Back view of people clapping for a person standing in the front.

In Fall, Scientists Rise High

Science awards remind us that seemingly overnight success takes years of hard work and patience.

Many people love the fall season for the colorful leaves, crisp air, and pumpkin spice lattes. Life science researchers have one more reason: It is the time of the year when winners of some of the most prestigious awards in science—the Nobel Prize, Lasker Awards, and Breakthrough Prize—are declared within a few weeks of one another.

Every year, the scientific community awaits these announcements to find out who has been bestowed with high honors for their groundbreaking research for the betterment of human life. While receiving these coveted awards is no doubt a triumphant moment for any scientist, their paths to glory rarely have been easy. 

A few years back, I interviewed Alfred Sommer, who won the Lasker Award for Clinical Research in 1997, about his scientific journey leading up to the award. He talked about the difficult early days when his findings were met with disbelief (by everyone, not just reviewer 2). The story of how he spent years collecting more data to convince his peers that a simple solution was not necessarily a wrong one stuck with me. 

Recently, Michel Sadelain, an immunologist who won the 2024 Breakthrough Award, narrated a similar saga about the initial “Why bother?” reaction to his work on engineering T cells. The common factor in both cases is that these scientists persisted in their efforts without knowing if the accolades would ever come. 

These stories serve as inspiring reminders that science is all about resilience and perseverance. Once the appreciation floodgates open, many of the awardees go on to receive multiple awards. I can’t help but think about the many unsung science heroes who never get their due recognition but keep going altruistically throughout their careers because it is the right thing to do. 

This awards season, let’s applaud all researchers who embody the true spirit of science; they hypothesize, experiment, and analyze, whether or not they win the prize.

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wrinkled hands held over blue water

Why Do Fingers Prune?

After a long soak in the tub, fingers emerge looking like raisins. The real reason for this curious phenomenon lies under the skin.

Einar Wilder-Smith
Einar Wilder-Smith, a neurologist at Luzerner Kantonsspital, found that vasoconstriction causes fingertips to wrinkle in water.
Einar Wilder-Smith

Why fingers shrivel up in water is an age-old question that every child asks at bath time, but the answer may come as a surprise. “The whole body doesn’t wrinkle, and that says a lot,” said Einar Wilder-Smith, a neurologist at Luzerner Kantonsspital. Unlike the surrounding skin, the outermost layer of the fingertip is highly innervated with and tethered to vasculature, setting the stage for pruney fingers. 

While osmosis, particularly into dead skin cells, seems like a compelling explanation for this curious phenomenon, Wilder-Smith clarified, “In fact, it's the opposite.” 

In the early 2000s, while working at the National University Hospital in Singapore, Wilder-Smith suspected that the surrounding vasculature drives the wrinkling. He found that after a long soak, blood vessels nestled just below the skin constrict, resulting in negative pressure and downward tugging of the outermost layer of skin. The uneven puckering pattern likely results from varied skin tautness, or tethering, throughout the fingertip. 

Scientists still do not understand how exactly water triggers vasoconstriction, although Wilder-Smith has his theories.1 “It's likely that there's a whole array of different electrolyte channels, and that these are selectively being stimulated,” he said.

Observational studies in patients with peripheral nerve damage further support the notion that wrinkling is an active process. The median nerve runs down the arm into the hand and regulates sweating and blood flow. Patients with nerve damage in their hands did not exhibit wrinkling in the affected fingers.2 In the 1970s, the mother of a child with nerve damage in the hand noticed the return of shriveling fingers following nerve repair. This observation inspired the hand surgeon Seamus O’Riain at University College to develop a simple test that uses wet fingertip wrinkling as a readout of nerve function, which is still used today.3 


  1. Wilder-Smith E, Chow A. Muscle Nerve. 2003;27(3):307-311.
  2. Wilder-Smith E. Clin Auton Res. 2004;14(2):125-131.
  3. O’Riain S. Br Med J. 1973;3(5881):615-616.

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Improving Microplate Reader Measurements

Researchers can choose their own microplate adventure with these critical considerations for application setup.

Learn More
Icino representing detection mode

Detection Mode

Multimode microplate readers include different detection modes. From absorbance to fluorescence, researchers can choose the mode that best suits the application.
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Gain Adjustment 

The right gain setting enhances the signal-to-background ratio and measurement sensitivity. Adjust the gain to ensure proper recording of all data points in a run.
Icons showing plate choices

Plate Choice

Microplates come in different formats, colors, and well shapes. Select the right plate to increase signal-to-background ratios and improve measurement sensitivity. 
Icon representing flash number

Flash Number

Flash settings influence total measurement times and data quality. Select an appropriate flash number to reduce variability and ensure reliable and accurate data.    
Icon showing reading direction

Reading Direction

Measuring from above or below the microplate well has different advantages. Choose the reading direction based on factors that affect target localization in the well.
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Focus Adjustment

Tunable focal height ensures the best results. Adjust the microplate reader to detect the focal plane where the intensity of the sample signal is at its highest. 
Human lung with viruses

Gut Signals Influence Lung Responses to Infection

Diet-derived molecules spur a biological mechanism in the lung barriers of mice that prevents viral lung injury.

Andreas Wack’s research at the Francis Crick Institute focuses on understanding what influences the severity of viral infections in the lungs. An immunologist by training, Wack studied immune and lung epithelial cells for years before realizing that the lung endothelial cells, which are part of the lung barrier, could be key to an organism’s response to a viral infection. 

Evidence suggested that the aryl hydrocarbon receptor (AHR) is essential for airway epithelia and gut barrier immunity.1,2 So, Wack led a team of scientists to investigate the function of AHR in the lung endothelium. In the journal Nature, he and his collaborators described how AHR signaling prevents endothelium damage after an infection and pinpointed the contribution of dietary AHR ligands to this end.3 

“Looking at the endothelium in terms of barrier function is not entirely new,” said Wolfgang Kuebler, a lung and cardiovascular physiologist at the Charité University Berlin who was not involved in the research. “But looking at how the endothelium regulates the epithelium and thereby improves barrier function, that is what matters because both cells compose the barrier and work together.” 

Wack’s team used mice that either lacked AHR or did not metabolize its ligands, leading them to build up. After a viral infection, mice lacking the receptor showed signs of lung injury that were prevented in animals with excess AHR ligands.

By assessing gene expression changes in endothelial cells, the team found that AHR-deficient mice showed disruption of the apelin signaling pathway, which is involved in vessel function regulation. Treating mice with apelin reduced lung damage after infection in wild type but not in AHR-deficient mice, suggesting a role for AHR-apelin signaling in lung protection.

AHR ligands come from the diet (mainly from cruciferous vegetables) or from the metabolism of gut bacteria, so the team next tested whether adding an AHR ligand to the mouse food would affect AHR activity and disease progression. The enriched diet led to fewer signs of lung damage, which according to Wack, provides an example of how gut-derived molecules can affect barrier integrity in other parts of the body.

“A lesson for all immunologists is that you want to embed your lung immune response research into a bigger context,” said Wack. “The lung is clearly communicating with other barrier sites and organs, and we need to think about this.”


  1. Villa M, et al. Nat Commun. 2016;7:12652.
  2. Schiering C, et al. Nature. 2017;542(7640):242-245.
  3. Major J, et al. Nature. 2023;10.1038/s41586-023-06287-y.
3d illustration of microscopic close up showing viruses and intestine villus into digestive tract.

The Viral Microbiome

Humans harbor both bacteria and viruses that help keep us healthy. Soon, they might cure us too.

          A picture of man with light skin and grey hair, wearing a grey suit jacket, a light blue shirt, a piece of red knitwear and a purple and grey tie.
Frederic Bushman is a microbiologist at the University of Pennsylvania where he researches the microbiome, COVID-19, and HIV, often in combination.
Ed Hille

As a researcher of the critters that live in human bodies, microbiologist Frederic Bushman at the University of Pennsylvania has broad interests, from how microbial communities colonize newborns to the interplay between the microbiome and COVID-19. After seeing the powerful effects that microbes can exert on human health, he looks forward to a time when we can use them to our advantage.

You study both the bacteria and the viruses in our microbiomes. What kind of viruses do we have, and are they bad for us?

We have a whole “virome” in our bodies, about a billion virus-like particles per gram of human gut content. Of the ones that we can identify, most are phages that infect the bacteria in our microbiomes, and some are viruses that infect human cells. 

They colonize us shortly after birth.1 Babies are born sterile, but then bacteria come in, and many of them have viral sequences integrated into their genomes that will eventually excise and grow until they explode the cell and take their chances as free viral particles. Human-associated viruses arrive shortly afterwards.

Some of those viruses are pathogenic, but the virome likely also modulates health in many ways. It may be that some amount of low level viral infection provokes a permanent weak immune response that is part of good health.

New effects of the microbiome seem to be discovered daily. What do you expect to see ten years from now?

We will be optimizing and composing microbial communities to advance human health and treat infections such as C. difficile infection, for which products have already been approved.There will be more of that. What useful metabolic outputs can we get from the numerous and diverse bacteria in the world? And what would it take to install them in the gut? I’m very optimistic that we will answer those questions and also about the long-term prospects of engineering the microbiome.

This interview has been condensed and edited for clarity.


  1. Bushman F, Liang G. Curr Opin Virol. 2021;48:17-22.
  2. Chehoud C, et al. MBio. 2016;7(2):e00322-16.
Orange bacteria on a green and orange background.

Bacterial Time Capsules May Inform Future Medicines

Historical samples of bloodstream infections hold secrets to Escherichia coli’s evolutionary history and the emergence of virulent clones.

Polysaccharide cloaks called capsules adorn bacteria to help them evade immune system detection and adapt to changing environments.1 Pathogens like Escherichia coli produce dozens of capsular types, but only a few associate with invasive diseases. In a paper published in Nature Communications, researchers mapped the genetic history of one particularly potent E. coli cloak—the K1 capsule—for understanding the secrets to its success.2 

Alex McCarthy, a microbiologist at Imperial College London, and his team analyzed global whole-genome sequencing data from more than 5,000 clinical samples of bloodstream infections, some predating the antibiotic era. They reconstructed the evolutionary history of the E. coli populations and mapped the emergence of genes encoding the K1 capsule. The results surprised McCarthy’s team.

Approximately 25 percent of the sampled bacteria encoded genes for the K1 capsule, and the genetic locus for the capsule emerged in multiple lineages over the last 500 years. “This was really exciting and interesting,” said McCarthy. “We didn't grasp beforehand the way in which this capsule has emerged independently in multiple different clones of bacteria.”

“One of the strengths that allowed them to get to this result is the use of unbiased databases,” said Olaya Rendueles, a microbiologist at the Pasteur Institute who was not involved in the study. McCarthy’s team used a blend of datasets, which allowed them to take a snapshot of all pathogenic E. coli.

The team also tested K1 capsule survival in human serum in vitro. When they added a bacteriophage enzyme to a blend of human serum and E. coli, it stripped the bacteria of its protective cloak, allowing the human immune system to attack the pathogen. 

In the future, McCarthy and his team hope to understand how the K1 capsule evolves to inform new measures to control and prevent infections. 


  1. Nucci A, et al. Nat Commun. 2022;13:4751.
  2. Arredondo-Alonso S, et al. Nat Commun. 2023;14:3294.
Image of cochlear implant and hearing aid.

Reversing Hearing Loss

Gene reactivation restored hearing after loss in mice, but the timing of intervention is key.

     Stained marginal cells of the stria vascularis of the cochlea.
Steel’s team imaged marginal cells (red) of the cochlea, which maintain EP necessary for hearing, in a Spns2 mutant mouse. Normal cellular function is shown in green, and the blue patches show the breakdown of cells associated with deteriorated hearing.
Elisa Martelletti

Hundreds of genes influence hearing loss, and although hearing aids and cochlear implants offer some reprieve, deafness reversal options do not exist.¹ In an early step to ameliorate one type of inner ear dysfunction, a recent study reported that timely activation of a gene associated with early onset deafness reversed hearing loss in mice.² This proof of concept approach may one day lead to a solution for people with hearing loss attributed to genetic causes.

“Most people tend to think that any neurological disease like deafness, or any sort of problem with brain function at all, represents an irreversible step, and there's no way of going back,” said Karen Steel, a geneticist at King’s College London who led this work. 

To study genetic hearing loss, Steel and her team mutated spinster homolog 2 (Spns2), a gene associated with early onset hearing loss and subsequent deficiency in endocochlear potential (EP), which acts as an inner ear battery by providing the electrical force for normal auditory function.³ They designed the mutation such that they could reverse it with a single tamoxifen injection. 

Mice lacking Spns2 experienced rapid hearing loss within two weeks after birth. “This is a window of opportunity to try to activate the gene,” explained Steel. The researchers injected mice with tamoxifen at 14 to 28 days post birth. Using scalp electrodes, they measured brainstem responses to various sound frequencies before and after the injections. 

They saw gradual hearing improvement in their mice after gene reactivation. The team also noted improved cell morphology in the cochlea, which generates EP, and higher EP levels in these mice compared to their counterparts that lacked Spns2. “This was really the first time that they had any realistic reasonable hearing level,” said Steel. Lastly, earlier reactivation in mice showed more effective sound registration at normal frequencies. 

These findings elucidate the developmental timeframe of intervention in this specific type of hearing loss. Jeffrey Holt, a neuroscientist at Harvard Medical School who was not involved in the study, said, “The field of biological therapies for hearing loss is really in its infancy, but I think there’s great potential.” 

Steel next plans to explore whether other forms of genetic deafness and mechanisms of pathology in hearing loss can also be reversed.


  1. Ingham NJ, et al. PLoS Biol. 2019;17(4):e3000194.
  2. Martelletti E, et al. PNAS. 2023;120(34):e2307355120.
  3. Chen J, et al. PLoS Genet. 2014;10(10):e1004688.
A dark haired man is asleep on a grey couch under a darker grey blanket. A box of tissues is under his arm, and he is holding a tissue in one hand.

Why Do I Sleep So Much When I Am Sick?

Some elements of human immune systems serve important functions beyond fighting infections.

Sickness often brings on fatigue. But why do we feel so tired when we are sick? “There’s not a simple answer,” said James Krueger, a neuroscientist at Washington State University who studies how sleep relates to infectious disease. 

To better understand this sickness-related fatigue, scientists like Krueger study the molecules from pathogens and the immune system that cause sleep during an illness. In the early 1980s, Krueger isolated muramyl peptide, a component of bacterial cell walls, from human urine samples and showed that it induced sleep in rabbits.1 

Muramyl peptide induces interleukin-1β (IL-1β), a cytokine that is part of an inflammatory response. With collaborators who were studying IL-1β, Krueger found that this cytokine also caused rabbits to sleep.Additional studies from other teams showed that IL-1β also correlates with sleeping behavior in humans.3-5 Researchers also identified other inflammatory cytokines triggered during infection that induce sleep in animals and humans.6-8 These may work in conjunction with neurotransmitters, genes, and the circadian rhythm, which regulate normal sleep.

One hypothesis for why immune proteins induce sleep alongside their inflammatory roles suggests that sleeping during illness is the body’s way of conserving energy.10 Fevers induced during infection are metabolically demanding.11,12 Additionally, sleep is important for responding to cellular stress, repairing damaged tissues, and even regulating immune cell proliferation and trafficking.13-15

While the exact reasons behind why we tend to sleep more when we’re sick aren’t fully pinned down, the research suggests that it is evolutionarily conserved across species to rest when the body is stressed. 

“Most people’s grandmothers or mothers have told them to get sleep to recuperate from a disease,” Krueger said. “That’s probably good advice.” 


  1. Krueger JM, et al. J. Biol. Chem. 1982;257(4):1664-9
  2. Krueger JM, et al. Am. J. Physio. 1984;246(6)R-994-R999
  3. Hohagen F, et al. Neuropsychobiology 2008;28(1-2):9-16
  4. Vollmer-Conna U, et al. Psychol Med 2004;34(7):1289-1297
  5. Covelli, V et al. Int J Neuro 1992;63(3-4):299-305
  6. Shoham S, et al. Am. J. Physio. 1987;253(1):R142-R149
  7. Hogan D, et al. J. Neuro. 2003;137(1-2):59-66
  8. Späth-Schwalbe E, et al. J. Clin. Endocr. 1998;83(5):1573-1579
  9. Garbarino S, et al. Commun Biol. 2021;4:1304
  10. Imeri L, Opp MR. Nat. Rev. Neurosci. 2009;10(3):199-210
  11. Baracos VE, et al. Can J Physiol Pharmacol. 1987;65(6)1248-1254
  12. Berger RJ, Phillips NH. Behav Brain Res. 1995;69(1-2)65-73
  13. Davis KC, Razien DM. Phsyiol. J. 2016;595(16): 5415-5424
  14. Elkhenany H, et al. Life Sci. 2018;214(1):51-61
  15. Besedovsky L, et al. Eur J Appl Physiol. 2012;463:121-137

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A female scientist holds up a burning funnel.

A Ticking Firebomb

Annalise Rogalsky finally got the potassium metal to react, but not during her experiment.

Photo of Annalise Rogalsky holding a burnt plastic funnel.
Annalise Rogalsky conducted her undergraduate research at Gonzaga University. She recently earned her PhD at Rush University.
Annalise Rogalsky

In 2017, I was a third-year undergraduate student at Gonzaga University in Stephen Warren’s group. Our team studied farnesol, a molecule used to potentially treat seizures in mice suffering from alcohol withdrawal syndrome. Farnesol treatment is short lived, and to find out how it is metabolized, I attempted nonenzymatic synthesis of its metabolite farnesol glucuronide.¹ 

To achieve this, I chose potassium metal as the strong base to remove a hydrogen molecule from glucose for facilitating the reaction. One late night during spring break, I was catching up on washing used glassware. I rinsed a container with an organic solvent and poured the refuse into the plastic funnel connected to the waste container inside the fume hood. Next, I repeated this step with water. 

The moment I poured the wastewater into the plastic funnel, it caught on fire! Horrified, I realized that there was unreacted potassium metal in the glassware. The waste jar contained a mix of solvents and water. It was a fireball.  

I froze for a moment but then quickly sprang into action. Terrified, I pulled the burning funnel off with tongs and extinguished the flames with a beaker of water. The fume hood was a mess, but I averted a potential lab explosion. When I nervously broke the news to my advisor, he was surprisingly calm. He simply laughed and said, “That must have been exciting, huh?” 

That memorable incident served as a cautionary tale about lab safety. Even during my graduate studies, this story reminded me to keep a cool head when my research work was literally or figuratively on fire.  

This interview has been edited for length and clarity. 


  1. Staines AG, et al. Biochem J. 2004;384(3):637-645.

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Genome sequence map concept

Mind the Genome Gap

Population geneticist Tábita Hünemeier seeks out isolated indigenous groups living in the Brazilian Amazon rainforest to expand understanding of the human genome.

A blonde woman is wearing a laboratory coat and smiling.
Tábita Hünemeier is a population geneticist who studies the genetic variability of Brazilian Native American populations.
Tábita Hünemeier

Tábita Hünemeier, a population geneticist at the University of São Paulo, travels by river for several days to reach the indigenous groups she studies. By focusing on these often overlooked populations, she hopes to expand scientists’ understanding of human genome diversity, disease susceptibility, and evolutionary history.

Why are you interested in the genetics of Native Americans?

We have very little genomic information about Native Americans. By studying these groups, we can better understand the admixture process that happened in several countries in America, where Native Americans are one of the ancestral populations, and how this process affected the health and evolution of the people living there. In addition, we can discover evidence of natural selection or adaptation in those groups, which was once thought to be nonexistent because America was occupied only 15,000 years ago. In 2018, for instance, we identified three new loci under positive selection in Andean Native populations, indicating adaptation to the high altitude of the Andes.1 

What are the broader implications of studying the genomes of these groups?

There might be clinical implications. For example, in a recent study, we looked at indigenous groups in the Amazon and found that there is a genetic basis for Chagas disease.We can also study other processes, such as migration. We might find out that an isolated population has a higher frequency of some genes that are related to diseases. In this sense, the genetic structure of a population can be used to study its health status. 

What are some of the challenges involved in doing this research?

We mostly work with Brazilian indigenous groups that live isolated in the Amazon rainforest. To reach them, it takes us almost a week by boat, so that is challenging. Also working with genomic data is expensive, and financial resources are not always available in Brazil. Despite the difficulties, this research helps indigenous groups gain more visibility because people interested in genetics will read about our studies and learn more about them.

This interview has been edited for length and clarity.


  1. Jacovas VC, et al. Sci Rep. 2018; 8(1):12733.
  2. Couto-Silva CM, et al. Sci Adv. 2023;9(10):eabo0234.
Orange rod-shaped bacteria over a red and purple background.

Macrophages Curtail Tuberculosis

Two autophagy genes work together to stop Mycobacterium tuberculosis dead in its tracks.

Purple cell with a cluster of green tubes
A lack of robust genetic tools has hindered experiments in human primary macrophages. Gutierrez’s team developed a novel human macrophage cell model to dissect the role that autophagy plays in curtailing Mycobacterium tuberculosis (false colored here in green).
Tony Fearns

Mycobacterium tuberculosis (Mtb) and the human immune system have been at war for centuries. In a study published in Nature Microbiology, researchers probed the genetic weapons used on both sides of the battle and revealed how host cells deploy autophagy as a first line of defense to prevent Mtb from gaining a foothold.1 

“Initial interactions are critical for disease outcomes, so understanding factors that drive pathogenic versus protective responses are really important,” said Robert Watson, a microbiologist at Texas A&M University who was not involved in the study. 

Infected macrophages engage two main autophagy pathways to package Mtb into phagosomes for removal, but the exact details of how they do this are unknown. Maximiliano Gutierrez, a cell biologist at The Francis Crick Institute, investigated two key genes, ATG7 and ATG14, to uncover the underlying mechanisms.

Gutierrez’s team infected macrophages generated from human induced pluripotent stem cells with Mtb. Using CRISPR-Cas9 tools, they deleted ATG7 or ATG14 from macrophages and observed increased Mtb replication in both cases, confirming that both genes are required to curtail the pathogen. 

Next, the researchers disarmed Mtb by deleting two defense genes. As expected, wild type cells and ATG7-deficient cells showed hindered Mtb replication. However, when they performed the same experiment in ATG14-deficient cells, the disarmed Mtb replicated successfully. 

This surprised Gutierrez. “We weren't expecting such a strong phenotype with ATG14 because there is still some [ATG7] autophagy operating in those cells.” In subsequent experiments, the authors found that ATG14 regulates the fusion of Mtb-containing phagosomes with lysosomes for disposal, thus identifying another mechanism by which autophagy restricts the pathogen’s escape into the cytosol. 

While the researchers observed these effects in vitro using human iPSCs, others reported mixed results using mouse models.2,3 “It will take the field still some time to sort out exactly why autophagy in myeloid cells in vivo is important for the bacterial control and inflammatory response,” said Jen Philips, a microbiologist at Washington University School of Medicine who was not involved in the study. 


  1. Aylan B, et al. Nat Microbiol. 2023;8:803-818.
  2. Golovkine G, et al. Nat Microbiol. 2023;8:819-832.
  3. Kinsella R, et al. PLoS Biol. 2023;21(6):e3002159.
Orange bacteria on a green and orange background.

Science Crossword Puzzle

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

          November 2023 crossword puzzle
Click the puzzle for a full-size, interactive version.
Stella Zawistowski

8. Like hydra reproduction, usually
9. Bud with a pungent flavor
10. Feature of some chins
11. Pores in a plant's epidermis
12. Cellular recycling process
14. Substance used in electrophoresis
16. Roll of turf
18. Semi-stable colloids
21. Domain once classified with bacteria
22. Follower of "human" or "living"
23. The "A" in AV
24. Greek letter used to characterize mass-to-light ratio


1. Protective clothing for scientists, often
2. Arid biome
3. Fine particles
4. Approximately 55% of a human's total blood volume
5. ELISA, LANA, and others
6. Leaped (up)
7. Basis of some COVID-19 vaccine technology
13. Hawk or coyote, ecologically
15. Viral reproduction by means of a bacterial host
17. Ten-year period
19. Planet whose signature blue-green color comes from methane
20. Orange-plumed blackbird relative
21. Not at home
22. Creosote ___ (plant also known as chaparral)