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A Forget

Publications and source records attributed to A Forget.

At least 19 recordsLinked to original sources
PubMed2006

Spin dynamics and magnetic order in magnetically frustrated Tb2Sn2O7.

We report a study of the geometrically frustrated magnetic material Tb2Sn2O7 by the positive muon-spin relaxation technique. No signature of a static magnetically ordered state is detected while neutron magnetic reflections are observed in agreement with a published report. This is explained by the dynamical nature of the ground state of Tb2Sn2O7: the Tb3+ magnetic moment characteristic fluctuation time is approximately 10(-10) s. The strong effect of the magnetic field on the muon-spin-lattice relaxation rate at low fields indicates a large field-induced increase of the magnetic density of states of the collective excitations at low energy.

Journal Article↗
PubMed2006

Nernst effect and disorder in the normal state of high-T(c) cuprates.

We have studied the influence of disorder induced by electron irradiation on the Nernst effect in optimally and underdoped YBa2Cu3O(7-delta) single crystals. The fluctuation regime above T(c) expands significantly with disorder, indicating that the T(c) decrease is partly due to the induced loss of phase coherence. In pure crystals the temperature extension of the Nernst signal is found to be narrow whatever the hole doping, contrary to data reported in the low-T(c) cuprate families. Our results show that the presence of intrinsic disorder can explain the enhanced range of the Nernst signal found in the pseudogap phase of the latter compounds.

Journal Article↗
PubMed2002

Evidence for two distinct energy scales in the Raman spectra of YBa2(Cu1-xNix)3O6.95.

We report electronic Raman scattering from Ni-substituted YBa2Cu3O6.95 single crystals with T(c) ranging from 92.5 to 78 K. The fully symmetrical A(1g) channel and the B(1g) channel which is sensitive to the d(x(2)-y(2)) gap maximum have been explored. The energy of the B(1g) pair-breaking peak remains constant under Ni doping while the energy of the A(1g) peak scales with T(c) ( E(A(1g))/k(B)T(c) = 5). Our data show that the A(1g) peak tracks the magnetic resonance peak observed in inelastic neutron scattering yielding a key explanation to the long-standing problem of the origin of the A(1g) peak.

Journal Article↗
PubMed2002

First-order transition in the spin dynamics of geometrically frustrated Yb2Ti2O7.

Using neutron diffraction, 170Yb Mössbauer and muon spin relaxation spectroscopies, we have examined the pyrochlore Yb2Ti2O7, where the Yb3+S' = 1/2 ground state has planar anisotropy. Below approximately 0.24 K, the temperature of the known specific-heat lambda transition, there is no long range magnetic order. We show that the transition corresponds to a first-order change in the fluctuation rate of the Yb3+ spins. Above the transition temperature, the rate, in the GHz range, follows a thermal excitation law, whereas below, the rate, in the MHz range, is temperature independent, indicative of a quantum fluctuation regime.

Journal Article↗
PubMed2000

Eradication of multiple myeloma and breast cancer cells by TH9402-mediated photodynamic therapy: implication for clinical ex vivo purging of autologous stem cell transplants.

High-dose chemotherapy combined with autologous transplantation using bone marrow or peripheral blood-derived stem cells (PBSC) is now widely used in the treatment of hematologic malignancies as well as some solid tumors like breast cancer (BC). However, some controversial results were recently obtained in the latter case. The presence of malignant cells in the autograft has been associated with the recurrence of the disease, and purging procedures are needed to eliminate this risk. The aim of this study was to evaluate the potential of the photosensitizer 4,5-dibromorhodamine methyl ester (TH9402), a dibrominated rhodamine derivative, to eradicate multiple myeloma (MM) and BC cell lines, while sparing more than 50% of normal pluripotential blood stem cells from healthy volunteers. The human BC MCF-7 and T-47D and MM RPMI 8226 and NCI-H929 cell lines were used to optimize the photodynamic purging process. Cell concentration and the cell suspension thickness as well as the dye and light doses were varied in order to eventually treat 1-2 L of apheresis. The light source consisted of two fluorescent scanning tubes emitting green light centered about 515 nm. The cellular uptake of TH9402 was measured during the incubation and washout periods and after photodynamic treatment (PDT) using spectrofluorometric analysis. The limiting dilution assay showed that an eradication rate of more than 5 logs is obtained when using a 40 min incubation with 5-10 microM dye followed by a 90 min washout period and a light dose of 5-10 J/cm2 (2.8 mW/cm2) in all cell lines. Agitating the 2 cm thick cell suspension containing 20 x 10(6) cells/mL during PDT was essential for maximal photoinactivation. Experiments on mobilized PBSC obtained from healthy volunteers showed that even more drastic purging conditions than those found optimal for maximal eradication of the malignant cell lines were compatible with a good recovery of hematopoietic progenitors cells. The absence of significant toxicity towards normal hematopoietic stem cells, combined with the 5 logs eradication of cancer cell lines induced by this procedure suggests that TH9402 offers an excellent potential as an ex vivo photodynamic purging agent for autologous transplantation in MM and BC treatment.

Breast Neoplasms↗
PubMed1994

Hydrolysis of retinyl esters in rat liver. Description of a lysosomal activity.

When incorporated into liposomes made of phospholipids, retinyl palmitate is an adequate substrate for an acidic REH (aREH). In rat liver, this activity is mainly localized in the lysosomal fraction. Kinetic parameters have been determined for retinyl palmitate (Km = 315 microM; maximal rate = 22.1 nmol retinol/h per mg protein). The aREH activity is different from the lysosomal acidic cholesteryl ester hydrolase (aCEH): cholesteryl oleate does not inhibit aREH activity, neither do some aCEH specific inhibitors, and aREH does not hydrolyse cholesteryl ester. Involvement of aREH in the hydrolysis of lipid droplets retinyl esters in fat storing cells is discussed.

Animals↗
PubMed1991

A role for gamma interferon, tumor necrosis factors, and soluble T-cell receptors in the depressed blastogenic response of spleen cells of Mycobacterium lepraemurium-infected mice.

Spleen cells of Mycobacterium lepraemurium-infected mice were cultured on petri dishes coated with mycobacterial antigens, and antigen-reactive cells were isolated. Upon incubation in mitogen- or antigen-free culture medium, these cells released mediators capable of depressing the in vitro proliferative response of normal splenocytes to specific antigen and to concanavalin A and lipopolysaccharide. One of these mediators was identified with gamma interferon (IFN-gamma), mainly on the basis that treatment of supernatants with monoclonal anti-IFN-gamma antibodies markedly reduced the suppressive activity contained therein. Detectable levels of tumor necrosis factor alpha (TNF-alpha) and TNF-beta were present in spleen cell culture supernatants of infected mice. Moreover, low doses of recombinant TNF-alpha and TNF-beta were found to potentiate the suppressive activity of exogenous IFN-gamma. Soluble T-cell receptors beta were also detected in the culture supernatants. The elimination of these molecules with monoclonal anti-T-cell receptor beta (F23.1) antibodies immobilized on a plastic surface partially reversed the depression of the response to mycobacterial antigen but did not affect the response to mitogens. These results revealed the complex nature of suppressor mediators that are produced by mycobacterial antigen-reactive cells and that regulate the in vitro proliferative response.

Animals↗
PubMed1990

Killing of Mycobacterium smegmatis by macrophages from genetically susceptible and resistant mice.

The bactericidal function of macrophages was investigated in congenic mice expressing the phenotype of susceptibility (B10.A, Bcgs) or resistance (B10.ABcgr) to mycobacterial infection. When splenic and peritoneal macrophages from these two mouse strains were infected in vitro with Mycobacterium smegmatis, the Bcgr macrophages were shown to inactivate M. smegmatis more efficiently than their Bcgs congenic counterparts. The mechanisms of this superior antimycobacterial activity was studied further. Addition of catalase did not abolish killing to a significant degree in either allelic type of macrophage, suggesting that hydrogen peroxide production was not involved in the killing activity controlled by the Bcg gene. Activation of Bcgs macrophages by exposure to crude lymphokines rendered them equally as efficient as their Bcgr counterparts in their capacity to destroy M. smegmatis. This finding suggests that both the genetically resistant and susceptible macrophages have the potential to kill M. smegmatis in vitro. This potential is expressed constitutively by the Bcgr but not Bcgs macrophages and can be induced, by lymphokine treatment, in the Bcgs macrophages. In a final set of experiments, the macrophage killing of M. smegmatis was evaluated as a test system to type for the Bcg gene allelic type in vitro, using a set of AXB and BXA recombinant inbred strains of mice. Results obtained show that typing of AXB/BXA recombinant inbred strains for the trait of bactericidal activity vs. M. smegmatis in vitro revealed a perfect match with the strain distribution pattern of resistance/susceptibility to Mycobacterium bovis BCG in vivo.

Animals↗
PubMed1990

Biological properties of factors secreted by antigen-reactive suppressor cells in mice infected with Mycobacterium lepraemurium.

Antigen-reactive cells were isolated from the spleens of Mycobacterium lepraemurium-infected C57BL/6 mice on petri dishes coated with mycobacterial antigens. When adoptively transferred to syngeneic mice, the mycobacterial antigen-reactive cells were found to depress the induction and expression of the delayed-type hypersensitivity (DTH) reaction to M. lepraemurium antigens. The adoptive transfer of soluble suppressor factors (SF) secreted by these cells inhibited only the expression of DTH. The cells depressing the induction of DTH mainly belonged to the L3T4+ (CD4+) T-lymphocyte subset, whereas those depressing its expression differed from the L3T4+ and Lyt-2+ (CD8+) subsets. Treatment of M. lepraemurium-infected mice with SF reduced their mean survival time and enhanced the multiplication of bacilli at the site of infection and their dissemination to the spleen and liver. In vitro at least, SF appeared to interfere at the level of mycobacterial antigen recognition by T lymphocytes rather than at the levels of antigen processing and presentation by macrophages.

Animals↗
PubMed1989

Linkage analysis of the Bcg gene on mouse chromosome 1. Identification of a tightly linked marker.

We have mapped and determined the gene order of five cloned genes in the vicinity of the murine host resistance gene Bcg on mouse chromosome 1. For this, we have used a RFLP-type analysis in panels of 43 recombinant inbred strains, 3 congenic mouse strains, and 186 segregating backcross progeny derived from inbred strains of Bcgr and Bcgs genotypes. The Bcg alleles of segregating animals were established by in vivo infection with Mycobacterium bovis (Bacillus Calmette-Guérin) strain Montreal. Genomic DNA prepared from progenitor mouse strains was isolated, digested with restriction endonucleases, and analyzed by Southern blotting to identify strain-specific RFLP for each DNA marker tested. Among a number of DNA markers tested, Len2, Fn, Vil, Alpi, and Achrg were found to co-segregate with Bcg in mouse strains congenic for this locus. Detailed segregation analysis of the five markers and Bcg showed that Vil was extremely close to Bcg with no recombinant identified, whereas Fn and Len2 were located 4.5 and 9 cM proximal of Bcg, respectively. Alpi and Achrg mapped 5 and 5.5 cM distal from Bcg, respectively. Pedigree analysis in the recombinant inbred strains and backcross animals indicated the gene order: centromere-Len2-Fn-Vil,Bcg-Alpi-Achrg. The tightly linked Vil marker can now be used as an entry point in recombinant genomic DNA libraries to clone sequences overlapping Bcg. This group of five genes flanking Bcg on mouse chromosome 1 is precisely conserved on the telomeric end of the long arm of human chromosome 2q. Our results suggest that a likely location for a putative human homologue to the murine host resistance gene Bcg is the long arm of human chromosome 2 (2q32-qter).

Animals↗
PubMed1989

Identification and characterization of a BCG antigen expressed at the membrane surface of in vitro infected mouse peritoneal macrophages.

A murine monoclonal antibody to Mycobacterium bovis (BCG) (230A4A6) was used to identify an antigenic determinant expressed at the surface of murine peritoneal macrophages infected in vitro. This determinant was shown to be expressed with a delay in infected macrophages following in vitro infection. Isolation of the 230A4A6 reactive antigen showed that it was part of a 12-kD molecule. This protein was shown to be capable of eliciting delayed-type hypersensitivity in infected mice in a standard footpad assay as well as provide stimulus for mitogenesis of BCG-primed spleen cells.

Animals↗
PubMed1988

Pleiotropic effects of the Bcg gene. II. Genetic restriction of responses to mitogens and allogeneic targets.

The response of Bcgr and Bcgs spleen cells to allogeneic Ag, mitogens, and in a system of oxidative mitogenesis using neuraminidase and galactose oxidase was investigated in two Bcg congenic systems. The Bcgr macrophages supported the MLR across H-2 barrier much better than the Bcgs macrophages. At sub-optimal or optimal doses of mitogens Bcgr mice were higher responders than their Bcgs counterparts. The superior response of Bcgr spleen cells to Con A was further investigated with the aim of identifying the population expressing this phenotype. T cells of either Bcgr or Bcgs type showed equal ability to respond to Con A in the presence of macrophages. Purified splenic macrophages from Bcgr mice contained a significantly greater percentage of Ia+-bearing macrophages compared to Bcgs mice. Splenic macrophages of the Bcgr type were more efficient than their Bcgs counterparts at restoring the Con A response of accessory cell-depleted spleen cells. Resident peritoneal macrophages as well as splenic dendritic cells from Bcgr and Bcgs mice were equally efficient at restoring this response. Glutaraldehyde-fixed Bcgr splenic macrophages were shown to be more efficient than the Bcgs cells at replenishing the response of Con A-unresponsive spleen cells when supplemented with IL-1.

Animals↗
PubMed1988

Pleiotropic effects of the Bcg gene. I. Antigen presentation in genetically susceptible and resistant congenic mouse strains.

The Ag-presentation ability of Bcgr and Bcgs spleen cells was studied in two sets of Bcg-congenic systems; namely, the BALB/c-BALB/c.Bcgr pair and the B10.A-B10.A-Bcgr pair, by using three sonicated soluble bacterial Ag (mycobacterium bovis bacillus Calmette-Guérin, Salmonella typhimurium, and Brucella abortus) as well as a particulate Ag (heat-killed Escherichia coli). Pulsed Bcgr spleen cells were shown to induce a stronger proliferation of the T cell-indicator system than their Bcgs counterparts. No difference in Ag-presenting ability could be shown between Bcgr and Bcgs peritoneal macrophages from normal animals. However, elicited peritoneal macrophages from immune Bcgr mice were superior in their Ag-presentation ability. Differences at the level of Ag presentation of Bcgr and Bcgs splenic cells were investigated further. Depletion of T cells and B cells did not alter the differences in Ag-presenting ability between Bcgr and Bcgs spleen cells. Furthermore, splenic dendritic cells of Bcgr or Bcgs allelic types were equally efficient in presenting bacillus Calmette-Guérin Ag to accessory cell-depleted T cells. In a final experiment, it was shown that spleen macrophages were the cell type involved in the superior Ag presentation by Bcgr splenic cells.

Animals↗
PubMed1988

Partial characterization of suppressor factors in spleen cell culture supernatants of Mycobacterium lepraemurium-infected mice.

Suppressor factors (SF) were released into the culture supernatant when spleen cells from M. lepraemurium-infected C57BL/6 mice were incubated at 37 degrees C in the absence of any inducing agents. Some of the SF appeared to be specific in that they inhibited the blastogenic response to mycobacterial antigens by opposition to the others which inhibited the blastogenic responses to PHA, Con A and LPS. All SF seemed to be produced in a cyclic manner. In mice infected 9 weeks earlier, the release of "specific" SF occurred early (4-8 h) during the incubation period whereas, the nonspecific SF were released later on (12-32 h). Adoptive transfers of SF-containing culture supernatants depressed the expression of DTH to M.1m antigens but not its induction.

Animals↗
PubMed1988

Pleiotropic effects of the Bcg gene: III. Respiratory burst in Bcg-congenic macrophages.

Macrophage respiratory burst, as assessed by H2O2 and O2- production, and HMS and chemiluminescence activity was investigated in a variety of conditions in macrophages from Bcg-congenic mice. Measurement of HMS and chemiluminescence in splenic macrophages challenged in vitro with BCG showed that the Bcgr cells were more stimulated by the challenge than their Bcgs counterparts. H2O2 production was measured in Bcgr and Bcgs splenic macrophages. PMA-triggering and LK-triggering were shown to stimulate a similar degree of H2O2 production Bcgr and Bcgs macrophages. In contrast, in vitro phagocytosis of BCG was shown to trigger superior production of H2O2 and O2- in the Bcgr splenic macrophages as compared to their Bcgs congenics. Finally, following the in vivo infection with BCG Montreal, Bcgr splenic macrophages were superior producers of H2O2 (both spontaneous and PMA-triggered) in the early phase of infection.

Animals↗
PubMed1987

Suppressor T cells for delayed-type hypersensitivity in susceptible mice infected with Mycobacterium lepraemurium.

Spleen cells from immunodepressed C3H mice, i.e., mice inoculated intravenously 4 months earlier with 1 X 10(7) Mycobacterium lepraemurium (Mlm) bacilli, were separated into different populations, and the T-cell-enriched population was treated further with gamma-irradiation or specific anti-Lyt antibodies plus complement. The cell populations obtained were then adoptively transferred to normal and Mlm-sensitized syngeneic mice in order to investigate whether or not suppressor cells regulate the delayed-type hypersensitivity (DTH) reaction to specific antigens. A radiosensitive cell population expressing the Lyt 1+, 2+ phenotype had the capacity to depress the induction (afferent phase) of DTH reaction. In contrast, a radioresistant cell population expressing the Lyt 1+, 2- phenotype possessed the capacity to depress the expression (efferent phase) of the cutaneous reaction. Thus, distinct populations of suppressor cells, each regulating a different phase of DTH, are induced in the spleen of Mlm-infected mice.

Animals↗
PubMed1986

Control of the Bcg gene of early resistance in mice to infections with BCG substrains and atypical mycobacteria.

The effect of the Bcg gene on the early host response to intravenous infection with a variety of BCG substrains and some atypical mycobacteria was investigated. The numbers of live bacilli of BCG Pasteur and BCG Tice recovered from the spleens of Bcgs mice (C57BL/6, B10.A and BALB/c) at 3 weeks following infection exceeded the bacterial dose injected, whereas the number of CFU recovered from the spleens of Bcgr mice (A/J, DBA/2 and C3H/HeN) did not exceed the number of CFU injected, thus following the pattern observed in Bcgr mice and Bcgs infected with BCG Montreal. BCG Russia failed to multiply in both test groups; however, the number of CFU recovered in Bcgr mice was significantly lower than in Bcgs mice. On the other hand, the presence of live bacilli in the spleens of either Bcgr or Bcgs mice injected with BCG Japan was undetectable in most cases. Involvement of the Bcg gene in the early resistance to infection with BCG Pasteur, BCG Russia, Mycobacterium kansasii and M. intracellulare was documented by the significant differences in the kinetics of infections in mice of the C.D2 (BALB/c-Bcgr) and BALB/c (Bcgs) congenic lines. In BCG Russia, M. intracellulare and M. fortuitum infections, the phenotypic expression of the Bcg gene resulted in a more rapid elimination of the bacteria in the spleens of Bcgr when compared with Bcgs mice. On the other hand, the hepatic granuloma formation correlated with bacterial load except when C.D2 mice were infected with a small dose of BCG Pasteur or M. kansasii where extensive granulomatous hepatitis developed although no bacterial multiplication occurred in the spleen. It is suggested that granuloma formation could depend of the properties of the mycobacteria as well as the genetic background of the host without implicating the bacterial burden.

Animals↗