Pneumatosis cystoides intestinalis and immunosuppression.
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Biomedical subjects
Publications and source records attributed to F Vincent.
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Steady-state levels of 12S rRNA and NADH dehydrogenase subunit 4 mRNA (ND4) mitochondrial transcripts were measured on rabbit articular chondrocyte in culture. In pseudosynchronized chondrocytes, changes of mitochondrial RNA levels were observed during the progression of the cells in the cell cycle. Oxidative stress generated by the hypoxanthine-xanthine oxidase system (HX-XO) induced a transient decrease in the levels of both ND4 and 12S rRNA. Mitochondrial RNA levels recovered 24 h after the oxidative stress. These RNA level changes were not associated with modifications in the structure or the copy number of the mitochondrial genome. Furthermore, the decrease in the amount of the mitochondrial transcripts observed may be related to a transient inhibition of mitochondrial transcription since the treatment of cells with ethidium bromide (a mitochondrial transcription inhibitor) resulted in the same decrease in 12S rRNA level as HX-XO treatment alone.
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The use of bioindicators to evaluate exposure to the biological effects of chemical pollutants in marine organisms constitutes a new tool in the monitoring field. The establishment of a North Sea monitoring network in 1991, involving such international organizations as the North Sea Task Force, the International Council for the Exploration of the Sea, and the Intergovernmental Oceanography Commission, led French researchers to develop an enzymatic biomarker to monitor biological effects within the National Observation Network. The biomarker, ethoxyresorufin-O-deethylase (EROD), dependent on the CP450 system, has been monitored biannually since 1992 in several species of fish (Callionymus lyra, Limanda limanda, Serranus sp., Mullus barbatus) in two coastal sites particularly exposed to industrial and domestic pollution. A rapid method is used to assay EROD enzymatic activity determined along a pollution gradient, and results are interpreted on a microplate reader. The strategy of this approach is to assess the effects on the marine ecosystem during prolonged exposure to specific pollutants such as polyaromatic hydrocarbons, polychlorinated biphenyls, and dioxins.
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A simple procedure is described that permits the simultaneous determination of trimipramine and its two major metabolites, desmethyl- and hydroxytrimipramine, in human plasma or red blood cells (RBCs) at therapeutic concentrations. The extracted biological fluids are injected into a capillary gas chromatograph with an OV-1 fused-silica column coupled to a nitrogen-phosphorus-selective detector. The limit of determination for trimipramine is 3 ng/ml and for that desmethyl- and hydroxytrimipramine is 4 ng/ml. The method permits the RBC/plasma ratios to be determined and to be correlated with the clinical response.
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Proteins of the complement system (C2, C3) are synthesized by human monocytes and macrophages, thus providing an important local source of these proteins in vivo which serve as a first-line host defense mechanism. In this study, we investigated the production of complement components C2, C4, and C9 by human monocytes/macrophages and by the pathologic cells of acute monocytic leukemia which represent a source of immature monocytic precursors. Human blood monocytes were collected and purified by cytapheresis and elutriation and leukemic cells by Ficoll gradient. Secretion of complement components was measured by a hemolytic assay. The evaluation of the mRNAs of the various complement components in the cells was performed by polymerase chain reaction (PCR) by adding 32P labeled deoxycytidinetriphosphate (dCTP) to the amplification step. Functional C2 was found to increase during in vitro maturation of macrophages up to the fourth week of culture. C2 mRNA was detected after amplification and increased during the maturation. Interferon-gamma (IFN-gamma) mediated a marked increase of the C2 mRNA. We found a decrease in synthesis of C4 mRNA during in vitro differentiation of human monocytes. The effect of IFN-gamma resulted in an increase in C4 mRNA. C9 mRNA was not detected although it was detected in the HepG2 hepatoma-derived cell line. Functional C2 was not detected by leukemic cells after 24 h of culture but little functional C4 was present in the cell supernatants. As they were by human monocytes and macrophages, C2 and C4 mRNAs were detected after amplification but C9 mRNAs were not detected.(ABSTRACT TRUNCATED AT 250 WORDS)
Differentiation of the U937 cell line can be induced by various agents. We have investigated the differentiation abilities of gamma-interferon (IFN-gamma), interleukin-6 (IL-6), macrophage and granulocyte-macrophage colony-stimulating factors (M-CSF + GM-CSF) or the combinations IL-6 + M-CSF + GM-CSF and IFN-gamma + M-CSF + GM-CSF on the U937 cells by studying the morphology, cytochemical activity and several functional properties. The expression of the Leu-CAM proteins (CD11a, CD11b, CD11c, CD18) was also evaluated during the culture period. Our results show that the cytokines used in this study inhibit to a certain extent the proliferation of the tumor cells and drive the cells toward a differentiation phenotype that has several characteristics in common with mononuclear phagocytes, such as the expression of CD14, phagocytosis and release of superoxide anions. The adhesion molecules CD11b alpha chain and CD18 beta chain were strongly induced on the U937 cells with a maximal expression of the CD11b on the cells cultured with either M-CSF + GM-CSF or the combinations of IL-6 and IFN-gamma with M-CSF + GM-CSF. Conversely, for CD11a and CD11c alpha chains a rather low enhancement of the expression was noticed. In our culture system, cells incubated with the combination of M-CSF + GM-CSF exhibited differentiation characteristics which appeared to be largely potentialized when cytokines such as IL-6 or IFN-gamma were added.
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Forty-seven patients with unresectable non small cell lung carcinoma, 15 stage IIIA, 31 stage IIIB, 1 stage IV (cervical lymphadenopathy) were treated with a combination of three courses of chemotherapy and hypofractionated irradiation followed after 3 weeks by split course radiotherapy. Each course was repeated every 3 weeks with the following sequence: Cisplatinum (CDDP) (20 mg/m2) was given in a 20-min infusion, followed by a 2-h infusion of 5-fluorouracil (5-FU) (400 mg/m2) on days 1, 2, 5 and 6. Radiation with a dose of 3 Gy on the target volume was given on days 3 and 4--in one fraction for the former 27 patients, in 2 fractions of 1.5 Gy for the latter 20 patients with a 6-h interval--after a 2-h infusion of 5-FU (400 mg/m2). The results remain disappointing: the objective response rate was 53%, the median survival was 10 months for the series, and the one-year survival 47%. The median survival was 14 months for IIIA, 10 months for IIIB and IV. Regarding the therapeutic regimen there seems to be less morbidity with 2 fractions per day for which the median survival is nearly the same at 10 months (1 fraction/day) versus 12 months (2 fractions/day).
BACKGROUND: After the publication of an uncontrolled trial of nine patients with streptococcus-associated psoriasis who appeared to benefit from a course of oral penicillin or erythromycin with the addition of rifampin in the last 5 days, we wished to confirm or refute the validity of this observation. OBJECTIVE: Our purpose was to confirm the effectiveness of antibiotics in the treatment of streptococcus-associated psoriasis. METHODS: Twenty patients were placed randomly into two groups. One group was given penicillin or erythromycin for 14 days with a placebo added during the last 5 of the 14 days. The other group received the same medication with the addition of rifampin in the last 5 days. RESULTS: Although all the patients studied met the criteria of the reported preliminary study, we were unable to detect any evidence of improvement in their psoriasis. CONCLUSION: There was no apparent benefit for patients with streptococcus-associated psoriasis from a course of oral penicillin or erythromycin with the addition of rifampin in the last 5 days in a 14-day trial.
The effects of long-term exposure to hyperthermia were studied on several cell cultures of cartilaginous or bone origin after a 4-day treatment at 40 degrees C. Chondrocytes proliferation, as well as mitochondrial activity were not modified by these culture conditions (40 degrees C) but protein content and cell volume were increased. In contrast, the proliferative capacity of osteoblasts, MC3T3.E1 a and ROS 17/2.8 was decreased and their protein content, cell volume and mitochondrial activity were increased. Chondrocytes appeared to be thermoresistant, and osteoblastic cells thermosensitive. Furthermore, temperature sensitivity was greater for the continuous established osteoblastic cell line MC3T3.E1 and for the cancerous established osteoblastic cell line ROS 17/2.8 than for chondrocytes.
The aim of this work was to study the proliferation pathological perturbations of cultured chondrocytes in response to menadione, an oxygen free radicals producing drug. Rabbit articular chondrocytes in monolayer culture were treated with 10(-5) M, 1.5.10(-5) M and 2.10(-5) M of menadione during three days. A dose dependent decrease of the proliferative capacity was observed. Flow cytometry analysis revealed a perturbation of the cell cycle progression consisting in an accumulation of cells in the S and G2 + M phases. This growth perturbation was due to oxygen radicals production since a treatment with catalase suppressed these toxic effects. Furthermore, to identify oxygen derived radicals in the cellular suspension of cultures treated with menadione, we used a technique of spin-trapping coupled with electron spin resonance (ESR). The ESR signal corresponding to the DMPO hydroxyl radical adduct (DMPO-OH) has been detected. The spectra observation indicated the actual production of hydroxyl radical. However, superoxide anions have not been identified; this fact can be explained by the low reactivity of these anions with DMPO and by the decomposition of signal DMPO-OOH to DMPO-OH.