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.rar Update : I have not tried RAR but I am not sure if it will work. You can try it. Abstract: As many as 200 million people suffer from sickle cell anemia (SCD), a single-gene disorder, and over 2,000,000 newborns are born every year with the disease in developed countries. Patients with SCD must treat the infirmities resulting from vascular problems, such as anemia, premature death due to increased susceptibility to infection and damage caused by sickled RBCs (sRBCs) in the circulatory system. SCD is very common in Africa, where it affects as many as two million people and may account for as much as a half of all childhood deaths. Thus, it is imperative that a highly effective cure for SCD be developed. Unfortunately, the early death of patients with SCD has prevented the study of the cellular and molecular events that are critical to the development of the disease. We show that purine depleting agents that deplete the adenosine and guanosine triphosphate (ATP and GTP) pools in cells, such as 6-N-hydroxymethyl-dA (6HMA), have the capacity to prevent the formation of the very sickled RBCs that are pathogenic and elicit a crisis in patients with the disease. In addition, we showed that adenosine deaminase (ADA) inhibitors can prevent the production of abnormally sickled RBCs in mice. Thus, we plan to study the mechanisms of the actions of these drugs in the prevention of the formation of abnormally sickled RBCs, as well as to develop new drugs that have the capacity to prevent the formation of the sickle RBCs that cause the vascular damage that are associated with the disease. We will also investigate how the ADA inhibitor causes a decrease in the production of superoxide by RBCs, and to study the mechanisms that are involved in the adverse production of superoxide by human RBCs. We also plan to develop new drugs that can specifically kill the overproduced of the deoxy-sickle hemoglobin (deoxy-HbS), as well as a drug that can decrease the formation of sRBCs. More specifically, we will investigate how adenosine and 2′-deoxyguanosine (dG), nucleosides that are metabolites of adenosine and that are normal by-products of the enzymatic turnover