Biomedical subjects
Publications and source records attributed to M Prats.
A description of time correction applied to the integrated Michaelis equation in view of cancelling a non-correct estimation of the Michaelis constant due to a lack of coincidence between time zero of measurement and time zero of reaction is presented. An estimation of kinetic parameters is made with time correction on the same experimental set of data using a classical least squares iterative procedure.
Proton conduction is known to be facilitated along phospholipid monolayers spread on aqueous phases. This property was monitored with mixed cetyltrimethylammonium bromide/phosphatidyl-ethanolamine monolayers. The film was shown to be metastable by surface pressure and fluorescence measurements. The detergent was leaving the interface for the bulk phase. Nevertheless, a fraction of the detergent remained in the lipid matrix, as shown by the binding of the fluorescent probe 8-anilino-1-naphthalensulfonate. Its dissociation constant decreased, and the nature of its binding site was affected, as shown by a shift of its emission spectrum. Apart from film expansion, the properties of the film were affected only at the water/membrane interface. Proton conduction was prevented only when the surface concentration of the detergent was larger than a critical value. Such an effect could be due either to the disruption in the continuity of the conducting hydrogen-bond network or to an electrostatic repulsion of the protons by the interface.
Adult female Swiss albino mice were infected intraperitoneally or subcutaneously with Listeria monocytogenes Serovar 4b or 1/2a and killed at intervals. Thymus, spleen, Peyer's patches and a variety of lymph nodes, including the jejunal (mesenteric), mediastinal, lumbar, mandibular and superficial inguinal, were examined by histopathology and by immunocytochemistry for detection of L. monocytogenes antigen. Similar results were obtained with both Serovars and by both routes of inoculation used. In the spleen, L. monocytogenes was detected, by immunoperoxidase staining, as soon as 4 h after inoculation, inside phagocytic cells located predominantly in the marginal zone of the white pulp. This was followed by inflammation, necrosis and depletion of lymphoid cells, which extended in extreme cases to the whole organ. Inflammatory lesions diminished progressively at 5 to 6 days after inoculation. In animals dying of the infection, a severe necrotizing splenitis was present. Depletion of lymphoid cells and inflammatory changes were widespread in the lymph nodes and to a lesser extent in the Peyer's patches. An extensive necrotizing lymphadenitis was the prominent lesion in severely affected nodes. Inflammatory lesions and detection of L. monocytogenes antigen started around the venules of high endothelium. A thymus depletion, not associated with the multiplication of bacteria in the organ, was also a constant feature of the infection. This study suggests that L. monocytogenes (1) is transported to the spleen and to the lymph nodes by phagocytes, entering the organs by the marginal sinus in the spleen and by the venules of high endothelium in the lymph nodes; (2) multiplies in these cells as well as in neutrophilic granulocytes (the latter rapidly migrate to the affected zones); and (3) induce a splenitis and lymphadenitis, involving predominantly T cell-dependent areas, with a necrotizing component in severe cases. From our observations it is concluded that infection of the lymphoid system is a major feature in the pathogenesis of murine listeriosis.
Studies have been carried out on the lateral proton conductance properties of monolayers of the major and minor phospholipids of extremely halophilic archaebacteria, 2,3-diphytanyl-sn-glycero-1-phospho-3'-sn-glycerol 1'-phosphate (PGP) and 2,3-diphytanyl-sn-glycero-1-phospho-3'-sn-glycerol (PG), respectively, as well as on their respective deoxy analogues: 2,3-diphytanyl-sn-glycero-1-phospho-1'-propanediol 3'-phosphate (dPGP), 2,3-diphytanyl-sn-glycero-1-phospho-1'-1',3'-propanediol (dPG), and 2,3-diphytanyl-sn-glycero-1-phospho-1'-propanol (ddPG). Lateral proton conduction was found to occur with monolayers of all ether phospholipids examined at reduced surface pressure (pi greater than 25 mN/m) on subphases of low (1 mM) and high (4 M) ionic strength. Proton conduction was also detected in highly condensed monolayers (greater than 35 mN/m) of the naturally occurring phospholipids (PGP, PG) but was abruptly terminated in tightly packed monolayers (greater than 35 mN/m) of the corresponding deoxy compounds (dPGP, dPG, ddPG) on subphases with low ionic strength. conduction did occur, however, along monolayers of the deoxy compounds at high surface pressure when spread on a subphase of high ionic strength (4 M). The abrupt termination of conduction with monolayers of the deoxy compounds at low ionic strength cannot be attributed to a lipid phase transition or to changes in the lateral fluidity of the monolayers, nor was the pK of the fluorescent interfacial proton indicator affected at high surface pressures.(ABSTRACT TRUNCATED AT 250 WORDS)
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A study has been carried out on 116 mammary neoplasias in which the prolactin receptors together with other clinical and hormonal parameters have been determined. A 46.3% frequency of PRLR+ has been obtained as well as a statistically significant correlation between these and blood estradiol (p less than 0.05). PRLR- have greater survival and PRLR may act as a growth factor.
Using a fluorescence method applied to phospholipids spread at the air-water interface, we showed the occurrence of a localized proton pathway along the phospholipid polar heads. From the systematic investigation of this phenomenon, we conclude that the protons diffuse through a hydrogen bond network which is a matrix of hydrated polar head groups.
A fluorescent indicator for the determination of pH in the vicinity of water/lipid interfaces was produced by the covalent linkage of fluoresceinisothiocyanate to Escherichia coli phosphatidylethanolamine. When embedded in monolayers spread on an air/water interface, its apparent pK was shown to be only slightly affected by the nature of the polar headgroups or the packing density of the host phospholipids. Its properties were not affected by the ion content of the subphase. For small unilamellar vesicles, its properties were only affected when localized in the inner layer. This probe could therefore be of value in the study of proton fluxes along biological membranes.
Fast lateral proton conduction was observed along the lipid/water interface using a fluorescence technique. This conduction can be detected for a large number of lipids, both phospholipids and glycolipids. The efficiency of the proton transfer is dependent on the molecular packing of the host lipid at a given surface pressure. The proton conduction which is present in the liquid expanded state is abolished by the transition to the liquid condensed state. The proton transfer is affected slightly by the ionic content of the aqueous subphase except in the case of calcium which can inhibit the conduction along phosphatidylglyceroethanolamine. We suggest that the transfer of the protons occurs along a bidimensional hydrogen-bond network formed from the polar head groups, their water molecules of hydration and the water molecules which are intercalated between the lipid molecules.
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Fast lateral proton conduction along the lipid/water interface has recently been experimentally demonstrated in our laboratory [Teissié, J., Prats, M., Soucaille, P. & Tocanne, J.F. (1985) Proc. Natl Acad. Sci. USA, in the press]. The present study gives a more precise description of the way various physical parameters can affect this process. The dependence of the distance covered by the proton on time is demonstrated to be quadratic. Increasing the speed of stirring in the injection compartment or the amount of injected acid or the contact between the monolayer and the acidic subphase increased the efficiency of the proton transfer. Raising the strength of the buffer in the bulk phase inhibited proton conduction. Results from experiments where the transfer of protons from the bulk phase to the interface was modified, suggested the occurrence of an 'energy barrier' limiting the access of protons from the bulk phase to the lipid polar head region.
Movements of H+ along the polar heads of phospholipids spread in monolayers were compared to movements of H+ in the aqueous subphase. The probe for detecting H+ movement along the monolayer was a pH-sensitive fluorescein chromophore covalently bound to the head group of phosphatidylethanolamine. The behavior of this probe was not affected by the electrical properties of the lipid/water interface. Lateral diffusion of H+ along the phospholipid/water interface was then studied by acid-jump experiments in which advantage was taken of the large size of the monolayer. H+ was injected a few centimeters away from the probe observation area. The time needed for H+ diffusion to the probe was monitored by the change in the fluorescence signal, fluorescein being nonfluorescent in an acid medium. Diffusion of H+ in the bulk phase was monitored by the fluorescence change of water-soluble fluorescein isothiocyanate. Diffusion along the lipid monolayer was found to be 20 times faster than in the bulk water phase and required a structured monolayer in order to occur, as revealed by variation of the molecular area occupied by the lipid molecules. The molecular basis of rapid H+ transfer along the lipid monolayer may be the existence of a hydrogen-bond network along the polar heads, capable of supporting a rapid "hop and turn" of H+.
A group of 32 patients with disseminated breast cancer were submitted to polychemotherapy following Cooper's protocol. Vincristine, cyclophosphamide, 5-fluorouracil, and prednisone were administered. The fifth drug used by Cooper, methotrexate, was not included in the therapy program because of difficulties in obtaining it. Both the objective and subjective results were similar to those of other authors using similar drug associations, while toxicity was moderate. Although this treatment is effective to some degree, the authors feel that further research should be carried out on more potent drugs, or in different combinations, in order to get a more definite chemotherapeutic effect in patients with breast cancer.
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The L-(+)-Lactate:cytochrome c oxidoreductase or cytochrome b2 from the yeasts Saccharomyces cerevisiae and Hansenula anomala were partially hydrolysed in various concentrations of trypsin. Conditions were found which allowed the isolation from the Hansenula enzyme of a 140 000 +/- 10 000-dalton flavoprotein. The prosthetic flavin groups were still reducible by substrate (spectroscopic evidence) but the flavoprotein was unable to form a complex with cytochrome c, the physiological acceptor in the enzymatic reaction. No such flavoprotein units could be found during proteolysis of the Saccharomyces enzyme. The heme prosthetic group of the Hansenula enzyme remained bound to a 15 500 +/- 1000-dalton protein unit which was larger than, but very similar to, the well known 'cytochrome b2 core' of the Saccharomyces enzyme. Moreover, the degradation of different enzyme samples by contaminated proteases allowed the isolation of a particular form of Hansenula enzyme: each tetramer had, on the mean, four bound flavins and only two heme groups. These molecules completely retained their ability to form a complex with cytochrome c.
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MCA serum levels were determined in 27 healthy subjects, 136 with benign pathology (42 breast) and in 289 patients with cancer (247 active). The last group includes 223 patients with breast cancer (96 without metastases, 89 with metastases and 38 no-evidence of disease). CEA and CA15-3 serum levels were determined in all the patients with breast diseases. The mean levels of MCA were 4.7 + 2.4 U/ml in the control group, considering less than 11 U/ml as normal. MCA values were abnormal in 15.4% of patients with benign pathology, mainly in those with liver cirrhosis (8/20) and lung diseases (4/20). In the majority of these cases, the rise was only moderate, lower than 15 U/ml in 97.5% of patients. In malignant diseases, important increments were found in breast cancer (19.8% Mo, 77.5% M1) and ovarian cancer stages III-IV (44.4%). When we compared MCA serum levels with CA15-3 and CEA in breast pathology, a similar specificity was observed: 92.3%, 92.3% and 100% in cases with benign pathology and 92.1%, 94.7%, and 97.4% in NED patients, respectively. MCA and CA15-3 sensitivity was similar in breast cancer without metastases (19.8%) and lower for CEA (16.7%). In patients with breast cancer without metastases, we found a relation between positivity of these tumor markers and prognostic factors (tumor size, nodal involvement). The disease free interval in patients with locoregional breast cancer was shorter in cases with abnormal presurgical levels of some of the tumor markers, but only the difference from MCA was significant (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)