Sodium is a hot topic that is being investigated to determine if its relationship is truely detremental to blood pressure levels which can impact its relationship with cardiac disease. Currently sodium is a major no no for those with high blood pressure and diets have been developed such as the DASH diet to eliminate sodium intake. The first article gives the Center for Disease Control's opinion on sodium based off previous findings. I feel that this could be a more informative than the french fries and heart article. The second link gives an interesting take on sodium from the opposing side aka the salt lovers.
http://www.cdc.gov/bloodpressure/sodium.htm
http://www.naturalnews.com/015820.html
29 February 2012
28 February 2012
Review: Innate and Adaptive Immunity in Inflammatory Bowel Disease (IBD)
Inflammatory bowel diseases are the results of a dysregulated mucosal immune system. The mucosal immune system have both innate and adapative immunity. This review article presents the cross-regulation between these two immune systems and understanding the cross-regulation can help us to better understand the disease and possibly identify the future therapeutic targets.
IBD is idiopathic disease, but many soursces say that there is a genetic component for the cause. Genome-wide association studies (GWAS) provided a strong evidence for a close link between the innate and the adaptive immune system in regulating the sensitive balance of the mucosal immune system.
In the intestine, innate immunity includes the epithelial barrier and phagocytic cells within the lamina propria. The genetic defects in innate immunity can increase the incidence of IBD according to the paper.
For the adaptive immunity, Th1-mediated immune responses are typically evoked in response to an intracellular pathogen presented by antigen-presenting cell in the presence of IL-12. Then, the consequencial response is to localize the infectious agent and secret other cytokines like IFN-gamma and cytotoxic T cell for apoptosis. Th17 secret IL-12 and IL-22 which are pro-inflammatory and in inflamed Crohn's disease (CD) mucosa, there was an increasing level of IL-17 and IL-22. There are Treg cells which secrete IL-10, a potent anti-inflammatory cytokine and IL-10 deficient mice develop intestinal inflammation. Another form of IBD, Ulcerative Colitis (UC) had increasing levels of IL-13 and IFN-gamma which targets the epithelial cell to become dysfunctional. So, UC is more of superficial epithelial injury disorder.
Under which conditions does dysregulation of innate and adaptive immunity occur? Luminal antigens cross the epithelial barrier, and this process is increased during intestinal inflammation. The antigens reaching the lamina propria will first activate the innate immune system via pattern recognition receptors (PRRs) and antigen presenting cells (APCs) show antigens to T cell to evoke an adaptive immunity.
This article picked two examples to illlustrate the cross-regulation of innate and adaptive immunity. One example is NOD2, a cytoplasmic protein acting as PRR that serves as a bacteria sensor for the proteins on the cell wall of bacteria. Mice lacking NOD2 showed a defect in intestinal innate defense. CD patients with mutant NOD2 were shown to have decreased defensins and an increase of bacterial translocation and thus activating the adaptive immune system. The second example this article gives is IL-12. IL-12 is a key Th1 cytokine and CD is classified as a Th1-mediated disease. IL-12 is produced a lot by macrophages and dendritic cells within the lamina propria after the translocation of the bacteria and it will ultimately lead to the inflammation by Th1-mediated process. A mutation in NOD2 is associated with increase in IL-12, thus linking a receptor of the innate immunity with the effector cascade of the adaptive immunity. So, anti-IL-12 treatment is effective in patients with CD.
Source: Siegmund, Britta, and Martin Zeitz. "Innate and adaptive immunity in inflammatory bowel disease." World Journal of Gastroenterology. 17.27 (2011): 3178-3183.
Inflammatory bowel diseases are the results of a dysregulated mucosal immune system. The mucosal immune system have both innate and adapative immunity. This review article presents the cross-regulation between these two immune systems and understanding the cross-regulation can help us to better understand the disease and possibly identify the future therapeutic targets.
IBD is idiopathic disease, but many soursces say that there is a genetic component for the cause. Genome-wide association studies (GWAS) provided a strong evidence for a close link between the innate and the adaptive immune system in regulating the sensitive balance of the mucosal immune system.
In the intestine, innate immunity includes the epithelial barrier and phagocytic cells within the lamina propria. The genetic defects in innate immunity can increase the incidence of IBD according to the paper.
For the adaptive immunity, Th1-mediated immune responses are typically evoked in response to an intracellular pathogen presented by antigen-presenting cell in the presence of IL-12. Then, the consequencial response is to localize the infectious agent and secret other cytokines like IFN-gamma and cytotoxic T cell for apoptosis. Th17 secret IL-12 and IL-22 which are pro-inflammatory and in inflamed Crohn's disease (CD) mucosa, there was an increasing level of IL-17 and IL-22. There are Treg cells which secrete IL-10, a potent anti-inflammatory cytokine and IL-10 deficient mice develop intestinal inflammation. Another form of IBD, Ulcerative Colitis (UC) had increasing levels of IL-13 and IFN-gamma which targets the epithelial cell to become dysfunctional. So, UC is more of superficial epithelial injury disorder.
Under which conditions does dysregulation of innate and adaptive immunity occur? Luminal antigens cross the epithelial barrier, and this process is increased during intestinal inflammation. The antigens reaching the lamina propria will first activate the innate immune system via pattern recognition receptors (PRRs) and antigen presenting cells (APCs) show antigens to T cell to evoke an adaptive immunity.
This article picked two examples to illlustrate the cross-regulation of innate and adaptive immunity. One example is NOD2, a cytoplasmic protein acting as PRR that serves as a bacteria sensor for the proteins on the cell wall of bacteria. Mice lacking NOD2 showed a defect in intestinal innate defense. CD patients with mutant NOD2 were shown to have decreased defensins and an increase of bacterial translocation and thus activating the adaptive immune system. The second example this article gives is IL-12. IL-12 is a key Th1 cytokine and CD is classified as a Th1-mediated disease. IL-12 is produced a lot by macrophages and dendritic cells within the lamina propria after the translocation of the bacteria and it will ultimately lead to the inflammation by Th1-mediated process. A mutation in NOD2 is associated with increase in IL-12, thus linking a receptor of the innate immunity with the effector cascade of the adaptive immunity. So, anti-IL-12 treatment is effective in patients with CD.
Source: Siegmund, Britta, and Martin Zeitz. "Innate and adaptive immunity in inflammatory bowel disease." World Journal of Gastroenterology. 17.27 (2011): 3178-3183.
Inflammatory Bowel Disease and Depression
For the March 5th, 2012 discussion about the Inflammatory Bowel Disease (IBD), there is one interesting lay article Dr. Cohen posted for our interesting discussion which was that the students who have had the symptoms of IBD were struggling academically by missing classes. The study from the Nationwide Children's Hospital in Columbus, Ohio noted that the students who have IBD are at a higher risk of getting the "internalizing" problems such as depression. This depression can lead kids not doing well in school. As I read this lay article, I wanted to know more about the possible relationship or association between the IBD and depression.
I came across with this Neuroscience paper to answer my curiosity:
From inflammation to sickness and depression: when the immune system subjugates the brain.
Dantzer, R. et al. Nature Reviews Neuroscience 9, 46-56 (January 2008).
It turns out that the inflammatory cytokines such as Interleukin-1a, Interleukin-1b, Interleukin-6, and TNF-a from IBD can play a role in the brain to induce the "sickness behavior" which is very similar to and hard to differentiate from the depression according to the paper. Out of these cytokines, Interleukin-6 released from the stimulated cells can cause the down-regulation of Treg and up-regulation of Th1 and Th17 which are very strong pro-inflammtory. These can activated M1, classically-activated macrophages and lead to chronic inflammation, in this case on the mucous membrane of the gut for IBD.
Overall, the inflammation can negatively affect the health of the brain in this case causing the depression via cumulative actions from cytokines.
Cool it!
I was sitting here like the nerd I am, not thinking of the
UofA basketball team or attractive ladies walking by, but of how to slow
ischemic stroke and decrease the stroke infarct volume. A very simple idea
popped into my head: hypothermia! What
do you do when you break your leg and it swells? You put ice on it! Why not do
that to the brain?
It is also already known that many who suffer heart attacks
or drowning in cold water have a much higher chance of survival than at non-hypothermic
conditions. So I started my research and was actually very surprised to
actually see people are studying/testing this. I had no idea this was an actual
concept! **Victory dance that I actually had a good idea! <(' -'<)
<( '-' )> (>'-')> ***
One group studied two ways of cooling; surface cooling and endovascular
cooling. Intravascular cooling is being studied now and is not included in this
article. Both trials (surface and endovascular) results show the feasibility of
the concept but cannot comment on the safety of the procedure.
Models of temporary ischemia with administration of
hypothermia show a reduction in infarct size and improvement in behavioral
outcomes.They show that hypothermia initiated after 5 minutes of ischemic
stroke onset protected the cortical ad hippocamplan neurons. However,
hypothermia was not effective when initiated 30 minutes after. This is much
different in animal studies. Both 2 and 6 hour delays show protective effects.
A 22 hour delay showed to be even more neuroprotective.
They hypothesize that the mode of protection comes from the
fact that it causes metabolic rate of the brain to slow as well as reduces release
of inflammation markers and free radicals. I would imagine it would also help
with reperfusion injury as well once the embolism is removed.
Surface cooling can use air blankets, water mattresses,
alcohol bathing, cooling jackets, and ice packing. Advantages are its
simplicity and ability to even be performed at home, in a crude way, while
waiting for the ambulance. However, this takes several hours to reach the
desired temperature.
Endovascular cooling uses catheters that can be inserted
directly into the central venous system transferring heat via transduction
through an internal circulation in the catheter. This is much quicker, tighter
temperature control and reduces shivering quite a bit.
With either case passive re-warming is used afterwards.
These therapies could be combined with neuroprotective agents to augment each
other.
http://stroke.ahajournals.org/content/38/2/794.long
27 February 2012
Woman suffers stroke after hickey
Just in case anyone was interested, here was the lay article that Dr. Cohen showed the class when I was taking Cardio. I guess the moral of the story is don't get hickeys after the age of 40 =]
http://www.dailymail.co.uk/health/article-1349201/Woman-suffers-stroke-amorous-partner-gives-love-bite.html
http://www.dailymail.co.uk/health/article-1349201/Woman-suffers-stroke-amorous-partner-gives-love-bite.html
26 February 2012
"They try to make me go to rehab.."
Since I have an interest in
rehabilitation, I wanted to look at what kinds of treatment are used for people
post-stroke and what kinds of things therapists do to try and prevent recurrent
ones. As a quick review, a stroke is when blood supply to the brain is
disturbed, due to an event such as lack of blood flow to the brain caused by a
blockage or a hemorrhage. Loss in brain function from a stroke may result in
inability to move limbs on a particular side of the body, inability to talk or
understand speech correctly, or visual impairment. According to the American Heart Association,
when considered independent to other cardiovascular diseases, strokes are the 3rd
leading cause of death in the US, and it is proposed that incidence may
continue with the growing population of elderly Americans, increasing rates of
diabetes and obesity, and great prevalence of cardiac problems and inactivity
among communities. Think of it this way… 1 person nearly every 45 seconds
suffers a stroke, 1/3 of which are recurrent. It is crazy to think about! Post stroke,
only about 14% of survivors are able to fully recover; about 25-50% still
require some assistance throughout their lives, and others, in severe cases, receive
partial paralysis. By implementing exercise training and physical activity,
stroke survivors strive to regain ability to do daily functions, such as dressing,
bathing, or walking, learn how to manage muscle or joint pain, and improve
cardiovascular fitness.
Rehabilitation programs asses each
patient and design a program around their current condition, medical history,
any neurological complications or other medical conditions, and lifestyle.
Programs typically address 3 main goals. The first goal for the patient is to
start a physical conditioning regimen to recover the prestroke level of
activity. The second goal is to prevent recurrent stroke and cardiovascular complications;
by starting aerobic conditioning programs, stroke survivors can enhance glucose
regulation, decrease in body weight and fat stores, lower blood pressure, lower
serum triglycerides and LDL cholesterol, and increase HDL cholesterol and
improve cardiovascular functions such as blood flow or coronary artery
endothelial function. The third rehabilitation goal is for patients to improve
aerobic fitness despite limitations. As for recommended exercise programming,
the American Heart Association recommended that patients should utilize aerobic training modes (leg,
arm or combo) ergometry at 40-70% peak oxygen consumption, and train 4-7 days a
week with duration of 20-60 minutes a day of exercise. Treadmill training in particular can be very beneficial, as patients can decrease
their body weight by holding on to the handrails while regaining their ability
to walk, as well as increasing the grade of incline or speed as they gain
mobility. It is remarkable that in incorporating exercises such as upper-body
and resistance training or stretching, patients can improve sensorimotor impairments
and performance time, as well as range of motion, respectively. The AHA provides a nice table that shows
programming recommendations for stroke survivors that is quick and easy to read
and understand! (http://circ.ahajournals.org/content/109/16/2031/T1.expansion.html). Although this information focuses on the physical rehabilitation, it is very important to recognize that other members of the rehab team are just as essential in the process; occupational therapists aid in finer tasks such as eating, or writing, a speech-language therapist can help with speech impairments or difficulty swallowing, and psychologists/psychiatrists are important in assessing the emotions a patient goes through.
It is very interesting to see how
different people recover from something as serious as a stroke. My friend’s
father, for example, completely hid that he had a stroke from his daughters for
a while and they never knew the difference, whereas my mother’s best friend from
nursing school had one post car accident and now has a speech impediment. I am
very interested to see what is in store for cardiac disease/stroke prevention
and rehabilitation as I continue my own career in healthcare.
If you would like to read more,
here is the full AHA article!
23 February 2012
Stroke of Insight
As most of you may already know, a stroke is somewhat of a "brain attack", or what happens when blood flow to a part of the brain stops. There are two main types of ischemic stroke: one in which a clot may form in an artery that is already very narrow creating a thrombotic stroke. In addition, a cerebral embolism, or an embolic stroke can occur in which a clot breaks off from some part of the body, or from a place in the blood vessels of the brain and travels up to the brain. Plaque built up on an artery wall or blood vessel from cholesterol, fat, and other substances can lead to a blood clot, which may block blood from reaching the brain and cause an ischemic stroke. On the other hand, a hemorrhagic stroke (less common) occurs when a blood vessel in part of the brain becomes weak enough to burst open, causing blood to leak into the brain.
The symptoms of stroke depend on what part of the brain is affected and usually develop suddenly and without warning. Symptoms of stroke are usually most severe at onset and may possibly slowly get worse, or they may occur on and off for the first day or two. The brain is an incredibly complex organ, with each area having a responsibility for a particular function or ability. The brain is divided into four primary parts: the right hemisphere, the left hemisphere, the cerebellum and the brain stem. The right hemisphere of the brain controls the movement of the left side of the body as well as analytical and perceptual tasks, such as judging distance, size, speed, or position and seeing how parts are connected to wholes. A stroke in the right hemisphere usually causes paralysis in the left side of the body known as left hemiplegia. Patients of right-hemisphere strokes may also have problems with their spatial and perceptual abilities in addition to changed behavior, judgment abilities, and short term memory difficulty. Similarly, survivors of left-hemisphere stroke may also develop memory problems, which can include shortened retention spans, difficulty learning new information and problems in generalizing and conceptualizing. The left hemisphere of the brain controls the movement of the right side of the body as well as speech and language abilities. A left-hemisphere stroke often causes paralysis of the right side of the body, known as right hemiplegia.
A stroke in the cerebellum can cause coordination and balance problems, dizziness, nausea, vomiting, and abnormal reflexes of the head and torso. The brain stem, however, is the area of the brain that controls all of our involuntary, "life-support" functions, such as heartbeat, blood pressure, and breathing rate. It also controls eye movements, hearing, speech and swallowing abilities. Survivors of a brain stem stroke may also develop paralysis in one or both sides of the body because of the impulses generated in the brain's hemispheres that must travel through the brain stem on their way to the appendiges.
Jill Bolte Taylor, a brain research scientist, experienced and studied her very own stroke in the left hemisphere, but after spending eight years recovering, she feels more enlightened and stronger than before. She gives a very emotional, captivating and detailed description of her experience during and after her stroke on T.E.D talks, for which I have provided the link below!
http://www.ted.com/talks/jill_bolte_taylor_s_powerful_stroke_of_insight.html
References:
http://www.stroke.org/site/PageServer?pagename=EFFECT
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001740/
The symptoms of stroke depend on what part of the brain is affected and usually develop suddenly and without warning. Symptoms of stroke are usually most severe at onset and may possibly slowly get worse, or they may occur on and off for the first day or two. The brain is an incredibly complex organ, with each area having a responsibility for a particular function or ability. The brain is divided into four primary parts: the right hemisphere, the left hemisphere, the cerebellum and the brain stem. The right hemisphere of the brain controls the movement of the left side of the body as well as analytical and perceptual tasks, such as judging distance, size, speed, or position and seeing how parts are connected to wholes. A stroke in the right hemisphere usually causes paralysis in the left side of the body known as left hemiplegia. Patients of right-hemisphere strokes may also have problems with their spatial and perceptual abilities in addition to changed behavior, judgment abilities, and short term memory difficulty. Similarly, survivors of left-hemisphere stroke may also develop memory problems, which can include shortened retention spans, difficulty learning new information and problems in generalizing and conceptualizing. The left hemisphere of the brain controls the movement of the right side of the body as well as speech and language abilities. A left-hemisphere stroke often causes paralysis of the right side of the body, known as right hemiplegia.
A stroke in the cerebellum can cause coordination and balance problems, dizziness, nausea, vomiting, and abnormal reflexes of the head and torso. The brain stem, however, is the area of the brain that controls all of our involuntary, "life-support" functions, such as heartbeat, blood pressure, and breathing rate. It also controls eye movements, hearing, speech and swallowing abilities. Survivors of a brain stem stroke may also develop paralysis in one or both sides of the body because of the impulses generated in the brain's hemispheres that must travel through the brain stem on their way to the appendiges.
Jill Bolte Taylor, a brain research scientist, experienced and studied her very own stroke in the left hemisphere, but after spending eight years recovering, she feels more enlightened and stronger than before. She gives a very emotional, captivating and detailed description of her experience during and after her stroke on T.E.D talks, for which I have provided the link below!
http://www.ted.com/talks/jill_bolte_taylor_s_powerful_stroke_of_insight.html
References:
http://www.stroke.org/site/PageServer?pagename=EFFECT
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001740/
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