The Necro-Omar
16-06-2005, 02:29
Charles Mikov shifted uneasily in his chair.
"I have been waiting for an hour! Where is that stupid scientist?" Just at that moment the supposed scientist walked in.
http://www.mxm.dk/images/maxm-mad-scientist-2-w150.jpg
"Uh hello great and wise Triumverate member!"
"What in the hell? Are you the guy I'm waiting on?"
"Yes."
"No matter. What have you got for me?"
"Well sir, we've developed a way to give large amounts of people Creutzfeldt-Jakob's disease at one time through germs, which will be usable in war."
"What was it's name?"
"Creutzfeldt-Jakob's disease Commander. You can call it CJD for short."
"Right. Well tell me about CJD"
"What do you want to know?"
"What is Creutzfeldt-Jakob Disease?"
"Creutzfeldt-Jakob disease (CJD) is a rare, degenerative, invariably fatal brain disorder. In the early stages of disease, patients may have failing memory, behavioral changes, lack of coordination and visual disturbances. As the illness progresses, mental deterioration becomes pronounced and involuntary movements, blindness, weakness of extremities, and coma may occur. It basically eats the brain, making large holes in it. Our biological agents can speed up the disease, allowing it to kill in 24 hours.
There are three major categories of CJD:
In sporadic CJD, the disease appears even though the person has no known risk factors for the disease. This is by far the most common type of CJD and accounts for at least 85 percent of cases.
In hereditary CJD, the person has a family history of the disease and/or tests positive for a genetic mutation associated with CJD. About 5 to 10 percent of cases of CJD in the United States are hereditary.
In acquired CJD, the disease is transmitted by exposure to brain or nervous system tissue, usually through certain medical procedures. There is no evidence that CJD is contagious through casual contact with a CJD patient. Since CJD was first described in 1920, fewer than 1 percent of cases have been acquired CJD.
CJD belongs to a family of human and animal diseases known as the transmissible spongiform encephalopathies (TSEs). Spongiform refers to the characteristic appearance of infected brains, which become filled with holes until they resemble sponges under a microscope. CJD is the most common of the known human TSEs. Other human TSEs include kuru, fatal familial insomnia (FFI), and Gerstmann-Straussler-Scheinker disease (GSS). Kuru was identified in people of an isolated tribe in Papua New Guinea and has now almost disappeared. FFI and GSS are extremely rare hereditary diseases, found in just a few families around the world. Other TSEs are found in specific kinds of animals. These include bovine spongiform encephalopathy (BSE), which is found in cows and is often referred to as “mad cow” disease; scrapie, which affects sheep and goats; mink encephalopathy; and feline encephalopathy. Similar diseases have occurred in elk, deer, and exotic zoo animals.
We will be using the sporadic CJD for our purposes."
"What are the Symptoms of the Disease?"
"CJD is characterized by rapidly progressive dementia. Initially, patients experience problems with muscular coordination; personality changes, including impaired memory, judgment, and thinking; and impaired vision. People with the disease also may experience insomnia, depression, or unusual sensations. CJD does not cause a fever or other flu-like symptoms. As the illness progresses, the patients’ mental impairment becomes severe. They often develop involuntary muscle jerks called myoclonus, and they may go blind. They eventually lose the ability to move and speak and enter a coma. Pneumonia and other infections often occur in these patients and lead to death."
"What Causes Creutzfeldt-Jakob Disease?"
"Some researchers believe an unusual "slow virus" or another organism causes CJD. However, they have never been able to isolate a virus or other organism in people with the disease. Furthermore, the agent that causes CJD has several characteristics that are unusual for known organisms such as viruses and bacteria. It is difficult to kill, it does not appear to contain any genetic information in the form of nucleic acids (DNA or RNA), and it usually has a long incubation period before symptoms appear. In some cases, the incubation period may be as long as 40 years. The leading scientific theory at this time maintains that CJD and the other TSEs are caused by a type of protein called a prion.
Prion proteins occur in both a normal form, which is a harmless protein found in the body’s cells, and in an infectious form, which causes disease. The harmless and infectious forms of the prion protein have the same sequence of amino acids (the "building blocks" of proteins) but the infectious form of the protein takes a different folded shape than the normal protein. Sporadic CJD may develop because some of a person’s normal prions spontaneously change into the infectious form of the protein and then alter the prions in other cells in a chain reaction.
Once they appear, abnormal prion proteins aggregate, or clump together. Investigators think these protein aggregates may lead to the neuron loss and other brain damage seen in CJD. However, they do not know exactly how this damage occurs.
We will use a special type of germ that will instigate the prions to change in a persons body. We call it the CJD Germ. It has a success rate of about 98.9%"
"How is the Disease Treated?"
"There is no treatment that can cure or control CJD. Researchers have tested many drugs, including amantadine, steroids, interferon, acyclovir, antiviral agents, and antibiotics. Studies of a variety of other drugs are now in progress. However, so far none of these treatments has shown any consistent benefit in humans.
Current treatment for CJD is aimed at alleviating symptoms and making the patient as comfortable as possible. Opiate drugs can help relieve pain if it occurs, and the drugs clonazepam and sodium valproate may help relieve myoclonus. During later stages of the disease, changing the person’s position frequently can keep him or her comfortable and helps prevent bedsores. A catheter can be used to drain urine if the patient cannot control bladder function, and intravenous fluids and artificial feeding also may be used."
"Execellent work! Begin production immeditly! This will be our secret ace up our sleave. But there is one problem I had..."
"What Great and Wise one?"
"Change the name of the gas.....TO COBRA VENOM! MHA HA HA HA HA HA HA HA!"
"I have been waiting for an hour! Where is that stupid scientist?" Just at that moment the supposed scientist walked in.
http://www.mxm.dk/images/maxm-mad-scientist-2-w150.jpg
"Uh hello great and wise Triumverate member!"
"What in the hell? Are you the guy I'm waiting on?"
"Yes."
"No matter. What have you got for me?"
"Well sir, we've developed a way to give large amounts of people Creutzfeldt-Jakob's disease at one time through germs, which will be usable in war."
"What was it's name?"
"Creutzfeldt-Jakob's disease Commander. You can call it CJD for short."
"Right. Well tell me about CJD"
"What do you want to know?"
"What is Creutzfeldt-Jakob Disease?"
"Creutzfeldt-Jakob disease (CJD) is a rare, degenerative, invariably fatal brain disorder. In the early stages of disease, patients may have failing memory, behavioral changes, lack of coordination and visual disturbances. As the illness progresses, mental deterioration becomes pronounced and involuntary movements, blindness, weakness of extremities, and coma may occur. It basically eats the brain, making large holes in it. Our biological agents can speed up the disease, allowing it to kill in 24 hours.
There are three major categories of CJD:
In sporadic CJD, the disease appears even though the person has no known risk factors for the disease. This is by far the most common type of CJD and accounts for at least 85 percent of cases.
In hereditary CJD, the person has a family history of the disease and/or tests positive for a genetic mutation associated with CJD. About 5 to 10 percent of cases of CJD in the United States are hereditary.
In acquired CJD, the disease is transmitted by exposure to brain or nervous system tissue, usually through certain medical procedures. There is no evidence that CJD is contagious through casual contact with a CJD patient. Since CJD was first described in 1920, fewer than 1 percent of cases have been acquired CJD.
CJD belongs to a family of human and animal diseases known as the transmissible spongiform encephalopathies (TSEs). Spongiform refers to the characteristic appearance of infected brains, which become filled with holes until they resemble sponges under a microscope. CJD is the most common of the known human TSEs. Other human TSEs include kuru, fatal familial insomnia (FFI), and Gerstmann-Straussler-Scheinker disease (GSS). Kuru was identified in people of an isolated tribe in Papua New Guinea and has now almost disappeared. FFI and GSS are extremely rare hereditary diseases, found in just a few families around the world. Other TSEs are found in specific kinds of animals. These include bovine spongiform encephalopathy (BSE), which is found in cows and is often referred to as “mad cow” disease; scrapie, which affects sheep and goats; mink encephalopathy; and feline encephalopathy. Similar diseases have occurred in elk, deer, and exotic zoo animals.
We will be using the sporadic CJD for our purposes."
"What are the Symptoms of the Disease?"
"CJD is characterized by rapidly progressive dementia. Initially, patients experience problems with muscular coordination; personality changes, including impaired memory, judgment, and thinking; and impaired vision. People with the disease also may experience insomnia, depression, or unusual sensations. CJD does not cause a fever or other flu-like symptoms. As the illness progresses, the patients’ mental impairment becomes severe. They often develop involuntary muscle jerks called myoclonus, and they may go blind. They eventually lose the ability to move and speak and enter a coma. Pneumonia and other infections often occur in these patients and lead to death."
"What Causes Creutzfeldt-Jakob Disease?"
"Some researchers believe an unusual "slow virus" or another organism causes CJD. However, they have never been able to isolate a virus or other organism in people with the disease. Furthermore, the agent that causes CJD has several characteristics that are unusual for known organisms such as viruses and bacteria. It is difficult to kill, it does not appear to contain any genetic information in the form of nucleic acids (DNA or RNA), and it usually has a long incubation period before symptoms appear. In some cases, the incubation period may be as long as 40 years. The leading scientific theory at this time maintains that CJD and the other TSEs are caused by a type of protein called a prion.
Prion proteins occur in both a normal form, which is a harmless protein found in the body’s cells, and in an infectious form, which causes disease. The harmless and infectious forms of the prion protein have the same sequence of amino acids (the "building blocks" of proteins) but the infectious form of the protein takes a different folded shape than the normal protein. Sporadic CJD may develop because some of a person’s normal prions spontaneously change into the infectious form of the protein and then alter the prions in other cells in a chain reaction.
Once they appear, abnormal prion proteins aggregate, or clump together. Investigators think these protein aggregates may lead to the neuron loss and other brain damage seen in CJD. However, they do not know exactly how this damage occurs.
We will use a special type of germ that will instigate the prions to change in a persons body. We call it the CJD Germ. It has a success rate of about 98.9%"
"How is the Disease Treated?"
"There is no treatment that can cure or control CJD. Researchers have tested many drugs, including amantadine, steroids, interferon, acyclovir, antiviral agents, and antibiotics. Studies of a variety of other drugs are now in progress. However, so far none of these treatments has shown any consistent benefit in humans.
Current treatment for CJD is aimed at alleviating symptoms and making the patient as comfortable as possible. Opiate drugs can help relieve pain if it occurs, and the drugs clonazepam and sodium valproate may help relieve myoclonus. During later stages of the disease, changing the person’s position frequently can keep him or her comfortable and helps prevent bedsores. A catheter can be used to drain urine if the patient cannot control bladder function, and intravenous fluids and artificial feeding also may be used."
"Execellent work! Begin production immeditly! This will be our secret ace up our sleave. But there is one problem I had..."
"What Great and Wise one?"
"Change the name of the gas.....TO COBRA VENOM! MHA HA HA HA HA HA HA HA!"