via ted.com
Another wonderful TED talk! Relevant to our discussion of Bacterial diversity and communication in Biol 1B this week.
What about Lindsay Clancy?
2 weeks ago
Showing posts with label medicine. Show all posts
Showing posts with label medicine. Show all posts
Thursday, March 18, 2010
Wednesday, March 17, 2010
Rebecca Skloot brings Henrietta Lacks to the Colbert Nation
I'm still reading Skloot's fascinating account The Immortal Life of Henrietta Lacks, which I started reading during Black History Month, and will finish soon before Women's History Month ends.
Tuesday, February 2, 2010
The immortal HeLa cells and their source, Henrietta Lacks
via abcnews.go.com
ABC World News aired this story last Sunday, which includes a short interview clip with Rebecca Skloot, whose book The Immortal Life of Henrietta Lacks is just hitting the stores. And yes, the woman's name is Lacks - but lame as it seems, the ABC website and video have misspelt it!! The story itself is quite remarkable, and really well told. I will try to post a review of the book here as I'm hoping to finish reading it soon.
Thursday, May 7, 2009
Your term papers better not have cited papers from these "journals" from Elsevier!
I expect it is unlikely that any of the evolution term papers just turned in may have cited from these "biomedical journals" published by Elsevier - but this breaking scandal in the world of scientific publishing highlights the need for good critical evaluation and thinking skills so you can separate the scientific wheat from the drug companies' (and other vested interests') chaff. If you haven't heard about this scandal, it started with the discovery that the big pharma company Merck had paid Elsevier to publish fake journals made to look like they were peer-reviewed! (quick, how many of their journals have you read/cited in the recent past?) Now it turns out, they published at least SIX such "journals":
Scientific publishing giant Elsevier put out a total of six publications between 2000 and 2005 that were sponsored by unnamed pharmaceutical companies and looked like peer reviewed medical journals, but did not disclose sponsorship, the company has admitted.
Elsevier is conducting an "internal review" of its publishing practices after allegations came to light that the company produced a pharmaceutical company-funded publication in the early 2000s without disclosing that the "journal" was corporate sponsored.
The allegations involve the Australasian Journal of Bone and Joint Medicine, a publication paid for by pharmaceutical company Merck that amounted to a compendium of reprinted scientific articles and one-source reviews, most of which presented data favorable to Merck's products. The Scientist obtained two 2003 issues of the journal -- which bore the imprint of Elsevier's Excerpta Medica -- neither of which carried a statement obviating Merck's sponsorship of the publication.
[via Elsevier published 6 fake journals :The Scientist [7th May 2009]]
If some of our students already had trouble telling if a particular journal is peer-reviewed - Elsevier just made it harder. And while students citing something from one of these fake journals for a term paper may not seem like such a big deal, the real problem here is, of course, the intended target readership for these "journals": doctors and other practitioners in the biomedical fields! How much time does your doctor have to look behind the curtain of such publications to decide if a paper about some drug trial is trustworthy? Do medical (and related professional) schools emphasize critical thinking skills enough to safeguard against such fraud? (I have some doubts about that given how many doctors are creationists - but that's another story).
What's even more unfortunate is that this scandal is breaking at a time when the anti-vaccination movement seems to be reaching a peak in the US (and increasing the casualty count of children around the world) - with Oprah jumping on that anti-science bandwagon last week! These purveyors of anti-science woo would probably eat up a story like this as further evidence that all of science is untrustworthy and how you cannot believe anything they say in any scientific journals! Why, oh why did Elsevier have to go and muddy the bathwater so much more when there's already a growing mob straining to tip over the tub, and toss out the baby (science) as well?!
Sunday, May 3, 2009
A perfect storm for viruses
According to Nathan Wolfe, a virus hunter interviewed last week in another TED Q&A, "We've created a perfect storm for viruses". An excerpt:
SARS, avian flu, swine flu ... what's going on here? Why are we suddenly seeing so many more outbreaks of viruses from animals?
Viruses have always passed from humans to animals. In fact, the vast majority of human diseases have animal origins. But the human population is different from what it once was. For most of our history, we lived in geographically disparate populations. So viruses could enter from animals into humans, spread locally and go extinct. But the human population has gone through a connectivity explosion. All humans on the planet are now connected to each other spatially and temporally in a way that's unprecedented in the history of vertebrate biology. Humans -- as well as our domestic animals and wild animals we trade -- move around the planet at biological warp speed. This provides new opportunities for viruses that would have gone extinct locally to have the population density fuel they need to establish themselves and spread globally.
We've created a "perfect storm" for viruses. And we'll continue to see -- as we have in the past few years -- a whole range of new animal diseases as outbreaks in human populations. But we have to stop being surprised by them. Right now, global public health is like cardiology in the '50s -- just waiting for the heart attack, without understanding why they occur or the many ways to monitor for them, detect them early and ultimately prevent them. Swine flu is not an anomaly. We know that swine flu -- like the vast majority of new outbreaks -- comes from animals. We should be monitoring those animals and the humans that come into contact with them, so we can catch these viruses early, before they infect major cities and spread throughout the world.
And here's Wolfe's TED talk:
Thursday, April 30, 2009
Laurie Garrett on Flu pandemics, past and future
Courtesy of TED, we have some useful media bringing typically well-informed perspectives on the flu now unfolding. Let's start of with a Q&A with Laurie Garrett, author of "The Coming Plague: Newly Emerging Diseases in a World Out of Balance":
TED took 20 minutes with Laurie Garrett this afternoon to follow up on her TEDTalk from 2007, posted today, about pandemic flu. Garrett is the author of The Coming Plague, and a fellow on the Council for Foreign Relations who studied global health and emerging diseases. (As you can imagine, she is very busy this week.) We asked Garrett: What has changed since the last pandemic panic, 2007's avian flu? What does she worry about now? And really, should we not wash our hands?
TED has also posted video of a lecture Garrett gave in 2007:
In 2007, as the world worried about a possible avian flu epidemic, Laurie Garrett, author of "The Coming Plague," gave this powerful talk to a small TED University audience. Her insights from past pandemics are suddenly more relevant than ever.
Tuesday, April 28, 2009
Applying phylogenetics: Did the California H1N1 swine flu come from Ohio?
Just as we (in Biol 105) finish up studying how phylogenetic trees are estimated, and how they might be used to answer interesting questions, comes this highly topical example - microbiologist and science blogger Sandra Porter spent a happy afternoon applying phylogenetic analyses to try and answer the health scare du jour:
This afternoon, I was working on educational activities and suddenly realized that the H1N1 strain that caused the California outbreak might be the same strain that caused an outbreak in 2007 at an Ohio country fair. Here's the data.
Once I realized that the genome sequences from the H1N1 swine flu were in the NCBI's virus genome resources database, I had to take a look.
And, like eating potato chips, making phylogenetic trees is a little bit addictive. Or maybe it was just the adrenaline rush that hit when I realized that every tree was telling me the same thing.
What did those trees say?
Read the full blog post to study the results yourself, and see what you think of the remarkable concordance between the trees, providing a plausible answer to the question of where this virus may have originated.
In the process, Dr. Porter has also given us all a glimpse at the working product of a fresh analysis - raw results hot off the computer before they are published in a peer-reviewed journal! Is this a first for the blogosphere? I don't know, but given the high level of public interest, I can see why one might want to get the results out quickly. Surely some top science journal would be interested in publishing this quickly as well?
Thanks to Porter's blog, we all get to see how genomic data available in the public domain can be used to help address problems that might affect us in real time! How cool is that?! As I try to impress upon my students every time we discuss the subject: Phylogenies are not just static graphic depictions of inferred relationships between organisms long gone - trees of dead wood, so to speak: they also serve as working models of ongoing evolutionary processes! And often enough, they help us pinpoint the origins of new diseases, in turn helping us develop treatment strategies before the outbreak gets too far out of hand. And how is that for putting those phylogenetic trees to work?
Meanwhile, Tara Smith, of Aetiology (also on ScienceBlogs) following up on Porter's big discovery, notes that the peer-reviewed paper describing the Ohio swine flu strain came out only recently. And here's the bit that really raises the eyebrow, if not the hair on your head:
I also assume this is where the human-avian-swine reassortant claim came from. The authors note that:
The H1N1 viruses contain the HA and NA from the classical swine virus and the internal genes from the triple reassortant H3N2 viruses (rH1N1); the H1N2 viruses contain the HA from the classical swine virus and the NA and internal genes from the triple reassortant H3N2 viruses (Karasin et al., 2002; Webby et al., 2004). Contemporary triple reassortant viruses were demonstrated to have acquired a PB1 gene of human virus origin; PA and PB2 genes of avian virus origin; and the remaining internal genes, M, NS, and NP, of swine virus origin, thus giving rise to the triple reassortant designation (Zhou et al., 1999).
So what it looks like to me is that this isn't a *new* reassortant virus, but is closely related to one that had already been identified in swine--and that had already caused an outbreak in humans right here in the US.
So why is the virus getting so much more media attention this time around? Is the strain in Mexico really the same or different? And if it is the same (or close) how did it get from Ohio to Mexico City and back to Texas and California? Gotta love that globalization, eh!
Wednesday, December 3, 2008
Modeling the emergence of multi-drug resistant TB hot zones
According to the World Health Organization (WHO), a “hot zone” is an area with >5% prevalence (or incidence) of Multi-Drug Resistant Tuberculosis (MDRtb). Sally M Blower and Tom Chou have been using a mathematical method to track the emergence and evolution of multiple strains of drug resistant tuberculosis, but they have now developed a new, more complex mathematical model. Before this model, there was only a two strain model, meaning it was only relevant to individuals that can be infected with a wild type pansensitive strain or a drug resistant strain, but there are many more strains then this. There are a resistant strains only to one drug and some resistant to multiple drugs. This means there is a multitude of strains in these hot zones and there was a need for a better way to track this (Blower and Chou 2004). Blower and Chou realized that a more complex mathematical model is necessary to capture the complexity of the epidemiology of the hot zones, and the evolution of hot zones was very unclear
Understanding drug resistance is important to understanding the, and Blower and Chou explain the evolving of resistance very well. They give three processes that are involved in generating drug resistance: Transmission of drug resistant strains to uninfected individuals, which is transmitted resistance; Conversion of wild pansensitive cases to drug resistant cases, which is acquired resistance; finally, cases where they have drug resistant strains and it becomes resistant to more antibiotics during treatment, which is amplified resistance. What everyone has had to do in the past is just study acquired and transmitted resistance, and now with the new model, they can incorporate amplification resistance. This was a big problem because it has been shown that inadequate treatment of DRtb can result in the amplification of drug resistant strains, which may be an important process of MDR epidemics (Blower and Chou 2004). So this is where Blower and Chou came in. They created a model, the call the amplifier model, that enables the tracking of emergence and evolution of MDR strains, the transmission of these strains and the amplification of these strains during repeated episodes of treatment.
Blower and Chou are really studying the effects of inadequate treatment programs, and how this may lead to a higher prevalence in MDRtb. One problem that this research cannot completely take into account yet is the transmittance ability of MDRtb compared to pansensitive tuberculosis. This is an area that is hazy right now, and so this cannot completely be incorporated into the model. Amazingly, they have measured a general fitness of MDRtb vs. pansensitive tuberculosis, by calculating the treatment fail rates and treatment cure rates of the each category of strains.
The authors were very clear with the purpose of the model. Even though the mathematical model is very complex, the idea and how they explain it is easily understandable. They use R0 to stand for the average number of secondary cases caused by one infectious case in a population where treatments are available. Their model breaks this up into four categories of strains: The wild type pansensitive [R0(1)], which is sensitive to all drugs; Pre-MDR [R0(2)], which is sensitive to one of the main drugs used to treat tuberculosis; MDR [R0(3)], which is resistant to both of the main treatment drugs; and post-MDR [R0(4)], which is resistant to both of the main antibiotics and others as well (Blower and Chou 2004). With the information gathered from over 30 years of date they constructed likely evolutionary trajectories of hot zones, and with this they also took into account low cure rates vs. high amplification probabilities in many areas. They also tried to incorporate which strains are more transmissible, but as I said before this was not really possible with their model and there was a large degree of uncertainty.
The results of their model matched the WHO predictions well, but there were some distinct differences, and I think these differences are what make this research so important. By using all for types (R01-4) they found great variability in incidence and prevalence. When treatments were originally started strains of pre-MDR strains emerged quickly, so incidence and prevalence of pre-MDR strains increased, and this subsequently led to possible amplification of resistance and MDRtb epidemics in certain areas. The question is: Why certain areas and not others? This question is explained by Blower and Chou. Interestingly, areas with bad treatment programs do not necessarily have a really high incidence of MDRtb, it has stayed pretty steady at a 5%-14% (Blower and Chou 2004). This to me seems like an argument that MDRtb is not as easily transmissible, because its rates overall have stayed pretty low, but there was no significant evidence for this. The WHO predictions state that a >5% prevalence OR incidence in MDRtb equals a hot zone. Blower and Chou found the mathematical relationship between MDR prevalence and incidence. MDR prevalence can be three times greater then MDR incidence. They used the results to evaluate the hot zones on prevalence or incidence. If it is by incidence then only 20% of those areas would be considered hot zones and 51% if criterion is prevalence (Blower and Chou 2004). I see this as an argument for the fitness of MDRtb to be very high and transmissible ability to be lower, because there are less new cases, and more cases that have just become more resistant.
When looking at the four strains the hot zones had a much lower R0 for pansensitive strains (median=.82), which suggests that the wild type strain should be slowly eradicated. The R0 for the pansensitive strains in non-hot zones were all above 1 (median=1.39) Looking at the rate of detection of cases and treatment rates in hot zones versus non-hot zones it is 55% to 25% (Blower and Chou 2004). This shows that places where they have control programs were successful at fighting pansensitive strains but ironically it created more MDRtb strains, making it more likely to become a hot zone.
The importance of this research is that they have figured out that the difference between incidence and prevalence rates is significant enough to change the view of an area as being a hot zone or not. Their research looks at many factors that go into the evolution of these hot zones. Out of the many factors they actually saw that case detection and treatment rates were the most important factors. They came to this conclusion because if case detection and treatment rates were low, and the amplification was high, it still did not generate a hot zone. Vise versa, if the case detection and treatment rates were high and the amplification rates were low; it was likely to become a hot zone. The point is that these areas with high case detection and treatment rates should not increase these rates unless high cure rates are achieved first. Blower and Chou have created a model that has multiple dimensions and can help the WHO in the future to prevent hot zones from popping up in high risk regions. The WHO already had a model for this but it was nowhere complex enough to correctly calculate prevalence and incidence of MDRtb, and how their mathematical relationship.
Reference:
Sally M Blower, Tom Chou (2004). Modeling the emergence of the 'hot zones': tuberculosis and the amplification dynamics of drug resistance Nature Medicine, 10 (10), 1111-1116 DOI: 10.1038/nm1102
Monday, October 27, 2008
Marking a quarter century of living and fighting with HIV
Scientific American has a special report out on: HIV--25 Years Later]. Check it out! Here's the editor's introduction:
In 1983 and 1984 scientists established that HIV (the human immunodeficiency virus) causes AIDS, which had recently begun cropping up in gay men in California and New York. The discovery quickly led to predictions that a preventive vaccine would soon be on tap. Similarly, in 1996, after powerful drug combinations began forcing HIV down to undetectable levels in the blood, prominent HIV researcher David D. Ho of the Rockefeller University voiced optimism that attacking the virus early and hard could prove curative.
Yet neither a vaccine nor a cure has materialized. Indeed, the most promising vaccine prospects have failed. And when aggressive treatment stops, the wily virus comes roaring back.
Where do we go from here? Scientific American asked two leading HIV researchers to address the biggest scientific challenges facing the field today: Is finding a vaccine even possible? And what, exactly, would it take to rid a person’s body of HIV and thus effect a cure? Their frank, thought-provoking answers follow.
And if you want to read a first hand account from the early days of what it was like to deal with the beast in the field, my favorite is Abraham Verghese's memoir of the period he spent as a doctor in the South (not those coastal cities) when HIV first hit small-town communities: My Own Country: A Doctor's Story
Sunday, September 28, 2008
A gene to save us from HIV?
Sandra Porter, over at Discovering Biology in a Digital World has a very interesting post up reviewing recent research on a gene that might protect us from HIV and other retroviruses. Well worth reading, given our recent classroom discussions of HIV, and the upcoming lectures where we will address resistance genes, fairly soon! Besides this post is also an excellent model for you to shoot for when writing your own critique/commentary/synthesis for this class!
Monday, May 5, 2008
Evolution of drug resistance in TB
Student post submitted by Pritha Singh
The author first describes the clinical circumstances for the resistance development in Mycobacterium tuberculosis. He states that the reason why drug therapy for tuberculosis is different than the most bacterial infections is due to the long generation time and ability of dormancy in M. tuberculosis. Apart from this, it has a very slow metabolic rate which makes it difficult to target. There are many different populations of the bacterium present within the host. M. tuberculosis may be found in the pulmonary cavities, empyema pus and solid caseous material. The location of the bacterium makes it very difficult for the antibiotics to penetrate or the low pH conditions interfere with the activity of the anti-TB drugs. Thus each of the anti-TB drugs has a unique role in dealing with these different populations of mycobacterium. For example, INH is a drug that is active only against aerobically growing organisms and so it plays a major role very early in the drug therapy against bacteria growing in pulmonary cavities. On the other hand, PZA is a drug only active in low pH conditions thus is used for killing bacilli residing inside the caseous necrotic foci. RIF is most effective in killing the mycobacterium that are metabolizing slowly. Hence, due to the specific roles of these drugs, poor adherence to the drug therapy can result in resistant strains in mycobacterium.
Gillespie goes on to explain the molecular mechanism for the emergence of drug resistance. The way the researchers have started to understand the molecular mechanism of resistance in M. tuberculosis is from the action of these anti-TB drugs. The resistance in this bacterium occurs through single step mutations at the chromosomal level. He states that rate at which resistance emerges is different for all the anti-TB drugs which could be calculated by using the mutation rate. Mutation rate rather than mutation frequency is used to calculate the rate of resistance because calculating frequency has a risk of recording mutation per cell division. However, mutation rate is more apt as it records the proportion of the mutant cells. The author provides an equation and hypothetical calculations for resistance rate in the mycobacterium which suggests that even a small deviation from the standard drug regimen may lead to the emergence of resistance in a TB patient.
To describe the development of drug resistance in M. tuberculosis, the author talks about two anti-TB drugs: streptomycin (SM) and rifampin (RIF). A point mutation in rpsL gene results in high level of resistance to SM which can be categorized into restrictive and nonrestrictive mutations. Restrictive mutations are associated with an attenuation of virulence, whereas nonrestrictive mutations are not. He lists various clinical studies that show that resistant strains were equally divided between restrictive and non-restrictive mutations. However, the author does not explain how SM works on the bacterium or how the mutation in a specific gene leads to resistant strains which could have helped in better understanding of this section. Moreover, he does not mention an additional mutation that takes place in rrs operon which could also lead to drug-resistance.
The mycobacterium strains that are resistant to RIF have a mutation on the beta subunit of rpoB gene encodes for DNA-dependent RNA polymerase. Experimental studies have shown that more than 70% of the RIF’s mutations are restricted to the rpoB gene. He also mentions the study conducted by using the model of guinea pigs that were infected with M. tuberculosis in which katG gene was inactivated. These studies showed that the virulence of the strains was far less than the parent strain. However, the virulence was restored when katG gene was reintegrated in the genome. The author does a fair job in stating the clinical studies, however does not mention anything about the drug mechanism. KatG gene encodes for enzymes that are involved in mycolic acid biosynthesis but there was no mention of how mutation in katG gene is what leads to the INH resistance.
Lastly, the author mentions about human studies of resistance emergence. He mentions a report in which a brother and a sister suffered multiple drug resistance due to non adherence to the drug therapy. This case provides the evidence that variation in biological fitness has an affect on outcome of the therapy. In this study, the bacterium in one case showed multiple-drug resistance (MDR) whereas in the other case, it was completely susceptible which suggested that fitness deficit was directly related to the difference in susceptibility. However, Gillespie also mentions that multidrug-resistant M. tuberculosis strains with identical susceptibilities have different in vitro fitnesses. He provides data of a study conducted on an infected human female that suggests that changes occur on passage in humans. Since initially resistant strains have a fitness deficit, transmission of the organism in a group of immunocomprised people may allow the bacterium to adapt and be transmitted while adapting. This also agrees with previous studies that show MDR numbers have increased in immunocomprised patients.
The author ends his articles by stating that these molecular and clinical studies have shown that resistant organisms over time can become fully virulent. Thus to prevent the multi drug resistance tuberculosis, steps must be taken that patients are effectively treated. Drug-resistance is a major threat to human population and to stop these numbers from rising, it is important to understand the mechanisms of resistance development in this organism. Treatment with internationally approved regimens is very effective in preventing the resistance development. This is due to the fact that combination of drugs involved in the therapy makes it very unlikely for spontaneous mutations to occur to all the antibiotics involved. Inadequate treatment of tuberculosis or treatment with only one type of drug can lead to resistant strains. When these strains that are resistant to single agents are exposed to the combination drug therapy, the effectiveness of the drug therapy is depleted which further leads to multiple-drug resistance.
The author of this article Stephen H. Gillespie is a Professor of Medical Microbiology at University College London. He has done a lot of research in the treatment and diagnosis of tuberculosis and other respiratory infections. The author provides plenty of reference articles and studies to refer for further clarification for the reader. He backs up his statements with evidence collected from various research studies. However, the author’s use and interpretation of the evidence was unclear to me in many sections. To wrap up, my opinion of this article is that it was very difficult to follow at times and the author should have included some basic information about the drug action on the mycobacterium before talking about the gene mutations that lead to the drug resistance.
Reference:
Gillespie, S.H. (2002). Evolution of Drug Resistance in Mycobacterium tuberculosis: Clinical and Molecular Perspective. Antimicrobial Agents and Chemotherapy, 46(2), 267-274.
Monday, April 28, 2008
A summary of Ted Peter's talk on the ethics of stem cell research
Student post submitted by Stephanie Chow.
Ted Peters discussed the topic of stem cell controversy at Wednesday’s ethics lecture. He brought a surprising amount of information about both sides of the debate. [I felt he was a little heavy on the pro-stem cell usage side, but he admitted that he was personally still on the fence for the issue.] A summary of what he discussed:
Regenerative medicine has the potential to offset diseases such as Parkinson’s disease, Alzheimer’s, and multiple sclerosis. This can be achieved using undifferentiated stem cells. These cells are obtained as blastocysts from fertilized eggs are broken apart. Most of the stem cells used in research come from fertility clinics. When women undergo fertility treatments, they fertilize several of their eggs at once. They use one or two at a time, and the rest are frozen. If that single treatment becomes a successful pregnancy, the woman often decides that they do not need the other eggs. Rather than be discarded, these fertilized eggs are used in research.
There are several ethical arguments against the use of stem cells. One is the embryo protection reason. Roman Catholics have taken the stance that scientists should not take apart the blastocyst to get stem cells. They feel that once an egg is fertilized (and is a zygote at that point), it has dignity because it has a soul. In other words, each unique genome correlates with a unique soul. The “14-day position” is another argument used within embryo protection. After 14 days, the fertilized egg adheres to the uterine wall and develops the primitive streak (the first stage of backbone development). Other religious groups used the 14-day position to explain their feelings towards stem cell usage.
Proponents for stem cell research contend that every fertilized egg should not automatically be considered a person. They give the statistic that 60-80% of all fertilized eggs are flushed from the woman’s body, known as fetal wastage. There is also the circumstance of chimerism, when two fertilized eggs join and a person will end up with extra genome. Stem cell advocates say that situations like these demonstrate that not every fertilized egg is a unique, soul-bearing being.
Regenerative medicine inspired by a Newt
Student post submitted by Sheena Edmonds
An experiment was done that utilized immature muscle cells of newts and mice. The two types of myoblasts were grown together and induced to differentiate into skeletal muscle fibers. Some of the newt myoblasts fused with the mouse myoblasts and created a hybrid. The hybrid cells were isolated and stimulated with serum (Cai, 2007). The serum was expected to cause the newt myotube to synthesize DNA but they did not expect the mouse myotube to do the same. Shockingly, the mouse myotube also began to synthesize DNA which indicated that there was something in the newt myotube nuclei that made the mouse myotube nuclei able to respond to the serum (Cai, 2007). In yet another experiment, the mouse myotube dedifferentiated when it was treated with extract derived form the regenerating limb of the newt implying the signal that initiates dedifferentiation was in the extract. Researchers subjected the extract to chemical and physical treatment including lipid removal, boiling, and trypsin digestion. The results proved the signal within the extract was a protein (Cai, 2007). Moreover, these two experiments confirm that mammalian cells can dedifferentiate when stimulated with the right factors. Identification of the exact molecules would aid in studying the mechanism for dedifferentiation which could eventually be used to regenerate tissue in vivo.
Researchers have now directed their attention to studying the dedifferentiation process that occurs in human myoblasts. They found that ciliary neurotrophic factor (CNTF) plays an important role in regulating many processes with in the nervous system. They also found that there are an abundance of CNTF receptors in human skeletal muscles (Cai, 2007). More excitingly they tested the affects of CNTF and found that it induced committed myoblasts to dedifferentiate into mulitpotent cells. Not only could these cells restore skeletal muscles, they also have the ability to differentiate into new tissues such as neurons, glial cells, and smooth muscle cells (Cai, 2007).
By investigating the way invertebrates adapt to the stresses and strains of their environment researchers have come closer to discovering the mechanism by which cells that were previously thought to be permanently differentiated can work backwards to their original pluripotent cells. This new method for regenerative medicine is one of the many breakthroughs in modern science. Dedifferentiation of one’s own cells offers many advantages over other researched treatments. It poses little threat of initiating an immune response and it is morally more correct then utilizing human embryonic stem cells.
Reference:
CAI, S., FU, X., SHENG, Z. (2007). Dedifferentiation: A New Approach in Stem Cell Research. BioScience, 57(8), 655. DOI: 10.1641/B570805
Additional related articles:
Mammalian myotube dedifferentiation induced by newt regeneration extract
Subscribe to:
Posts (Atom)
Posts
