**7. Cardiovascular diseases**

*Drug Design - Novel Advances in the Omics Field and Applications*

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**Figure 4.**

**Figure 3.**

*Single-strand DNA binding aziridine and carbamate.*

*clinical trials for treating bran cancer.*

*Gold medal for Dr. Khan. Dr. A. Hameed Khan, a scientist at the National Institutes of Health (NIH), USA, an American scientist of Indian origin was awarded on April 2, 2004. Vaidya Ratna, the gold medal, one of India's highest awards in Medicine for his discovery of AZQ (US Patent 4,146,622) which is now undergoing* 

Coronary artery disease is complex involving about 60 genomic variants (genes). All variants are not clustered on any specific chromosome. These variants are dispersed across the entire genome. Although all variants have not been sequenced, we can shut off only the mutated gene without knowing the sequence of all other genes. As I mentioned above in the "Cancers" section, the mutated gene grows rapidly forming the tumor. As it grows, it uses glucose as a source of energy, which is broken down to produce pyruvic acid. In the presence of acid, the analogs of aziridine and carbamate are activated to generate carbonium ion which attack the tumor DNA shutting off their genes. While we may someday be able to sequence all 60 genes associated with the coronary artery disease, presently, we can single out and identify the mutated gene bound complex using radiolabeled aziridine and carbamate. The following example explains how some arrhythmias causing genes could be identified and how drug could be designed to shut off these genes.

The term "QT" refers to the segment of an electrocardiogram, which measures the duration of time for the heart to relax after a heartbeat. In long QT syndrome, the duration of time is abnormally prolonged and creates a vulnerability to dangerous arrhythmias [22]. Ever since the syndrome was described in 1957, researchers have engaged in a genetic race to identify the genes associated with long QT syndrome, which currently includes 17 genes. Three genes, *KCNQ1*, *KCNH2*, and *SCN5A*, had sufficient evidence to be implicated as "definitive" genetic causes for typical long QT syndrome. Four other genes had strong or definitive evidence supporting their role in causing atypical forms of long QT syndrome, presenting in the newborn symptoms associated with heart block, seizures, or delays in development. Once the mutated genes are identified, we could design drugs to shut off these genes as described in the "Cancers" section.
