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In contrast, the mechanical theory suggests that severe malaria is attributable to excessive sequestration of P. falciparum-infected erythrocytes (IEs) in the microvasculature of vital host organs leading to mechanical obstruction of blood flow, hypoxia, tissue damage and, ultimately, organ failure [8].
A few different approaches have been used to prevent excessive sequestration of IGF-1 and restore its bioavailabity in pathological conditions.
Incubation of cells with ANC resulted in excessive sequestration of the NPs into the SCC (Fig. 7A, arrows), as well as into smaller, more isolated vacuoles, where the particles were packed with higher density (Fig. 7A, arrowheads).
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We thus propose the existence of a similar mechanism in pSap deficiency, i.e. excessive lysosomal sequestration of the ubiquitin-tagged proteins released most probably from damaged neuronal membranes or resulting from impaired downstream pSap signaling [ 2, 23].
Overexpression of PiCdc14 may misregulate proteins through excessive dephosphorylation or sequestration of its substrates.
Therefore the 'calcium auxotrophy' possibly results from excessive vacuolar calcium sequestration, causing cytosolic calcium deprivation.
In the case of impaired permeability induced by inflammation, this strategy usually results in excessive interstitial fluid sequestration.
Thrombocytopenia in malaria probably occurs through peripheral destruction, sequestration or excessive removal of the platelets by the spleen, as well as platelet consumption by the process of disseminated intravascular coagulation [ 25- 28].
Although sequestration of excessive iron by microglia in the hypoxic PWM may be a microglia's attempts to protect the immature OLs against its toxic effects, iron accumulation in the PVL may affect the immature OLs directly through oxidative stress, resulting in their death.
However, disadvantages of this approach include excessive sebum within the follicle, sequestration of drug within the follicle, and lack of appendages in some areas of the body [40].
It involves the sequestration of dysfunctional or excessive mitochondria within double-membrane autophagosomes, which then fuse with the vacuole/lysosome to deliver these mitochondria for degradation.
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