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Chap. 1 - CELL INJURY AND CELL DEATH
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- By Adone Baroni, Second University of Naples, Eleonora Ruocco, Second University of Naples, Maria Antonietta Tufano, Second University of Naples, Elisabetta Buommino, Second University of Naples
- Edited by Ronni Wolf, Batya B. Davidovici, Jennifer L. Parish, Lawrence Charles Parish
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- Book:
- Emergency Dermatology
- Published online:
- 07 September 2011
- Print publication:
- 17 January 2011, pp 1-11
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Summary
WHEN CELLS are damaged, as often occurs during trauma and metabolic stress, the organism has to choose whether to repair the damage by promoting cell survival or remove irreparably injured cells. Cell injury occurs when an adverse stimulus reversibly disrupts the normal, complex homeostatic balance of the cellular metabolism. In this case, after injury the cells attempt to seal breaks in their membranes, chaperone the removal or refolding of altered proteins, and repair damaged DNA. On the contrary, when cell injury is too extensive to permit reparative responses, the cell reaches a “point of no return” and the irreversible injury culminates in programmed cell death (PCD). Specific properties or features of cells make them more or less vulnerable to external stimuli, thus determining the kind of cellular response. In addition, the characteristic of the injury (type of injury, exposure time, or severity) will also affect the extent of the damage.
We present a short overview of the best-known PCD pathways. We emphasize the apoptotic pathway, considered for years the hallmark of PCD, and the different stimuli that produce cell injury.
CELL INJURY
The survival of multicellular organisms depends on the function of a diverse set of differentiated cell types. After development is complete, the viability of the organism depends on the maintenance and renewal of these diverse lineages. Within each lineage homeostasis is maintained through a delicate balance between cell proliferation and cell death.
Chap. 11 - STAPHYLOCOCCAL SCALDED SKIN SYNDROME
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- By Eleonora Ruocco, Second University of Naples, Adone Baroni, Second University of Naples, Sonia Sangiuliano, Second University of Naples, Giovanna Donnarumma, Second University of Naples, Vincenzo Ruocco, Second University of Naples
- Edited by Ronni Wolf, Batya B. Davidovici, Jennifer L. Parish, Lawrence Charles Parish
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- Book:
- Emergency Dermatology
- Published online:
- 07 September 2011
- Print publication:
- 17 January 2011, pp 109-114
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- Chapter
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Summary
STAPHYLOCOCCAL scalded skin syndrome (SSSS) is the term used to define a potentially life-threatening, blistering skin disease caused by exfoliative toxins (ETs) of certain strains of Staphylococcus aureus. The syndrome belongs to a wide spectrum of staphylococcal infections that range in severity from localized bullous impetigo to a generalized cutaneous involvement characterized by extensive blistering with superficial denudation and subsequent desquamation of the skin. SSSS is so-named because of its staphylococcal etiology and its remarkable resemblance to the clinical picture of scalding.
HISTORY
The original description of the syndrome dates back to 1878, when Ritter von Rittershain, director of an orphanage in Prague, reported approximately 300 cases of dermatitis exfoliativa neonatorum. A relationship between the disease and staphylococci was perceived at the beginning of the 20th century, but only in the early 1950s did the link between bullous impetigo and phage group 2 staphylococci become evident. Lyell's report on toxic epidermal necrolysis (TEN) in 1956 drew attention to the similarities between this drug-induced condition and the appearance of extensive scalding, but also led to a period of confusion between nonbacterial (immune-mediated) TEN and bacterial (staphylococcal) toxin-mediated scalded skin syndrome. In the early 1970s, the development of a murine model of the staphylococcal disease clarified the situation.
Nowadays, SSSS is clearly distinguished from other diseases of generalized epidermal necrolysis and the term Ritter's disease is still used to describe generalized SSSS in newborns.