Inherit the Wind – The Battle of the Century
Inherit the wind is a fictionalized account of the notorious “Scopes Monkey Trial of 192 ”. Jerome Lawrence and Robert E. Lee wrote this explosive courtroom drama 30 years after the original trial on which it is based. The issue of creationism vs. Darwinism and the right to think and express ideas is as relevant today as it was 50 years ago when this play was written.
The Florida Repertory Theatre is an intimate, cozy place from which to view this emotionally charged play. In the middle of a scorching hot summer, the famous monkey trial began in Dayton, Texas. The town in the play is called Hillsboro and the music, clothing and appearance of extreme heat bring this small town of 500 alive on the stage.
In 1925 a high school teacher, John Scopes, stood accused of violating the Butler Act, a law that prohibited the teaching of evolution in public schools. The famous civil rights attorney, Clarence Darrow, defended Scopes. While 3-time presidential candidate William Jennings Bryan prosecuted the case.
Nearly 200 reporters descended on this small town including H.L. Mencken of the Baltimore Evening Sun. Dayton, Tennessee took on a carnival like atmosphere during the trial. 30 years later the writers of the play fictionalized the names and circumstances of the trial but the essence of the story comes through, that is the right to think and question and the right to express those thoughts and ideas openly and without fear of persecution.
When the play opens Bertram Cates (Scopes) in is jail. Cates played by Justin Lakes is quiet, almost shy but is emphatic about his right to express his ideas. He is depressed and misses his girlfriend, Rachel, who is played brilliantly by Aria McKenna. Rachel visits Bert in jail and begs him to apologize for teaching evolution so “this whole thing will go away”. Their pain, love and longing for each other can be felt by all. Scopes was not imprisoned but free and interacting with the townspeople in a friendly manner while the trial was going on.
In reality the Civil Liberties Union had advertised for someone to challenge the law. Citizens of Dayton approached Scopes as a possible candidate in hopes of bringing publicity that would benefit their town. Scopes was a math teacher and coach but had substituted as a biology teacher briefly. He did not remember teaching evolution but had used a standard textbook, which contained a small section on Darwinism. Scopes actually knew very little about Darwin’s theory so the defense kept him off the stand to avoid embarrassment.
The play keeps you in the frame of mind of a small town with picnics, prayer meetings and the mass mentality against Cates (Scopes). The religious fanaticism comes through on the stage, putting you on edge, trying to wish these small town bigots away. The motherless Rachel is torn by her love for Cates and her conservative religious upbringing, her father being the town preacher. At one point her father becomes angry with her and pushes her to the ground. It was shocking, you could hear and feel the thud as Rachel hit the stage and wished you could shelter and protect her.
John Newton does a splendid job of portraying agnostic defense attorney, Henry Drummond (Darrow). He appears to be sincere about defending the righteous from unjust laws and the type of person you’d like to invite over for dinner and get to know better.
E.K. Hornbeck, the reporter from Baltimore is played by Greg Longenhagen. His bow tie adorned costume is wonderful, as is his typical hard- nosed reporter attitude. He is full of one liners - “ I may be rancid butter but I’m on your side of the bread.”
During the course of the trial Brady is confident and self-righteous. The town sides heavily with Brady and his literal biblical views. Brady, played by Niels Miller, is quirky and likable though close minded. He is prone to long-winded speeches while tucking his thumbs in his suspenders. He made this author laugh out loud many times, especially when he kept sneaking food whenever his wife wasn’t watching him. He comes across as kind and fair, as well as old and vulnerable. It was a superb performance by Mr. Miller.
After the judge excludes defense testimony from scientists, Drummond, desperate for a defense calls Brady himself to the stand. Brady testifies as an expert witness on the Bible. Drummond ruthlessly challenges and confuses Brady until the crowd is laughing at his ridiculous responses. Brady is humiliated and his vulnerability comes across when he seeks comfort in the arms of his wife. The jury finds Cates guilty. The judge issues a token fine of .00. In the real trial the fine was $1.00. It was a triumph for Drummond, Cates and free speech.
Brady vehemently protested the light punishment. During his closing speech he becomes so distraught that he sputters and shouts and finally collapses. Shortly after, he dies. This is a very distressing scene. At the end of the trial Cates loses his right to teach, but in reality Scopes’ job was open to him even after the verdict. The trial is over and Drummond, Cates and Rachel all head to the train station together to leave this small, steamy town behind. In the real story, Scopes received a scholarship for graduate school and went to the University of Chicago to study geology. He went on to have an active career as a geologist.
The blending of history and theater is interesting. The dialog is powerful and well done by all. The real point: the right to express ideas and think freely comes through and leaves you feeling uplifted and relieved.
Mutant Genes and Their Effect On HIV Infection
Mutant Genes and Their Effect On HIV Infection
Imagine it is the year 2025. Some things have not changed. The sun still rises, the sky is blue and the birds continue to sing each morning to welcome the new day. Your doctor just informed you that you have contracted HIV. You are not too concerned because genetic research has brought with it effective medications. Your physician will test your blood with a microchip to determine any genetic defects you may have and treat you accordingly with effective drugs and gene therapy..
Mutant genes that prevent or slow the progression of HIV have recently been identified. Scientists now have a better idea of how the disease process works. This exciting new discovery has led to great hope for more effective and less toxic treatments for HIV and other diseases.
HIV infects the white blood cells that orchestrate the immune system. HIV is referred to as AIDS (Acquired Immune Deficiency Syndrome) when a person has lost their ability to fight off fatal infections such as pneumonia, toxoplasmosis, cryptosporidiosis, karposis sarcoma and other infections that are easily killed by normally functioning immune systems. According to the Centers for Disease Control, (CDC par.1) the Human Immunodeficiency Virus is passed through contact with body fluids that contain white blood cells. These fluids include blood, semen, vaginal fluid and breast milk. Other fluids that may transmit HIV and are a cause of concern for health care workers are spinal cord fluid, fluid around the bone joints and amniotic fluid (CDC par.3).
Scientists have long known that HIV infects the body by attaching to CD4 receptors (proteins located on the surface of the healthy cell). The virus binds to the white blood cell via the protruding CD4 receptor just like a key in a lock. It was recently discovered that to infect a cell HIV requires a second protein known a CCR5. HIV is a type of retrovirus that can only reproduce in a living cell because it has RNA but no DNA of its own. HIV uses the DNA of the host cell to model its own DNA. The virus then begins to replicate and destroy the immune system. Once HIV has penetrated the healthy cell’s genes, it is referred to as a provirus (Avert par.2).
Today the virus that causes AIDS is transmitted throughout every country in the world. It is expected that thirty to forty million people will have been infected by the year 2000 (UNAIDS par.3). According to UNAIDS (par.6), half of all infections have been in the 15 to 24 year old age group. AIDS has become the leading cause of death among adults under 45 (Avert par.13). Approximately 43% of adults infected with HIV are women and one in three children orphaned by HIV/AIDS is under the age of five. Fourteen million people have died from AIDS so far, 95% of them in developing countries.
The CCR5 gene normally controls cell migration (McNicholl par.24). It was discovered recently that mutant CCR5 genes could slow progression of HIV infection or even prevent infection altogether (Cohen, Heterozygosity par.2). According to Liu (par.32), CCR5 is not necessary for good health. There seems to be no downside to the mutation. Sternberg (par. 21) says that it is unusual for a genetic mutation to be harmless. A genetic mutation found in black individuals prevents malaria (Sternberg par. 22) but causes sickle cell anemia.
According to Garrett (par.18) persons with two copies of the mutant CCR5 gene, one inherited from each parent, are immune to HIV infection. They do not produce the CCR5 protein needed by HIV to successfully invade a cell.
Those with only one copy of the mutation progress to full-blown AIDS more slowly than those with two normal copies of the CCR5 gene. One in five Caucasian Americans have one copy of the mutant gene (Radetsky par.40). Researchers have found that people with one copy of the mutant gene produce four to ten times less HIV than usual (The Dallas Morning News par.20). Long-term non-progressors are defined as persons who have been HIV infected for more than seven years with no symptoms. Most, but not all, long-term non-progressors have one copy of the mutant CCR5 gene. The mutation is not the only factor involved with their slow progression (Cohen, Heterozygosity par. 27). This author agrees with Dr. Cohen as she has been infected with HIV for twenty years with no disease progression.
CCR5 is a complicated protein. It is called a “seven-transmembrane” protein because it extends out from the white blood cell in seven places. Asthma medications target seven transmembrane receptors, so scientists are familiar with it. This has given researchers an advantage in their search. HIV must connect with CD4 and CCR5 to infect a cell. If a cell lacks the CCR5 protein, the virus cannot enter the cell (Radetsky par. 19).
This author’s physician, Dr. Oren J. Cohen is a researcher at the National Institute of Allergy and. Infectious Disease. Dr. Cohen discovered that a person who is homozygous (possessing two mutant CCR5 genes) is protected from infection with HIV (Cohen, email par.8). HIV is unable to bind with the cell when CCR5 is not present. Individuals with one mutant copy of the CCR5 gene (Liu par.21) do not have as many docking sites for HIV to lock onto so the virus replicates less efficiently than usual. Research to mimic the action of these mutant genes is in progress.
It is estimated (Gorman par.4) that there are two thousand to five thousand genes that can cause or predispose a person to disease. For example (Collins par. 17), an abnormality in the alpha-synuclein gene predisposes one to Parkinson’s disease. Breast cancer can be hereditary (Collins par.17) due to mutant BRCA1 and BRCA2 genes. This type of information can be used to screen people for disease and then preventative therapy can be started.
Unlike the AIDS virus, the mutant CCR5 gene does discriminate. Research done by Huang (1241) found that this mutation of CCR5 is not found in Asians or Africans. It is exclusively found in Caucasians. According to Dean (1861) this is a relatively new mutation probably due to an epidemic. There is a high frequency of the mutation in Caucasians of northern European descent (about 10%) and is not seen in Asians or Africans. The mutation probably offers protection from other infectious diseases (O’Brian par.4). Another mutation that slows the progression of HIV disease has been discovered. Mutations of CCR2 genes offer protection to both Caucasians and Africans (O’Brian par.6). The genetic selectivity of CCR5 probably goes back to the 14th century when the “Black Death” spread through Europe (McNicholl par. 23) killing one out of three people (Sternberg par.1). Apparently the mutation that protects this author from AIDS today, also protected her ancestors from the plague. Falko, from Stanford is currently testing the hypothesis that the plague epidemic of the 14th century played some role in the selection of a mutant gene that appears to provide resistance to HIV. The research will be completed in a few months (Sternberg par. 34).
The mutation in the gene is the deletion of a 32-bp segment resulting in a non-functioning CCR5 receptor (McNicholl par.13). Koup and Landau of the Aaron Diamond AIDS Research Center in Manhattan discovered a hole in the middle of the gene’s DNA. The CCR5 is so deformed that instead of appearing on the surface of the cell, the cell kills it (Radetsky par. 37).
Dr. Murphy of the National Institute of Allergy and Infectious Disease believes that recent discoveries give scientists a better understanding of the molecular structure of HIV and provide a target for drug design (Niaid News par.10). New approaches to combat HIV hold great promise for the future (O’Brian par.15). Dr. Fauci of the National Institute of Health has his researchers searching for drugs to block CCR5 but the search is just beginning (Minneapolis Star par. 26). Dr. Koup of the Diamond Center is working on a type of antibody that would attach to normal CCR5 genes and block infection from HIV (Garrett par. 21). Drug companies are working avidly on developing new drugs as well (Garrett par. 21).
A research team at the National Institutes of Health is working to design a vaccine to boost the immune system. Many of the top selling drugs target seven transmembrane receptors like CCR5 so scientists are familiar with this and feel positive and hopeful about their hunt for effective vaccines and gene therapy (Radetsky par. 47). Scientists hope to transfer the defective gene to patients via bone marrow transplants. There is a lot of optimism because the mutant gene seems to cause no ill effects (Radetsky par. 49). The new findings have led to fresh, new and exciting approaches to vaccines to prevent HIV (McNicholl par. 24).
Other research has sprung from these findings: studies of the host factor in infectious diseases, the distribution of genetic differences in certain groups and the social ramifications of these genetic differences (McNicoll par. 24). HIV disease is a challenge, says Dean (1856),
for current genetic researchers and will lead to new techniques in disease treatment. Soon doctors will be able to check your genetic profile and prescribe the best medications for your disease. Scientists will soon produce very specific, effective drugs by using synthesized strands of DNA to copy the RNA they want to block (Gorman par. 21). In the future microchips that are capable of analyzing millions of gene sequences simultaneously from one blood sample will be available. They will be used to screen patients for genetic weaknesses and predisposition to disease (Gorman par. 21). Information that now takes decades to discern will be done in minutes. The DNA chips are still experimental and the cost for genetic testing is about but is predicted to drop in the next few years. Use of the microchips will then become more routine (Collins par.36). The Human Genome Project has already identified more than half of the human genes. They are hoping to decode all of the three billion pairs by the year 2003 (Collins par.11). Once a genetic mutation has been identified, good things happen. Diagnostic tests are most often the first result of these new discoveries. Scientists would ultimately like to treat diseases with gene therapy in which the gene is the drug (Collins par.20). Nine years ago a genetic mutation that causes cystic fibrosis was discovered. Since then, thanks to gene therapy, a normal copy of the mutant gene is introduced into the body through the cells that line the lungs (Collins par. 22). The body responds to this treatment, but only briefly. Still doctors are hopeful that they will someday be able to apply this gene therapy with lasting results (Collins par.24). Genetic profiles provide essential data for treating and preventing disease (O’Brian par. 7). Hopefully the insight into how HIV and CCR5 interact will provide a therapeutic breakthrough for patients (O’Brian
par.8). According to Liu (375) the new findings provide unique insight into the complex interaction between HIV and its human host. The science of genetics has become the forerunner in medical research and will provide many new diagnostic tools in the first decade of the coming millennium (Collins par.48). Collins asserts that all disease with the exception of illnesses caused by trauma has a genetic component and that none of us is genetically perfect (par.2). Hemochromatosis is a disease that causes the body to absorb too much iron. The genetic defect that causes this disorder had been identified. It is easy to test for and doctors hope to begin screening and identifying people who are high risk and treating them within 5 years.
Dr. Mark Asperilla is an infectious disease specialist in Charlotte county, Florida. In an interview with this author he stated, “ There is much hope for the future. We are already beginning to think of HIV as a chronic manageable illness, like diabetes. Great breakthroughs in HIV research are being made. So there is hope and, when all else fails, there is prayer.”
According to this author (215) “We have moments of joy and ecstasy and also sadness and fear. We have moments of strength and moments of vulnerability. We laugh, we cry, we live – just like everyone else.”
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Global Warming
An increase in temperature of 9 degrees F. in next 200 years would be extremely disruptive to our planet. Ice at the poles would melt. Glaciers would retreat. Tropical plants and animals would migrate north. Tropical diseases would spread further away from the equator. Bleaching would destroy coral reefs. As the atmosphere warms, water evaporation would increase causing more precipitation and flooding. Sea levels would rise; as the oceans warm, the water would expand. Melting ice would also add more water to the oceans, as would the increase in precipitation.
The poles would warm up and ice would begin to melt (this is already occurring). Northern ice sheets would break up. In a warmer world there is more water vapor in the atmosphere, which leads to more snowfall as well as more melting. Maybe ice sheets would become smaller in area but thicker. Icebergs might be found around England and Norway. Northern Europe would experience a year round winter. They would burn more coal for heat, increasing global warming even more. This melting of ice would add water to the sea, increasing sea level and decreasing salinity. Deep ocean currents could be disrupted; they are driven by density and winds. Currents move heat from one place to another and keep dissolved carbon dioxide in the deep sea. Density of the oceans would change because of freshwater being added to the ocean by melting ice and rainfall. The ability of the ocean to absorb excess carbon dioxide would be reduced, again increasing global warming. The depth of the surface (mixed) layer of the ocean could increase. To sink to the deep ocean, water needs to be particularly dense (cold and salty). There would be a reduction of density and salinity in the surface water from the melting ice, preventing water from sinking and altering ocean circulation. This could affect the Gulf Stream, possibly deflecting it to the south. England, France, Germany and Norway would then be very cold.
There would be an increase in water temperature, an increase in evaporation, and an increase in clouds. Would these clouds shade us or trap the heat? Warmer ocean temperatures would mean more energy release, leading to more frequent and intense storms. Precipitation in some areas would increase causing flooding and thus disrupting agriculture. Plant growth could be affected by plant eating insects that would breed quickly in the warmer environment. Mold and weeds that flourish in warm climates could also affect food production. Plant crops and seafood would be decreased in low-lying coastal areas. Areas such as Bangladesh, India and China where rice is grown would be affected. Fisheries would be disrupted. Since water has such a high heat capacity, changes in ocean temperature would be gradual; they could be measured accurately by measuring changes in the travel time of sound. The sound would travel faster in warmer water. Satellites can measure ocean conditions at the surface and could be used to measure temperature, track ocean currents, and monitor the amount of plant life.
The rise in sea level would cause some beaches to disappear. Manhattan and the Florida Keys would cease to exist. Low-lying islands such as the Cook and Marshall Islands would be submerged under water. Many people would have to migrate inland. This mass migration of one third of our population could cause social disorganization and instability. Wetlands and mangrove swamps contain much bio-diversity and are extremely productive. Many fish caught for human consumption as well as many birds and animals depend on coastal marshes and swamps for their life cycles, so they are vital to global ecology. These areas could adjust to a slow rise in sea level but a rapid increase could be devastating, leading to the loss of agricultural land and salt intrusion into freshwater resources. Plants and animals might not be able to adapt and migrate quickly enough and some species could become extinct. The natural ecosystem could become increasingly out of sync with the environment. The changes in ocean temperature and circulation patterns could result in changes in areas where upwelling occurs and fish congregate. Some fisheries might collapse while others explode.
There would be changes in the weather. The heat would not be evenly distributed; some places would be very hot while others would become extremely cold. There would be an increase in heat related deaths. The intensity of hurricanes, tornadoes and other violent weather would increase. El Nino would become more frequent, affecting upwelling and preventing the needed nutrients that come from the colder levels of the ocean from reaching the surface. Increases in El Nino seem to cause a decrease in monsoons. As ocean temperature increases, the warm air rises over the sea forming storms that drop most of their moisture as rain before they move off over land. This lack of much needed rain over land could cause serious droughts. An increase in ocean temperature and the addition of fresh water could cause coral bleaching. Productive coral reefs could be destroyed as well as the fish and other organisms dependent on the reef. Reefs reduce the intensity of incoming waves and protect the shore from erosion and storms the same way barrier islands protect mainland coasts. If sea level rises more rapidly than the upward growth of coral reefs, waves would wash over the reefs and penetrate the beach causing erosion. An ocean warming of only 1-degree C. can kill coral and other reef organisms. Warm waters during El Nino have been suspected of causing the death of Pacific corals. The disruption of corals could disrupt the food chain and kill an entire ecosystem.
Global warming is a natural process but it seems that man is aggravating it. This would be particularly disruptive to the area that we live in here in Southwest Florida.
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