Scicomm: Diverse roles in the vast world of science communications

*Special Article*

Written by: Rebecca Tweedell

In the age of the internet and rapid-fire communication, you see stories about science all over the place. Science communications (or scicomm for short) have become an integral part of our world. All kinds of people contribute to scicomm, on spectrums ranging from the casual conversationalist to the full-time writing professional; from the high school student to the highest-ranking academic professor. No matter where on the spectrum we fall, the core goal of good scicomm is always the same: to deliver information about scientific findings as clearly and accurately as possible to the intended audience.

Scicomm professionals write about science in a variety of formats to pass information along to others.

As the calls for accurate and timely information grow and more people join the ranks of the full-time scicomm professional, people are often curious about these careers and what exactly people in these jobs do. Since we get this question so frequently, here’s a brief look at some of the most common scicomm jobs. Please note, this is by no means an extensive list, and new types of jobs are being created all the time.

• Science writer: This term encompasses a very diverse group of professionals. People in this job often cover emerging scientific discoveries and interview scientists to write news articles, magazine features, social media posts, television news stories, and many other forms of content. This is most often, though not always, targeted for a general audience. These writers could work for newspapers, magazines, academic institutions, or other research centers. Depending on the focus of the organization, this job can come with other responsibilities, such as managing publications for an academic department or helping with grant submissions.

• Medical writer: A quick LinkedIn search will tell you that this is the type of job I have. In this role, writers are typically writing about science for other scientists, often with a clinical focus. These writers will frequently write scientific journal articles, congress materials, and strategically driven documents for pharmaceutical or biotech companies.

• Technical writer: This job typically involves writing the documents required by law or institutional guidelines to ensure quality and safety in biological processes and studies. As with medical writers, these writers are usually writing science for other scientists. Their work could include writing specific protocols used to produce a drug, standard operating procedures for use in a lab, or reports for submission to regulatory authorities.

• Journal editor: Every scientific journal has an editorial board. Some of these boards are made up of academic professors who volunteer their time, but there are typically full-time editors on staff as well. These editors are responsible for evaluating each article submitted to the journal to decide whether it is of interest and a good fit for that specific journal. They are also responsible for reaching out to the researchers to shape the scientific narrative for their journal, making them integral players in the scicomm network.

As you can see, the jobs within scicomm are many and diverse, as are the forms of communication that result. Most importantly, beyond these full-time jobs, each member of society can play a role in scicomm by just talking about science. So remember, whether you are a full-time scicomm professional or someone with a more casual interest, you can be part of the ever-important conversation and share your knowledge and the scientific facts with others. Welcome to the scicomm world.

Molecules found in soy and red clover… to treat a rare muscle disorder?

Written by: Ken Estrellas

Original Article: Banerji et al. Human Molecular Genetics 2019

The Gist of It:

Facioscapulohumeral muscular dystrophy, or FSHD, may not receive as much press as other muscle disorders such as ALS (Lou Gherig’s Disease), DMD (Duchenne Muscular Dystrophy), or SMA (Spinal Muscular Atrophy), but it’s fairly prevalent – affecting 1/8,333 people worldwide. FSHD, which primarily affects the muscles of the face, back, and upper arms, currently has no cure. Treatments in development are focused on reducing the negative effects of the mutation that causes FSHD, but almost none use strategies to do the opposite and specifically promote proper growth of the muscle itself. In this paper, Banerji and colleague closely studied the differences between healthy skeletal muscle cells and those from patients with FSHD, focusing specifically on how both types of cells grow. When grown in a dish, diseased muscle cells grew in less regular patterns than healthy muscle cells; they also matured slower and formed smaller myotubes (a precursor to mature muscle fibers). The amounts of several genes in both healthy and FSHD muscle cells were also compared over time, and two were shown to be reduced in FSHD: ESRRA and PPARGC1A. Lower levels of these genes resulted in lower levels of the proteins ERRα and PGC1α, which help make the mitochondria required to power muscle cell growth. One class of compounds called isoflavones, which are commonly found in soy and red clover, promote the activity of ERRα and could potentially correct abnormal muscle cell growth. Consequently, when FSHD muscle cells were treated with various isoflavones, they were able to grow and mature normally, with increased levels of the muscle protein myosin heavy chain. Future treatments for FSHD could focus on designing molecules to increase the expression of ERRα, or even incorporate the isoflavones themselves, to promote proper muscle regeneration in FSHD patients.

Compounds from soy and red clover flowers corrected the improper growth of muscle cells from patients with FSHD.

The Nitty Gritty

In this study, Banerji et al employed a high-throughput analysis of morphogenesis to characterize the developmental differences in myotube formation between healthy human skeletal myoblasts and immortalized human skeletal myoblasts derived from patients with FSHD1. Following standard protocols for in vitro culture and differentiation, FSHD myoblasts formed smaller myotubes than healthy controls over the course of three days, with significantly lower levels of myosin heavy chain expression. Dynamic morphometry revealed that the processes of myoblast alignment and fusion, which are crucial to myotube formation, were delayed in FSHD myoblasts. Transcriptomic analysis was performed at several time points between initial myoblast confluence and myotube maturation and revealed significantly decreased expression of ESRRA and PPARGC1A in FSHD myoblasts and myotubes. siRNA-mediated knockdown of PPARGC1A in healthy control myoblasts significantly impaired myogenesis as visualized with fluorescence microscopy and quantified with RT-qPCR revealing significantly decreased myosin heavy chain expression; these defects were corrected with the inclusion of 10 μm of the isoflavone and known ERRα agonist biochainin A in the differentiation medium. Treatment of differentiating FSHD myoblasts with 10 μm of the isoflavones biochainin A, daidzein, or genistein improved myofiber morphology and increased myosin heavy chain expression over the course of three days, rescuing their hypotrophic phenotype. Although current FSHD therapies in development are focused primarily on the consequences of ectopic expression of DUX4 (which leads to excessive macrosatellite D4Z4 repeats), improvement of mitochondrial biogenesis through targeting of ERRα and/or PGC1α could serve as an attractive alternative or combinatorial therapeutic strategy to ameliorate this hypomyogenic phenotype.

Original Research Article: Banerji, C.R.S., et al. “Dynamic transcriptomic analysis reveals suppression of PGC1α / ERR  drives perturbed myogenesis in facioscapulohumeral muscular dystrophy.” Human Molecular Genetics (2018). Doi: 10.1093/hmg/ddy405.

Fighting mosquito-borne diseases from above: Using drones to find breeding sites

Written by: Rebecca Tweedell

Original Article: Carrasco-Escobar et al. PLoS Neglected Topical Disease 2019

The Gist of it:

Recently, drones have become exciting new toys for many people. Drones can be used to photograph landscapes from a new perspective, capture video sequences for movies, or even deliver packages. But they can also play an important role in the war against mosquito-borne diseases, such as malaria, dengue, and Zika. These diseases are often difficult to treat, so one of the major strategies for disease control is to reduce the population of mosquitoes that carry the pathogens. This is most frequently done using insecticide-treated bed nets and indoor residual spraying. Unfortunately, these strategies only work if the mosquitoes are living and biting inside homes. Some mosquito populations live and bite exclusively outdoors. To control these populations, a key strategy is to identify and treat breeding sites to reduce the number of mosquito eggs and larvae. Here’s where the drones come in. Surveying every body of water by hand to identify whether it is a mosquito breeding ground is an overwhelming task, especially in areas like the Amazon in Peru where it is difficult to travel by foot or car. A new study found that drones could do the surveying for us. Researchers sent out drones to take high-resolution, multispectral images of the landscape. They also tested the bodies of water for mosquito larvae to identify which were breeding sites. Using the multispectral images and the results of the water tests, the researchers created computational models that used different features of the images, such as the red/green/blue (RGB) banding, to predict whether a given body of water would be a breeding site. Their models were able to predict with 87% to 97% accuracy where mosquitoes were breeding. Using this drone surveillance technique could improve our ability to roll out targeted mosquito control strategies to fight against mosquito-borne illnesses.

Drone surveillance can be used to identify mosquito breeding sites for targeted population control strategies

The Nitty Gritty:

Carrasco-Escobar et al. surveyed 4 communities in the Peruvian Amazon for the major mosquito vector of malaria in the region, Nyssorhynchus darlingi (formerly Anopheles darlingi). They used DJI Phantom 4 Pro drones with DJI 4K cameras to capture RGB images and 3DR Solo drones with Parrot Sequoia sensors to capture multispectral images. Larval collections were performed in the bodies of water in the same areas using standard dippers. The images from the drones were processed to create 3 different orthomosaics for each community: 1) a 3-band RGB image from the DJI 4K camera, 2) a 4-band multispectral image from the Parrot Sequoia camera, and 3) an 8-band composite image that merged images 1 and 2 and added a normalized difference vegetation index. Images were then classified using Google Earth Engine with a Random Forest algorithm in three different approaches. The first approach differentiated classifications of land cover (bare soil, low vegetation, high vegetation, or water); this method was 86.73% accurate at predicting breeding sites. The second approach included the differentiation of bodies of water based on the presence or absence of Ny. darlingi larvae in the previous 6 months per the results of standard dipper sampling; this method was 87.58% accurate. The third approach masked the 8-band composite image using the water class from the first approach and had the highest accuracy, with an average of 96.98%. Using these models, the researchers could consistently, and with high accuracy, use the drone images to distinguish bodies of water used as breeding grounds by Ny. darlingi from those not being used.

Original Research Article: Carrasco-Escobar G., et al. “High-accuracy detection of malaria vector larval habitats using drone-based multispectral imagery.” PLoS Neglected Tropical Disease 13.1: e0007105 (2019). doi:10.1371/journal.pntd.0007105.

Feeling weak after a bad case of the flu? IL-6 might be to blame.

Written by: Kaitlyn Sadtler

Original Article: Radigan et al. Journal of Immunol 2019

The Gist of It:

‘Tis the season. For influenza, that is. Every year more than 20,000 people in the United States die from the flu. Through vaccination it is possible to dampen the symptoms of the flu and even completely prevent it. However, if you don’t get the vaccine and end up with a bad case of the flu, there are long-lasting effects even after you recover from the fever, muscle aches, congestion, and malaise associated with acute infection. One of the side effects of our immune system’s fight against the infection is muscle wasting. Recently, researchers have tied a specific protein secreted by immune cells fighting the flu in the lungs to loss of muscle mass in other parts of the body. When our body is fighting influenza, our immune system produces inflammatory proteins like IL-12, TNFα, IFNγ, and IL-6. Radigan and colleagues looked at infection in humans and mice and noted lots of IL-6 throughout the body. IL-6 interacts with the surface of muscle cells to activate a protein inside cells called STAT3. Furthermore, scientists were able to directly connect IL-6 to a degradation and recycling pathway within cells – called ubiquitin ligation. They found that when IL-6 interacted with muscle cells, it started a chain reaction that resulted in muscle proteins being tagged for degradation, which leads to muscle wasting.  Importantly, if scientists stopped IL-6 from interacting with the cell using an FDA-approved antibody, they saw that muscle wasting decreased in the context of the flu. So, the bottom line? Get vaccinated! When you receive a flu vaccine, even if you get the flu, your symptoms (both short-lived and long-lasting) will decrease and you will recover faster – or not even get the flu at all! At the same time, you’re protecting those that cannot get the vaccine, like kids with cancer who have no immune system, or other immunocompromised people, due to genetic or other diseases.

A bad case of the flu can cause long-lasting detriments to your health — including muscle wasting, caused by the inflammatory protein IL6.

The Nitty Gritty:

Using a mouse model, Radigan et al. showed that mice experienced muscle wasting after infection with influenza A as determined by muscle mass and fiber cross-sectional area (CSA), which both decreased. In mice lacking atrogin-1 (atrogin-1^-/-; E3 ubiquitin ligase), the CSA does not decrease as much as it does in a wild-type control after influenza infection. Influenza induces high systemic levels of IL-6, which were not affected by genetic loss of atrogin-1. However, when mice were treated with tocilizumab (a murine version of the FDA-approved anti–IL-6 therapeutic blocking antibody), CSA measurements and muscle mass recovered. When STAT3, an intracellular signaling protein of IL-6, was knocked down using siRNA in C2C12 cultured myotubes, myotube diameter decreased compared to the diameter when a scrambled control siRNA was used. Furthermore, when transcription factor FoxO3a, but not FoxO1, was knocked down, the same effect was observed as with STAT3 knockdown. The same was repeated with atrogin-1 siRNA knockdown. These studies suggest that IL-6, which is upregulated by the lung epithelium in response to influenza infection, induces muscle wasting through a STAT3-FoxO3a-atrogin1 pathway that can be mitigated by antibody-mediated blocking of IL-6 activity.

Original Research Article: Radigan, K.A., et al. “Influenza A virus infection induces muscle wasting via IL-6 regulation of the E3 ubiquitin ligase atrogin-1.” The Journal of Immunology 202.2 (2019): 484-493.