Search PubMed⌕ Search

Biomedical subjects

M Fabre

Publications and source records attributed to M Fabre.

At least 145 records · Page 8Linked to original sources
PubMed1990

Cloning and characterization of cDNAs for murine macrophage inflammatory protein 2 and its human homologues.

A cDNA clone of murine macrophage inflammatory protein 2 (MIP-2) has been isolated from a library prepared from lipopolysaccharide (LPS)-stimulated RAW 264.7 cells and the nucleotide sequence determined. This cDNA was used to clone cDNAs for human homologues of MIP-2 from a library prepared from phorbol myristate acetate-treated and LPS-stimulated U937 cells. Two homologues were isolated and sequenced. Human MIP-2 alpha and MIP-2 beta are highly homologous to each other and to a previously isolated gene, human gro/melanoma growth-stimulating activity (MGSA). These three human genes, MIP-2 alpha, MIP-2 beta, and gro/MGSA, constitute a sub-family within the cytokine family represented by platelet factor 4 and interleukin 8.

Amino Acid Sequence↗
PubMed1990

Human epidermal Langerhans cells express only the 40-kilodalton Fc gamma receptor (FcRII).

In man, three distinct classes of receptors for the Fc fragments of IgG (FcRI, II, III) have been defined. The FcRI has a Mr of about 72 kDa, binds human IgG-coated E, and is recognized by mAb such as 32. The FcRII has a Mr of 40 kDa, binds murine IgG1-coated E, and reacts with the mAb IV.3 and CIKM5, which recognize CDw32 moieties. Lastly, the FcRIII has a Mr of 50 to 70 kDa and is recognized by anti-CD16 mAb. In the present study we have shown that i) only murine IgG1-coated E form rosettes with 49 +/- 1.5% (mean +/- SEM, n = 9) of CD1a+ epidermal cells (EC) (which represent Langerhans and indeterminate cells) and that ii) the mAb anti-FcRII CIKM5 prevents this rosette formation. Among the mAb reacting with the three different types of FcR, only those recognizing FcRII i) stain about 55 +/- 1.5% (mean +/- SEM, n = 9) of the CD1a+ EC and ii) reveal the presence of dendritic cells in epidermal sheets obtained by suction blister. Under the electron microscope i) apparently all the cells forming rosettes or reacting with the gold-labeled anti-FcRII mAb (CIKM5 or the F(ab) fragment of IV.3) contained Birbeck granules and ii) the gold-labeled mAb were internalized in unfixed Langerhans cells by receptor-mediated endocytosis and accumulated in lysosomes. Labeling by the anti-FcRII mAb of the CD1a+ cells in suspension disappears after 48 h of culture. All these observations strongly suggest that CD1a+ EC express only the FcRII. This conclusion was confirmed by immunoprecipitation experiments, whereas no specific immunoprecipitate was noted with the anti-FcRI or anti-FcRIII mAb, the anti-FcRII mAb immunoprecipitated a protein of Mr 40 kDa.

Antibodies, Monoclonal↗
PubMed1990

Nodular regenerative hyperplasia of the liver, peliosis hepatis, and perisinusoidal fibrosis. Association with angioimmunoblastic lymphadenopathy and severe hypoxemia.

Three different liver lesions were found in a 20-year-old woman with angioimmunoblastic lymphadenopathy. The lesions included nodular regenerative hyperplasia of the liver, perisinusoidal fibrosis, and peliosis hepatis. It is suggested that the association of angioimmunoblastic lymphadenopathy with this broad spectrum of liver lesions was not fortuitous.

Adult↗
PubMed1990

Deficiency of long-chain 3-hydroxyacyl-CoA dehydrogenase: a cause of lethal myopathy and cardiomyopathy in early childhood.

A child presented in early childhood with episodes of coma and hypoglycemia and a rapidly evolutive myopathy and cardiomyopathy leading to death at 9 mo of age. Ketosis was decreased (blood beta-hydroxybutyrate: 0.07 mmol/L) despite normal plasma levels of fatty acids (0.81 mmol/L). The patient's urine contained excessive amounts of the C6 to C10 dicarboxylic acids present in almost all defects of fatty acid mitochondrial oxidation. More specifically, gas chromatography-mass spectrometry identified an accumulation of medium- and long-chain (C8 to C14) 3-hydroxy-dicarboxylic acids, suggesting a defect of the mitochondrial enzyme that normally dehydrogenates these 3-hydroxyacyl-CoA esters. Biochemical studies in the patient's cultured fibroblasts confirmed the impairment of medium- and long-chain fatty acid oxidation, and allowed the recognition of the deficiency of long-chain 3-hydroxyacyl-CoA dehydrogenase. The activities of long-, medium-, and short-chain acyl-CoA dehydrogenases and 3-ketoacyl-CoA thiolase were normal. These results describe a disorder of fatty acid metabolism that affects the liver, skeletal muscles, and myocardium. It is important to point out that long-chain 3-hydroxyacyl-CoA deficiency shares many clinical similarities with systemic carnitine deficiency, as well as with carnitine-palmityl-CoA transferase and long-chain acyl-CoA dehydrogenase deficiencies. The differential diagnosis of this disease relies on the demonstration of long-chain urinary dicarboxylic acids with a hydroxyl group in 3-position and the study of the enzyme activity in cultured fibroblasts.

Acyl-CoA Dehydrogenase, Long-Chain↗
PubMed1990

[Unusual cause of ascites: the POEMS syndrome].

A 39-year-old woman presented with polyneuropathy, hepatomegaly, splenomegaly, endocrinopathy, monoclonal protein and skin changes, several of the many clinical features of the recently described POEMS syndrome. In addition, she had a Castleman's disease (angiofollicular lymph node hyperplasia). In this case ascites was a main presenting feature. Thus, the POEMS syndrome must be added to the list of rare causes of ascites. Electron microscopy of the liver showed perisinusoidal fibrosis.

Adult↗
PubMed1990

[Effect of alcohol and cirrhosis on the presence of Helicobacter pylori in the gastric mucosa].

The aim of this study was to determine whether there was any relationship between alcohol consumption, cirrhosis and Helicobacter pylori associated antral gastritis. One hundred and forty-four patients undergoing upper gastrointestinal endoscopy were prospectively included and classified in four groups. The first group of 23 patients had cirrhosis and an alcohol consumption below 80 g per day. The second group of 31 patients had cirrhosis and an alcohol consumption over 80 g per day. The third group of 34 patients had an alcohol consumption over 80 g per day without cirrhosis. The fourth group of 56 patients had an alcohol consumption below 80 g per day without any preexisting liver disease and underwent upper gastrointestinal endoscopy for non specific digestive symptoms. The diagnosis of Helicobacter pylori was made at histological examination using the hematoxylin and eosin stain and the Whartin-Starry stain in each case. Histopathological results were confirmed by a bacteriological study in 15 cases. One hundred and twelve of 144 patients (78 percent) had gastritis. Gastritis was more frequent (p less than 0.01) when Helicobacter pylori was present than when it was not (90 percent vs 68 percent). Gastritis was more frequent when alcohol consumption was high (86 percent vs 72 percent). Helicobacter pylori was found in 26 percent of the first group, 48 percent of the second group, 65 percent of the third group and 45 percent of the fourth group. These differences were significantly different (p less than 0.05). A statistically significant relationship between high alcohol consumption and the presence of Helicobacter pylori was noted, even in the presence of cirrhosis (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Familial hyperinsulinism with nesidioblastosis of the pancreas: further evidence for autosomal recessive inheritance.

We report on a brother and sister with hyperinsulinism and nesidioblastosis of the pancreas. In addition, one brother and one sister who died in the neonatal period were probably affected. The parents of these children were healthy and consanguineous. We think that this is strongly suggestive of autosomal recessive inheritance. Seven other reports of presumed autosomal recessive hyperinsulinism are reviewed. To our knowledge, we report the first case in sibs whose parents were consanguineous. We think that early recognition of the condition is of obvious importance not only for therapy, but also for purposes of genetic counseling.

Consanguinity↗
PubMed1989

Quantitative study of centrolobular hepatic fibrosis in alcoholic disease before cirrhosis.

In an attempt to determine the importance of perivenular fibrosis (PVF) in alcoholic liver disease, we studied 71 liver biopsies using histological grading and a morphometric method. The histological grading used 7 variables which allowed us to classify the patients into 7 groups: controls, patients without alcoholic hepatitis but with steatosis, steato-fibrosis, portal fibrosis and patients with mild, moderate, or severe alcoholic hepatitis. The quantitative analysis examined 3 parameters: (1) The inner diameter of the terminal hepatic veins (THV). (2) The thickness of the THV rims, related to perivenular fibrosis (PVF). (3) Centrolobular fibrosis (CLF) which represented the association of perivenular and perisinusoidal centrolobular fibrosis. No changes in the inner diameter of the terminal hepatic veins was observed for the different groups except in the case of severe alcoholic hepatitis. This fact indicated the absence of veno-occlusive lesions in early stages of mild and moderate alcoholic disease. In severe alcoholic hepatitis, THV were destroyed by centrolobular scars and most of them were indistinguishable and unmeasurable. Of the 26 cases with steatosis (with or without portal fibrosis) only two cases with steatofibrosis showed perivenular fibrosis. In contrast, a significant increase in PVF and in CLF appeared in patients with alcoholic hepatitis. CLF is easier to quantify and more significative than PVF. Thus, it seems to us that CLF is a better indicator of the intensity of sclerosis and of the risk of developing cirrhosis than PVF alone.

Fatty Liver, Alcoholic↗
PubMed1989

ATPase and morphologic changes in Langerhans cells induced by epicutaneous application of a sensitizing dose of DNFB.

We have previously described an ATPase Langerhans cell (LC) staining technique allowing progression from light to electron microscope observation. Using this technique we have studied, following epicutaneous application of a sensitizing dose of a hapten, 2,4-dinitro-1-fluorobenzene (DNFB), the fate of the epidermal LC located in the sensitization zone. We wanted to know, under the light microscope, if the density and/or morphology of the LC are modified by such a treatment and, under the electron microscope, what are the ultrastructural changes accompanying the possible light microscope modifications. Under the light microscope, the observation of LC during the 5 d necessary for the development of contact sensitivity to DNFB shows that their number drops in the course of the first 24 h to normalize again 3 d later. Under the electron microscope, observations over the first 24 h revealed that LC remained in the epidermis, but were ATPase-negative. The disappearance of the membrane ATPase activity took place while the LC presented an increased number of coated pits, coated vesicles, endosomes, and lysosome organelles which characterize, at the ultrastructural level, the process of receptor-mediated endocytosis (RME). Following RME, many Birbeck granules (BG) appeared in the cytoplasm. Thus, epicutaneous application of DNFB leads to an endocytic activation of LC. However, the ligand(s) and/or the cell-surface components, which probably internalize during the RME process, remain unknown.

Adenosine Triphosphatases↗
PubMed1989

[Idiopathic granulomatous hepatitis and lymphoma of serous membranes].

We described the case of a woman with idiopathic granulomatous hepatitis who developed a type B lymphoma with serous effusion six years later. This association raised the hypothesis that sarcoidosis or lymphoma could present as idiopathic liver granuloma. We suggest that lymphoma developed in our patient as a consequence of the granulomatous hepatitis. This lymphoma was particular because only sera were involved.

Ascitic Fluid↗
PubMed1989

[Does nimodipine improve the outcome of perioperative complications of aneurysm rupture? Results of systematic treatment].

Morbidity after aneurysmal subarachnoid hemorrhages is proceeding from many factors; ischemic etiology is underestimated and frequently thought to be vasospasm related only. Other undoubted mechanisms are in the setting of ischemic disorders after ruptured aneurysms. The management of these disorders is relevant of new calcium blockers. Early administration of prophylactically oral nimodipine, with temporary intravenous administration of the therapy after surgery or in the setting of delayed ischemic deterioration, were assigned to 36 patients with aneurysm surgery. Efficacy was judged on prevention and outcome of ischemic disorders at discharge and three months later using the Glasgow Outcome Scale. On all, twenty-nine patients were disabled from any etiology; twenty made full or improved recoveries at discharge; twenty-eight get independent conditions of life at 3 months. Fourteen patients have return to their pre-rupture activity. Twenty-two surgical patients (61%) set an undoubtly ischemic disability during any time of their hospitalization, but many etiologies were identified in majority of cases. Spasm is the main factor of stroke in only 6 patients, and one of the ischemic factors in 15 cases. Among these ischemic deteriorations, twenty improved or made full recovery at discharge and get independent life at 3 months. No death with spasm. These data support the assumption that vasodilatating is not the only mode of nimodipine action. Hypervolemia must be adjunct with nimodipine to prevent regional hypoperfusion.

Adolescent↗
PubMed1988

Plasma prolidase and prolinase activity in alcoholic liver disease.

Prolidase (EC 3.4.13.9) and prolinase (EC 3.4.13.8) activity was measured in the plasma of 53 patients with alcoholic liver disease. Plasma prolinase activity was not correlated with histological characteristics in liver biopsies. In contrast, prolidase activity rose significantly (p less than 0.02) in cirrhotic patients with alcoholic hepatitis in comparison with those without alcoholic hepatitis. It also showed a significant positive correlation with ASAT activity (r = 0.505, p less than 0.001) and with the ASAT/ALAT ratio (r = 0.452, p less than 0.001). Plasma prolidase activity did not allow the differentiation of patients with reversible fibrosis from those with cirrhosis. The interest of this new marker is discussed.

Adult↗
PubMed1988

Light chain deposition disease with liver dysfunction.

Light and transmission electron microscopic study as well as immunohistochemical investigation were performed on three cases of light chain deposition disease (LCDD) with severe liver dysfunction. In two cases, the amount of light chain deposits in the liver was moderate and did not correlate with the severity of clinical and biological symptoms. Ultrastructural study demonstrated a collagenization of the Disse's space, with basement membrane-like material in association with light chain deposits. Immunohistochemical investigation showed a marked increase of collagen types I, III, and IV, as well as fibronectin and laminin in perisinusoidal space. This study suggests that collagenization of the Disse's space has a minor role in liver dysfunction. The analogy between kidney and liver lesions in diabetes and in LCDD is stressed, but the mechanism of this abnormal accumulation of matrix proteins remains unknown.

Aged↗
PubMed1988

Appearance of Birbeck granule-like structures in anti-T6 antibody-treated human epidermal Langerhans cells.

We have previously demonstrated by immunogold labeling techniques that the T6 surface antigen of living human Langerhans cells (LC) of the skin is internalized by a process of receptor-mediated endocytosis (RME). Receptor-mediated endocytosis induced by the binding of the monoclonal anti-T6 antibody BL6 involves coated pits, coated vesicles, endosomes, the smooth endoplasmic reticulum, and lysosomes. After RME, gold-labeled Birbeck granules (BGs) appear in the cell center. In the present study, by modifying the experimental conditions but retaining the presence of gold-labeled BL6, we have observed (in addition to the above-mentioned gold-labeled organelles) images that appear to correspond to BG-like structures. These structures, like the intracytoplasmic BGs, are pentalaminar and gold-labeled, but they differ from the intracytoplasmic BGs by their attachment to the cell membrane, their length, the frequent presence of a coat, and by prolongation by one or more coated pits. Birbeck granule-like structures seem to result, at the ultrastructural level, from receptor ligand interactions and from modifications of the LC shape.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1988

A method for the rapid isolation of human epidermal Langerhans cells using immunomagnetic microspheres.

Because Langerhans and indeterminate cells are the only epidermal cells that express the specific CD1a surface antigen T6, we have used immunomagnetic monodisperse polymer microspheres for positive selection of human epidermal Langerhans and indeterminate cells. Epidermal cells in suspension are successively incubated with a murine monoclonal anti-T6 antibody of the IgG1 subclass and then with magnetic beads coated with a sheep anti-mouse IgG1. Rosetted cells are obtained and then easily separated from the non-rosetted cells using a magnet. The two cell fractions are characterized by phase contrast microscopy, immunofluorescence, electron microscopy, and the skin cell-lymphocyte reaction. All the rosetted cells (1.5 to 5% of the total epidermal cells) express T6 antigen by indirect immunofluorescence and under the electron microscope possess all the ultrastructural characteristics of Langerhans cells. Moreover, the rosetted Langerhans cells remain functional: Under the electron microscope they internalize by receptor-mediated endocytosis gold labeled anti-T6 antibody, and in the skin cell-lymphocyte reaction they stimulate allogeneic lymphocytes. In contrast, the rosette depleted cell fraction is deprived of T6 positive cells and unable to stimulate allogeneic lymphocytes. The immunomagnetic depletion of epidermal cells is a simple and rapid method to isolate functional human Langerhans cells with good yield and high purity (97%). This technique should be of value in the study of the pharmacology of Langerhans cells and in the investigation of the interactions of Langerhans cells with keratinocytes or lymphocytes.

Cell Count↗
PubMed1988

Light chain deposition disease presenting with hepatomegaly: an association with amyloid-like fibrils.

We report an unusual case of lambda light chain deposits without overt plasma cell dyscrasia. The clinical presentation was hepatomegaly without biochemical sign of renal involvement. Portal hypertension, spontaneous rupture of the spleen and fracture of the 12th thoracic vertebra occurred during the course of the disease. Ultrastructural studies showed that lambda light chain deposits were associated with amyloid-like deposits. This case suggests that light chain deposition disease and amyloidosis could be two expressions of the same disease.

Amyloidosis↗