The three tiers of science communication

Perhaps one of the most important yet widely ignored skills that us scientists need to cultivate is to communicate our science better. By “communicate science”, I am not simply referring to publishing research articles and reviews in journals and publications. This is about conveying ideas, research, theories, and facts to a wide audience. This is harder than it seems. On a day-to-day basis, we are so engrossed in our little scientific bubble that we hardly engage with people from outside our labs, departments, and universities. For example, I can prepare to present my work during our weekly group meetings with an accurate understanding of how to introduce my research project to my fellow lab members and what data to present during my talks. Most individuals in my program or department have an understanding of the common scientific language and the several jargons that are overused during the talks and seminars.

I would like to think that being in my research group has given me a better understanding of communicating my work to my fellow peers.  My lab is a “hybrid” wet and dry lab i.e., it is comprised of computer scientists, computational chemists, synthetic chemists, and biologists. Our group meetings are extremely interdisciplinary covering a multitude of topics ranging from machine learning and molecular dynamics to immunology and cancer biology. At this point in my career, I am certain and confident with my ability to convey the scope of my project and the several particular aspects of my current research.

The most challenging audience are individuals who are completely outside the realm of our scientific bubble. These individuals serve critical roles in our society but are overlooked by us all the time. I have interacted with my friends and family from different professions and they’re always intrigued by my work and more specifically about *what* we do in the lab and *how* we do science. These are important questions that not only establishes confidence in the scientific community but also bridges the gap between our worlds. Questions that may seem simple or even silly to us may be important in the large scheme of things. For example, the other day, my friend asked me “How do the lab mice get Alzheimer’s disease?” To answer this, I could have just said that there are several transgenic models of mice with genetic mutants that spontaneously develop Alzheimer’s over time. This is an answer that I would have had for someone in the scientific community. But for my friend who happens to be a business associate, I candidly described genetics of the disease, how mice are bred in laboratories, and how they develop plaques that can be viewed in their brain tissue sections. In order for the public to trust us, first and foremost, they need to be aware and educated on the basic scientific methods and principles. This includes communication about the bases of experimental design, process of gathering significant data, peer reviewing, reproducibility, etcetera.

This brings me to what I consider are “the three tiers of science communication” that scientists should cultivate. We need to learn how to communicate our science to:

  1. Our fellow peers in the field i.e., individuals from our specific area of research
  2. Our scientific colleagues from different areas of research
  3. The general public including individuals from other professions

Tier #1 is a no-brainer. Individuals from this tier read and review our work. They are critical of every aspect of our research and question the scientific methods used. They make signifiant contributions to our work and provide guidance for the growth of our research. Tier #2 is tricky. Why would I, a neurobiologist want to communicate my work to a computer scientist or a meteorologist even? A major aspect of creating new solutions to old problems is to collaborate with scientists from outside our specific focus areas. Drug discovery is not possible without computer scientists teaming up with chemists and biologists. Many of the problems in the areas of neuroscience such as understanding of neural circuits and systems, cognitive and behavioral neuroscience, etcetera would not be solvable without the help of electrical and mechanical engineers.

tier three
Source: SMBC-comics.com

Individuals from tier #3 are probably one of the most significant yet overlooked in this regard. Science communication to the general public does not happen until there is a problem affecting people from the both worlds. Involving this tier should not be limited to the difficult times but should be an ongoing process. It should be a part and parcel of our work. Much has already been said about this. How do we make science outreach a regular part of our work? Should the burden of outreach not be imposed on scientists at all? We need more science communicators breaking out of our bubble and out into the real world. Furthermore, many grad students and researchers make contributions in their own way. For example, using social media (#scicomm on twitter and instagram) for science outreach is a great way to reach thousands of individuals from your fingertips while working in your lab. No fancy equipment, no travel money, no event organization necessary! Well established senior scientists with the means and resources should strive to connect with and impact a larger audience.

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Science vs. the scientist

A common thought in the entertainment industry is whether an artist and their art can be held in mutually exclusive standards. Do you like a song because you like the musician or do you like a musician because you like their song? Can the two be separated from one another? People boycott Woody Allen films because they do not want to support his career or his power in the entertainment industry. By watching his movies, do we validate his actions by contributing to his growth as an artist? Same goes with Harvey Weinstein and many others.

Similar parallels can be drawn with scientists and their science. For example, James Watson may have contributed to one of the most significant discoveries in science -the discovery of the double helix structure of DNA- or may have led a great scientific undertaking with the Human Genome Project, but relinquished his reputation when his racist and sexist remarks were made apparent. Lawrence Krauss (theoretical physicist, cosmologist, famous atheist, and a “liberal crusader“) was recently accused of sexual harassment which was followed by more allegations and expose by female academics on social media. I have thoroughly enjoyed Krauss’ popular science opinions as well as supported his science and public policy advocacy in the past. The recent allegations and accusations have left me transfixed about whether his work deserves my support at this point. Will I (indirectly) validate Krauss’ ghastly actions by supporting his scientific literacy and the skeptic movement? The deep dark spaces on the Internet harbors more stories about prominent scientists. Do scientific contributions become less significant due to the scientists’ reprehensible actions and behavior? One may argue that science is larger than one individual where do we draw the line?

The fact of the matter is that scientific principles, discoveries, and inventions do not stem from one individual. The credibility of scientist is validated by several other scientists in charge of legitimizing the science with a proof of approval. Does continuing to fund and support such researchers mean validation of bad behavior? The forthcoming ripple effect and propagation of a toxic environment will eventually affect others in the community. Science is scrutinized and validated by peer review over and over again. Is it time to scrutinize and peer review scientists as well?

More: Harassment case opens dialogue and When will science get its #metoo moment?

Officially a PhD Candidate!

On November 16th, I successfully defended my original proposal in front of my preliminary committee and officially became a PhD candidate! I was looking forward to this day all through the summer and fall. [I have written about the entire process of our preliminary examination in my previous blog post.] I submitted my written proposal a month before my oral defense date and received feedback from my committee about the experiments proposed and the validity of my hypothesis. I am extremely grateful for each and every one of my preliminary committee members for taking the time to review my proposal and for providing their valuable feedback and criticism. This entire process helped me grow as a scientist and helped me think and write critically. I am also grateful for my family and friends who took the time to review my proposal, attended my practice talks, and provided useful comments.

As mentioned in my previous post, our graduate program requires us to pick a topic outside our main research area and develop an NIH-style original proposal related to the chosen topic. I chose to study the role of Myeloid-Derived Suppressor Cells (MDSCs) in Type 1 Diabetes (T1D). MDSCs are a heterogeneous population of immune cells that suppress or down-regulate the effector T cell responses in various immune microenvironments. In tumor microenvironments, T cells help kill the tumor cells and prevent the tumor cells from growing. However, MDSCs suppress these T cells and prevent them from killing the tumor cells thereby causing the cancer cells to proliferate. An autoimmune microenvrionment is opposite to the tumor microenvironment. In T1D, the T cells become autoreactive i.e., the T cells start killing the innocent insulin-producing beta cells in the pancreas. This leads to reduced insulin production and increased glucose in the bloodstream in the body. Insulin is an important hormone that helps in the transfer of glucose molecules into the cells that can then serve as the energy source for the cells and tissues. The destruction of the pancreatic beta cells therefore leads to an imbalance in the glucose homeostasis in the body. In such a microenvironment, we require MDSCs to suppress the T cells and prevent them from destroying the beta cells in the pancreas. The first question to ask here is, are MDSCs induced during T1D? The answer is yes. It was shown in 2014 that T1D patients have an increased MDSC induction in their peripheral blood. As to the best of my knowledge, this is the ONLY study that focusses on the native (body’s own) MDSCs during T1D. However, not much is known about the MDSCs and the different subpopulations of these cells that exists that are responsible for interacting with T cells in the pancreas. MDSC subsets and their mechanism of action are dependent on the specific tissue or the site of inflammation. Understanding the role of MDSCs in T1D and the specific MDSC subsets involved in T1D lead to several questions. I chose to investigate a few in my proposal:

  1. If MDSCs are induced in T1D patients, why are they unable to suppress the T cell responses in the pancreas? i.e., Are MDSCs defective during T1D?
  2. What are the specific subsets of MDSCs induced during T1D that are specific to the pancreatic microenvironment? MDSCs are incredibly heterogeneous and can exhibit several phenotypic and molecular states. These subsets are unique to the local tissue microenvironment.
  3. What is an MDSC-specific immune regulatory molecule and its corresponding pathway implicated in T1D that may contribute to disease pathogenesis? 

Without going into the details of each question posed, I proposed several experiments and techniques ranging from single-cell RNA sequencing analysis of the MDSC populations in the pancreas to generating MDSC-specific conditional gene knockout experiments in mice to answer these key questions. There were a few flaws in my experiments that were brought up during the presentation and I tried to address them to the best of my ability by proposing alternative approaches. Overall, my committee members were impressed with the breadth of background knowledge and experiments presented. The most important factor was to develop a hypothesis-driven proposal with a solid premise to back my hypothesis. The presentation didn’t feel one-sided and eventually developed into a curiosity-driven discussion.

Transitioning from a PhD student to a PhD candidate is a backbreaking process. Perhaps it is meant to be this way. Even though I felt numb for a few hours after the conclusion of my presentation, I could feel the academic apocalypse building up in a cloud over my head already. Here’s hoping for more successes and vital experiences in the future!

It’s brain awareness week!

Hello all!  I wanted to take a few minutes to write something for the brain awareness week. This is important to me because my research focusses on understanding the role of the immune system in the brain. For a very long time, the brain was thought to be an “immune privileged” organ i.e., it was thought that the brain is protected from all the peripheral insults and that it is “divorced” from the rest of the body. In 2015, it was shown that there exists certain lymphatic vessels that connect the CNS to the rest of the body (1). The lymphatic system carries immune cells through a network of vessels and tissues; it connects the bloodstream and tissues in order to remove dead cells and other debris. The discovery of the new “glymphatic system” has opened new avenues to study the connection between the brain and the rest of the body. This is especially helpful in understanding the role of the peripheral immune system on the CNS during infections, injury, and other disease insults.

glymphatic system
Old lymphatic system (left) and newly discovered lymphatic system in the CNS (right). Source: University of Virginia Health System

My work focusses on a specific cell type in the brain known as microglia which are are the resident macrophages of the CNS (they eat up and clear out the bad stuff in the brain like dead cells and mis-folded proteins). Microglia are the only known immune cells of the brain. Compared to all that’s known about the cells of our body’s immune system (B cells, T cells, NK cells, neutrophils, basophils, Treg cells, MDSCs, TH1, TH2, and many many more with several subtypes of each cell), it is safe to say that cells of the CNS are poorly understood. My efforts are focussed towards understanding the role of microglial cells in neurodegenerative diseases such as Alzheimer’s Diseases (AD) , Parkinson’s Disease (PD), Multiple Sclerosis (MS), etcetera. These diseases are characterized by mis-folded proteins that aggregate in the different regions of the brain tissues causing the neurons to degenerate and eventually die. The microglial cells in these disorders play a major role in disease progression by regulating many pathways involved in cell-cell communication, cell survival, and cell death. This is a relatively new and an exciting area of study with many missing links and questions to be answered. I will try my best to keep this space alive with updates and stories! In the meantime, here’s a fun read on Leonardo da Vinci’s contributions to neuroscience: http://www.sciencedirect.com/science/article/pii/S0166223600021214

And here’s a 1504-1506 drawing of the human brain by da Vinci:

Leonardo da Vinci's contributions to neuroscience
In the upper figure, the three ventricles are labeled imprensiva (anterior ventricle, corresponding to the paired lateral ventricles), senso comune (third ventricle), and memoria (posterior or fourth ventricle). Below the ventricles, seven pairs of cranial nerves are shown. The lower figure shows a human head in an exploded view, with the skull raised over the brain and from the head. Source: 

Sources:

  1. Louveau A, et al. Structural and functional features of central nervous system lymphatic vessels. Nature. 2015;523(7560):337–341. doi: 10.1038/nature14432.

Thoughts on lab rotations

The thing with first-year rotations in a Ph.D. program is that anxiety starts kicking in somewhere along the way when you consciously identify the lab that you want to join and want to get started right away. Having realized that this is going to be a long journey and rushing into things may not help, I am now gaining patience and perspective, and hope to make the most of the remaining time of my first year.

Rotations are a great way to learn about a lab and get involved in the nitty-gritty of research. I was warned at the beginning by a few seniors that I would either love a lab or reject it within the first few weeks of the rotation. Mind you – this has nothing to do with the science pursued in the lab (one wouldn’t decide to rotate in a lab if they didn’t find the research interesting in the first place). This is more about getting comfortable with the way a lab functions and deciding if the environment is a good fit for you. An eight-week lab rotation is really like an eight-week long interview with a potential PI and the lab! It is essential to identify the kind of relationship you foresee having with your advisor for the next couple of years (and beyond). This is perhaps one of the most important aspects of a rotation for me, next to the research work. A good mentor-mentee relationship can go a long way and can be extremely beneficial to one’s academic/professional career. I prefer having an open channel of communication with my mentor and learn as much as possible from him/her.

Not all graduate programs require laboratory rotations. Many departments or programs accept or reject students simply based on their application and/or an interview. In the UK for example, students are recruited to work on specific projects and grants as a part of their Ph.D. for the time period of around 3 years. This may not benefit the candidates who wish to propose their own ideas and develop their own thesis based on their individual research interests. In the US, for most graduate programs in the life sciences (mainly biology and chemistry), the average time for graduation is around 5-6 years. I believe that the freedom and independence of this system trump the short graduation time of the other systems. Although I am certain that both sides have their set of merits and demerits, at the end of the day, the journey is unique to each one of us and what we make of the experience matters the most.

I got a grant!

I got a grant for my ion channel research project! Receiving the graduate research grant award has immensely boosted my morale, and has encouraged me towards the scientific career path that I wish to pursue.

On behalf of the Graduate Studies Office, I am pleased to inform you that you are a recipient of a Graduate Research Grant for the 2014-2015 Academic Year. Those who evaluated your proposal were impressed with the project.  We congratulate you and look forward to your successful completion of the proposed research. We will be interested in your progress as you move along in your research, and look forward to hearing your presentation at Student Research Day next spring.

The Graduate School seeks, through such awards, to encourage the highest standards of scholarship among its graduate students and we are extremely gratified to provide this opportunity for you to pursue your theory.

***

Our lab finally got a new fluorescence/chemiluminescence imager and it has been great for our investigations so far. I have also been getting many positive western blot results. Evaluating the right antibody concentrations for the blots and tweaking the immunoprecipitation protocols to fit my experiments was a considerable amount of work. My next goal is to quantify the protein bands and figure out the statistical significance of GIRK channel subunit interactions. I am so glad to have had worked on it during the fall semester. I can now concentrate on putting my findings together by the time I graduate in spring(!).

Besides this, I am looking forward to working on the electrophysiology rig with my lab mates next semester. We have been concentrating on the biochemical experiments since the past couple of months. It would be interesting to perform preliminary patch clamping experiments on the cells expressing the mutated and wildtype channel subunits.

I finally got down to updating this space after a long break. I have been very busy with the research work, classes and teaching. It feels great to finally break the writing dry-spell.

Giraffe and Evolution – Not just a long (neck) story

Feeding on acacia leaves
Feeding high up on acacia leaves

In the early 19th century, Lamarck proposed a theory of evolution by studying the behaviour of giraffes. He believed that giraffes evolved to have long necks as they began reaching for higher leaves on trees. He called this “change through use and disuse”. According to this theory, an organ or a character that is used more often becomes stronger and better. Therefore, over the course of history, giraffe’s neck got longer as it began stretching it a lot more than usual. Lamarck also proposed the “law of inheritance of acquired characteristics” according to which the improved characteristics of an organism are passed on from one generation to the next. These improved features persists and the disadvantageous features disappear.

The Lamarckian theory was eventually abandoned* as it could not explain the genetic basis for inheritance of acquired characteristics (traits obtained after birth due to environmental changes, accidents, use and disuse; these traits are not inheritable). Lamarckism also predicts that simpler life forms will disappear from the earth once organisms become more complex. While we see some organisms evolving into more complex systems with intricate functions, the simpler life forms like the single celled prokaryotic cells still exist to this day.

Darwin’s theory of evolution on the other hand, can account for the continued existence of the simpler life forms on earth. Darwin believed that complexity is a result of adaptation to the environment from one generation to the next. In the Origin of Species, Darwin proposed a theory of evolution driven by natural selection. According to this theory, there is variation seen amongst individuals. Certain environmental conditions favours certain variations and the species exhibiting these variations adaptsurvive. The unadapted species which do not exhibit the favoured variations do not survive and become extinct over generations of time.

Applying this to giraffes, the long neck species are considered dominant and have greater chances of survival during harsh drought conditions compared to the short neck species that have to rely on ground habitation for food. This of course is just one theory amongst many other. The long necks are also used to reach deep inside trees that other competing animals cannot reach, and is therefore more advantageous. One of the latest proposal is the theory of sexual selection. Male giraffes fight with other males by “necking” to compete for female partners. As it turns out, females prefer males with longer and stronger necks. Natural selection again, favours long neck males.

“Animal Autopsy”, a show on National Geography channel dug deep into giraffes – quite literally! – to explore the physiological and anatomical features of this intriguing mammal to unravel some of its evolutionary secrets.

During the autopsy, Richard Dawkins talks about one of the evolutionary disadvantages caused due to the long laryngeal nerve that starts off in the brain and ends in the larynx (which is in fact situated very close to the brain). This nerve runs all the way down the neck, loops around one of the arteries in the chest and returns to the larynx on top. Why does the nerve take such a long route when it can simply connect from the brain to the larynx directly without having to pass through the entire neck? Also, consider this – giraffes with a long necks must also bend much lower to drink water from the ground. The contracting of the muscles along with the tension in the elastic tissue in the neck utilises way more energy, and is considered to be another evolutionary flaw. Another interesting fact to chew upon is that due to its long neck, giraffes have to pump blood to the brain that is ~2.5 meters above the heart – against gravity – by using extremely high blood pressure. How does the long neck favour such distant positioning of the heart and the brain?

Biologists consider different perspectives to understand the evolutionary reasoning behind the advantages as well as the flaws caused due to the long necks of giraffes. As more pieces of this puzzles are put together, it is quite remarkable to think about the imperfections that are caused due to evolution. Imperfections that somehow adds up to the making of such a marvellous mammal on our planet.

*New research reveals the epigenetic basis for the inheritance of acquired characteristics. In the article “A Comeback for Lamarckian Evolution?”, Emily Singer of the Tufts University School of Medicine provides evidence for the largely abandoned Lamarckian theory of evolution. Read article on MIT tech review here.