On the afternoon of May 12, 2008, a magnitude-8 earthquake hit Sichuan province, a mountainous region in western China. Official figures stated that 69,197 were confirmed dead, including 68,636 in Sichuan province, and 374,176 injured, with 18,222 listed as missing.

The earthquake left about 4.8 million people homeless,though the number could have been as high as 11 million. Although this disaster itself was so devastating, many inspiring stories still managed to surface during that time.

a graphic of a heart with bandages over itIt’s amazing that it is within this horrific tragedy that I find one of the most moving stories I’ve ever heard. On May 13, the day after this earthquake, rescuers saw a woman lying motionless in the ruins of Beichuan County.

Through a pile of reinforced concrete space, people could see the position of her body. She was kneeling down, prostrated, as if worshipping the ancients. Her upper body was creeping forward, and her hands were on the ground for support. Her body was so disfigured from the disaster that no one could bear to look at her.

After the rescuers confirmed her death, the leader of the rescue team found a living child under her. This 3- or 4-month-old baby was wrapped with a small, red, flowered quilt. Because of his mother’s protection, he was not injured at all and was still peacefully asleep.

When the accompanying doctor untied the small quilt for physical examination, he found a mobile phone with a message written on the screen that said: “Dear baby, if you can live, please always remember that I love you!”

I cannot say how shocked I was the first time I heard this story. The only thought I have is that it’s never been clearer to me that love is the most amazing and powerful thing in the world. I hope we all can learn from the unconditional love epitomized in this story and give our love to the people around us to make our world a better place.

About the Author

Xin Liu

Xin Liu is a postdoctoral fellow in biological chemistry. She loves her research, writing, singing and is really happy to make new friends here.

What do faulty brakes on a car and cancer cells have in common? For one, cancer cells have found ways to evade checkpoints that the body’s cells use as brakes to stop them from dividing out of control. By this same analogy, the accelerator in a cancer cell is always pushed to the floor, and the brakes are ineffective, causing cancer cells to multiply uncontrollably.

Though chemotherapy and surgery have been treatment staples for decades, they are not without unwanted side effects, expenses and resistances, in which the cancer cells find ways to circumvent the treatments. Therefore, instead of using exhaustive and expensive chemotherapies, what if doctors could use the patients’ own immune systems to fight cancer?

boxing glove punching a cancer virusDubbed Science magazine’s Breakthrough of the Year1 in 2013, cancer immunotherapy offers new hope for combating difficult-to-treat cancers by invoking the power of the patients’ own T cells and B cells: the body’s natural immune defense mechanisms.

As early as the 1990s, biologists in Japan found that T cells have a brakelike mechanism that prevents their aberrant activation. This molecule, known as programmed cell death protein 1, or PD-1, is a protein expressed on the surface of both T cells and naive B cells. Along with that, other reports published around the same time showed that drugs inhibiting PD-1 released this brake on T cell function and subsequently overcharged the immune system.

However, the potential power of these immune checkpoint mechanisms wasn’t recognized until Drew Pardoll, M.D., Ph.D., of The Johns Hopkins University began using PD-1 inhibitors in the clinical setting. Specifically, in a clinical trial he pushed for, cancer patients with refractory disease treated with PD-1 inhibitors saw their tumors shrink.

A year after immunotherapy gained its Breakthrough of the Year moniker, Suzanne Topalian, M.D., director of the Melanoma Program and professor of surgery and oncology at Johns Hopkins, helped pioneer and solidify the field of immunotherapy in cancer treatment. Recently listed as one of Nature’s Top 10 people of 2014, Dr. Topalian is paving the way to make these treatments a reality through clinical trials she initiated at Johns Hopkins using the PD-1 inhibitor nivolumab in partnership with Bristol-Myers Squibb. Having completed a promising trial of nearly 300 patients that was published in the New England Journal of Medicine, Topalian found that nivolumab was effective in combating treatment-refractory lung cancer, melanoma and kidney cancers.

Most recently, a follow-up phase 3 clinical trial demonstrated that the PD-1 inhibitor is superior to chemotherapy, with significant improvements in overall survival and progression-free survival in melanoma patients. This is particularly encouraging given that lung cancer and melanoma remain some of the most deadly cancers to treat today.

Doctors and researchers have barely scratched the surface of immunotherapy’s potential, and more trials and research are currently being conducted on advanced cancers that were previously thought to be untreatable. Nevertheless, researchers such as Pardoll and Topalian are proceeding cautiously yet optimistically as the landscape of treatment options broadens for cancer patients with advanced disease.

1. Science 20 December 2013: Vol. 342 no. 6165 pp. 1432-1433 DOI: 10.1126/science.342.6165.1432

About the Author

Paul Sirajuddin

Paul Sirajuddin is a postdoctoral fellow in radiation oncology, a writer and a photographer. When he isn’t zapping cells or shooting photos, he’s writing about science.

Imagine a new restaurant just opened downtown and you want to check it out. You hop on the bus and take it a few stops. Once you get off, you have no sense of where you are or how to get to your destination.

You look around to collect your bearings: Camden Yards is to your right, and you see the Bromo Seltzer tower in the distance. You understand where you are and make your way to dinner, and on your way back you find the exact location, knowing that it is the bus stop. How did this internal mapping occur? Researchers, led by postdoc Joe Monaco under the mentorship of Jim Knierim, a professor of neuroscience at The Johns Hopkins University, have found that this mapping is due, in part, to the initial scanning behavior that allowed you to gather your bearings once you got off the bus.

a maze in the shape of a brainHow brains create an internal perception of the environment of the external world uses the hippocampus — a seahorse-shaped structure within the brain — and specific “place cells.” These cells will only fire when they recognize that small region of the external world. They are thought to create a spatial framework onto which memories are added, similar to how one hangs clothes on a clothesline.

Though the discovery of these cells was a monumental milestone in the field of neuroscience — in fact, the person who discovered them was one of this year’s recipients of the Nobel Prize — how the place cells acquire their specific area of activation, or “place field,” is unclear.

Johns Hopkins scientists looked into1 exactly this by training rats to walk around a circular track while researchers recorded from their hippocampi. They also recorded the animals with a video camera to match behavior with brain activity. When they analyzed the data, they found cells that were active only after the animal paused, looked around, then resumed moving. On initial laps, a cell was not active on any part of the track, but once the animal scanned its environment, that cell was active in that same location for the rest of the day.

This is very similar to when you looked around at the bus stop, creating a new part of your internal map. Without looking around, these cells would have remained silent, and neither you nor the rat would recall the exact position if it happened again.

The ability to recall environments and what happens where is an incredible function of the nervous system. Without this ability, we would only be able to navigate one environment at a time and would fail to gain our bearings as we pass into new locations. By taking the time to look around a new environment, you’re giving yourself the resources your brain needs to update your internal map.


1. Joseph D Monaco, et al (2014) Attentive scanning behavior drives one-trial potentiation of hippocampal place fields. Nature Neuroscience 17, 725-731. doi: 10.1038/nn.3687

About the Author

Kevin Monk

Kevin Monk is a neuroscience graduate student who enjoys sharing scientific discoveries with anyone interested in reading about them.

As 2014 ended, Medscape released “The Year in Medicine 2014: News That Made a Difference.” Among the notable stories were the Dr. Oz Senate hearings, in which the celebrity doctor was censured for “perpetuating weight loss fraud.” He defended himself, saying he believed in his products, though still admitting the products’ claims were not backed by scientific evidence.

A prospective observational study1 recently published in BMJ found that in 40 episodes of The Dr. Oz Show, existing evidence contradicted 15 percent of the host’s claims, while 39 percent weren’t supported by scientific evidence.

Though the validity of popular health celebrities such as him might be easy for us as scientists to disregard, we would be remiss to simply shake our heads and ignore the problem. Much of the lay public relies on personalities like Dr. Oz for their health information, and last year he attracted over 3 million viewers a day. Instead of simply ignoring the issue, we could use this information to effect positive change.

pull quote reading: We need to recognize when medical jargon is appropriate and when it is not

As Johns Hopkins University School of Medicine students, we are in the unique position of being able to bridge the gap between the language of the lay public and health professionals.

When I came to Johns Hopkins, I didn’t know what a hernia was. Nor a hemorrhoid. Nor a hemorrhage. Really, it seemed medical H-words were all made of foreign stuff.

Yet now I am in my fourth year, spouting a vocabulary my first-year self would have registered as not unlike Flemish. And the truth is, I often forget how much I have learned. I was reminded of this recently while teaching a group of first years, and one commented on how much information I seemed to have packed into my brain. She said the system must really work if I was anywhere near her level when I started. I remember feeling the same way toward my upperclassmen, and yet I had not realized I had crossed to that other side.

It is this inherent transition that we need to capitalize on: We need to remember what it was like before we stepped over to the “informed scientist side.” We need to recognize when medical jargon is appropriate and when it is not.

Please don’t get me wrong: I love the intellectualization of medicine. I love knowing and using the obscure vocabulary while rounding outside patient rooms, but as soon as we walk in, that language has to change. It needs to be clear and facilitate better patient education. Simple language can be used to teach concepts, while detailed terminology can be left outside the room.

Dr. Oz and his contemporaries may be misinforming, but their popularity among the general public means they cannot be overlooked. By speaking at a basic level, they appeal to the need for an accessible means of medical communication.

Instead of simply shunning Dr. Oz, let’s learn from him.

Let’s be encouraged to educate our patients in simple language. But this time, let’s give a message based on evidence-based medicine and clear, appropriate clinical intention.


1. BMJ 2014; 349 doi: http://dx.doi.org/10.1136/bmj.g7346 (Published 17 December 2014)

About the Author

Arielle Medford

Arielle Medford is a fourth-year medical student who spent this past year doing cancer research. She is also a dancer and a writer, and she loves everything science.

An interdisciplinary team of scientists from the Lieber Institute and Johns Hopkins has discovered more than 50,000 regions of the genome that show different levels of activity in the brain across six stages of human development. Their report1, published online on Dec. 15 in Nature Neuroscience, highlights the complexity of genes associated with brain growth as well as the link between these age-associated fingerprints and neurological and psychiatric diseases.

Previous studies relied on predefined sets of genes to analyze changes in gene expression, but the authors’ used a statistical model that allowed them to identify gene regions with differential expression without the need for existing gene databases. By combining this model with high-throughput genomic sequencing technology, the authors were able to find many known and unknown gene regions that are expressed at different levels throughout brain development.

illustration of a human brain glowingFor each region, the researchers evaluated which developmental stage showed the highest activity. Most regions (81.7 percent) have the highest activity in the fetal brain. Not surprisingly, these gene regions are enriched for genes linked to neuronal growth, connectivity and signaling.

More intriguing still is the fact that a large fraction of these “differentially expressed regions” map to areas of the genome not previously associated with gene expression. For many genes, not all of the RNA sequence is useful for making proteins. Some of the RNA regions that do not encode for protein (called "introns") must be removed before the RNA enters the main body of the neuron.

Because the vast majority of the analyzed RNA came from the neuron body, the researchers expected to find very few introns. However, the authors found that 41.5 percent of their differentially expressed regions were attributable to areas of the genome previously annotated as introns. From this work, the researchers were able to conclude that these RNA regions were unlikely to be introns, suggesting that a large fraction of previously unknown sequences in the genome could potentially be made into protein.

The researchers then used bioinformatic methods to explore the association of these differentially expressed regions with genetic risk factors previously linked to neuropsychiatric diseases. They found significant enrichments of known risk factors for conditions including schizophrenia, autism, intellectual disability, Parkinson’s disease and Alzheimer’s disease. For age-related diseases such as Parkinson's and Alzheimer's, risk factors were enruched in regions with high expression late in life. In contrast, schizophrenia risk factors were enriched in regions with high expression early in life.

Findings such as these could support the neurodevelopmental hypothesis of schizophrenia, which proposes that disruptions to early brain wiring may increase the risk of schizophrenia later in adulthood. Overall, this study provides a useful resource for those in the scientific community interested in brain gene expression changes across the human lifespan and the relationship between these changes and neuropsychiatric disease.


1. Andrew E Jaffe, et al (2015) Developmental regulations of human cortex transcription and its clinical relevance at single base resolution. Nature Neuroscience 18, 154-161. doi:10.1038/nn.3898

About the Author

Alisa Mo

Alisa Mo is an M.D./Ph.D. student who's passionate about the intersection of neuroscience, genomic medicine and society. She’s also a pianist and enjoys cooking.

Anyone who has taken a biology or biochemistry class is familiar with the central dogma of the biological sciences, which describes the flow of genetic information. It dates back to Francis Crick in 1956 and can be simplified to the following concept: DNA encodes for RNA, and RNA encodes for proteins.

alzheimers word cloud with other words like healthA new study1 from the University of Utah reveals that this linear flow of information might not be as straightforward as we once thought.
The study takes a close look at the quality control process involved in protein synthesis. Protein-making machines known as ribosomes are responsible for stitching together the amino acid building blocks of proteins by using the sequence of messenger RNA (mRNA) as a blueprint.

When an error occurs, the ribosome will stall. This recruits an assembly of proteins charged with disassembling the ribosome, removing the faulty RNA and degrading the improperly made protein.
One particular quality control protein, known as Rqc2p, was found to play a surprising role. This protein — which is conserved across numerous species, from yeast to humans — binds to the stalled ribosome and promotes the continuation of protein synthesis without the use of the template mRNA sequence. Rqc2p accomplishes this unique function by binding to transfer RNA (tRNA) molecules carrying alanine or threonine amino acids.

The binding of specific tRNAs to the ribosome is generally facilitated by the sequence of the mRNA, but this protein manages to bypass what was once perceived as a crucial step in the protein-making process. This results in a nonsensical tag of alanines and threonines added to the end of improperly made proteins.
One potential purpose of this tag may be to target the dysfunctional protein for degradation. Accumulation of degenerate proteins has been linked to neurodegenerative diseases, such as Alzheimer’s and Huntington’s. The study authors suggest this new method of protein synthesis could contribute to disease prevention.

Peter Shen, Ph.D., and co-authors first arrived at this interesting finding when they used cryo-electron microscopy to determine the structure of the quality control proteins bound to a stalled ribosome. They observed that Rqc2p was bound to both the ribosome and a tRNA, which it had positioned adjacent to the improperly made protein chain. Seeing is not always believing, though, so the scientists involved in the study carried out numerous biochemical assays to validate this new method of protein synthesis.

The next steps will be to determine when this process takes place in the grand scheme of the cell cycle and what occurs when this process fails. While those key points are still unclear, what we know for sure is that our notion of how nature works is far more complicated than once perceived, and that old dogmas are subject to change with time and innovation.
The study was published in the Jan. 2, 2015, edition of Science


1. Rcq2p and 60S ribosomal subunits mediate mRNA-indpendent elongation of nascent chains. Peter S. Shen, Joseph Park, Yidan Qin, Xueming Li, Krishna Parsawar, Matthew H. Larson, James Cox, Yifan Cheng, Alan M. Lambowitz, Jonathan S. Weissman, Onn Brandman, Adam Frost. Science. Jan. 2, 2015: Vol. 347 no. 6217 pp. 75-78.

About the Author

Shannen Cravens

Shannen Cravens is a Ph.D. student in molecular biophysics with a passion for teaching who enjoys weaving art into her lab life.

While we’ve all heard the tired warning to wear our coats outside so we don’t get sick, it’s fair to wonder how much validity there is to such reasoning. Are we really more likely to catch a cold in colder weather?

woman sneezing

Lucky for us, scientists at Yale are looking into it. Their recent article1, published in Proceedings of the National Academy of Sciences, looked at the effect that colder temperatures had on rhinovirus growth in mouse airway epithelial cells (AECs). It was already known that rhinoviruses grow better at cooler temperatures — around 33 degrees Celsius — but the mechanisms by which this preferential growth occurred remained largely unknown. However, in this article, scientists presented new findings that suggest the mechanism is more related to impaired immune function in the infected cells than directly virus intrinsic.

Specifically, the researchers used ex vivo treatment of mouse AECs infected with a mouse-adapted rhinovirus to test differences in cellular processes at varying temperatures.

When compared to those cells grown at 37 degrees Celsius, the cells grown at 33 degrees Celsius had a significantly decreased amount of immune response elements, including both type 1 and type 3 interferon subtypes and interferon-stimulated genes.

Intriguingly, it is known that interferons limit viral growth and have been specifically reported to limit rhinovirus growth2, and interferon-stimulated genes are known to aid in immune response to viruses.

Taken together, these findings provide a potential mechanism by which growth of rhinovirus might be inhibited at higher temperatures. The paper goes on to further elucidate cellular mechanisms for this differential interferon production. Specifically, the researchers discovered that the recognition of viral replication intermediates, namely, dsRNA, by RIG-I-like receptors (RLRs), was responsible for the increased interferon response at higher temperatures. RLRs are part of our innate immune system and are responsible for recognition of “nonself” antigens, such as viral RNA.

But how is the temperature difference affecting the interferon response? Through a series of experiments, the researchers identified two mechanisms that affect viral growth at differing temperatures. Essentially, they found that at 33 degrees Celsius, decreased RLR enzyme activity was responsible for the less potent interferon response. At 37 degrees Celsius, enhanced signaling through type 1 interferon receptors resulted in increased interferon production.

The the authors’ findings suggest there is a temperature-based growth advantage in cells infected with rhinovirus, and this advantage is mediated through cell-intrinsic mechanisms. While more research is needed, this study could help explain why cold temperatures could lead to more cases of the cold virus.


1 Foxman EF, et al. (2015) Temperature-dependent innate defense against the common cold virus limits viral replication at warm temperature in mouse airway cells. Proc Natl Acad Sci USA [Epub ahead of print].
2 Becker TM, et al. (2013) Exogenous interferons reduce rhinovirus replication and alter airway inflammatory responses. Ann Allergy Asthma Immunol 111(5):397–401.

About the Author

Bree Yanagisawa

Bree Yanagisawa is an aspiring scientist who is passionate about the unique opportunity represented in engaging science through the use of mass media sources.

In a year where scientists have turned back the clock on aging and designed robots to think as a group, choosing a standout success is a charge that is near impossible.

However, when Science magazine released its annual short list of the most outstanding contributions to the scientific field, it ultimately made the difficult decision of naming the Breakthrough of the Year. From the 19 exceptional candidates of the past year, one soared high above the rest. The 2014 Breakthrough of the Year is the landing of Philae on Comet 67P/Churyumov-Gerasimenko.

The descent is a feat 10 years in the making, and the exciting trek of the lunar lander appears borrowed from the pages of science fiction novels. The project, spearheaded by the European Space Agency with a price tag of 1.4 billion euros, began with the launch of the Rosetta vessel in 2004. Over the next decade, Rosetta was flung through the orbits of Earth and Mars, gaining the momentum necessary to align with the 6.5-year orbit of the Comet 67P. Once Rosetta entered the orbit of 67P, scientists could breathe a sigh of relief.

The entry marked a first in the history of space travel and meant the mission was on the whole a success, as Rosetta itself contains most of the payload for the discovery portion of the launch. Because Rosetta is trapped in the orbit of 67P, sometimes nearing 10 kilometers from the surface, the comet's movements can be tracked for the foreseeable future. Onboard are powerful spectrometers and instruments with the capability to scan the comet visually and analyze the composition of its atmosphere. These two pieces of data will give scientists the ability to postulate on the comet’s formation billions of years ago, ultimately providing some answers to our universe’s origin.

After relaxing into orbit, Rosetta’s next daunting mission was to launch the Philae lander. Researchers watched nervously as Philae emerged from Rosetta and made its seven-hour journey to 67P. Philae neared the surface in what should have been a perfect entrance, but for reasons unknown, its rear thrusters and anchoring harpoons failed to attach the tiny lander into the ground of the comet. Instead, Philae bounced around in the low-gravity environment, causing fear of its loss to the depths of space.

In the end, Philae stuck its landing, albeit in the darkened shadow of rocks. Since the solar panels couldn’t be effectively recharged, scientists had 57 hours of battery life to conduct their groundbreaking measurements. Data from the first science sequence was transmitted from Philae to Rosetta and eventually to the mission headquarters before Philae powered down, finding solid ice, a vast amount of dust and a rich array of organic molecules. Further analysis is needed to validate the findings, but the crew is optimistic.

Philae’s beloved Twitter account ends this nail-biting saga on a hopeful note about its future activity: “My #lifeonacomet has just begun @ESA_Rosetta. I'll tell you more about my new home, comet #67P soon… zzzz #CometLanding.”

About the Author

Kirstie Keller

Kirstie Keller is a classically trained ballerina-turned-scientist with a penchant for 90s music. She enjoys piecing together the details of a discovery into the larger puzzle of life.