Thursday, April 29, 2010
Seeing Disease Symptoms May Make One's Immune System More Aggressive
Seeing Disease Symptoms May Make One's Immune System More Aggressive
Seeing an ill person on the street, in a building, or even in a picture, may make one's immune system work harder. Though most people have a psychological response to seeing a sick person (they want to stay away), scientists have recently discovered that seeing an ill person may trigger an aggressive physical response by the immune system. In the University of British Columbia a study was done that showed different people pictures of sick people to see it there was a response from the immune system. "It seems like it's probably good for the immune system to be responding especially aggressively at times when it looks like you are likely to be coming into contact with something that might make you sick." says Mark Schaller. He also says that his may help fight off pathogens. Pathogens are barteria, viruses or basically anything that can cause a disease. The researchers found that seeing sick people make other people have a physiological response and want to stay away from the sick person.
The researchers also wanted to find out if a person's immune system acts differently when they see a sick person. So, they set up an experiment to test this. They showed 10 minute slides to people on 2 different days. There were 3 types of slide shows. First a neutral one that was not expected to trigger any reaction from the immune system which was of furniture. Then the subjects were shown either a slide show of ill people, or a slide show of guns. Before and after each showing a blood sample was taken from each individual. The scientists added a little bacteria to the sample to test for a specific component called interleukin-6 which protects the immune system cells. The results of the experiment showed that the people who watched the disease sideshow had a stronger response by their immune system than the people who watched the gun or furniture slide shows.
Acknowledgments: None.
Questions to Consider:
Do you think that there could be other responses in the body like this one that could be useful to our health or well-being?
Do you think that this is a reasonable response to seeing a sick person? For example, when you see a sick person do you want to stay away from them or do you not notice this response?
Do you think the researchers could have done anything differently that would have made the experiment better? What would you have done if you had to come up with an experiment to test the researchers second question?
Works Cited:
ScienceDaily. Retrieved April 29, 2010, from http://www.sciencedaily.com /releases/2010/04/100427111248.htm
Herbert, Wray. "'I feel your disease.'" Association for Psychological Science.
N.p., Apr. 2010. Web. 29 Apr. 2010.
Allergy details: Retrieved April 29, 2010, from http://www.allergy-details.com/health-t/wikipedia-features-immune-system/
Lily, Arielle and Arianne- Section 2 Magenta
Epigenetics
Epigenetics
The remote large areas of northern Sweden are an unlikely place to begin a story about genetic science. The kingdom's northern county, Norrbotten, has barely any human life. An average of six people live in each square mile and this tiny population can reveal a lot about how genes work in our everyday lives.
Norrbotten is very isolated. In the 19th century, if the harvest was bad, people starved. The years people starved were the hardest for their vulnerability. For example, 1800, 1812, 1821, 1836 and 1856 were years of total crop failure and extreme suffering. But in 1801, 1822, 1828, 1844 and 1863, the land spilled so much wealth that the same people who had gone hungry in previous winters were able to feed themselves for months.
In the 1980s, Dr. Lars Olov Bygren, a preventive-health specialist who is now at the prestigious Karolinska Institute in Stockholm, began to think what long-term effects the celebration and famine years might have had on children growing up in Norrbotten in the 19th century and not just on them but on their kids and grandkids as well. He picked a random group of 99 individuals born in the Overkalix parish of Norrbotten in 1905 and used historical records to trace their parents and grandparents back to birth. By analyzing accurate natural records, Bygren and two colleagues figured how much food was available to the parents and grandparents when they were young.
Around the time he started collecting the data, Bygren had become interested with research showing that conditions in the womb could affect your health not only when you were a fetus but well into adulthood. In 1986, the Lancet published the first of two groundbreaking papers showing that if a pregnant woman ate poorly, her child would be extremely higher than the average possibility for heart disease as an adult. Bygren thought whether that effect could start before pregnancy: Could parents' experiences early in their lives somehow change the traits they passed to their offspring?
It was a different idea. After all, we have had a lasting deal with biology: whatever choices we make during our lives might ruin our short-term memory or make us fat or hurry to death, but they won't change our genes — our actual DNA. Which meant that when we had our own kids, the genetic slate would be wiped clean.
Also, any such effects of nurture (environment) on a species' nature (genes) were not supposed to happen so quickly. Charles Darwin, whose On the Origin of Species celebrated its 150th anniversary in November, taught us that evolutionary changes take place over many generations and through millions of years of natural selection. But, now, Bygren and other scientists have collected historical evidence showing that powerful environmental conditions (near death from starvation, for instance) can somehow leave an imprint on the genetic material in eggs and sperm. These genetic imprints can short-circuit evolution and pass along new traits in a single generation.
For instance, Bygren's research showed that in Overkalix, boys who enjoyed those rare overabundant winters — kids who went from normal eating to gluttony in a single season — produced sons and grandsons who lived shorter lives. Far shorter: in the first paper Bygren wrote about Norrbotten, which was published in 2001 in the Dutch journal Acta Biotheoretica, he showed that the grandsons of Overkalix boys who had overeaten died an average of six years earlier than the grandsons of those who had endured a poor harvest. Once Bygren and his team controlled for certain socioeconomic variations, the difference in longevity jumped to an astonishing 32 years. Later papers using different Norrbotten cohorts also found significant drops in life span and discovered that they applied along the female line as well, meaning that the daughters and granddaughters of girls who had gone from normal to gluttonous diets also lived shorter lives. To put it simply, the data suggested that a single winter of overeating as a youngster could initiate a biological chain of events that would lead one's grandchildren to die decades earlier than their peers did. How could this be possible?
Bygren's data — along with those of many other scientists working separately over the past 20 years — have given birth to a new science called epigenetics. At its most basic, epigenetics is the study of changes in gene activity that do not involve alterations to the genetic code but still get passed down to at least one successive generation. These patterns of gene expression are governed by the cellular material — the epigenome — that sits on top of the genome, just outside it (hence the prefix epi-, which means above). It is these epigenetic "marks" that tell your genes to switch on or off, to speak loudly or whisper. It is through epigenetic marks that environmental factors like diet, stress and prenatal nutrition can make an imprint on genes that is passed from one generation to the next.
Tuesday, April 27, 2010
PTSD is linked to genes
Post Traumatic Stress Disorder (PTSD) is a psychiatric illness that affects the brain after it goes through a traumatic experience. It was first identified in Vietnam veterans who have experienced traumatic event. The types of traumatic events range from losing a loved one, experiences in prison, assault, domestic abuse, rape, war experiences. Symptoms of the disorder may be immediate or delayed up to 6 months after the event. It can affect individuals of any age, race, or gender. Everyone experiences some stress from traumatic events but not every one gets PTSD. Physicians and psychologists can interview patients with symptoms of PTSD, though there is no definite test to diagnose it. Diagnosis is based on the onset of symptoms, history of trauma, and history of traumatic event.
A recent study identified genes as potential biologic markers linked to PTSD. Scientists involved with the study screened surviving victims of the Rwandan genocide. The death toll of the genocide has been estimated at 1 out of 5 people or at least 500,000 people. Exact numbers are not available, but estimates have determined most Rwandans experienced significant trauma by witnessing traumatic events or losing loved one. The study evaluated blood samples and reviewed medical records from 424 Rwanda genocide survivors living in the Nakivale refugee camp in southwestern Uganda. All participants experienced trauma but one group was diagnosed with PTSD orwith and one group was PTSD-free. Scientist hypothesized that a "traumatic load" can be calculated to quantify the amount of trauma a person experiences. A traumatic load was defined as "the number of traumatic events he or she experiences." Basically they concluded the higher the traumatic load, the higher the chance of developing PTSD. The study found a "dose-response" relationship between traumatic load and the widespread appearance of lifetime PTSD. The hypothesis suggests a direct relationship where the higher amount of traumatic load, the more likely the chance of developing PTSD. Scientists also found genetic biomarkers directly linked to the "traumatic load" The COMT (catechol-O-methyltransferase) is an enzyme produced by all individuals with some variability. COMT "digests" the chemicals produced when stress occurs. Previously, COMT has been linked with the feeling of fear. With this in mind, The people with less COMT have a higher stress load leaving them more vulnerable to PTSD. This study may provide information putting us one step closer to finding a biologic intervention for prevention or treatment of mental disorders related to stress like PTSD .
questions:
Is PTSD an issue
do you think that if scientist continue to study the COMT enzyme do you think they will cure PTSD?
Do you think this experiment makes sense?
Do you think some people can be less likely to have a mental disorder
Is it okay to study people who have already gone through such an ordeal like genocide
If you could run the experiment, what changes would you make to it
New Technique Strengthens Immune Cells to Fight Cancer
Monday, April 26, 2010
By Ben Irving, Georgina Johnson, Scott Kaufman
Stem cells are non-specialized cells that are both capable of renewing themselves and becoming specialized tissue and organ cells through cell division (cloning/asexually reproducing). In some organs or tissue, like bone marrow, stem cells regularly divide to repair and replace worn out or damaged tissues. In other organs, however, such as the pancreas and the heart, stem cells only divide under special conditions. Their ability to regenerate and repair tissues and organs makes them a fascinating area of exploration and hope for curing disease.
Until recently, two kinds of stem cells from animals and humans were used: embryonic stem cells and non-embryonic "somatic" or "adult" tissue stem cells. Embryonic stem cells are undifferentiated cells taken from embryos, whereas adult stem cells are undifferentiated cells found in some organs. The controversy over embryonic stem cells has raged on since their usefulness was discovered. Many believe that the gathering of embryonic stem cells kill innocent children, thus never giving them a chance to experience the world. Others believe that by doing this, they save an unwanted child, and help someone receive urgent medical care. Adult stem cells are rare to find and also have a limited capacity for reproducing and differentiating. So adult stem cells are not very useful.
In 2006, researchers developed a way to genetically "reprogram" some specialized adult cells to become stem cell-like. This new type of stem cell is called induced pluripotent stem cells (iPSCs). It is not known how iPSCs differ from embryonic stem cells. IPSCs have been created from mouse embryos as well as human embryos.
Now scientists at the University of Missouri have developed new a way of creating stem cells from regular cells taken from pig tissue, known as fibroblasts. These scientists have have been able to convert the fibroblasts to stem cells through inserting four specific genes into the fibroblast cells. Being able to use pigs is helpful because they are more similar to humans as opposed to mice. In addition, the pigs have a longer lifespan than mice, allowing the scientist to observe the long term effects. However, the scientists have not yet figured out how to program the stem cells to develop into one type of specialized cell rather than a mixture. They will need to learn how to achieve this before the new tissues can be transplanted back into the animal.
Despite all the progress made it could still take years before these stems cells can be put to the test. A major benefit of this research would be having tissue that could be transplanted back into the donor, so as to eliminate incompatibility between donor and receiver (rejection). The stem cells could also be used to create good cells to try out therapies, such as drug therapies, on tissues more similar to humans than mice tissues. They also provide a good testing opportunity to research how to reprogram the cells. However, other problems with stem cell research may not be solved with pig tissues, such as the problem of tumor growth. Finally, some may wonder if it is ethical or humane to sacrifice pigs for this research.
Here is the link to the article - http://www.sciencedaily.com/releases/2009/06/090625141508.htm
A New Way to Create Stem Cells?
By Ben Irving, Georgina Johnson, Scott Kaufman
Stem cells are non-specialized cells that are both capable of renewing themselves and becoming specialized tissue and organ cells through cell division (cloning/asexually reproducing). In some organs or tissue, like bone marrow, stem cells regularly divide to repair and replace worn out or damaged tissues. In other organs, however, such as the pancreas and the heart, stem cells only divide under special conditions. Their ability to regenerate and repair tissues and organs makes them a fascinating area of exploration and hope for curing disease.
Until recently, two kinds of stem cells from animals and humans were used: embryonic stem cells and non-embryonic "somatic" or "adult" tissue stem cells. Embryonic stem cells are undifferentiated cells taken from embryos, whereas adult stem cells are undifferentiated cells found in some organs. The controversy over embryonic stem cells has raged on since their usefulness was discovered. Many believe that the gathering of embryonic stem cells kill innocent children, thus never giving them a chance to experience the world. Others believe that by doing this, they save an unwanted child, and help someone receive urgent medical care. Adult stem cells are rare to find and also have a limited capacity for reproducing and differentiating. So adult stem cells are not very useful.
In 2006, researchers developed a way to genetically "reprogram" some specialized adult cells to become stem cell-like. This new type of stem cell is called induced pluripotent stem cells (iPSCs). It is not known how iPSCs differ from embryonic stem cells. IPSCs have been created from mouse embryos as well as human embryos.
Now scientists at the University of Missouri have developed new a way of creating stem cells from regular cells taken from pig tissue, known as fibroblasts. These scientists have have been able to convert the fibroblasts to stem cells through inserting four specific genes into the fibroblast cells. Being able to use pigs is helpful because they are more similar to humans as opposed to mice. In addition, the pigs have a longer lifespan than mice, allowing the scientist to observe the long term effects. However, the scientists have not yet figured out how to program the stem cells to develop into one type of specialized cell rather than a mixture. They will need to learn how to achieve this before the new tissues can be transplanted back into the animal.
Despite all the progress made it could still take years before these stems cells can be put to the test. A major benefit of this research would be having tissue that could be transplanted back into the donor, so as to eliminate incompatibility between donor and receiver (rejection). The stem cells could also be used to create good cells to try out therapies, such as drug therapies, on tissues more similar to humans than mice tissues. They also provide a good testing opportunity to research how to reprogram the cells. However, other problems with stem cell research may not be solved with pig tissues, such as the problem of tumor growth. Finally, some may wonder if it is ethical or humane to sacrifice pigs for this research.
Here is the link to the article - http://www.sciencedaily.com/releases/2009/06/090625141508.htm
Sunday, April 25, 2010
Is This The "Silver Bullet" of Antivirals?
Benhur Lee, a professor at UCLA has possibly discovered an antiviral that can stop Pandemic HIV, Ebola, flu, and any virus you can think of.That isn't even the best part. Lee believes that viruses will not be able to become resistant to this antiviral.
So why aren't we using this to get rid of all viruses in the world? Well, this has only worked in the labs at UCLA.
Then what is it? It is a compound that inhibits viral entry by disabling the viral envelope. It does not destroy the virus it just stops it from entering our cells, therefore, rendering it harmless. More specifically, the compound binds to the lipids in the viral envelope and to the cell the virus is invading. The virus does not have any repair mechanisms, unlike our cells. Therefore, the virus cannot work its magic, while our cells can easily repair the lipids.
This finding is amazing. Unfortunately, Lee says that this compound is not quite ready for mass production. The researchers at UCLA say that this compound may be more toxic to the human body than they had thought in the beginning of their research. It has not proven to very toxic in their research, but there haven't been any trials of the compound to date.
The compound should be researched more heavily and studied before trials start. However, this is an incredible finding. An antiviral that renders all viruses harmless? Seems legendary, but we have to find out how we can safely use this compound in our favor.
"The breadth of antiviral activity is fascinating but I fear that with the underlying mechanism of membrane disruption, there might be a lot more toxicity than is currently appreciated. Primary cells often are much more sensitive than laboratory-adapted cells," -UCLA researcher.
We will see if this "silver-bullet" lives up to the hype.
Works Cited: http://www.scientificamerican.com/article.cfm?id=broad-spectrum-anti-viral
More On Antivirals:
http://en.wikipedia.org/wiki/Antiviral_drug
www.cdc.gov/flu/professionals/treatment/
-Nathaniel B. Chumley
Startling Link Between Our Immune and Nervous Systems
Recently, many scientists have found new leads as to how our immune system might actually cause certain nervous system diseases while fighting other pathogens. A few years ago it was discovered that neurons have major histocompatibility complex (MHC) class I molecules on their surface. These proteins, are antigens, which allow our immune system to recognize cells that have been infected by a virus and mark them for destruction. It was thought for many years that neurons were the only cells in the body that did not have the MHC class I molecules.
This discovery prompted testing on mice that lacked this MHC class I molecule. It was discovered that this molecule acts as a “‘molecular brake’ on synaptic plasticity, the ability of brain cells to rewire themselves”. This ability which the MHC class I molecules block is essential to learning and memory functions. These studies also revealed the possibility that these MHC class I molecules may trigger neurodegenerative diseases such as Alzheimer’s and Parkinson’s by causing the immune system to attack brain cells. This same issue is seen in rheumatoid arthritis where the immune system attacks the joints of a person.
Another immune system protein, immunoglobulin-like receptor-B (PirB), was more recently discovered to be expressed by neurons. This protein could lead to the inability to repair neurons damaged in s spinal cord injury or stroke.
These new discoveries unlock a possible cause to disease like Alzheimer’s and Parkinson’s, which are currently incurable. If these discoveries can lead to preventative and curative measures then it would be a great leap for medical science.
However, with a discovery like this the question of whether or not this discovery is a matter of science overstepping its bounds. Some may wonder if because these diseases are caused by our body, whether or not it is our right to stop them.
Society For Neuroscience. "Immune System Research Hold Promise For Alzheimer's, Stroke, And Mental Disorders." ScienceDaily 7 November 2007. 25 April 2010
-Graham
HIV Patients Hold Clues to Salmonella Vaccine Development
As we all know, HIV causes deficiencies in the immune system which lead to infections that the body would otherwise be able to fight off. In most cases these infections can be fatal and are part of what makes HIV/AIDS so destructive. Though the links between certain conditions and HIV are known, not all have been scientifically explained. One such case, until recently was Non-Typhoidal Salmonella. Thursday, April 8, 2010
Bacteria on Easter Island
Bacteria on Easter Island
Rapamycin is a drug that keeps the immune system from attacking and potentially destroying transplanted organs (heart, lungs, kidneys, etc.). This drug has another use, which fights Alzheimers. The drug was first found isolated in soil on Easter Island (Rapa Nui). A team from The University of Texas Health Science Center at San Antonio reported that the drug rescued memory in a mouse with Alzheimers. The team also found a reduced amount of brain lesions, similar to the ones found in humans that die of Alzheimers. Because Rapamycin is a approved United States drug it could be used to start fighting Alzheimers. Three institutions reported that the life of the lab mice was extended. It was the first pharmacologic intervention shown to extend the life of an aging animal.
During a 10 week period mice with Alzheimers were fed chow containing the drug Rapamycin. Each mouse 6 months old (age of a young adult), and showed signs of having Alzheimers. At the end of the 10 weeks the mice were put through the Morris water maze (miniature swimming pool used for memory testing). The brains were then tested to see if the Rapamycin made a difference on the lesions. The drug is also being tested on cancer mice to see if it can stop or help cancer. The conductors of the test are still unsure as to whether or not this could work on humans.
By Venice Gordon, Cindy Cochran, Matthew Winter
Source:
http://www.sciencedaily.com/releases/2010/02/100224165259.htm
Wednesday, April 7, 2010
There May be a Way to Stop Cancer Growth
Sources:
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