Amoxicillin with milk

Khan is the first Indian to receive one of America’s highest awards in Medicine.

Hameed Khan, discoverer of anticancer AZQ, after receiving 2004, Vaidya Ratna, the gold medal, one of India’s highest awards in Medicine at the Rashtrapati Bhavan (Presidential Palace), in Delhi, India, during a reception held on 02 April 2004.

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 clinical trials for treating bran cancer. 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

Alois Alzheimer identified the microscopic changes in the brain of a patient with the memory loss. He was the first physician to identify the disease in a 50-year-old woman who suffered from psychosis and who died within 4 years. Using special dyes, he stained the brain tissues which carried abnormal protein deposit around her brain which controlled brain function. He identified two kinds of legions of amyloid patches which he mistakenly thought was fatty patches and now turned out to be proteins. He observed a patch of fatty deposit on the top of the brain cells called plaques and the legions inside the nerve cells called tangles. He accurately correlated the abnormal protein deposits around brain cells with the controlled of brain function [23, 24, 25, 26]. Today, we know that the age is the single most risk factor for developing Alzheimer.

By age 65 or older, the risk for developing Alzheimer is about 10%, and by age 85 or older, the risk factor is as high as 40 or 50%.

When he performed the autopsy of many senile persons, Dr.

Alzheimer found the same plaques and tangles in many other samples.

Early onset or late onset of Alzheimer resulted in the epidemic of Alzheimer. When comparing a normal brain with the Alzheimer brain, we find that the Alzheimer brain has shrunken and there is a concentration of plaques and tangles in neurons. In healthy brain cells, we see occasional plaques and tangles. It defines the disease; the plaque and tangles start building up as we

grow

Early onset affects cognition which encompasses memory and other mental functions such as erosion of attention, thinking, reasoning, visual functions, spatial function, and dementia with memory loss and other cognitive erythromycin and amoxicillin functions resulting in mental impairment which affects to the degree interfering with the daily life.

Recent studies confirm that Alzheimer is an irreversible brain disorder which slowly destroys memory and thinking skills. The damage to the brain is not particularly associated to any specific gene, but the presence of the one form of the apolipoprotein E (APOE) is a suspect gene whose presence does increase a patient’s risk for developing Alzheimer. The early onset of Alzheimer is associated with three single gene mutations: first, the presence of an amyloid precursor protein (APP) located on chromosome-21; the presence of presenilin 1 (PSEN1) on chromosome-14 and the presence of presenilin 2 (PSEN2) located on chromosome-1.

All three chromosomes are very large and carry hundreds of genes. For example, chromosome-1 is the largest chromosome in the genome.

It is made of 163 million nucleotide bases carrying 2610 genes. Chromosome-21 is made of 50 million nucleotide bases carrying 337

genes

Mutations on these genes may be associated with the onset of Alzheimer. Of all the genes on these chromosomes, only five single-gene mutations are associated with the early onset of the Alzheimer, it is the greatest challenge to design drugs to attack only the mutated genes. As I said above in the “Cancers” section, the good news is that the only mutated genes grow rapidly using glucose as a source of energy.

It is the acid which activates the aziridine and carbamate moieties producing powerful carbonium ion which attack N-7 guanine of DNA and shut off only the mutated genes. Using C-14 radiolabeled aziridines, we can identify the mutated gene which form the aziridine/protein complex as described in the “Cancers” section.

It is well known that using the TFT dye, which is 3,6-dimethyl-2-(4-dimethlaminophenyl)-benzothiazoline, could be used to stain the plaques and tangles of Alzheimer tissues. Using TFT dye as a carrier for the aziridine and carbamate moieties, we could design drugs to attack the mutated DNA to shut off genes which form plaques and tangles to prevent the progress of Alzheimer. In the above “Cancers” section, I have described in detail how I

had

Could I use the same rational drug design and introduce a novel method for treating breast tumor?

Although mutations on BRCA1 gene located on chromosome-17 (which is made of 92 million nucleotide bases carrying 1394 genes) have been identified years ago responsible for causing breast cancer, we wonder why it has been so difficult to design drugs on rational basis to treat breast cancer.

By the time the breast cancer diagnosis is confirmed in a patient, the BRCA1 has accumulated more than 3000 mutations. Genotyping of the blood would also show the existence of many cells carrying mutated cells responsible for creating secondary deposits.

It is also believed that by the time breast cancer is confirmed, metastatic cancer cells have already been spread from liver lung on its way to brain. Since all other organs including breast and liver could be removed and replaced by organ transplant except brain, I thought that protecting brain is utmost important to save life. Once AZQ is developed to protect the brain, I could focus on the breast and prostate cancers.

Recent, radiolabeled studies showed that male hormone testosterone has great affinity for female organs like breast, ovary, and fallopian tube cells. On the other hand, estrogen, the female hormone, has great affinity for male prostate gland. By attaching multiple aziridine rings and carbamate ions to both hormones, I could design novel drugs to attack the breast and the prostate cancer.

Now, I found that I could go even further by attaching more than four aziridine and carbamate moieties to both male and female hormones.

In a breast tumor, within the start and stop codons, BRCA1 gene has captured over 200,000 nucleotide bases. These mutations are caused by exposure to radiations, chemical or environmental pollutants, viral infection, or genetic inheritance.

To attack the mutated nucleotides among the 3000 cells in BRCA1 gene, I could use male hormone, testosterone, and bind multiple radiolabeled aziridine and carbamate ions to attack BRCA1 mutations.

By using three-dimensional MRI, I could show how many radiolabeled nucleotides were bound to which mutations.

Out of 17 positions available for substitutions on testosterone ring system, there are only three positions, that is, 1, 3, and 17 available for substitution on testosterone ring system.

Carl Djerassi [27] had demonstrated that we could activate positions 9 and 10 by

reacting

I could increase or decrease the number of aziridine and carbamate ions to get the maximum benefit by further brominating positions 15 and 16 to introduce additional aziridine and carbamate moieties. Similarly, I could use the female hormone estrogen and by attaching multiple aziridine and carbamate ions to attack prostate tumor.

Since there are 17 positions also available on estrogen ring as well; again, I could increase or

decrease

Ethical issues (the impact of science on society) By 2050, novel drug design would have produced new class of medicine to treat all known 6000 genes. We would not only produce new treatment but also we would have new food, new fuel, and new medicine to treat every disease known to mankind to protect, preserve, and prolong human life beyond 100 years. This section discusses the impact of prolonging human life beyond 100 years. Our attempt to prolong human life by shutting off the genes of the old age diseases raises several ethical and moral questions.

We face the same population problem when we succeed in shutting off genes of all three old age diseases, that is, cancer, cardiovascular disease, and Alzheimer. What happens after we achieve that goal of reaching 100 years? By exercises and good nutrition, if the body mass is not retained, the centenarians are most likely to be fragile and weak.

They need the help of caretakers to perform the daily routine. By 2050, if we increase the age of about 100 years of about a billion people, we need another billion caretakers.

The society is hardly likely to accept such a proposal. To cure diseases to prolong human life,

several

Second approach is to design drugs to shut off genes of old age to prolong life.

Next attempt to increase human life would be to prevent the loss of telomeres, the six-letter code (TTAGGG) that shorten our DNA and shorten our lifespan.

During replication, each chromosome loses about 30 telomeres each year. If we prevent the loss of telomeres by using the enzyme telomerase reverse transcriptase (TRT), we could slow down the aging process. elegance that we could increase its lifespan several fold.

Now, we could translate this work in human being; we could try by making a less virulent flu virus carrying TRT gene when injected to a volunteer who comes down with a mild flu. When he recovers from the flu, the TRT gene would have inserted in the entire genome of every cell in his body (we can confirm the insertion by sequencing). Suppose at each replication, only 15 telomeres are deleted instead of 30 telomeres.

Also, suppose the sequencing of his genome would confirm that every cell of his body carries the TRT gene.

Since the longevity treatment with the flu virus is safe, inexpensive, and would be easily available to everyone, should we provide the treatment to every man, woman, and child on the face of the Earth?

Such studies are likely to raise two serious ethical questions. First, we have to ask ourselves, do people have a right to live and second do we have a right to live as long as we wish, no matter how old, how weak, or how sick we are?

The answer to first question is, according to the UN charter, we all have the right to life, liberty, and pursuit of happiness.

Do people have a right to extent their lives as long as they wish? Most amoxicillin and sore throat people are reluctant to answer this question either No or Yes. First, they argue that there are seven and a half billion people live on planet Earth and we are adding 90 million additional people each year.

According to UN estimate, by 2050, the population of the world is likely to reach 9 billion.

Does our planet Earth have all resources to support such a population explosion?

Can we provide food, fuel, and medicine to all the people of the world? By extending life, we will have serious problems such as lawlessness, riots, and chaos in the streets. The current population of Earth has polluted the water, the air, and the land. Today, they wonder if the water they drink is safe, the food they eat is safe, and the air they breathe is safe.