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Since the supply oxygen tension increases, proliferation near y = 0 increases and, hence, there are more live cells near to the blood vessel.
Rolling continues until integrins take over; they strengthen the adhesion and allow the cells to crawl out of the blood vessel into the tissue.
In normal wound healing, angiogenesis (new blood vessel formation from pre-existing vessels) occurs in areas undergoing repair.
For simplicity, we restrict attention to one-dimensional models, with the spatial dimension being outward from the blood vessel.
We couple the behaviour of the blood vessel into the model for the oxygen tension.
However, durability of this coil in blood vessel was 2 to 3 hours.
A feature of some lesions was a centrally located small blood vessel presenting fibrinoid necrosis with infiltration by polymorphonuclear leucocytes.
There is an imbalance of signals from the corresponding retinae because one is shadowed by the blood vessel and the other receives normal stimulation.
After the cells away from the blood vessel have died, they are degraded.
During re-endothelialisation of wounds to the blood vessel wall, endothelial cells extend protrusive contacts in order to close gaps in the cell layer.
These, in turn, cause the blood vessel to open or close, and drive the movement of the live and dead cells.
This creates space away from the blood vessel.
Increased vascular supply to the tumour via the induction of new blood vessel formation (angiogenesis) encourages tumour growth and facilitates metastasis to distant sites.
Once a constricted blood vessel falls below a critical size, it supplies no oxygen to the system.
You put the mechanical surgeon inside the blood vessel, and it goes into the heart and 'looks' around.
