Next time you have a kid and you are searching for first names, don’t forget about the middle name !!!
If she/he becomes a scientist, she/he will definitely have less problem than me when searching for her/his publications in Pubmed…
If I want to see all my publications, here is my pubmed search !
Sigh…
Surely, I know that I did travel for work and conferences before we all had iPads and smart phones. Still, I can’t understand how I survived it all. Especially not when my husband can now placate my homesickness with adorable stuff like this…
April and May are incredibly busy months for me. This is when all of our major scientific meetings happen. At the end of April is the Experimental Biology meeting. There, I get to get my geek on and learn about new and exciting physiology, but really from a “basic science” perspective. (I put “basic science” in scare quotes, because I think it’s not a relevant term in physiology, especially given how many of are doing applied research. Still, my clinician friends love it, so onward we march.) Then, at the beginning of May I attend the Pediatric Academic Societies(PAS) meeting. This meeting tends to be more clinically-oriented, with focuses on model-based research, patient population research, and clinical practice. I like this mix and I almost always leave with more questions than I could ever answer in a lifetime.
I’m at PAS now and one of the major themes, as it was last year, is stem cell therapy to treat pediatric diseases. Diseases like bronchopulmonary dysplasia, type 1 diabetes, acute respiratory distress syndrome in the intensive care unit, etc. One of the statements that I’ve heard repeatedly is that stem cells traffic to the damaged/affected/diseased tissue, do that thing they do, someone usually says “inflammation”, and then the cells “disappear.” Some of the theories commonly thrown around are that they either differentiate or undergo apoptosis when their work is done (a programmed cell death).
That would be very noble of those little cells, either fading away into the background or throwing themselves on their proverbial caspase swords after their the job is done. Wouldn’t it?
(Image and quote sources here, here and here)
I don’t think it’s that simple and, every time I hear someone suggest that stem cells just “go away”, I want to grab them and yell, “BUT HAVEN’T YOU SEEN THIS???!?! OMFG, IT’S THE MOST AMAZING THING I’VE EVER SEEN! EVER!!1!!11!!!!ELEVENTY!1!”
The “THIS” I refer to is work done by my colleague, respiratory physiologist Dr. Jahar Bhattacharya and his group at Columbia University. At the last two Experimental Biology meetings, Jahar presented his findings that the reparative prowess of bone marrow derived stromal cells comes from their ability to transfer their mitochondria. That is, in a mouse model of experimentally-induced lung injury, BMSCs create channels to the damaged alveolar epithelium and send their mitochondria over to repair the injury. The mitochondria transfer restores the normal metabolic function of the damaged cell. To demonstrate this, the group stained the cells green and mitochondria red. Then, using intravital microscopy, the group observed the transfer of mitochondria between the BMSCs and alveoli and the associated increase in ATP production.
This is part of Figure 1 from the paper. Note the cells in green and mitochondria in red. License for non-profit use granted by Nature Publishing Group.
As I mentioned, I’ve heard Jahar speak about this work on a couple of occasions. Most recently, he showed video of the mitochondrial transfer during a banquet in which he was talking about serendipity in science. It’s still the coolest damned thing I have ever seen. He noted that his group only noted this phenomenon because they had originally grown their BMSCs too densely. When they examined the cells, they found all of these projections. Each time I’ve heard about his work, I have wondered what other organelles these cells might be transferring.
I think this organellar transfer hypothesis might be important in explaining some inconsistent results in the literature. In a paper last year in Pediatrics Research, Sutsko, et al. examined the efficacy of MSCs versus their growth media in a rat model of bronchopulmonary dysplasia, also called chronic lung disease of prematurity. Several groups have investigated the use of growth media because 1) it seems to be at least partially efficacious and 2) people are still concerned about the long-term safety of stem cell injection. Especially in the lung. These authors followed the rats for 100 days after treatment and found that both media and MSCs improved lung development, but the MSCs were more effective. They tracked MSCs engraftment by instilling MSCs whose nuclear DNA had been transfected with green fluorescent protein (GFP, or that stuff that people use to make glow-in-the-dark sheep). This should cause the MSCs to make GFP and glow green. They instilled the stem cells into the trachea and, after 100 days, stained for GFP and found little remaining fluorescent signal. These authors concluded that the cells had not engrafted into the lung and, thus, the cells and media must be working by releasing mediators (a so-called paracrine mechanism). This puzzled me though. What mediators would the cells release that wouldn’t be in the media? Perhaps, as Jahar’s work would suggest, the effects aren’t paracrine at all. Perhaps in this case the MSCs were more effective because they could transfer their mitochondria. Because the GFP gene wouldn’t be in the mitochondrial DNA, they’d never find them using this technique.
I offer the caveat, though, that this is all probably pretty speculative.
So, where have all the stem cells gone? And how do they repair damaged tissue? I have a feeling the answer is even more amazing than we think…
I am happy to announce that I am the Guest Editor, along with Phil Ainslie and Niels Secher, of a Research Topic titled “Cerebral oxygenation in health and disease states“. This great opportunity will permit to bring together the leaders in cerebrovascular physiology around this exciting topic.
Are you interested in contributing to our Research Topic ? You are welcome to send us an abstract/outline of work related to cerebral oxygenation (no longer than one page) by clicking on the “Submit Abstract” link on this page. Authors will then be notified by the host editors whether their abstract/outline has been accepted. If accepted, authors will have the possibility to submit their manuscript online.
You can find more information regarding our Research Topic and instructions for authors HERE.
(This entry is cross-posted from Le Physiologiste)
In my last post, I looked at the influence of energy drinks on ambulatory blood pressure in healthy volunteers. Here, I will look at another study dealing with Red Bull energy drinks.
In that study, Astorino et al. investigated the influence of one serving of Red Bull energy drink (80 mg of cafeine and 1000 mg of taurine) on sprint performance and rating of perceived exertion in women athletes.
More specifically, this study used a randomized, placebo-controlled, single-blind crossover design, where one can of Red Bull (255mL; 110 kcal) or placebo (190 mL of Canada Dry Gingerale containing 91 kcal mixed with one package of lemon-favored Crystal Light containing 5kcal and 64 mL of cold water) was consumed one hour before exercise.
Then, following a dynamic warm up, repeated ‘all-out’ sprinting (24 sprints separated into three sets of eight trails of the t Test) were performed on a soccer field by each subject where sprint time, heart rate and rating of perceived exertion were assessed on a regular basis. On a second day of testing (at least 72 h after the first experimental day, but no more than 96 h), this protocol was repeated.
The figures below (source) show the main results of this study:
Sprint performance
Although sprint time was different across bouts, the energy drink had no beneficial impact on that variable vs. the placebo. In addition, Red Bull had no impact on mean sprint time between the 3 sets of eight sprints.
Interestingly, the authors reported that 5 of 15 subjects (3 caffeine users and 2 non-users) improved their performance with Red Bull, 5 (4 caffeine users and 1 non-user) improved their sprint performance with the placebo, while the remaining 5 subjects showed no difference in performance between experimental drinks.
Rating of perceived exertion (RPE in the figure)
Although rating of perceived exertion was different across bouts, the energy drink had no influence on this variable vs. the placebo.
Heart rate
Heart rate increased from the beginning (after 4 sprints) until the end (after 24 sprints) of the exercise protocol but again, the energy drink had no beneficial impact on that variable vs. the placebo.
The authors suggest that the caffeine content in the energy drink may have not been enough to enhance performance. In addition, since this study was performed in women athletes, these results may not be generalized to inactive individuals or men athletes.
In conclusion, findings suggest little benefit of one serving of Reb Bull containing caffeine, taurine, and carbohydrate on repeated sprint performance in women athletes
So, does Red Bull give you wings ??
Reference
Astorino TA, Matera AJ, Basinger J, Evans M, Schurman T, Marquez R. Effects of red bull energy drink on repeated sprint performance in women athletes. Amino Acids 2011 (Ahead of print) doi:10.1007/s00726-011-0900-8
As I have already mentioned in a previous post over at Scientopia’s Guest Blogge, the regulation of energy drinks is currently inadequate and considering the growing number of reports describing serious adverse effects following inappropriate energy drink consumption, there is a need for well-designed studies that investigate the influence of these drinks on human health.
A pilot study recently published looked at the impact of a commercially available energy drink vs. an equivalently dosed caffeine control supplementation on 24-hour ambulatory blood pressure in 9 healthy volunteers (mean age: 28 years; body mass index: 28 kg/m2).
The volunteers were required to randomly consume study beverages (80 mg of caffeine in an 8-oz bottle of water OR 8.3-oz can of Reb Bull Energy Drink containing 80 mg of cafeine and 1000 mg taurine) at 4 scheduled times (08:00, 11:00, 15:00 and 19:00). Blood pressure was measured every 20 minutes during the day and every 30 minutes during the night by an ambulatory blood pressure monitoring.
Different variables such as systolic, diastolic and mean blood pressure, systolic and diastolic blood pressure load (the percent of blood pressure readings exceeding a given blood pressure threshold) and percent nocturnal dipping and dipping status (dipper or nondipper; defined as a decline of 10% or more in nighttime blood pressure) were also determined.
The figure below (source) shows systolic and diastolic blood pressure patterns from the ambulatory blood pressure monitoring during each condition.
Overall, mean 24-hour systolic, diastolic and mean blood pressure measurements were higher with the consumption of the energy drink vs. the caffeine supplementation. In addition, daytime diastolic blood pressure was elevated and trends toward higher daytime systolic and mean blood pressure and nightime diastolic blood pressure were reported with the consumption of the energy drink vs. the caffeine supplementation.
Systolic and diastolic loads were higher during with the energy drink supplementation. No difference was reported regarding nocturnal dipping. Further analyses included in this manuscript suggest that estimated average usual daily caffeine intake had no impact on the results.
As suggested by the authors, other ingredients contained in Red Bull Energy drinks may potentiate the blood pressure response to caffeine (pharmacodynamic or pharmacokinetic interactions). In fact, the combination of caffeine and taurine (with purported effect on cardiac force of contraction) could contribute to the more important elevation in blood pressure with the consumption of the energy drink compared to the caffeine supplementation.
The fact that the subjects randomly consumed both experimental drinks definitely represents a strength of this study. However, the authors underline that these observations are limited by the small sample size of healthy individuals and cannot be extrapolated to other energy drinks. Another important limitation is that the investigators did not directly observe the consumption of the experimental drinks.
The consumption of the drinks in an unblinded manner, the absence of a placebo drink without caffeine and the absence of a strict control regarding the consumption of other beverages and food during each 24-hour study periods are other limitations of this pilot study.
Although this study provides very interesting preliminary observations, further studies are warranted to support these results in healthy individuals.
References
Franks, A. M., Schmidt, J. M., McCain, K. R., & Fraer, M. (2012). Comparison of the Effects of Energy Drink Versus Caffeine Supplementation on Indices of 24-Hour Ambulatory Blood Pressure. Annals of Pharmacotherapy, 46(2), 192–199. doi:10.1345/aph.1Q555
A few months ago, I’ve decided that my other blog would be solely dedicated to cerebrovascular physiology and I’ve started to archive posts that are unrelated to the brain. Two of these posts are about energy drinks.
I’m interested in the influence of these drinks on health since the end of my postdoc and I would really like to continue blogging about it in the future and I consider that The Boundary Layer would be a great place to do so.
As an appetizer, I will thus present you these two posts about the impact of Red Bull on 1) ambulatory blood pressure and 2) exercise performance.
I’m sure that you’ve all felt dizzy at least once in your life when standing up from a supine position. This sudden change in position is associated with a lowering in the amount of blood returning to your heart (venous return), the amount of blood going out of your heart (cardiac output) and blood pressure. Although the reduction in blood flow to your brain (and thus oxygen level) is limited because of its capacity of autoregulation, orthostatic intolerance with associated symptoms such as dizziness is not uncommon in healthy individuals like you and me. However, in healthy individuals, postural hypotension rarely leads to a loss of consciousness (syncope).
This being said, its not the same ball game for individuals prone to syncope. In these subjects, prolonged standing is associated with vasodilatation and a reduction heart rate (vasovagal reaction). These changes are triggered, in most part, by a lowering in central blood volume, a consequence of the pooling of blood in their legs. These individuals may experience numerous losses of consciousness, from several times a year to several times a day !
Are these individuals sentenced to lose consciousness their entire life? Is there a way to attenuate orthostatic intolerance? Some researchers have been interested in that issue and found that, in healthy volunteers, the reduction in brain blood flow (and oxygen level) is attenuated by muscle tensing (that is pressing the legs against each other). Interestingly, leg crossing and muscle tensing are also associated with increased orthostatic tolerance in individuals prone to syncope. So, a simple movement can delay, or even prevent, a loss of consciousness in these individuals.
So, next time you see a move like this…
and there is no boom box nearby, it’s not a new breakdance move, it’s most likely muscle tensing!
Yesterday, I’ve been interviewed by a journalist who will write a series of articles related to the future of young researchers in our Faculty. Several themes, unrelated to our research interests (these articles will appear in a newspaper, not a scientific journal), will be covered over a couple of articles. I have been chosen by my Faculty to participate to that series.
Although the journalist made it clear that the focus of the article wouldn’t be about my area of expertise, she nevertheless asked me to present myself and to talk about my background that led to my position as an assistant professor at the Department of Kinesiology at Université Laval.
Me: Oh…tricky question !
Journalist: Why ??
Me: Well…
I’ve a bachelor degree in Kinesiology (obviously!)…
I’ve a master’s degree in Experimental Medicine, with a focus in exercise physiology (no, I’m not a physician)…
I’ve a PhD degree in Pharmacy, with a focus in exercise physiology (no, I’m not a pharmacist)…
During my postdoc, I’ve worked in a department of anesthesia with a focus in cerebrovascular physiology…
Journalist: hmmm
Me:
I admit that I don’t have the most straight forward path for a physiologist who works in a Department of Kinesiology !
Can you beat my sinuous path ??
My son and I are huge fans of the Big Bang Theory. While I will admit to feeling conflicted about the stereotypical portrayal of geeky, awkward, unattractive scientists a la Amy Farrah Fowler, this is far outweighed by how darned loveable I find Sheldon Cooper. Any time I am feeling down, I watch the Rock, Scissors, Paper, Lizard, Spock bit and my mood is instantly improved.
Last week’s episode in which the ladies attempt to play hooky to go to Disneyland but end up having to talk to a group of girls about being “women scientists” left me with a lot to think about. You see, part of being a woman and a scientist (at least if you happen to be me) is that you get asked to talk ~20% of the time about your science. ~80% of the time, you get asked to talk to people more junior about being a woman with a family who happens to be a scientist. A lot of the time, these end up being really meaningful conversations. But, some of the time, it ends up going like it did on the Big Bang Theory…
…where you get asked to give what I would call a “pep talk” to girls. To tell them that they can be anything they want to be.
And, you always get asked to give these sorts of talks in your free time when you really just want to be playing hooky with your friends.
I find these sorts of talks trite and out of touch and I don’t think it’s the sort of information young women really want. I don’t think that girls believe they couldn’t be scientists, per se. The question is, why would they want to be scientists? And, why would they want to stay scientists after all the years of training they endure. That’s a hard question to answer and, I’ll be honest, I don’t know that I necessarily know the answer. No single woman scientist can really be expected to espouse on the enormity of “women in science.”
I’ve come to realize that the only thing I can do that feels truthful when I’m asked to give these sorts of talks is to speak honestly about the experiences that I’ve had and the strategies that I use to survive my life. I once felt bad for not being able to fully discuss the totality of the problem, but I also don’t believe that’s what people really want to hear.
Mostly, they just want to hear about how we “balance” work and family. I don’t know how other women answer that question, but for me there really is no “balance.” I heard an analogy a few years ago that I now use when I answer this question. My life is most like an endless game of Whac-a-Mole. I just whack whatever’s sticking up and try to pretend the other stuff doesn’t exist for the moment. Good enough.
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