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  6. Keywords
  7. Topics
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We are analyzing https://link.springer.com/article/10.1007/s10495-008-0187-8.

Title:
Secondary necrosis in multicellular animals: an outcome of apoptosis with pathogenic implications | Apoptosis
Description:
In metazoans apoptosis is a major physiological process of cell elimination during development and in tissue homeostasis and can be involved in pathological situations. In vitro, apoptosis proceeds through an execution phase during which cell dismantling is initiated, with or without fragmentation into apoptotic bodies, but with maintenance of a near-to-intact cytoplasmic membrane, followed by a transition to a necrotic cell elimination traditionally called “secondary necrosis”. Secondary necrosis involves activation of self-hydrolytic enzymes, and swelling of the cell or of the apoptotic bodies, generalized and irreparable damage to the cytoplasmic membrane, and culminates with cell disruption. In vivo, under normal conditions, the elimination of apoptosing cells or apoptotic bodies is by removal through engulfment by scavengers prompted by the exposure of engulfment signals during the execution phase of apoptosis; if this removal fails progression to secondary necrosis ensues as in the in vitro situation. In vivo secondary necrosis occurs when massive apoptosis overwhelms the available scavenging capacity, or when the scavenger mechanism is directly impaired, and may result in leakage of the cell contents with induction of tissue injury and inflammatory and autoimmune responses. Several disorders where secondary necrosis has been implicated as a pathogenic mechanism will be reviewed.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Science
  • Telecommunications

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {💸}

The income method remains a mystery to us.

Earning money isn't the goal of every website; some are designed to offer support or promote social causes. People have different reasons for creating websites. This might be one such reason. Link.springer.com could be getting rich in stealth mode, or the way it's monetizing isn't detectable.

Keywords {🔍}

google, scholar, pubmed, cas, article, cell, apoptosis, death, cells, apoptotic, necrosis, biol, med, immunol, clearance, neutrophil, necrotic, macrophages, disease, injury, neutrophils, inflammation, differ, respir, role, mol, lung, secondary, res, exp, tissue, rev, care, physiol, sci, mechanisms, systemic, nature, autoimmunity, crit, clin, mice, acute, phagocytosis, human, henson, elastase, silva, membrane, curr,

Topics {✒️}

month download article/chapter anti-fas mab-induced apoptosis death receptor-induced apoptotic transforming growth factor-beta cigarette smoke-induced blockade plasma membrane ca+atpase coordinately induce anti-inflammatory ps-dependent phagocytic clearance mitochondrial love-hate triangle mfg-e8-deficient mice galactosamine-induced liver injury plasmid-encoded virulence factor suppress pro-inflammatory eicosanoid glucocorticoid-induced cell death hepatic ischemia/reperfusion injury glutamate-induced neuronal death endotoxin-induced pulmonary inflammation fas-triggered phosphatidylserine exposure devd-specific caspase activation full article pdf ischemia-reperfusion prevents inflammation epithelial cell death wattiaux-de coninck renal epithelial cells van de water acute lung injury neutrophil-derived serine proteases secondary necrosis induced mycobacterium ulcerans required dendritic cells mediated anti-fas antibody article apoptosis aims privacy choices/manage cookies tumor cell death necrotic ca2+ overload secondary necrosis ensues plasma membrane disruption cultured human fibroblasts hepatic ischemia-reperfusion induces autoantibody production krysko dv molecular switches deciding cell death induced necrotic tumor cells ischemia/reperfusion injury de bruin hg melanoma cell lines induce macrophage release atp levels occurs bovine mammary gland

Questions {❓}

  • Albert ML (2004) Death-defying immunity: do apoptotic cells influence antigen processing and presentation?
  • Aliprantis AO, Diez-Roux G, Mulder LC, Zychlinsky A, Lang RA (1996) Do macrophages kill through apoptosis?
  • Gregory CD, Devitt A (2004) The macrophage and the apoptotic cell: an innate immune interaction viewed simplistically?
  • Maher JJ, Gores GJ (1998) Apoptosis: silent killer or neutron bomb?
  • Munoz LE, Gaipl US, Franz S et al (2005) SLE—a disease of clearance deficiency?
  • Naylor EJ, Bakstad D, Biffen M et al (2007) Haemophilus influenzae induces neutrophil necrosis: a role in chronic obstructive pulmonary disease?
  • Proskuryakov SY, Konoplyannikov AG, Gabai VL (2003) Necrosis: a specific form of programmed cell death?
  • Uller L, Persson CG, Erjefalt JS (2006) Resolution of airway disease: removal of inflammatory cells through apoptosis, egression or both?
  • Uncontrollable catastrophe, or is there order behind the chaos?
  • Vincent JL, Zambon M (2006) Why do patients who have acute lung injury/acute respiratory distress syndrome die from multiple organ dysfunction syndrome?
  • Viorritto IC, Nikolov NP, Siegel RM (2007) Autoimmunity versus tolerance: can dying cells tip the balance?

Schema {🗺️}

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         description:In metazoans apoptosis is a major physiological process of cell elimination during development and in tissue homeostasis and can be involved in pathological situations. In vitro, apoptosis proceeds through an execution phase during which cell dismantling is initiated, with or without fragmentation into apoptotic bodies, but with maintenance of a near-to-intact cytoplasmic membrane, followed by a transition to a necrotic cell elimination traditionally called “secondary necrosis”. Secondary necrosis involves activation of self-hydrolytic enzymes, and swelling of the cell or of the apoptotic bodies, generalized and irreparable damage to the cytoplasmic membrane, and culminates with cell disruption. In vivo, under normal conditions, the elimination of apoptosing cells or apoptotic bodies is by removal through engulfment by scavengers prompted by the exposure of engulfment signals during the execution phase of apoptosis; if this removal fails progression to secondary necrosis ensues as in the in vitro situation. In vivo secondary necrosis occurs when massive apoptosis overwhelms the available scavenging capacity, or when the scavenger mechanism is directly impaired, and may result in leakage of the cell contents with induction of tissue injury and inflammatory and autoimmune responses. Several disorders where secondary necrosis has been implicated as a pathogenic mechanism will be reviewed.
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      headline:Secondary necrosis in multicellular animals: an outcome of apoptosis with pathogenic implications
      description:In metazoans apoptosis is a major physiological process of cell elimination during development and in tissue homeostasis and can be involved in pathological situations. In vitro, apoptosis proceeds through an execution phase during which cell dismantling is initiated, with or without fragmentation into apoptotic bodies, but with maintenance of a near-to-intact cytoplasmic membrane, followed by a transition to a necrotic cell elimination traditionally called “secondary necrosis”. Secondary necrosis involves activation of self-hydrolytic enzymes, and swelling of the cell or of the apoptotic bodies, generalized and irreparable damage to the cytoplasmic membrane, and culminates with cell disruption. In vivo, under normal conditions, the elimination of apoptosing cells or apoptotic bodies is by removal through engulfment by scavengers prompted by the exposure of engulfment signals during the execution phase of apoptosis; if this removal fails progression to secondary necrosis ensues as in the in vitro situation. In vivo secondary necrosis occurs when massive apoptosis overwhelms the available scavenging capacity, or when the scavenger mechanism is directly impaired, and may result in leakage of the cell contents with induction of tissue injury and inflammatory and autoimmune responses. Several disorders where secondary necrosis has been implicated as a pathogenic mechanism will be reviewed.
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         Oncology
         Biochemistry
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         Virology
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