Prolonged stress disorder may increase the risk of heart disease, according to resarchers from the Harvard School of Public Health.
Anxiety disorder may be triggered by traumatic memories such as from military combat, from natural disasters, terrorist attacks, as well as from physical or sexual abuse. Symptoms of this anxiety disorder includes flashbacks, anger and difficulty of sleeping, emotional deadening, increased blood pressure, rapid heartbeat, and muscle tension.
The study published in the Archives of General Psychiatry analyzed data from the Veterans Administrative Normative Aging Study, a research project that examined the health of military veterans. Responses of male World War II and Korean War veterans showed that those with stronger post traumatic stress disorder symptoms suffered higher rates of coronary heart disease.
Laura Kubzansky, who analyzed the responses suggests that "prolonged stress and significant levels of PTSD symptoms may increase the risk of coronary heart disease in older male veterans."
Wednesday, October 10, 2007
Tuesday, October 09, 2007
Scientists Explains How Sunburn Causes Skin Cancer
Researchers from the US have found a new mechanism that explains not only how the body repairs damage done by the sun but might explain why some people are more prone to cancer.
The study was tested in mice but researchers believe their findings will translate to human beings.Researchers believe our body has many known mechanisms for fixing damaged DNA in cells or killing damaged cells so they do not start the out-of-control growth that leads to the tumors.
"We have shown that the body has an innate defense against the accumulation of genetic mutations that arise from sun exposure. You get DNA damage almost everytime you go out. This can be translated over to mutations. If you can get rid of the cells containing the DNA damage, you get rid of the cancer," said Laurie Owen-Schaub of the M.D. Anderson Cancer Center at the University of Texas in Houston.
This is how the experiment was done. The researchers shaved and zapped laboratory mice with a dose of ultraviolet light, roughly equivalent to 45-minute exposures of humans at noon on a sunny day. Within 3 to 6 hours, skin cells of mice were producing both Fas and FasL. Explaining in the journal Science where the findings was reported, the team said a gene called p53 causes damaged cells to die. It controls another gene, called Fas. Another critically important gene is called Fas ligand or Fas L, which works independently of p53.When the group tested mice bred to lack FasL, the mice had much more damage to their cells, even if p53 kicked in and tried to kill off the damaged cells.
The group also subjected both kinds of mice to regular ultraviolet exposure, about an hour and a half a day, for a week or two. Results showed five percent of the normal mice had genetic damage to their skin cells, as opposed to 70 percent of the mice lacking FasL. Their conclusion was "Fas is like the lock and FasL is like the key. If you lose the key, you can't undergo cell death. When this defense mechanism fails or is inactivated, sunlight exposure induces the genetic alterations that then persist,eventually resulting in skin cancer."
The study was tested in mice but researchers believe their findings will translate to human beings.Researchers believe our body has many known mechanisms for fixing damaged DNA in cells or killing damaged cells so they do not start the out-of-control growth that leads to the tumors.
"We have shown that the body has an innate defense against the accumulation of genetic mutations that arise from sun exposure. You get DNA damage almost everytime you go out. This can be translated over to mutations. If you can get rid of the cells containing the DNA damage, you get rid of the cancer," said Laurie Owen-Schaub of the M.D. Anderson Cancer Center at the University of Texas in Houston.
This is how the experiment was done. The researchers shaved and zapped laboratory mice with a dose of ultraviolet light, roughly equivalent to 45-minute exposures of humans at noon on a sunny day. Within 3 to 6 hours, skin cells of mice were producing both Fas and FasL. Explaining in the journal Science where the findings was reported, the team said a gene called p53 causes damaged cells to die. It controls another gene, called Fas. Another critically important gene is called Fas ligand or Fas L, which works independently of p53.When the group tested mice bred to lack FasL, the mice had much more damage to their cells, even if p53 kicked in and tried to kill off the damaged cells.
The group also subjected both kinds of mice to regular ultraviolet exposure, about an hour and a half a day, for a week or two. Results showed five percent of the normal mice had genetic damage to their skin cells, as opposed to 70 percent of the mice lacking FasL. Their conclusion was "Fas is like the lock and FasL is like the key. If you lose the key, you can't undergo cell death. When this defense mechanism fails or is inactivated, sunlight exposure induces the genetic alterations that then persist,eventually resulting in skin cancer."
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About Me
- Teresita Tayanes
- I am a college librarian, a passionate reader, and a seeker of God's truth.