The Newsweek article posted talks about all of the wonders and benefits of probiotics and reminded me of a news story I had heard. I guess Dannon (yogurt company) is one of those companies that has been using probiotics and marketing the effects of them, especially in digestion. Anyways, there's been a recent lawsuit placed against them, claiming that Dannon has mislead consumers and claiming that the benefits of the probiotics are just claims with no scientific support. I don't know what's worse: Dannon making claims and charging the consumer extra money for it or people being sue-happy. Here's some info on the suit.
http://www.webmd.com/digestive-disorders/news/20080125/yogurt-maker-sued-over-health-claims
http://www.importantlawsuits.com/lawsuits/dannon-activia-lawsuit/
26 February 2008
"Translational Research in IBD" (Abreu et al)
As mentioned by Lian, Inflammatory Bowel Disease (IBD) is an overactive and uncontrolled immune response in the digestive tract. The article assigned this week, “Translational Research in Inflammatory Bowel Disease” (Abreu et. al) contains a good amount of information regarding the disease. The researchers identify that IBD is caused by a dysregulated mucosal immune response to a luminal antigen. Furthermore, people with IBD have an imbalance of T-helper effector cells and T regulatory cells being activated. The effector cells are identified as being responsible for producing the proinflammatory cytokines whereas the latter are responsible for producing the anti-inflammatory cytokines. The imbalance of these immune cells (more effector cells) results in inflammation and this leads to the protective layer of the gut being less effective, leaving the gut exposed and vulnerable.
The article notes that there are many causes and risk factors associated with IBD. A major risk factor includes genetic predisposition and therefore, people who have had occurrences of IBD in their family are more susceptible to the disease. The NOD2/CARD15 and OCTN1/2 genes and mutations of them are the primary genes associated with risk for IBD. The CARD15 gene is responsible for recognizing antigens and will release proinflammatory cytokines as a response. A mutation in this gene will lead to greater inflammatory responses. The OCTN genes function in carnatine transport across the membrane of epithelial cells in the GI. Mutations of OCTN lead to a greater amount of harmful antigens being transported across the membrane, which then warrants a greater immune response, which means more inflammation.
They also mention Toll-like Receptors (TLR) and Dendritic cells. The TLRs are expressed on cells in the GI and function in recognizing and binding antigenic ligands and after doing so, warrant an immune response. So basically, the TLRs contributes to a greater and more sensitive immune response. The Dendritic cells, they note, sample the contents in the lumen of the GI and upon sensing antigens/bacteria, will then signal T cells to either inhibit or activate an immune response.
It goes on by mentioning treatments, therapies, and ideas on how to treat IBD. They mention restoring the balance of all the cytokines and T cells involved in the immune response. This would help keep the inflammation in check. Another treatment is through the use of antibiotics/probiotics. The idea here is to repopulate the GI with the good or beneficial bacteria while ridding it of the bad bacteria.
They end off by mentioning the “IBD chip”. This chip would provide a personal and specific solution for the person with IBD. The chip would identify all of the genes and proteins expressed in that person’s mucosa and provide sort of a map on where and what to attack.
Abreu M, Sparrow M. Translational Research in Inflammatory Bowel Disease.
The article notes that there are many causes and risk factors associated with IBD. A major risk factor includes genetic predisposition and therefore, people who have had occurrences of IBD in their family are more susceptible to the disease. The NOD2/CARD15 and OCTN1/2 genes and mutations of them are the primary genes associated with risk for IBD. The CARD15 gene is responsible for recognizing antigens and will release proinflammatory cytokines as a response. A mutation in this gene will lead to greater inflammatory responses. The OCTN genes function in carnatine transport across the membrane of epithelial cells in the GI. Mutations of OCTN lead to a greater amount of harmful antigens being transported across the membrane, which then warrants a greater immune response, which means more inflammation.
They also mention Toll-like Receptors (TLR) and Dendritic cells. The TLRs are expressed on cells in the GI and function in recognizing and binding antigenic ligands and after doing so, warrant an immune response. So basically, the TLRs contributes to a greater and more sensitive immune response. The Dendritic cells, they note, sample the contents in the lumen of the GI and upon sensing antigens/bacteria, will then signal T cells to either inhibit or activate an immune response.
It goes on by mentioning treatments, therapies, and ideas on how to treat IBD. They mention restoring the balance of all the cytokines and T cells involved in the immune response. This would help keep the inflammation in check. Another treatment is through the use of antibiotics/probiotics. The idea here is to repopulate the GI with the good or beneficial bacteria while ridding it of the bad bacteria.
They end off by mentioning the “IBD chip”. This chip would provide a personal and specific solution for the person with IBD. The chip would identify all of the genes and proteins expressed in that person’s mucosa and provide sort of a map on where and what to attack.
Abreu M, Sparrow M. Translational Research in Inflammatory Bowel Disease.
23 February 2008
A leading cause of stroke
One of the leading causes of stroke is atrial fibrillation, a condition which causes the upper two chambers of the heart to beat irregularly. In atrial fibrillation, the electrical impulses that are normally generated by the sinoatrial node are replaced by disorganized activity in the atria, leading to irregular conduction of impulses to the ventricles that generate the heartbeat. The result is an irregular heartbeat. Usually atrial fibrillation is asymptomatic but can result in palpitations, fainting, chest pain, or congestive heart failure. For these reasons, patients are at a 2-7 percent higher risk of stroke. Often patients are treated with medicine to slow down the heart beat or with anticoagulants. These anticoagulants come with their own risks and generally require frequent blood tests. Reasearchers have developed a potential alternative to these treatments called The Watchman procedure. For this procedure they place a small, parachute-like device near the left appendage of the heart. Once places, the device employs and blocks clots from leaving the heart and going to the brain.
The full article can be seen at
http://www.sciencedaily.com/videos/2005/1203-stopping_strokes.htm
The full article can be seen at
http://www.sciencedaily.com/videos/2005/1203-stopping_strokes.htm
Quick Overview of Inflammatory Bowel Disease (IBD) - Crohn's Disease and Ulcerative Collitus
Inflammatory Bowel Disease is a general categorization for multiple diseases that are distinguished by an abnormal immune response found in the digestive tract. Often healthy microbes such as certain types of bacteria are mis recognized, and the immune system responds by sending white blood cells to the intestinal lining. This immune response unfortunately results in chronic inflammation causing further damage throughout the digestive tract such as blockages, ulcers, and malnutrition. IBDs do not exhibit a "clear cut pattern of inheritable", but are a result of multiple factors: genetics, the immune system, and the environment. High rates of prevalence are found in white European races and also in Jews. Often 10%-20% affected patients have a relative with the same disorder. The two major diseases belonging to this IBD category are Crohn's Disease and Ulcerative Collitus. The symptoms between the two are somewhat similar.
Crohn's Disease is usually found to effect the smaller intestine and upper colon, throughout all layers of the intestinal lining (the entire thickness of the bowel wall). Diagnosis often occurs in children and young adults. Since there is not a specific cure for Crohn's disease, treatment consists of suppressing the immune response and treating the symptoms (with various drugs and medications) in the hopes of allowing the affected intestinal tissue to heal. Once the symptoms are brought somewhat under control, treatments are aimed to prevent future flare ups. In response to the chronic inflammation the bowel wall can thicken as a result of scar tissue formation, thus narrowing the passageway. Deep ulcers can also further develop into fistulas; which become tracts that can burrow into surrounding tissues such as the bladder, vagina or skin. These fistulas can result in further infection and if large enough, have to be repaired through surgery.
Ulcerative Collitus is often isolated to affecting the superficial layers (mucosa) of the colon. Sores and Ulcers are created on the mucosa of the colon and can result in pus production and bleeding. The different types of Ulcerative Collitus are identified by the area of the colon that is effected. Ulcerative Collitus can be set apart from Crohn's disease in that it affects the tissue in a continuous manner. On average the age of diagnosis is mid 30's and is more commonly found in men. Symptoms are very similar to Crohn's Disease and include abdominal cramping, bloody loose stools, diarrhea, appetite and weight loss, nausea, and fever. Treatments include medications, antibiotics, adjustments to diet, nutritional supplements, and also surgery.
Here is a clear and interactive website from the CCFA - Crohn's and Collitus Foundation of American. This website describes the cause, symptoms, treatments, medication details, and latest procedures used in the treatment of IBDs. Take a look because it presents a very nice overview of the disease.
http://www.ccfa.org/
Crohn's Disease is usually found to effect the smaller intestine and upper colon, throughout all layers of the intestinal lining (the entire thickness of the bowel wall). Diagnosis often occurs in children and young adults. Since there is not a specific cure for Crohn's disease, treatment consists of suppressing the immune response and treating the symptoms (with various drugs and medications) in the hopes of allowing the affected intestinal tissue to heal. Once the symptoms are brought somewhat under control, treatments are aimed to prevent future flare ups. In response to the chronic inflammation the bowel wall can thicken as a result of scar tissue formation, thus narrowing the passageway. Deep ulcers can also further develop into fistulas; which become tracts that can burrow into surrounding tissues such as the bladder, vagina or skin. These fistulas can result in further infection and if large enough, have to be repaired through surgery.
Ulcerative Collitus is often isolated to affecting the superficial layers (mucosa) of the colon. Sores and Ulcers are created on the mucosa of the colon and can result in pus production and bleeding. The different types of Ulcerative Collitus are identified by the area of the colon that is effected. Ulcerative Collitus can be set apart from Crohn's disease in that it affects the tissue in a continuous manner. On average the age of diagnosis is mid 30's and is more commonly found in men. Symptoms are very similar to Crohn's Disease and include abdominal cramping, bloody loose stools, diarrhea, appetite and weight loss, nausea, and fever. Treatments include medications, antibiotics, adjustments to diet, nutritional supplements, and also surgery.
Here is a clear and interactive website from the CCFA - Crohn's and Collitus Foundation of American. This website describes the cause, symptoms, treatments, medication details, and latest procedures used in the treatment of IBDs. Take a look because it presents a very nice overview of the disease.
http://www.ccfa.org/
21 February 2008
source of Interleukin 10 in cerebral ischaemia
As we read in this weeks articles, interleukin 10 (IL10) is an anti-inflammatory cytokine that helps reduce the damage caused by inflammation after a stroke. I did more research on this cytokine and found in the paper, Interleukin-10 Modulates Neuronal Threshold of Vulnerability to Ischaemic Damage, that the source of IL-10 in the brain is activated microglia. This superised me, because last week we read in the article, The Inflammatory Response in Stroke, that activated microglia may contribute to brain injury during a stroke. The paper does not detail the mechanism or outline a possible mechanism about how IL-10 gets released from activated microglia and I was unable to find more papers on this in a Pubmed search, but it is interesting information.
http://www.blackwell-synergy.com.ezproxy1.library.arizona.edu/doi/abs/10.1046/j.1460-9568.2000.00090.x
http://www.blackwell-synergy.com.ezproxy1.library.arizona.edu/doi/abs/10.1046/j.1460-9568.2000.00090.x
I am also very interested in why Mexican Americans are more suseptible to stroke. I looked up a bunch of articles and found one study that showed a much lower average age of Mexican American stroke sufferers to that of non-hispanic whites. They also found a that Mexican Americans were less likely to have graduated high school and more likely to make less than 20K per year, which could have been one explanation for the disproportionate numbers. However, they found no differences in the rate of having a primary care physician! This seems very strange. Has anybody found further research on this?
To answer Kim...I read up on stroke and Pima Indians and did not find any major differences, but I did find some inderesting info reguarding Pima Indians and their decreased SNS response to high fat % and insulin levels, which may account for a lower prevalance of hypertension. Here is a brief overview about it if you are interested.
http://hyper.ahajournals.org/cgi/content/abstract/36/4/531
To answer Kim...I read up on stroke and Pima Indians and did not find any major differences, but I did find some inderesting info reguarding Pima Indians and their decreased SNS response to high fat % and insulin levels, which may account for a lower prevalance of hypertension. Here is a brief overview about it if you are interested.
http://hyper.ahajournals.org/cgi/content/abstract/36/4/531
20 February 2008
Another agent that may prevent stroke in some people.
The basic science paper assigned this week (“Levels of Anti-Inflammatory Cytokines and Neurological Worsening in Acute Ischemic Stroke” by Nicolas Vila et. al.) Another element that plays a role in reducing the damaging effects of ischemic stroke was introduced: Interleukin-10 (IL-10). IL-10 is a cytokine which acts as an anti-inflammatory agent, by inhibiting the production of some proinflammatory cytokines, such as IL-6 and TNF-alpha. In this study 249 patients were observed after they were admitted for treatment within 24 hours of the onset of stroke symptoms. In this group about 36% showed signs of neurological worsening within 48 hours after the stroke began. Also noticed in this group was a significantly lower concentration of the IL-10 cytokine. The conclusions of this paper suggest that lower concentrations of IL-10 result in more damage from ischemic stroke than in cases where the levels are normal.
An interesting point brought up towards the end of this paper is the issue that some people express genes which lead to such low levels of IL-10 production. If this is found to be true in further research, this can be used as a method to detect individuals who are predisposed to stroke or those who have a greater risk of mortality from stroke. If this can be detected early, the last few statements suggest that treatment with IL-10 can prevent stroke or at least decrease the damage from acute stroke. Like the claims made concerning E-selectin tolerance, this too seems to be another potential method of preventing stroke.
Fucoidin and sushi
I noticed in two of the four readings that there was the mention of using fucoidin. So I thought I would look up to see what fucoidin is and where it comes from. Fucoidin is a sulfated polysaccaride found in types brown seaweed and also within animals such as the sea cucumber. There are two types of fucoidin (also spelled fucoidan and fucidin) F-fucoidin which is composed of greater then 95% sulfated esters of fucose and U-fucodin which is about 20% glucronic acid. Interestingly, along with enhancing recovery from ischemic strokes found in the papers read, in a japanese study in 2005 it was found that fucoidin could induce apoptosis in human lymphoma cell lines. Another study conducted in France in 2002 found that fucoidin inhibited hyperplasia in rabbits. So as mentioned in a early post about drinking next time you get slammed while saki bombing, mix in a little wine and a sushi roll and your body will love all that much more.
19 February 2008
As if one stroke weren't enough...
So this article basically tells the dangers that mexican-americans deal with as a risk for stroke. However, the article describes other risk factors for stroke; poor diet, physical inactivity, smoking, not going to the doctor proceeding a stroke, high blood pressure and cholesterol, diabetes, etc. Why do you think this would target mexican-americans over any other race. Americans pretty much have the same diet, physical inactivity and so forth. Maybe people don't go to the doctor after a stroke because they don't have health insurance?? Just an idea.
If these other risk factors are such a big deal, I'd be interested to know where the Pima Indians stand as a risk factor. If anyone comes across someting will you let me know. If I find something, I'll post it as well. Thanks everyone. Have a great week
If these other risk factors are such a big deal, I'd be interested to know where the Pima Indians stand as a risk factor. If anyone comes across someting will you let me know. If I find something, I'll post it as well. Thanks everyone. Have a great week
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