Agent Orange: The Peloponnesian War

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It’s interesting to see the progression of weapons from the early beginnings to now. Most people believe that chemical warfare agents were first introduced during the World Wars. Interestingly enough, the concepts of these agents were developed as early as 600 B.C. They weren’t known as chemical warfare agents however; the techniques that were used mimic the action of these agents that are being used today. During the Peloponnesian War between Sparta and Athens, the Spartan army used a mixture of chemicals in what they called the “Greek fire.” It was found to be that the “Greek Fire” was actually a mixture of sulfur, resin, pitches, naphtha, lime and saltpeter (Grey, 2006). In the early stages of World War I was when we first saw the use …show more content…
Peripheral neuropathy is a condition which impacts the peripheral nervous system and impacts the communication between the brain and spinal cord to the other areas of the body. Neuropathy can be caused by damage to the axons or the myelin sheath that provides a protective coating and a form of insulation to the axon. If the connections between the main brain and spinal cord are severed, there are certain symptoms that occur including miscommunication between muscles and the neurons that react to the certain stimulus. The word neuropathy is defined as nerve damage and thus the nerves that could be referred to are motor, sensory or autonomic nerves. As a result, symptoms can range anywhere from numbness and tingling to paralysis or organ dysfunction depending on the type of nerves(s) that are damaged. Motor nerve damage can result in muscle damage or uncontrolled movements. Depending on the size of the sensory nerve that is damaged, patients may become over sensitive or even desensitized to environmental stimuli. In addition, sensory nerve damage can cause loss in coordination of body movements and inability to maintain balance. Damage to autonomic nerves causes loss of control of major organ systems (Institute of Medicine, …show more content…
This pathway highlights the “rapid intracellular increase in Ca2+ concentration, enzymatic activation of cytosolic phospholipase A2 (cPLA2) and that of Cox-2 are taking place through the nongenomic action of the ligand-activated AHR” (Dong & Matsumura, 2008). There was an observation of an increase in free arachidonic acid in the medium of MCF10A human breast epithelial cells when treated with TCDD. The enzyme that correlates to this is cPLA2 since its primary role is to release free arachidonic acid from the plasma membrane of cells. Free arachidonic acid also is a “precursor of many inflammation-inducing metabolites such as prostaglandins and leukotrienes.” Ca2+ is also known to be the initial step for the nongenomic pathways as it is a well known activator of cPLA2. This was shown in a study that determined maximal Ca2+ concentration was observed within 30 seconds after addition of TCDD (Hanneman, et al., 1996). So this nongenomic pathway shows that once TCDD is introduced, there is a influx of Ca2+ intracellularly and that results in the release of free arachidonic acid by cPLA2 causing an inflammatory reaction releasing prostaglandins and

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