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cardiolipin/nécrose
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Intravascular coagulation necrosis of the skin associated with cryofibrinogenemia, diabetes mellitus, and cardiolipin autoantibodies.
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Intravascular coagulation necrosis of the skin is rare and appears as hemorrhagic infiltrates that may develop ulcerating necrosis, mainly on the acral areas. The face, arms, and legs were severely involved in our patient. In this patient intravascular coagulation necrosis was associated with
Cardiolipin plays a role in KCN-induced necrosis.
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Cardiolipin (CL) is a unique anionic, dimeric phospholipid found almost exclusively in the inner mitochondrial membrane and is essential for the function of numerous enzymes that are involved in mitochondrial energy metabolism. While the role of cardiolipin in apoptosis is well established, its
Widespread cutaneous necrosis associated with cardiolipin antibodies.
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Many clinical phenomena have been described in association with antiphospholipid antibodies, which are measured by a variety of techniques. The relationship of each assay is not completely clear, nor is it apparent which assay correlates best with the various clinical conditions. We describe a
Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) induced mitochondrial pathway to apoptosis and caspase activation is potentiated by phospholipid scramblase-3.
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Tumor Necrosis Factor (TNF)-Related Apoptosis-Inducing Ligand (TRAIL) initiate pathways of cell death in which caspase activation is mediated either directly (without mitochondrial amplification), or indirectly via the release of apoptogenic factors from mitochondria. Phospholipid scramblases (PLS)
Overexpression of glutaredoxin-2 reduces myocardial cell death by preventing both apoptosis and necrosis.
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Mitochondrial glutaredoxin-2 (Glrx2) has been recognized as an important redox regulator in mammalian organs including heart. To date no investigations have addressed the potential role of Glrx2 in cardiac disorders. The present study examined if myocardial overexpression of Glrx2 in the heart could
Abnormal IgG cardiolipin antibody titers in patients with Raynaud's phenomenon and/or related disorders: prevalence and clinical significance.
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BACKGROUND
The prevalence of antibodies to cardiolipin (a-CL) in patients with Raynaud's phenomenon (RP) and/or related disorders (rD) is not known.
OBJECTIVE
The purpose of this study was to determine the prevalence of these antibodies.
METHODS
We assayed IgG a-CL in 230 consecutive patients with
[Study on the effects of mitochondrial pathways on apoptosis in colon carcinoma cells induced by tumor necrosis factor related apoptosis inducing ligand].
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OBJECTIVE
To explore the effects of mitochondrial pathways on apoptosis in colon carcinoma cells induced by Tumor necrosis factor related apoptosis inducing ligand and offer evidences for TRAIL application in clinic.
METHODS
Apoptosis, integration of mitochondria (including DeltaPsim, cardiolipin),
Cardiolipin and apoptosis.
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Cardiolipin (CL) is recognized to be an essential phospholipid in eukaryotic energy metabolism so that physiological and pathological perturbations in its synthetic and catabolic pathways play key roles in maintaining mitochondrial structure and function, and ultimately cell survival. This review
Human anticardiolipin monoclonal autoantibodies cause placental necrosis and fetal loss in BALB/c mice.
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OBJECTIVE
To analyze the structure, specificity, and in vivo pathogenetic potential of 2 human anticardiolipin (aCL) monoclonal antibodies (MAb).
METHODS
Human aCL IgG MAb were generated from hybridized Epstein-Barr virus-induced B cell lines from a healthy subject (MAb 519) and from a patient with
Cardiolipin deficiency releases cytochrome c from the inner mitochondrial membrane and accelerates stimuli-elicited apoptosis.
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Cardiolipin (CL) is a mitochondria-specific phospholipid synthesized by CL synthase (CLS). We describe here a human gene for CLS and its analysis via RNAi knockdown on apoptotic progression. Although mitochondrial membrane potential is unchanged in cells containing only 25% of the normal amount of
Placental thrombosis and fetal loss after passive transfer of mouse lupus monoclonal or human polyclonal anti-cardiolipin antibodies in pregnant naive BALB/c mice.
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In the present study we evaluated the effect of passive transfer of a mouse monoclonal (CAM) or a human polyclonal anti-cardiolipin IgG on pregnancy outcome in BALB/c mice. The mice were immunized through the tail vein immediately after mating with 10 micrograms of monoclonal or polyclonal
Mitochondrial kinases and their molecular interaction with cardiolipin.
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Mitochondrial isoforms of creatine kinase (MtCK) and nucleoside diphosphate kinase (NDPK-D) are not phylogenetically related but share functionally important properties. They both use mitochondrially generated ATP with the ultimate goal of maintaining proper nucleotide pools, are located in the
Augmentation and suppression of release of tumor necrosis factor from macrophages by negatively charged phospholipids.
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We recently reported that some lipid species of cell membranes and lipoproteins induced the growth of peripheral macrophages. In this study, the effects of phospholipids on tumor necrosis factor (TNF)-releasing activity of macrophages were examined. Ten to 20 micrograms/ml of cardiolipin, which is a
Levamisole-contaminated cocaine: an emergent cause of vasculitis and skin necrosis.
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The prevalence of cocaine adulterated with levamisole-induced vasculitis is increasing and physicians should be aware of this unique entity. There have been many reports of cutaneous vasculitis syndrome caused by cocaine which is contaminated with levamisole. Levamisole was used as an antihelminth
Role of mitochondrial cardiolipin peroxidation in apoptotic photokilling of 5-aminolevulinate-treated tumor cells.
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In 5-aminolevulinic acid (ALA)-based photodynamic therapy (PDT), ALA taken up by tumor cells is metabolized to protoporphyrin IX (PpIX), which sensitizes photodamage leading to apoptotic or necrotic cell death. Since lipophilic PpIX originates in mitochondria, we postulated that photoperoxidation of
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