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Archive for December, 2010

STRESS BREAKDOWN: FIRST SYMPTOM – HIGH LEVELS OF SENSORY INPUT CAUSE DISTRESS

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Information comes in to the brain through sensory nerve fibres. Usually sensory nerves are activated by tiny sense organs or ‘receptors’ which respond to certain sensations and fire off the nerve. There are receptors for heat sensation, touch, position sense, balance, acceleration, cold, light, sound, taste and smell. As well, the muscles and the joints are supplied with stretch receptors which provide the information necessary for the body to know where its various parts are.
There doesn’t seem to be a specific receptor for pain impulses. We experience pain from over-stimulation of nerves which don’t have specific sense receptors, and also whenever specific sensor receptors are over-stimulated. Thus a too-loud noise, a too-cold stimulus, a too-hot stimulus, or a too-bright light, will all cause the person to feel pain.
Pain is experienced, therefore, when the sensory nerve fibres are over-stimulated. There is a corresponding hypersensitivity which occurs not when the incoming fibres are over-stimulated, but when the receiving brain cells are over-sensitive. Receiving brain cells become over-sensitive when they are over-stimulated in stress breakdown. Thus the over-stimulation of brain cortex cells in stress breakdown may have the effect of making the incoming information disagreeable, just as excess actual stimulation makes the sensory input disagreeable or painful.
In stress breakdown which has gone beyond second stage, the receiving brain cells are so over-sensitive that strong sensory stimulation becomes actually disagreeable.
Even stimulation which has previously been highly enjoyable, such as sexual stimulation, music and perfume or exotic tastes can become disagreeable in the third stage.
In third stage breakdown, women who previously enjoyed an active sex life might claim to be totally uninterested in sex and, even more than that, actually turned off it. ‘I can’t stand him to even touch me, doctor. What’s wrong with me?’ In the third stage, over-stressed people who normally love music might be irritated by the very music they previously enjoyed. This leads to over-stressed people complaining that the radio or TV is too loud, and that they have ‘gone off’ their favorite programmes or activities.
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STRESS BREAKDOWN: FIRST SYMPTOM – HIGH LEVELS OF SENSORY INPUT CAUSE DISTRESS
Information comes in to the brain through sensory nerve fibres. Usually sensory nerves are activated by tiny sense organs or ‘receptors’ which respond to certain sensations and fire off the nerve. There are receptors for heat sensation, touch, position sense, balance, acceleration, cold, light, sound, taste and smell. As well, the muscles and the joints are supplied with stretch receptors which provide the information necessary for the body to know where its various parts are.There doesn’t seem to be a specific receptor for pain impulses. We experience pain from over-stimulation of nerves which don’t have specific sense receptors, and also whenever specific sensor receptors are over-stimulated. Thus a too-loud noise, a too-cold stimulus, a too-hot stimulus, or a too-bright light, will all cause the person to feel pain.Pain is experienced, therefore, when the sensory nerve fibres are over-stimulated. There is a corresponding hypersensitivity which occurs not when the incoming fibres are over-stimulated, but when the receiving brain cells are over-sensitive. Receiving brain cells become over-sensitive when they are over-stimulated in stress breakdown. Thus the over-stimulation of brain cortex cells in stress breakdown may have the effect of making the incoming information disagreeable, just as excess actual stimulation makes the sensory input disagreeable or painful.In stress breakdown which has gone beyond second stage, the receiving brain cells are so over-sensitive that strong sensory stimulation becomes actually disagreeable.Even stimulation which has previously been highly enjoyable, such as sexual stimulation, music and perfume or exotic tastes can become disagreeable in the third stage.In third stage breakdown, women who previously enjoyed an active sex life might claim to be totally uninterested in sex and, even more than that, actually turned off it. ‘I can’t stand him to even touch me, doctor. What’s wrong with me?’ In the third stage, over-stressed people who normally love music might be irritated by the very music they previously enjoyed. This leads to over-stressed people complaining that the radio or TV is too loud, and that they have ‘gone off’ their favorite programmes or activities.
*30/129/5*

ASTHMA IN CHILDREN: THE INHALED ALLERGENS – ANIMALS AS ALLERGENS

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Some animals and insects are known to act as allergens and cause asthma.
Animals. Henry Hyde Salter has given the first accurate description of the attacks of asthma caused by an exposure to a cat. In his book on asthma published around the middle of the nineteenth century, he wrote:
‘This singular phenomenon is, I imagine, almost peculiar to myself. The cause of this asthma is the proximity of a common domestic cat; the symptoms are very similar to those of hay fever, and, as in the case of hay fever, are occasioned by some sudden influence inappreciable by the senses. I cannot recollect at what time I first became subject to the cat asthma, but I believe the susceptibility has existed
from the earliest period of even a pet dog can cause life. I believe there are even some asthma symptoms even if I were sitting by the fire and the cat sleeping on the hearthrug; but the effect is much greater when the cat is at the distance of about one or two feet or closer; it is further increased by the rising of the fur and moving and rubbing about; but most of all when it is in the lap, just under the face…. The asthmatic spasm is immediate and violent and accompanied with sneezing, burning and watery condition of the eyes and nose and excessive itching of the skin…., I believe that if the cause were suffered to continue, all or most of the other symptoms of hay fever would ensue, only with a more excessive and conspicuous asthma. After the removal of the cause, and if the paroxysm is not very severe, the cure is effected in five or ten minutes, leaving, as in all other cases of asthmatic spasm, a tendency to mucus at the top of the wind pipe, which being repeatedly removed in the ordinary way the last symptom disappears, and the lungs and throat resume their normal condition’.
*30\260\8*

ASTHMA IN CHILDREN: THE INHALED ALLERGENS – ANIMALS AS ALLERGENSSome animals and insects are known to act as allergens and cause asthma.Animals. Henry Hyde Salter has given the first accurate description of the attacks of asthma caused by an exposure to a cat. In his book on asthma published around the middle of the nineteenth century, he wrote:’This singular phenomenon is, I imagine, almost peculiar to myself. The cause of this asthma is the proximity of a common domestic cat; the symptoms are very similar to those of hay fever, and, as in the case of hay fever, are occasioned by some sudden influence inappreciable by the senses. I cannot recollect at what time I first became subject to the cat asthma, but I believe the susceptibility has existedfrom the earliest period of even a pet dog can cause life. I believe there are even some asthma symptoms even if I were sitting by the fire and the cat sleeping on the hearthrug; but the effect is much greater when the cat is at the distance of about one or two feet or closer; it is further increased by the rising of the fur and moving and rubbing about; but most of all when it is in the lap, just under the face…. The asthmatic spasm is immediate and violent and accompanied with sneezing, burning and watery condition of the eyes and nose and excessive itching of the skin…., I believe that if the cause were suffered to continue, all or most of the other symptoms of hay fever would ensue, only with a more excessive and conspicuous asthma. After the removal of the cause, and if the paroxysm is not very severe, the cure is effected in five or ten minutes, leaving, as in all other cases of asthmatic spasm, a tendency to mucus at the top of the wind pipe, which being repeatedly removed in the ordinary way the last symptom disappears, and the lungs and throat resume their normal condition’.*30\260\8*

BIOBOMBS: DESIGNER BUGS

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One of the scenarios that surfaces in discussions of biological terrorism is the possibility of a genetically engineered superbug for which there is no defense. The ability of molecular biology to accomplish such an engineering feat is limited, however. A superbug would need to have the right mix of transmissibility and virulence, and the interplay between different genes in the genome is not sufficiently well understood to allow this kind of designer bug to be generated. Nasty variants can certainly be created in laboratories by trial and error, but this possibility existed long before the precision of molecular engineering arrived on the scene.
Animal models won’t do the trick either, because repeated transferring of a pathogen between animals of a given species tends to adapt the pathogen to that species and makes it less able to live in and harm humans. One can therefore obtain a highly lethal and transmissible pathogen for mice that is unpredictable in humans. To generate a pathogen that would be both highly damaging and transmissible after being released in a human population, pathogens would need to be transferred among humans in the same way that virulent pathogens can be generated in an animal species—by transferring the pathogen among many individuals of that host species. This option is so abhorrent to most people that we should be able to suppress it. Even if a psychotic individual was willing to do such research, the project would have to be so large, and the probability of being appalled would be so great for those involved, that word would probably get out; when the word did get out, it would most likely be possible to obtain overwhelming approval for drastic measures to end the work and remove from power those who instigated it. The project would be so self-destructive that only the most foolish would engage in it. Still there are self-destructive psychopaths, and there are historical precedents, such as the experiments by the Japanese on prisoners during World War II. The knowledge that superbugs could be created by using humans as experimental subjects should generate multinational public support for efforts to monitor any research activities using human subjects and to place the investigations and dismantling of any such projects above any pleas of national sovereignty.
The potential dangers of such a superbug are illustrated by the history of contact between people during the colonial period. Before this contact, something akin to an experimental passaging of pathogens in humans was carried out. This passaging occurred over thousands of years in European populations, who coevolved resistance to endemic pathogens such as measles, mumps, and smallpox. When these pathogens were introduced into human populations who did not share this co-evolutionary history, the lethality of each was ferociously elevated. Whereas smallpox killed one in ten in Europe, it killed most of the New World people it infected. Measles was transformed from a disease that killed about one out of every thousand infected Europeans to a disease that killed New World people the way smallpox killed Europeans. Mumps, which killed less than one in a hundred thousand Europeans, killed New World populations the way measles killed Europeans. The net result was the destruction of New World populations by more than 90 percent. Throughout the arms race between Europeans and pathogens, the pathogens were continually selected to break through human defenses and be transmissible. The evolved and acquired immune defenses of Europeans caused the pathogens to evolve particularly aggressive characteristics that, though held in check in European populations, met with little defense in populations native to the New World.
This natural experiment of human history should keep us from being complacent about the damage pathogens could cause if they acquired the appropriate mix of characteristics. But fear of this scenario should be tempered by the knowledge that this natural experiment cannot be repeated. Human pathogens are now so thoroughly and continuously mixed that we cannot generate the coevolutionary arms races in one area that would leave the humans who were not running in the race vulnerable when they eventually encountered the pathogens. No more New World populations of humans are left to discover, contact, and destroy.
Another problem with the designer bug strategy is the continued evolution of virulence and transmissibility after the bug is released. A key characteristic of the designer bug would be transmissibility, but once transmission occurs, the evolutionary future of the bug is out of the hands of the terrorists. It would rapidly evolve to a level of virulence that is most suited to the environments in which it is being transmitted. In other words, it would evolve into an organism with more familiar characteristics. The organism may cause terrible damage during the process of evolutionary equilibration and thereafter. But, as noted above, it would still leave the target population intact, ready to take revenge on the terrorists. The influenza pandemic of 1918 illustrates something like a worst-case scenario. Here was a pathogen that was probably overly exploiting its host during most of the pandemic; as it swept around the world, the most virulent viruses eventually lost out in competition with viruses of reduced virulence. The generation and maintenance of high virulence was permitted by natural selection only when the dependence of transmission on ambulatory hosts was temporarily relaxed under the unusual conditions of the Western Front and the masses of densely packed populations transported at the end of the war. It killed about 1 percent of humanity, yet it hardly seemed to influence the ability of the afflicted countries to keep the social cogs moving. Within a year or two the nasty variants of the influenza viruses vanished and never resurfaced in epidemic form. For more than eight decades, they have been replaced by the more traditional influenza viruses, which have been less lethal than the 1918 viruses by one or two orders of magnitude. The nasty strains did not disappear because of any heroic control efforts. Rather, they probably disappeared because they were too damaging for their own transmission under normal conditions. Terrorists would have little control over such a virus.
*55\225\2*

BIOBOMBS: DESIGNER BUGSOne of the scenarios that surfaces in discussions of biological terrorism is the possibility of a genetically engineered superbug for which there is no defense. The ability of molecular biology to accomplish such an engineering feat is limited, however. A superbug would need to have the right mix of transmissibility and virulence, and the interplay between different genes in the genome is not sufficiently well understood to allow this kind of designer bug to be generated. Nasty variants can certainly be created in laboratories by trial and error, but this possibility existed long before the precision of molecular engineering arrived on the scene.Animal models won’t do the trick either, because repeated transferring of a pathogen between animals of a given species tends to adapt the pathogen to that species and makes it less able to live in and harm humans. One can therefore obtain a highly lethal and transmissible pathogen for mice that is unpredictable in humans. To generate a pathogen that would be both highly damaging and transmissible after being released in a human population, pathogens would need to be transferred among humans in the same way that virulent pathogens can be generated in an animal species—by transferring the pathogen among many individuals of that host species. This option is so abhorrent to most people that we should be able to suppress it. Even if a psychotic individual was willing to do such research, the project would have to be so large, and the probability of being appalled would be so great for those involved, that word would probably get out; when the word did get out, it would most likely be possible to obtain overwhelming approval for drastic measures to end the work and remove from power those who instigated it. The project would be so self-destructive that only the most foolish would engage in it. Still there are self-destructive psychopaths, and there are historical precedents, such as the experiments by the Japanese on prisoners during World War II. The knowledge that superbugs could be created by using humans as experimental subjects should generate multinational public support for efforts to monitor any research activities using human subjects and to place the investigations and dismantling of any such projects above any pleas of national sovereignty.The potential dangers of such a superbug are illustrated by the history of contact between people during the colonial period. Before this contact, something akin to an experimental passaging of pathogens in humans was carried out. This passaging occurred over thousands of years in European populations, who coevolved resistance to endemic pathogens such as measles, mumps, and smallpox. When these pathogens were introduced into human populations who did not share this co-evolutionary history, the lethality of each was ferociously elevated. Whereas smallpox killed one in ten in Europe, it killed most of the New World people it infected. Measles was transformed from a disease that killed about one out of every thousand infected Europeans to a disease that killed New World people the way smallpox killed Europeans. Mumps, which killed less than one in a hundred thousand Europeans, killed New World populations the way measles killed Europeans. The net result was the destruction of New World populations by more than 90 percent. Throughout the arms race between Europeans and pathogens, the pathogens were continually selected to break through human defenses and be transmissible. The evolved and acquired immune defenses of Europeans caused the pathogens to evolve particularly aggressive characteristics that, though held in check in European populations, met with little defense in populations native to the New World.This natural experiment of human history should keep us from being complacent about the damage pathogens could cause if they acquired the appropriate mix of characteristics. But fear of this scenario should be tempered by the knowledge that this natural experiment cannot be repeated. Human pathogens are now so thoroughly and continuously mixed that we cannot generate the coevolutionary arms races in one area that would leave the humans who were not running in the race vulnerable when they eventually encountered the pathogens. No more New World populations of humans are left to discover, contact, and destroy.Another problem with the designer bug strategy is the continued evolution of virulence and transmissibility after the bug is released. A key characteristic of the designer bug would be transmissibility, but once transmission occurs, the evolutionary future of the bug is out of the hands of the terrorists. It would rapidly evolve to a level of virulence that is most suited to the environments in which it is being transmitted. In other words, it would evolve into an organism with more familiar characteristics. The organism may cause terrible damage during the process of evolutionary equilibration and thereafter. But, as noted above, it would still leave the target population intact, ready to take revenge on the terrorists. The influenza pandemic of 1918 illustrates something like a worst-case scenario. Here was a pathogen that was probably overly exploiting its host during most of the pandemic; as it swept around the world, the most virulent viruses eventually lost out in competition with viruses of reduced virulence. The generation and maintenance of high virulence was permitted by natural selection only when the dependence of transmission on ambulatory hosts was temporarily relaxed under the unusual conditions of the Western Front and the masses of densely packed populations transported at the end of the war. It killed about 1 percent of humanity, yet it hardly seemed to influence the ability of the afflicted countries to keep the social cogs moving. Within a year or two the nasty variants of the influenza viruses vanished and never resurfaced in epidemic form. For more than eight decades, they have been replaced by the more traditional influenza viruses, which have been less lethal than the 1918 viruses by one or two orders of magnitude. The nasty strains did not disappear because of any heroic control efforts. Rather, they probably disappeared because they were too damaging for their own transmission under normal conditions. Terrorists would have little control over such a virus.*55\225\2*