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Biomedical subjects

E Moreau

Publications and source records attributed to E Moreau.

At least 19 recordsLinked to original sources
PubMed2006

Powerful strategy for polymerase chain reaction-based clonality assessment in T-cell malignancies Report of the BIOMED-2 Concerted Action BHM4 CT98-3936.

Polymerase chain reaction (PCR) assessment of clonal T-cell receptor (TCR) and immunoglobulin (Ig) gene rearrangements is an important diagnostic tool in mature T-cell neoplasms. However, lack of standardized primers and PCR protocols has hampered comparability of data in previous clonality studies. To obtain reference values for Ig/TCR rearrangement patterns, 19 European laboratories investigated 188 T-cell malignancies belonging to five World Health Organization-defined entities. The TCR/Ig spectrum of each sample was analyzed in duplicate in two different laboratories using the standardized BIOMED-2 PCR multiplex tubes accompanied by international pathology panel review. TCR clonality was detected in 99% (143/145) of all definite cases of T-cell prolymphocytic leukemia, T-cell large granular lymphocytic leukemia, peripheral T-cell lymphoma (unspecified) and angioimmunoblastic T-cell lymphoma (AILT), whereas nine of 43 anaplastic large cell lymphomas did not show clonal TCR rearrangements. Combined use of TCRB and TCRG genes revealed two or more clonal signals in 95% of all TCR clonal cases. Ig clonality was mostly restricted to AILT. Our study indicates that the BIOMED-2 multiplex PCR tubes provide a powerful strategy for clonality assessment in T-cell malignancies assisting the firm diagnosis of T-cell neoplasms. The detected TCR gene rearrangements can also be used as PCR targets for monitoring of minimal residual disease.

Gene Amplification↗
PubMed2006

Connection between the Burgers equation with an elastic forcing term and a stochastic process.

In this paper, a complete analytical resolution of the one dimensional Burgers equation with the elastic forcing term -k2x + f(t), k is an element of R is presented. Two methods existing for the case K=0 are adapted and generalized using variable and functional transformations, valid for all values of space and time. The emergence of a Fokker-Planck equation in the method allows the establishment of a connection between the Burgers equation and the Ornstein-Uhlenbeck process.

Journal Article↗
PubMed2005

Humoral and cellular immune responses to Fasciola gigantica experimental infection in buffaloes.

Humoral and cellular immune responses to Fasciola gigantica experimental infection in buffaloes were studied. The results showed that 33.4+/-9.1% of the infection dose was recovered as adult flukes from infected animals at necropsy. Significant differences of weight gain between infected and non-infected buffaloes was observed at 4 MPI (months post-infection). Anti F. gigantica excretory-secretory products (FgESP)-IgG levels increased significantly from 3 WPI (weeks post-infection) and displayed a peak at 13 WPI. Western blot indicated that in FgESP six major bands of 11.5, 19.0, 23.4, 29.8, 47.5 and 53.2kDa were recognized by F. gigantica-infected buffaloes sera after 0 WPI. Eosinophil numbers increased significantly from 3 WPI in F. gigantica-infected buffaloes and displayed a peak at 8 WPI. Peripheral blood mononuclear cells (PBMC) proliferation induced by FgESP increased from 2 WPI with a peak at 5 WPI. IFNgamma secretion by FgESP-stimulated PBMC appeared early from 1 WPI with three peaks at 2, 5 and 8 WPI, respectively. IL-10 production was observed from 2 WPI with two peaks at 4 and 9 WPI, respectively. Our results suggested that buffaloes were highly susceptible to F. gigantica infection, and this susceptibility could be associated with the late and weak cellular immune response in the early phase of infection and the Th0-like response throughout the infection.

Animals↗
PubMed2005

Fasciola hepatica and Fasciola gigantica: comparison of cellular response to experimental infection in sheep.

Cellular responses to Fasciola gigantica and to Fasciola hepatica infection in sheep were compared. Eosinophil numbers increased more quickly and strongly in F. gigantica-infected sheep than in F. hepatica-infected sheep. In both groups, peripheral blood mononuclear cell (PBMC) proliferation in response to the parasitic excretory-secretory products (ESP) showed similar kinetics. Interferon-gamma (IFN-gamma) production by ESP-stimulated PBMC was early and showed similar kinetics in both groups. Interleukin-10 (IL-10) production by FhESP-stimulated PBMC was very high throughout infection even at 0 weeks post-infection (WPI) in F. hepatica-infected sheep, while in F. gigantica-infected sheep, IL-10 production by FgESP-stimulated PBMC increased between 1 and 4 WPI. IL-10 production in F. gigantica-infected sheep was significantly lower than in F. hepatica-infected sheep during infection. The lower susceptibility to F. gigantica infection in sheep could be explained by the more intense cellular response induced by the parasite and the weaker capacity of F. gigantica to evade the immune response.

Animals↗
PubMed2005

Comparison of modulation of sheep, mouse and buffalo lymphocyte responses by Fasciola hepatica and Fasciola gigantica excretory-secretory products.

In order to explain the difference in susceptibility to Fasciola hepatica and F. gigantica between animal species, the activity of their excretory-secretory products (FhESP and FgESP, respectively) on concanavalin A (ConA)-induced proliferation of different animal species (sheep, mouse and buffalo) lymphocytes was compared. At high doses, FhESP inhibited proliferation of lymphocytes of all the animal species tested, and at low doses they inhibited the proliferation of sheep lymphocytes and increased the proliferation of buffalo and mouse lymphocytes. The effects of FgESP were similar but the intensity of FgESP inhibition was less than FhESP. The immunomodulatory effects of FhESP or FgESP could not alone explain the susceptibility level of hosts to Fasciola spp. The immunomodulatory molecules of FhESP and FgESP and their role in the course of Fasciola spp. infection should be further investigated.

Animals↗
PubMed2004

Comparison of humoral response in sheep to Fasciola hepatica and Fasciola gigantica experimental infection.

Humoral response of sheep to F. gigantica was compared with the well known humoral response to F. hepatica, in order to explain the difference of susceptibility of sheep to these two parasites. In this work, a lesser susceptibility of sheep to F. gigantica than to F. hepatica infection was confirmed. Humoral response to F. hepatica infection is similar to that previously described by several authors. IgG level of F. gigantica infected sheep increased from week 2 post-infection (2WPI) and displayed a peak at 13WPI. F. gigantica excretory-secretory products (FgESP) analyzed by SDS-PAGE showed at least 31 bands from 12.0 to 127.6 kDa in FgESP. Western blot indicated that F. gigantica infected sheep sera recognized, in FgESP, at least 30 antigens from 7.8 to 119.2 kDa of which 12 major bands recognized after OWPI. In FhESP and FgESP, F. hepatica infected sheep serum reacted only with the lower molecular mass antigens, while F. gigantica infected sheep serum reacted with the lower and the higher molecular mass antigens. These differences of antigenic recognition might be associated with the difference of susceptibility of sheep. Further investigation must be done to study the mechanism of resistance between the sheep infected with F. hepatica or F. gigantica.

Animals↗
PubMed2004

Important B-cell epitopes for neutralization of human immunodeficiency virus type 1 Tat in serum samples of humans and different animal species immunized with Tat protein or peptides.

The Tat regulatory protein of human immunodeficiency virus type 1 (HIV-1) is secreted by infected cells and plays a key role in viral pathogenesis and replication. Tat protein has been proposed as a target antigen for vaccine design since anti-Tat antibodies may interfere with virus spread and disease progression. The aim of this study was to analyse the serum antibody response of mice, rabbits, macaques and humans immunized with recombinant Tat, synthetic Tat, Tat toxoid or Tat peptides and to examine the biological properties of these antibodies in terms of Tat-induced transactivation and HIV-1 replication. Only sera with antibody specificity to both N-terminal and basic functional domains were able to inhibit extracellular Tat-dependent transactivation significantly in vitro. Antibodies from a human subject immunized with Tat also reduced HIV-1 replication in acutely infected T cells and blocked reactivation of virus replicating low levels in chronically infected cells by exogenous Tat. These results demonstrate that immunization with Tat protein or a combination of synthetic Tat peptides elicits the production of Tat-neutralizing serum antibodies and suggest that Tat vaccination could be used to block in vivo extracellular Tat autocrine/paracrine transactivation of HIV-1 replication.

AIDS Vaccines↗
PubMed2003

Development of the foetal and neonatal testis.

The foetal testis originates from a proliferation of the mesonephric and the coelomic epithelia which are colonized by the primordial germ cells. In the foetal testis, the development and functions of the three main cell type precursors (Leydig, Sertoli and germ cells) do not depend upon gonadotropins. Numerous intra- and extra-testicular factors are candidates for the control of its development and functions. To study the potential involvement of these factors, we developed an organotypic culture system. In absence of any growth factors or hormone, this system allows a development of the three main cell types which mimics that observed in vivo. The effects of different regulators (gonadotropin-releasing hormone, follicle-stimulating hormone, transforming growth factor-beta, insulin-like growth factor-I, anti-Mullerian hormone, retinoic acid, oestrogens) were tested in this system. Whether or not some of the effects observed in vitro have a physiological relevance was evaluated using appropriate transgenic mice. It is concluded that the foetal testis cannot be considered as an adult mini-testis since it has a specific physiology which largely differs from that of the immature or adult testis.

Animals↗
PubMed2001

Heterocyclization of functionalized vinylic derivatives of imidazo.

Heterocyclization of functionalized vinylic derivatives of imidazo[1,2-a]pyridines was explored experimentally and theoretically using semiempirical AM1 and ab initio methods. A range of functionalized vinylic derivatives (azido, amino, and carbodiimide groups) were prepared for conversion into pyrroloazaindoles 19-22, imidazo[1,x]-, (x = 5, 6, 7, 8), [2,6]-, and [2,7]naphthyridines 28-30, 35-38 by thermal reaction. In the case of vinylic groups in the 5 position, peri annulation also was observed. The experimental and theoretical data are compared and discussed.

Animals↗
PubMed2001

Construction and functional evaluation of a single-chain antibody fragment that neutralizes toxin AahI from the venom of the scorpion Androctonus australis hector.

9C2 is a murine monoclonal IgG that participates in the neutralization of Androctonus australis hector scorpion venom. It recognizes AahI and AahIII, two of the three main neurotoxins responsible for almost all the toxicity of the venom when injected into mammals. Using PCR we cloned the antibody variable region coding genes from 9C2 hybridoma cells and constructed a gene encoding a single-chain antibody variable fragment molecule (scFv). This scFv was produced in the periplasm of Escherichia coli in a soluble and functional form and purified in a single step using protein L-agarose beads yielding 1-2 mg.L(-1) of bacterial culture. scFv9C2 was predominantly monomeric but also tended to form dimeric and oligomeric structures, all capable of binding toxin AahI. The affinity of scFv and the parental mAb for toxin AahI and homologous toxin AahIII was of the same magnitude, in the nanomolar range. Similarly, purified forms of scFv9C2 completely inhibited the binding of toxin AahI to rat brain synaptosomes. Finally, scFv9C2 was efficient in protecting mice against the toxic effects of AahI after injection of the toxin and scFv to mice by the intracerebroventricular route in a molar ratio as low as 0.36 : 1. Thus, we produced a recombinant scFv that reproduces the recognition properties of the parent antibody and neutralizes the scorpion neurotoxin AahI, thereby opening new prospects for the treatment of envenomation.

Amino Acid Sequence↗
PubMed2001

Overexpression of human insulin-like growth factor binding protein-1 in the mouse leads to nephron deficit.

IGFs and their binding proteins are important regulators of fetal development. We have previously reported that overexpression of the human IGF binding protein-1 in mice is associated with glomerulosclerosis. The aim of this study was to investigate whether, in that model, decreased bioavailability of IGFs also affected nephrogenesis. When the mothers expressed human IGF binding protein-1, pups were growth retarded and had a reduced number of nephrons. Even nontransgenic pups born to heterozygous mothers had a nephron reduction, indicating that renal hypoplasia was secondary to fetal growth retardation. When the transgene was expressed only in the fetus, pups had a normal birth weight and the kidney was normal at birth, as indicated by histologic studies. However, a significant reduction in the nephron number was observed at 3 mo of age. Because nephrogenesis continues for a few days after birth in the mouse, this indicated that human IGF binding protein-1 overexpression altered postnatal nephrogenesis. In addition, exogenously added IGF-II, but not IGF-I, was effective in stimulating in vitro nephrogenesis. Together these elements suggest that reduced amounts of circulating IGFs, presumably IGF-II, impair kidney development.

Animals↗
PubMed2000

Interactions between red blood cells and a lethal, partly quaternized tertiary polyamine.

Partially quaternized poly[thio-1-(N,N-diethyl-aminomethyl) ethylene]s, Q-P(TDAE)(x) with x indicating the percentage of quaternized subunits, have been proposed as potential carriers for drugs insoluble in water. However these cationic polyelectrolytes form emboli upon intravenous administration. In order to study the mechanism, Q-P(TDAE)(11) was incubated in vitro with red blood cells (RBCs) suspended in various aqueous media such as autologous plasma, autologous serum, albumin dissolved in phosphate buffer, plasma-serum mixtures and Tris buffer. The deformability of the RBC membrane studied by viscometry was not affected by the polycation. Q-P(TDAE)(11)-induced hemagglutination was studied by optical microscopy. It depended on the polymer concentration and on the presence of plasma proteins. As ghosts were formed in some cases, hemolysis was investigated by measuring potassium and hemoglobin released from RBCs. Fibrinogen and serum proteins, except albumin, protected RBCs from hemolysis. Moreover the order of addition of the suspension components modulated dramatically the Q-P(TDAE)(11)-induced hemolysis. Addition of Q-P(TDAE)(11) to whole blood caused hemolysis whereas addition of the polymer to plasma prior to contact with RBCs did not affect the cell integrity. In contrast, addition of the polymer to RBCs suspended in albumin solution caused greater hemolysis than the addition to whole blood, and the contact between Q-P(TDAE)(11) and albumin prior to RBC addition still enhanced cell lysis. Two conclusions can be drawn from these observations: (i) Q-P(TDAE)(11) induces both hemagglutination, probably through electrostatic interaction, and hemolysis, because Q-P(TDAE)(11) disrupted the RBC lipid bilayer; (ii) proteins can decrease or increase the deleterious effects of Q-P(TDAE)(11) on RBCs.

Blood Proteins↗
PubMed1999

Nephrotoxin exposure in utero reduces glomerular number in sclerosis-prone but not sclerosis-resistant mice.

BACKGROUND: We have previously found that nephron number was not fixed, that is, there was a direct correlation between low birth weight and decreased nephron number in infants. In sclerosis-prone rats, we found that gentamicin exposure in utero induced a reduction in glomerular number and aggravated glomerulosclerosis in adults. In mice, we found that an inborn 50% reduction in nephron number, caused by the Os mutation, was associated with glomerulosclerosis in sclerosis-prone (ROP+/+) mice, but not in sclerosis-resistant (C57BL/6J) mice. Because the genetic background determined the response to decreased nephron number, we asked whether the susceptibility changes in glomerular number and glomerulosclerosis were linked. METHODS: Gentamicin was administered before and after the onset of fetal nephrogenesis. (1) Prior to the onset of nephrogenesis, two groups of pregnant mice were treated from embryonic day (E) E8 to E12. In group A, early glomerular development was studied by placing ureteric ridges removed on E12 in vitro for four days, following which the ureteric bud branches and glomeruli were counted using lectin staining. In group B, nephron number was determined in spontaneously delivered 14-day-old (14PN) pups by counting glomeruli. (2) After the onset of nephrogenesis, to determine the direct effects of gentamicin on nephron induction, ureteric ridges were placed in organ culture at E12 of normal gestation, in the presence or absence of gentamicin. The number of glomeruli and ureteric bud branches were counted after six days in culture. RESULTS: A decrease in glomerular number and ureteric bud branches was observed in sclerosis-prone (ROP+/+) mice, irrespective of whether gentamicin was administered prior to or after the onset of nephrogenesis. Glomerular number and ureteric bud branching were not decreased by gentamicin in sclerosis-resistant (C57BL/6) mice. CONCLUSIONS: These data provide evidence that there is a positive correlation between the susceptibility to glomerulosclerosis in adulthood and a reduction in nephron number in utero. Thus, exposure to nephrotoxins in utero compounds the risk of renal failure as an adult in sclerosis-prone individuals.

Animals↗
PubMed1998

Mild vitamin A deficiency leads to inborn nephron deficit in the rat.

BACKGROUND: Vitamin A plays a critical role in fetal organogenesis, and its severe deficiency during pregnancy is known to result in malformations of several organs, including the kidney. However, the consequences of mild vitamin A deficiency (VAD) has received little attention. In the present study, we examined the effect of in utero exposure to mild VAD on renal organogenesis. METHODS: A rat model of mild VAD compatible with normal gestation was developed. Plasma retinol was determined by reverse phase HPLC in mothers and fetuses. Nephron counting was performed in kidneys of fetuses and pups issued from control and VAD mothers. Metanephroi explanted from 14-day-old fetuses from both groups were cultured in the presence or absence of retinoic acid (RA), and growth and differentiation were assessed. c-ret expression was analyzed from fetuses exposed in utero to VAD or to normal vitamin A status and also in metanephroi grown in culture with or without RA using RT-PCR. RESULTS: The 50% reduction in circulating vitamin A levels induced by vitamin A deprivation in pregnant rats did not affect the overall fetal development. However, the number of nephrons was reduced by 20% in 21-day-old VAD fetuses. The number of nephrons was closely correlated with circulating vitamin A level in both VAD and control fetuses. Metanephroi taken from VAD fetuses developed to a lesser extent in vitro, but their capacity to respond to exogenous retinoic acid was not altered. Finally, we found that the expression of the proto-oncogene c-ret was modulated according to the retinoid environment. CONCLUSION: We conclude that vitamin A supply to the fetus is critical in determining the number of nephrons. Data available thus far on the frequency of mild VAD during pregnancy and on the long-term consequences of inborn nephron deficit highlight the clinical relevance of the present study.

Animals↗
PubMed1998

IFN gamma and IL-10 production by hepatic lymph node and peripheral blood lymphocytes in Fasciola hepatica infected sheep.

The present study was designed to determine whether IFN gamma and IL-10 were secreted by peripheral blood mononuclear cells (PBMC) and hepatic lymph node mononuclear cells (HLNMC) from 17 Fasciola hepatica infected sheep after in vitro stimulation by Fasciola hepatica excretory-secretory products (FhESP) during the first six weeks of two different infections. The IFN gamma concentration in mononuclear cells (MC) culture supernatants was determined by sandwich ELISA. The presence of IL-10 in MC culture supernatants was determined by the capacity of these to inhibit, with or without monoclonal antibodies to IL-10, the NO production of recombinant bovine IFN gamma (rBoIFN gamma) activated monocytes. FhESP-stimulated PBMC and HLNMC produced IFN gamma in culture supernatants from DPI 7 (day post-infestation 7) to DPI 14. Culture supernatants of PBMC stimulated with FhESP first induced an increase in the NO production of rBoIFN gamma activated monocytes. After 2 or 3 weeks of infection, MC culture supernatant reduced the NO production of rBoIFN gamma activated monocytes. From DPI 35, anti-IL-10 antibodies addition restored or enhanced NO production. During sheep fasciolosis, IFN gamma production increased only until the first two weeks post infection. IL-10 could be secreted throughout the first six weeks of infection and could inhibit monocytes from DPI 35.

Animals↗
PubMed1998

Regulation of c-ret expression by retinoic acid in rat metanephros: implication in nephron mass control.

Vitamin A and its derivatives have been shown to promote kidney development in vitro in a dose-dependent fashion. To address the molecular mechanisms by which all-trans-retinoic acid (RA) may regulate the nephron mass, rat kidneys were removed on embryonic day 14 (E14) and grown in organ culture under standard or RA-stimulated conditions. By using RT-PCR, we studied the expression of the glial cell line-derived neurotrophic factor (GDNF), its cell surface receptor-alpha (GDNFR-alpha), and the receptor tyrosine kinase c-ret, known to play a major role in renal organogenesis. Expression of GDNF and GDNFR-alpha transcripts was high at the time of explantation and remained unaffected in culture with or without RA. In contrast, c-ret mRNA level, which was low in E14 metanephros and dropped rapidly in vitro, was increased by RA in a dose-dependent manner. The same is true at the protein level. Exogenous GDNF barely promotes additional nephron formation in vitro. Thus the present data establish c-ret as a key target of retinoids during kidney organogenesis.

Amino Acid Sequence↗