Anna Kramer
Author: Loyola University Health System
Published: April 23, 2014
URL: http://www.medicalnewstoday.com/releases/275751.php
Summary:
There is a very difficult decision that doctor's have to make when treating patients with the rare lung disease, lymphangioleiomyomatosis (LAM), that causes a growth of muscle cells that invade the lungs and make it difficult for air to pass through the airways. The drug, sirolimus, can decrease the progression of the disease and help with the shortness of breathe, but, it often causes fatal complications following a lung transplant that make it difficult for the wound to heal and the attachment points of the lung do not hold. The Food and Drug Administration has issued a warning attached to this drug, so patients on the waiting list for a lung transplant are not allowed to go on sirolimus. The drug has a long half-life, so it stays in the body longer, making it not predictable on the results of the transplant even if the patient is taken off of the drug. But, there is another drug, everolimus, which does not last as long in the body once the patient stops taking it. A patient who uses this strategy usually doesn't have an issue with the wound healing after the transplant. Members of the LAM foundation agree that more research needs to be done on the rapamycin-class of drugs (the class that includes sirolimus and everolimus). But, because LAM is such an uncommon disease, there are still many unknowns.
Connection:
This article connects to our unit on the respiratory system because LAM is a disease that occurs in the lungs. The lungs are a very significant organ that function in breathing. LAMS blocks the airways and makes it so that air can not travel throughout the lungs. This proposes a very serious issue because without the airflow in the lungs, this affects not only the respiratory system, but also the circulatory system. If the lungs can not provide oxygen to diffuse into the blood, the heart won't have sufficient amounts to pump to the rest of the body. The body needs oxygen to make ATP, and without it, the body can not function. The issue that sirolimus causes with the wound not being able to heal is a very large issue for the immune system because it damages the first-response of the immune system and could lead to an infection of the wound if pathogens were to enter.
Wednesday, May 21, 2014
Middle Eastern Respiratory Syndrome
Everett Han
May 21st, 2014
Published: May 12, 2014
URL: http://www.ibtimes.com/what-mers-all-about-middle-east-respiratory-syndrome-photo-1583183
Summary: A 44 year old man came to the United States to visit his family, and last Friday, he was admitted to the hospital. He is thought to have an respiratory disease known as Middle Eastern Respiratory Syndrome. Middle East Respiratory Syndrome is caused by a beta coronavirus, a common virus that causes mild to moderate respiratory illness in those whom it effects. Most people who suffer from the MERS-CoV infection go on to develop severe acute respiratory illnesses. Its symptoms include fever, coughing and shortness of breath. This disease kills about a third of its victims. It also does not have a cure or a treatment. This virus first appeared in 2012, and the disease then infected the Arabian peninsula, with Saudi Arabia, the United Arab Emirates, Qatar, Oman, Jordan, Kuwait, Yemen and Lebanon all reporting cases of the disease within their countries.The origins of MERS is unknown, although it is believed that animals, such as camels and bats, were the source of the disease. The virus currently spreads from human to human when people infected with MERS come in close contact with someone who has the disease.
Connection: This connects to our unit in bio because the respiratory system was a large part of this unit. This disease relates to the respiratory system because it is a respiratory disease and affects the system. It causes coughing and shortness of breath, suggesting that homeostasis is being disrupted. Coughing is the way of removing bacteria and pollutants from our body which suggests that bacteria has entered our bodies. Shortness of breath suggests that this disease if affecting your ability to take in oxygen which suggests some damage to a structure in the respiratory system.
May 21st, 2014
Published: May 12, 2014
URL: http://www.ibtimes.com/what-mers-all-about-middle-east-respiratory-syndrome-photo-1583183
Summary: A 44 year old man came to the United States to visit his family, and last Friday, he was admitted to the hospital. He is thought to have an respiratory disease known as Middle Eastern Respiratory Syndrome. Middle East Respiratory Syndrome is caused by a beta coronavirus, a common virus that causes mild to moderate respiratory illness in those whom it effects. Most people who suffer from the MERS-CoV infection go on to develop severe acute respiratory illnesses. Its symptoms include fever, coughing and shortness of breath. This disease kills about a third of its victims. It also does not have a cure or a treatment. This virus first appeared in 2012, and the disease then infected the Arabian peninsula, with Saudi Arabia, the United Arab Emirates, Qatar, Oman, Jordan, Kuwait, Yemen and Lebanon all reporting cases of the disease within their countries.The origins of MERS is unknown, although it is believed that animals, such as camels and bats, were the source of the disease. The virus currently spreads from human to human when people infected with MERS come in close contact with someone who has the disease.
Connection: This connects to our unit in bio because the respiratory system was a large part of this unit. This disease relates to the respiratory system because it is a respiratory disease and affects the system. It causes coughing and shortness of breath, suggesting that homeostasis is being disrupted. Coughing is the way of removing bacteria and pollutants from our body which suggests that bacteria has entered our bodies. Shortness of breath suggests that this disease if affecting your ability to take in oxygen which suggests some damage to a structure in the respiratory system.
Monday, May 19, 2014
Urine Test Could Help Clinicians Spot Blood Clots in At-risk Patients
Jonathan Liu
May 19th, 2014
Published: May 18th, 2014
URL: http://www.sciencedaily.com/releases/2014/05/140518164105.htm
Summary: Researches from California and Canada have conducted a study that shows that a urine test can indicate whether the patient has a venous thromboembolism. A venous thromboembolism is a blood clot that has broken free from where it originated, where it travels through the bloodstream and eventually ends up in some vein. The test indicates the levels of fibrinopeptide B, which is a small peptide that is released when a thrombosis forms. It is able to test this because the peptide is removed from the body through urine. The study lead author claimed that this urine test is better for determining risk of clots because it doesn't require the removal of blood and it can proved more accurate results than the D-dimer test (which is the blood test). The researchers say that this test could be useful to be used with other tests to produce very accurate results. For example, the urine test can be used with the D-dimer blood test to provide accuracy.
Connection: In the second unit of the term, we studied the cardiovascular system and also how the body removes waste. When we studied the cardiovascular system we talked about blood clots. This article relates to how the body gets rid of waste and it relates to blood clots. It also relates to the homeostatic imbalance of risk of blood clots, such as a stroke. It relates to waste by telling us that the peptide used for clots is removed as waste through urine.
May 19th, 2014
Published: May 18th, 2014
URL: http://www.sciencedaily.com/releases/2014/05/140518164105.htm
Summary: Researches from California and Canada have conducted a study that shows that a urine test can indicate whether the patient has a venous thromboembolism. A venous thromboembolism is a blood clot that has broken free from where it originated, where it travels through the bloodstream and eventually ends up in some vein. The test indicates the levels of fibrinopeptide B, which is a small peptide that is released when a thrombosis forms. It is able to test this because the peptide is removed from the body through urine. The study lead author claimed that this urine test is better for determining risk of clots because it doesn't require the removal of blood and it can proved more accurate results than the D-dimer test (which is the blood test). The researchers say that this test could be useful to be used with other tests to produce very accurate results. For example, the urine test can be used with the D-dimer blood test to provide accuracy.
Connection: In the second unit of the term, we studied the cardiovascular system and also how the body removes waste. When we studied the cardiovascular system we talked about blood clots. This article relates to how the body gets rid of waste and it relates to blood clots. It also relates to the homeostatic imbalance of risk of blood clots, such as a stroke. It relates to waste by telling us that the peptide used for clots is removed as waste through urine.
human stem cells cure disease in rats
Cole Winsor
Author: University of Utah Health Sciences
Published: may 15, 2014
link: http://www.sciencedaily.com/releases/2014/05/140515123204.htm
summary: Mice with multiple sclerosis were able to walk after two weeks following treatment with human stem cells. It was first expected that the mice would reject the stem cells much like an organ transplant. However the scientist were all very surprised when the transplant worked and the rats were cured of their multiple sclerosis. after 10 to 14 days the rats could move again and after six months they still seemed fine. The treatment seemed to have a reversal of symptoms and could help people with more progressive forms of MS, which has no cure right now. in fact after i week there were no stem cells left in the mice, however in the time that the stem cells were present they sent out chemical signals, which caused a repair of the myelin. this could point to the possibility that drugs could be developed that mimicked these effects in a patient.
connection: This article connects to the systems of the human body. In this case it is focusing on the nervous system. multiple sclerosis is a disease which we learned about during the presentation on the nervous system by our classmates.It is an autoimmune disease which we also learned about in class. It talks about myelin sheaths, which are important in quickening nervous responses. that is how it connects to what we have learned about in class.
Author: University of Utah Health Sciences
Published: may 15, 2014
link: http://www.sciencedaily.com/releases/2014/05/140515123204.htm
summary: Mice with multiple sclerosis were able to walk after two weeks following treatment with human stem cells. It was first expected that the mice would reject the stem cells much like an organ transplant. However the scientist were all very surprised when the transplant worked and the rats were cured of their multiple sclerosis. after 10 to 14 days the rats could move again and after six months they still seemed fine. The treatment seemed to have a reversal of symptoms and could help people with more progressive forms of MS, which has no cure right now. in fact after i week there were no stem cells left in the mice, however in the time that the stem cells were present they sent out chemical signals, which caused a repair of the myelin. this could point to the possibility that drugs could be developed that mimicked these effects in a patient.
connection: This article connects to the systems of the human body. In this case it is focusing on the nervous system. multiple sclerosis is a disease which we learned about during the presentation on the nervous system by our classmates.It is an autoimmune disease which we also learned about in class. It talks about myelin sheaths, which are important in quickening nervous responses. that is how it connects to what we have learned about in class.
Why Athletes Are More Likely to Need Pacemakers in Old Age
Shaina Sikka
Period 2/Mr. Mathieu
Author: Unknown, Source is Manchester University Published: May 13, 2014
URL: http://www.sciencedaily.com/releases/2014/05/140513113254.htm
Summary:
The University of Manchester has conducted a study in rodents that explains why athletes are more likely to need pacemakers in old age. Elder athletes can have arrhythmias, or heart rhythm disturbances. Their resting heart rate tends to be 30 beats per minute, while the average resting heart rate is 60 or more beats per minute. At first, scientists thought that the overuse of the vagal nerves, which lower heart rate, was a cause of the low heart rate in athletes. However, this study shows that the heart changes in training. In rodents, the heart’s pacemaker changes molecularly when exercising. Research shows that the amount of a pacemaker protein, HCN4, decreases in response to exercise and is the cause of lower heart rate. Researchers also say that by looking at the sinus node, which is a cardiac structure that generates heart rhythm, there can be a broader understanding of heart rhythm disturbances in athletes. However, frequent long-term exercise may have more advantageous effects that harmful.
Connection:
This connects to our curriculum on the systems in the human body. The pacemaker, or Sinoatrial node, is controlled by the autonomic nervous system. This system controls involuntary actions such as breathing and heartbeat. We learned how this system is divided into two parts, the sympathetic and parasympathetic division. The sympathetic raises the heartbeat, while the parasympathetic lowers that heartbeat. This is because sympathetic division increases the body’s activity, while the parasympathetic returns the body to its regular functions. This experiment also relates to our study on rats. Though this experiment used mice, rats have similar internal organs to humans, and since rats and mice are alike, it is possible that the scientists used a mouse for more accurate results.
Period 2/Mr. Mathieu
Author: Unknown, Source is Manchester University Published: May 13, 2014
URL: http://www.sciencedaily.com/releases/2014/05/140513113254.htm
Summary:
The University of Manchester has conducted a study in rodents that explains why athletes are more likely to need pacemakers in old age. Elder athletes can have arrhythmias, or heart rhythm disturbances. Their resting heart rate tends to be 30 beats per minute, while the average resting heart rate is 60 or more beats per minute. At first, scientists thought that the overuse of the vagal nerves, which lower heart rate, was a cause of the low heart rate in athletes. However, this study shows that the heart changes in training. In rodents, the heart’s pacemaker changes molecularly when exercising. Research shows that the amount of a pacemaker protein, HCN4, decreases in response to exercise and is the cause of lower heart rate. Researchers also say that by looking at the sinus node, which is a cardiac structure that generates heart rhythm, there can be a broader understanding of heart rhythm disturbances in athletes. However, frequent long-term exercise may have more advantageous effects that harmful.
Connection:
This connects to our curriculum on the systems in the human body. The pacemaker, or Sinoatrial node, is controlled by the autonomic nervous system. This system controls involuntary actions such as breathing and heartbeat. We learned how this system is divided into two parts, the sympathetic and parasympathetic division. The sympathetic raises the heartbeat, while the parasympathetic lowers that heartbeat. This is because sympathetic division increases the body’s activity, while the parasympathetic returns the body to its regular functions. This experiment also relates to our study on rats. Though this experiment used mice, rats have similar internal organs to humans, and since rats and mice are alike, it is possible that the scientists used a mouse for more accurate results.
Sunday, May 18, 2014
Citrus Fruit and Kidney Cysts
Sophie Antonioli
Mr. Mathieu
April 18, 2014
Published: October 3, 2013
Royal Holloway, University of London
Summary:
It has recently been stated in the British Journal of Pharmacology than a component of grapefruit and other citrus fruits, called naringenin can inhibit the formation of kidney cysts. These cysts on kidneys are known as polycystic kidney disease. If someone has this disease, they would have cysts on their kidneys that would grow and in most cases eventually lead to the loss of kidney functions when the cysts reach a certain size. The disease can lead to high blood pressure, need for dialysis and even death. Because there are not many treatments for this disease, this should be very helpful in the future and can provide insite on how to control the disease. According to the article, naringenin regulates a protein called PKD2 and this protein is responsible for polycystic kidney disease. As a result of this protein being regulated, the formation of cysts is blocked. To discover this, scientists used mammal kidneys and triggered cysts to form on them. They then added naringenin and observed that as the amount of PKD2 proteins decreased, the cysts growth decreased as well.
Connection:
This article connects to what we have learned this year for a few reasons. One being about the protein PKD2 and how it is specifically connects to one genetic trait, the formation of cysts and polycystic kidney disease. And another because the disease effects the kidneys, which are part of the excretory system, which we have yet to learn but will in the near future. The effects of this disease are also aspects of the curriculum we have already talked about, for example high blood pressure. The disease itself causes also homeostatic imbalance by affecting the function of the kidneys. We discussed many different homeostatic imbalances in class and this is just another one.
Nano Pacemaker Implanted in Long Island Patient's Heart
Sonali Deshpande
May 18, 2014
Author: Delthia Ricks
Published May 4, 2014
http://www.newsday.com/news/health/nano-pacemaker-implanted-in-long-island-patient-s-heart-1.7917824
Summary:
Doctors at St. Jude Medical have created a "nano" pacemaker, a small self-contained device without wires, which was inserted into the heart of 50-year-old Robert Johnson without surgery. Johnson was home within 24 hours of the procedure, which in itself lasted only 20 minutes. The device, which is still being tested for safety and efficacy, is much less bulky than a standard pacemaker, and lacks a lead wire. The device is routed into the heart's right ventricle through a tube known as a catheter, after being inserted into the femoral vein in one's leg. The device has a battery that lasts to 10 years, and another can be added when the old one dies, without removing the old one. The device works by monitoring electrical rhythms in the heart and sending an electrical simulation when the beat is too slow. This nano pacemaker, however, is only targeted towards people who only need a pacemaker in one chamber of the heart, and people whose heartbeat is too slow.
Connection:
This relates to our study of the circulatory system. The heart must contract regularly in order pump blood to the lungs and arteries, and thus, transport nutrients, gases, and hormones through our body. The regulation of these contractions is done by a pacemaker, a specific region of heart muscle located in the right atrium. The pacemaker generates electrical impulses that spread over the walls of both atria and cause them to contract. The impulses then spread to the AV nodes, causing the ventricles to the contract. These contractions happen in a rhythmic cycle. The pacemaker is controlled by two opposing nerves which either speed it up or slow it down. It can also be controlled by hormones. Some diseases can disrupt the function of the pacemaker, causing arrhythmia: an irregular heartbeat. In these cases, doctors can insert a pacemaker in a patient, controlling their heartbeat.
May 18, 2014
Author: Delthia Ricks
Published May 4, 2014
http://www.newsday.com/news/health/nano-pacemaker-implanted-in-long-island-patient-s-heart-1.7917824
Summary:
Doctors at St. Jude Medical have created a "nano" pacemaker, a small self-contained device without wires, which was inserted into the heart of 50-year-old Robert Johnson without surgery. Johnson was home within 24 hours of the procedure, which in itself lasted only 20 minutes. The device, which is still being tested for safety and efficacy, is much less bulky than a standard pacemaker, and lacks a lead wire. The device is routed into the heart's right ventricle through a tube known as a catheter, after being inserted into the femoral vein in one's leg. The device has a battery that lasts to 10 years, and another can be added when the old one dies, without removing the old one. The device works by monitoring electrical rhythms in the heart and sending an electrical simulation when the beat is too slow. This nano pacemaker, however, is only targeted towards people who only need a pacemaker in one chamber of the heart, and people whose heartbeat is too slow.
Connection:
This relates to our study of the circulatory system. The heart must contract regularly in order pump blood to the lungs and arteries, and thus, transport nutrients, gases, and hormones through our body. The regulation of these contractions is done by a pacemaker, a specific region of heart muscle located in the right atrium. The pacemaker generates electrical impulses that spread over the walls of both atria and cause them to contract. The impulses then spread to the AV nodes, causing the ventricles to the contract. These contractions happen in a rhythmic cycle. The pacemaker is controlled by two opposing nerves which either speed it up or slow it down. It can also be controlled by hormones. Some diseases can disrupt the function of the pacemaker, causing arrhythmia: an irregular heartbeat. In these cases, doctors can insert a pacemaker in a patient, controlling their heartbeat.
Why athletes are more likely to need pacemakers in old age
Article Title: Why athletes are more likely to need pacemakers in old age
Date Published: May 13, 2014
Summary:
The University of Manchester studied the effects of exercise on the heartbeat by measuring the heartbeat of seasoned athletes in their older age. The normal resting heart rate for an adult is between 60-100 BPM (beats per a minute) while the heartbeats of endurance athletes beat at 30 BPM when they are resting. It used to be believed that this condition was caused by an increased activity in the autonomic nervous system. The pacemaker was controlled by the vagal nerves, part of the autonomic nervous system, which is responsible for lowering the heart rate. But, according to another study by Manchester, there are molecular changes in the pacemaker of rodents when they are exposed to exercise training. A deficiency in an important pacemaker protein , called HCN4 , leads to the abnormally low heart rate. The protein is used in the sinus node(pacemaker), which controls the heart’s rhythm. This whole problem leads to older athletes to need an artificial pacemaker
Connection:
During this term, we learned about how the heartbeat is controlled. The pacemaker sets the rate for contraction by creating electrical impulses which then go to the AV node. We learned that the pacemaker is controlled by the nervous system, more specifically the autonomic part. Also, one of the primary reasons that a rat was used in the other study is because their body organs and body systems are very similar to ours. We even did a whole two day dissection where we saw the similarities. we also learned about the autonomic nervous system. The autonomic nervous system is further divided into the sympathetic division and parasympathetic division . The sympathetic division increases body activity while the parasympathetic division returns the body to it’s normal functions. But more relevantly, the parasympathetic division decreases heart rate by controlling the pacemaker.
Manchester University. "Why athletes are more likely to need pacemakers in old age." ScienceDaily. ScienceDaily, 13 May 2014. <www.sciencedaily.com/releases/2014/05/140513113254.htm>.
Sleeping Pills Can Cause Higher Cardiovascular Risk
Thanoshi Balasuriya
May 18, 2014
Link: http://www.hngn.com/articles/31583/20140518/sleeping-pills-increases-cardiovascular-risk-heart-failure-patients-study.htm
Author: Vishakha Sonawane
Published: May 18, 2014
Summary: In Japan, scientists did a study on heart failure patients. The patients were tracked after being discharged from the hospital. The endpoint for their tracking was if and when they had a cardiovascular event or were taken back to the hospital for a heart failure. Since not being able to sleep is common with heart failure patients, many had sleeping pills prescribed for them. However, these pills were shown to be worse for the patients with the data collected by the scientists. It seems that the sleeping pills cause cardiovascular events to take place. Many of the patients that were prescribed sleeping pills were readmitted to the hospital within the 180 days of tracking, whereas most other patients without the pills were found not to have any attacks within those 180 days. Obviously, this is a serious problem for patients with heart failure, especially because it is extremely common to want to sleeping pills with the condition of heart failure, which causes sleeping problems. The scientists plan to do a larger study, so that they can figure out the exact processes going on with the sleeping pills
Connection: In class, we have been studying the circulatory system. The heart is a major organ in the body, and plays a key role in the circulatory system. Also, we recently watched the presentation on the circulatory system, where all of the diseases were heart diseases. Heart failure is a common form of heart disease as well. With this study, scientists can possibly figure out how heart failure works, the exact causes and problems caused, etc. Also, if sleeping pills can cause more problems with the heart, there may be other medicines that might have fatal side effects as well. The chemical composition of these medicines may affect the heart drastically, affecting the whole circulatory system and body, ultimately causing homeostatic imbalance.
May 18, 2014
Link: http://www.hngn.com/articles/31583/20140518/sleeping-pills-increases-cardiovascular-risk-heart-failure-patients-study.htm
Author: Vishakha Sonawane
Published: May 18, 2014
Summary: In Japan, scientists did a study on heart failure patients. The patients were tracked after being discharged from the hospital. The endpoint for their tracking was if and when they had a cardiovascular event or were taken back to the hospital for a heart failure. Since not being able to sleep is common with heart failure patients, many had sleeping pills prescribed for them. However, these pills were shown to be worse for the patients with the data collected by the scientists. It seems that the sleeping pills cause cardiovascular events to take place. Many of the patients that were prescribed sleeping pills were readmitted to the hospital within the 180 days of tracking, whereas most other patients without the pills were found not to have any attacks within those 180 days. Obviously, this is a serious problem for patients with heart failure, especially because it is extremely common to want to sleeping pills with the condition of heart failure, which causes sleeping problems. The scientists plan to do a larger study, so that they can figure out the exact processes going on with the sleeping pills
Connection: In class, we have been studying the circulatory system. The heart is a major organ in the body, and plays a key role in the circulatory system. Also, we recently watched the presentation on the circulatory system, where all of the diseases were heart diseases. Heart failure is a common form of heart disease as well. With this study, scientists can possibly figure out how heart failure works, the exact causes and problems caused, etc. Also, if sleeping pills can cause more problems with the heart, there may be other medicines that might have fatal side effects as well. The chemical composition of these medicines may affect the heart drastically, affecting the whole circulatory system and body, ultimately causing homeostatic imbalance.
New tool helps doctors better predict, prevent deadly respiratory failure after surgery, multicenter study says
Isabelle Terranova
Author: American Society of Anesthesiologists (ASA)
Date: April 22, 2014
Source: http://www.sciencedaily.com/releases/2014/04/140422084509.htm
Summary:
Author: American Society of Anesthesiologists (ASA)
Date: April 22, 2014
Source: http://www.sciencedaily.com/releases/2014/04/140422084509.htm
Summary:
Doctors, participating in a large multi-center study, have discovered a new prediction tool that can help identify patients who are at a high risk of Acute Respiratory Distress Syndrome (ARDS) after surgery. Acute Respiratory Distress Syndrome is a sudden failure of the lungs that can be brought on by many different things. This new prediction tool ranks patients' risk levels based on nine factors. The factors include, "blood infection (sepsis), liver disease, high-risk surgery on the heart or aorta, emergency surgery, admission from a location other than home, an increased respiratory rate, and two measures that show the patient has lower-than-normal oxygen levels in the blood." With this new method, doctors could save many of lives 30% of the 200,000 americans who have this condition every year, die from it. Using this new prediction method, doctors can take measures during surgery to prevent this from happening. They can use different methods to ventilate the lungs and they can also restrict the administered volume of fluids. Even though only 3% of patients considered at risk actually have this happen, this new method could still save many lives.
Connection:
There are many connections with the human body systems. One very broad connection is that it relates to the respiratory system because it prevents a respiratory disease. Also, the Acute Respiratory Distress Syndrome causes many types of homeostatic imbalance, which we discussed in class. Homeostatic imbalance is when the body isn' t able to maintain a stable internal environment. Some include, difficulty getting air to the lungs and low blood-oxygen levels. Also, some of the factors used to rank patients are related to other organs that we have discussed in the past unit. For example, liver disease and surgery on the heart or aorta, which we studied during class with the circulatory system. There are many different connections, however these are the main ones.
Effective Treatment for Mitochondrial Disease
Jessica Lim
Author: not given (info provided by the University of Helsinki)
Published: April 7, 2014
Summary:
The mitochondria within cells create fuel or energy that power all functions of the body, also known as ATP. Mitochondrial disorders are caused by the malfunction of the mitochondria, and therefore mitochondrial myopathy, a form of mitochondrial disorders, results in muscle weakness, cramps, and pain. These diseases are inherited, and they are the most common form of a mitochondrial disorder found in adults. There is currently no cure for these diseases.
Recently, researchers from the University of Helsinki and École Polytechnique Fédérale de Lausanne announced that Vitamin B3 is a possible therapy that could be used for treating adults with mitochondrial myopathies because researchers were able to conclude, by testing Vitamin B3 on mice that had the disease, that the vitamin can slow down the progress of mitochondrial myopathies. "These results clearly showed the potential of this vitamin B form, a natural constituent of milk, to activate dysfunctional mitochondrial metabolism" (sciencedaily.com).
Connection:
This article connects to what we learned about the muscular system and homeostatic imbalance because mitochondrial myopathies cause muscle weakness, cramps, and pain which affect the muscular system. Within the muscular system, there are muscles that carry out the daily activities that we perform everyday, and if these diseases cause muscle weakness, it will affect the way you move and it will cause you to feel tired easily which prevents you from performing your normal activities. This results in homeostatic imbalance, and it creates an unsteady environment within your body because your body can no longer function properly due to the loss of strength in your muscle and pain.
Sleep May Help Move Harmful Molecules From The Brain
Andrew Robbertz
Author: Christopher Thomas
Published: October 17, 2013
Source: http://www.nih.gov/news/health/oct2013/ninds-17.htm
Summary:
In a study done my the National Institute of Neurological Disorders and Stroke (NINDS), Researchers made discoveries on the importance of sleep in cleaning the brain. The researchers injected a dye into the brain to see the flow of fluid through the brain.They found that during sleep, there is a 60% increase in interstitial fluid in the brain during sleep. They noticed a greater exchange of all molecules throughout the brain and a great decrease of amyloid B, which can have neurotoxic effects. This led them to the conclusion that your brain cells actually change in size between when you are awake, and when you are asleep. Previous studies have shown that some neurodegenerative diseases are caused by the accumulation of toxic molecules between brain cells. The researchers then injected another toxin into the mice brains both while asleep and while awake to see how quickly they were cleared from the brain. It disappeared faster in the brains of the mice that were asleep, further confirming that sleep continuously clears toxic chemicals from the brain.
Connection:
The study fully confirmed that sleep is directly connected to the functionality of the glymphatic system that clears the waste in your central nervous system. This in important because the brain and spinal cord lack any lymphatic tissue. Without any lymphatic tissue, the body cannot filter any matter flowing through there. Having these neurotoxins in your brain slows your ability to control ion concentrations across cellular membranes, diminishing the speed of your nerves. Knowing that the function of the glymphatic system is linked to the shrinking of brain cells while sleeping can help scientists create new treatments for neurodegenerative diseases.
Author: Christopher Thomas
Published: October 17, 2013
Source: http://www.nih.gov/news/health/oct2013/ninds-17.htm
Summary:
In a study done my the National Institute of Neurological Disorders and Stroke (NINDS), Researchers made discoveries on the importance of sleep in cleaning the brain. The researchers injected a dye into the brain to see the flow of fluid through the brain.They found that during sleep, there is a 60% increase in interstitial fluid in the brain during sleep. They noticed a greater exchange of all molecules throughout the brain and a great decrease of amyloid B, which can have neurotoxic effects. This led them to the conclusion that your brain cells actually change in size between when you are awake, and when you are asleep. Previous studies have shown that some neurodegenerative diseases are caused by the accumulation of toxic molecules between brain cells. The researchers then injected another toxin into the mice brains both while asleep and while awake to see how quickly they were cleared from the brain. It disappeared faster in the brains of the mice that were asleep, further confirming that sleep continuously clears toxic chemicals from the brain.
Connection:
The study fully confirmed that sleep is directly connected to the functionality of the glymphatic system that clears the waste in your central nervous system. This in important because the brain and spinal cord lack any lymphatic tissue. Without any lymphatic tissue, the body cannot filter any matter flowing through there. Having these neurotoxins in your brain slows your ability to control ion concentrations across cellular membranes, diminishing the speed of your nerves. Knowing that the function of the glymphatic system is linked to the shrinking of brain cells while sleeping can help scientists create new treatments for neurodegenerative diseases.
Iron Deficiency and Heart Failure: The Great Predictor
Doran Teverovsky
May 18 2014
European Society of Cardiology
Published May 17 2014
http://www.sciencedaily.com/releases/2014/05/140517085837.htm
Summary:
Researchers in Greece attempted to look at the connection between iron deficiency and heart failure. They measured iron deficiency in a completely new way be looking at two variables, circulating hepcidin, an indicator of low iron stores. And high amounts of transferrin receptors circulating in the blood, which indicate high iron requirements by cells. It was found that patients who exhibited both of these characteristics were more likely to die in the twelve months following heart failure. If only one of the two indicators was expressed, it was a much lower chance of death after heart failure. This has great bearing for predicting mortality after heart failure. This study also used traditional iron measuring methods which were not able to accurately predict death in patients.
Connection:
This article was talking about how deficiency in one micro nutrient can radically increase mortality rates. This is a direct example of homeostatic imbalance. This also relates to what certain types of cells need to function, for example, muscle cells require some iron in order to function well, without, cardiac muscle can have reduced efficiency. This also relates to the circulatory, as the article was talking about heart failure specifically and the prevention of many issue that can spawn off of it.
May 18 2014
European Society of Cardiology
Published May 17 2014
http://www.sciencedaily.com/releases/2014/05/140517085837.htm
Summary:
Researchers in Greece attempted to look at the connection between iron deficiency and heart failure. They measured iron deficiency in a completely new way be looking at two variables, circulating hepcidin, an indicator of low iron stores. And high amounts of transferrin receptors circulating in the blood, which indicate high iron requirements by cells. It was found that patients who exhibited both of these characteristics were more likely to die in the twelve months following heart failure. If only one of the two indicators was expressed, it was a much lower chance of death after heart failure. This has great bearing for predicting mortality after heart failure. This study also used traditional iron measuring methods which were not able to accurately predict death in patients.
Connection:
This article was talking about how deficiency in one micro nutrient can radically increase mortality rates. This is a direct example of homeostatic imbalance. This also relates to what certain types of cells need to function, for example, muscle cells require some iron in order to function well, without, cardiac muscle can have reduced efficiency. This also relates to the circulatory, as the article was talking about heart failure specifically and the prevention of many issue that can spawn off of it.
Surface area of the digestive tract much smaller than previously thought
Jake Urso
Source: University of Gothenburg
Summary:
The internal surface area of the gastro-intestinal tract was
once thought to be between 180 and 300 square meters. Biologists at the
Sahlgrenska Academy have used new and improved microscopic techniques that
allowed them to see the internal surface area was actually between 30 and 40
square meters. The reason previous measurements were so far off was because the
measurements were taken when the tissue was relaxed. In the new methods of
measuring the surface area scientists use radiological methods, along with
studies of the structures of the digestive system, taken through the use of endoscopes to obtain samples of the mucous membrane of the intestines. The scientists said that these were average measurements that can vary from person to person based on the healthfulness of their lifestyle.
Connection:
This connects to our recent studies of the human body
because it is about the digestive system. It was interesting because when we
talked about the surface area of the digestive system in class it was compared
to the surface area of a tennis court. In this article it says specifically how
scientists once thought the same thing, but these new microscopic techniques
allowed for this to be proven wrong.
New treatment targeting versatile protein may protect brain cells in Parkinson's disease
Madhuri Raman
May 17, 2014
No author given
Published: May 16, 2014
Source: http://www.sciencedaily.com/releases/2014/05/140516092046.htm
Summary:
Researchers from Lund University have recently discovered a possible solution to the extreme decrease in dopamine in Parkinson's Disease (PD) patients. Dopamine is a neurotransmitter produced in specific neurons and helps control the body's movement. In PD, these cells are unable to produce dopamine, leading to a patient acquiring some type of movement disorder. The researchers have decided to approach this issue by looking at a protein in the brain called Sigma-1, "that improves the brain's capacity to cope with a host of harmful processes." By activating this protein in mice, they found that inflammation decreased, dopamine levels increased, and a noticeable improvement of motor symptoms was shown in mice with a Parkinson-like condition. Although this method has never been tested on humans with PD, it has, however, worked successfully on mice and humans suffering from motor neuron disease or stroke. Professor Cenci Nilsson said, "...The Sigma-1 receptor is widely expressed in many cell types, [so] the treatment could intervene in many of these damaging processes ." Scientists believe that this treatment will become a potential therapy for Parkinson's Disease in the future
Connection:
This article directly relates to our classes studies of the Nervous System. Parkinson's Disease, itself, is involved with the nonproduction of dopamine. Since dopamine is a key neurotransmitter in synapses, a loss of it causes signals to not be sent to other neurons in the brain. In class, we learned about the structure of a neuron and the important role of neurotransmitters to send message to and from neurons. We also discussed the term "homeostatic imbalance." In PD, the body is faced with a homeostatic imbalance when it cannot produce a sufficient amount of dopamine. However, with the discovery of the new protein, Sigma-1, a body suffering from PD will be able to overcome this homeostatic imbalance by producing more dopamine. Furthermore, we learned about the different types of neurons in the body; mainly sensory and motor neurons. In PD, motor neurons play a major role because they are the neurons carrying signals to the brain regarding movement. With more dopamine available, patients' motor symptoms will also increasingly improve.
Stem cell therapy regenerates heart muscle damaged from heart attacks in primates
Sunday, May 18, 2014
Stem cell therapy regenerates heart muscle damaged from heart attacks in primates
Ronak Shah
No specific author given, but is from University of Washington
Published April 30, 2014
Summary:
Dr. Charles Murray at University of Washington led a research team to conduct an experiment: Can human embryonic stem cells from muscle cells regenerate non-human primate hearts? To perform the experiments they preformed controlled myocardial infarctions in a type of old world monkey called a Macaque. The researchers blocked the coronary artery for 90 minutes to simulate the heart attack, because in humans, heart attacks most often occur from a block in the coronary artery. 2 weeks after the myocardial infarctions, researchers injected human embryonic heart cells into the infarcted (all monkeys were put on immunosuppressives to stop the rejection of the cells). The researchers found over the next weeks, the stem cells infiltrated the damaged tissue, then matured into muscle fibers, and then began to work in the monkey hearts. After three months, they were fully integrated. The cells regenerated 40% of the damaged heart tissue. Researchers say they now the scale and procedure for possibly trying this on humans, and may be able to come up with a new procedure. The most common complications were arrhythmias, a few weeks after the transplant, but these subsided after the electric signal became more stable and the arryhthimias subsided so researchers are very optimistic.
Connection:
This clearly connects to our studies in the circulatory system, stem cells, and the complications that can arrise in the two. We studied something called homeostasis, which is the bodies ability to maintain a stable inner environment. Myocardial infarction's impair this ability by killing the heart tissue, making the part of the heart not pump so some of the crucial tasks of the circulatory system, such as delivering oxygenated and deoxygenated blood, and fighting infection are impaired. This article provides a possibility for actually treating the damaged heart tissue, rather than just unblocking the artery, using stem cells. We studied stem cells earlier in the year when we talked about how they could specialized as they mature and turn into different kinds of cells depending on the environment. The heart stem cells will provide a way to return homeostasis to first the heart, then the circulatory system, and then finally the entire body.
New Effective Treatment for High Blood Pressure? Removing tiny organ
Becky Nitschelm
Author: University of Bristol
Published: Sep 3 2013
http://www.sciencedaily.com/releases/2013/09/130903113300.htm
Summary:
New research has been discovered that removing a small organ on the carotid arteries could decrease hypertension, or high blood pressure. When there is a decreased amount of oxygen in the blood, the brain responds by sending a signal to the heart to beat faster and breath faster, increasing the blood pressure and breathing rate. This gets the oxygen levels back to normal. The small organ, known as the carotid body, sends the nervous signal to the brain that the oxygen levels are low. Keeping the blood pressure at a normal rate is important to supply the brain with enough blood. However, researchers have discovered that removing the carotid body rapidly decreases blood pressure and keeps it at the constant low rate. A human test is going on now to see the results between different patients on a larger scale at the University of Bristol.
Connection
In our study of the human body, we learned about the circulatory system and the many problems that can occur that result in a loss of homeostasis. One of those problems that we studied was hypertension. Therefore this article relates to what we have studied because it talks about a way to resolve this problem and bring the circulatory back to its homeostatic balance. In addition, we learned about reactions to the oxygen level in blood being too low. This article talks about an increased breathing rate, which we talked about in class, caused by a signal sent by the nervous system. We also studied the nervous system in class and how these signals are sent to the brain.
Author: University of Bristol
Published: Sep 3 2013
http://www.sciencedaily.com/releases/2013/09/130903113300.htm
Summary:
New research has been discovered that removing a small organ on the carotid arteries could decrease hypertension, or high blood pressure. When there is a decreased amount of oxygen in the blood, the brain responds by sending a signal to the heart to beat faster and breath faster, increasing the blood pressure and breathing rate. This gets the oxygen levels back to normal. The small organ, known as the carotid body, sends the nervous signal to the brain that the oxygen levels are low. Keeping the blood pressure at a normal rate is important to supply the brain with enough blood. However, researchers have discovered that removing the carotid body rapidly decreases blood pressure and keeps it at the constant low rate. A human test is going on now to see the results between different patients on a larger scale at the University of Bristol.
Connection
In our study of the human body, we learned about the circulatory system and the many problems that can occur that result in a loss of homeostasis. One of those problems that we studied was hypertension. Therefore this article relates to what we have studied because it talks about a way to resolve this problem and bring the circulatory back to its homeostatic balance. In addition, we learned about reactions to the oxygen level in blood being too low. This article talks about an increased breathing rate, which we talked about in class, caused by a signal sent by the nervous system. We also studied the nervous system in class and how these signals are sent to the brain.
Experimental Technique Coaxes Muscles Destroyed By War To Regrow
Julia Friend
Author: Rob Stein
Published: April 30th, 2014
Link (NPR)
Summary:
A medical team has discovered a way to encourage the regeneration of muscle tissue after its destruction in some sort of trauma. The experiment subjects were five men disabled from war - one, for instance, stepped on a land mine. The scientists found a way to stimulate muscle growth using extracellular matrix, a substance surrounding cells. It is similar to glue in that it keeps all of the cells together; in addition, the matrix has signals that can instruct the cells in certain ways. By transferring new, unaffected matrix from pig bladders to the damaged leg muscles of the men, scientists were successful in promoting new muscle growth. The matrix signaled to dormant, immature muscle cells to grow, thus regenerating the muscles. The men subjected to the experiment all saw improvements on various levels: some could now walk without their canes, and some could even complete harder tasks such as jumping jacks or hiking - men who originally had trouble even getting out of a chair independently. This method is being developed further as a replacement for ineffective options, such as muscle replacements and physical therapy.
Connections:
The muscles affected in these men were voluntarily controlled, and were thus skeletal muscles (as opposed to the involuntary cardiac and smooth muscles). The damage to these muscles came from an acute form of trauma: a single particular action destroyed those muscles, such as stepping on a land mine. This trauma is a form of homeostatic imbalance, where the muscles cannot function as they are supposed to. The leg muscles of these men could not support their body or aid in physical movement. The regeneration of their muscles restored, or partially restored, homeostasis so that those men could take part in the activities they once did before their injuries. The article as a whole relates to the muscular system, its parts, and its functions - all of which we discussed as a class with the powerpoint and book notes.
Author: Rob Stein
Published: April 30th, 2014
Link (NPR)
Summary:
A medical team has discovered a way to encourage the regeneration of muscle tissue after its destruction in some sort of trauma. The experiment subjects were five men disabled from war - one, for instance, stepped on a land mine. The scientists found a way to stimulate muscle growth using extracellular matrix, a substance surrounding cells. It is similar to glue in that it keeps all of the cells together; in addition, the matrix has signals that can instruct the cells in certain ways. By transferring new, unaffected matrix from pig bladders to the damaged leg muscles of the men, scientists were successful in promoting new muscle growth. The matrix signaled to dormant, immature muscle cells to grow, thus regenerating the muscles. The men subjected to the experiment all saw improvements on various levels: some could now walk without their canes, and some could even complete harder tasks such as jumping jacks or hiking - men who originally had trouble even getting out of a chair independently. This method is being developed further as a replacement for ineffective options, such as muscle replacements and physical therapy.
Connections:
The muscles affected in these men were voluntarily controlled, and were thus skeletal muscles (as opposed to the involuntary cardiac and smooth muscles). The damage to these muscles came from an acute form of trauma: a single particular action destroyed those muscles, such as stepping on a land mine. This trauma is a form of homeostatic imbalance, where the muscles cannot function as they are supposed to. The leg muscles of these men could not support their body or aid in physical movement. The regeneration of their muscles restored, or partially restored, homeostasis so that those men could take part in the activities they once did before their injuries. The article as a whole relates to the muscular system, its parts, and its functions - all of which we discussed as a class with the powerpoint and book notes.
Young Blood May Hold Key to Reversing Aging
Gabriella Ricciardone
May 18, 2014
Author: Carl Zimmer
Published: May 4, 2014
Summary:
This past Sunday, studies were published that show that blood from young mice can effectively rejuvenate the muscles and brains of old mice. Continuing this research could lead to the discovery of treatment for diseases such as Alzheimer’s and heart disease. These studies build on the centuries-old idea that the blood of young people contains substances that might revitalize older people. A few decades ago, it became clear that stem cells are essential for keeping tissues alive. Stem cells produce new cells to replace dying ones when tissues are damaged. As people age, their stem cells weaken. In the early 2000s, scientists came to the realization that stem cells were not dying off in aging tissues; rather, they just were not getting the correct signals. There were still plenty of stem cells there. So, researchers joined old and young mice together, in a procedure known as parabiosis, just as Dr. Clive McCay did back in the 1950s to try to find the answer to the same question. The experiment proved that there were certain compounds in the blood of young mice that could awaken stem cells and rejuvenate aging tissues. Similarly, the blood of old mice had compounds that weakened the resilience of the young mice, and made the young mice grow prematurely old, with slower muscle healing ability and slower stem cell productivity. One scientist, Dr. Amy J. Wagers, screened the blood of the mice and found that protein GDF11 was abundant in young mice but scarce in old mice. She and her team also found that GDF11, even on its own, could effectively rejuvenate the hearts and stem cells in old muscles of the mice. A study at Stanford in 2011 reported that the blood of younger mice gave bursts of new neurons in the hippocampus of older mice when injected, and allowed for better memory formation. The same team from Stanford decided to remove the cells and platelets from the blood of young mice and inject them into the old mice through the remaining plasma, which ended up causing the old mice to perform better on memory tests. Scientists hope to one day use this technique and data to help reverse aging in humans as well.
Connection:
During our studies of Chapter 30, we discussed the functions of blood, platelets, and plasma in the body. This article is mainly about the role of young blood and platelets in the rejuvenation of old blood and platelets. We also studied brain functions and neurons during our discussions of Chapter 28, and part of the studies shown above included the improvements in the functions of the hippocampus in older mice when injected with blood of younger mice. We also briefly covered Alzheimer's disease in class, and this research will hopefully be, one day, used to help reverse the effects of Alzheimer's in human beings. During Chapter 30 we also discussed the heart and heart disease and these studies are being done to help reverse the effects of heart disease as well. Stem cells, tissues, and muscles were also discussed during our learning in class.
May 18, 2014
Author: Carl Zimmer
Published: May 4, 2014
Summary:
This past Sunday, studies were published that show that blood from young mice can effectively rejuvenate the muscles and brains of old mice. Continuing this research could lead to the discovery of treatment for diseases such as Alzheimer’s and heart disease. These studies build on the centuries-old idea that the blood of young people contains substances that might revitalize older people. A few decades ago, it became clear that stem cells are essential for keeping tissues alive. Stem cells produce new cells to replace dying ones when tissues are damaged. As people age, their stem cells weaken. In the early 2000s, scientists came to the realization that stem cells were not dying off in aging tissues; rather, they just were not getting the correct signals. There were still plenty of stem cells there. So, researchers joined old and young mice together, in a procedure known as parabiosis, just as Dr. Clive McCay did back in the 1950s to try to find the answer to the same question. The experiment proved that there were certain compounds in the blood of young mice that could awaken stem cells and rejuvenate aging tissues. Similarly, the blood of old mice had compounds that weakened the resilience of the young mice, and made the young mice grow prematurely old, with slower muscle healing ability and slower stem cell productivity. One scientist, Dr. Amy J. Wagers, screened the blood of the mice and found that protein GDF11 was abundant in young mice but scarce in old mice. She and her team also found that GDF11, even on its own, could effectively rejuvenate the hearts and stem cells in old muscles of the mice. A study at Stanford in 2011 reported that the blood of younger mice gave bursts of new neurons in the hippocampus of older mice when injected, and allowed for better memory formation. The same team from Stanford decided to remove the cells and platelets from the blood of young mice and inject them into the old mice through the remaining plasma, which ended up causing the old mice to perform better on memory tests. Scientists hope to one day use this technique and data to help reverse aging in humans as well.
Connection:
During our studies of Chapter 30, we discussed the functions of blood, platelets, and plasma in the body. This article is mainly about the role of young blood and platelets in the rejuvenation of old blood and platelets. We also studied brain functions and neurons during our discussions of Chapter 28, and part of the studies shown above included the improvements in the functions of the hippocampus in older mice when injected with blood of younger mice. We also briefly covered Alzheimer's disease in class, and this research will hopefully be, one day, used to help reverse the effects of Alzheimer's in human beings. During Chapter 30 we also discussed the heart and heart disease and these studies are being done to help reverse the effects of heart disease as well. Stem cells, tissues, and muscles were also discussed during our learning in class.
Heart attack gene, MRP-14, triggers blood clot formation
Heart attack gene, MRP-14, triggers blood clot formation
Matthew He
5/18/14
Author: Case Western Reserve UniversityLink: http://www.sciencedaily.com/releases/2014/04/140401172910.htm
Summary:
Scientists at Case Western Reserve School of Medicine and University Hospitals Case Medical Center have studied humans and mice and discovered how MRP-14 (myeloid related protein-14 ) generates dangerous clots that could trigger heart attack or stroke, and what happens by manipulating MRP-14. A whole new pathway was discovered that shows clotting platelets have MRP-14 inside them, that platelets secrete MRP-14 and that MRP-14 binds to a platelet receptor called CD36 to activate platelets. In detailed studies using MRP-14-deficient mice, the investigators discovered MRP-14 in action. A key fact is that, while MRP-14 is required for pathological blood clotting (Heart disease), it does not appear to be involved in the natural response to prevent bleeding. This is potentially groundbreaking because if a drug could be developed that stops pathological clotting without interfering with the body's natural clotting to heal cuts, you would have a safer medication to treat clotting for heart attack or stroke.
Impact:
This article connects to the circulatory system, and in particular, pathological clotting. Pathological clotting is a major part of Atherosclerosis, and Myocardial Infarction. In the current class unit, we learned that the circulatory system's imbalances are often clot related, as clotting blocks the circulatory system's function of bringing oxygen and nutrients to cells. In addition, we learned about natural clotting with platelets and fibrin. This connects to pathology of the circulatory system because it identifies a specific gene that is involved with pathological clotting, showing that heart disease has genetic factors in it.
Matthew He
5/18/14
Author: Case Western Reserve UniversityLink: http://www.sciencedaily.com/releases/2014/04/140401172910.htm
Summary:
Scientists at Case Western Reserve School of Medicine and University Hospitals Case Medical Center have studied humans and mice and discovered how MRP-14 (myeloid related protein-14 ) generates dangerous clots that could trigger heart attack or stroke, and what happens by manipulating MRP-14. A whole new pathway was discovered that shows clotting platelets have MRP-14 inside them, that platelets secrete MRP-14 and that MRP-14 binds to a platelet receptor called CD36 to activate platelets. In detailed studies using MRP-14-deficient mice, the investigators discovered MRP-14 in action. A key fact is that, while MRP-14 is required for pathological blood clotting (Heart disease), it does not appear to be involved in the natural response to prevent bleeding. This is potentially groundbreaking because if a drug could be developed that stops pathological clotting without interfering with the body's natural clotting to heal cuts, you would have a safer medication to treat clotting for heart attack or stroke.
Impact:
This article connects to the circulatory system, and in particular, pathological clotting. Pathological clotting is a major part of Atherosclerosis, and Myocardial Infarction. In the current class unit, we learned that the circulatory system's imbalances are often clot related, as clotting blocks the circulatory system's function of bringing oxygen and nutrients to cells. In addition, we learned about natural clotting with platelets and fibrin. This connects to pathology of the circulatory system because it identifies a specific gene that is involved with pathological clotting, showing that heart disease has genetic factors in it.
Researchers Discover How ALS Spreads
Adhirath Bollapragada
18 May 2014
University of British Columbia
Published: 18 February 2014
Summary:
The fatal neurodegenerative disease ALS, also known as Lou Gehrig's disease, has been under investigation by researchers, and in particular, how it spreads. New findings suggest that transmission can be blocked, and that misfolded non-mutant SOD1 can be transmitted from region to region in the nervous system, offering a molecular explanation for the progressive nature of the spread. ALS is a disease that affects nerve cells in the brain and the spinal cord. There are approximately 140,000 new cases diagnosed worldwide each year.
Connection:
This connects to our first unit on the Human Body, where we learnt about the Nervous System. We learnt about the motor neurons and how they send the information back to where the sensory neurons received received information. This article connects to the nervous system as it talks about how ALS can break down the motor neurons in the nervous system. In addition to connecting with the nervous system, this article also talks about mutation and how genetic mutation can cause mutation in protein. As a result, this article relates back to our unit on DNA and RNA.
Origin of Huntington's disease found in brain; insights to help deliver therapy
Shruti Suresh
Period 2 Mathieu
Biology Honors
19 May 2014
Published: 28 April 2014
No author, but article is based on materials given by University of California, Los Angeles (UCLA), Health Sciences
Source: http://www.sciencedaily.com/releases/2014/04/140428120654.htm
Summary:
A research that was published on April 28, 2014, gives new awareness on the origins of Huntington's disease. The research helps advocate new targets and routes for drugs to help delay the disease. Huntington's disease is caused by a genetic mutation in the gene, huntingtin, which is present in every somatic cell. A repetitive area of DNA at one end of the mutated gene called a genetic "stutter" is what scientists hold responsible for the cause of the degeneration of the neurons. Professor X. William Yang and Nan Wang, a postdoctoral researcher used genetic scissors to cut the "stutter" off and turned off the mutated gene in neurons of the cortex and the striatum in a mouse model. Scientists at UCLA unearthed that diminishing huntingtin in the cortex partially recovered the symptoms of Huntington's disease. But when reducing huntingtin in both the cortex and in the striatum, and leaving the gene in the rest of the brain, resulted in a correction in symptoms of the disease in the mouse model.
Connection:
This article directly relates to our curriculum because it focuses on a specific brain disease that affects a particular part of the human brain, which we studied. Due to this research, new ways to target the mutated gene have been found. For example, by finding precise locations of the origins of Huntington's disease and by using genetic scissors to cut the repetitive part of DNA in huntingtin scientists are able to reduce the symptoms of brain atrophy and help patients affected with Huntington's disease.
Viagra as a Therapy for Heart Failure
Viagra as a Therapy for heart Failure: Effectiveness on Male vs Female
David Chen
17 May 2014
John Hopkins University School of Medicine
Published: 16 May 2014
http://medicalxpress.com/news/2014-05-gender-differences-impact-viagra-therapy.html
Summary:
When we think of Viagra, we don't think of a treatment for heart failure. We think of those awkward advertisements... Or what the drug was made for, erectile dysfunction. However, within the last decade, scientists have realized another use for Viagra. Sildenafil, the active ingredient in Viagra, can help with heart problems. Sildenafil, when taken, can activate an enzyme that causes a protein called "titin" to relax. This protein is responsible for the elasticity of a cell, and in muscle tissue, it can often cause stiffening. In Viagra's normal application, it dilates the blood vessels, leading to increased blood flow to the penis. However, with further testing, Takimoto, an assistant professor of medicine and a researcher at the Heart and Vascular Institute at John Hopkins, and his team discovered something peculiar between male and female mice models. All of the mice recieved cardiac remodeling. The effectiveness of Sildenafil on females were different from the males. Upon further research, scientists discovered that the hormone estrogen played a role in interacting with Sildenafil. As of now, it appears to help in repairing the heart muscle. Takimoto says this could be an explanation for why a Sildenafil based drug: "RELAX", does not work effectively, as most of its female participants were 70 or older, when menopause had already struck, and estrogen was lower.
Connection:
This article has several connections to what we are learning in biology. Firstly, the main way Sildenafil works is by activating an enzyme, which interacts with a protein. This connects with our unit where we learned about enzymes and proteins. Also, titin connects with how muscles work, as it adds on to our knowledge about how the basic units of muscles, sarcomeres, work. Second, this connects with the circulatory system, in our current unit about the human body. Specifically, it connects with heart failure, which is a condition brought on by many of the diseases explored by the Circulatory Presentation group (I'm in it). Third, the hormone estrogen will connect with a later unit that we will go over, in which we explore the hormones of the body.
David Chen
17 May 2014
John Hopkins University School of Medicine
Published: 16 May 2014
http://medicalxpress.com/news/2014-05-gender-differences-impact-viagra-therapy.html
Summary:
When we think of Viagra, we don't think of a treatment for heart failure. We think of those awkward advertisements... Or what the drug was made for, erectile dysfunction. However, within the last decade, scientists have realized another use for Viagra. Sildenafil, the active ingredient in Viagra, can help with heart problems. Sildenafil, when taken, can activate an enzyme that causes a protein called "titin" to relax. This protein is responsible for the elasticity of a cell, and in muscle tissue, it can often cause stiffening. In Viagra's normal application, it dilates the blood vessels, leading to increased blood flow to the penis. However, with further testing, Takimoto, an assistant professor of medicine and a researcher at the Heart and Vascular Institute at John Hopkins, and his team discovered something peculiar between male and female mice models. All of the mice recieved cardiac remodeling. The effectiveness of Sildenafil on females were different from the males. Upon further research, scientists discovered that the hormone estrogen played a role in interacting with Sildenafil. As of now, it appears to help in repairing the heart muscle. Takimoto says this could be an explanation for why a Sildenafil based drug: "RELAX", does not work effectively, as most of its female participants were 70 or older, when menopause had already struck, and estrogen was lower.
Connection:
This article has several connections to what we are learning in biology. Firstly, the main way Sildenafil works is by activating an enzyme, which interacts with a protein. This connects with our unit where we learned about enzymes and proteins. Also, titin connects with how muscles work, as it adds on to our knowledge about how the basic units of muscles, sarcomeres, work. Second, this connects with the circulatory system, in our current unit about the human body. Specifically, it connects with heart failure, which is a condition brought on by many of the diseases explored by the Circulatory Presentation group (I'm in it). Third, the hormone estrogen will connect with a later unit that we will go over, in which we explore the hormones of the body.
New Molecule Found to Treat Asthma
Marisa Patel
Author: Sanford-Burnham Medical Research Institute
Link: http://www.sciencedaily.com/releases/2014/05/140512154856.htm
Summary:
A new study at the Sanford-Burnham Medical Research Institute, Max Planck Institute, Free University of Berlin, UC San Diego, and Shinshu University has recently found a new molecule that prevents Asthma that is caused by Allergies. This new synthetic molecule (sulfate monosaccharide) inhibits the signals sent by T-cells that are sent to the lungs to trigger an asthma attack. It is also able to lessen the symptoms that are followed by asthma such as inflammation, mucus production, and airway constiction. A study showed that the sulfate monosaccharide blocks the interaction between CCL20 and heparin sulfate which stalls the recruiting of the T-cells that trigger inflammation. This new molecule can be used by injection intravenously or by inhalation. Although billions of dollars are spent trying to find a cure for asthma, it is still on the rise for being the most common chronic disease in children. There is no cure for asthma, but many treatments are used to reduce the risk for asthma being deadly, like this new molecule. The pulmonary inhalation of this molecule is used to surpress chemokine (CCL20) initiated inflammatory responses which helps to reduce the symptoms.
Connection:
This connects to the Respiratory System, specifically Asthma. This disease helps to increase the easy flow of oxygen into the cells and Carbon dioxide out of the body. In this chapter, the respiratory has many homeostatic imbalances such as the lack of oxygen to the cells and one of the main reasons for that is inflammation in the bronchi and this helps to decrease that inflammation therefore creating a balance. This also connects to the molecules and cells chapters because it explains the use of monosaccharides which is a term we learned as one protein molecule where as polysaccharide is a chain of proteins.
Author: Sanford-Burnham Medical Research Institute
Link: http://www.sciencedaily.com/releases/2014/05/140512154856.htm
Summary:
A new study at the Sanford-Burnham Medical Research Institute, Max Planck Institute, Free University of Berlin, UC San Diego, and Shinshu University has recently found a new molecule that prevents Asthma that is caused by Allergies. This new synthetic molecule (sulfate monosaccharide) inhibits the signals sent by T-cells that are sent to the lungs to trigger an asthma attack. It is also able to lessen the symptoms that are followed by asthma such as inflammation, mucus production, and airway constiction. A study showed that the sulfate monosaccharide blocks the interaction between CCL20 and heparin sulfate which stalls the recruiting of the T-cells that trigger inflammation. This new molecule can be used by injection intravenously or by inhalation. Although billions of dollars are spent trying to find a cure for asthma, it is still on the rise for being the most common chronic disease in children. There is no cure for asthma, but many treatments are used to reduce the risk for asthma being deadly, like this new molecule. The pulmonary inhalation of this molecule is used to surpress chemokine (CCL20) initiated inflammatory responses which helps to reduce the symptoms.
Connection:
This connects to the Respiratory System, specifically Asthma. This disease helps to increase the easy flow of oxygen into the cells and Carbon dioxide out of the body. In this chapter, the respiratory has many homeostatic imbalances such as the lack of oxygen to the cells and one of the main reasons for that is inflammation in the bronchi and this helps to decrease that inflammation therefore creating a balance. This also connects to the molecules and cells chapters because it explains the use of monosaccharides which is a term we learned as one protein molecule where as polysaccharide is a chain of proteins.
Role of calcium in familial Alzheimer's disease clarified, pointing to new therapeutics
Megan Zhou
No author given, but is based on materials provided by the University of Pennsylvania School of Medicine.
Published: May 13, 2014
http://www.sciencedaily.com/releases/2014/05/140513175211.htm
Summary:
A research team from 2008 had shown that mutations in two proteins associated with familial Alzheimer's Disease disrupted the flow of calcium ions in neurons; the same team, now led by Kevin Foskett, has found that suppressing the hyperactivity of calcium channels subdued the FAD-like symptoms in mice. Foskett says that these new observations suggest approaches for therapies based on modulating calcium signaling, as current treatments for the pathology of Alzheimer's are experimental. The presenilin proteins 1 and 2 (PS1 and PS2) interact with the calcium release receptor, the IP3R, in the endoplasmic reticulum. The mutant forms of the protein increase the activity of the IP3R, thus increasing calcium levels in cells. The team observed in their mice experiment that the reduced expression of IP3R1 decreased amyloid plaque accumulation in brain tissue and the buildup of tau protein, which are characteristics of advanced Alzheimer's disease. The team's results indicate that the IP3 signaling pathway could be a potential medicinal target for patients that have the mutations in presenilins linked to Alzheimer's. Foskett says that even though the assumption is that FAD is just an earlier, more aggressive onset of AD, no one really knows if the causation of FAD is the same to the common AD. The team's findings is important to find effective treatments that target the IP3R and calcium signaling, specifically for the FAD patients.
Connection:
This article connects to our class' study about the nervous system and its related diseases. Homeostasis is the process by which organisms maintain a relatively stable environment. Alzheimer's disease creates homeostatic imbalance with part of the nervous system's function, starting with the hippocampus and affecting memory. It can spread to all parts of the brain, further inhibiting normal nervous system actions. Even though Alzheimer's disease is the 6th leading cause of death in the US, there is no known cure for it. This relates to the article because their study shows a possibility of a way to prevent the restriction on the nervous system's major functions. The article describing Foskett's team's experimental findings offers an idea for new treatments regarding FAD, a more recurrent version of AD with similar symptoms. The team, by testing on mice with similar FAD-causing mutation presenilins, may be able to use their research to find treatments that will be able to help maintain homeostasis in the nervous system for people with FAD.
No author given, but is based on materials provided by the University of Pennsylvania School of Medicine.
Published: May 13, 2014
http://www.sciencedaily.com/releases/2014/05/140513175211.htm
Summary:
A research team from 2008 had shown that mutations in two proteins associated with familial Alzheimer's Disease disrupted the flow of calcium ions in neurons; the same team, now led by Kevin Foskett, has found that suppressing the hyperactivity of calcium channels subdued the FAD-like symptoms in mice. Foskett says that these new observations suggest approaches for therapies based on modulating calcium signaling, as current treatments for the pathology of Alzheimer's are experimental. The presenilin proteins 1 and 2 (PS1 and PS2) interact with the calcium release receptor, the IP3R, in the endoplasmic reticulum. The mutant forms of the protein increase the activity of the IP3R, thus increasing calcium levels in cells. The team observed in their mice experiment that the reduced expression of IP3R1 decreased amyloid plaque accumulation in brain tissue and the buildup of tau protein, which are characteristics of advanced Alzheimer's disease. The team's results indicate that the IP3 signaling pathway could be a potential medicinal target for patients that have the mutations in presenilins linked to Alzheimer's. Foskett says that even though the assumption is that FAD is just an earlier, more aggressive onset of AD, no one really knows if the causation of FAD is the same to the common AD. The team's findings is important to find effective treatments that target the IP3R and calcium signaling, specifically for the FAD patients.
Connection:
This article connects to our class' study about the nervous system and its related diseases. Homeostasis is the process by which organisms maintain a relatively stable environment. Alzheimer's disease creates homeostatic imbalance with part of the nervous system's function, starting with the hippocampus and affecting memory. It can spread to all parts of the brain, further inhibiting normal nervous system actions. Even though Alzheimer's disease is the 6th leading cause of death in the US, there is no known cure for it. This relates to the article because their study shows a possibility of a way to prevent the restriction on the nervous system's major functions. The article describing Foskett's team's experimental findings offers an idea for new treatments regarding FAD, a more recurrent version of AD with similar symptoms. The team, by testing on mice with similar FAD-causing mutation presenilins, may be able to use their research to find treatments that will be able to help maintain homeostasis in the nervous system for people with FAD.
Saturday, May 17, 2014
Researchers discover how vascular disease activates autoimmune disorders
Carter Terranova
Author: Cell Press
Date: Jan. 9, 2014
Source: http://www.sciencedaily.com/releases/2014/01/140109132303.htm
Summary:
In a recent study, the University of Texas Health and Science Center found that a molecule that causes atherosclerosis also activates T cells that are responsible for autoimmune disorders. First, the team led by Yeonseok Chung speculated that since patients with T cell-mediated autoimmune disorders have a much higher risk of getting atherosclerosis, then the correlation between those diseases could be explained by the activation of T cells from oxLDL. OxLDL stands for oxidized low-density lipoprotein, which is a type of molecule that activates the immune system and is more abundant in patients with vascular diseases, such as atherosclerosis. To get their results, the team exposed atherosclerotic mice to an autoimmune disease causing molecule, and then treated the mice with an agent that prevents the activity of Th17 cells (cells that increase in numbers from oxLDL). After that, symptoms of the autoimmune diseases improved. The study shows that the circulatory system has an impact on immune diseases and that in treatment controlling oxLDL levels could improve the efficiency of treatment.
Connection:
This article connects to what we have been learning by including things like the circulatory system and its diseases, as well as autoimmune diseases such as rheumatoid arthritis. In class, we have learned that the circulatory system's main function is to bring nutrients, oxygen, and blood to and from the cells. Also, atherosclerosis, a circulatory system disease, is caused by the build up of plaque from fat, cholesterol, and other substances in your arteries and over time hardens and narrows those arteries, limiting the flow of oxygenated blood to the rest of the body. This disease can lead to heart attacks, strokes, or death and is connected to autoimmune diseases as mentioned in the article above. Lastly, when studying skeletal system diseases, we learned about rheumatoid arthritis which is a type of autoimmune disease that leads to inflammation of joints and other tissues and is also a type of T cell-mediated autoimmune disease that increases the risk of getting atherosclerosis and was one of the autoimmune diseases targeted in the study above.
Summary:
In a recent study, the University of Texas Health and Science Center found that a molecule that causes atherosclerosis also activates T cells that are responsible for autoimmune disorders. First, the team led by Yeonseok Chung speculated that since patients with T cell-mediated autoimmune disorders have a much higher risk of getting atherosclerosis, then the correlation between those diseases could be explained by the activation of T cells from oxLDL. OxLDL stands for oxidized low-density lipoprotein, which is a type of molecule that activates the immune system and is more abundant in patients with vascular diseases, such as atherosclerosis. To get their results, the team exposed atherosclerotic mice to an autoimmune disease causing molecule, and then treated the mice with an agent that prevents the activity of Th17 cells (cells that increase in numbers from oxLDL). After that, symptoms of the autoimmune diseases improved. The study shows that the circulatory system has an impact on immune diseases and that in treatment controlling oxLDL levels could improve the efficiency of treatment.
Connection:
This article connects to what we have been learning by including things like the circulatory system and its diseases, as well as autoimmune diseases such as rheumatoid arthritis. In class, we have learned that the circulatory system's main function is to bring nutrients, oxygen, and blood to and from the cells. Also, atherosclerosis, a circulatory system disease, is caused by the build up of plaque from fat, cholesterol, and other substances in your arteries and over time hardens and narrows those arteries, limiting the flow of oxygenated blood to the rest of the body. This disease can lead to heart attacks, strokes, or death and is connected to autoimmune diseases as mentioned in the article above. Lastly, when studying skeletal system diseases, we learned about rheumatoid arthritis which is a type of autoimmune disease that leads to inflammation of joints and other tissues and is also a type of T cell-mediated autoimmune disease that increases the risk of getting atherosclerosis and was one of the autoimmune diseases targeted in the study above.
Breakthrough model holds promise for treating Graves' Disease
Sarah Jackman
Author: Endocrine Society
Published: September 13, 2013
http://www.sciencedaily.com/releases/2013/09/130903101545.htm
Summary:
Graves' disease is caused by an autoimmune response, meaning the immune system attacks its own tissues. The thyroid gland produces too much not enough hormones because antibodies are attacking it. If untreated, this disease could cause major heath problems such as heart disease. One problem caused by Graves' Disease are eye problems, which are called Graves' orbitopathy. Swelling tissues press up against the back of the eye causing pain and potentially blindness in the eye. Currently, Graves' orbitopathy is treated with steroids, but they are not an ideal treatment. Dr. J. Paul Banga created an experiment to create an animal model of Graves' orbitopathy in order to find a better treatment. His team of researchers used mice to perform the experiment. To stimulate Graves' orbitopathy, researchers used plasmids, and electric pulses to ensure the plasmids had inserted themselves self into the cells. After three months, the mice that had received the plasmids exhibited the same problems humans with Graves' Disease expressed.
Connection:
This connects to our unit that we will be learning about this term about the immune system. It connects to a major theme of the human body, homeostatic imbalances. In Graves' disease, the thyroid is over or under active depending on whether one has hyperthyroidism or hypothyroidism. The over and under productions of hormones causes homeostatic imbalance. This article also connects to an idea from a previous unit. Plasmids were discussed a term or two ago when we discussed recombiant DNA technology and cloning.
Author: Endocrine Society
Published: September 13, 2013
http://www.sciencedaily.com/releases/2013/09/130903101545.htm
Summary:
Graves' disease is caused by an autoimmune response, meaning the immune system attacks its own tissues. The thyroid gland produces too much not enough hormones because antibodies are attacking it. If untreated, this disease could cause major heath problems such as heart disease. One problem caused by Graves' Disease are eye problems, which are called Graves' orbitopathy. Swelling tissues press up against the back of the eye causing pain and potentially blindness in the eye. Currently, Graves' orbitopathy is treated with steroids, but they are not an ideal treatment. Dr. J. Paul Banga created an experiment to create an animal model of Graves' orbitopathy in order to find a better treatment. His team of researchers used mice to perform the experiment. To stimulate Graves' orbitopathy, researchers used plasmids, and electric pulses to ensure the plasmids had inserted themselves self into the cells. After three months, the mice that had received the plasmids exhibited the same problems humans with Graves' Disease expressed.
Connection:
This connects to our unit that we will be learning about this term about the immune system. It connects to a major theme of the human body, homeostatic imbalances. In Graves' disease, the thyroid is over or under active depending on whether one has hyperthyroidism or hypothyroidism. The over and under productions of hormones causes homeostatic imbalance. This article also connects to an idea from a previous unit. Plasmids were discussed a term or two ago when we discussed recombiant DNA technology and cloning.
Human Stem Cells Get Mice With MS Walking Withing 2 Weeks
Katie Liu
Author: Rebekah Marcarelli
Published: May 16 2014
Link: http://www.hngn.com/articles/31494/20140516/human-stem-cells-get-mice-with-ms-like-disease-walking-within-2-weeks.htm
Summary: A recent study had shown that mice that suffered from a form of Multiple Sclerosis were able to walk after being treated with stem cells that came from humans. The mice that were affected by the stem cells were showing signs of change within only two weeks. Multiple Sclerosis is an autoimmune disease, meaning it is cause by the body system attacking itself. The body’s own immune system damages the myelin sheaths and causing symptoms such as difficulty walking or impaired vision. However, in treated mice, the symptoms were reversed. Instead of the myelin sheaths becoming more and more damaged in the mice, the sheaths were shown to have started to repair itself. Among those lists of changes, the immune system’s attacks on the body were abated. However, the stem cells were rejected after a period of time in the mice’s body as expected. Despite that, the period of time the stem cells were in the body was enough to transmit signals to slow down the body’s attacks on itself and begin myelin sheath repair.
Connection: This article connects to our current unit relating to the human body systems. In this case, the article is directly related to immune system and the nervous system. The immune system is talked about in this article as damaging the myelin sheaths, leading to this disease. The myelin sheaths that are talked about make up neurons, which are part of the nervous system. This article also talks about Multiple Sclerosis, a disease which we mentioned in class. It is also an autoimmune disease and we discussed them in class as well.
Author: Rebekah Marcarelli
Published: May 16 2014
Link: http://www.hngn.com/articles/31494/20140516/human-stem-cells-get-mice-with-ms-like-disease-walking-within-2-weeks.htm
Summary: A recent study had shown that mice that suffered from a form of Multiple Sclerosis were able to walk after being treated with stem cells that came from humans. The mice that were affected by the stem cells were showing signs of change within only two weeks. Multiple Sclerosis is an autoimmune disease, meaning it is cause by the body system attacking itself. The body’s own immune system damages the myelin sheaths and causing symptoms such as difficulty walking or impaired vision. However, in treated mice, the symptoms were reversed. Instead of the myelin sheaths becoming more and more damaged in the mice, the sheaths were shown to have started to repair itself. Among those lists of changes, the immune system’s attacks on the body were abated. However, the stem cells were rejected after a period of time in the mice’s body as expected. Despite that, the period of time the stem cells were in the body was enough to transmit signals to slow down the body’s attacks on itself and begin myelin sheath repair.
Connection: This article connects to our current unit relating to the human body systems. In this case, the article is directly related to immune system and the nervous system. The immune system is talked about in this article as damaging the myelin sheaths, leading to this disease. The myelin sheaths that are talked about make up neurons, which are part of the nervous system. This article also talks about Multiple Sclerosis, a disease which we mentioned in class. It is also an autoimmune disease and we discussed them in class as well.
Dangerous Bacteria Exploiting Human Blood
Link: http://www.sciencedaily.com/releases/2014/05/140502102429.htm
Summary: At the University of York, recent research explains how bacteria use human proteins during infection to their advantage. Professor Jennifer Potts of York’s Biology Department studied the way Staphylococcus aureus can attach itself to two proteins found in the blood of humans. S.aureus is a bacterium that causes deadly infections in people. The two proteins it can attach to are fibronectin and fibrinogen. Both of these proteins play a key role in blood clotting and wound healing. S.aureus binds to fibronectin and fibrinogen to cause the dangerous heart infection endocarditis. Professor Jennifer Potts stated: "Bacteria have evolved various mechanisms to exploit human proteins to cause infection. Understanding these mechanisms might not only lead to the development of new therapeutics but can also provide important information regarding the normal role of these human proteins in the body."
Connection: This recent article relates to our studies of bacteria and the cardiovascular/circulatory system as well as the immune system. In class we learned about bacteria being able to manipulate it's DNA as needed, and doing so to fit with a specific protein is not impossible for the mighty bacteria. S.aureus's ability to do this is a prime example. We also learned in class about blood's key role in the body, including mending injuries and fighting infection. And under normal circumstances our white blood cells, which are also part of our immune system, do not attack their own kind so by binding to our proteins S.aureus can be overlooked. This article is something that fits perfectly into our curriculum.
Summary: At the University of York, recent research explains how bacteria use human proteins during infection to their advantage. Professor Jennifer Potts of York’s Biology Department studied the way Staphylococcus aureus can attach itself to two proteins found in the blood of humans. S.aureus is a bacterium that causes deadly infections in people. The two proteins it can attach to are fibronectin and fibrinogen. Both of these proteins play a key role in blood clotting and wound healing. S.aureus binds to fibronectin and fibrinogen to cause the dangerous heart infection endocarditis. Professor Jennifer Potts stated: "Bacteria have evolved various mechanisms to exploit human proteins to cause infection. Understanding these mechanisms might not only lead to the development of new therapeutics but can also provide important information regarding the normal role of these human proteins in the body."
Connection: This recent article relates to our studies of bacteria and the cardiovascular/circulatory system as well as the immune system. In class we learned about bacteria being able to manipulate it's DNA as needed, and doing so to fit with a specific protein is not impossible for the mighty bacteria. S.aureus's ability to do this is a prime example. We also learned in class about blood's key role in the body, including mending injuries and fighting infection. And under normal circumstances our white blood cells, which are also part of our immune system, do not attack their own kind so by binding to our proteins S.aureus can be overlooked. This article is something that fits perfectly into our curriculum.
Thursday, May 15, 2014
New Important Immune Discovery
Immune discovery article
Summary:
Scientists have discovered a new kind of immune system response where the cells do not circulate throughout the body, but instead only reside in a single organ. This discovery could lead to a whole new set of opportunities to use immune cells to help fight cancers and viral infections. The liver, skin and uterus each have their own set of immune cells that never leave, which are called tissue-resident natural killer cells. If scientists are able to create specialized medications to activate only these organ specific cells, they would be a massive selective weapon against tumors and infections. Results of further testing suggest that there are four types of natural killer cells, instead of just one; which was previously thought.
Connection:
This article relates to a few key human body systems and ways to treat certain threats that the body faces. The immune system is a system that we are yet to learn about, but it plays a key role to protect other organs, such as the liver which aids in the digestive system. It also resides in the integumentary system in the sense that these specialized cells reside in the skin to help protect the body from pathogens.
Summary:
Scientists have discovered a new kind of immune system response where the cells do not circulate throughout the body, but instead only reside in a single organ. This discovery could lead to a whole new set of opportunities to use immune cells to help fight cancers and viral infections. The liver, skin and uterus each have their own set of immune cells that never leave, which are called tissue-resident natural killer cells. If scientists are able to create specialized medications to activate only these organ specific cells, they would be a massive selective weapon against tumors and infections. Results of further testing suggest that there are four types of natural killer cells, instead of just one; which was previously thought.
Connection:
This article relates to a few key human body systems and ways to treat certain threats that the body faces. The immune system is a system that we are yet to learn about, but it plays a key role to protect other organs, such as the liver which aids in the digestive system. It also resides in the integumentary system in the sense that these specialized cells reside in the skin to help protect the body from pathogens.
Be Happy, Be Healthy
Victoria Zhou
Author: Jo Marchant, Nature Magazine
Published: November 27, 2013
Link: http://www.scientificamerican.com/article/how-happiness-boosts-the-immune-system/
Summary:
A branch of science which is usually scoffed at by esteemed biologists and chemists knows as psychoneuroimmunology(PNI) has recently attracted a lot of attention. PNI is a field which studies how moods connect to the immune and nervous system. Stress and sickness has been a long linked duo but with little explanation. Steve Cole, a current professor at the University of California, has performed studies with his colleagues regarding negative states of mind and their affects on the human genome. The research identified 209 genes which differed in self-labeled lonely people and people who had strong social connections. these genes were found to be associated with inflammation, which were upregulated in lonely people, and genes with roles in fighting viruses, which were downregulated in the lonely people. Cole's explanation for this is that it would make sense from an evolutionary standpoint as people in large packs were exposed to more viruses and would need to be able to fend them off, and people who traveled in smaller packs or in solitary would be more likely to be cut, in which inflammation would help with healing. However, in modern times the constant inflammation could lead to diseases such as cancer, atherosclerosis, and diabetes. Other projects were conducted with different scenarios, regarding both negative and positive states of mind, with varying populations leading to the idea that mental state has much to do with physical state. Regardless, there are still many who are skeptical of the data and wary of PNI, but it is still an up and coming field.
Connection:
This article connects to our unit on the nervous system and the immune system. We learned that the systems all rely on the other to survive and the article highlights the connections between the two systems and how one may affect the other. The immune system helps fight off diseases using inflammation which too much of is also related to diseases regarding the circulatory system, atherosclerosis. Thus, we are able to see just how thoroughly entwined the body systems are. The article similarly connects to our study of genetics and evolution as it linked the connection of the immune system and moods to a varying set of genes within people with different social activity levels. Genetic variation would allow the 209 genes mentioned in the article to be overactive or more sedative, respectively, in groups of humans who would stay more solitary versus humans in larger groups.
Wednesday, May 14, 2014
Sophia Li
Author: Hui Chen
Published: April 1, 2014
http://www.sciencedaily.com/releases/2014/04/140401173136.htm
Summary
Dimethyl fumarate (DMF) has recently been approved in Europe as a basic therapy for multiple sclerosis, a chronic inflammatory disease of the central nervous system that affects nerve fibers by damaging their myelin sheaths. The cause of multiple sclerosis is uknown and the disease has no cure, but there are several possible treatments for affected people. Basic MS therapy usually involves beta interferons or glatiramer acetate, which are administered by injections under the skin or into the muscle, causing great discomfort to many patients. However, DMF can be taken as a tablet and has much less side effects. Scientists from the Max Planck Institute for Heart and Lung Research and the Institute of Experimental and Clinical Pharmacology and Toxicology at the University of Lubeck used a standardized mouse model of multiple sclerosis, whereby drugs trigger an autoimmune response. Using this model, they induced neurological deficits similar to those observed in multiple sclerosis. In this experiment, the group treated with DMF had significantly less problems in motor function than the control group. Researchers also discovered that DMF's protective effect is due to the HCA2 receptor. The activation of the HCA2 receptor is responsible for infiltration of the CNS, and DMF blocks this infiltration, theryby preventing inflammation. In mice without the HCA2 receptor, DMF was unable to prevent the signs or paralysis caused by multiple sclerosis. Scientists believe that patients respond differently to DMF treatment because individual genetic differences infulence the efficacy of DMF. Researchers also intend to search for additional substances that bind to the HCA2 receptor that may even have a greater efficacy with fewer side effects.
Connection
This article connects to our study of nervous system, the immune system, and autoimmune diseases. We learned in class that autoimmune diseases are caused when the immune system turns against some of the body's own molecules or "self"cells. While studying about the immune and nervous system, we learned that multiple sclerosis is an autoimmune disease that attacks the central nervous system. T cells attack the myelin sheaths that cover the axons of neurons. Multiple sclerosis can cause fatigue, tingling, and numbness, as well as interfere with memory, talking, and concentration. As mentioned in the article, while there is no cure for multiple sclerosis, there are many treatments. Medicines for autoimmune diseases usually replace the destroyed "self cells," suppress the immune response, or treat specific symptoms. DMF is an example of one of these medicines.
Author: Hui Chen
Published: April 1, 2014
http://www.sciencedaily.com/releases/2014/04/140401173136.htm
Summary
Dimethyl fumarate (DMF) has recently been approved in Europe as a basic therapy for multiple sclerosis, a chronic inflammatory disease of the central nervous system that affects nerve fibers by damaging their myelin sheaths. The cause of multiple sclerosis is uknown and the disease has no cure, but there are several possible treatments for affected people. Basic MS therapy usually involves beta interferons or glatiramer acetate, which are administered by injections under the skin or into the muscle, causing great discomfort to many patients. However, DMF can be taken as a tablet and has much less side effects. Scientists from the Max Planck Institute for Heart and Lung Research and the Institute of Experimental and Clinical Pharmacology and Toxicology at the University of Lubeck used a standardized mouse model of multiple sclerosis, whereby drugs trigger an autoimmune response. Using this model, they induced neurological deficits similar to those observed in multiple sclerosis. In this experiment, the group treated with DMF had significantly less problems in motor function than the control group. Researchers also discovered that DMF's protective effect is due to the HCA2 receptor. The activation of the HCA2 receptor is responsible for infiltration of the CNS, and DMF blocks this infiltration, theryby preventing inflammation. In mice without the HCA2 receptor, DMF was unable to prevent the signs or paralysis caused by multiple sclerosis. Scientists believe that patients respond differently to DMF treatment because individual genetic differences infulence the efficacy of DMF. Researchers also intend to search for additional substances that bind to the HCA2 receptor that may even have a greater efficacy with fewer side effects.
Connection
This article connects to our study of nervous system, the immune system, and autoimmune diseases. We learned in class that autoimmune diseases are caused when the immune system turns against some of the body's own molecules or "self"cells. While studying about the immune and nervous system, we learned that multiple sclerosis is an autoimmune disease that attacks the central nervous system. T cells attack the myelin sheaths that cover the axons of neurons. Multiple sclerosis can cause fatigue, tingling, and numbness, as well as interfere with memory, talking, and concentration. As mentioned in the article, while there is no cure for multiple sclerosis, there are many treatments. Medicines for autoimmune diseases usually replace the destroyed "self cells," suppress the immune response, or treat specific symptoms. DMF is an example of one of these medicines.
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