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Biomedical subjects

A Barat

Publications and source records attributed to A Barat.

At least 19 recordsLinked to original sources
PubMed1992

Acquired symmetric lipomatosis of the soles. A plantar form of the Madelung-Launois-Bensaude syndrome.

Benign symmetric acquired lipomatosis is a rare condition characterized by multiple, diffuse, subcutaneous collections of nonencapsulated mature adipose tissue. A thick and disfiguring deposit of fat is symmetrically distributed in the subcutaneous tissue of the neck, upper trunk and proximal portions of the upper extremities. The face, distal extremities, hands, and feet are characteristically spared. We describe a case in which only plantar involvement was present.

Adipose Tissue↗
PubMed1992

[The immunological characterization of 63 cases of Hodgkin's disease with a panel of 8 antibodies].

Sixty three cases of Hodgkin's disease are studied (two with lymphonodular predominance, 15 with diffuse lymphocyte predominance, 26 nodular sclerosis, 15 mixed cell and 5 lymphocyte depletion) with a panel of 8 monoclonal antibodies, material routinely used and included in paraffin: Ber H2 (CD30), Leu M1 (CD15), Common Leukocyte Antigen (CD45), L26 (CD20), MB2, UCHL1 (CD45 RO), MTI (CD43) and Epithelial Membrane Antigen. Ber H2 turned out to be the most usefull marker, positive in 100% of cases, independently of the histologic type. Positiveness with Leu M1 ranged from 100% (2/2 cases) of lymphonodular predominance, to 53.3% (8/15 cases) of diffuse lymphocyte predominance. The reactivity of the rest was variable, 1 though it is note worthy the positiveness of B markers (L26, MB2) in the two cases with lymphonodular predominance. In the other subtypes, reactivity with L26 was greater than that with MB2. T cell marker expression was minimal, except for the positiveness in 40% of cases (2/5) of the lymphocyte depletion type. In addition, the results of other series are revised and as a result the possible histogenesis of Hodgkin's disease is discussed.

Antibodies, Monoclonal↗
PubMed1991

Chondroitinases release acetylcholinesterase from chick skeletal muscle.

Bacterial chondroitinases (both ABC and AC types) release asymmetric and globular forms of AChE from chick skeletal muscle samples. Heparinases, however, including heparitinase I, fail to do so under different incubation conditions. These results do not support the direct implication of the heparin/heparan sulfate family of GAGs in the interaction of the different AChE molecular forms with the muscle ECM. GAGs of the chondroitin/dermatan sulfate group could however be involved, either directly or indirectly, in the attachment of the AChE collagen-like tail to the muscle basal lamina.

Acetylcholinesterase↗
PubMed1991

Solubilization of asymmetric acetylcholinesterase by polyanions.

A number of polyanions, including polysulfates (sulfated glycosaminoglycans (GAGs), dextran and pentosan sulfates, and polyvinylsulfate), polyphosphates (tetrapolyphosphate, polyadenylate) and polycarboxylates (polyaspartate, polyglutamate) solubilize asymmetric acetylcholinesterase (AChE) from chick muscle at low ionic strength, and partially or totally displace AChE tailed forms bound to heparin-agarose columns. The previously reported solubilization of asymmetric AChE by heparin, or the proven affinity of the tailed enzyme forms for this GAG, cannot therefore be taken as direct proof of the involvement of heparin-like heparan sulfate proteoglycans in the anchorage of the collagenous tail of the enzyme to the basal lamina in skeletal muscle.

Acetylcholinesterase↗
PubMed1991

Malignant combined nevus.

This report describes an example of combined nevus with malignant transformation. The clinical impression was blue nevus. Histologically, the lesion was composed of a cellular blue nevus in the reticular dermis and an overlying compound melanocytic nevus. The junctional component of the melanocytic nevus showed transition to malignant melanoma in situ. A review of the literature failed to find a precedent for the present case.

Cell Nucleus↗
PubMed1991

Erythema elevatum diutinum mimicking porphyria cutanea tarda.

A case of erythema elevatum diutinum (EED) closely resembling porphyria cutanea tarda (PCT) is reported. The initial skin biopsies were suggestive for PCT but porphyrin levels in the urine, stool and plasma were normal. A further biopsy from an early cutaneous lesion showed a leucocytoclastic vasculitis with fibrinoid necrosis of the vessel walls.

Adult↗
PubMed1991

Localized epidermal necrolysis (erythema multiforme-like reaction) following intravenous injection of vinblastine.

We report a case of localized epidermal necrolysis that developed 24 hours after an intravenous injection of vinblastine. Clinically, the lesions consisted of erythematous macules, vesicles, and bullae with a linear arrangement over the injected vein. Histologically, the lesions showed features closely resembling erythema multiforme (epidermal necrolysis). We discuss the pathogenesis of this curious cutaneous drug reaction and review the literature concerning local cutaneous complications associated with intravenously administered chemotherapeutic agents.

Erythema Multiforme↗
PubMed1991

Postlymphography linear dermatitis.

Cutaneous effects secondary to lymphography are rare events. We herein report a patient with Hodgkin's disease who developed a linear dermatitis in both lower limbs 6 days after a pedal lymphography. Histopathologic examination of the lesions demonstrated a subacute dermatitis. Patch tests with the substances used in the lymphography yielded negative results. We discuss the possible pathogenic mechanisms of this striking linear dermatitis.

Adult↗
PubMed1991

Erythema elevatum diutinum in a patient with acquired immunodeficiency syndrome. Another clinical simulator of Kaposi's sarcoma.

Several types of vasculitis have been described in patients with human immunodeficiency virus infection. Erythema elevatum diutinum is a rare variant of cutaneous leukocytoclastic vasculitis which, with the exception of the case reported herein, has been described only once in human immunodeficiency virus-infected patients. Our male patient, a longtime intravenous drug abuser, had cutaneous lesions, closely resembling Kaposi's sarcoma, on the extensor surfaces of the lower extremities. Cutaneous biopsy specimens, however, demonstrated leukocytoclastic vasculitis with fibrinoid necrosis of the vessel walls and areas of basophilic degeneration of collagen bundles in early lesions, whereas late lesions showed dense diffuse fibrosis with proliferation of dermal spindle cells and some foci of residual leukocytoclastic vasculitis. Oral therapy with dapsone resulted in marked clearing of the cutaneous lesions within few days. This case raises the necessity of histologic confirmation for all cases of suspected Kaposi's sarcoma in patients with acquired immunodeficiency syndrome. We discuss the possible pathogenesis of leukocytoclastic vasculitis in human immunodeficiency virus-infected patients.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Localized hyperkeratosis lenticularis perstans (Flegel's disease).

A case of hyperkeratosis lenticularis perstans involving only the back of a thirty-nine-year-old woman is reported. Histologic examination showed foci of compact and eosinophilic hyperkeratosis overlying a thinned stratum malpighii. In the underlying papillary dermis there was no evidence of inflammatory infiltrate. This case demonstrates that hyperkeratosis lenticularis perstans may appear as a localized disorder, and that the inflammation is not an essential pathogenic process in this disorder.

Adult↗
PubMed1990

Asymmetric acetylcholinesterase is absent from chick retina, but present in choroid, ciliary muscles and iris.

Freshly dissected chick neural retina and pigmented epithelium do not apparently contain asymmetric molecular forms (A-forms) of acetylcholinesterase (AChE). The neighboring choroid, and the ciliary muscles and iris, are however rich in type II A-forms (high salt/EDTA-extractable). Most if not all the asymmetric AChE activity detected in chick 'whole retina' preparations could then be explained in terms of contamination by non-retinal eye tissues.

Acetylcholinesterase↗
PubMed1990

Co-existence of hepatocyte ground-glass inclusions from several causes.

Two patients with two and three types respectively of ground-glass hepatocyte inclusions are described. Both were hepatitis B surface antigen (HBsAG) positive and received cyanamide for alcohol aversion therapy. In addition, one of them had taken benzodiazepines and barbiturates. In one patient, cyanamide and HBsAg inclusions co-existed in the same hepatocytes.

Adult↗
PubMed1990

Interaction of asymmetric and globular acetylcholinesterase species with glycosaminoglycans.

Chicken muscle and retina, and rat muscle asymmetric acetylcholinesterase (AChE) species were bound to immobilized heparin at 0.4 M NaCl. Binding efficiency was between 50 and 80% for crude fraction I A-forms (AI; muscle), and nearly 100% for fraction II A-forms (AII; muscle and retina). Antibody-affinity-purified AI-forms (chicken) were, however, quantitatively bound to heparin-agarose gels, whereas diisopropylfluorophosphate-inactivated high-salt extracts partially prevented the binding of both AI and AII AChE forms, thus suggesting the presence in crude AI extracts of heparin-like molecules interfering with the tail-heparin interaction. All bound A-forms were progressively displaced from the heparin-agarose columns by increasing salt concentrations, with maximal release at about 0.6 M. They were also efficiently eluted by heparin solutions (1 mg/ml), other glycosaminoglycans being much less effective. Chicken globular AChE forms (G-forms, both low-salt-soluble and detergent-soluble) also bound to immobilized heparin in the absence of salt. Stepwise elution with increasing NaCl concentrations showed maximal release of G-forms at 0.15 M, all globular forms being totally displaced from the column at 0.4 M NaCl. Heparin (1 mg/ml) had the same eluting capacity as 0.4 M NaCl, whereas other glycosaminoglycans were only marginally effective. We conclude that the molecular forms of AChE in these vertebrate species interact with heparin, at salt concentrations that are characteristic for asymmetric and globular forms. Within the A and G molecular form groups, no differences were found in the behavior of the different fractions or subtypes, provided that the enzyme samples were free of interfering molecules.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholinesterase↗
PubMed1990

Detection and characterization of circulating and glomerular immune complexes in experimental IgA nephropathy.

The different models of experimental IgA nephropathy described so far have provided insight into pathogenesis; however, the evidence for a role of IgA immune complexes (IC) has only been gained in passive systems. In an active model of IgA nephropathy, induced in mice by repeated injections of dextran, some of the mechanisms that could explain the formation of glomerular IgA deposits are studied in this report. Serum total IgA and anti-dextran IgA antibody levels increased significantly over the period of immunization. Only 13-30% of mice had total and/or specific IgA IC, determined by Raji cell and PEG assay in ELISA. Analytical ultracentrifugation showed that IgA IC were of small (7-13 S) or intermediate (13-17 S) size. There was a close correlation between total serum IgA levels and the presence of IC-containing IgA anti-dextran antibodies, with the existence of IgA in the mesangium. The percentage of animals (n = 76) with IgA mesangial deposits increased over the immunization period (88% at 10 weeks). Forty-three per cent of mice had polymeric IgA in the mesangium; by contrast, only 12% had dextran deposits. On the whole, these data suggest that in the dextran-induced IgA nephropathy, the glomerular IgA could be the result of circulating IgA complexes and/or IgA polymers deposition.

Animals↗
PubMed1989

Compartmentalization of acetylcholinesterase in the chick retina.

Using selective inhibitor treatments, we have studied the distribution of asymmetric (A) and globular (G) forms of acetylcholinesterase (AChE) in the extra- and intracellular compartments of chick retina, a specialized region of chick central nervous system (CNS). Our results show that the chick retinal collagen-tailed AChE (an example of class II asymmetric molecular forms) is essentially an extracellular form of the enzyme; this is the first demonstration of the extracellular localization of asymmetric AChE in the vertebrate CNS. The active site of most of the hydrophobic, membrane-bound G4-form is also exposed to the external environment. In turn, the smaller molecular weight G-forms (G2 and G1) are localized within the cells, where they may represent intermediate components in the assembly or degradation of the more complex enzymatic molecular species. Histoenzymatic ultrastructural techniques show internal AChE in amacrine as well as in ganglion cell bodies, and external enzyme, specifically associated with synapses and axons, in the inner plexiform layer. The probable cooperation of the extracellular A12-forms and the membrane-bound G species (mainly G4) of the enzyme to the hydrolysis of acetylcholine (ACh) released into the external compartment is suggested and discussed.

Acetylcholinesterase↗