calf following S1 radiculopathy; the second had a hypertrophy of tibialis anterior muscle, five years after a compressive injury of the common peroneal nerve. The third case is a global hypertrophy of leg muscles after intensive care or legionella neuropathy. Previous cases of the literature are reviewed and the various pathophysiological hypothesis are considered. Among these hypothesis, the role of abnormal electrophysiological activities in most previous cases, as well as in ours (namely complex repetitive discharges and fasciculations), seems the most consistent.

Adult↗
PubMed1995

Interleukin-6 signal transducer gp130 has specific binding sites for different cytokines as determined by antagonistic and agonistic anti-gp130 monoclonal antibodies.

The cytokines interleukin (IL)-6, IL-11, ciliary neurotrophic factor (CNTF), leukemia inhibitor factor (LIF), oncostatin M (OSM) and probably the recently cloned cytokine cardiotrophin-1, signal, in combination with their specific receptors, through the common signal transducer gp130. Here, we report that the signaling activities of IL-6, IL-11, CNTF and OSM/LIF can be specifically blocked by different anti-gp130 monoclonal antibodies (mAb). Furthermore, we found two mAb, B-P8 and B-S12, which directly activate gp130 independently of the presence of cytokines or their receptors. This agonistic activity includes induction of cytokine-dependent cell proliferation and stimulation of acute-phase protein synthesis in liver cells. Compared to B-P8 mAb, the B-S12 mAb exhibited the strongest agonistic activity, while both mAb are synergistic in their action. This activity could not be blocked by inhibiting mAb against IL-6 and the IL-6 receptor. In contrast to F(ab')2 of B-S12 which still could activate gp130, Fab fragments completely lost their agonistic activity. Activation by tyrosine phosphorylation of the transcription factors Stat1 and APRF/Stat3 was also induced by B-S12 and B-P8, suggesting that both mAb induce homodimerization of gp130. Since hematopoietic stem cells express gp130 on their plasma membrane, it was anticipated that the agonistic anti-gp130 mAb could stimulate the proliferation of these stem cells. Indeed, B-S12 and B-P8 were able to stimulate CD34+ cells. In summary, our data show for the first time that mAb against gp130 can specifically block the action of distinct IL-6-type cytokines that signal through gp130. Such mAb might be of great value for therapeutic applications in diseases where a single cytokine action needs to be inhibited. In addition, the agonistic gp130 mAb may be used as growth factors for maintenance and expansion of stem cells prior to grafting.

Animals↗
PubMed1995

Acute normovolaemic haemodilution does not reduce the inflammatory process induced by facial surgery.

The place of preoperative acute normovolaemic haemodilution (haematocrit = 28%-32%) in reducing postoperative inflammation was evaluated after facial surgery. Thirty-two patients scheduled for mandibular osteotomy were randomized to a nonhaemodiluted group or to a haemodiluted group. The degree of postoperative inflammation was evaluated: first by an x-ray technique (radiotelemetry) providing measurements of the tissue thickness (quantitation of facial oedema), and second by the measurement of four acute phase protein plasma concentrations during the first postoperative week. Throughout the study, no changes in facial oedema or in variation of acute phase proteins were detected after haemodilution. It is concluded that acute normovolaemic haemodilution has no effect on the intensity of facial oedema and the biological inflammation process after facial surgery.

Acute-Phase Proteins↗
PubMed1995

Clinical experience with an inactivated hepatitis A vaccine.

Clinical trials of an inactivated hepatitis A vaccine have encompassed 104 studies completed by December 1993 in 27 countries. Studies involved 50,677 subjects and administration of > 120,000 vaccine doses. Results show that the vaccine is safe, clinically well-tolerated, and highly immunogenic in all age groups. A seroconversion rate of 100% is achieved 1 month after primary vaccination. Vaccine-induced antibody titers persist after a primary vaccination course for > or = 1 year with a single dose of 1440 ELISA units (EL.U.) in adults and after two doses of 360 EL.U. in children. A booster dose 6-12 months after the first vaccine dose induces very high antibody titers, which according to a mathematical model, are expected to protect against hepatitis A for > 20 years. The vaccine is equally immunogenic when administered simultaneously with other traveler vaccines, therefore enabling flexible and convenient vaccination against hepatitis A.

Adult↗
PubMed1994

Functional coupling between the cyclic adenosine monophosphate pathway and cholecystokinin secretion in RIN cells.

The cellular events associated with cAMP-dependent cholecystokinin (CCK) release were investigated with an X-ray induced rat pancreatic tumor cell line (RIN 1056 E). Forskolin dose-dependently stimulated the release of CCK. Agents that increase [Ca2+]i (thapsigargin, Bay K 8644, ionomycin) also stimulated the release of CCK. Conversely, absence of extracellular Ca2+ or cell treatment with various calcium channel blockers strongly reduced the forskolin-induced CCK release. Finally, the cAMP-kinase inhibitor H89, the calmodulin antagonist W7 and the Ca/calmodulin-dependent protein-kinase II inhibitor KN62 strongly inhibited the forskolin-evoked CCK secretion. We conclude that the release of CCK via a cAMP-dependent pathway is dependent on the activation of voltage-dependent calcium channels and may implicate protein kinase A, calmodulin and the Ca/calmodulin-dependent protein kinase II.

Adenoma, Islet Cell↗
PubMed1994

Cloning and characterization of the gene encoding Schistosoma mansoni glutathione peroxidase.

Antioxidant enzymes are thought to play a crucial role in the survival of the parasite, Schistosoma mansoni, during its migration through the tissues of the definitive host. We recently cloned the cDNA encoding one such enzyme, glutathione peroxidase (Gpx). In order to elucidate the regulation of expression of this gene, we describe the cloning and characterization of a Gpx gene of S. mansoni. An initial screen of a lambda EMBL4 genomic library using the corresponding cDNA sequence as a probe yielded 14 positive clones, two of which have so far been analyzed in detail. The complete Gpx gene contains five introns, four of which, located at the 5' end, are extremely short (30-51 bp) and the last of which is approximately 6 kb long. We present the sequence of the gene including 73 bp at the 5' end, the complete sequence to 137 bp downstream from the penultimate exon, 164 bp upstream and 131 bp downstream from the last 3' exon. The potential mRNA cap site is situated 219 bp upstream from the ATG start codon. All intron/exon junctions correspond to the conventional eukaryotic splice signal. Analysis of the 5' flanking region revealed the presence of a potential TATA box at--26 bp from the cap site, but no CAAT-like element is present. Southern blot analysis showed a unique Gpx gene organisation in the S. mansoni genome.

Amino Acid Sequence↗
PubMed1994

Correlation between detection of plasminogen cross-reactive antibodies and hemorrhage in dengue virus infection.

Although dengue fever (DF) is usually self-limited, some patients experience severe and prolonged illness characterized by capillary leakage, which may progress to hypovolemic shock (dengue hemorrhagic fever/dengue shock syndrome; DHF/DSS) with hemorrhage of unknown etiology. Development of antibodies potentially cross-reactive to plasminogen has been reported in a high percentage of Thai patients with DF and DHF/DSS. Correlation between detection of plasminogen cross-reactive antibodies and hemorrhage was evaluated in 88 Tahitian children with dengue virus type 3 infection who presented with (n = 59) or without (n = 29) hemorrhage. Plasminogen cross-reactive antibodies were found in acute and convalescent sera of 33 and 11 children, respectively (56% vs. 31%, P < .05), and closely paralleled antibodies to the cross-reactive site in dengue virus E protein. Antibodies were more frequent in children with secondary than primary infections (60% vs. 32%, P < .05). Plasminogen cross-reactive antibodies did not correlate with occurrence of DHF/DSS or thrombocytopenia. These results are consistent with the possibility that plasminogen cross-reactive antibodies play a role in the etiology of hemorrhage in dengue virus infection.

Adolescent↗