Cracking your knuckles

We all hear people say, "Don't crack your knuckles! It will give you arthritis!” But is this an old-wives’ tale or is there some truth to this? Afterall, it does seem like the joint becomes stressed repeatedly.

Before we can decide we should see what is happening in the joints when that popping happens.  Gases are continuously dissolved in this fluid. This capsule is stretched when you crack your knuckle and lowers the pressure inside the joint. This creates a vaccum that becomes filled with the gases previously dissolved in the synovial fluid. A “bubble” is formed which then bursts and creates the popping sound.  These gases take a while to re-dissolve which explains why you cant re-crack your knuckles immediately after. 

However, there is no evidence cracking your knuckles does any damage or cause complications later. The only reports of injury come from over stretching ligaments or dislocating tendons. A study did find that habitual knuckle crackers may have reduced grip strength. So for now there has not been any link found in popping your knuckles and arthritis. Although, there have not been many studies done on this subject either. I would not be surprised if in the future this link may be found.


http://www.hopkins-arthritis.org/arthritis-news/2007/knuckle-cracking-and-arthritis.html

Platelet-RIch Plasma Therapy

Hey guys, so today in class on the arthitis discussion, our first lay article discussed the woman who had the platelet- rich plasma therapy done on both of her knees. We all were curious as to exactly what the goal of it was and what not so I decided to do a quick search and see what basics came up on the subject. So when searching it one of the frist results led me to a site about the Orthohealing Center, it has some interesting stuff on the site (Link at the end). So they claim the PRP is a a way to heal tendon injuries and osteoarthiritis without a significant risk. Well in my point of view they still do not have good explanations or studies proving that this is not a significant risk to the patient. The main aspect of the platelet they are looking at is the many growth factors they have and their ability to help in wound healing. The goal is to gather many growth factors to enhacne and accelarate healing but I am not sure how well it really works or safe it is, I would still be tenative to do this. What they are now trying to do is specifically isolate certain proteins to help healing and decrease inflammation. Since they use the patients own blood they explain how you cannot just use anybodys platelets to do the procedure. I would suggest clicking on the link within here to cytokine therapy, it is within the text and is kind of interesting. It basically discusses how everyone reacts differently to the procedure and therefore they uses cytokines to help drive the PRP and either increase or decrease the rate of someones healing based on how they are reacting to the procedure. Overall I found it interesting that this PRP therapy is more out there than I thought it was considering I was not completely aware of this therapy until reading the article for today.

Hope you guys find this interesting in some way!

Link: http://www.orthohealing.com/plateletrichplasmatherapy-prp/

Michele J

p38 & arthritis inflammation- p495k Hwisun Lee

Hi, I am hwisun Lee PSIO 495k discussion class. When we discussed The article that was concerned about CNS controlling arthritic join inflammation... But it did not mention about how important p38 signal is affecting the inflammation. So people do not really have any idea of how p38 works in actual system. So here is my suggestion for you to look at it. This is the general signal cascade in our system. http://www.sabiosciences.com/pathway.php?sn=P38_Signaling Please look at P38-alpha, Beta, gamma and Delta right before it signals to nucleic level where Gene expression occurs. It does make some sense why they want to control the level of p38 signal for treatment of inflammation. Thanks. P.S p38 does not only affect by inflammation but other stresses such as diabetes, etc.

Alternative Remedies for Knee Osteoarthritis? Quite Possibly!

Reading about alternative remedies that claim to treat arthritis, I was naturally interested in if they actually worked. The major ones in the articles I read were boswellia, chondroitin sulfate, glucosamine, and MSM. I was able to find articles on each the specifically studied how effective it was in treating symptoms of  knee osteoarthritis.

Boswellia Serrata is the resinous gum (guggulu) of the boswellia tree. In a double-blind, placebo-controlled study (http://www.sciencedirect.com/science/article/pii/S0944711304701890), Boswellia demonstrated beneficial effects on knee osteoarthritis. 30 patients were given either 333 mg Boswellia capsules or placebo 3 times a day (~1000mg daily) for 8 weeks. Those that received BSE (Boswellia Serrata) in the first intervention crossed over to receive the placebo in the second intervention and vice-versa. Before and after each intervention patients were asked to grade the pain intensity, loss of function, and swelling. Patients in the Boswellia group experienced a significant decrease in pain and swelling and increase in range of motion compared to the placebo.

A similar study was done on knee osteoarthritis but instead measured the efficacy of methylsulfonylmethane (MSM). http://www.sciencedirect.com/science/article/pii/S1063458405002852. A similar randomized, double-blind, placebo-controlled trail was conducted but with 50 men and women. Patients were given 3 g of MSM or placebo twice a day for 12 weeks.

Results conclude that MSM improved symptoms of pain and physical function during the short intervention without major adverse events but long-term improvements cannot be concluded. Researchers suggest that MSM be used for short term intervention when NSAIDs and COX-2 drugs are ineffective.

Finally I chose to research chondroitin sulfate and glucosamine in a combined study on knee osteoarthritis (http://www.nejm.org/doi/pdf/10.1056/NEJMoa052771). Once again, a double-blind placebo study was conducted but with over 1500 patients. Patients received 1500  mg  of  glucosamine  daily,  1200  mg  of  chondroitin  sulfate  daily,  both glucosamine and chondroitin sulfate, or placebo for 24 weeks. Overall, glucosamine and chondroitin sulfate were not significantly effective compared to the placebo group in reducing knee pain. But the study does point out that in moderate-to-severe knee pain patients, both chondroitin sulfate and glucosamine revealed more effective results.

Based on these 3 studies, MSM and Boswellia Serrata seem to be effective in treating knee osteoarthritis BUT due to their small group size and short experimental period, this may only be effective for short term intervention. In comparison to the glucosamine and chondroitin sulfate study, it had a much larger group size and testing period but was not significant in treating symptoms of OA. It would be interesting to retest MSM and Boswellia Serrata with a larger group size and experimental period to see if it shows the same results. In addition, it would be interesting to test on other parts of the body or other forms of arthritis such as RA. 

Not all (round)worms are created equal...

As discussed in class, clinical studies are now underway to determine if helminth-based therapies are effective against IBD. Helminth-based treatments seem to switch the intestinal immune response from Th1 to Th2, thus calming down the symptoms that are associated with IBD. As life with IBD is certainly unpleasant, people are starting to self-diagnose and treat with helminths purchased online (yikes!). However, even though the human body may have evolved in sync with particular helminths, it is important to note that the associated mortality of parasitic infection far outweighs the morbidity that accompanies IBD. 


First off, it is shocking to me that nearly 9 million children (ages 0 - 5) die every year. The United Nations' Reduce Child Mortality Fact Sheet notes that these deaths are "related to malnutrition and lack of access to adequate primary health care and infrastructure, such as water and sanitation". Of these 9 million children, it is estimated that 1.5 million die from acute diarrhea, which is still the leading cause of child mortality  in developing nations. 


Diarrhea has a impressive list of causes but for this discussion let's focus on helminth infections. Trichuriasis and ascariasis infections are the most common chronic diseases that infect the poorest populations of developing nations. Both trichuriasis and ascariasis are caused by roundworms.Trichuriasis is estimated to infect 100 million people annually while there are 84 million cases of ascariasis per year. 


Trichuriasis is a roundworm infection that mainly affects children. Symptoms include bloody diarrhea, anemia, fecal incontinence, and rectal prolapse. Ascariasis is also caused by the digestion of roundworm eggs. The larvae start in the small intestine but move through the bloodstream and into the lungs. From the lungs, the parasite moves up and out, is swallowed back into the stomach and the cycle repeats itself (seriously... I think I just puked in my mouth a little...). The symptoms include bloody sputum, vomiting worms, and passing the little guys in your stool. If there is a large number of the roundworms present they can actually cause an intestinal blockage! 


It's interesting that in "developed" nations, the environment has become so clean that we've essentially created a new list of problems (case and point: IBD). However, with the excitement of helminth-based therapies for the treatment of IBD, it is important not to forget the true cost of parasitic infections around the world. 

Exercise Effects on IBD

So as I mentioned in class, I was interested in finding further information on the effects of exercise (in particular, anaerobic or higher resistance training) on IBD. While I could not find any specific articles about reistance training and IBD, I did come across a few articles that were interesting:

This first article (link to summary: http://www.nature.com/ajg/journal/v94/n3/abs/ajg1999153a.html) discusses how low intesnity exercises are beneficial for IBD patients. These patients simply did walking routines 3/day for 12 weeks, and they found that it improved the morbidity in these patients. What I find interesting in what
There (I could not find a link to the full pdf, so this may be mentioned somewhere in the full article) was no information on higher intensity exercise, and why it would not also be beneficial, or detrimental, to the patient's health.

When I read the paper the first time through, I assumed that this was intended for sedentary patients with moderate to severe CD, but the study was actually done on subjects with low to non active CD. It would be very interesting to know how more moderate exercise would effect their symptoms, if at all.

This next article (link: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2660805/?tool=pubmed) was very interesting, because it talked about different types of exercises and different studies done comparing exercise and IBD. One thing I didn't think about was the relationship between stress, exercise, and IBD. This paper brings up the point that exercise helps to lower stress levels. Since stress is considered a contributor to IBD, this paper theorized that this was one way in which exercise contributed.

Another interesting point this article brought up was that CD is linked to muscle deterioration in the lower limbs, but not the upper limbs. Based off of this, I think it is safe to say mild to moderate resistance training can be beneficial in patients suffering from CD, or are at risk for it.

The paper goes on to say in the summary (this was also mentioned at the beginning) that many of the clinical studies used to conclude that exercise is beneficial were too limited in their parameters, and more work needs to be done to conclude this. The authors of the paper believe that while exercise is good for treating symptoms of IBD, it does not alter the course of the disease.

If you have a chance, read this- it is a good read, even though it is basically just bringing in other papers to put together its information.

Obesity plus Pregnancy....more bad news

I saw this article earlier this month as I was reviewing for my Mineral Metabolism Exam.  In an earlier blog "ManasaK495" had discussed an article from WebMD which spoke of various birth defects that are linked with obesity.  The article, "Maternal Obesity Puts Infants at Risk of Iron Deficiency" adds another fear factor for the obese mother. 
  According to the author, obese mothers may also be putting their child at risk for iron deficiency anemia and thus possible brain development issues.  Iron deficiency for infants can be possibly even more harmful than in adults.  For the newborn/infant "50% of iron" obtained prior to birth is what is needed for growth. 
  Iron metabolism and usage is a very complicated and extensive network of pathways but put simply iron enables red blood cells to be made.  Without these, how can a human survive?  More importantly, how can a fetus develop properly without the iron that is neccessary being present?  Along with the aforementioned / discussed birth defects and issues, these fact may be some key talking points for a medical professional to an obese woman who is considering having children in her future.  As no woman ever wants to put her child in any sort of danger, this information may motivate the patient/individual to make the lifestyle changes towards improving her metabolic/weight profile that will decrease the morbidity risks for herself and her future child.

Article link:    http://www.sciencedaily.com/releases/2011/04/110430133125.htm

American Academy of Pediatrics (2011, April 30). Maternal obesity puts infants at risk of iron deficiency. ScienceDaily. Retrieved March 19, 2012, from http://www.sciencedaily.com­ /releases/2011/04/110430133125.htm

Flavones in citrus fruit lower the risk of ischemic stroke

You've all seen countess news articles claiming that some natural product found in food reduces the risk of cancers, heart disease, and other complications.  In order to pose any semblance of credibility, the writers of these articles generally reference supporting studies and list a few facts, including popular "buzz words."  While I'd venture to say that a majority of these articles are written in order to gain publicity, some are actually worth reading.

This article in The Clinical Advisor (Citrus Fruit linked to Lower Ischemic Stroke Risk briefly describes the findings of a study in Stroke (Cassidy A et al. StrokeDietary Flavonoids and Risk of Stroke in Women).  The study found that women who intake a higher dose of flavone from natural citrus juices are less likely to experience stroke over a 14 year period than those intaking a lower dose in juices.  The same trend held for whole fruits and supplements.  However, the news article author claims that total flavonoid intake is not (proportionally) related to reduction of stroke.  The author did not elaborate on this confusing point, but the study article reported that it was merely the flavone subclass found in citrus fruits that reduced the risk of stroke, not the overall total flavonoid intake.

The writer of the news article did a good job of including some numbers from the study, including p-test statistical values.  And while the article did not give too much detail on the study or specific reasons as to why flavone intake reduced stroke risk, the author did link the study article towards the bottom.  Overall, I think the writer did a decent job of portraying the "tip of the iceberg" of the Stroke study, just enough to peak someone's interest in reading the paper.  While many factors contribute to stroke risk besides possibly flavone intake, no harm generally comes from eating fresh citrus fruit, and it can be a tasty method of contributing to your health.  Just don't overdo it!!!

Quickly Identifying a Stroke

I’ve heard of quick assessments for emergency situations before, but I did a little search and found a way to remember what to do in a ‘stroke’ situation!

The onset of the damage from a stroke is not always immediate; there can be up to a period of a couple hours in which someone can be treated and the effects of the stroke would be less fatal. Like learning first aid and CPR, there are some simple questions one can use as a basic determinant on whether you might think someone has had a stroke, and to act immediately.

These questions focus on facial weakness, arm weakness, and speech disturbance

Just remember the first 3 letters of “stroke” – STR

S= SMILE!  Ask the person to smile. Another test that is common is to ‘STICK’ out their tongue. If it is crooked to the side, that can be an indication of a stroke

T=TALK and Speak a simple sentence. Ask the person to say a short sentence such as “It is sunny out today”

R= RAISE both arms!

If the person has trouble with any one of these symptoms, get them help quickly! You may save someone’s life!

http://medicine.uab.edu/neurology/DivsPgmsCtrs/cerebrovascular/CSRC/72348/

Second Hand Smoking and IBD

Hey all, as you all have read (or will read), there is an article called Smoking, Nicotine, and IBD. There is a vague reference to SHS and IBD, and I was interested, so I looked up some information.  The following link is to an article analyzing just that:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2998445/

This article suggests that second hand smoking, especially in developing countries, can have detrimental effects on children, the effect this article analyzed being IBD. The article essentially says that a reduction in exposure to SHS will mean a reduction in children with IBD, but there needs to be more extensive studies done in developing countries.

What I didn't like about this article was that the researchers just pulled together a bunch of other scholarly articles, and based their findings and opinions from this. While their results and conclusions are interesting, I would really like to see some more research done in developing countries where instances of IBD are high.

Ethan Burns

Reduced reperfusion injury from decreased expression of P-selectin

Hello All,
   After the discussion of the stroke articles this week I started to think that there are a lot of studies being done to reduce reperfusion injury after a stroke by manipulating inflammation. However, inflammation is our bodies way of healing itself and it wouldn't activate if there wasn't a good reason, so why would we want to interfere with something that's designed to help us? Then after thinking over some of the articles it seemed to me that it's not inflammation that causes reperfusion injury, rather it's over activation that causes damage due to inflammation. Thus, thinking that there had to be a better method of reducing reperfusion injury, other than manipulating inflammation, I searched the internet and found an awesome research article in the Journal of Immunology that did just that.
   The article "Complement-Dependent P-selectin Expression and Injury Following Ischemic Stroke" Looks at the affects of reperfusion injury on three groups of mice 1) wild type normal, 2)C3-deficient (complement deficient), and 3) CR2-Crry induced mice. CR2-Crry is a complement inhibitor that inhibits complement at the C3 stage and targets to sites of complement activation. Furthermore, by reducing complement the researchers were also looking to see a reduction in P-selectin expression, as P-selectin has been linked to promoting leukocyte adhesion, platelet aggregation and coagulation, and may also increase complement activation. In reducing these factors, the researchers were hoping to see a significant reduction in reperfusion injury in C3-deficient mice and the CR2-Crry induced mice.
   According to the experiment the mice were subjected to 60min MCAO (Middle Cerebral Arterial Occlusion) induced ischemia and 24hrs of reperfusion. With the results showing 62% survival rate of the normal group, 100% survival rate of the C3-deficient group, and an 80% survival rate for the CR2-Crry induced mice. Furthermore, both the C3-deficient and the CR2-Crry group mice were shown to have statistically significant protection from tissue and neuronal damage, as well as improved neurological function compared to the control group.
   Moreover, when looking at the presence of P-selectin, it was found that there was great expression in the control group, no expression in the C3-deficient group, and very little or no expression in the CR2-Crry group. Furthermore, expression of P-selectin mRNA levels in the cerebro-vasculature were high in the control group but were significantly reduced in the the other two groups. The results further go on to reveal that the presence of micro-thrombi and residual thrombus were less present in the C3-deficient and CR2-Crry mice than in the control.
   Of all the results however, the discussion focused on the CR2-Crry group as this was the group of interest through out the experiment. The results from this group for all tests performed showed similar results to the C3-deficient group. More importantly, according to the researchers the CR2-Crry complement inhibitor was shown to "provide appropriate bioavailabity in cerebral injury to enable complement inhibition, at a dose that will not significantly affect systemic levels of serum complement activity or host immunity to infection.
   Overall, I thought this article was really cool, especially with what the researchers did with the CR2-Crry group. According to the article they administered .25mg of the complement inhibitor via an I.V. tube 90min post ischemia and 30min post repurfusion. I didn't find anything in the article that explained why they chose that specific dosage or time to administer the inhibitor though. Regardless though, I truly liked how the researchers aimed to find a method that could reduce the activation of complement without shutting it down completely and putting the host at risk for infection. Moreover, the colored scans and graphs this paper contains really helps put the data into perspective. More experiments definitely need to be done regarding this procedure, but I could see this as a feasible method for use on human stroke sufferers to help the recovery process. Well I think I've talked enough, you've heard me hit the high points of this paper and give my thoughts, so why don't you follow the link, read the paper yourself and give me your thoughts on it?

http://www.jimmunol.org/content/177/10/7266.full.pdf