It's a region of DNA that binds DNA Polymerase to begin replication.
Clinical death is the medical term for cessation of blood circulation and breathing, the two necessary criteria to sustain human and many other organisms' lives.
It occurs when the heart stops beating in a regular rhythm, a condition called cardiac arrest.
Brain injuries start to accumulate almost immediately after Clinical Death.
Full recovery of the brain after more than 3 minutes of clinical death at normal body temperature is rare.
Usually brain damage or later brain death results after longer intervals of clinical death even if the heart is restarted and blood circulation is successfully restored.
Although loss of function is almost immediate, there is no specific duration of clinical death at which the non-functioning brain clearly dies.
The most vulnerable cells in the brain, CA1 neurons of the hippocampus, are fatally injured by as little as 10 minutes without oxygen.
However, the injured cells do not actually die until hours after resuscitation.
Brain failure after clinical death is now known to be due to a complex series of processes called Reperfusion Iinjury that occur after blood circulation has been restored, especially processes that interfere with blood circulation during the recovery period.
Hope this helps!!!
~Alkka♥
egg (female) and sperm ( male)
Answer:
Neutrophils help fight infections because they ingest microorganisms and secrete enzymes that destroy them. A neutrophil is a type of white blood cell, a type of granulocyte and a type of phagocyte.
Explanation:
Neutrophils display adhesion glycoproteins on their surface to bind endothelial and subendothelial structures. They move randomly until they find a damaged site. Unless neutrophils are activated, endothelial cells do not tend to adhere. When inflammation mediators (IL-1, FNT) activate endothelial cells, they express P-selectin and E-selectin on the surface. The expression of glycoproteins and L-selectin cause the initial adhesion of the non-stimulated neutrophil to the activated endothelium, slowing it down by rolling it over the endothelium. Activated endothelial cells, opsonized particles, immune complexes, FEC-G, FEC-GM and chemoattractants produce factors that stimulate neutrophil activation. Expressing β2 integrin (endothelium adhesion molecule) Neutrophils expand and form pseudopods. Neutrophil activation also promotes degranulation, superoxide generation, and arachidonate metabolite production.
Tropical rain forest biome :)
