Thursday, April 23, 2009

Conslusion

As already seen in the discussion part, the hypothesis which expressed there is no relationship between activation/inhibition of the platelets and externalization the phosphatidylserine would be, based on the results, ruled out.
Another hypothesis which expresses the relation ship is still on the table. It is not possible to declare:
-Activation of the platelets by Thrombin causes externalization of phosphatidylserine on the surface of the platelets.
-In this experiment the same results could be not applied to ADP as the test was performed for different concentrations of ADP but satisfactory results were not reached. Changing method in this regard in suggested.
-Inhibition of the platelets by Aspirin causes internalization of phosphatidylserine on the surface of the platelets. This statement has been approved by comparing the results of controls with and with out Aspirin.
In addition, having seen the papers, we would realize that COHEN Zoƫ and colleagues conducted a research in 2004 and their find out declare that if platelets become activated, they would express phosphatidylserine on the outer leaflet of the plasma membrane. They have working with ADP as they say ADP-induced PS exposure. They wanted to realise the role of Caspase in this process as well, while we were not. It can be a suggestion for further works as well to consider different enzymes in this process. Their findings could be useful to prove the activatory role of ADP as well.
Finally, the characteristics of Annexin V have been approved again. The property which they bind with negatively charged phospholipid on the surface of the cells, although it is not the main statement of this experiment but this viable facts could be used to be applied in other experiments as well.

6.1. Suggestions for further works
It should be realised how Thrombin/ADP or Aspirin apply their changes on the platelets. If we were working on cells which have nuclei the possibility of effect on the nuclei could be mentioned. But the platelets which are circulating in blood are not same cell. Therefore changing the expression of a gene which is highly possible for physiological reactions is ruled out. The other and simple way which comes to mind is acting by the aid of a second messenger. Further studies should be based on understanding the mechanism of this effect.
Repeating this experiment with different activators is suggested as well, in particular due to unclear results from ADP.
Further experiments should investigate about the role of Caspase and try to find out the mechanism of inhibition and activation with more details.
As stated about the receptors of ADP and Thrombin. The mechanism of action of stimulation (activation or inhibition) should be considered to find more relationship between the factor of change and response.

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