Café Scientifique tonight: Epidemiology of Lung Cancer in the Central Valley

Each year 160,000 Americans die from lung cancer and another 220,000 are diagnosed with the disease. About 85-90% of lung cancer is attributable to cigarette smoking and other tobacco related exposures; however, one in five American adults continue to smoke. Although there has been a decline in smoking during the last several decades, recent national data suggest the decline has leveled off, especially among young adults. In this presentation, the worldwide distribution of lung cancer, state and local patterns of lung cancer will be presented, as well as data on smoking habits and other risk factors for this deadly disease.

via valleycafesci.org

For those of you in Fresno tonight - a reminder: the above is the topic for tonight's talk at the Central Valley Café Scientifique by Dr. Paul Mills of the UCSF-Fresno Medical Education Program. And note that we meet at a new venue tonight. Enjoy - even if some of us regulars have to miss it!

Posted via web from a leaf warbler's gleanings

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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:

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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?

Read her responses on the TED website.

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.

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How the influenza virus can drift and shape-shift to keep us on our toes

As you may have read by now, the new swine flu virus, this new strain H1N1 which is threatening to turn into a pandemic according to the WHO (even though there is much confusion about the actual number of infected/dead victims confirmed to have this strain), is actually an interesting genetic mixture, a chimera if you will with a potpourri of genes from different influenza strains: these may be from multiple host taxa — birds (thought to be the original source of all influenza viruses), humans, and, of course, pigs (from North America and Asia!) — or perhaps all from pigs (the picture is still cloudy). In any case, if you are wondering how such reassorted viruses form, the following video paints a cartoon picture to help you understand. The key thing to remember is that viruses, like many other microbes, are rather promiscuous when it comes to swapping bits of DNA - even across "species" - and such lateral transfer can allow new strains to evolve, even drug-resistant ones, much more rapidly. Here's how influenza may be able to shift the shape of its antigens, and potentially jump between host species:

But, that is not the only trick up this virus' sleeve. Ever wonder why, unlike with other vaccinations which are often a once-in-a-lifetime deal, you've got to take that flu shot over every single year? Because, even in the absence of opportunities to hook-up and swap genes with other viruses, i.e., even when a host is infected by just a single strain of the flu, the virus is constantly changing shape. Mutations arise all the time, and those that change the shape of the antigen such that it is no longer recognized by host antibodies will be naturally selected. Antigen shape therefore drifts around constantly, making it a much more fun game for the host immune system - and our vaccines - to keep up with the flu! It's evolution in action, right within our own bodies and those of animals we cohabit with! You didn't think we had quite liberated ourselves from the clutches of evolutionary processes now, did you? As you ponder that, here's another cartoon depicting antigenic drift:

[Hat-tip: GrrlScientist for finding the videos]

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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!

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Modeling the emergence of multi-drug resistant TB hot zones

Rebecca Freeman submitted this essay for the Evolution class.

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

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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.

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Darn those scientists, confounding our politics again!

Unbelievable!! This is the leadership we are supposed to look forward to?!

As someone who came to the US because of the opportunities this country offered to pursue scientific research, and having seen science get bipartisan lip service (at least) over the past 4 presidential election cycles (when I have been here), despite the decline in science funding over the past 8 years, I find it really bizarre to see this "team of mavericks" tilting against the windmills of science in this fashion! First it was McCain railing against "pork-barrel" earmark funding to study the genetics of grizzly bears (a very successful project, btw, that he had actually voted for, before turning it into a convenient flogging-horse on the campaign trail), and now Palin takes on the iconic model organism of modern genetics, Drosophila!! Talk about clueless chutzpah, bashing research on the very organism which has yielded, among myriad other insights, important clues about autism, the cause she claims she would fund by cutting off these "earmark" projects!! But, as has been clear from the day she joined the ticket, and as Rachel Maddow demonstrates yet again, this hockey-mom continues to operate in a completely irony-free zone - how can one make fun of her when she embodies the joke so completely? (remember how people chuckled when someone initially suggested that she had foreign policy expertise because of Alaska's proximity to Russia; until she actually took that line seriously and ran with it?)

Science - cutting-edge basic science - has surely been one of the defining characteristics of this country's global leadership over the past half-century or more, no?! Why do these "mavericks" now suddenly think it is ok to throw that away, and that they will win more votes if they bash science and scientists? I've wondered about the curious dichotomy in this culture, where science and technology provide the basis of so much of everyday life, yet science and scientists, and intellectuals in general, are feared/reviled as nerds/dangerous elitists. Is the anti-intellectual strain in this society so strong that McCain/Palin can drum up a few more votes to win this election by continuing to bash science, and further entrench the age of american unreason? Please tell me that is not the case, that things haven't gone that far wrong... or should I be packing my bags as another soon-to-be-unwanted scientist who has been wasting his life and taxpayer money studying birds??!! While remaining a foreigner, to boot!!

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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!

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Impressions from the Central California Research Symposium

Kara Ward shares her experience attending the 29th Annual Central California Research Symposium held recently on campus.

Overall Impression:

The 29th annual CCRS symposium, held at Cal State-Fresno, was without doubt an experience to remember. Although I cannot say that it was my preferred activity for the afternoon, I can definitely say that when I left the symposium I had acquired a greater knowledge of how many undergraduate and graduate science talks and public presentations progress. I myself have not attended many of the weekly Friday Biology seminars they have here at Fresno State so it was definitely a treat to attend this symposium and I was actually very interested in seeing work produced by my peers.

Out of the six presentations that were actually presented to us, it was apparent that each presenter had a different angle and strategy in the planning and preparation of his or her presentation. Of the six presentations, a few presenters actually did an excellent job in presenting their topic thoroughly in the sparse time allotted to them. These few presenters stood out because of their ability to utilize all of their skills to present a complete presentation. Others, however, failed in many areas such as utilizing their allotted time efficiently, in using the correct grammar and speech necessary to give a public presentation, and most importantly, in presenting the material and data in a manner that we the audience could understand. It is my opinion that these presenters would defiantly [sic] benefit from more practice and possible lessons in how to give public presentations. I can definitely understand that they had to present a lot of information and data in a very short time, but more practice on the presentation itself may have produced much smoother delivery and pace. It was apparent that many of the presenters were nervous and a public speaking course could and would serve them well. Overall my assessment of this symposium is fair, and based on my experience attending this symposium, I would positively attend next year should I be afforded the opportunity and recommend that all science majors do the same.

Critique 1: The Identification of Brachyuran Megalopae of the San Francisco Bay Estuary

Presented by: Vanessa Gonzales

I chose this presentation to critique because I had heard a few things about the Chinese mitten crab in prior classes; however I had never actually been presented with such detailed facts about the crab’s lifecycle and I was extremely intrigued by it. I liked the flow of the presentation and appreciated how she began her talk explaining the problem before going into the details of the experiment. I thought Gonzales did and great job of explaining how the presence of the crabs negatively affected the habitat by competition with and predation of some of the native species; however, I would have liked her to speak a little more about some of the native species which were affected. I also thought that the presenter did an excellent job of providing graphs, charts and tables which illustrated the facts and stressed the points that she was trying to make. As I stated earlier, I feel that the presenter did a great job of going through all of the important stages in the life cycle of the crab. This background information would be vital to know prior to being able to understand the full extent of the problem at hand as well as understanding how the experiment was set up and I feel that she was wise to include it. As the presentation continued and Gonzales entered the research portion of the presentation, I felt that she entered into somewhat of a read and speak mode. By read and speak mode I mean that it almost seemed like she was just reading lines from her note cards and it was apparent that she may have gotten lost in her notes, because between every sentence she would say phrases akin to “um” and “like”. Aside from these minor areas, I felt that the presenter did a good job of presenting the information in an organized manor. The presentation flowed and each section was explained well by Gonzales who utilized her time well.

Critique 2: Potential Impacts of Selenium on California Red-Legged Frog (Rana draytonii)

Presented by: Foung Vang

I chose this presentation to critique because I had never heard of the primary organism of this study, the Red-Legged Frog, and just the name was enough to warrant my interest. After reading the abstract, provided by the presenter, my initial thoughts went to the Zebrafish experiment we conducted in our Developmental Biology lab in which we treated the fish with varying amounts of ethanol. Based on my experiences with the Zebrafish lab, I knew that most experiments monitoring early development are quite interesting and could really go either way so I was definitely interested in seeing the outcome of this experiment. Overall I felt that there were some strong areas of the presentation as well as some weak areas. The weak areas in the presentation for me, was the lack of background information on the frogs as well as the lack of graphics and illustrations. Where the presenter did a great job of providing us with a background of selenium and the issues presented by selenium in the environment, he hardly spoke at all about the history and life cycle of the frogs. It almost seemed as if the presenter was too eager to begin the discussion of the hypothesis and results section of the experiment, but in doing so, the presentation came off as being unbalanced and dry. Although this lecture presented a lot of facts and data, I still felt as if something was lacking in the overall presentation. Perhaps the problem for this presenter was merely a time management issue, trying to put too much information in a twelve minute presentation; however, this should not be an excuse. My overall assessment of this talk was that it was very informative and the presenter was well spoken, however, I still would have preferred a little more background information on the target organism as well as a little more visual stimulation.

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Evolution of MRSA

Student post submitted by Trevor Clark.

The article, Evolution and pathogenesis of Staphylococcus aureus: lessons learned from genotyping and comparative genomics, is well written and also well diagramed. The article is looking to obtain an understanding of what the exact biologic role of methicillin resistant S. aureus (MRSA) is. The authors want to understand the existence and the mechanism of evolution for the genesis of C-MRSA. The paper gives a clear background of MRSA but it does not go into depth about the history of how it has evolved to what it is now. It is clearly stated by the authors that, not much is known about how MRSA is able to evolve as quickly as it does to medications.

The body of the paper dives right into the evolution of the core genome of MRSA. My focus is more towards how MRSA has evolved in the hospital and medial setting and the effects that it has had on humans. The research conducted for the paper was vital for them to understand the clonal structure so they could compare it to the strains that common today. They were able to obtain an understanding of what genes it had by running it through a multilocus sequence typing (MLST). “MLST is currently the most popular typing method through the sequencing of seven housekeeping genes (arcC, aroE, glpF, gmk, pta, tpi, and yqiL). For each gene, the different sequences are assigned as alleles and the alleles at the seven loci provide an allelic profile, which unambiguously define the sequence type (ST) of each isolate.” From the data collected from the MLST they were able to analyze and conclude that point mutations have given rise to new alleles more frequently than recombination. Their data shown in figure 1 is good, but I still do not have a clear understanding on how their calculations came about. I would have liked to see a side-by-side comparison of the genes from each individual strains that they were able to sequence successfully. Anyone can talk about what they have found, but I need to see proof through more data.

Fig. 1. Protein homology between nine sequenced Staphylococcus aureus genomes. In each box is the number of orthologues shared by the corresponding strains and median nucleotide divergence that reflects divergence between the two strains. The orthologue was constructed by the orthomcl program (Li et al., 2003). Nucleotide divergence is defined as the number of mismatch bases divided by the number of comparable bases. The color intensity in each box is in inverse proportion to the nucleotide divergence. The accession numbers of the S. aureus genomes are: NC_002745 (N315), NC_002758 (Mu50), NC_003923 (MW2), NC_002953 (MSSA476), NC_002951 (COL), NC_007795 (NCTC8325), NC_007793 (USA300), NC_002952 (MRSA252), NC_007622 (RF122).

The second half of the paper was geared more towards what I was interested in. They talked about how MRSA enters a host and clearly explained the life cycle of MRSA on what they gathered from their studies. Community-acquired MRSA (C-MRSA) has become a problem and is considered to be a super bug since doctors and scientist have not yet found a cure or a drug to fight it. The evolution of MRSA to become what it has become today has interested the medical community and also has sparked an interest in me. This paper does a good job in bringing some light towards possible ways to fight MRSA; “staphylococcal species are one of the most important topics in the research of the evolution and pathogenesis of S. aureus”.

Fig. 4. Illustration of the hypothetical Staphylococcus aureus evolutionary history. The whole S. aureus species can be divided into two putative subspecies (Robinson et al., 2005a). The circles with different colors represent different agr groups, and the circles with numbers inside represent the corresponding clonal complexes. The arrows on the right side indicate the important phases during the S. aureus evolution.

The table and figures that were used were well done overall. They were clearly explained and could be understood. The way the paper was written and put together made is so those who have taken an entry-level genetic course would be able to understand and follow what was being said.

References:

Feng, Y., Chen, C., Su, L., Hu, S., Yu, J., Chiu, C. (2007). Evolution and pathogenesis of Staphylococcus aureus: lessons learned from genotyping and comparative genomics. FEMS Microbiology Reviews DOI: 10.1111/j.1574-6976.2007.00086.x

Robinson, D.A. (2005). Evolutionary Genetics of the Accessory Gene Regulator (agr) Locus in Staphylococcus aureus. Journal of Bacteriology, 187(24), 8312-8321. DOI: 10.1128/JB.187.24.8312-8321.2005

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Is stem cell therapy ok if it comes from the East?

Here's something to ponder in the wake of Jason Bush's talk, as we await the next lecture (on April 23rd) in the Ethics Center Seminar series where theologian Ted Peters (author of The Stem Cell Debate) will take up some of the more sticky moral controversies that Jason punted on last week! While a lot of the opposition to stem cell research in the US comes from the religious right, especially over the issue of embryonic stem cell research, there is opposition from the left as well - especially the "alternative medicine" left which sees everything in western medicine as being somehow tainted and unnatural. And then, by (illogical) extension, that any other "alternative" to western medicine is therefore much better for you, even if practitioners of said alternative don't have a clue about how their medicine works, if it works at all! But what if "eastern" medicine starts offering therapies based on stem cell research (and other products of "western" science)? And start doing so when such therapies are not available here in the west? Skeptico raises this question in an interesting commentary on an NPR story about how some Americans are heading to China seeking stem cell therapies not available in the US. In addition to the welcome and enjoyable bashing of irrational "skeptics" like Bill Maher, Skeptico makes this important point:

The truth is, ancient people, who did not understand how the body works or what really made people ill, just made stuff up about these things. The ancient Chinese made up stuff about meridians and chi. Ancient Indians made up stuff about chakras. Ancient Europeans made up stuff about humors. We now know better, and so have abandoned humors and bloodletting. The only mystery is why people still insist that chi and chakras are real. But whatever you believe is real, the distinction clearly is not between “western” and “eastern” (fill in your preferred country) therapies. The distinction is between therapies that work and those that don’t. Scientists in China are researching real medicine, and trying to find out what works and what doesn’t, just like scientists in the west. Maybe some have oversold their results, but scientific procedures, not ancient myth, will ultimately decide what works and what doesn’t.

So can we now please abandon this pretence that doctors in the west practice something called “western medicine”, while the Chinese have access to some secret knowledge that “western science” still hasn’t yet caught up with? There is only medicine that works – or at least, is backed by reliable evidence that it does – and pre-scientific superstitious quackery that doesn’t. The East/West labels mean nothing. And the next time some twit like Maher intones gravely against “western medicine”, just say, “yeah, I don’t fancy bloodletting either” - and advise him to go visit Doctor Hu in Hangzhou. Preferably on a one-way ticket.

I've always thought that the main criterion in medicine is whether it works. Even if we don't fully understand underlying mechanisms! Any good medicine should aim to cure the afflicted, without getting caught up in its own dogmas about how the human body is supposed to work. Figuring out the "how" and "why" of any successful medicine - well that's the job of science. That's why you can have many "alternative" medicines, but only one science - for there is no western or eastern science once we understand how any particular disease and its cure works, is there? And on the flip side (and this may raise some of your hackles), that's why medicine (even in the west) isn't always necessarily a science either!

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Time to Fight HIV in Our Genes

A lot of scientists are aware of the CCR5 gene and the mutant form of this gene that has a base pair deletion at position 32. The normal CCR5 gene codes for a receptor protein that gets HIV into the cell and people with the mutant form are resistant to HIV because the virus is unable to enter into the cell. It is an exciting time in the medical community because researchers have discovered a new promising gene that could potentially prevent the virus from forming. HIV is a rapidly mutating virus that is hard to stop with vaccines and cocktail drugs. It has been scientists’ objective to find new ways of fighting HIV despite its constant evolution, and they might have discovered a way to fight it naturally.

So what is this magical gene that is located in every cell of our body? It is called the TRIM22 gene and it has the amazing ability to prevent the assembly of the virus in our cells. A team of Canadian researchers at the University of Alberta discovered this gene and are excited to continue doing experiments to see how it works exactly. When the gene was placed into cells it actually prevents the virus from forming and intern prevents the onset of AIDS. In another experiment, the research team prevented cells from turning on the TRIM22 gene which caused the coordinating interferon to become ineffective at blocking the HIV infection. Under normal conditions this interferon coordinates attacks by the TRIM22 gene against infections. This means the TRIM22 gene is a crucial part of our defense against HIV. These research findings can be found in the public library of science pathogens.

Further research is necessary to answer more questions about this gene and its ability. For instance, the TRIM22 gene does not work in people who are already infected with HIV. Reasons for this are still unknown and mind boggling to scientists. Other studies are being done to see what other viruses the TRIM22 gene can fight. The tests done here were conducted using computer analysis and cell cultures, so it will be interesting to see what happens when they test the genes on model organisms.

The prospects of this research are promising and scientist hope to use this natural means for fighting the HIV virus to synthesize drugs that mimic the TRIM22 gene. Science and technology are allowing medicine to go in directions that it has never gone before. With dedicated scientists and proper funding it is possible that we will find a cure to HIV in the next few decades.

[contributed by Sheena Edmonds]

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Bush to speak on the ethics of stem cell culture - Mar 12 noon @ Fresno State

No... not that Bush / Shrub! Rather, its our own department's Jason Bush, who actually knows a little something about stem cell research as a scientist, and who happens to be from north of the border - the northern border of the US, that is. Our Bush will be speaking as part of the CSU-Fresno Center For Ethics spring lecture series:

March 12
Jason A. Bush: “The Art, Mystery, and Controversy of Stem Cell Culture”
As stem cell research has exploded in the past 5 years, fundamental concepts have changed and we have made technical advancements. Scientists see the potential and opponents see the slippery slope. This lecture will discuss the complex issues that engulf stem cell research.
Jason Bush has a Ph.D. in Experimental Medicine from the University of British Columbia. He did post-doc work in Cancer Biology at The Burnham Institute. He is Assistant Professor in the Biology Department at Fresno State.
[From Upcoming Ethics Center Events and Lectures]

The lecture will be in the Alice Peters Auditorium at 12:00 PM on March 12, 2008. Should be fun, so try to be there!

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Superbug Nightmare - on Nightline tonight

I don't know how many of you students watch ABC's Nightline (after all, it competes with Leno and Letterman!), but even if you are not in the habit - and especially if you are thinking about writing your term paper on this or a related topic - you might want to watch/TiVo it tonight (11:35 Pm on our local Channel 30), because it promises a segment on antibiotic resistant bacteria! A highly relevant evolutionary topic in the mainstream media can't really be missed now, can it? Well, let's see how much evolution they talk about... at least the accompanying article on their website contains the e-word twice! Here's a blurb about what's on for tonight:

Killer "Superbug"

MRSA is a million-year-old bacterium that kills 19,000 Americans a year, claiming more lives in the US than even AIDS. Though once confined mainly to hospitals, the bacterial infection is now increasingly common outside of medical facilities. Once contracted, MRSA is hard to treat because it's resistant to most antibiotics. ABC's Vicki Mabrey reports on the fight against this "superbug."

And you can also watch a somewhat cheesy "promotional" video if you like.
[From ABC News: 'It's Everywhere': Superbug Nightmare]

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