Dendritic cells are an important component of the immune system. They reside in our tissues and bloodstream in their immature form. When they are exposed to a pathogen, they use sucker like projections from their many “arms” to capture it and eat it. Once ingested, they break the pathogen down and isolate the antigens that are specific to this pathogen, after which they travel through the blood system or the spleen to one of the Lymph nodes. Here they attempt to find the B and T-cells that allow our bodies to fight off pathogens. Interestingly, the dendritic cells also appear to determine if killer T-cells or antibodies are produced as a response to the pathogen.
Some scientists are attempting to use this phenomenon to inoculate our bodies against cancer. With some cancer patients, scientists are taking monocytes, cells that become either macrophages or dendritic cells, and culturing them along with antigens of the specific cancer the patient has. Once the dendritic cells mature and are ready to present the antigen to B and T-cells, the scientists inject them back into the patient. Although this does not cure cancer, or allow the body to completely fight it off, it has been show to make patients immune responses stronger than they would have been. However, there are some problems with this technique. Because cancers are mutating by definition, it is possible that the cancer could stop presenting the antigen that the body was targeting, rendering the vaccine useless. Also, if the antigen the scientists have isolated is present elsewhere in the body, it could lead to the body destroying other things than the cancer.
Another thing scientists are attempting to learn about dendritic cells is how to shut them down. In autoimmune diseases, dendritic cells appear to be hyperactive. For example, when a patient has lupus, it appears that their dendritic cells mature in their blood stream, due to a protein that their cells release, and then ingest the patient’s DNA, which they then present to a B and T-cell, creating an immunity to the bodies own DNA. By learning more about the mechanisms that control dendritic cells, scientists hope to eventually be able to control our immune system responses.
-Dylan Karle
Source: Scientific American, November 2002 issue
Monday, May 3, 2010
Sunday, May 2, 2010
New HIV model may help in finding T cells that can fight against the virus
Chinese researches have recently developed a new HIV model in hopes of incorporating HIV’s behavioral dynamics into the modeling system. This new model suggests that a particular type of T cell could be useful in fighting HIV in a vaccine. Scientists from Xiamen University have been able to incorporate the ways HIV responds to antibodies, and its random mutations, into their model. This new model is able to act like the actual HIV virus does in real life.
-Emma G.
Sources:
http://www.medicalnewstoday.com/articles/187222.php
http://www.sciencemuseum.org.uk/on-line/lifecycle/images/1-2-5-3-5-2-2-0-0-0-0.jpg
http://biology.kenyon.edu/slonc/gene-web/Lentiviral/hiv_image.jpg
(The structure of HIV)
In the past, clinical trials have shown that in the acute first phase of human infection (about 2-6 after the virus enters the host body), HIV behaves normally. Our body sends T Cells to fight the virus, which is growing stronger. T cells work when they are activated by the presence of their specific pathogen in the body. They have markers on the outside of their cells that bind to an antigen that is only on the HIV virus. They then begin to reproduce and go to the part of the body that is infected, where they begin to attack the virus. This is different from how the innate immune system works in that T cells are not only limited to attacking the virus when it is in the blood stream, since they can also kill infected cells, killing the virus before it can produce more viruses in that infected cell.
(A T cell attacking a virus)
In most viruses, T cells are able to completely fight off the virus and use their memory to patrol the bloodstream in case the virus ever comes back, in which case they would be able to recognize the virus immediately and fight it off again. However, in HIV, the T Cells are not able to completely kill the virus, which stores itself away and spends years recuperating its strength. HIV has the ability to target CD4+ T cells, which are the master regulators of our immune system. They also have many mutating properties. Researchers believe that these two factors are what allow HIV to escape total annihilation. During the time HIV hides and regains strength, it is also slowly attacking our immune system.
-Emma G.
Sources:
http://www.medicalnewstoday.com/articles/187222.php
http://www.sciencemuseum.org.uk/on-line/lifecycle/images/1-2-5-3-5-2-2-0-0-0-0.jpg
http://biology.kenyon.edu/slonc/gene-web/Lentiviral/hiv_image.jpg
Thursday, April 29, 2010
Seeing Disease Symptoms May Make One's Immune System More Aggressive
Check out this SlideShare Presentation:
Seeing Disease Symptoms May Make One's Immune System More Aggressive
Study Relates Seeing Disease Symptoms to Increase in Immune System Aggressiveness
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
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.
Epigenetics presentation
View more presentations from Student Wilsonsbiologylab.
Tuesday, April 27, 2010
PTSD is linked to genes
A neurological disorder is now being linked to DNA
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 .
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 .
Ptsd
View more presentations from Student Wilsonsbiologylab.
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
Konstantine Adamopoulos
New Stanford University Research has recently begun to show, enhance, and grow T-cells in living mice and in human cell cultures. These breakthroughs may be the key to pote
ntially surpassing the drawbacks of current immune cell therapy, which has not proven to be the most effective mechanism for the human body.
The way this new mechanism works is by means of a relatively new branch of biology, synthetic biology, "in which researchers can build new functions into cells by integrating pre-designed genetic components," or simply, in which researchers can alter cells with existing genetic makeups of other molecules.
Where the bar is raised between the old method of immune cell care and this new method, is to a height at which the adoptive immunotherapy targets the events that occur when the immune system cannot detect a pathogen or disease. This system works by harvesting T-cells from a patient, modifying the cells, then injecting them back into the place in the body where the disease is most prevalent.
In the past, this has been quite ineffective, due to the fact that the T-cells have not been able to destroy the pathogen on its own without help from other molecules. The new approach, is to further engineer the T-cells so that they can be self-dependent. In other words, 'fix' them and make them strong enough to battle pathogens and bacteria on their own.
Monday, April 26, 2010
A New Way to Create Stem Cells?
By Ben Irving, Georgina Johnson, Scott Kaufman
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
Acknowledgements:
http://www.animaldefense.com/A_images/pig.jpg
http://dawnofanewera.files.wordpress.com/2009/09/baby-pig.jpg
http://www.innocentenglish.com/wp/wp-content/uploads/2008/02/valentines-day-pig.jpg
http://9freepictures.com/d/file/animals-pictures/200908/baby-pig-68-2.jpg
http://www.hedweb.com/animimag/piglets.jpg
http://www.troedyrhiw.com/Kune%20Kune%20Pigs/kune%20kune%20piglets.jpg
http://blogs.guardian.co.uk/food/piglets440.jpg
http://oldstersview.files.wordpress.com/2007/11/four-piglets-front-view-jpg.jpg
https://www.shopelysiumartists.com/images/Piglets---w.jpg
http://www.vetscite.org/publish/articles/000075/Figure%2010.%20Piglets%20in%20nursery%20pen%20without%20sowverkl.jpg
http://www.animalpicturesarchive.com/animal/a1/White_Domestic_Piglets_J01.jpg
http://www.hedweb.com/animimag/piglet2.jpg
http://www.museums.norfolk.gov.uk/img/Piglets.jpg
http://www.hedweb.com/animimag/pig.jpg
http://www.uth.tmc.edu/schools/med/neurology/specialty-programs/ut-stroke/images/stem-cells.jpg
http://trickyrelativity.files.wordpress.com/2009/11/fetus.jpghttp://www.sciencedaily.com/releases/2009/06/090625141508.htm
http://stemcells.nih.gov
http://www.isscr.org/science/faq.htm#2
http://www.heritage.org/Research/Reports/2005/05/Federal-Stem-Cell-Research-What-Taxpayers-Should-Knowhttp://docs.google.com/present/edit?id=0AXCgd83IlAm3ZGducDQ2OTlfOTBkcjUyajNkcw&hl=en
A New Way to Create Stem Cells?
A New Way to Create Stem Cells?
By Ben Irving, Georgina Johnson, Scott Kaufman
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
Acknowledgements:
http://www.animaldefense.com/A_images/pig.jpg
http://dawnofanewera.files.wordpress.com/2009/09/baby-pig.jpg
http://www.innocentenglish.com/wp/wp-content/uploads/2008/02/valentines-day-pig.jpg
http://9freepictures.com/d/file/animals-pictures/200908/baby-pig-68-2.jpg
http://www.hedweb.com/animimag/piglets.jpg
http://www.troedyrhiw.com/Kune%20Kune%20Pigs/kune%20kune%20piglets.jpg
http://blogs.guardian.co.uk/food/piglets440.jpg
http://oldstersview.files.wordpress.com/2007/11/four-piglets-front-view-jpg.jpg
https://www.shopelysiumartists.com/images/Piglets---w.jpg
http://www.vetscite.org/publish/articles/000075/Figure%2010.%20Piglets%20in%20nursery%20pen%20without%20sowverkl.jpg
http://www.animalpicturesarchive.com/animal/a1/White_Domestic_Piglets_J01.jpg
http://www.hedweb.com/animimag/piglet2.jpg
http://www.museums.norfolk.gov.uk/img/Piglets.jpg
http://www.hedweb.com/animimag/pig.jpg
http://www.uth.tmc.edu/schools/med/neurology/specialty-programs/ut-stroke/images/stem-cells.jpg
http://trickyrelativity.files.wordpress.com/2009/11/fetus.jpghttp://www.sciencedaily.com/releases/2009/06/090625141508.htm
http://stemcells.nih.gov
http://www.isscr.org/science/faq.htm#2
http://www.heritage.org/Research/Reports/2005/05/Federal-Stem-Cell-Research-What-Taxpayers-Should-KnowSunday, 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. Non-Typhoidal Salmonella, in high income countries, is essentially what we consider food poisoning. It causes vomiting, diarrhea, and results from eating raw foods. In low income areas it is much more destructive and for people with immune system deficiencies, in this case HIV infected people, it can be fatal. There are antibiotics for the condition but it has built an increased immunity to many of these treatments.
Though it was known that HIV prevented the body from killing the NTS cells, it was not known why. One of the researchers said of the old assumptions, "We normally think of HIV patients as being more susceptible to bacterial infections because of deficiencies in their immune systems, and often they have problems making antibodies when given vaccinations."
Yet the discovery proved quite to the contrary.
In order to kill invaders like NTS, antibodies bind to the proteins on the membranes of the invaders and consequently kill it in two ways. First, the antibody marks, or opsonizes the microbe which signals the phagocytes to ingest the cell. Secondly, some of the components collect on the membrane to form MACs or membrane attack complexes, which as we know open up a hole in the membrane.
It was discovered that in fact, HIV patients had very high levels of these antibodies which combat salmonella, yet they were still not functioning. These HIV patients had high levels of certain types of antibodies which instead of attaching to the proper point on the NTS membrane would latch on to LPS or lipopolysaccharides. The large numbers of antibodies bind to the LPS structures which effectively blocks the "killing" antibodies from binding to the cell. Though the antibodies are present, they are prevented from killing by these 'blocking' antibodies that bind to the wrong place on the cell.
When the blocking antibodies were removed, the killing antibodies went back to successfully opsonizing and MAC assembling. "In the present study, we found that it's actually an excess of antibodies that causes the problem," explained Dr MacLennan, a researcher on the project.
These findings and further investigations of LPS may lead to a vaccine which will allow those with HIV to survive NTS, a condition that is treatable for some, and should be for all.
More on antibodies:
http://en.wikipedia.org/wiki/Antibody
Supplementary info on NTS:
http://www.cdc.gov/eid/content/13/3/501.htm
-hp
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
Lately researchers from the University of Texas, Anderson Cancer Center, and Memorial Sloan-Kettering Cancer Center have been researching the Skp2 gene. Many scientists believe that if they understand the Skp2 gene well enough they should be able to make novel agents, which could stop or suppress tumor growth in many common types of cancer. After conducting experiments the scientists saw that certain types of cancer could be prevented or controlled by disabling the Skp2 gene. The Skp2 controls cell proliferation, cell cycle regulation, and the growth of new cells. In cancer where the cells are out of control the deactivation of Skp2 completely halts tumor growth.A special kind of cancer cell called an oncogene which has the power to become or make other cells cancer cells has also been shown to be directly linked to the Skp2. In these progressive forms of cancer the oncogenes are heavily expressed by the Skp2.When the Skp2 is deactivated however not only does it stop the over expression of the oncogenes but it also stops the growth of the newly cancerous cells through a process known as senescence.Senescence is the irreversible loss of a cells ability to divide or grow.
Sources:
Researchers performed experiments on mice to confirm whether they could feasibly create a therapeutic drug as well as whether or not the cancer was stopped. They found that they were able to stop the growth of the tumors in mice who were deficient in two chemicals Pten and p19Arf these chemicals usually suppress cancer growth but are deficient in most kinds of human cancer.By deactivating the Skp2 they were able to stop cancer in mice with both deficiencies even though it was previously thought to only be able to stop cancer in p19Arf-deficeint models. Further testing on mice showed that not only can the Skp2 halt tumors taking advantage of faulty tumor suppressor chemicals it also emits oncogenic activity all by itself so its permanent removal reduces likelihood of cancer in the future.
Although the deactivation of the Skp2 gene will be revolutionary break through the application and usage still is flawed. In most forms of senescence the DNA is destroyed thus halting growth. But with Skp2 when the cells stop dividing they release proteins which protect their DNA. These proteins however cause inflammation and damage to their surrounding tissue. This damage has been proven to accelerated aging as well as lead to age related diseases including cancer (irony).
Hui-Khan-Lin lead researcher, said that the researchers would try to find out if the Skp2 or other genes can cause senescence in HER2-decient model to determine whether the Skp2 "is globally required for an oncogenic event."
Sources:
Wednesday, March 17, 2010
Do Brains Process Melodies and Lyrics Separately or Together
Does the brain process the lyrics of a song separately from the music, or are the two elements processed as one? Daniela Sammler of the Max Planck Institute and a team of scientists may have uncovered the truth about the human brain. The group observed an MRI brain scan of a person listening to music, in order to identify when regions of the brain were processing just music and just lyrics. There were also some parts in which the music and lyrics were being processed together. Prior to their experiment, they were aware that people with aphasia (who are not able to speak), are still able to "hum a tune". This suggests that music and lyrics are each processed independently. Sammler believed that if she were to alter the tu
ne of a song, but keep the same lyrics, the inactive areas of the brain would be processing the lyrics (and vice versa). Areas of the brain that were inactive when both the tune and the lyrics remained the same were believed to be processing both.
The group conducting the experiment wrote 6 different sets of songs to determine if 12 volunteers were having different brain functions. Some songs had different melodies, but had the same lyrics. Another set had different lyrics, but the same melodies. In a third set, all the songs had different lyrics and melodies. From the MRI scans, the team was able to see that one part of the brain, the superior temporal sulcus, was mainly responsible for responding to the songs. In the middle of the STS, the lyrics and melodies were being processed as a single, uninterrupted signal. Though in the front of the STS, only the lyrics seemed to be processed, while the melody was nowhere to be found. The team did not find the portion of the brain for processing the melodies, possibly because there may be no individual process for them in an average brain (although experienced musicians may have this process).
After the experiment was completed, Sammler concluded that the brain first processes the music and lyrics together. Then, Sammler explained, a more complex process is used to decode the significance of the lyrics, and the music is treated separately. "The more they are processed, the more they are separated" she says. She argues that the level of inactivation in the superior temporal sulcus was not what would be expected if the music and lyrics were, in fact, being processed at the same time.
Although Sammler has come to her conclusion, there are still varied opinions among the researchers and other scientists. Martin Braun of Neuroscience of Music is not convinced that the brain is ever processing both the music and lyrics at once. "Activation of a particular brain area by different stimuli doesn't imply that these different stimuli are integrated. The stimuli might just have a similar effect on the area." he argues. If the truth is discovered, it should be a major factor in gaining further knowledge about the brain.
Sources
http://www.newscientist.com/data/images/ns/cms/dn18626/dn18626-1_536.jpg
http://www.newscientist.com/article/dn18626-music-and-lyrics-how-the-brain-splits-songs.html?DCMP=OTC-rss&nsref=life
By Emily Siegel and James Buchsbaum
ne of a song, but keep the same lyrics, the inactive areas of the brain would be processing the lyrics (and vice versa). Areas of the brain that were inactive when both the tune and the lyrics remained the same were believed to be processing both.The group conducting the experiment wrote 6 different sets of songs to determine if 12 volunteers were having different brain functions. Some songs had different melodies, but had the same lyrics. Another set had different lyrics, but the same melodies. In a third set, all the songs had different lyrics and melodies. From the MRI scans, the team was able to see that one part of the brain, the superior temporal sulcus, was mainly responsible for responding to the songs. In the middle of the STS, the lyrics and melodies were being processed as a single, uninterrupted signal. Though in the front of the STS, only the lyrics seemed to be processed, while the melody was nowhere to be found. The team did not find the portion of the brain for processing the melodies, possibly because there may be no individual process for them in an average brain (although experienced musicians may have this process).
After the experiment was completed, Sammler concluded that the brain first processes the music and lyrics together. Then, Sammler explained, a more complex process is used to decode the significance of the lyrics, and the music is treated separately. "The more they are processed, the more they are separated" she says. She argues that the level of inactivation in the superior temporal sulcus was not what would be expected if the music and lyrics were, in fact, being processed at the same time.
Although Sammler has come to her conclusion, there are still varied opinions among the researchers and other scientists. Martin Braun of Neuroscience of Music is not convinced that the brain is ever processing both the music and lyrics at once. "Activation of a particular brain area by different stimuli doesn't imply that these different stimuli are integrated. The stimuli might just have a similar effect on the area." he argues. If the truth is discovered, it should be a major factor in gaining further knowledge about the brain.
Sources
http://www.newscientist.com/data/images/ns/cms/dn18626/dn18626-1_536.jpg
http://www.newscientist.com/article/dn18626-music-and-lyrics-how-the-brain-splits-songs.html?DCMP=OTC-rss&nsref=life
By Emily Siegel and James Buchsbaum
Over Protective Parents
Over Protective Parents
By Alex Scheman and Amanda Shepherd
Overprotective and controlling parents may mean well, but in the long run could be slowing down their child's brain growth which are linked to mental illnesses. Children with parents who are highly protective or neglectful may be more likely to psychiatric disorders which are also related to defects in part of the prefrontal cortex. The prefrontal cortex is the part of the brain that concerns behavior, learning, judgment and personality. To test this, Kosuke Narita of Gunma University, Japan, scanned the brains of 50 people in their 20s and told them to fill out a questionare concerning their relationship with their parents throughout the first 16 years of their life. The questionare was called the Parental Bonding Instrument and was known internationally to unravel relationships between children and their parents.
Narita and his team discovered that children with overprotective parents had less grey matter in the area surrounding the prefrontal cortex than those who had healthy parent-child relationships. The grey matter is part of your nervous system that is in your brain. An interesting observation was that neglectful fathers, not mothers, stimulated less grey matter. This part of the brain develops during childhood and abnormalities there are common for people with schizophrenia and other mental illnesses. Narita thinks that an over release of stress hormone cortisol, either from neglect or too much attention, and the reduced making of dopamine due to poor parenting causes the grey matter growth to stop.
Stephen Wood, who studies adolescent development at the Melbourne Neuropsychiatry Centre in Australia, challenges this. He claims that these children may be born with abnormalbilites and other mental illnesses thus causing a rocky parent to child relationship. This brings up the potencial for a reverse order variable. Wood also points out that the test excluded people with a lower status and economic class, which may be contributing factors of childhood. These observations have opened up possible data flaws in the experiment. Although this test might not have been a success, the experiment opened up the eyes of many people in the parental and scientific community.
Acknowledgements: none
Sources:
http://www.newscientist.com/article/dn18633-mom-and-dad-stop-stifling-me--its-damaging-my-brain.html?DCMP=OTC-rss&nsref=life
http://www.google.com/search?hl=en&safe=active&client=firefox-a&hs=hhy&rls=org.mozilla%3Aen-US%3Aofficial&q=define%3A+prefrontal+lobe&btnG=Search
http://www.shockmd.com/wp-content/dorsolateral-prefrontal-cortex3.jpg
Over Protective Parents
View more presentations from Student Wilsonsbiologylab.
IVF Babies have High Risk of Diabetes, Obesity and other Metabolic Disorders
In 1978, the first test tube baby was born. A test tube baby is created through the process of In Virto Fertilisation (IVF), which is when egg cells are fertilized by sperm outside the womb. Scientists extract the ova (egg) from the ovaries of the woman. They then put the egg in a liquid with the sperm, which allows the egg to be fertilized.
Factors that affect the result of the IVF include the age of the woman, the normalcy of the uterus and semen quality, the success or failure of fertilization, and the number of embryos transferred. Now, more than three million babies are born through IVF. Risks have increased from about one in 15,000-20,000 to one in 4,000 cells.
First clues of problems with babies born through IVF was in 2001 with animal cloning studies. Scientists realized that in IVF there was a higher chance in offspring syndrome (abnormalities) and heart defects. Since they used the same procedures with animals, they predicted that it would affect babies too.
Though most test tube babies are born healthy, a large group are at a risk for low birth weight, which is associated with obesity, hypertension and type 2 diabetes (high blood sugar). At Temple University School of Medicine, Carmen Sapienza, a geneticist, is observing to groups of children. One group is born naturally, and the other is born through IVF. Sapienza was especially interested to see a chromosomal modification in the children born through IVF. Found out that 5 to 10 percent of modifications were in test tube babies. Sepienza says that these chromosomal modifications altered nearby genes, and that several of these genes express the metabolic disorders, such as obesity and type 2 diabetes.
After the egg is fertilized, the embryos are either killed purposefully or accidentally, or frozen. Many people believe that IVF is inhuman and wrong. But others believe that infertile people must be able to have children. The survival rate of each embryo is 36% for a mid-aged woman (30-50).
Acknowledgments:
-http://www.scientificamerican.com/article.cfm?id=assisted-reproduction-genetics
-http://en.wikipedia.org/wiki/In_vitro_fertilisation
-http://images.google.com/
By Dominic, Vahimir, and Giancarlo
Factors that affect the result of the IVF include the age of the woman, the normalcy of the uterus and semen quality, the success or failure of fertilization, and the number of embryos transferred. Now, more than three million babies are born through IVF. Risks have increased from about one in 15,000-20,000 to one in 4,000 cells.
First clues of problems with babies born through IVF was in 2001 with animal cloning studies. Scientists realized that in IVF there was a higher chance in offspring syndrome (abnormalities) and heart defects. Since they used the same procedures with animals, they predicted that it would affect babies too.
Though most test tube babies are born healthy, a large group are at a risk for low birth weight, which is associated with obesity, hypertension and type 2 diabetes (high blood sugar). At Temple University School of Medicine, Carmen Sapienza, a geneticist, is observing to groups of children. One group is born naturally, and the other is born through IVF. Sapienza was especially interested to see a chromosomal modification in the children born through IVF. Found out that 5 to 10 percent of modifications were in test tube babies. Sepienza says that these chromosomal modifications altered nearby genes, and that several of these genes express the metabolic disorders, such as obesity and type 2 diabetes.
After the egg is fertilized, the embryos are either killed purposefully or accidentally, or frozen. Many people believe that IVF is inhuman and wrong. But others believe that infertile people must be able to have children. The survival rate of each embryo is 36% for a mid-aged woman (30-50).
Acknowledgments:
-http://www.scientificamerican.com/article.cfm?id=assisted-reproduction-genetics
-http://en.wikipedia.org/wiki/In_vitro_fertilisation
-http://images.google.com/
By Dominic, Vahimir, and Giancarlo
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