Watu Wala watu wenzao
- Thread starter Sophist
- Start date
Kitia
JF-Expert Member
- Dec 2, 2006
- 418
- 74
The main cause of deadly brain-wasting diseases might be just what the researchers have for long been prodding into - cannibalism. Abnormal proteins called the prions resultantly cause a brain-wasting disease called Creutzfeld Jacob disease (CJD) and bovine spongiform encephalopathy, or mad cow disease in humans. The presence of this protein causes other proteins to be clumped together. CJD is usually found in large numbers// in people who take flesh with infectious prions. These as a result kill the brain cells. This disease is found in about one in a million people. A disease called kuru common among the Fore people in Papua New Guinea was mainly due to eating their deceased relatives in the mortuary feasts. There are genetic mutations called polymorphisms which resist the disease. Researchers have reported that natural selection appears to have spread through the population.
Pinpointing the selection pressure Research on women who feasted on the deceased ones was carried out. It suggested that there is a certain genetic variation and mutation which is more prevalent in women over 50 than young women. Some women who feasted on the deceased ones and yet were living were tested by the researchers. Ample evidence suggests that the protective mutation through generations had protected them from disease. The mutation protects against CJD too. Mutations do protect from diseases, with evidences from pre-historic age. There is much skepticism about the fact that all the early human being were cannibals.
The protective mutations now appear in the DNA of people around the world. Other prion researchers want to verify the findings with data from larger population samples. Since prions can cross between species, it is also possible that eating animals with prion diseases could have contributed to the spread of the protective gene. The protective mutations now appear in the DNA of people around the world. Other prion researchers want to verify the findings with data from larger population samples. Since prions can cross between species, it is also possible that eating animals with prion diseases could have contributed to the spread of the protective gene.
Source.
Pinpointing the selection pressure Research on women who feasted on the deceased ones was carried out. It suggested that there is a certain genetic variation and mutation which is more prevalent in women over 50 than young women. Some women who feasted on the deceased ones and yet were living were tested by the researchers. Ample evidence suggests that the protective mutation through generations had protected them from disease. The mutation protects against CJD too. Mutations do protect from diseases, with evidences from pre-historic age. There is much skepticism about the fact that all the early human being were cannibals.
The protective mutations now appear in the DNA of people around the world. Other prion researchers want to verify the findings with data from larger population samples. Since prions can cross between species, it is also possible that eating animals with prion diseases could have contributed to the spread of the protective gene. The protective mutations now appear in the DNA of people around the world. Other prion researchers want to verify the findings with data from larger population samples. Since prions can cross between species, it is also possible that eating animals with prion diseases could have contributed to the spread of the protective gene.
Source.
Kitia
JF-Expert Member
- Dec 2, 2006
- 418
- 74
Kuru (disease)
From Wikipedia, the free encyclopedia
Kuru is an incurable degenerative neurological disorder (brain disease) that is a type of transmissible spongiform encephalopathy found in humans.
It is believed to be caused by prions and is related to Creutzfeldt-Jakob disease.[2] It is best known for the epidemic that occurred in Papua New Guinea in the middle of the twentieth century, and earlier.
Although it is considered a transmissible prion disease, there is some evidence that the origin of the outbreak was due to consumption of an individual (cannibalism) with sporadic CJD, thus implying a common pathophysiology.
Kuru causes physiological as well as neurological effects that ultimately lead to death. It was endemic among the Fore tribe of Papua New Guinea and was confined to the Fore population and those nearby populations with whom they intermarried. It is characterized by truncal ataxia, preceded by headaches, joint pains and shaking of the limbs, with the clinical stage lasting an average of 12 months.
Trembling is present in almost all patients with transmissible spongiform encephalopathy.
Terminology
The word kuru is taken from the Fore word "kuria/guria", 'to shake'.It is also known as the laughing sickness due to the pathologic bursts of laughter people would display when afflicted with the disease.
History
Kuru was first noted in the Fore tribe of the Eastern Highlands Province of Papua New Guinea as Australian administrators explored the area in 1957–1959. It was in the late 1950s that the full extent of the disease was realized, after it had reached large infection rates in the South Fore of the Okapa Subdistrict, though the agent was unknown.
The disease was researched by Daniel Carleton Gajdusek who, along with Baruch S. Blumberg, was awarded the Nobel Prize in Physiology or Medicine in 1976 for his showing that kuru was transmissible to chimpanzees. This was the first time that this group of encephalopathies had been demonstrated to be infectious and therefore a major step forwards in their investigation. As kuru is the only epidemic of human prion disease in known human history, it has provided important insights into the variant CJD.
Transmission
It is believed by some that the disease spread easily and rapidly in the Fore people due to their endocannibalistic funeral practices, in which relatives consumed the deceased to return the "life force" of the deceased to his hamlet, a Fore societal subunit. The dysmorphism evident in the infection rates-kuru was 8-9 times more prevalent in women and children than in men at its peak-is because while the men of the village took the choice cuts, the women and children would eat the rest of the body including the brain, where the prion particles were particularly concentrated. There is also the strong possibility that it was passed on to women and children more easily because they took on the task of cleaning relatives after death and may have had open sores and cuts on their hands. Although ingestion itself of the prion particles would not lead to the disease, there was a high degree of transmission if the prion particles could reach the subcutaneous tissue. With elimination of cannibalism because of Australian law enforcement and local Christian missionaries' efforts, Kuru rapidly declined among the Fore. However, the mean incubation period of the disease is 14 years and cases were reported with latencies of 40 years for those who were most genetically resilient.
From Wikipedia, the free encyclopedia
Kuru is an incurable degenerative neurological disorder (brain disease) that is a type of transmissible spongiform encephalopathy found in humans.
It is believed to be caused by prions and is related to Creutzfeldt-Jakob disease.[2] It is best known for the epidemic that occurred in Papua New Guinea in the middle of the twentieth century, and earlier.
Although it is considered a transmissible prion disease, there is some evidence that the origin of the outbreak was due to consumption of an individual (cannibalism) with sporadic CJD, thus implying a common pathophysiology.
Kuru causes physiological as well as neurological effects that ultimately lead to death. It was endemic among the Fore tribe of Papua New Guinea and was confined to the Fore population and those nearby populations with whom they intermarried. It is characterized by truncal ataxia, preceded by headaches, joint pains and shaking of the limbs, with the clinical stage lasting an average of 12 months.
Trembling is present in almost all patients with transmissible spongiform encephalopathy.
Terminology
The word kuru is taken from the Fore word "kuria/guria", 'to shake'.It is also known as the laughing sickness due to the pathologic bursts of laughter people would display when afflicted with the disease.
History
Kuru was first noted in the Fore tribe of the Eastern Highlands Province of Papua New Guinea as Australian administrators explored the area in 1957–1959. It was in the late 1950s that the full extent of the disease was realized, after it had reached large infection rates in the South Fore of the Okapa Subdistrict, though the agent was unknown.
The disease was researched by Daniel Carleton Gajdusek who, along with Baruch S. Blumberg, was awarded the Nobel Prize in Physiology or Medicine in 1976 for his showing that kuru was transmissible to chimpanzees. This was the first time that this group of encephalopathies had been demonstrated to be infectious and therefore a major step forwards in their investigation. As kuru is the only epidemic of human prion disease in known human history, it has provided important insights into the variant CJD.
Transmission
It is believed by some that the disease spread easily and rapidly in the Fore people due to their endocannibalistic funeral practices, in which relatives consumed the deceased to return the "life force" of the deceased to his hamlet, a Fore societal subunit. The dysmorphism evident in the infection rates-kuru was 8-9 times more prevalent in women and children than in men at its peak-is because while the men of the village took the choice cuts, the women and children would eat the rest of the body including the brain, where the prion particles were particularly concentrated. There is also the strong possibility that it was passed on to women and children more easily because they took on the task of cleaning relatives after death and may have had open sores and cuts on their hands. Although ingestion itself of the prion particles would not lead to the disease, there was a high degree of transmission if the prion particles could reach the subcutaneous tissue. With elimination of cannibalism because of Australian law enforcement and local Christian missionaries' efforts, Kuru rapidly declined among the Fore. However, the mean incubation period of the disease is 14 years and cases were reported with latencies of 40 years for those who were most genetically resilient.
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