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At least 145 records · Page 8Linked to original sources
PubMed1982

[LE cell test].

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Humans↗
PubMed1978

[LE cells].

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Humans↗
PubMed1997

[LE cell death].

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Biomarkers↗
PubMedDate not supplied

[Neuropathies due to vasculitis in infancy].

INTRODUCTION: Vasculitis are characterised by the inflammatory infiltrate, chiefly of mononuclear cells, in the walls of the blood vessels, which can lead to occlusion with necrosis and the subsequent infarction of the affected tissue. AIMS: The Objective of this study was to determine the clinical, anatomicopathological and neurophysiological aspects of vasculitic neuropathies in infancy. PATIENTS AND METHODS: Each patient was submitted to the following tests: a complete hemogram, systemic lupus erythematosus cells (LE cells), lupus anticoagulant, antinuclear antibodies, neutrophil anticytoplasmic antibodies, venereal disease research laboratory test (VDRL), erythrocyte sedimentation rate, liver transaminases, serological testing for hepatitis C, B and A, cytochemical study of the cerebrospinal fluid, study of motor and sensory conduction, electromyography and nuclear magnetic resonance, when required; a biopsy of the sural nerve was performed, which was replaced by a necropsy if the patient died. RESULTS: 15 patients from a total of 25 who were studied had vasculitic neuropathies; the most usual presentation was multiple mononeuropathy; aetiologies found included microscopic polyangiitis, systemic lupus erythematosus, JRA, overlap syndrome and several undetermined vasculitis. Of the patients who were submitted to a biopsy, 75% showed signs of vasculitis, which affected the small and medium sized vessels in 62.5% of patients. CONCLUSIONS: The presence of neuropathy in association with symptoms and signs of systemic involvement suggested the possibility of a neuropathy in the course of a vasculitis. The examination of biopsy specimens of the sural nerve is useful for the diagnosis and classification of the aetiology of vasculitis. Response to treatment with immunosuppressant drugs was good, both in the case of the neuropathy and of the underlying disease.

Adolescent↗
PubMed2006

Acquisition of apoptotic resistance in cadmium-induced malignant transformation: specific perturbation of JNK signal transduction pathway and associated metallothionein overexpression.

Prior work has shown that chronic cadmium exposed rat liver epithelial cells (CCE-LE) become malignantly transformed after protracted low level cadmium exposure. Acquisition of apoptotic resistance is common in oncogenesis and the present work explores this possibility in CCE-LE cells. CCE-LE cells were resistant to apoptosis induced by etoposide or an acute high concentration of cadmium as assessed by flow cytometry with annexin/FITC. Three key mitogen-activated protein kinases (MAPKs), namely ERK1/2, JNK1/2, and p38, were phosphorylated in CCE-LE cells after acute cadmium exposure. However, the levels of phosphorylated JNK1/2 were markedly decreased in CCE-LE cells compared to control. JNK kinase activity was also suppressed in CCE-LE cells exposed to cadmium. Epidermal growth factor (EGF), used as a positive control for stimulating JNK phosphorylation, was much less effective in CCE-LE cells than control cells. Ro318220 (Ro), a strong activator of JNK, increased phosphorylated JNK1/2 to levels similar to the cadmium-treated control cells and also enhanced apoptosis in response to cadmium in CCE-LE cells. Metallothionein (MT), which is thought to potentially inhibit apoptosis, was strongly overexpressed in CCE-LE cells. Further, in MT knockout (MT-/-) fibroblasts, JNK1/2 phosphorylation was markedly increased after cadmium exposure compared with similarly treated wild-type (MT+/+) cells. These results indicate cadmium-transformed cells acquired apoptotic resistance, which may be linked to the specific suppression of the JNK pathway and is associated with MT overexpression, which, in turn, may impact this signal transduction pathway. The acquisition of apoptotic resistance may play an important role in cadmium carcinogenesis by contributing to both tumor initiation and malignant progression.

Animals↗
PubMed1974

Hyperreactivity to cow's milk in an infant with LE and tart cell phenomenon.

LE and tart cells were demonstrated in a black male infant whose serum contained milk-percipitating antibodies and who had pulmonary infiltrates. Immunoblasts, plasmocytoid lymphocytes, and an LE cell were found in a milk-stimulated skin window. The presence of LE cells corresponded to the presence of ENA antibody. Tart cells varied with oral milk challenge. A large Arthus type of skin reaction to injected milk was demonstrated. An oral feeding of milk resulted in a decrease in plasma C3. Lymphocyte transformation resulted from in vitro milk stimulation. ENA (extractable nuclear antigen) antibody and resulting LE cell formation possibly represented the combination of nuclear protein with milk antigen. The pulmonary infiltrates may represent a hypersensitivity pneumonitis characterized by both Arthus and cell-mediated reaction to milk.

Animals↗
PubMed1995

Lens epithelial cell mRNA, II. Expression of a mRNA encoding a lipid-binding protein in rat lens epithelial cells.

A lens epithelial (LE) cell cDNA clone, designated pLELBP, was isolated by subtraction-hybridization methods between a 4-week-old rat LE cell and rat lens fiber cell lambda ZAP cDNA libraries. The cDNA contained 683 bp, an ATG at bp 42, and an open reading frame (ORF) encoding a protein of 135 amino acids (aa), and a poly(A) signal at bp 641 (GenBank/EMBL accession No. U13253). Northern blot analysis showed that the lens mRNA was at a concentration that exceeded 100-fold that found in non-ocular tissues examined, except in skin it was found at levels equal to about 1/15 of the lens levels. In the retina, it was also found at about 1/15 of that present in the lens. By in situ hybridization analysis, the sense RNA was localized to the LE cells and to the glial cells of the retina, and negligibly to the lens fiber cells. Search of GenBank, EMBL and SwissProt data bases revealed that the LE cell mRNA and its aa encoded protein showed extensive sequence homology to members of the cytosolic lipid-binding protein (LBP) family. It matched to 91% in aa sequence homology to the protein encoded by ORF of mal1 cDNA, isolated from mouse skin squamous cell carcinoma [Krieg et al., J. Biol. Chem. 268 (1993) 17362-17369], and 99% in aa sequence homology to the protein encoded by ORF of rat skin LBP mRNA [Watanabe et al., Biochem. Biophys. Res. Commun. 200 (1994) 253-259]. Occurrence of high levels of mRNA for a specific LBP in the LE cells relative to other non-ocular tissues is consistent with a hypothesis that the encoded protein may be involved in several lens epithelial cell-specific mechanisms, possibly including differentiation, protective and nutritional processes.

Animals↗