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cytochrome c/feber
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Sensitization to CD95 ligand-induced apoptosis in human glioma cells by hyperthermia involves enhanced cytochrome c release.
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CD95L-induced apoptosis involves caspase activation and is facilitated when RNA and protein synthesis are inhibited. Here, we report that hyperthermia sensitizes malignant glioma cells to CD95L- and APO2L-induced apoptosis in the absence, but not in the presence, of inhibitors of RNA and protein
Enhancement of hyperthermia-induced apoptosis by a new synthesized class of benzocycloalkene compounds.
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The aim of this study was to examine whether, a new synthesized class of benzocycloalkene derivatives (BCs), enhances apoptosis induced by hyperthermia. The combined effects of hyperthermia (44 degrees C, 20 min) and BCs on apoptosis in human lymphoma U937 cells were investigated. Among the tested
Enhancement of hyperthermia-induced apoptosis by a free radical initiator, 2,2'-azobis (2-amidinopropane) dihydrochloride, in human histiocytic lymphoma U937 cells.
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To elucidate the mechanism how a free radical initiator, 2,2'-azobis (2-amidinopropane) dihydrochloride (AAPH), induces cell death at hyperthermic temperatures, apoptosis in a human histiocytic lymphoma cell line, U937, was investigated. Free radical formation deriving from the thermal decomposition
Enhancement of hyperthermia-induced apoptosis by sanazole in human lymphoma U937 cells.
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Sanazole has been tested clinically as a hypoxic cell radiosensitizer. The aim of the present study was to investigate whether sanazole enhances apoptosis induced by hyperthermia at 44 degrees C for 20 min in human lymphoma U937 cells. Sanazole alone induced continuous increase in the intracellular
A free radical initiator, 2,2'-azobis (2-aminopropane) dihydrochloride enhances hyperthermia-induced apoptosis in human uterine cervical cancer cell lines.
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Hyperthermia-induced apoptosis and its enhancement in the presence of a temperature-dependent free radical initiator, 2,2'-azobis (2-aminopropane) dihydrochloride (AAPH) were examined in human uterine cervical cancer cell lines, CaSki and HeLa. When both cell lines were treated with hyperthermia at
Alterations in mitochondrial morphology are associated with hyperthermia-induced apoptosis in early postimplantation mouse embryos.
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BACKGROUND
Previously, we showed that teratogens such as hyperthermia activate the mitochondrial apoptotic pathway in day nine mouse embryos. Activation of this pathway involves an initial release of cytochrome c from intermembranous spaces of the mitochondria into the cytoplasm. Cytoplasmic
Modulation of p53 cellular function and cell death by African swine fever virus.
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Modulation of the activity of tumor suppressor p53 is a key event in the replication of many viruses. We have studied the function of p53 in African swine fever virus (ASFV) infection by determining the expression and activity of this transcription factor in infected cells. p53 levels are increased
The role of Bcl-xL in synergistic induction of apoptosis by mapatumumab and oxaliplatin in combination with hyperthermia on human colon cancer.
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Colorectal cancer is the third leading cause of cancer-related mortality in the world. The main cause of death because of colorectal cancer is hepatic metastases, which can be treated using isolated hepatic perfusion (IHP), allowing treatment of colorectal metastasis with various methods. In this
Effect of hyperthermia and environmental acidity on the proteolytic activity in murine ascites tumor cells.
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The influence of hyperthermia and environmental pH on proteolytic activity was studied in murine ascites tumor cells in vitro. PNJ ascites tumor cells were incubated with [125I]cytochrome c at 42.5 or 37 degrees C in a modified Krebs-Ringer buffer adjusted to pH 7.2 or 6.4. Incubation at normal
Induction of apoptosis by carboplatin and hyperthermia alone or combined in WERI human retinoblastoma cells.
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This paper investigated the induction of apoptosis and perturbation of cell cycle progression caused by carboplatin (CPt) and hyperthermia alone or combined in WERI human retinoblastoma cells in vitro. An incubation of the cells with 25 or 50 microm of CPt at 37 degrees C caused apoptosis, which
Reversal of TNF-alpha resistance by hyperthermia: role of mitochondria.
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The aim of this study is to examine the effect of hyperthermia on tumour necrosis factor-alpha (TNF-alpha) resistance in L929-11E cells. L929-11E is a TNF-alpha resistant variant derived from L929 cells, a commonly used model for TNF-alpha study. Based on the results from flow cytometry and Western
Apoptosis and its relation with clinical course in patients with Crimean-Congo hemorrhagic fever.
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Crimean-Congo hemorrhagic fever (CCHF) is a tick-mediated viral infection. Patients with CCHF may show various clinical presentations. The cause of this difference in the clinical course is not completely understood. Apoptosis is programmed cell death and plays an important role in regulating the
Molecular Differentiation of the African Yellow Fever Vector Aedes bromeliae (Diptera: Culicidae) from Its Sympatric Non-vector Sister Species, Aedes lilii.
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BACKGROUND
Yellow fever continues to be a problem in sub-Saharan Africa with repeated epidemics occurring. The mosquito Aedes bromeliae is a major vector of yellow fever, but it cannot be readily differentiated from its non-vector zoophilic sister species Ae. lilii using morphological characters.
Molecular evidence indicates that Phlebotomus major sensu lato (Diptera: Psychodidae) is the vector species of the recently-identified sandfly fever Sicilian virus variant: sandfly fever turkey virus.
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Sandfly fever turkey virus (SFTV) is a recently-discovered sandfly fever Sicilian virus (SFSV) variant (family Bunyaviridae, genus Phlebovirus), characterized during retrospective evaluation of febrile disease outbreaks in Turkey. In addition to causing sandfly fever, SFTV was observed to induce
Cytochrome c release from mitochondria of early postimplantation murine embryos exposed to 4-hydroperoxycyclophosphamide, heat shock, and staurosporine.
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Cell death is an early and common event in the pathogenesis associated with the abnormal development induced by a variety of teratogens. Previously, we showed that the cell death induced in day 9 mouse embryos by three teratogens, hyperthermia (HS), 4-hydroperoxycyclophosphamide (4-CP), and sodium
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