Teflon for Teeth


I may come to regret the title of this post given the chemophobia and fear surrounding fluoride and water fluoridation, but recent research suggests that fluoride may help prevent bacteria from causing cavities by creating a non-stick surface on teeth.

Read more at PLOS Blogs.


Cultural Comic Books for Educating Asian Americans about Hepatitis B

photonovels 750

May is Asian-Pacific American Heritage Month and also Hepatitis Awareness Month. Coincidentally, Asian Americans are at great risk for hepatitis B, yet have the lowest rates of screening and vaccination. According to the CDC, of the estimated 1 million Americans with chronic hepatitis B about half are from the Asian/Pacific Islander (API) communities. For comparison, Asian Americans make up roughly 5% of the US population. Nearly 1 in 12 Asian Americans are chronically infected with hepatitis B, but many are unaware of their status.

How might we raise hepatitis B awareness for this cultural diverse group? Why, cultural comic books (sorta) of course!

There’s the story of a young Chinese American couple planning on getting married, but on the day of the proposal the bride-to-be confesses to her fiance that she has hepatitis B. Then there’s the one about a Korean immigrant family in which the father, who prefers traditional Asian medicine over Western medicine, discovers that his brother has liver cancer. Lastly, there’s the story of a Vietnamese American nail salon owner whose husband is diagnosed with hepatitis B, which was probably contracted by sharing razors with an infected roommate in college. No, these are are not vignettes from an Asian American film about coincidence. These are cautionary tales used in cultural, comic book-like photonovels that were developed to raise hepatitis B awareness among Asian Americans–the racial/ethnic group with the greatest risk of contracting hepatitis B.

You can read more of my post at PLOS Blogs

Immigration Reform: A Second Chance for Undocumented Immigrant Health?

When the Affordable Care Act was signed into law in March of 2010, many immigration advocates were disappointed that the bill left undocumented immigrants out in the cold. While the law kickstarts the process of bridging the gap for millions of uninsured Americans, specific language was written into the legislation to bar undocumented immigrants from being “eligible for public insurance or any type of private coverage obtained through exchanges.” At the time of the bill’s signing, approximately 7 million out of an estimated 11 million undocumented immigrants in the US were without insurance, and many of whom were living in poverty. These numbers are only expected to increase [1]. With immigration reform highly visible in Obama’s second term, immigration advocates are now viewing this as a second chance to address a growing public health concern.

Read more at PLOS Blogs…

Drug Resistance in MRSA is Finely-tuned

Cross-posted at PLOS Public Health Perspectives.

In hindsight, shoving my hand into a narrow drinking glass wasn’t such a good idea.  I learned this the hard way a few years ago while vigorously scrubbing the inside of a glass with a sponge. When the glass shattered in my hands, one of the shards cut the base of my index finger–right by the the knuckle–and required a trip to the local urgent care center. After being stitched up, I was sent home with some antibiotic ointment, extra gauze, and instructions to keep the wound clean. And that’s when things got worse.

Several days later, my finger became red, inflamed, and tender to the touch. There was also stomach-turning pus oozing out of the wound. Fearing that it was infected, I went back to the the urgent care center where the doctor took one look at my wound and then stated the obvious, “That looks infected.” A swab sample was taken from my wound to start a bacterial culture, which would be used to identify the nature of the infection. Since it would take a few days for the results to come back from the lab, she preemptively started me on a course of antibiotics. At the end of the week, there was a message left on my voicemail. The culture was positive for methicillin-resistant Staphylococcus aureus (MRSA).

MRSA-infected finger

This was cause for concern because MRSA is a bacterial pathogen that, once it enters the bloodstream, can cause severe to life-threatening infections. MRSA is also notoriously difficult to treat because it is resistant to β-lactams, a class of antibiotics generally prescribed as the first line of defense against normal staph infections. β-lactams, which include drugs like penicillin, oxacillin, and methicillin, kill bacteria by preventing the synthesis of bacterial cell walls–without which bacteria cannot survive. These drugs accomplish this by glomming onto and inactivating penicillin-binding protein (PBP), an enzyme that makes an essential component of bacterial cell walls. MRSA strains, however, are resistant to β-lactam drugs because they carry a gene called mecA. The mecA gene encodes a different form of penicillin-binding protein, PBP2a, which β-lactam drugs cannot inactivate, thus allowing normal cell wall synthesis to occur even in the presence of these drugs.

Methicillin-resistant Staphylococcus aureus (MRSA) Bacteria2
Scanning electron micrograph of methicillin-resistant Staphylococcus aureus bacteria (yellow) killing and escaping from a human white cell.

MRSA infections have long been associated with health care settings such as hospitals and nursing homes. These settings, characterized by a sick general population coupled with high antibiotic usage which selects for drug-resistance, are a perfect environment for MRSA strains to gain a foothold. Given that I had my stitches done at an urgent care center I just assumed that’s where I came into contact with MRSA.

In recent years, however, community-acquired MRSA (CA-MRSA) infections have been on the rise. These are infections contracted from settings like schools, childcare centers, gyms, and prisons. Infections caused by CA-MRSA strains are a particular concern because they are more virulent, spread more rapidly, and can cause more severe infections than its healthcare-acquired MRSA (HA-MRSA) counterparts. What’s worse is the line between the two are blurring as HA-MRSA strains move out into the community and CA-MRSA moves into the hospitals. Because of the increased virulence of CA-MRSA strains there are fears that these strains will eventually replace HA-MRSA strains in healthcare settings–although a recent model published in PLOS Pathogens suggests otherwise[1].

How MRSA developed β-lactam resistance is still unclear. While there are quite a few different strains of MRSA (some of which have also developed resistance to other classes of drugs) they all carry the mecA gene. The mecA gene, in turn, is part of a larger piece of foreign DNA known as the SCCmec element, which is not normally found in S. aureus. Since bacteria are quite adept at exchanging DNA with each other, scientists speculate that the SCCmec element found its way into a normal staph strain from an as-of-yet identified trading partner. This process of swapping and transferring DNA is known as horizontal gene transfer.

Interestingly, MRSA has a finely-tuned, “on-demand system” that turns mecA expression on in the presence of β-lactam drugs, while keeping expression turned off in the absence of these drugs. This regulation is carried out by proteins whose genes are also found on the SCCmec element. In the absence of β-lactams–when the bacteria doesn’t need the drug-resistant PBP2a protein around– the expression of mecA is kept in check by the protein MecI. MecI binds to the DNA promoter region of mecAand prevents gene transcription. However, in the presence of β-lactam drugs the bacteria needs PBP2a around in order to survive. In this case, expression of mecA is turned on through the action of the cell surface protein MecR1 whose job is to keep an eye out for β-lactams. When MecR1 detects the presence of β-lactams, it instructs the bacterial cell to break down the MecI inhibitor. This allows expression of the mecA gene that is essential for the bacteria’s survival to occur.

Figure 10. Model for the mecA induction by MecR1-MecI-MecR2.In the presence of a β-lactam antibiotic, MecR1 is activated and rapidly induces the expression of mecA and mecR1-mecI-mecR2. The anti-repressor activity of MecR2 is essential to sustain the mecA induction since it promotes the inactivation of MecI by proteolytic cleavage. In the absence of β-lactams, MecR1 is not activated and a steady state is established with stable MecI-dimers bound to the mecA promoter and residual copies of MecR1 at the cell membrane [2].

Recently, researchers from Portugal have identified and characterized another gene on the SCC element called mecR2 [2]. As it turns out the MecR2 protein is another component of the finely-tuned, “on-demand system”that regulates mecA expression. When MRSA bacteria encounter β-lactam drugs it starts ramping up the production of MecR2 protein. MecR2, in turn, knocks the MecI inhibitor protein off of the mecA gene promoter, thereby increasing mecA expression. The researchers speculate that the dislodged MecI protein becomes unstable and is then degraded inside the bacterial cell.

Importantly, the researchers demonstrated that in order to get the optimal expression of mecA that would confer resistance to β-lactam drugs, the bacteria needed MecR2 protein around. When they removed the mecR2 gene, the bacteria once again became sensitive to the β-lactam drug oxacillin, which coincided with a decrease in mecA expression. This research not only helps further our understanding of drug resistance in MRSA but also highlights new targets for therapeutics. For instance, drugs could be designed that either short circuit the ability of MecR1 to alert the bacterial cell to the presence of β-lactam drugs or prevent MecR2 from dislodging the MecI inhibitor from the mecA promoter, thereby keeping mecAexpression in check.

As for my finger and me, we made it out of the MRSA scare relatively unscathed–other than a barely noticeable scar at the base of my index finger. Once the lab results came back positive for MRSA, the doctor switched my prescription to Bactrim. Luckily for me, I wasn’t dealing with one of the multi-drug resistant varieties of the bug so the infection cleared in a few days.

Featured image: Scanning electron micrograph of methicillin-resistant Staphylococcus aureus (MRSA, yellow) surrounded by cellular debris. Credit: NIAID


1. Kouyos R, Klein E, & Grenfell B (2013). Hospital-Community Interactions Foster Coexistence between Methicillin-Resistant Strains of Staphylococcus aureus. PLoS Pathogens, 9 (2) PMID: 23468619 doi:10.1371/journal.ppat.1003134

2. Arêde P, Milheiriço C, de Lencastre H, & Oliveira DC (2012). The anti-repressor MecR2 promotes the proteolysis of the mecA repressor and enables optimal expression of β-lactam resistance in MRSA. PLoS Pathogens, 8 (7) PMID: 22911052 doi:10.1371/journal.ppat.1002816

Glaucoma Is not an Equal Opportunity Thief

Wrapping up Glaucoma Awareness Month over at PLOS Public Health Perspectives blog with a post on the ethnic disparities in the risk of developing glaucoma as well as current research in identifying the genetic basis for glaucoma in Asians:

Glaucoma isn’t exactly an equal opportunity thief, either. While it is estimated that over 4 million Americans have glaucoma, the prevalence of glaucoma in African Americans and Latino (particularly Mexican) Americans is significantly greater than in Caucasian Americans. African Americans are also more likely to develop glaucoma at a younger age and suffer blindness from the disease. While roughly 90% of all glaucoma cases in the US are what is known as primary open angle glaucoma (POAG), Asian Americans are at the greatest risk of all ethnicities to develop a different form of glaucoma called primary angle closure glaucoma (PACG)(1). The genetic causes underlying glaucoma remain unclear, but these ethnic disparities in the risk of developing glaucoma suggest a genetic basis that is ethnicity-specific. Read more

Dengue Fever, GMOsquitos, and a “Wolbachian” Invasion

In my recent Public Health Perspectives post for PLOS Blogs, I discussed two ways to control the transmission of dengue fever. The first was through the release of genetically-modified (GM) male mosquitoes that mate with wild females and pass on a gene that is lethal to its offspring–a strategy called Release of Insects carrying a Dominant Lethal (RIDL) (1). If released in sufficient numbers, the GM male mosquitoes will cause a collapse of the mosquito population.

Diagram of the RIDL transgene (image from Oxitec website)
Diagram of the RIDL transgene (image from Oxitec website)

The RIDL transgene (a) that has been engineered into the OX513A strain of mosquitoes carries instructions for the production of a protein called tetracycline transactivator (tTA). tTA , itself, is a product of genetic engineering, created by the fusion of parts of two proteins. One “half” of tTA acts as transcriptional activator–it can turn on and amplify the expression of certain genes. The other “half” can bind to specific DNA sequences called tetO binding sites. By engineering tetO binding sites into the RIDL transgene this allows the tTA protein, itself, to amplify expression of the tTA gene thereby producing even more tTA protein (b). This results in what is known as a positive feedback loop. At high enough levels, the tTA protein interferes with cellular process causing mosquito larvae to die. The expression of the tTA gene can be turned off by tetracycline, however (c). Tetracycline binds to the tTA protein and prevents it from binding to DNA, which short circuits the feedback loop.

“This allows scientists to raise the mosquitoes in the lab by adding tetracycline to the diet of the larvae. Without a source of tetracycline in the wild, however, any mosquito offspring that inherits the gene will live not beyond the larval stage.”

The other strategy I discussed was using Wolbachia infection of mosquitos to prevent dengue transmission. Wolbachia is an symbiotic bacteria that has been shown to protect mosquitos against dengue infection by interfering with the ability of the dengue virus to replicate. Wolbachia can invade and establish itself in insect populations quite rapidly and stably–an ideal characteristic if Wolbachia is to be used in limiting the transmission of dengue. It accomplishes this by employing a cunning strategy called “cytoplasmic incompatibility (2).” In short, when Wolbachia-infected males mate with uninfected females all their offspring die. However, the offspring of Wolbachia-infected females are viable regardless of the infection status of the male. This means that Wolbachia infection confers a reproductive advantage to infected females over uninfected females–infected females are more likely to have offspring because they can mate with both infected and uninfected males. Furthermore, Wolbachia infection is passed on from mother to offspring. It is through this process that Wolbachia “invades” and secures its place in an insect population.

Field studies conducted in Australia showed that when  mosquitoes infected with the wMel Wolbachia strain are released into the wild, within several months stable wMel infection became established in two wild A. aegypti populations (3). The speed at which wMel invaded the natural mosquito populations demonstrated the potential of using Wolbachia infection to control the spread of dengue.

You can read more about this topic here:

Could Wolbachia be an alternative to dengue-fighting GMOsquitos?


1) Phuc HK, Andreasen MH, Burton RS, Vass C, Epton MJ, Pape G, Fu G, Condon KC, Scaife S, Donnelly CA, Coleman PG, White-Cooper H, Alphey L. Late-acting dominant lethal genetic systems and mosquito control. BMC Biol. 2007 Mar 20;5:11. PubMed PMID: 17374148; PubMed Central PMCID: PMC1865532.

2) Walker T, Johnson PH, Moreira LA, Iturbe-Ormaetxe I, Frentiu FD, McMeniman CJ, Leong YS, Dong Y, Axford J, Kriesner P, Lloyd AL, Ritchie SA, O’Neill SL, Hoffmann AA. The wMel Wolbachia strain blocks dengue and invades caged Aedes aegypti populations. Nature. 2011 Aug 24;476(7361):450-3. doi: 10.1038/nature10355. PubMed PMID: 21866159.

3) Hoffmann AA, Montgomery BL, Popovici J, Iturbe-Ormaetxe I, Johnson PH, Muzzi F, Greenfield M, Durkan M, Leong YS, Dong Y, Cook H, Axford J, Callahan AG, Kenny N, Omodei C, McGraw EA, Ryan PA, Ritchie SA, Turelli M, O’Neill SL. Successful establishment of Wolbachia in Aedes populations to suppress dengue transmission. Nature. 2011 Aug 24;476(7361):454-7. doi: 10.1038/nature10356. PubMed PMID: 21866160.

Featured image:
Detail from the original by Emil August Goeldi (1859 – 1917) [Public domain or Public domain], via Wikimedia Commons

by Viet Le

I’ve joined the Public Health team at PLOS Blogs!


As some of you probably know by now, this week I’ve joined a talented team of writers over at the PLOS Public Health Blog. I’m excited for this opportunity to explore new topics in public health (with a particular focus on minority health) and to share my writing with the PLOS blog audience. I will continue to writing about science here as well.

My first post about the challenges in diagnosing diabetes in Asian Americans is up over at the PLOS Public Health Blog now, so have a read and let me know what you think!


And thanks for reading everyone!

Voters also have a right to know the science behind GMOs

On November 6th, California voters will decide if foods containing genetically modified organisms (GMO) will require labeling. Prop37 argues that consumers have a right to know so that they can make informed choices regarding the foods they buy. One of the issues that scientists have with this initiative is that Prop37, as well as media coverage of GMOs, contain misleading language that distorts the science behind how GMOs are made and how safe they are for consumption. This raises, then, the question of how useful would labeling of GMO foods be if there is general public misconception of the topic.

Katie PhD explains “what exactly IS a genetically modified plant” on her blog.

Many scientists and science communicators are seizing this opportunity to educate the public about GMOs. Some are taking the opportunity to explain to the public what a GMO actually is while others are providing insight concerning the safety of GMO foods. Others are exposing flaws in a recent study that claims GMO maize causes cancer (More related links can be found in Keith Kloors’ article in Slate).

Unsurprisingly, those entering the fray can also expect to have their credibility questioned. The food industry corporations, having spent a considerable amount of money in an effort to defeat Prop37, have provided the anti-GMO/pro-labeling crowd with a convenient way to dismiss or discredit scientists defending GMOs: they are all corporate shills (or worse). This, of course, is absurd. Could industry money be swaying scientist’s stance on GMOs? Maybe. But if scientists are that easily corruptible by money, why aren’t more scientists anti-climate change? Absent polling data, it’s unclear to me where scientists fall on the issue of GMO labeling (although, you can help by filling out this survey being conducted by @Katie_PhD). Anecdotally, in my interactions with other scientists, the stances on GMO labeling are not monolithic. Some are pro, some are anti, while others are ambivalent.

The issue for most scientists, I think, is not so much the labeling requirement itself, but the distortion of information being used to justify it and how that ultimately undermines science. The difficulty of course is that scientists are trying to engage the public dispassionately about a topic the public takes very personally. In my view, I don’t think GMO foods require labeling, but I certainly respect the public’s right to vote on this issue. However, by Prop37’s logic, if the consumer has a right to know if their foods contain to GMOs so that they can make informed decisions, then the public has the right to information so they can make an informed vote. Scientists are just making sure that they are getting accurate information.

Related Reading:

How California’s GMO Labeling Law Could Limit Your Food Choices and Hurt the Poor

The transfer of genes between unrelated organisms happens. All. The. Time.

Maybe we should just not eat anything

It seems like every week the news runs a story, based on some new study, that either touts the health benefits or demonizes the hazards of a particular food. One week, it’s eat walnuts if you want healthy spermies. Other weeks, it’s eating red meat could raise the risk of bowel cancer. Unfortunately, many of these stories lack, well, journalistic vigor, which can often lead to a regurgitation of the study’s press release, sensationalization of the studies claims, or worse, outright distortion of its conclusions. Other times, it overlooks just plain, old bad science. And to add to the confusion, this week’s story might contradict the findings of past nutrition research–leaving many of us wondering, “What CAN I eat, then?”

Luckily, capable science writers and communicators often step in to fill in the gap. Take for instance, Cassandra Willyard’s dissection of the actual study that many news outlets declared demonstrated eating eggs was almost as bad for your arteries as smoking cigarettes.

Or biochembelle’s breakdown of the link between Alzheimer’s and exposure to diacetyl, an ingredient in popcorn butter flavoring–pointing out that most of the articles failed to mention who was really at risk (industry workers) and also, that the “two major manufacturers, ConAgra and PopWeaver, removed diacetyl from their microwave popcorn.” Lastly, for a longer read, Gary Taubes writes on the limits of observational epidemiology, after reports that “meat-eating apparently causes premature death and disease” and “that chocolate is a food we should all be eating to lose weight” were published earlier this year.

These science writers provide insight and perspective into the science involved in food research by pointing out the limitations of these studies, illustrating what the news simply got wrong, or even  reminding us that sometimes we need to take these studies…with a grain of salt. And maybe, that’s why some of these journalists take the easy road. They know that someone else will come in later and do the hard work.

Related Reading:

Pink Slime: My beef with Jamie Oliver and Food Blogs

Is Sugar Really Sugar?

Image credits:

Walnuts courtesy of Marco Bernardini

Egg and Cigarette courtesy of Benjamin Maubach

Popcorn courtesy of  Jeff Baxter 


Histamine, Hygiene Hypothesis, & Hookworms

If you’re like me and millions of other Americans you’ve spent this spring being an itchy, sneezing, mucous-y mess. In this week’s Worldwide Wednesday I’m talking about allergies– the immune system’s reaction to pollen and otherwise harmless substances (dubbed allergens) and the ruiner of my favorite season.

Scanning electron microscope image of pollen grains from a variety of common plants.


We’ve all heard of them before, but what is histamine and what does it do? Histamine is a chemical compound produced by cells of the immune system, such as mast cells, and is the primary culprit that causes the miserable symptoms of allergies. That is because histamines induce capillaries to leak out fluids resulting in sneezing, watery eyes, and a runny nose. Learn how the release of histamines from mast cells is triggered by allergens and how anti-histamine drugs work:

(Note: I liked the videos about allergies and antihistamines on about.com better, but I couldn’t figure out a way to embed them.)

Hygiene Hypothesis Challenged

As I mentioned, allergies are actually an immune response and the main players have other roles in immunity. For instance, the class of antibodies called Immunoglobulin E (IgE), which bind to allergens and triggers the release of histamines, appears to be the main line of defense against parasitic infections. Histamine, on the other hand, is part of the inflammatory response.

So what would cause the immune system to react to otherwise innocuous substances? One widely accepted explanation that takes into account the prevalence of allergies in developed countries is the hygiene hypothesis. Since we have effectively eradicated parasitic infections and live in increasingly cleaner and relatively sterile environments, we have reduced our exposure to infections pathogens and parasites especially during childhood. As a result the body’s immune system, which would normally be pre-occupied dealing with parasitic infections, becomes “bored” and starts mistaking harmless substances for potentially hazardous ones. Recently, however, some scientists have begun to look at allergies not as our immune system going rogue but rather that “runny noses, coughs and itchy rashes keep toxic chemicals out of our bodies, they argue, and persuade us to steer clear of dangerous environments.”


The concept underlying the hygiene hypothesis has inspired some squirmy solutions. Some people, desperate for allergy relief, have turned to infecting themselves with parasites such as the hookwormNecator americanus. The idea behind this treatment, known as helminthic therapy, is to keep the immune system’s hands tied up dealing with the parasitic infection so that it can’t trigger allergies.

N. americanus. “What’s it going to be, me or allergies?”

While there is some evidence that this therapy works, its efficacy is still being studied. But that isn’t stopping this doctor from experimenting on himself. Neither is it stopping Jasper Lawrence, who deliberately infected himself to combat allergies and asthma. You can catch the story of how he took it one step further and started selling hookworms as a business and how shortly after he had an ominous visit from the FDA.

Related Reading:

While most allergy treatments focus on blocking histamines, Finnish scientists are taking a different approach: vaccination.

Scientists at the University of Eastern Finland led by Professor Juhu Rouvinen, in cooperation with Professors Kristiina Takkinen and Hans Söderlun from VTT, a technical research center in Finland, discovered unique IgE‐binding structures in allergens. They say these structures can be genetically modified so they do not bind IgE anymore, but they can still induce the production of the immunoglobulin G (IgG). IgG protects you from allergic symptoms by actually prohibiting the formation of IgE-allergen complexes and could, in theory, prevent the degranulation and histamine release from white blood cells. The modified allergens are produced using modern molecular biology and biotechnology.

It seems a little vague since I can’t find anything published, but it would appear to be a lot of work since I imagine for the vaccine to prevent all allergies it would require modifying ALL allergens.

Meanwhile, a study from the Fred Hutchinson Cancer Center links allergies to higher blood cancer risk. But as the report concedes, “the added risk is so small that no new screening guidelines are currently planned.” Which made me wonder why this was even reported on the first place. As with the vaccination report, I couldn’t find anything published to read and evaluate.