Shipping CratesAccording to a new study just released in the current issue of Science, “over half a million shipments of wildlife containing >1.48 billion live animals have been imported by the United States since 2000…[and] the majority (92%) of imports were designated for commercial purposes, largely the pet trade.” Most of these imports were fish and species of coral, although all major groups of animals were imported.

That is a lot of animals; roughly 4.8 animals per person in the Unites States (estimated population in US is 304,000,000 according to Google)! Unfortunately, this study also found that a large number of these shipments did not contain the proper information to determine what exactly was being imported. According to this study, almost a third of the shipments were only labeled generically, using labels like “marine fish” or “live invertebrate.” This may be cause for concern, considering most of the imported animals were from wild populations in places like Southeast Asia, which has a high threshold of emerging diseases, which may be transmissible between animals and humans.

The authors of this study, including scientists from the Wildlife Trust, Brown University, Pacific Lutheran University, the Centers for Disease Control and Prevention, and the Global Invasive Species Programme, suggest that new measures are needed to decrease the risk of new pathogen introduction and to protect not only people, but also local animals and the health of our ecosystem. Unfortunately, there is currently no national strategy, legislative authority, or funding devoted to oversight of the live wildlife trade to implement any changes, but this study recommends much more strict record keeping of imported animals, third-party surveillance of imports and testing of pathogens in imported animals, and better public education about the dangers of diseases that may be brought in to the country.

The CDC’s “Healthy Pets, Healthy People” Web site advises pet owners about zoonotic diseases associated with some wildlife, but not only do pet owners need to be more aware of what they are bringing into their homes. Pet stores, veterinarians, and animal advocates should also be more educated on the risks of imported wildlife and how possible diseases may effect their businesses.

Imagine not being able to buy a new pair of pants or even shoes that fit. Imagine not being able to buy lunch today. Or yesterday and the day before.  Imagine not being able to feed your children. Is this poverty? To some, yes. To others it is just the beginning. Now envision not being able to take your infant for her first check up and vaccinations. Or not being able to pay $0.50 for medication to treat your children’s hookworm infection. All over the world, these problems are happening right now.

You may think, “what does poverty have to do with science and medicine?” But increases in poverty have been linked with many infectious diseases including hookworm infection, Chagas disease, malaria, and syphilis as well as other health problems such as obesity, diabetes, asthma, and dental disease.

Not only do these ailments exist mainly in poverty stricken areas, but these diseases actually promote the continuation of poverty. These diseases have numerous detrimental effects on pregnancy and healthy childbirth, the growth and development of children, and the productivity of adults. This vicious cycle of poverty and disease are close bedfellows and both need to be addressed to take a step towards eradicating poverty on a global scale.

If you search poverty and disease on pubmed, you come up with over 3,500 hits. Many researchers have shown correlations between poverty and health problems, and some are trying to do something about it. The Global Network for Neglected Tropical Diseases Control is a partnership formed in 2006 as the first ever global effort to combat these diseases. Working with the World Health Organization, these groups are trying to increase awareness of the problems associated with the injurious poverty-health cycle, as well as change how these problems are dealt with.

It is not enough just to treat the disease. Likewise, it is not enough just to improve sanitation and housing. In addition to these steps, which are already being done, education in destitute areas, monitoring for new outbreaks, and continuing research and development of vaccines to prevent instead of merely treat disease are crucially important.

sources include:

Hotez. Hookworm and Poverty. Ann N.Y. Acad Sci. 200825 Jul. 1136: 38-44

Hotez et al. Neglected Infections of Poverty in the United States of America. PLos Neglected Tropical Diseases 2(26): e 256

Vogt R. Evaluation of riske factors and a community intervention to increase control and treatment of asthma in a low income semi-rural California community. J Asthma. 2008 Sep; 45(7): 568.

Squassi A, et al. Reationship between oral health in children and poverty related factors. Acta Odontal Latinoam. 2008; 21(1): 49.

Hotez, et al. The anti-poverty vaccine. Vaccine. 2006 26 July 24(31-32); 5787.

An Astrocyte

A Koosh Ball

When a brain is injured, cells called astrocytes change their shape (and probably their function too). An astrocyte is a cell in the brain that has many processes (think of a Koosh Ball) and these “arms” may help repair damage to your brain. In a “normal” injury, such as trauma or stroke, these astrocytes become enlarged and their arms grow in size and number. However, in an article published by PLosOne today Dr. Lowenstein, from Cedars-Sinai Medical Center and UCLA, and his collaborators demonstrate a new reaction by astrocytes to immunological insults in the brain (they looked at what happens during your body’s response to viral infections and autoimmunity in the brain).

This group of researchers demonstrates that when our own body’s cells attack astrocytes, instead of getting bigger, astrocytes, pull in all of their arms and form one large protrusion to interact with the attacking cell, called a T cell which is part of your immune system. This is a dramatic change in the shape of an astrocyte and may indicate a dramatic change in function as well. In the paper, the authors suggest that this change in shape may help fend off the attacking cell, either by blocking its way or even by engulfing the cell.

 Although there is only speculation at this point as to what this finding means, astrocytes have many functions in your brain; including protecting the barrier to your brain, helping transmit signals through your brain, promoting myelinating activity (health of your brain), as well as possibly regulating stem cells in your brain. All of these functions play a major role in your brain activity and, thus, your overall health. Understanding the interactions between immune cells and brain cells is an important part of treating immune responses in the brain, such as with Multiple Sclerosis, brain tumors, or viral infections in the brain (like West Nile Virus or HIV).

I know that this wasn’t a big-ticket news items today, but I work on the mechanisms of T cell activation during Multiple Sclerosis (an autoimmune disorder that attacks the myelin sheath protecting the nerves in your brain and spinal cord). So, I thought that this was pretty interesting and has many implications!

Just to update you on the new and exciting “exercise pill”….

Frank Booth, a University of Missouri expert on the science of inactivity, says in a news release that the “exercise pill” study did not test all of the commonly known benefits of exercise and taking the pill cannot be considered a replacement for exercise. In fact, he lists a number of benefits derived from exercise that were not tested after use of the “exercise pill” that I talked about in my previous post. This list includes:

• Decreased resting and submaximal exercise heart rate
• Increased heart stroke volume at all exercise work loads
• Increased maximal exercise cardiac output
• Lower blood pressure and arterial stiffness
• Increased aerobic capacity
• Increased strength and cross-sectional area of skeletal muscle
• Delayed loss of muscle mass and strength with aging and physical frailty
• Improved balance and coordination
• Improved flexibility
• Reduced osteoporosis
• Reduced joint stress and back pain
• Decreased gallstone disease
• Improved endothelial function
• Decreased incidence of myocardial ischemia
• Less myocardial damage from ischemia
• Decreased oxidative stress
• Decreased inflammation
• Improved immune function
• Decreased liver steatosis and fatty liver disease
• Improved insulin sensitivity and reduced risk of type 2 diabetes
• Less likelihood of depression, anxiety, stress and poor psychological well-being
• Ameliorating hyperlipidemia: lower total cholesterol, higher HDL, and decreased blood triglycerides
• Improved cognitive function in the elderly
• Increased blood flow and neurogenesis in the dentate gyrus of the hypothalamus
• Prevention of the loss of brain volume in the elderly
• Delay in decline of physiological reserve in organ systems with aging

I’m glad someone has stepped up and highlighted some of the benefits of exercise not gained from a pill. However, I am still waiting to see what side-effects (if any, and I bet there are some) these pills carry with them.


After the big blow up, which is still being discussed, between Tom Cruise and Brooke Shields in 2005, many people wondered whether postpartum depression is ‘real’ or not. A news release from the NIH claims that researchers Istvan Mody and Jamie Maguire may have found a mechanism behind this disease (published in Neuron).



Researchers have pinpointed a mechanism in the brains of mice that could explain why some human mothers become depressed following childbirth. The discovery could lead to improved treatment for postpartum depression. Supported in part by the National Institute of Mental Health, of the National Institutes of Health, the study used genetically engineered mice lacking a protein critical for adapting to the sex hormone fluctuations of pregnancy and the postpartum period. – NIH News Release

Although it was first thought that this depression related to fluctuations in hormone levels, this theory was mostly disproved. Now, it seems that the hormones actually change the levels of a receptor in the brain. A mutation in this receptor in women suffering from postpartum depression may be the cause of this disorder (if women are anything like the mice used here).

The question now is, will this research have Tom eating his words? Probably not, but we have to keep trying…

Honey Bee image:

There has been much talk in the last few years about the rapid decline of honeybees and what that decline means for farmers. Honeybees are not only used for making honey, but actually pollinate many of the food supply crops we consume. Although a ‘Colony Collapse Disorder’ has occurred before, this time it seems as though it is due to the varroa mite. Unfortunately, this clever little bug is becoming resistant to the pesticides previously used to control their numbers.

ScienceDaily (July 28, 2008 ) — One of the biggest world wide threats to honey bees, the varroa mite, could soon be about to meet its nemesis. Researchers at the University of Warwick are examining naturally occurring fungi that kill the varroa mite. They are also exploring a range of ways to deliver the killer fungus throughout the hives from bee fungal foot baths to powder sprays.

Although this new breakthrough seems encouraging and eco-friendly (no use of pesticides), whenever I hear plans to introduce a new species to control a pest problem I always wonder if the new species will cause more of a problem than the initial menace. In this case, introducing a new fungus to control the varroa mites may have implications for other insects or plants in the area. Hopefully, we learn from past experiences (like introducing the cane toad in Australia to ward off sugar-cane pests) and are more prudent about introducing a new species to places where they do not belong.

At the beginning of the year, I read an interesting book by Dr. Temple Grandin, a professor of animal science who happens to have Asperger’s Syndrom (a form of autism), called Thinking in Pictures. This interesting and enlightening book describes Grandin’s experience with autism and how it helps her relate to animals.

In this book, she touches on the fact that many people who have autism have trouble interpreting the unsaid innuendos, social cues, and sarcastic remarks often used in everyday conversation. This can cause a feeling of confusion and isolation which often times results in the person pulling away from people around them

In a new study published in the journal Social Neuroscience, a team of researchers from Carnegie Mellon University tries to pin point the underlying mechanism of this experience. Here, they show evidence suggesting that this trouble is a result of faulty social network connections and inefficient neuronal pathways. In other words, messages important for understanding non-verbal social cues in an autistic brain are slow or have lower levels of transmission than in a normal brain.

This research highlights an important study published in Science earlier in the month in which the researches searched the genome of families with shared ancestry to find inherited factors for autism. During the course of their research, they noticed that all of the genes in common within a family had high levels of expression in the brain. They go on to show that many of these genes may mediate neuronal synaptic development and plasticity. Here is an excerpt from their conclusions:

Early brain development is driven largely by intrinsic patterns of gene expression that do not depend on experience-driven synaptic activity. Mutations in the genes active in early development can lead to brain malformations or severe mental retardation. In contrast, postnatal brain development requires input from the environment that triggers the release of neurotransmitter and promotes critical aspects of synaptic maturation. During this process, neural activity alters the expression of hundreds of genes, each with a defined temporal course that may be particularly vulnerable to gene dosage changes. The connection between experience-dependent neural activity and gene expression in the postnatal period forms the basis of learning and memory, and autism symptoms typically emerge during these later stages of development. Our finding that deletions of genes regulated by neuronal activity or regions potentially involved in regulation of gene expression in autism suggests that defects in activity-dependent gene expression may be a cause of cognitive deficits in patients with autism. Therefore, disruption of activity-regulated synaptic development may be one mechanism common to at least a subset of seemingly heterogeneous autism-associated mutations.

Every time you learn something new, a new connection forms in your brain. As you are reading this, you are making new connections! So, according to the authors, before you are born your brain develops according to a set plan but during childhood certain genes need to be working to make these new connections.

The findings from this research suggests that in children with autism there may be a defect in early learning due to genetic mutations which makes it more difficult to form new connections and, therefore, to process and learn new things. Although this makes things more difficult, it is not impossible to make these connections but it will take longer and require more repetition, which is why it is so important for this disease to be diagnosed as early as possible and start teaching these children in a way that benefits them the most.