Disseminated blue nevus: abnormal nevoblast migration or proliferation?
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Adult↗
Biomedical subjects
V Mallet
Publications and source records attributed to V Mallet.
[Pachydermoperiostosis with extramedullary hematopoiesis without myelofibrosis].
BACKGROUND: In three previous reports of primary hypertrophic osteoarthropathy, an associated extramedullary hematopoiesis was related to myelofibrosis. CASE REPORT: A 44-year-old male patient with primary hypertrophic osteoarthropathy diagnosed when he was 34-year-old was referred to our hospital with an abdominal mass fortuitously detected. DISCUSSION: The present case is unique for the patient developed an extramedullary hematopoïesis without associated myelofibrosis. It suggests the possible intervention of growth factors common to the skin fibroblasts and the blood progenitor cells in the pathogenesis of primary osteoarthropathy.
Abdomen↗
Interferon-gamma rescues HLA class Ia cell surface expression in term villous trophoblast cells by inducing synthesis of TAP proteins.
Human placental trophoblast cells that constitute the materno-fetal interface during pregnancy escape maternal alloimmune attack. The different trophoblast cell subpopulations have developed efficient regulatory mechanisms to prevent expression of beta2-microglobulin-associated HLA class Ia molecules at their cell surface. We previously reported the presence of HLA class Ia messages in villous cytotrophoblast cells and in the syncytiotrophoblast differentiated in vitro purified from term placenta. In this study, we found that these transcripts are translated in heavy chain proteins that are endoglycosidase H sensitive and thus retained in the endoplasmic reticulum or cis-Golgi. Moreover, these class Ia heavy chains can be co-immunoprecipitated with the chaperone protein calnexin resident in the endoplasmic reticulum. When these trophoblast cells are treated with interferon (IFN)-gamma, part of the class Ia heavy chains become endoglycosidase H resistant, demonstrating that they have left the endoplasmic reticulum. Furthermore, after such a treatment, these heavy chains are detectable at the cell surface of these trophoblast cells, as assessed by two-color flow cytometry analysis and immunoprecipitation of cell surface biotinylated proteins using the W6/32 anti-HLA class I monoclonal antibody (mAb). IFN-gamma treatment induces a significant enhancement of the transcription of transporters associated with antigen processing (TAP1 and TAP2) rather than an increase of HLA class I or beta2-microglobulin messages. Finally, we demonstrate that an anti-TAP1 mAb co-immunoprecipitates TAP1 proteins and HLA class Ia heavy chains in these IFN-gamma-treated trophoblast cells. Thus, the constitutive absence of HLA class Ia cell surface expression in term villous cytotrophoblast and syncytiotrophoblast is likely to be due to a lack of transporter proteins that participate in the proper assembly of these molecules in the endoplasmic reticulum. Such a defect can be modified upon IFN-gamma treatment.
ATP Binding Cassette Transporter, Subfamily B, Mem↗
Endothelial cells in chorionic fetal vessels of first trimester placenta express HLA-G.
Using four different HLA-G-recognizing monoclonal antibodies (mAb), we investigated whether this nonclassical HLA class I molecule could be expressed in placental cell types other than extravillous cytotrophoblasts (evct) in which HLA-G has already been detected. Immunohistochemical analysis was performed on serial cryosections of first trimester placenta as well as on maternal decidual tissue. In addition to some proliferative evct, the recently described BFL.1 mAb also slightly stained some villous cytotrophoblast (vct) stem cells located near cell columns and cell islands, which until now have been considered as HLA-G negative. The same staining pattern was obtained with the 16G1 mAb raised against the soluble HLA-G isoform, whereas neither 87G nor HCA2 reacted with vct but did strongly label the invasive populations of evct, including interstitial and endovascular trophoblasts. Surprisingly, BFL.1 strongly and reproducibly stained endothelial cells in the fetal capillaries present in the mesenchymal core of the chorionic villi, whereas none of the other surrounding cellular components were stained. The same specific labeling was obtained, although with less intensity, with the three other HLA-G-recognizing mAb. In contrast, maternal endothelial cells present in spiral arteries of the decidua parietalis remained unstained. This unexpected cellular localization suggests that HLA-G may be present as a soluble form during the whole period of fetal vascularization and/or exert a nonimmunological function related to the endothelial cell type, in particular in the angiogenesis process which is highly active, until term, in chorionic villi.
Blood Vessels↗
DNA vaccination using expression vectors carrying FIV structural genes induces immune response against feline immunodeficiency virus.
Following inactivated virus vaccination trials, the surface glycoprotein gp120 of the feline immunodeficiency virus (FIV) was considered as one of the determinants for protection. However, several vaccination trials using recombinant Env protein or some peptides failed to induce protection. To understand the role of the gp120 protein in vivo, we vaccinated cats with naked DNA coding for FIV structural proteins gp120 and p10. We analyzed the ability of these vaccinations to induce immune protection and to influence the onset of infection. Injection in cat muscles of expression vectors coding for the FIV gp120 protein induced a humoral response. Cats immunized twice with the gp120 gene showed different patterns after challenge. Two cats were, like the control cats, infected from the second week after infection onwards. The two others maintained a low proviral load with no modification of their antibody pattern. The immune response induced by gp120 DNA injection could control the level of viral replication. This protective-like immune response was not correlated to the humoral response. All the cats immunized with the gp120 gene followed by the p10 gene were infected, like the control cats, from the second week but they developed a complete humoral response against viral proteins after challenge. Furthermore, they showed a sudden but transient drop of the proviral load at 4 weeks after infection. Under these conditions, one injection of the p10 gene after one injection of the gp120 gene was not sufficient to stimulate protection. On the contrary, after a period, it seems to facilitate virus replication.
Animals↗
HLA-G and pregnancy.
Recent studies of the nonclassical HLA-G class I gene provide insight into its function(s) during pregnancy. The HLA-G gene can be transcribed in different isoforms resulting from alternative splicings and encoding membrane-bound and soluble proteins. These different mRNA species have been found in the various trophoblast cell subpopulations that constitute the maternofetal interface in the human placenta. The raising of antibodies to HLA-G has introduced new tools to determine in which types of trophoblast cells and in which other tissues these transcriptional isoforms are translated in functional proteins. The HLA-G gene exhibits a certain amount of polymorphism, the exon three that encodes the alpha 2 external domain showing the most extensive nucleotide variability. It remains to be determined whether the homozygosity of some HLA-G alleles constitutes a real disadvantage in terms of pregnancy or resistance to specific pathogens. Regarding the potential antigen-presenting function(s) of HLA-G, two isoforms are capable of binding an identical set of nonamer peptides derived from a variety of intracellular proteins. The ligand motif contains three anchor residues and is similar to that of classical HLA class I molecules. Experiments are being performed to identify the recognizing cells and to determine whether HLA-G induces a cytolytic (including anti-viral) T-cell response or in some other way represses natural killer-cell functions.
Alleles↗
Placental expression of HLA class I genes.
This article presents an overview of the more recent data dealing with the constitutive, transcriptional, and translational expression of classical class Ia and nonclassical HLA-E and -G class Ib products in the different trophoblast cell subpopulations that constitute the maternofetal interface during human pregnancy. Of particular interest is the expression of alternatively spliced HLA-G transcriptional isoforms that may be translated in membrane-bound or soluble protein products. Molecular regulatory mechanisms that may control the differential expression of class Ia and class Ib molecules, according to the cell types, state of differentiation, and stages of gestation are also examined. They may operate at the levels of transcription, translation and/or transport of proteins to the cell surface. Functional significance of the absence of detectable cell surface expression of class Ia molecules in all trophoblast cell subpopulations, and of the presence of membrane-bound HLA-G products in extravillous cytotrophoblast cells is finally questioned.
Female↗
Detection of membrane-bound HLA-G translated products with a specific monoclonal antibody.
A monomorphic anti-HLA-G monoclonal antibody (mAb) was obtained by immunization of HLA-B27/human beta 2-microglobulin double-transgenic mice with transfected murine L cells expressing both HLA-G and human beta 2-microglobulin. This mAb, designated BFL.1, specifically recognizes, by flow cytometry analysis, the immunizing HLA-G-expressing cells, whereas it does not bind to parental untransfected or to HLA-B7- and HLA-A3-transfected L cells, suggesting that it distinguishes between classical HLA-A and -B and nonclassical HLA-G class I molecules. This was further assessed by the absence of BFL.1 reactivity with a number of human cell lines known to express classical HLA class I proteins. In addition, we showed that the BFL.1 mAb also labels HLA-G-naturally-expressing JEG-3 and HLA-G-transfected JAR human choriocarcinoma cell lines as well as a subpopulation of first-trimester placental cytotrophoblast cells. Further biochemical studies were performed by immunoprecipitation of biotinylated membrane lysates: BFL.1, like the monomorphic W6/32 mAb, immunoprecipitated a 39-kDa protein in HLA-G-expressing cell lines, a size corresponding to the predicted full-length HLA-G1 isoform. However, in contrast to W6/32, which immunoprecipitates both classical and nonclassical HLA class I heavy chains, BFL.1 mAb does not recognize the class Ia products. Such a mAb should be a useful tool for analysis of HLA-G protein expression in various normal and pathological human tissues and for determination of the function(s) of translated HLA-G products.
Animals↗
Methylation status and transcriptional expression of the MHC class I loci in human trophoblast cells from term placenta.
Of the various molecular regulatory mechanisms that may be used by human trophoblast cells to down-regulate expression of HLA class I genes, we chose to investigate the methylation of DNA, generally associated with inhibition of transcription. We analyzed the methylation status of different HLA class I loci in villous and extravillous cytotrophoblast cells and in vitro-differentiated syncytiotrophoblast, purified from human term placenta, as well as in the human trophoblast-derived JAR and JEG-3 cell lines. We then compared methylation status and transcriptional activity. An inverse relationship was established between JAR and JEG-3: HLA-A, -B, and -G are methylated and repressed in JAR, whereas in JEG-3, HLA-A is methylated and repressed but HLA-B and -G are partially methylated and transcribed. HLA-E is unmethylated and transcribed in both cell lines. Apart from HLA-E, which is always unmethylated and transcribed, no such relationship exists for the other class I loci in trophoblast cells. Whereas nonclassical HLA-G and classical HLA-A and -B class I genes are undermethylated in both cytotrophoblast and syncytiotrophoblast, they are clearly transcribed in the former but minimally transcribed in the latter subpopulation. Thus, the down-regulation of class I gene expression in the in vitro-differentiated syncytiotrophoblast is unlikely to be caused by DNA methylation. Furthermore, there is no detectable expression of any class I molecule at the cell surface of either trophoblast cell subpopulation, suggesting a negative control on translation and/or on the secretory pathway to the plasma membrane.
Base Sequence↗
Neutrophilic dermatoses during granulocytopenia.
BACKGROUND AND DESIGN: Noninfectious cutaneous neutrophilic lesions can occur during granulocytopenia, but their mechanism remains unknown. We undertook a retrospective study of the neutrophilic dermatoses that developed during granulocytopenia induced by chemotherapy for acute myelogenous leukemia. RESULTS: Seven men and one woman were included (2.6% of treated cases of acute myelogenous leukemia); half had acute myelogenous leukemia subtypes 4 and 5. The male-to-female ratio was 7:1. Neutrophilic eccrine hidradenitis was diagnosed in five cases, Sweet's syndrome in two cases, and difficult-to-classify neutrophilic dermatoses in one case. Cutaneous lesions appeared 12.5 days after the start of chemotherapy, and the mean leukocyte count was 0.426 x 10(9)/L. Three patients needed corticosteroids systemically. CONCLUSION: Neutrophilic dermatoses during chemotherapy-induced granulocytopenia seem to occur more frequently in men with acute myelogenous leukemia subtypes 4 and 5.
Adult↗
[Cutaneous cicatrizing agents].
Cutaneous healing is an important field of dermatology for it concerns superficial wound, as well as little surgery action, leg ulcer, eschar or burn. In spite of the claiming of their healing properties and their profusion, only a few have been tested and have proved their efficiency. Use precautions must be complied with paying the highest attention among others to the condition of the wound before product applying, the sensitization risk and the systemic risk particularly for young child. After topics, colloids appeared about ten years ago. New technics in development are reflecting, the research perseverance in dermatology.
Cicatrix↗
[Clinical aspects and therapeutic approach in cutaneous lesions of lupus erythematosus].
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Biopsy↗
[Palmoplantar punctate keratosis].
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Adult↗
[Diagnosis and treatment of photodermatoses].
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Humans↗
[Tinea of the scalp in the region of the river Meuse: a current renaissance?].
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Antifungal Agents↗
Simultaneous determination of captan and captafol in apples and potatoes by thin layer chromatography and in situ fluorometry.
A simple method is described for the simultaneous quantitative determination of captan [N-(trichloromethylthio)-3a,4,7,7a-tetrahydrophthalimide] and captafol [N-(1,1,2,2-tetrachloroethylthio) -3a,4,7,7a - tetrahydrophthalimide] in apples and potatoes. The fungicide residues are extracted with acetonitrile, partitioned into a solution of methylene chloride in petroleum ether, separated from each other and the co-extractives on a thin layer chromatographic plate impregnated with aluminum chloride, sprayed with sodium chlorate, and heated. The fluorescence is then measured directly from the chromatogram. Recoveries were greater than 90% in the test crops at the 0.2 ppm level.
Captan↗
Determination of quinomethionate (6-methylquinoline-2,3-diyldithiocarbonate) residues in crops by in situ fluorometry.
A simple method is described for the quantitative determination of quinomethionate (6-methylquinoline- 2,3 - diyldithiocarbonate) in crops. The pesticide residue is extracted with acetonitrile and partitioned in petroleum ether. After separation from the co-extractives by thin layer chromatography (TLC), the fluorescence is measured directly on a silica gel TLC plate. An average of 89% recovery is obtained at the 0.05 ppm level in apples, peaches, pears, and tomatoes.
Chromatography, Thin Layer↗