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C Renaud

Publications and source records attributed to C Renaud.

At least 19 recordsLinked to original sources
PubMed2006

[Perinatal consequences of maternal connective tissue diseases: a prospective study of 73 cases].

AIM: To describe a group of newborns born from mothers with connective tissue diseases, to determine their perinatal characteristics and the neonatal morbidity, and to assess the possible role of drugs received by mothers on the obstetrical and neonatal morbidity. PATIENTS AND METHODS: During a 34-month period, newborns born from mothers with connective tissue diseases and followed in a single center were prospectively included in the study. In all cases, maternal treatments (i.e. hydroxychloroquine and/or prednisone) were continued during pregnancy. RESULTS: Among the 73 included infants, 18 (25%) were born before 37 weeks of gestation and 3 (4%) were small for gestational age. A neonatal lupus syndrome with facial rash and thrombopenia was observed in 1 case. No neonatal congenital heart block was observed and maternal treatment did not significantly influence the mean PR or QT intervals. Four infants had minor congenital abnormalities and 3 had feto-maternal infection. CONCLUSION: These data show that perinatal morbidity is lower than that previously published. We postulate that a strict follow-up during pregnancy may have played a significant positive role in these results.

Adult↗
PubMed2004

[Surgical management of emphysema].

Surgery is an important therapeutic option for emphysema patients with invalidating dyspnea and poor quality-of-life. Preoperative tests must determine the degree of functional impairment (dyspnea score, walking test, quality-of-life) and evaluate lesion reversibility (imaging, function tests, TLCO, blood gases, scintigraphy, right microcatheterism) and assess the patient's general health status. Besides lung transplantation, the only surgical alternative is resection which, depending on the type of parenchymal damage, can involve excision of bullae or volume reduction. Several modalities can be proposed: atypical resection of the apexes via sternotomy, multiple unilateral atypical resection, simple lobectomy. The choice depends on the distribution of the parenchymal destruction and also on the severity of the emphysema and the patient's age. Operative mortality is now well below 10%. Volume reduction provides significant functional improvement in 80% of patients but with a temporary effect (4-5 years). Bullae excision is particularly important since functional recovery is achieved early and persists.

Dyspnea↗
PubMed1995

12(S)-HETE is a mitogenic factor for microvascular endothelial cells: its potential role in angiogenesis.

12(S)-HETE [12(S)-hydroxyeicosatetraenoic acid] is a lipoxygenase metabolite of arachidonic acid. Treatment of murine-lung-derived microvascular endothelial cells (CD clone 4) with exogenous 12(S)-HETE promoted wound healing of injured endothelial cell monolayers. 12(S)-HETE, in a time- and dose-dependent manner, enhanced the growth of CD clone 4 cells. Thymidine incorporation assays demonstrated that 12(S)-HETE increased the DNA synthesis by > 4 fold. In addition, normal endothelial cell growth stimulated by serum could be dose-dependently inhibited by a select 12-lipoxygenase inhibitor (BHPP), suggesting that 12(S)-HETE is a physiological mitogenic factor for microvascular endothelial cells.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1995

Solid tumor cells express functional "tethered ligand" thrombin receptor.

Previous work demonstrated that alpha-thrombin promoted tumor cell adhesion to endothelium and extracellular matrix as well as enhanced the metastatic capacity of tumor cells. This study was initiated to investigate whether the thrombin effect on tumor cells is mediated through the "tethered ligand" thrombin receptor. RT-PCR analysis using primers based on the human thrombin receptors detected mRNA in human colon adenocarcinoma cells (clone A), whose authenticity was confirmed by Southern hybridization. The presence of thrombin receptor mRNA in rat (W256 carcinosarcoma) and mouse (melanoma) tumor cells was demonstrated by RT-PCR/Southern blotting using species-specific PCR primers. Sequencing of the PCR fragment of clone A cells revealed complete homology with the reported human cDNA sequence. Subsequently, tumor cells derived from three species, i.e., human, rat, and mouse, were found to express the thrombin receptor protein as revealed by immunoblotting using ligand peptide-derived mAb ATAP138, whose reactivity towards the M(r) approximately 66,000, potential thrombin receptor was blocked by preincubating the antibody with the immunogen peptide SFLLRNPNDKYEPF (TRP 14). Finally, peptides TRP 14 and TRP 7 (SFLLRNP), but not TRP 5 (FLLRN), were found to mimic alpha-thrombin in stimulating tumor cell adhesion to fibronectin, suggesting that the thrombin receptors expressed on solid tumor cells are biologically functional.

Amino Acid Sequence↗
PubMed1995

Haemolytic uraemic syndrome: prognostic factors in children over 3 years of age.

Previous studies have shown that age at onset of primary haemolytic uraemic syndrome (HUS) is a feature of prognostic significance, the disease being of much better outcome in paediatric patients younger than 3 years than in older children. In an attempt to find an explanation for such a difference, we analysed the clinical and pathological features of 42 children over 3 years of age who presented with HUS between 1955 and 1990 in our department. On the basis of the presence of a prodromal diarrhoea, we divided our patients into two groups: 21 children presented with the diarrhoea-associated (typical or D+) form of HUS, whereas 21 had the non-diarrhoea-associated (atypical or D-) form. Of the 42 children, 20 (47.5%) progressed to end-stage renal failure. However, our study shows that age at onset of HUS is not a prognostic feature per se. The difference in outcome between children and infants is most likely related to the high incidence of the atypical subset of HUS in children over 3 years, a subset that is very uncommon in infants. The ominous features which characterise this form of the disease are: (1) the absence of a diarrhoeal prodrome, (2) normal urine output, (3) marked proteinuria, (4) hypertension, (5) the occurrence of relapses or recurrences and (6) the presence of widespread and severe arteriolar changes on renal biopsy. The poor prognosis of the atypical form of HUS warrants the use of fresh-frozen plasma infusions and/or plasma exchange as early as possible in the course of the disease.

Adolescent↗
PubMed1995

[Comparative study of nebulized sambutol against placebo in the acute phase of bronchiolitis in 33 infants aged 1 to 6 months].

BACKGROUND: The therapeutic role of bronchodilators in bronchiolitis remains controversial. The aim of this study is to evaluate the safety and the clinical response to nebulized salbutamol in infants with mild acute bronchiolitis. PATIENTS AND METHODS: Thirty-three infants, aged 1 month to 5 months and 22 days (mean: 92.4 days) were included in the study. Patients received either nebulized salbutamol (0.15 mg/kg per dose: 16 infants) or a placebo (normal saline aerosol: 17 infants), delivered by an oxygen propellent, three times at intervals of 1 hour, as part of a double-blind randomized trial. Effect of treatment was evaluated by measuring respiratory and heart rate, clinical scores based on the degree of retraction and wheezing, and oxygen saturation. Clinical assessment was repeated 30 minutes after each nebulization. A nasopharyngeal swab was obtained for detection of respiratory syncytial virus (VRS) antigens by immunofluorescence assay in all patients. RESULTS: Patients in the salbutamol group exhibited significantly greater improvement in respiratory rate (P = 0.01), accessory muscle score (P < 0.001) and wheezing score (P < 0.001). There was no significant difference in oxygen saturation between both groups. Infants treated with salbutamol exhibited a non-significant increase in heart rate after the three sprays; no other adverse effects were noted. VRS was identified in 78% of the children tested. CONCLUSIONS: Salbutamol is safe and effective in relieving the respiratory distress of young infants with acute bronchiolitis. Our study confirms previous observations that infants younger than six months of age respond as well as older children when given three doses of nebulized salbutamol. Responders could not be differentiated from non responders by personal or family histories of atopy and VRS isolation. A longitudinal study could establish a correlation between response to bronchodilator therapy and later development of asthma.

Acute Disease↗
PubMed1994

Tumor cell-derived 12(S)-hydroxyeicosatetraenoic acid induces microvascular endothelial cell retraction.

Our previous work demonstrated that the 12-lipoxygenase metabolite of arachidonic acid, 12(S)-hydroxyeicosatetraenoic acid [12(S)-HETE] induced a nondestructive and reversible retraction of cultured endothelial cells. In the current study we tested the hypothesis that tumor cells produce 12(S)-HETE during their interactions with endothelial cells which in turn induces endothelial cell retraction. Coincubation of Lewis lung carcinoma cells or elutriated B16 amelanotic melanoma (B16a) cells but not 3T3 fibroblasts with microvascular endothelial cells (CD3) resulted in a time- and concentration-dependent retraction of the CD3 monolayers as revealed by quantitative binding assays and phase contrast microscopy. Lewis lung carcinoma cell-induced endothelial cell retraction was blocked by specific lipoxygenase inhibitors but not by cyclooxygenase inhibitors, suggesting the involvement of a lipoxygenase metabolite(s). Radioimmunoassay and high-performance liquid chromatography analysis of tumor cell extracts identified 12(S)-HETE as the major lipoxygenase metabolite of arachidonic acid and tumor cell generation of 12(S)-HETE was specifically blocked by a select 12-lipoxygenase inhibitor N-benzyl-N-hydroxy-5-phenyl-pentamide. The identity and stereochemistry of tumor cell-derived 12-HETE was substantiated by gas chromatography-mass spectrometry analysis and chiral phase high-performance liquid chromatography, respectively. Lewis lung carcinoma cell adhesion to CD3 monolayers was accompanied by an enhanced 12(S)-HETE biosynthesis by tumor cells, which paralleled the tumor cell-induced endothelial cell retraction in a cell number-dependent manner. Pretreatment of tumor cells with N-benzyl-N-hydroxy-5-phenylpentamide inhibited both increased 12(S)-HETE biosynthesis and tumor cell-induced endothelial cell retraction. Highly metastatic variants of elutriated B16a cells which had been shown to produce large quantities of 12(S)-HETE induced significant CD3 cell retraction, while low metastatic subpopulations of B16a cells which synthesized no or little 12(S)-HETE did not induce endothelial cell retraction. These results suggest that 12(S)-HETE synthesis during tumor cell-endothelial cell interactions may represent a key contributory factor in cancer metastasis.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1994

Enhanced endothelial cell retraction mediated by 12(S)-HETE: a proposed mechanism for the role of platelets in tumor cell metastasis.

Platelets have been hypothesized to contribute to tumor cell metastasis, but the underlying mechanism(s) remain unknown. We demonstrate here that one mechanism whereby platelets may facilitate metastasis is by potentiating tumor cell-induced endothelial cell retraction, a prerequisite for the extravasation of most tumor cell types. The integrity of cultured microvascular endothelial cell (CD3 cells) monolayers was perturbed by 12[S]-hydroxyeicosatetraenoic acid (12(S)-HETE), a lipoxygenase metabolite of arachidonic acid, as well as by tumor cells (i.e., Lewis lung carcinoma cells or 3LL). 3LL cells induced a concentration- and time-dependent retraction of the CD3 monolayers, as assessed by quantitative binding assays as well as by phase-contrast microscopy. In contrast, normal murine fibroblasts (3T3) did not induce endothelial cell retraction. 3LL cell-induced endothelial cell retraction was potentiated, in a dose- and time-dependent manner, by homologous murine platelets while platelets alone did not induce endothelial cell retraction. Platelet-enhanced, tumor cell-induced endothelial cell retraction was inhibited by treating either tumor cells or platelets with the lipoxygenase inhibitors nordihydroguaiaretic acid or N-benzyl-N-hydroxy-5-phenylpentanamide (BHPP) as well as by PGI2 or its analogs iloprost and ZK96.480 (cicaprost), but not by the cyclooxygenase inhibitor aspirin (ASA). Tumor cells, upon adhesion to endothelium, initiated 12(S)-HETE biosynthesis, which was inhibited by pretreating tumor cells with BHPP but not with ASA. Additionally, 12(S)-HETE biosynthesis during tumor cell-endothelial cell adhesion was significantly enhanced by the addition of homologous platelets. Collectively, these results suggest that tumor cell-platelet-endothelial cell interactions lead to enhanced biosynthesis of 12(S)-HETE by tumor cells and/or platelets, which in turn induces endothelial cell retraction, thus facilitating tumor cell extravasation and metastasis.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1994

A thirty-year retrospective study of hospitalization among severely mentally ill patients.

This study examines the effects of deinstitutionalization policies on psychiatric hospitalization rates over a thirty-year period. It is based on a retrospective study of successive hospitalizations in severely disabled patients. The data indicate that in any five-year period these patients still spend over 20% of their time in hospital. For patients who have stayed for a total of more than one year every five years in hospital, the average length of stay has been decreasing far less rapidly in the last fifteen years than it had previously. Patients who were first admitted after 1971 spent proportionally as much time in hospital as those whose first stay was earlier. These results show that the groups primarily affected by deinstitutionalization are those who were first hospitalized prior to the 1970s and those who are the heaviest hospital users. However, the data from the patients admitted since the seventies seem to reveal that the process of change may have reached its limits.

Adolescent↗
PubMed1993

The lipoxygenase metabolite, 12(S)-HETE, induces a protein kinase C-dependent cytoskeletal rearrangement and retraction of microvascular endothelial cells.

We previously reported that a lipoxygenase metabolite of arachidonic acid, 12(S)-hydroxyeicosatetraenoic acid [12(S)-HETE], induced large vessel endothelial cell (EC) retraction and increased tumor cell adhesion to exposed extracellular matrix (Honn et al., FASEB J. 3, 2285-2293, 1989). Here, we present evidence that 12(S)-HETE induces the retraction of microvascular ECs in a time- and concentration-dependent manner. The EC retraction was observed 15 min after 12(S)-HETE treatment and reached a peak level between 1 and 2 h. The monolayer reformed by 24 h. Silver staining and "gap-FRAP" experiments suggest that 12(S)-HETE altered the normally apposed cell junctions and impaired gap junction-mediated cell-cell communication. It appears that the 12(S)-HETE effect was mediated by cytoskeletal alteration. The first observed alteration in EC cytoskeleton following 12(S)-HETE stimulation is vimentin bundling, followed by the rearrangement and disruption of vinculin-containing adhesion plaques and/or simultaneous redistribution of alpha-actinin and disruption of spectrin. These changes are accompanied by progressive microfilament dissolution. During the same time interval, alpha-actinin is mobilized to the cell periphery at cell "ruffles." However, 12(S)-HETE showed little or no effects on actin-binding proteins filamin and tropomyosin or on microtubules. 12(S)-HETE effects on these cytoskeletal elements were fully reversible by 24 h and appeared to be mediated through enhancing protein phosphorylation. Following 12(S)-HETE (0.1 microM) treatment increased phosphorylation of proteins that comigrated with myosin light chain (20 kDa), actin (42 kDa), and vimentin (57 kDa) were observed. The enhanced phosphorylation of these cytoskeletal proteins was confirmed by 2D gel analysis. The phosphorylation-promoting effect of 12(S)-HETE on cytoskeletal proteins could be totally abolished by calphostin C, partially inhibited by staurosporine, but was not influenced by N-[2-(methylamine)ethyl]-5-isoquinolinesilfonamide dihydrochloride (HS), suggesting that the 12(S)-HETE effect was mediated via protein kinase C. This was further substantiated by quantitative experiments demonstrating that calphostin C, but not H8, inhibited 12(S)-HETE-induced EC retraction.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1993

Activity and protein distribution of 12-lipoxygenase in HEL cells: induction of membrane-association by phorbol ester TPA, modulation of activity by glutathione and 13-HPODE, and Ca(2+)-dependent translocation to membranes.

The understanding of the intracellular regulation of 12-lipoxygenase requires a knowledge of the distribution of both enzyme protein and its activity. In human erythroleukemia cells, the membrane fraction contains about 90% of the total cellular 12-lipoxygenase activity, whereas only approximately 10% of 12-lipoxygenase activity resides in the cytosol. However, the majority of the cellular 12-lipoxygenase protein is found in the cytosol. Pretreatment of cells for 0-3 days with 160 nM TPA caused a marked, time-dependent increase in membrane-bound 12-lipoxygenase activity and protein, respectively. In contrast, the cytosolic amount of 12-lipoxygenase protein and activity, respectively, were minimally altered by this TPA treatment. Recombining the active membrane fraction with cytosol resulted in no significant inhibition of its 12-lipoxygenase activity, but the addition of GSH to the membrane fraction inhibited 12-lipoxygenase activity in a dose-dependent manner. On the other hand, the cytosolic enzyme can be rendered active in the presence of 1 microM 13-hydroperoxyoctadecadienoic acid. In HEL cell homogenates, a partial translocation of the cytosolic enzyme to the membrane takes place in a Ca(2+)-dependent manner, resulting in an increase in membrane-associated 12-lipoxygenase activity and a concomitant decrease in cytosolic 12-lipoxygenase activity above 0.1 microM Ca2+.

Arachidonate 12-Lipoxygenase↗
PubMed1993

[Disclosure by neurologic signs of right subclavian aneurysm. Post-traumatic aneurysm?].

BACKGROUND: Aneurysms of the subclavian artery are rare in childhood and may be due to traumatic, infectious or congenital causes. CASE REPORT: A 15 year-old boy presented with a sudden left visual disturbance plus decreased muscle strength and paresthesias of the left arm; these manifestations disappeared within 15 minutes. His neurological examination on admission was normal. The right arm radial pulse was weak and the blood pressures of the right and left arms were significantly different. Doppler showed a right subclavian artery aneurysm containing several clots, that was confirmed by angiography. There were no signs of inflammation or indication of autoimmune disease. This aneurysm might have been caused by trauma as the patient had had a violent cervical traumatism after a diving accident 2 years earlier. The aneurysm was surgically removed and the right vertebral artery arising from it was reimplanted. Histological examination of the aneurysm gave no evidence of etiology. The post-surgical MRI showed no brain abnormaly. CONCLUSIONS: This aneurysm is probably of post-traumatic origin. The cerebral disturbance could be due to embolism or transient ischemia; the latter is more compatible with the normal NMR.

Adolescent↗
PubMed1992

Protein-kinase-C inhibitor calphostin C reduces B16 amelanotic melanoma cell adhesion to endothelium and lung colonization.

We recently reported that the Ca(2+)- and phospholipid-dependent protein kinase, protein kinase C (PKC), was involved in rat Walker carcinosarcoma cell adhesion to large-vessel endothelium. We extended our studies to explore the role of this kinase in the adhesion to small-vessel endothelium and lung colonization of murine B16 amelanotic melanoma (B16a). Subpopulations of B16a cells, which differ in lung-colonization potentials, were isolated by centrifugal elutriation from solid tumors. In this study, we demonstrate that cells from a high metastatic sub-population (HM340), when compared with cells from a low metastatic sub-population (LM180), exhibit elevated levels of total cellular as well as membrane-bound PKC. The increase in PKC in cells from the HM340 correlates positively to their increased ability to adhere to murine pulmonary-microvessel endothelial-cell monolayer, and to form pulmonary colonies in syngeneic mice. Calphostin C, a potent and selective PKC inhibitor, decreases in a dose-dependent manner the adhesion to endothelium and the lung colonization of cells from both the low and the high metastatic sub-populations with IC50 at sub-micromolar concentrations. In conclusion, our results suggest that PKC may be a key element in regulating tumor-cell metastasis and that PKC inhibitors may be anti-metastatic agents.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗