Image of balancing geometric spheres.

Work and Life: Balance or Blend?

Some scientists strive to separate work from life, while some prefer to mix them.

Image Credit:

© istock.com, eileen

About a decade ago, a few lab mates and I set off on a mission to explore a newly opened local karaoke joint. Hours passed by with us singing away our troubles, and only when we realized the threat of missing the last bus did we surrender our microphones. As the bus dawdled along, one of my lab mates prepared to disembark a couple of stops ahead of her home. On seeing our puzzled expressions, she succinctly explained, “My cells need me.” We all nodded understandingly. 

These words, or some version of them, have been uttered by most scientists during their stints in the lab. None of us were strangers to tending cells on weekends or staying up nights in the hopes of collecting publication worthy data. I remember thinking at the time how burdensome the expectations—imposed by the system or by scientists themselves—are in academia. On social media platforms, I regularly come across researchers voicing their concerns about the extraordinary number of hours they feel compelled to invest in the competitive academic environment, which often hampers their work-life balances. 

A couple of years ago though, I came across a fresh perspective on this topic. When I questioned a panel of successful women scientists about their work-life balances, they opined that the term is misleading. One joked that she is very much alive at work. Another researcher agreed; when one doesn’t stop being a spouse or a parent at work, why should they stop working outside the lab or office, she questioned. If spending hours on her work truly excites her, why does that imply that she is not balancing life?  

I found it interesting that some scientists require defined boundaries, while others prefer no demarcation between the two concepts. Which side do you land on in the work-life balance versus blend debate?

Share your opinion.

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A man with glasses that looks distressed as he stands in front of a laboratory bench with his failed experiment.

Voltage Ventured, Nothing Gained

A common mistake and a well intentioned but misguided gesture led Allison Mackay’s experiment awry in the lab.

Image Credit:

Modified from © istock.com, lioputra; Designed by Erin Lemieux

     A man stands in front of a cabinet of reagents.
Allison Mackay conducted his research at Queens University. He is now a laboratory technician at Ontario Veterinary College.
Allison Mackay

In the late 1990s, I was a fourth-year undergraduate student at Queens University in Dan Lefebvre’s laboratory. For my senior research project, I worked with potatoes and their genetic clones to extract and purify DNA from a genomic library. 

Much of my work involved running DNA gel electrophoresis. I was new to working in the laboratory, and you practically had to tell me not to make my running buffer with tap water. But I was eager to do science! 

One day, I placed my gel into the buffer and loaded all of my samples into the wells. When I stepped back to appraise my work, something was wrong. A wave of despair washed over me as I stood frozen; I had loaded my gel backward. This experiment was already a disaster!

I took a deep breath. I couldn’t turn my gel around without losing my samples, so I decided to do the next best thing to salvage my experiment; I reversed the black and red electrical leads at the power supply so that my samples wouldn’t run off the gel. 

Feeling content, I set my timer and left to drink coffee. However, the rollercoaster of these events was far from over. When I returned to check on my gel, I realized that a well meaning colleague had fixed my “mistake” in connecting the electrical leads, unintentionally running my samples backwards into the buffer. My colleague apologized for this mishap, and thankfully we did not lose any expensive or rare samples in the accident.

Even though this is a common mishap, it felt like a major disaster in that moment. Consequently, the lesson that stuck with me throughout my career was empathy. Everyone did what they did with a good heart, but mistakes happened. 

Now, I work as a laboratory technician in the reproductive biology laboratory at Ontario Veterinary College. I interact with students often, and empathy helps me reassure them whenever something goes wrong that feels like the ends of their worlds. 

This interview has been edited for length and clarity. 

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Conceptual image of mulitcolored cells on a black background.

Explore Life in the Fast Lane With Single Cell Dispensing

Benchtop analytics get a boost from automated single cell dispensing technology that combines microfluidics, flow cytometry, and liquid dispensing.

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© istock.com, Yuuji

Learn More

Single cell sorting and isolation are fundamental techniques for analyzing cells. The downstream applications are almost endless and include diverse research fields such as cell engineering, cell line development, synthetic biology, rare cell isolation, monoclonal antibody development, and single cell genomics. Traditionally, scientists use methods such as fluorescence activated cell sorting (FACS) or limiting dilution assays to sort and isolate single cells for further investigation. Although these approaches are widely used and effective, they involve multiple steps, are time consuming, and yield a limited number of viable cells.

     Photo of the Namocell Pala Single Cell Dispenser benchtop cell sorting and isolation instrument.
The NamocellTM Pala Single Cell Dispenser streamlines cell sorting and isolation workflows using rapid, simple, and gentle cell isolation.
Namocell

For example, the high pressure required to sort cells using FACS instruments causes stress to cells, altering key molecular pathways and diminishing their viability.1,2 Moreover, this approach has multiple manual steps that increase the risk of cell contamination and device challenges such as blockages. In contrast, limiting dilution assays offer scientists a gentler approach to single cell sorting and isolation, but the process is long, labor intensive, and less efficient. As a result, researchers seek new approaches to streamline single cell dispensing workflows and improve the reliability and reproducibility of scientific data.

Innovative technologies pave the way for cell sorting solutions that recognize the limitations of traditional techniques. For example, the NamocellTM Pala Single Cell Dispenser combines cutting-edge microfluidics, flow cytometry, and liquid dispensing technologies for automated, high-throughput single cell sorting and isolation. This benchtop single cell dispenser is faster, easier, and gentler than conventional cell sorting techniques, allowing scientists to preserve cell viability, increase productivity, and decrease contamination and clogging. New technologies such as this are designed to be affordable, maintenance-free, FDA-compliant, and intuitive, allowing researchers to reallocate valuable resources and streamline cell analysis workflows.

Read more about automated single cell dispensing here.

A female scientist holding a pen and clipboard as she stands next to a piece of forensic evidence on the table.

Solving Forensic Puzzles

Colby Duncan uses a powerful criminal justice tool to decode DNA evidence.

Image Credit:

Modified from: © istock.com, Flashvector, Rudzhan Nagiev; Designed by Erin Lemieux

  Headshot of Colby Duncan, a forensic scientist at the DNA unit of a crime lab.
Colby Duncan is a forensic scientist who works in the DNA unit of a crime lab to aid law enforcement in processing evidence.
The Lounge Booth

Colby Duncan, a forensic scientist at a crime lab in Southern California, aspired to be a lawyer growing up due to her interest in criminal justice. However, when she watched The New Detectives, it sparked a profound calling to use biology to unravel criminal mysteries. With a bachelor’s degree in forensic science with a concentration in biology and a master’s degree in criminalistics, she now has her dream job. She seamlessly blends her dual passions to help bring justice to victims and their families.  

What background do you need as a forensic scientist?

There’s a misconception that you can enter this field with a criminal justice degree. While it depends on the lab, they largely look for people who have a science degree. Many of my colleagues have science backgrounds. The training is rigorous though. I am undergoing an intense 18-month training program performing mock cases, moot courts, and competency tests before I am allowed to handle official casework.

How is the collected evidence processed in the laboratory?

We process thousands of cases annually that range from homicide to sexual assault to property crimes. Our initial serology testing involves presumptive tests to identify body fluids. Positive stains undergo DNA analysis, and we check for DNA profile matches with a national database. Then we present our work with clear information about the statistics in court. 

What challenges do you face when handling evidence, and how do you overcome them?

Sample quantity used to be a huge limitation. We needed a dime- or quarter-sized amount of blood. Today, by using enhanced-sensitivity DNA analysis tools, we can process an almost-invisible speck of blood. New amplification kits offer a range of sensitivity or specificity by incorporating more dyes and primers. These kits enable multiplex detection and improve intracolor signal balance, aiding in differentiating between DNA profiles to include or exclude in the investigation. The downside of high sensitivity assays is the detection of junk DNA, but additional purification helps in those cases.

This interview has been edited for length and clarity. It expresses Colby Duncan’s personal opinions. 

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Different types of finger food

Why Do Travelers Get Upset Stomachs?

Diet influences the microbiome. When new foods enter the mix, it gets complicated.

Image Credit:

© istock.com, sorendls

Trying a new cuisine while traveling can be an exciting experience, but sometimes unfamiliar bites don’t agree with travelers even when the food sits fine with the local residents. After ruling out pathogenic bacteria, the next culprit could be commensal bacteria disagreeing with the unusual fare. 

“I would say that the microbiome has to be involved,” said Jonathan Clayton, a microbial ecologist at the University of Nebraska Omaha. 

The gut microbiome breaks down many food substances that would be otherwise indigestible to humans and provides nutrients in return. However, what we eat influences the composition of our microbiomes, and that shapes the community’s digestion skillset, such as the ability to digest fiber, carbohydrates, or even starches in seaweed.1-5 Our diet also influences the biochemistry of the microbiota, as diets high in protein and fat use more amino acid degradation pathways compared to those found in plant product-heavy diets, which rely on more amino acid biosynthesis. 

New dietary elements not only expose our commensal microbes to foods that they may not be equipped to digest, but also to potentially brand-new food-associated bacteria that may try to compete with our microbial residents. A new diet, even for a short period, can transiently shift the microbiome, leading to altered intestinal mobility and possibly localized inflammation, causing discomfort, as these new microbes interact with the resident immune system.6 

“We know that there are things that microbes do to reduce and buffer inflammation. We know there are things that microbes can do to promote it,” Clayton said. 

Upset stomachs in travelers may come from an inflammatory effect, a temporary shift in microbial composition, a struggle to break down new foods, or something else entirely that is still on the table.

A blue neuron extends into the distance with many protrusions.

Promoting Parenting Practices

Pregnancy hormones help mice prepare to take care of their young by altering activity in neurons.

Image Credit:

© istock.com, koto_feja

If you’re expecting to add any miniatures to your family this season, hormones may help you prepare for them by rewiring your brain. Pregnancy hormones cause many changes in the body to prepare for offspring, and in rodents, this includes promoting parenting behaviors.1,2 However, the changes to neurons and their activity that drive these behaviors are poorly understood.3,4

Johannes Kohl, a neuroscientist at the Francis Crick Institute and coauthor of a recent study, and his team explored the influence of these hormones on neurons that control parental behavioral in mice.5 Understanding these changes could help researchers find interventions for postpartum depression or anxiety.

“The brain can prepare itself for specific future behavioral challenges,” Kohl said. “The way it does this is by just listening to the body.”

The team assessed parenting behaviors in female mice, such as retrieving pups and crouching over them, before, during, and after pregnancy by placing two pups into their cages. They also investigated the influence of estradiol (E2) and progesterone (P4) on these activities and on activity in galanin-expressing (Gal+) neurons in an area of the hypothalamus that controls many of these activities.

Even mice that only saw pups before and at the end of pregnancy exhibited more parenting behaviors as pregnancy progressed. However, the loss of either the E2 or P4 receptor impaired these behaviors. Using patch-clamp electrophysiology, the team showed that E2 decreased the baseline of Gal+ neurons but maintained their excitability after stimulation, while P4 increased the number of inputs that these neurons received. 

“This is really getting into the details of what different types of hormones are doing in very specific sets of neurons,” said Frances Champagne, a neuroscientist at the University of Texas at Austin who was not involved in the study. “It's really doing a nice job at bringing in some of the newer tools that we have now that weren't available back in the 1980s to really dissect out that plasticity and how it's represented with a particular focus on behavior.”

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A Glowing Mouse Map

A whole-body immunostaining method allowed researchers to achieve cellular resolution at the whole-organism level.

          The mouse peripheral nervous system with nerve cells farther away from the camera represented in yellow and pink, while nerves closer to the camera are shown in blue tones.
Researchers used an antibody that targets neurons to visualize the entire mouse peripheral nervous system.
Ertürk lab, Helmholtz Munich

For years, researchers have aspired to look under the skin at the organism level, but limitations in available technologies hindered their progress. Now, researchers led by Ali Ertürk, a neuroscientist at the Helmholtz Munich, developed a novel chemical method dubbed wildDISCO that enables whole-body immunostaining using off-the-shelf antibodies.1 

The secret to wildDISCO’s success is a cholesterol-removing compound that extracts the lipid from the cell membranes without disrupting the cell’s structure. “This is kind of a magical chemical,” said Jie Luo, a postdoctoral researcher in Ertürk’s lab who helped develop the method and coauthored the paper. According to Luo, the compound helps standard antibodies penetrate the cells more easily and homogeneously. 

The team first applied this method to map the mouse’s peripheral nervous system. After fixing the mouse’s body, Luo and his colleagues pumped solutions containing the cholesterol-removing molecule, followed by addition of a pan-neuronal marker (PGP9.5) coupled to a fluorescent tag, through the mouse’s circulatory system. The team next made the whole mouse body transparent using a method that Ertürk previously developed.2 Using light-sheet microscopy, they imaged the entire mouse body and then stitched the images together using software to create a 3D representation of the mouse’s peripheral neuronal network. 

The resulting image reveals different levels of the peripheral nervous system, which the team color-coded such that nerves deeper in the animal’s body show up in yellow and pink, while nerves closer to the camera appear in blue tones. This whole-body mapping enabled the team to clearly see how different organs are innervated, revealing connections that may help other researchers better understand the roles of these projections in health and disease states. 

The successful labeling motivated the team to continue validating other antibodies using the technique, said Luo, and it highlighted the potential of wildDISCO for improving researchers’ understanding of complex biological systems.

a woman in a red shirt stands outside a car, holding her head and looking nauseous.

The Culprits Behind Motion Sickness

Scientists identified neurons that drive the disagreeable symptoms of motion sickness in mice.

Image Credit:

© istock.com, nicoletaionescu

     Albert Quintana wears a lab coat and stands against a background of laboratory equipment.
Albert Quintana uses mouse models to probe the neural mechanisms of motion sickness.
Roser Bastida

From astronauts to roadtrippers, most people have likely experienced the cold, sweaty, stomach-churning sensation of motion sickness. Humans aren’t alone in this affliction: dogs, mice, and even fish share in this familiar misery.1

Despite its prevalence, motion sickness mechanisms are incompletely understood, and many available treatments cause problematic drowsiness. Now, a team of neuroscientists, including Albert Quintana and Elisenda Sanz at the Autonomous University of Barcelona and Richard Palmiter at the University of Washington, have pinpointed the neurons that control motion sickness symptoms in mice, suggesting new therapeutic avenues.2

First, the scientists created a rotation device—like a cross between a carnival ride and NASA’s high-G training centrifuge—to produce motion sickness symptoms like reductions in body temperature, food intake, and locomotion. Building on previous research showing that glutamatergic neurons in the vestibular nuclei (VN) mediated responses to hypergravity, the neuroscientists demonstrated the importance of these neurons in rotation-induced physiological responses as well.3 

Next, the researchers analyzed the neurons’ mRNA transcripts to identify subpopulations within this diverse group of cells. One subpopulation expressed cholecystokinin (CCK), a peptide implicated in nausea and reduction in food intake. When researchers stimulated these neurons optogenetically, they recapitulated many symptoms of motion sickness. Even more promising from a translational perspective, a CCK antagonist blocked some of the rotation-induced symptoms.

The treated animals displayed normal levels of movement. “That was one of the cool things about this study,” said Quintana. “We have identified a different mechanism to prevent motion sickness that doesn’t seem to affect the alertness circuitry in the brain.”

“This was a fantastic study,” said Rebecca Lim, a neuroscientist at the University of Newcastle, Australia who was not involved in the research. “It was great to see this really comprehensive work examining behavioral and neural responses to this motion sickness-eliciting stimulus.”

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Ferret and DNA composition

Ferreting Out the Causes of Cystic Fibrosis

Transgenic ferret models ratted out how a rare cell type affects airway function.

Image Credit:

Modified from © istock.com, DrAfter123, GlobalP; Designed by Erin Lemieux

     Blue cells with yellow spots releasing smaller yellow dots.
Pulmonary ionocytes contain specialized apical caps (yellow) enriched in CFTR and other channels that mediate salt absorption and secretion in the airway to control airway surface liquid volume.
Feng Yuan

Five years ago, researchers discovered a rare cell type in the lungs: pulmonary ionocytes.1 Although ionocytes account for only one percent of all cells lining the airway epithelium, they have the highest expression of cystic fibrosis transmembrane conductance regulator (CFTR), a protein that shuttles water and salt across the lung surface.2 In a recent study published in Nature, researchers used an uncommon animal model, the ferret, to show that ionocytes control airway function.3 The findings have important implications for cystic fibrosis therapeutics.  

Transgenic mice are the gold standard for disease models, but researchers studying cystic fibrosis struggled to recapitulate key phenotypes. “We had to have newer models,” said John Engelhardt, a geneticist at The University of Iowa. He turned to ferrets, whose lung biology and anatomy more closely resembles humans, in the late 1990s, and found that they develop spontaneous bacterial colonization in the airways, a hallmark of cystic fibrosis.4

To determine whether these CFTR-rich cells are the lung’s airway traffic controllers, Engelhardt’s team developed transgenic ferret models to track, tweak, and delete ionocyte function, which helped them identify the mechanisms by which ionocytes regulate airway surface fluid volume, viscosity, and clearing. In his favorite experiment, Engelhardt’s team used single-cell imaging to visualize ionocytes trafficking anions through CFTR portals. “That approach is very powerful moving forward to identify things we didn't even discover within the paper that are still unknown about ionocyte function,” said Engelhardt.

“This paper is really a landmark paper and a technical tour de force,” said Darrell Kotton, a cell biologist at Boston University who was not involved in the study. “It really sets the bar very high for what ionocytes are doing in human lungs and really refocuses our attention on whether the cystic fibrosis drugs might be tailored to modulate ionocytes.”

  1. Montoro DT, et al. Nature. 2018;560:319-324.
  2. Plasschaert LW, et al. Nature. 2018;560:377-381.
  3. Yuan F, et al. Nature. 2023;621:857-867.
  4. Keiser NW, Engelhardt JF. Curr Opin Pulm Med. 2011;17(6):478-483.
A hummingbird hovers next to a red and yellow feeder.

Why Don’t Hummingbirds Get Diabetes?

Astronomically high blood sugar is no problem for these tiny speed demons.

Image Credit:

Brock and Sherri Fenton

          Kenneth Welch Jr. wears a red collared shirt and smiles against a background of trees.
Kenneth Welch Jr. studies the physiology and metabolism of hummingbirds at the University of Toronto Scarborough.
Ken Jones

It’s no secret that hummingbirds are sugar fiends. To fuel their energy-intensive hovering flight, a wild hummingbird consumes approximately 2 grams of sugar per day—the equivalent of a person consuming about 90 pounds of the stuff.1 In keeping with their sugar-rich diet, hummingbirds have exceptionally high blood glucose levels, up to 42 mM.2 In humans, levels over 10mM are cause for concern and can lead to diabetes-related cardiovascular disease, nerve damage, and even blindness. Yet hummingbirds appear to weather this hyperglycemic state without ill effects and, in fact, are quite long-lived considering their diminutive size.

According to Kenneth Welch Jr., an ecological physiologist at the University of Toronto Scarborough, hummingbirds’ high metabolisms and intense daily workout regimes likely help counteract some of the negative effects of high sugar consumption. Protein glycation—the binding of sugars to proteins—may also play a role. Excessive protein glycation can result in an abundance of advanced glycation end-products, which are implicated in many of the complications of diabetes.3

Yet hummingbirds seem resistant to this glycation stress. Despite their high blood sugar, hummingbirds have lower levels of glycated hemoglobin (sometimes called HbA1c) than humans with diabetes.2 No one knows exactly how hummingbirds accomplish this, but it’s a question that Welch is currently exploring. In the case of chickens (all birds are relatively hyperglycemic), one protein called albumin has evolved to have fewer exposed lysine residues, which may render it glycation resistant.4

Welch said that it’s currently unclear whether hummingbird physiology research can prompt development of new therapies for metabolic disease in humans. However, he said, “Knowing more about how evolution can produce solutions to these functional problems in metabolic physiology can only help us formulate more creative solutions in the human biomedical context.”

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a Taenia solium parasite, a human brain, and lines that represent an electroencephalogram (EEG) recording.

How a Parasite Excites the Brain

Tapeworm larvae may cause seizures by releasing excitatory amino acids into the brain.

Image Credit:

Illustrated by Ashleigh Campsall

Brain infections caused by larvae of the tapeworm Taenia solium are common in many developing countries.1 Once nestled in the brain, the parasite causes neurocysticercosis, an infection characterized by recurrent seizures. Scientists knew that the host’s inflammatory response to the larvae contributed to seizures in neurocysticercosis, but it was unclear whether the larvae directly altered neurons’ electrical activity. 2,3

Now, researchers from the University of Cape Town report that tapeworm larvae directly affect neuronal firing by releasing excitatory amino acids, mainly glutamate, in their surroundings.4 Their findings, published in eLife, pave the way for developing potential new treatment options for seizures in neurocysticercosis. 

For the study, the researchers applied extracts of the larvae or their secretions to brain slices while recording the cells’ electrical activity using the patch clamp technique. Since T. solium larvae are difficult to find, Anja de Lange, a postdoctoral researcher at the University of Cape Town and coauthor of the study, and her colleagues used Taenia crassiceps, a tapeworm that infects rodents and is genetically similar to T. solium, for most of the experiments.

In normal conditions, exposure to parasite preparations caused neurons to fire, but when the team blocked neuronal glutamate receptors, they found no signal. Elevated glutamate levels in the parasite preparations further confirmed glutamate’s involvement.

Finally, to confirm that T. solium exposure showed similar results, the team hunted for T. solium larvae in an endemic region of South Africa and harvested a few from local infected pigs. Puffing T. solium preparations onto human brain slices induced neuronal firing, an effect also mediated by glutamate.  

Accumulating clinical evidence suggests that neurocysticercosis causes seizures in people with epilepsy who live in areas where T. solium is endemic, explained Jorge Burneo, a neurologist at Western University who was not involved in the research. “But we never had basic science evidence that that's the case.” 

Moving forward, the team plans to zoom in on T. solium by examining the effects of the parasite at different life stages on human brain slices and the interplay between the parasite and the inflammatory changes it induces in the brain. “We are quite passionate about this disease being studied more,” said de Lange.

  1. World Health Organization. Taeniasis/cysticercosis. 2022.
  2. Stringer JL, et al. Exp Neurol. 2003;183(2):532-536. 
  3. Robinson P, et al. PLoS Pathog. 2012;8(2):e1002489.
  4. de Lange A, et al. Elife.2023; 12:RP88174.
February 2024 Crossword image

Science Crossword Puzzle

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

Image Credit:

Ertürk lab, Helmholtz Munich

          February 2024 crossword image
Click the puzzle for a full-size, interactive version.
STELLA ZAWISTOWSKI


ACROSS

1. Having no traces of life    
4. Angiosperm's reproductive organ    
8. Invertebrate's eyespot    
9. Insect that produces a gall    
10. Award for a fun and unusual scientific achievement
12. Pulls on    
13. Adjusts to a new environment    
16. Rodent known for its wrinkly pink skin    
18. Catchall survey category    
20. Teeth also known as cuspids    
21. Organisms with offspring    
22. Visibly emotional, in a way    

DOWN

1. Receptor-activating substance    
2. One who studies the seas    
3. Adjust to a standard, as a centrifuge    
4. Rock formed from rapidly cooling lava    
5. Some reproductive cells    
6. Mental health disorder that may be linked to DNA methylation    
7. Most frequent value in a data set    
11. Name for Mars that comes from the oxidized iron in its soil 
14. Meet the expectations of    
15. Protective gear for scientists or painters    
17. Saponification product    
19. Go fast on foot    

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