Friday, May 12, 2017

Could Parasites Be Causing Prostate Cancer?

Long ago in the mid-1600s, a fellow named Antonie van Leeuwenhoek started making lenses…as a hobby (remember, Facebook and Netflix were not invented yet). He was so adept at grinding glass that his lenses were able to magnify objects about 270 times their normal size. Leeuwenhoek soon discovered a whole new universe right here on earth, a universe of creatures so tiny that only his microscope could reveal them. He called them "animalcules."

With his powerful microscope, Leeuwenhoek became the first person to see amoebae, bacteria, and blood cells. For these revolutionary discoveries, he is considered “the father of microbiology.”

But after looking at endless water samples, the ever-curious Leeuwenhoek wondered what bodily fluids looked like under his microscope. While Leeuwenhoek examined blood, sweat, and tears (and a lot of dental plaque), a medical student in 1677 named Johan Ham told Leeuwenhoek that he spotted animalcules swimming in the semen he collected from a gonorrhea patient.

Believing these animalcules might be a result of disease, Leeuwenhoek procured a clean semen sample from his own stock - obtained fresh after proper lovemaking with his wife, he insisted. Leeuwenhoek confirmed Ham's finding and went on to discover the same tiny eel-like critters teeming in the semen from many other species. This is how we came to make the “seminal” discovery of sperm cells.

Other people in Leeuwenhoek’s day mistook these microscopic beasties squiggling around in the semen to be "merely" parasites, referring to them as “seminal Worms.” In fact, we didn’t realize that these “semen parasites” played a key role in fertilization until the 1870s when Oscar Hertwig spotted the fusing of nuclei from sperm and egg after contact…in sea urchins of all places.

We didn’t figure out where babies come from until fairly recently – 1870. White studying sea urchins, Oscar Hertwig noticed that the nucleus in the sperm fuses with the nucleus in the egg (the nucleus is the cellular organelle housing DNA).

While the mystery of sperm has been solved, we have indeed discovered a variety of pathogens that can inhabit our nether regions. Trichomoniasis, scrotal filariasis, and Chlamydia are just some of the unpleasant conditions caused by these most intimate of uninvited guestsAn unsettling new study led by graduate student Darrelle Colinot at the Indiana University School of Medicine may have found yet another.

In experiments performed in mice, researchers found that the common single-celled parasite called Toxoplasma gondii disseminates to the prostate within two weeks after infection. And there it remains in the form of latent tissue cysts for at least sixty days, but probably for the rest of the host’s life. The presence of these parasitic cysts led to chronic inflammation in the prostate, which is a precursor to benign prostatic hyperplasia (BPH), the reason why older men have to get up multiple times to pee at night. Chronic inflammation in the prostate is also connected to prostate cancer, which afflicts more than 200,000 men in the US each year.

Parasites in prostates. The control panel shows cells from an uninfected mouse prostate (the nuclei are stained blue). The other panel shows the presence of a Toxoplasma tissue cyst (green) in the prostate 14 days post-infection (14 D.P.I.).

If Toxoplasma is also found to trigger chronic inflammation in human prostate, the finding takes on added significance given the prevalence of the parasite in the human population. According to the CDC, up to 22% of Americans are infected with the parasite, which is transmitted through oocysts that are excreted into the environment by infected cats or through tissue cysts present in game and livestock. 

Women are commonly advised to avoid gardening, changing the litterbox, and consuming undercooked meat while pregnant so the parasite doesn’t transmit to the fetus. Men may need to heed these warnings as well to avoid a prostate full of parasites, but a lot of critical work still needs to be done before we can ascertain whether this discovery has relevance to prostate issues in humans. Regardless, our study introduces Toxoplasma-infected mice as a powerful new model for the study of prostatic inflammation.

Prostate cancer is believed to arise from a constellation of events that can involve a person’s genes and environmental exposures. Infectious agents and carcinogens have previously been proposed as agents that can injure the prostate and lead to the development of chronic inflammation. Numerous types of bacteria and viruses have been shown to infect the prostate and cause an inflammatory response; this new study in mice suggests that the parasite Toxoplasma might be added to this list.

Contributed by:  Bill Sullivan

Note:  Bill Sullivan is a co-author on the study highlighted in this article.


Colinot, D., Garbuz, T., Bosland, M., Wang, L., Rice, S., Sullivan, W., Arrizabalaga, G., & Jerde, T. (2017). The common parasite induces prostatic inflammation and microglandular hyperplasia in a mouse model The Prostate DOI: 10.1002/pros.23362

Saturday, April 22, 2017

We Support The March For Science

In person or in spirit, scientists and science enthusiasts MARCH FOR SCIENCE today. Why? Science is the most reliable method that humanity has devised that teaches us how things work - it is the beacon that leads us to the truth. Truths that are often well-disguised, beyond our intuition, and shielded behind our preconceived notions. The truth can upset worldviews and bottom lines, but those who resist it cannot be allowed to jeopardize the reality reasonable people have come to accept. When we forego the evidence to maintain a faulty reality, we fail to progress. A world that doesn’t invest in science will pay for it with another Dark Age.

Support science, education, and evidence-based policy.

Friday, April 21, 2017

You've Gotta Learn to Walk Before You March

March For Science Logo
Saturday, April 22, 2017, is Earth Day. So it is appropriate that organizers have scheduled a large-scale march on Washington, DC (and over 500 other satellite marches planned), in support of evidence-based policy decisions. It is interesting that in the year 2017 we require marches to get across the point (hopefully) that scientific evidence should be a critical aspect of policy development. But alas, here we are.

So, in the spirit of marching along with our fellow scientists and science enthusiasts who understand the importance of scientific inquiry, and who want to advocate for sustained and predictable federal funding for science, we at THE 'SCOPE thought it would be fun to take a closer look at the funny (dare I say, silly?) way that humans, march: on two legs, or bipedally as it is called.

We briefly covered the evolution of bipedal walking in an earlier post, so we will not rehash the anatomical adaptations that allow for this type of locomotion. Suffice it to say that our skeleton has undergone several changes to the spine, pelvis, and lower limbs, that allow us to keep our knees under our center of mass while standing and walking. Instead, we will focus on HOW we accomplish walking along on two legs.

The phases of the gait cycle. From Anatomy Reference Center.
When walking, our lower limbs alternate between being planted on the ground and swinging through the air in order to be planted as the next step. We refer to these two different positions as the two phases of the "gait cycle": stance phase, or when the foot is planted; and swing phase, or when the foot is.... wait for it.... swinging.

Transfer of the weight across the foot during stance phase.
Let's now put the gait cycle "under the scope" for a moment. The gait cycle is defined as the period from stance phase of one limb to the next stance phase of the same limb - never mind for now that the other limb is in its own gait cycle! The stance phase begins when the heel strikes the ground, at which point the body weight is transferred from the heel to the lateral side of the foot, across the ball of the foot, and toward the base and ultimately distal end of the big toe (referred to as "push off" or "toe off"). At push off, the limb enters the swing phase, which itself ends when the heel strikes the ground again.

So as you can see, the stance phase accounts for a higher proportion of the gait cycle (about 60%) than does the swing phase. But remember this is for one limb only... the other limb is also in one of the two phases of the gait cycle. Over the combined gait cycles of both limbs, the two limbs together contact the ground (double support) only about 25% of the time. So roughly 75% of the combined gait cycles involves support over a single limb. As walking speed increases, the percentage of the gait cycle spent in single support also increases. During running, for example, there is no period of double support!

Even with the silly type of locomotion that humans employ, it is highly energetically efficient because bipedal walking is essentially a series of controlled falls over the supported limb (the limb in stance phase). In other words, the lower limb acts like an inverted pendulum which uses the force of gravity and the principles of angular momentum to propel the body forward. Combine the low input energy required to sustain level walking with the fact that 60-70% of the input energy is recovered through anatomical function of the lower limb that reduces the vertical and lateral displacement of the center of mass during the gait cycle, and what you have is a recipe for efficient locomotion on two legs.

So, to those who are marching on behalf of the scientific enterprise, remember this: you can stride a great deal before you tire out simply because you are the product of 6-7 million years of evolution for bipedal locomotion.

Jason Organ is Assistant Professor of Anatomy & Cell Biology at Indiana University School of Medicine. Follow Jason on Twitter.

Mochon S, & McMahon TA (1980). Ballistic walking. Journal of biomechanics, 13 (1), 49-57 PMID: 7354094

Lovejoy, C. (1988). Evolution of Human Walking Scientific American, 259 (5), 118-125 DOI: 10.1038/scientificamerican1188-118

Gait cycle illustrations from: Organ JM. 2017. Gait. Amirsys Anatomy Reference Center, Elsevier: Salt Lake City, UT.

Thursday, April 20, 2017

Unsung Heroes In Our Battle Against Infectious Disease

Humanity has always been at war with infectious agents, but it wasn’t until 1860 when Louis Pasteur famously theorized that microbes (first observed by Antony van Leeuwenhoek in the 1600s) cause disease. It took another 70 years before Alexander Fleming noticed that Penicillium mold produced a substance that killed bacteria. While most people are familiar with these luminaries in the field, have you heard of Francesco Redi, Ignaz Semmelweis, Theobald Smith, Mary Hunt, and a cow named Blossom? In this presentation, we celebrate some of the “unsung heroes” whose victories are often neglected from the infectious disease saga.

In the talk below, Dr. Bill Sullivan, a professor at the Indiana University School of Medicine, takes us on a fascinating tour through medical history, answering these questions and more:

How did we figure out that microscopic creatures can make us sick?
Why were milkmaids considered to be so beautiful and what does that have to do with vaccination?
How were starfish important to the discovery of the immune system?
What do you mean penicillin wasn't the first antibiotic?