Illustration showing in-person conference on the left and at-home virtual conference attendee on right

Scientific Conferences Get Virtually Real

Between online and in person options, is there a right medium for attending a conference?

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modified from © istock.com, Natalia Kolosova, Rudzhan Nagiev; designed by erin lemieux

On the first day of one of the biggest conferences of the year, the website clocked more than 20,000 registrants. But for once, I was in no rush to grab a seat for the keynote. One minute before the talk started, I plugged right in from the comfort of my ergonomic office chair. 

With the rise of online portals, it was only a matter of time before we submitted to a virtual world. The COVID-19 pandemic catalyzed this transition, coaxing researchers to connect digitally. For a brief period, the experience of attending a conference went from lugging bags on train platforms to simply logging into a platform. 

For a while, scientists believed that they could commit to this medium and save some credit, both monetary and carbon. Academics across the globe imagined a world where they would not miss a conference because of travel fund limitations or visa restrictions. Institution heads dreamed of reallocating budgets dedicated to overpriced hotels, and online attendees breathed better by avoiding the breathless runs across the venue between sessions.

Yet, despite the cost savings that virtual platforms offered for researchers, scientists flew to conferences in throngs once the pandemic restrictions were lifted. The allure of in person congregation begs the question: Why is the digital medium good but not good enough? 

One guess is that the convenience of sitting at home costs the experience of the meeting. Presenting to people sitting in the same room or walking through a poster hall allows for an interaction that can transform into a meaningful conversation. Networking, an important aspect of conferences, relies on human connection, and as failed virtual happy hours have demonstrated, is hard to replicate online.   

Personally, I prefer a mix. If attending a conference in person is not possible, having a virtual option keeps science open. With three clicks, as long as I can avail myself of all presentations, I say, “There’s no place like home.”

What’s your take on the virtual versus in person conference conundrum? 

Submit Your Opinion

Murine cells stained pink and purple.

Learning About Pain from a Master Manipulator

Leishmania parasites often cause puzzlingly painless lesions. Scientists are beginning to dig into the mechanisms underlying this pain-blocking effect.

Image Credit:

Abhay Satoskar

          Abhay Satoskar stands in a science lab wearing a tie and a white lab coat.
Abhay Satoskar studies how Leishmania parasites interact with host immune systems.
Parag Pathak

For decades, researchers around the world have been investigating the molecular mechanisms by which microbes cause pain. Abhay Satoskar, a parasite immunology researcher at Ohio State University, is interested in the opposite question: How can a microbe relieve pain?

More specifically, Satoskar wants to explore the relationship between mammalian hosts and Leishmania mexicana, a unicellular parasite that causes chronic but surprisingly painless skin lesions. In a study published in iScience, Satoskar and his colleagues identified changes in host cell metabolism that may underlie these analgesic effects.1

“It is fascinating to learn how this bug is evading host detection by manipulating not only the immune system, but in this case, even the sensory system,” said Satoskar.

By using mass spectrometry, his team measured differences in metabolites between infected and noninfected tissues in a mouse model of the disease. They found that L. mexicana infection altered purine metabolism at the lesion site; some of the upregulated purine metabolites, including xanthine, hypoxanthine, and inosine, are thought to play relevant roles in anti-nociception. Researchers also identified enrichment of certain pain-numbing endocannabinoid metabolites.  

“There is still a lot to explain,” said Ricardo Silvestre, an immunometabolism researcher at the University of Minho who was not involved in the study. “The work was mainly descriptive, and they are very honest in the paper about the limitations of the study. [However], I believe it opens a new field of research that many will follow.” 

One major limitation—the use of a mouse model—Satoskar hopes to remedy soon by validating these findings in human L. mexicana lesions. He also wants to dig deeper into the mechanisms governing infection-related shifts in these metabolic pathways, and noted that elucidating how L. mexicana manipulates nociception could have far-reaching effects. “If we find the mechanism—let's say a parasite molecule—it could be an important pain killer that could be used for other diseases,” said Satoskar.

Reference

  1. Volpedo G et al. iScience. 2023;26(12):108502.
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3D rendered DNA strand and cancer cell

Translating ctDNA Detection into Breast Cancer Research Breakthroughs

Noninvasive methods to monitor traces of cancer left over after treatment may lead to better early interventions.

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© ISTOCK.COM, CIPHOTOS

Isaac Garcia-Murillas is a molecular biologist at the Institute of Cancer Research. Following PhD training and a postdoctoral fellowship where he studied lipids and intracellular signaling in model organisms, his focus shifted to translational liquid biopsy research and pioneering the clinical utility of breast cancer circulating tumor DNA (ctDNA). 

          Isaac Garcia-Murillas standing in a laboratory. 
Isaac Garcia-Murillas has pioneered the clinical utility of ctDNA and liquid biopsies in breast cancer for over a decade. 
Image provided by Isaac Garcia-Murillas

Q: How do you detect ctDNA?

We showed more than a decade ago that we can detect amplifications in ctDNA using droplet digital PCR (ddPCR),1 for example, with HER2 gene amplifications. This led to our work detecting mutations in ctDNA in the blood of patients with primary breast cancer, which associated with recurrence risk. This was the first time that association was demonstrated for any solid tumor. We did this by combining next generation sequencing (NGS) and ddPCR.2 Most approaches nowadays rely on NGS to identify mutations in tumor samples before detecting them in ctDNA. This allows us to define smaller panels of patient-specific mutations to track in liquid biopsies using NGS or ddPCR. New ddPCR and other digital PCR technologies that identify more events might rival the use of NGS in the future in terms of sensitivity, with the bonus that these approaches do not require complex bioinformatics analysis pipelines.

Q: Why is ctDNA detection important?

Detection before cancer progression is called minimal residual disease (MRD) detection, which refers to the minute amounts of cancer that remain after initial treatment. We now know that MRD drives cancer progression, and detecting it allows us to identify which patients are at risk of progression or recurrence. This in turn has led to prospective interventional clinical trials to eradicate residual disease before metastasis at a point when we believe the disease is more homogeneous and could better respond to therapies.

Learn more about detecting ctDNA for cancer research with ddPCR technologies.

This interview has been condensed and edited for clarity.

References

  1. Gevensleben H, et al. Clin Cancer Res. 2013;19(12):3276-3284
  2. Garcia-Murillas, et al., Sci Transl Med. 2015;7(302):302ra133.
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The Shape of Cilia

Three dimensional images of human pancreatic islet cells provide an unprecedented view of the enigmatic primary cilia.

          An antenna-like cellular structure emerges from the surface of a human pancreatic islet cell. The surface of the cell is covered with small structures called microvilli.
Researchers used scanning electron microscopy to image the cytoskeletal components of the human pancreatic primary cilia.
Sanja Sviben and Alexander Polino, Washington University in St. Louis.

In her lab at Washington University in St. Louis, endocrinologist Jing Hughes studies a peculiar structure that sticks out of the surfaces of human pancreatic islet cells: the primary cilium. The cilia are antenna-like organelles that sense shifts in the extracellular environment and communicate these changes to the intracellular space.

Although scientists first identified primary cilia in human pancreatic islets 60 years ago and know that dysfunction of cilia affects the development and function of the pancreas, there are still many unanswered questions about their role and appearance.1 “That, to me, was just screaming to be followed up on,” Hughes said. 

Hughes decided to begin by finding a way to visualize primary cilia on human islets. Over months, she and her collaborators optimized a protocol for peeling away the entire cell membrane to see the cytoskeletal components of the cilia. Then they applied this method to donated human pancreatic samples and used scanning electron microscopy to obtain a 3D view of cilia morphology.2

The resulting image reveals the richness of the surface of a pancreatic islet cell. Emerging from the microvilli-covered surface is a lone few microns-long primary cilium. Circular rings around its base form the transition zone of the cilium, from which nine parallel microtubules project into the extracellular space. About halfway through, the microtubules wind around each other, producing a directionality that was consistent across all cilia analyzed. Its effect on cilia function remains unclear, Hughes noted. 

By studying the structure of pancreatic cilia, Hughes hopes to understand their basic functions, which may help scientists determine how cilia defects can lead to disease. “It's a peculiar structure. It's long, it's awkward, it's vulnerable to a lot of mechanical stress, but certainly it has evolved to be that way to perfect a function that it serves,” Hughes said. “It really captured my imagination.”

References

  1. Lodh S, et al. Birth Defects Res C Embryo Today. 2014;102(2):139-158
  2. Polino AJ, et al. Proc Natl Acad Sci USA. 2023;120(22):e2302624120.
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A stock image featuring a render of an influenza virion in the bottom-right corner.

Staying Ahead of Influenza

Researchers access a wide range of tools and reagents to keep pace with seasonal influenza.

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© istock.com, feellife

          Stylized rendering of an influenza virus, focusing on virion surface proteins. One large virion is prominent in the foreground while four float in the background.
Influenza viruses mutate regularly, forcing scientists to rapidly adapt when performing disease research or vaccine development.
Sino Biological

Influenza represents a major health concern, with seasonal outbreaks causing an estimated 250,000-500,000 deaths worldwide every year. Furthermore, influenza has the capability to cause a pandemic, having already done so in 1918, 1957, 1968, and 2009. Vaccination represents the best method for limiting influenza mortality and morbidity.1,2

However, developing influenza vaccines is complex. Influenza viruses constantly mutate, resulting in a diverse and constantly changing array of strains. The World Health Organization (WHO) monitors influenza virus antigenic phenotypes throughout the year, an essential process for influenza-centric research efforts including the development of pan-influenza vaccines.2

The most prominent circulating strains differ between distinct geographical regions and vary from year to year. As a consequence, combatting seasonal influenza currently entails the annual development of new vaccines targeting what is predicted to be the most prominent strains for the upcoming season in a given region.2

To fight influenza, researchers need access to tools that let them comprehensively capture the depth and breadth of the virus’s diversity and gauge vaccine-induced antibody responses. Recombinant influenza antigens are particularly useful for simulating responses to viral infection, and companies like Sino Biological maintain sizable antigen libraries derived from prominent strains of recent years. Sino Biological, in particular, covers recombinant antigens for influenza strains spanning 2015 to 2025 and offers hemagglutinin (HA), HA trimer, neuraminidase (NA), and nucleoprotein (NP) proteins from all WHO-recommended vaccine strains in recent years. Tools such as these help scientists examine influenza pathogenesis, design new assays, and develop new vaccine candidates.

Learn more about the available tools for influenza research. 

References

  1. Paules CI, et al. Immunity. 2017;47(4):599-603
  2. Cox N. Bull World Health Organ. 2014;92(5):311
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An illustration of a guy in shorts and flip flops presenting data on a screen to an audience.

The Poster Projector

Alok Wessel was well prepared to present his conference poster, or so he thought.

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Modified from © istock.com, Volodymyr KryshtalThinkNeo, vectornation, AlonzoDesign; Designed by Erin Lemieux

          Alok Wessel working on laser mounting blocks in a machine shop.
Alok Wessel was a biophysics graduate student at the University of Goettingen in 2014. He is now a software development team lead at Abberior Instruments, a microscope company.
Alok Wessel

In 2014, I was in the final year of my graduate studies in biophysicist Christoph Schmidt’s group at the University of Goettingen. I had collected decent data from my project investigating the mechanical properties of Drosophila embryos, so my advisor encouraged me to present at an international conference in Boston that summer. 

The day of my poster presentation, I had spare time before my session. Feeling well prepared for the event, I explored the beach before heading to the conference venue. When I entered the presentation hall, I noticed two shocking details. First, most attendees were dressed in formal clothes, while I stood there in my shorts and flip flops. Second, and much worse, there were no poster stands in sight; instead, a giant screen stood at the front of the room. That’s when I pieced together that my work had been selected for an oral presentation, not a poster. 

Mortified about how I had missed this detail in the acceptance email, I experienced both cold and hot sweats simultaneously. I realized that I could flee the situation or face it, and decided in favor of the latter. I rushed to my hotel, grabbed my laptop, and loaded the digital version of my poster. When it was my turn to present, I projected the poster on the screen, zooming in and out of sections as I spoke. The situation felt awful at the time, but I survived. I even got asked a few questions at the end of my talk. 

Thankfully, my advisor found the situation amusing rather than upsetting. Another silver lining of my debacle was that it served as an excellent networking catalyst; people recognized me as the “poster guy” for the rest of the conference. 

Although the incident was embarrassing, I learned that there’s always a way to go on. Scientific presentations seem like a big thing as a student, but in the end, this problem wasn’t as catastrophic as it seemed. 

This interview has been condensed and edited for clarity.

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Purple and blue antibodies rendered in 3D

Problems and Solutions for Rapid Antibody Production

Antibody production requires myriad steps with distinctive challenges, but there are solutions for speeding up this process.

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© stock.adobe.com, Corona Borealis

Antibody production can slow research to a crawl. As senior vice president of Biointron, Lei Shi works with scientists around the globe to optimize and expedite their antibody projects, from start to finish.

          A head shot of Dr. Lei Shi, senior vice president at Biointron
Lei Shi advocates for an improved antibody production process that leads to rapid results.
www.biointron.com, Katherine Zhang

How does antibody production typically work?

The process involves multiple steps from gene synthesis to the final product. First, researchers have to synthesize their antibody gene and make an expression construct. This involves primer design, cloning into an expression plasmid, extracting the plasmid from bacteria, and transfecting it into mammalian cells. After culturing for multiple days, the cells secrete antibodies into the medium. Scientists then perform several purification steps that capture the antibodies and remove contaminants to get a pure product. This process can take eight weeks. 

Why does antibody production take so long?

There are challenges at every step. Scientists often outsource the gene synthesis, which can take between one to three weeks, and mistakes can occur during this process. Subcloning into a desired plasmid, which researchers outsource or take on themselves, can take from one to two weeks and includes challenges such as sequence verification for multiple clones. Transfection and cell culture last another one to two weeks before researchers can finally collect their products. 

Researchers must choose a cell line with good transfection efficiency. Even experienced protein biochemists can have trouble during purification because different antibodies have properties that require specific conditions, without which products degrade and aggregates form. 

What advice do you have for scientists engaging in antibody research?

The connection between gene synthesis and antibody production needs to be optimized. Biointron performs gene synthesis and antibody production together. Scientists who come to us have one order number that takes their project from primer design to the end product, seamlessly connecting every step. By doing this, we get a plasmid ready for transfection in three days. Then by using optimized cell lines, transfection processes, and culturing conditions, we produce antibodies at yields of hundreds of milligrams per liter within four to six days. This shortens the whole process to one to two weeks, which is a tremendous improvement. 

Learn more about optimized antibody production.

This interview has been condensed and edited for clarity.

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A scientist is at his desk with two computer monitors in front of him.

Behind the Scenes of the Publication Process

What happens on the other side of the paper publication submission portal? Christopher Rodrigues, who serves as a journal associate editor, revealed the process.

Image Credit:

Modified from © istock.com, Lyudinka; Designed by Ashleigh Campsall; Adapted from reference 1

          Photograph of a man in a collared blue shirt facing the camera and smiling.
Christopher Rodrigues serves as an associate editor for MicrobiologyOpen in addition to his academic roles at the University of Warwick.
George Archer Photography

Christopher Rodrigues, a molecular microbiologist at the University of Warwick, and his team study the development of spore formation in bacteria. His publication record caught the attention of MicrobiologyOpen, a peer-reviewed journal. Three years ago, he accepted their invitation to serve as an associate editor alongside his full-time role as an academic scientist 

Why did you choose to serve as an associate editor, and what do you do in this role?

I wanted to learn how the publication process worked, and I felt that serving as an editor was an opportunity to contribute to my scientific community in addition to publishing my own research. The tasks provide credentials that can help my career profile, so that’s another benefit. 

As the associate editor, I preview manuscripts to determine if the content fits the scope of the journal. I am required to disclose conflicts of interest such as being a current or recent collaborator with a study author. If the paper fits the scope, I reach out to potential reviewers. I use their comments to decide if the manuscript will be published or needs revision. 

What are the challenges of taking on this role as a full-time academic scientist?

It takes me about 45 minutes to an hour to determine if a study is suitable for the journal, and then I contact the first set of reviewers. Sometimes, I don’t have time to get to my reviews during the week, so they eat into my weekend. However, I don’t have manuscripts every week, so on average, I would say that this role only takes up about a half an hour of my week. The biggest challenge is finding reviewers because people decline or may not respond right away, so I need to keep checking and inviting more people to review the paper. 

This interview has been edited for length and clarity

Reference

  1. Meeske AJ, et al. PLoS Biol. 2016;14(1):e1002341
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DNA molecules.

Genetic Imprints in the Brain

Neuroscientist Anthony Isles studies how the epigenetic phenomenon of genomic imprinting influences the brain and its functions.

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© istock.com, anusorn nakdee

          A man wearing a blue shirt and glasses looks at the camera and smiles.
Anthony Isles, a neuroscientist at Cardiff University, explores how genomic imprinting affects the brain and behavior.
Catrin Hopkins, Cardiff University.

As an undergraduate student, Anthony Isles, now a neuroscientist at Cardiff University, was fascinated by the study of behavior and genetics. When applying for graduate programs, he accidentally landed an interview for a different graduate program at the University of Cambridge than the one he had originally considered. This fortuitous event set him on a journey to understand how the epigenetic phenomenon of genomic imprinting affects the brain.

What is genomic imprinting?

The concept of genomic imprinting emerged about 40 years ago. At that time, embryologists wanted to understand whether the DNA we inherit from each of our parents is functionally equivalent. To do this, they created diploid embryos that had two copies of either maternal or paternal DNA. They found that these embryos did not survive mid-gestation, suggesting that there is a distinction between the maternal and paternal genomes. They called the phenomenon in which some genes are expressed only from the maternal copy while others are expressed only from the paternal copy genomic imprinting. Over the past 20 years, researchers have identified a number of imprinted genes and the epigenetic mechanisms—DNA methylation, histone modification, and noncoding RNA—that make their expression parent dependent.    

How do imprinted genes affect the brain and behavior?

The concept that genomic imprinting is important for parenting, defined as social behaviors that help the offspring survive and develop optimally, emerged in the late 1990s.1 However, researchers haven’t explicitly tested whether imprinted genes are more likely to affect parenting. In a recent study, we looked at publicly available transcriptomic data from a known hypothalamic region involved in parenting in mice. We found that imprinted genes are enriched in this area, supporting the idea that they are essential for parental care. We then induced changes in maternal and paternal parental behavior by knocking out one of these genes and observed deficits in parental behavior, revealing a functional link.2

This interview has been condensed and edited for clarity.

References

  1. John RM, et al. Nat Rev Genet. 2023;24(11):783-796.
  2. Higgs MJ, et al. PLoS Genet. 2023;19(10):e1010961.
Creativity concept with a brain exploding in colors.

Understanding the Symphony of Human Brain Development

Paola Arlotta discussed her journey to become a leader in brain organoid research.

Image Credit:

© STOCK.ADOBE.COM, StockSnap

As a stem cell and regenerative biology researcher at Harvard University, Paola Arlotta seeks to understand how the human brain is formed and what makes it unique. After being inspired by her high school science teacher, Antonio Vecchia, Arlotta pursued a research path that led to her current work exploring the cerebral cortex by growing human organoids in 3D cell culture and investigating their development with single cell sequencing techniques. 

In this Science Philosophy in a Flash podcast episode, Niki Spahich spoke with Arlotta to learn more about her path from a curious child in Italy to her current work exploring the complexities of human brain development using organoid models.

Learn more about Paola Arlotta and brain organoid research.

     A headshot of Harvard developmental neurobiologist Paola Arlotta
Paola Arlotta, PhD
Chair and Golub Family Professor
Stem Cell and Regenerative Biology
Harvard University
Associate Member, Stanley Center for Psychiatric Research Broad Institute
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Soybeans growing against a black background.

How Do Plants Know Which Way is Up?

Despite centuries of study, scientists still make new discoveries about the mechanisms of gravitropism.

Image Credit:

© istock.com, Darkves

          Sophie Farkas wears a white button-down and smiles against a grey backdrop.
Sophie Farkas studies the molecular mechanisms that direct plant root growth.
Barnabás Lévai and Barbara Rozmán

“My dear sir,” wrote botanist Thomas Andrew Knight in 1806. “It can scarcely have escaped the notice of the most inattentive observer of vegetation, that in whatever position a seed is placed to germinate, its radicle invariably makes an effort to descend towards the center of the earth.”1

More than two hundred years later, attentive observers of vegetation are still working out the molecular mechanisms involved in this process. One of the first major discoveries—the identification of statocytes—occurred in the early 1900s.2 These cells located in root tips contain heavy, starch-filled granules called amyloplasts that settle to the bottom of the cell. However, said Sophie Farkas, a molecular physiologist at the University of Freiburg, the molecular mechanisms that amyloplasts use to signal which way is down have only recently been elucidated.

     A microscopy image of a root, with cells at the very tip highlighted in red.
Cells in the root tip (red) contain small circular amyloplasts, which settle to the bottom of the cell and help direct root growth.
Sophie Farkas

In 2023, researchers found that tipping a plant 90 degrees triggered phosphorylation of proteins called LAZY.3 This caused the LAZY proteins to hop from the cell membrane onto the amyloplasts. Then as the amyloplasts slowly sedimented to the new bottom of the cell, they brought the LAZY hitchhikers with them. When the amyloplast reached its destination, the LAZY proteins hopped off and attached themselves to the membrane on the lower side of the cell.

“From there, we know that the LAZY proteins recruit other proteins,” said Farkas. Eventually, this leads to recruitment of PIN-FORMED 3 (PIN3), a transporter for the growth-regulating hormone auxin. Subsequently, auxins move to the lower side of the root, where they inhibit growth. If the root is positioned horizontally and grows faster on the upper side than on the lower side, the root is forced to curve downwards, toward the center of the earth.

Studying the mechanisms that control the growth and structure of roots may help scientists figure out how to engineer plants that are more drought resistant.

References

  1. Knight TA. Philos Trans R Soc. 1806;96:99-108.
  2. Prankerd TL. Botanical Gazette. 1920;70(2):148-152.
  3. Chen J et al. Cell. 2023;186(22):4788-4802.e15.
May 2024 Digest crossword

Science Crossword Puzzle

Put on your thinking cap, and take on this fun challenge.

Image Credit:

SANJA SVIBEN AND ALEXANDER POLINO, WASHINGTON UNIVERSITY IN ST. LOUIS

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