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Thanks to Themes4CMS for our new website!

Posted by admin at 11:07 PM Friday, December 23, 2011

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The Harvard Science Review deeply thanks Themes4CMS (www.themes4cms.com) for helping us design and launch our sparkling, new website. They have been easy to work with, creative, and on-time; we recommend them to anyone looking to bring an organization online. If you have any suggestions for the website, or are interested in managing the Harvard Science Review page as our webmaster, please email harvard.sci.review@gmail.com

You Are the Germs You Eat aka How Human Culture Shapes Evolution

Posted by admin at 10:01 PM Friday, April 16, 2010

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Your gut is filled with trillions of bacteria that feed on the remains of your every meal(1). These bacteria, however, are not simply freeloaders that take advantage of a cozy habitat where food is always abundant; they serve many important functions. Among these functions are the salvaging some nutrients which our bodies cannot digest, production of vitamin K and maintaining the proper functioning of the immune system(2).

Life is not easy for an intestinal resident bacterium. There is intense competition for the available resources, in this case what is left of the food we eat after our stomach and intestinal enzymes have broken down most of the complex compounds. Therefore, bacteria that can better break down what is left will survive and multiply better. For example, humans cannot break down the polysaccharides in the plants which we feed on (think “dietary fibers”), so these compounds are fair game for the intestinal flora. Therefore, one would think that the resident bacteria (those that have won, for now, the natural selection contest) have accumulated a lot of these “glycosidases” (enzymes that break down carbohydrates), and indeed this is what research has shown(3). So the bacteria that live in our gut are proficient at breaking down our dietary remains, which makes a lot of sense from an evolutionary perspective.

The question that one can ask is how these bacteria have evolved to have so many genes for breaking down specifically the carbs that we eat and can’t digest (especially since not all of us eat the same carbs)? Well, one general way bacteria evolve is by a mechanism called “lateral gene transfer”, which basically means bacteria can share DNA with each other. Lateral gene transfer is responsible for specifically hard to control infections: the disease pathogens get the genes for antibiotic resistance from other bacteria, process which makes them harder to kill. It is also possible that lateral gene transfer is responsible for the accumulation of glycosidase genes in gut bacteria.

On April 8, 2010, Hehemann et al.(4) reported a rather interesting example of such genetic transfer. The team was studying a glycosidase known as porphyranase, which breaks down the polysaccharide porphyran. Porphyran is found mainly in a type of marine red algae named Porphyra (hence its name). Though the researchers started studying this enzyme in a marine bacterium that shares an ecosystem with the algae, they soon discovered it was also found in a gut bacterium (Bacteroides plebeius). Now the real twist: the gut bacteria only possess porphyranase in Japanese individuals, not in Americans(3, 5). The probable reason for this: people in Japan eat seaweed in large amounts, while people in the USA do not. The fascinating conclusion is that bacteria in our diets help shape the bacteria in our gut. The different eating habits of humans across the world contribute to them having different intestinal floras, a discovery which might have big implications in the current global context. The food we eat today in the developed world is significantly “cleaner” that the food that has shaped our evolution. Also, global trade allows us to eat foods that were previously unavailable to us because of geography. All these mean that the ecosystem of our intestines is changing faster than ever before, but also that we are depriving our residents of the marine bacteria they used to see very often. This could have major implications for our health, though at this point what those implications are is anyone’s guess. What better way to end this discussion than the scientist’s favorite phrase: More research is required to…

  • 1. L. Dethlefsen, M. McFall-Ngai, D. A. Relman, Nature 449, 811 (2007).
  • 2. F. Guarner, J.-R. Malagelada, The Lancet 361, 512 (2003).
  • 3. P. J. Turnbaugh et al., Nature 457, 480 (2009).
  • 4. J.-H. Hehemann et al., Nature 464, 908 (2010).
  • 5. K. Kurokawa et al., DNA Res 14, 169 (January 1, 2007, 2007).

Butterflies and Climate Change

Posted by admin at 1:25 PM Thursday, April 8, 2010

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One of the biggest challenges for climate change scientists is pinpointing direct evidence of disturbing changes in the global climate. In Australia, however, a small but significant shift in the timing of spring events may be the place to start. In the last 65 years, a striking increase of 0.14 degrees Celsius in air temperature per decade has taken place in Melbourne. On top of this, scientists at the University of Melbourne have discovered a biological change in the common butterfly Heteronympha merope: the butterfly is emerging from its cocoon 1.6 days early each decade over the same 65 year period.

Butterflies raised in the laboratory with a controlled climate mirroring the rise in Melbourne’s temperature also revealed a shift in the timing of the butterflies’ emergence from the chrysalis (1.3 days earlier). Furthermore, there is strong evidence that the actual 0.14 degree increase in temperature measured in Melbourne is the result of human activity and cannot be explained but natural variations in temperature over time (1). The evidence for the human-induced climate change only grows harder and harder to ignore.

String vision

Posted by admin at 3:40 AM Thursday, April 1, 2010

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Check out this ophthalmotrope, found at Harvard’s Putnam Gallery!
(photograph by the blogger)

The device, which served to demonstrate muscular control of ocular vision, was made by Max Kohl in Germany at around 1893. The device consisted of lead weights on strings, which could be pulled to show movements of the muscles that bring the eyeballs together.

At this time, refrigeration was not widely used yet, so cadavers reeked too much for anatomy students to work with. Instead, machines like these offered an alternative way to interactively teach anatomical details. We’ve sure come a long way since 1893… all thanks to formaldehyde!

Want to live longer? Take two of these every morning before breakfast!

Posted by admin at 8:12 PM Tuesday, March 30, 2010

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How many of us would like to hear something like that from their doctor? Probably most. But is it really possible to devise a drug that will make you live longer? You may be surprised that the answer is “probably”, and in fact we seem to not be very far from developing one. In July 2009, Harrison et al.(1) reported in Nature that feeding middle-aged mice a drug called rapamycin significantly extended their lifetime, regardless of their genetic background.

This incredible breakthrough was possible because of a radical revolution that is happening in the field of aging biology. For a long time it was thought that aging was simply a result of wear and tear brought about by reactive oxygen species, molecules that form naturally in each of our cells as a result of our aerobic metabolism(2). However, now a dramatically different paradigm is replacing the wear and tear view. Though it is still regarded as possible that reactive oxygen species are somehow involved in the aging process, most scientists now regard aging as a programmed event which can be seen as an extension of normal development. If this is indeed the case, specific inhibitors of key enzymes in the pathway should be able to increase lifespan, much like antiretrovirals postpone the progression of AIDS.

One of the biochemical pathways that have surfaced in recent years as a key player in the aging process is the so-called TOR pathway, at the heart of which lies an enzyme known as the TOR kinase. By inhibiting the TOR pathway, researchers have successfully extended the lifespan of organisms as diverse as brewer’s yeast(3), nematodes(4) and fruitflies(5). Until now, however, it was not known if this was possible in mammals because mammals do not possess the TOR kinase, though they do have a related enzyme referred to as mTOR. Now, Harrison et al. prove that feeding an mTOR inhibitor (rapamycin) to mice late in their life increases lifespan by as much as 14%.

This study holds great promise for increasing human life span for a number of reasons. Firstly, the authors used genetically heterogeneous mice, as opposed to the usual highly-inbred laboratory mice. This is a crucial distinction, because inbred strains usually die of a particular disease, while “normal” mice, like people, die of various causes. Thus rapamycin does not only decrease the risk of a particular disease, it is a real inhibitor of aging. This is further supported by the disease profile of rapamycin-fed mice, which was identical to that of control mice. Secondly, the rapamycin was fed late in the life of the mice. This means that – in case this is ever confirmed in humans – each individual could choose if he or she wants to live longer.

Thus, it seems that the new paradigm is paying off. Of course, results like these need to be confirmed, and there must be a certainty that administering rapamycin to humans does not have any serious side effects. If this turns out to be the case, it may not be so unrealistic to hope that in twenty years clinical trials for a scientific fountain of youth will be underway.

- S. Andrei Anghel
[From September 10, 2009]

  • 1. D. E. Harrison et al., Nature 460, 392 (2009).
  • 2. M. L. Genova et al., Annals of the New York Academy of Sciences 1011, 86 (2004).
  • 3. R. W. Powers, M. Kaeberlein, S. D. Caldwell, B. K. Kennedy, S. Fields, Genes & Development 20, 174 (2006).
  • 4. K. Jia, D. Chen, D. L. Riddle, Development 131, 3897 (2004).
  • 5. P. Kapahi et al., Current Biology 14, 885 (2004).

The Placebo Effect: A very basic neurological process

Posted by admin at 8:07 PM Tuesday, March 30, 2010

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The placebo effect – the curious phenomenon in which a patient feels better and even gets better when he thinks he is receiving treatment but in fact is not – has received great attention by the scientific and medical communities and by the general public in the recent decades. After its discovery, experimental medical trials had to be redesigned to account for it, and a race began among scientists to elucidate how this extraordinary “treatment” works. Many of the following studies have focused on the placebo effect of relieving pain (1) and considerable data now indicates that this occurs through the endogenous opioid system (the same neurological circuit activated by painkillers such as morphine) (2,3).

In this month’s edition of Neuron, Eippert et al. (4) produce solid data supporting a role of the opioid system in the placebo effect. They do this through an elegant study in which patients were given an inert treatment for a mild burn, and half of them were further administered naloxone, a drug that blocks the opioid circuits in the brain. The authors then employed a combination of two state-of-the-art medical imaging techniques – functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) – to visualize which areas of the brain “light up” in the presence and absence of the naloxone.

Their results are groundbreaking: not only do they show a clear correlation between administration of naloxone and the decrease in placebo pain relief, but they identify some very “primitive” brain components – the amygdala, the hypothalamus and part of the brainstem – as part in the placebo effect circuitry. This comes as a great surprise: because the phenomenon is the result of voluntary expectation (the patient thinks he is receiving treatment) it would be more intuitive that it mainly involved the more “evolved” and human-specific parts of the cortex.

Given these new data, one cannot help wondering: if the placebo effect is so deeply rooted in one’s brain, does that mean it is somehow connected to more crucial brain functions? And when and more importantly why, did the placebo effect evolve? Like is often the case with science, this groundbreaking discovery seems to generate more questions than it answers.

- S. Andrei Anghel
[From September 7, 2009]

  • 1. V. De Pascalis, C. Chiaradia, E. Carotenuto, Pain 96, 393 (Apr, 2002).
  • 2. P. Grevert, L. H. Albert, A. Goldstein, Pain 16, 129 (Jun, 1983).
  • 3. J. D. Levine, N. C. Gordon, H. L. Fields, Lancet 2, 654 (Sep 23, 1978).
  • 4. F. Eippert et al., Neuron 63, 533 (Aug 27, 2009).

Single Factor Reprogramming of Human Fetal Neural Stem Cells with Oct4: A Step Towards Translating iPSC Research to the Bedside

Posted by admin at 8:02 PM Tuesday, March 30, 2010

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The ethically fraught field of embryonic stem cell research received much attention in late 2007 when induced pluripotent cells stem cells (iPSCs) were derived from somatic cells manipulated with the Yamanaka factors– Oct3/4, Sox2, Klf4, c-Myc. These genes, which are highly expressed in embryonic stem cells, induce pluripotency and “embryonic stem cell-like” characteristics in human and mouse cells when overexpressed. Such cells hold promise for the field of regenerative medicine, and they dodge the controversy surrounding embryonic stem cells, since iPSCs can be derived from somatic cells, not embryos. Furthermore, they have demonstrated therapeutic benefit similar to that of embryonic stem cells. However, iPSCs are not free from drawbacks, and use could be limited in humans if viral transgenes are used in the induction process. This is especially true for oncogenes c-Myc and KLF4; reactivation of these in the host genome can lead to tumor formation. This has led researchers to examine the precise mechanisms of the Yamanaka factors and seek out combinations of 1-2 factors that are equally efficacious but pose less risk of tumorigenicity. Kim et al. (1) demonstrated in Feburary of this year that exogenous Oct4 expression was sufficient to reprogram adult mouse neural stem cells into iPSCs with capacity to differentiate into cells of endodermal, ectodermal, and mesodermal lineage. In a Nature Letter, Kim et al. showed that ectopic expression of Oct4 is sufficient to induce pluripotency in human fetal neural stem cells. In vitro, neural stem cells were retrovirally infected with human Oct4 and KLF (two factor) or Oct4 alone (one factor). Eight days after infection, cells were replated on feeder layers, and 10 weeks later, colonies with neural rosettes were observed. Within 5-6 days, the rosette could be removed from the colony, and the rest of the human ES-cell-like colony could be replated and cultured, with an overall reprogramming efficiency of 0.004% in the single factor colony. To confirm that the Oct4 reprogramming was sufficient, epigenetic analysis showed that the levels of methylation of the Oct4 promoter in the reprogrammed cells and embryonic stem cells were similar. The reprogrammed cells retained normal karyotypes, suggesting that single-factor reprogramming is not only feasible, but also not harmful to cell differentiation capacity and phenotype. It is possible that reprogramming of these neural stem cells is possible with only a single factor because their genetic and epigenetic profile is similar to that of embryonic stem cells. Future work is necessary to examine whether non-viral manipulation of cells can induce pluripotency with enough efficiency to create therapeutic cell lines, and which cell sources are ideal reprogramming candidates.

- Katie Ransohoff
[From September 3, 2009]

  • 1. J.B. Kim et al., Nature (Aug 28, 2009)
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