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Neuroscience

The Benefits of Exercise in a Pill? Science Is Closer to That Goal – Neuroscience News

Summary: Researchers have identified a molecule in the blood that is produced during exercise. The molecule, Lac-Phe, can effectively reduce food intake and obesity in mouse models.

Source: Baylor College of Medicine

Researchers at Baylor College of Medicine, Stanford School of Medicine and collaborating institutions report today in the journalNaturethat they have identified a molecule in the blood that is produced during exercise and can effectively reduce food intake and obesity in mice.

The findings improve our understanding of the physiological processes that underlie the interplay between exercise and hunger.

Regular exercise has been proven to helpweight loss, regulate appetite and improve the metabolic profile, especially for people who are overweight and obese, said co-corresponding author Dr. Yong Xu, professor of pediatricsnutrition and molecular and cellular biology at Baylor.

If we can understand the mechanism by which exercise triggers these benefits, then we are closer to helping many people improve their health.

We wanted to understand how exercise works at themolecular levelto be able to capture some of its benefits, said co-corresponding author Jonathan Long, MD, assistant professor of pathology at Stanford Medicine and an Institute Scholar of Stanford ChEM-H (Chemistry, Engineering & Medicine for Human Health).

For example, older or frail people who cannot exercise enough, may one day benefit from taking a medication that can help slow down osteoporosis, heart disease or other conditions.

Xu, Long and their colleagues conducted comprehensive analyses of blood plasma compounds from mice following intense treadmill running. The most significantly induced molecule was a modified amino acid called Lac-Phe. It is synthesized from lactate (a byproduct of strenuous exercise that is responsible for the burning sensation in muscles) and phenylalanine (an amino acid that is one of the building blocks of proteins).

In mice with diet-induced obesity (fed ahigh-fat diet), a high dose of Lac-Phe suppressed food intake by about 50% compared to control mice over a period of 12 hours without affecting their movement or energy expenditure. When administered to the mice for 10 days, Lac-Phe reduced cumulativefood intakeandbody weight(owing to loss of body fat) and improved glucose tolerance.

The researchers also identified an enzyme called CNDP2 that is involved in the production of Lac-Phe and showed that mice lacking this enzyme did not lose as much weight on an exercise regime as a control group on the same exercise plan.

Interestingly, the team also found robust elevations in plasma Lac-Phe levels following physical activity in racehorses and humans. Data from a human exercise cohort showed that sprint exercise induced the most dramatic increase in plasma Lac-Phe, followed by resistance training and then endurance training.

This suggests that Lac-Phe is an ancient and conserved system that regulates feeding and is associated withphysical activityin many animal species, Long said.

Our next steps include finding more details about how Lac-Phe mediates its effects in the body, including the brain, Xu said. Our goal is to learn to modulate this exercise pathway for therapeutic interventions.

Author: Press OfficeSource: Baylor College of MedicineContact: Press Office Baylor College of MedicineImage: The image is in the public domain

Original Research: Closed access.An exercise-inducible metabolite that suppresses feeding and obesity by Jonathan Long et al. Nature

Abstract

An exercise-inducible metabolite that suppresses feeding and obesity

Exercise confers protection against obesity, type2 diabetes and other cardiometabolic diseases. However, the molecular and cellular mechanisms that mediate the metabolic benefits of physical activity remain unclear.

Here we show that exercise stimulates the production ofN-lactoyl-phenylalanine (Lac-Phe), a blood-borne signalling metabolite that suppresses feeding and obesity.

The biosynthesis of Lac-Phe from lactate and phenylalanineoccurs in CNDP2+cells, including macrophages,monocytes and otherimmune and epithelial cells localized to diverse organs. In diet-induced obese mice, pharmacological-mediated increases in Lac-Phe reduces food intake without affecting movement or energy expenditure.

Chronic administration of Lac-Phe decreases adiposity and body weight and improves glucose homeostasis. Conversely, genetic ablation of Lac-Phe biosynthesis in mice increases food intake and obesity following exercise training.

Last, large activity-inducible increases in circulating Lac-Phe are alsoobserved in humans and racehorses, establishing this metabolite as a molecular effector associated with physical activity across multiple activity modalities and mammalian species.

These data define a conserved exercise-inducible metabolite that controls food intake and influences systemic energy balance.

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The Benefits of Exercise in a Pill? Science Is Closer to That Goal - Neuroscience News

Neuroscience

Who Benefits From Brain Training and Why? – Neuroscience News

Summary: People who are competent at near transfer, or skilled ability at similar games, are more likely to also have far transfer skills, meaning a greater ability to focus on daily living activities.

Source: UCR

If you are skilled at playing puzzles on your smartphone or tablet, what does it say about how fast you learn new puzzles, or, more broadly, how well you can focus, say, in school or at work? Or, in the language of psychologists, does near transfer predict far transfer?

A team of psychologists at UC Riverside and UC Irvinereports inNature Human Behaviorthat people who show near transfer are more likely to show far transfer.

For a person skilled at playing a game, such as Wordle, near transfer refers to being skilled at similar games, such as a crossword puzzle. An example of far transfer for this person is better focus in daily living activities.

Some people do very well in training, such as playing a video game, but they dont show near transfer perhaps because they are using highly specific strategies, said first authorAnja Pahor, an assistant research psychologist at UCR and a project scientist in the Department of Psychology at the University of Maribor in Slovenia.

For these people, far transfer is unlikely. By better understanding why this type of memory training or intervention works for some people but not others, we can move forward with a new generation of working memory training games or use approaches that are more tailored to individuals needs.

The researchers conducted three randomized control trials involving nearly 500 participants and replicated the same finding: The extent to which people improve on untrained tasks, that is, tasks they are not familiar with (near transfer), determines whether far transfer to an abstract reasoning task is successful.

By analogy, if a person running on a treadmill in the gym (training or intervention) proceeds to be able to run faster outdoors (near transfer), then this improvement predicts whether this person would be better prepared to engage in other physical activities (far transfer), such as cycling or playing a sport.

Whether and the degree to which working memory training improves performance on untrained tasks, as in fluid intelligence, the ability to think and reason abstractly and solve problems, remains a highly debated topic. Some meta-analyses show a small but significant positive effect on fluid intelligence; others argue no evidence exists that training generalizes to fluid intelligence.

What working memory researchers get most excited about is whether there is transfer to fluid intelligence, said coauthorAaron Seitz, a professor ofpsychologyat UCR and the director of the UCRBrain Game Center for Mental Fitness and Well-Being. What we say in our paper is simple: If you get near transfer, it is very likely that you also get far transfer.

But not everybody gets near transfer for a variety of reasons, such as participants disengaging during training or because that particular training is ineffective for them. These people appear not to get far transfer.

Seitz noted that people are constantly being sold brain training games.

Some studies claim these games work; other studies claim the opposite, making it difficult to interpret the interventions, he said. Further, some of these studies have lumped together people who show near transfer with people who show no near transfer. Our paper clarifies some of this confusion.

To further explore those issues, the team has launched a large-scale citizen science project that will engage 30,000 participants in various forms of brain training. The researchers welcome anyone over 18 to participate bysigning upor learn more about their ongoing work.

Susanne Jaeggi, a professor of education at UCI and director of the UCIWorking Memory and Plasticity Laband a coauthor on the research paper, cautioned that companies claims that their games improve core cognitive functions need to be carefully evaluated.

Almost everyone has access to an app or plays a game on a computer and it is easy to get seduced by the claims of some companies, she said. If we can understand how and for whom brain training apps work, we can improve them to get more out of them than just fun. Such improved apps would be especially meaningful for older adults and certain patient groups.

Funding: The research was funded by a grant to UCR and UCI from the National Institute of Mental Health of the National Institutes of Health.

Author: Iqbal PittalwalaSource: UCRContact: Iqbal Pittalwala UCRImage: The image is credited to UCR

Original Research: Open access.Near transfer to an unrelated N-back task mediates the effect of N- back working memory training on matrix reasoning by Anja Pahor et al. Nature Human Behavior

Abstract

Near transfer to an unrelated N-back task mediates the effect of N- back working memory training on matrix reasoning

The extent to which working memory training improves performance on untrained tasks is highly controversial.

Here we address this controversy by testing the hypothesis that far transfer may depend on near transfer using mediation models in three separate randomized controlled trials (RCTs).

In all three RCTs, totalling 460 individuals, performance on untrainedN-back tasks (near transfer) mediated transfer to Matrix Reasoning (representing far transfer) despite the lack of an intervention effect in RCTs 2 and 3. UntrainedN-back performance also mediated transfer to a working memory composite, which showed a significant intervention effect (RCT 3).

These findings support a model ofN-back training in which transfer to untrainedN-back tasks gates further transfer (at least in the case of working memory at the construct level) and Matrix Reasoning.

This model can help adjudicate between the many studies and meta-analyses of working memory training that have provided mixed results but have not examined the relationship between near and far transfer on an individual-differences level.

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Who Benefits From Brain Training and Why? - Neuroscience News

Neuroscience

How the brains of social animals synchronise and expand one another – Aeon

Humans are not the only creatures that show a refined grasp of social norms. If a group of adult male rhesus monkeys (Macaca mulatta) find themselves sitting around a turning table set with food, they will display an I scratch your back, you scratch mine ethos of reciprocity. One monkey will offer another one a piece of fruit and, whats more, will expect the gesture to be reciprocated. If the offer isnt forthcoming, the first monkey is likely to retaliate by refusing to give up anything on his turn. The monkeys also like to group together in cliques; if they see one monkey has been kind to another, they collectively show kindness to the first monkey. If youre observing, it looks like nothing so much as a group of friends buying each other rounds of drinks at a bar.

While decades of research have dispelled the myth that sociality is unique to our species, scientists are still unclear about just how individual animals retain information about the structure of the society in which theyre embedded. Are the monkeys simply copying each other and sharing food via a sophisticated form of mirroring? Or are they truly keeping track of their own and others behaviour in order to make decisions within a broader social dynamic?

Over the years, biologists have used a variety of lenses to try and answer these sorts of questions. While 19th-century naturalists looked at animal behaviour with a focus on its psychological and physiological aspects, it was only after the groundbreaking work of zoologists such as Nikolaas Tinbergen and Karl von Frisch in the 1930s that the field returned to a focus on how social behaviour might be explained in evolutionary terms.

Following the emergence of the modern discipline of ethology the study of animal behaviour weve been left with two main ways of framing enquiries into the social lives of animals. One approach takes data from observations of animals in the field, trying to understand the group dynamic by looking from the outside in. Yet this necessarily makes it hard to fathom whats happening inside an individual creatures mind. By contrast, the second approach is based on detecting an individuals brain activity, and then on trying to draw a map between patterns of neuronal spiking or firing the oscillating electrical activity that produces brain waves and how the animal acts. Yet this data comes from the inside out, and often struggles to encompass group dynamics. Both of these frames tend to capture an incomplete picture.

Now a new generation of scientists is pushing for a third, more nuanced paradigm for studying animal sociality. Known as collective neuroscience, this research programme proceeds from the idea that brains have evolved primarily to help animals exist as part of a social group rather than to solve problems per se and should be studied as such. Since embedding a brain within a social structure changes how it and other brains perform, it makes no sense to only study individual minds in isolation, because it doesnt provide the full picture. Based on the notion that intelligence is a dynamic of looping cause and effect among multiple brains, researchers are drawing on the latest neuroimaging techniques to try to obtain a more detailed understanding of multiple animals brain states as they engage in a variety of social activities. The hope is that this could lead us to answers about how animals perceive their social world, and how that perception is neurally encoded.

Beyond nonhuman animals, collective neuroscience could also help us decipher some of the complexities of human society as well. Since brains appear to work differently when placed in relationships with others, we might begin to recognise the necessity to tailor interventions to improve mental health in terms of the wider social environment, rather than focusing on individual pathologies. And, in quite a different domain, if sociality is a necessary step on the road to intelligence, its unclear whether machine-learning algorithms really stand a chance of approximating a human intellect unless theyre embedded in a rich society of other algorithms.

In mainstream approaches to cognitive neuroscience in animals, portions of the brain are labelled as relating to perception, action, memory, attention, decision, sociality. But when we examine animal behaviour through a more collective lens, we begin to see that large portions of complex brains are hungry to work in harmony with others, according to Emmanuelle Tognoli, a researcher at the Center for Complex Systems and Brain Sciences at Florida Atlantic University. Like many others, Tognoli is convinced that the brain likely evolved to deal with the informational complexity of navigating and coordinating social relationships. If thats true, cognitive neuroscience that ignores sociality is probably pointless, Tognoli believes.

Much research in cognitive science examines how one brain responds to basic stimuli such as how we work through a problem a friend is recounting, or how we remember that same conversation weeks later. But even a study looking at the dynamic between two individuals lacks certain aspects of the diversity of interactions that emerge naturally in organic, more complex social groups including attention allocation, creating subgroups, and recruiting allies, says Julia Sliwa. She is a neural-systems researcher at the Paris Brain Institute who penned a seminal paper on the need for more collective neuroscience in animal research. What she and others are trying to upend, she says, is the orthodoxy that intelligence, and in this case social intelligence of a species, derives solely from the workings of the single brain. What people have been studying so far is how groups of neurons in single brains can create information in the brain; what we also need to look at, though, is how such information is processed among and between multiple brains working together.

There appear to be neurons responsible for taking note of friends complex social behaviour

The problem with trying to vindicate this idea has largely been a technical one so far, especially for nonhuman animals. Animal neuroscience research has largely relied on attaching animals to clunky machines in a lab and encouraging them to interact within a pair. But these artificial parameters will of course distort social dynamics present in the wild. Now, though, new portable technologies such as wireless neurophysiological recording devices have made it possible to observe creatures in their natural environment, where they interact organically, and in much larger groups.

Recall our friendly macaques, the subjects of a Harvard neurosurgery study published in Science in late 2021. The researchers peered into the macaques brains with recording helmets that could track brain activity in specific neurons with great precision. They observed that each kind of interaction appeared to involve several hallmark neurons lighting up in the dorsomedial prefrontal cortex, the section of the brain that is believed to play a role in social interactions. Different neurons responded differently depending on the circumstances with some neurons firing when someone didnt give a piece of fruit and going silent when someone reciprocated, while other neurons behaved in the opposite way. There were also neurons that seemed to encode information about choices, outcomes and interactions among other monkeys who were simply being observed. In other words, there appeared to be neurons responsible for taking note of friends complex social behaviour.

The Harvard researchers pulled these observations into a neuronal map, which allowed them to anticipate whether the macaques would reciprocate or retaliate on the screen before they did so in real life. These predictions were remarkably accurate, indicating that specific neurons can represent defined pieces of social information. To establish this more decisively, the researchers also worked the other way around. They applied a very small electrical current to temporarily disrupt neuronal activity in specific parts of the monkeys brains, in order to see whether that would stop the macaques from carrying out the social actions but still leave them able to perform their other cognitive functions, such as remembering or making decisions. And, just like that, the monkeys ability to perform social actions slumped, and they failed to reciprocate as expected.

The second experiment Sliwa points to focuses on brain-to-brain synchronisation. In a pivotal study from 2010, Guillaume Dumas, assistant professor of computational psychiatry at the University of Montreal, showed that the brains of human participants mirrored each other on a neurological level when engaging in activities together, such as making funny, meaningless gestures with their hands while watching each other. Another study including Dumas involved giving one of two romantic partners a painful stimulus either alone in a room, in a room with their partner, or in a room with their partner while holding hands and monitoring the effects on brain synchronisation. Unsurprisingly, hand-holding produced the most similarity in partners brain signals, and the person in pain reported that it also eased the pain. (Other studies had already shown that the analgesic effect is much lower if youre holding hands with a stranger.)

This work has widened into other contexts. Uri Hasson, a researcher at the Princeton Neuroscience Institute, has shown that a good storyteller can induce synchronisation between her and her listeners brains (if theres shared common ground, experiences and beliefs); and, in a classroom setting, how well a students brain waves sync up with their peers can serve as a good predictor of how engaged they are, and how much they feel like they get along with the group, according to research by Suzanne Dikker, a senior research scientist at the Max Planck NYU Center for Language, Music and Emotion.

Is this phenomenon present among nonhuman animals? Neuroscientists at the University of California, Berkeley, also published a paper in Science, in which they used the collective neuroscience lens to see whether the same happens for fruit bats a sociable animal that spends most of its life in a group, huddled together in small nooks during the day, and foraging for food in groups during the night.

The bats neurons spiked in similar ways, bringing their brains quite literally onto the same wavelength

The researchers tracked bats brain activity using wireless neurophysiological recording devices as the animals flew around freely in their enclosures and talked to one another with their signature high-pitched screeches. Just like the rhesus monkey study, different patterns of neuronal firing were evident while the bats were recognising and distinguishing between the calls of different members of the group. A cry from one bat stimulated activity in one set of neurons in the listener, while a vocalisation from a different bat stimulated another set of neurons. The mapping was so clear that, when in a silent room observing only the bats brain activity on a screen, researchers could identify which bats had called out.

In addition, the study found that the whole group synchronises its brain states when engaged in communication. Their neurons spiked and oscillated in similar ways, bringing their brains quite literally onto the same wavelength. And if the bats were friendly, having spent significant time together, their brains synchronised even more strongly an effect, perhaps, similar to the finding from Dumass study of hand-holding. The same effect was observed within social subgroups; members of these cliques also had a much clearer neuronal representation when one of their number was vocalising.

The neuroscientists also experimented with playing recordings of bat sounds to some of the bats, in isolation, but this failed to provoke activity in the relevant brain areas perhaps indicating that the bats knew this wasnt a genuine social interaction. This effect could partly arise from how the animals process one anothers presence using vision and olfaction in addition to hearing. But, tantalisingly, it could also indicate that another brain needs to be present for an individuals neurons to even register the existence of a social dynamic. The social context, that is, modulates activity both within and between brains.

Theres much we still dont know. Yes, specific neurons are called into action and synchronised when two bat friends call to one another, and specific neurons light up when two monkeys share food. But whether these neurons are doing the synchronisation, the recognising, or the encoding of information about what is being communicated is still to be determined. We also dont know the extent to which social information is retained over time, or whether its just for the duration of the social activity at hand. Nonetheless, the collective neuroscience agenda has undoubtedly made strides; in most previous studies, researchers couldnt even detect why a neuron was firing or not, Sliwa says, and whether it was because the animal had recognised it was interacting with their friend or because it was interacting with another animal at all.

These preliminary studies are important pieces of a much larger puzzle, according to Sliwa. Their results corroborate the idea that its possible for scientists to discover entirely new capacities when brains are scrutinised all together. Crucially, it also means giving up the clean division between stimuli and inputs versus behaviour and outputs; rather, collective neuroscience involves reckoning with the science of complex systems, where causation is not linear but looping, and social and neuronal structures mesh in unpredictable ways.

Take a sports team. Statistics about each player can tell you a lot about whether theyre going to make good additions to the team or not, but whether the group vibes together, whether they have synchronicity, whether they work together in a group, cant be quantified by the number of their scores or assists. Yet this collective X factor can be what makes a good team into a dream team.

Collective neuroscience offers a different way of seeing neuropsychiatric conditions

In the context of social-animal neuroscience, this means looking at how individual brains both affect and are affected by the social context, rather than starting from the perspective of a single brain. A complex-systems lens would demand that we study animal neuroscience across multiple interlocking scales: starting from neurons, moving into brains and embodied organisms, then across to pairs and groups, looking all the time at how all these levels relate to one another, according to Tognoli. Cognition, in this view, is a dynamical process that happens not only within and between brains, but across a variety of biological, behavioural and social levels of organisation.

Mapping how neuronal activity relates to specific social interactions, and understanding the effects of group social dynamics on the biology of the brain, could shed light on aspects of human society, too. Collective neuroscience offers a different way of seeing neuropsychiatric conditions such as depression and schizophrenia, for example not as instances of individual dysfunctions in the brain, but as phenomena that emerge from multiple dynamic physiological and social processes. How does one get to the bottom of human cognition if we are intrinsically social beings, for whom culture has had a profound impact upon our evolution? Experiments such as the macaque study helped to identify brain areas linked to abnormal or normal social behaviour; related research in humans could yield new therapies or possibilities for intervention.

In the field of AI, embracing the collective neuroscience paradigm could mean the difference between genuine intelligence and useful, but limited, algorithms. If humans complex cognitive architecture arises from their ability to engage in social and cultural learning, computer scientists ought to take note. For example, Dumas, the computational psychiatrist behind the hand-holding study, says social interaction in AI is like dark matter in the field of physics: We know well that it exists, but we do not know how to study it directly just yet. So far, AI has been somewhat solipsistic and individualistic in seeing social cognition as a potential task, rather than as a constitutive aspect of complex cognition, Dumas says. Hes now working on creating frameworks to include this multidimensional form of social intelligence in how artificial intelligence is coded, leveraging our understanding of social learning to help machines advance towards a human-level cognition.

To tackle the challenges ahead, Sliwa reminds me, its not a matter of completely ditching single-brain neuroscience. Interactions in a network might account for much of the social intelligence we see in nonhuman animals but thats also due to their brains being able to independently analyse social interactions. Its still vital to continue to study how a single brain possesses this advanced cognitive ability, as well as how those individual brains then come to work in groups. If intelligence is about dynamic of feedback loops among multiple brains, Sliwa notes, the way we study it also needs to be a system of different looping frameworks feeding into each other a lot of loops of different levels of investigation.

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How the brains of social animals synchronise and expand one another - Aeon

Neuroscience

The Sensations Experienced in Reading Poetry – Neuroscience News

Summary: Using neuroscience concepts, researchers evaluate the emotional sensation and analytical representations that occur as we read poetry.

Source: Tallinn University

In addition to searching for the meaning of poems, they can also often be described through the emotions that the reader feels while reading them.

Kristiine Kikas, a doctoral student at the School of Humanities of Tallinn University, studied which other sensations arise whilst reading poetry and how they affect the understanding of poems.

The aim of the doctoral thesis was to study the palpability of language, i.e. sensory saturation, which has not found sufficient analysis and application so far.

In my research, I see reading as an impersonal process, meaning the sensations that arise do not seem to belong to either the reader or the poetry, but to both at the same time, Kikas describes the perspective of her thesis.

In general, the language of poetry is studied metaphorically, in order to try to understand what a word means either directly or figuratively. A different perspective called affective perspective usually studies the effects of pre-linguistic impulses or impulses not related to the meaning of the word on the reader.

However, Kikas viewed language as a simultaneous proposition and flow of consciousness, i.e. a discussion moving from one statement to another as well as connections that seem to occur intuitively while reading.

She sought to identify ways to approach verbal language, that is considered to trigger analytical thinking in particular, in a way that would help open up sensory saturation and put their observation in poetic analysis at the forefront along with other modes of studying poetry.

To achieve her goals, Kikas applied Gilles Deleuzes method of radical empiricism and compared several other approaches with it: semiotics, biology, anthropology, modern psychoanalysis and cognitive sciences.

Kikas describes reading in her doctoral thesis as a constant presence in verbal language, which is sometimes more and sometimes less pronounced. This type of presence can be felt like colour, posture or birdsong.

Following the neuroscientific origins of metaphors, I used the human organisms tendency to perceive language at the sensory-motor level in my close reading to help replay it using body memory. This trait allows us to physically experience the words we read, explains Kikas.

According to her, the sensations stored in the body evoked by words can be considered the oneness of the reader and the words, or the readers becoming the words. Kikas emphasises that this can only happen if the multiplicity of sensations and meanings that arise during reading are recognized.

Although the study showed that the saturation associated with verbal language cannot be linked to a broader literary discourse without representational and analytical thinking, the conclusion is that noticing and acknowledging them is important in both experiencing and interpreting the poem, summarises Kikas her doctoral thesis.

As her research was only the first attempt in examining sensations in poetry, Kikas hopes to provide material for further discussion.

Above all, she encourages readers in their attempts to understand poetry to notice and trust even the slightest sensations and impulses triggered while reading, as these are the beginning of even the most abstract meaning.

Author: Kristiine KikasSource: Tallinn UniversityContact: Kristiine Kikas Tallinn UniversityImage: The image is in the public domain

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The Sensations Experienced in Reading Poetry - Neuroscience News

Cell Biology

Heated Debate Persists over the Origins of Complex Cells – Scientific American

For billions of years after the origin of life, the only living things on Earth were tiny, primitive cells resembling todays bacteria. But then, more than 1.5 billion years ago, something remarkable happened: One of those primitive cells, belonging to a group known as the archaea, swallowed another, different one a bacterium.

Instead of being digested, the bacterium took up permanent residence within the other organism as what biologists call an endosymbiont. Eventually, it integrated fully into its archaeal host cell, becoming what we know today as the mitochondrion, the crucial energy-producing component of the cell.

Its acquisition has long been viewed as the key step in what is arguably the most important evolutionary leap since the origin of life itself: the transition from early primitive cells, or prokaryotes, to the more sophisticated cells of higher organisms, or eukaryotes, including ourselves.

Its a neat story youll find in most biology textbooks but is it quite that simple? In the last few years, new evidence has challenged the notion that mitochondria played a seminal role in this transition. Researchers sequencing the genomes of modern-day relatives of the first eukaryotes have found many unexpected genes that dont seem to come from either the host or the endosymbiont. And that, some scientists suggest, might mean that the evolution of the first eukaryotes involved more than two partners and happened more gradually than suspected.

Others dont see a reason yet to abandon the theory that the acquisition of the mitochondrion was the spark that ignited the rapid evolution of eukaryotes giving rise, eons later, to plants, animals, vertebrates, ourselves. Fresh evidence from genomics and cell biology may help resolve the debate, while also pointing to knowledge gaps that still need to be filled to understand one of the foundational events in our own ancestry, the origin of complex cells.

Uncertainties arose when mystery genes turned up in the last decade when researchers including Toni Gabaldn, an evolutionary genomicist at the Barcelona Supercomputing Centre, and his colleagues took advantage of todays cheap gene sequencing technology to explore the genomes of a wide range of eukaryotes, including several obscure, primitive, modern-day relatives of early eukaryotes.

They expected to find genes whose lineage traced back to either the archaeal host or the mitochondrial ancestor, a member of a group called the alphaproteobacteria. But to their surprise, the scientists also found genes that seemed to come from a wide range of other bacteria. Gabaldn and colleagues hypothesized that the cellular ancestor of eukaryotes had acquired the genes from a variety of partners. Those partners could have been additional endosymbionts that were later lost, or free-living bacteria that passed one or a few of their genes to the ancestral host in a common process called horizontal gene transfer. Either way, the tango that led to eukaryotes involved more than two dancers, they suggested.

It is clear now that there are additional contributions from additional partners, says Gabaldn, who wrote about the early evolution of eukaryotes in the 2021 Annual Review of Microbiology.

Its tough to know exactly where those ancient foreign genes came from because so much time has elapsed. But there are many more recent, looser endosymbioses where the origin of foreign genes is easier to identify, says John McCutcheon, an evolutionary cell biologist at Arizona State University in Tempe who wrote about endosymbiont evolution in the 2021 Annual Review of Cell and Developmental Biology. Studying these might, by analogy, give us a shot at understanding how mitochondria and the first eukaryotes could have evolved, he says.

A prime example is a roughly 100-million-year-old partnership between insects called mealybugs and two bacterial endosymbionts, one nested inside the other in the mealybugs cells. (The endosymbionts make essential amino acids that the mealybug cant get from its diet.) Based on a genomic analysis, McCutcheon and his colleagues found that the mealybugs metabolic pathways are now a mosaic made up of genes that originated with the bugs themselves, came in with their endosymbionts or were picked up by horizontal transfer from other microbes in the environment. To make this work, McCutcheons team showed, mealybug cells had to evolve an apparatus that transports proteins to and fro between what were once independent organisms allowing ones from the mealybug cell nucleus to journey across two sets of endosymbiont membranes for use by the innermost endosymbiont

Something similar occurs in a single-celled, amoeba-like eukaryote called Paulinella. Paulinella has an endosymbiont, engulfed tens of millions of years ago, that allows it to harvest energy from sunlight without the chloroplast organelles that usually power photosynthesis. Eva Nowack, who leads a lab at the University of Dusseldorf in Germany, discovered that Paulinelllas genome now contains genes from the endosymbiont along with others that were acquired through horizontal gene transfer.

Remarkably, the endosymbiont imports more than 400 proteins from the host nucleus, so it also must have evolved a complicated protein transport system like the mealybugs. Thats quite exciting, says molecular evolutionist Andrew Roger, who studies the evolution of organelles at Dalhousie University in Halifax, Canada, because it suggests that evolving these transport systems anew isnt as difficult as previously thought.

These examples illustrate how endosymbionts become integrated with their hosts and suggest that horizontal gene transfers from various sources could have been quite frequent early in the evolution of eukaryotes, too. It doesnt show that is what happened in the formation of the mitochondria, but it shows that its possible, says McCutcheon.

Others agree. Theres lots of strong evidence for horizontal gene transfer in eukaryotes, so theres really no reason to say that it couldnt have happened during that period of the prokaryote-eukaryote transition. In fact, it almost certainly did happen, Roger says.

The implication is that the ancient host could have gradually acquired eukaryotic traits one at a time, like a shopper picking up items in a shopping bag, via horizontal gene transfers or by gobbling a series of endosymbionts, explains John Archibald, a comparative genomicist at Dalhousie University. Some of those newly acquired genes could have been useful to the host as it evolved the rest of the machinery found in modern eukaryotic cells.

If so, by the time the ancient host engulfed the precursor of mitochondria, it would have already possessed many eukaryotic features, perhaps including some organelles, the internal compartments surrounded by membranes meaning that mitochondria would have been not the main driver of eukaryotic evolution but a late addition.

But despite all the evidence supporting a gradualist hypothesis for the evolution of eukaryotes, there are some reasons for doubt. The first is that these more recent endosymbioses may not tell us much about what happened during the origin of eukaryotes after all, in these cases the modern host cells were already eukaryotes. These examples tell us how easy it is, once you have a eukaryotic cell, to establish intracellular endosymbioses, says Bill Martin, an evolutionary biologist who studies the origins of eukaryotes at the University of Dusseldorf. But eukaryotes already have all the intracellular machinery needed to engulf another cell. Its not at all clear that the ancestral proto-eukaryote had that ability, Martin says which would make the barrier to that first endosymbiosis much higher. That, to him, argues against a gradual evolution of the eukaryotic cell.

In fact, some evidence suggests that key eukaryotic features were acquired all at once, rather than gradually. All eukaryotes have the exact same set of organelles familiar to anyone who has studied cell biology: nucleus, nucleolus, ribosomes, rough and smooth endoplasmic reticulum, Golgi apparatus, cytoskeleton, lysosome and centriole. (Plants and a few other photosynthetic eukaryotes have one extra, the chloroplast, which everyone agrees arose through a separate endosymbiosis.) That strongly suggests the other cellular components all originated at about the same time if they didnt, different eukaryotic lineages ought to have different mixes of organelles, says Jennifer Lippincott-Schwartz, a cell biologist at the Howard Hughes Medical Institutes Janelia Research Campus in Virginia.

Some biochemical evidence points that way, too. The ancestral host and endosymbiont belonged to different branches of the tree of life archaea and bacteria, respectively that use different molecules to build their membranes. None of the membranes of eukaryotic organelles are exclusively archaeal in structure, so its unlikely they came from the ancestral host cell. Instead, this suggests that the archaeal host was a relatively simple cell that evolved its other organelles only after the arrival of the mitochondrial ancestor.

But what about all those mysterious foreign genes recently found in the eukaryotic family tree? Theres another possible explanation, Martin says. All those foreign genes could have arrived in a single package with the endosymbiont that evolved into the mitochondrion. Later in the 1.5 billion years following that event those genes could have been scattered among many bacterial groups, courtesy of the ease with which bacteria swap genes to and fro. That would give the erroneous impression that multiple partners contributed genes to the early eukaryote.

Moreover, Martin adds, if the gradualist idea is correct, different lineages of eukaryotes should have fundamentally and measurably different collections of genes, but he has shown they do not. There is no evidence to suggest that there were serial acquisitions, Martin says. A single acquisition of mitochondria at the origin of eukaryotes is enough.

The debate is unlikely to be settled soon. Its very hard to find data thats going to make us clearly distinguish between these alternatives, says Roger. But if further studies of obscure, primitive eukaryotes revealed some that have only a subset of eukaryotic organelles, this could lend weight to the gradualist hypothesis. On the other hand, if evidence was found for a way that a simple archaeal cell could acquire an endosymbiont, that would make the mitochondria early hypothesis more plausible.

People are drawn to big questions, and the harder they are to answer, the more people are drawn to them and debate them, says Archibald. Thats what makes it fun.

This article originally appeared in Knowable Magazine, an independent journalistic endeavor from Annual Reviews. Sign up for the newsletter.

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Heated Debate Persists over the Origins of Complex Cells - Scientific American

Cell Biology

Lect/Assist Prof in Plant Cell Biology & Biotech job with UNIVERSITY COLLEGE DUBLIN (UCD) | 297237 – Times Higher Education

Applications are invited for a Temporary post of a Lecturer / Assistant Professor in Plant Cell Biology and Biotechnology within UCD School of Biology & Environmental Biology

The School of Biology & Environmental Science at University College Dublin is seeking to appoint a Lecturer (Above the Bar) in Plant Cell Biology and Biotechnology.

The School offers a diverse portfolio of programmes at both undergraduate and postgraduate levels, including BSc degrees in Cell and Molecular Biology, Plant Biology, Zoology, Environmental Biology and Genetics, and MSc degrees in Plant Biology, Applied Environmental Science, Environmental Sustainability, Global Change and Biological & Biomolecular Science (by negotiated learning).

We are looking for a candidate who has a demonstrated passion for student engagement and teaching and will join a team within the School delivering lectures in the broad area of plant cell biology and biotechnology. The purpose of this post is to provide undergraduate teaching (and associated administrative tasks) covering general aspects of plant cell and molecular biology, within plant, animal and fungal kingdoms. The successful candidate would also be expected to contribute to the supervision of final year and MSc project students and participate in the scholarly activities of the School where appropriate. The candidate should complement and engage with current academic staff and research programmes within the School and wider UCD community Candidates should have a PhD in an appropriate discipline and alongside their teaching and administration duties, will have the opportunity to develop their own research agenda. The School has central facilities enabling plant cell and tissue culture, molecular biology and extensive greenhouse space and state of the art climate control chambers. The successful applicant will be afforded laboratory space and will be supported in developing their research programme

95 Lecturer / Assistant Professor Above the Bar salary scale: 55,951 - 88,601 per annumAppointment will be made on the appropriate scale in accordance with UCD and Department of Finance guidelines.

Closing date: 17:00hrs (local Irish time) on 14th July 2022

Applications must be submitted by the closing date and time specified. Any applications which are still in progress at the closing time of 17:00hrs (Local Irish Time) on the specified closing date will be cancelled automatically by the system. UCD are unable to accept late applications.

UCD do not require assistance from Recruitment Agencies. Any CV's submitted by Recruitment Agencies will be returned.

Note: Hours of work for academic staff are those as prescribed under Public Service Agreements. For further information please follow link below: https://www.ucd.ie/hr/t4media/Academic Contract.pdf. Prior to application, further information (including application procedure) should be obtained from the Work at UCD website: https://www.ucd.ie/workatucd/jobs/

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Lect/Assist Prof in Plant Cell Biology & Biotech job with UNIVERSITY COLLEGE DUBLIN (UCD) | 297237 - Times Higher Education

Cell Biology

Nearly $3 Million Awarded to Study Sickle Cell Disease at UConn Health – UConn Today – UConn

In honor of World Sickle Cell Day, marked each June 19, we share that UConn Healths Dr. Marja Hurley has recently received nearly $3 million in research funding from the NIH and a pharmaceutical company to advance scientific knowledge about sickle cell disease and its related bone loss.

Hurley, a pioneering physician-scientist, is renowned for her three decades of NIH-funded bone research. She is a UConn Board of Trustees Distinguished Professor of Medicine and Orthopedic Surgery at UConn Health.

Sickle cell disease is a painful inherited red blood cell condition impacting the bloods circulation due to abnormally hook-shaped red blood cells. Individuals born with the disease have severe pain episodes due to blockages that can form inside their smaller blood vessels, capillaries, and even bone marrow, when their abnormally shaped cells cannot pass through smoothly. The dangerous blockages can reduce blood flow, may cause deadly blood infections, or profound anemia, an unhealthy level of oxygen-rich red blood cells.

While the sickling of red blood cells inside bone marrow causes severe bone pain episodes it also can cause bone infarctions or damaged areas. However, little is known why a high prevalence of sickle cell patients also experience musculoskeletal frailty and brittle and broken bone complications such as osteoporosis.

To study this phenomena The National Institute of Diabetes and Digestive and Kidney Diseases has awarded a4-year $2,211,239 grantto Hurley as principal investigator with co-investigators Dr. Liping Xiao, assistant professor of medicine and psychiatry, and Siu-Pok Yee, Ph.D, associate professor of cell biology at UConn School of Medicine.

Together the research team will study how sickle cell disease contributes to impaired bone mineralization. Specifically, the researchers will research in mouse models the molecular mechanism impacting the phosphate regulating hormone Fibroblast Growth Factor 23 (FGF23). These studies will aim to identify whether FGF23 is a novel contributor to the pathogenesis of sickle cell disease-related bone loss and anemia and if it can be prevented in the laboratory with the findings translated someday to patient care.

Our hope is that we can develop a useful therapy to prevent bone loss in sickle cell disease patients in the very near future, stresses Hurley. There is much needed intervention to further fuel scientific discoveries to not only curb the pain suffered by sickle cell patients but further enhance their overall musculoskeletal health and well-being.

In addition, the pharmaceutical company, Global Blood Therapeutics(GBT), has provided Hurley with a3-year $535,000 grantto study bone and muscle function in sickle cell disease mouse models.

The drug Voxelotor is a currently FDA-approved drug for treatment for the anemia caused by sickle cell disease. However, little has been determined about the efficacy of the drug to also increase muscle strength and bone mineral density in sickle cell disease patients or mouse models. Hurleys research will be investigating this drugs promise further.

More than 3.5 million are affected worldwide by sickle cell disease, including approximately 100,000 Americans, and in Connecticut, at least 1,000 adults and 600 children. African-Americans and Latinos are predominantly affected in the U.S., with life expectancy for the majority of people with sickle cell disease is now age 40 or greater thanks to advanced health management.

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Nearly $3 Million Awarded to Study Sickle Cell Disease at UConn Health - UConn Today - UConn

Cell Biology

Different Forms of Autism Have Opposite Problems with Brain Precursor Cells – The Scientist

The primordial cells that give rise to most other brain cells do not proliferate in a typical way in autistic peopleand that could explain how common traits emerge from a range of genetic origins, according to a new study.

The idea that autism disrupts the proliferation of neural precursor cells isnt new, but until now, few studies had investigated how that difference arises.

In the new study, scientists fashioned neural precursor cells out of cord blood cells from five autistic boys ages 4 to 14 and, to serve as controls, either their non-autistic brothers or unrelated non-autistic people. Three of the autistic children have idiopathic cases, in which there is no known genetic cause for their autism; the other two have deletions in 16p11.2, a chromosomal region linked to autism and other neuropsychiatric conditions. Three of the autistic children havemacrocephaly, or a large head.

Neural precursors from the autistic boys all proliferated in atypical ways, the scientists found. Among children with macrocephaly, this growth was accelerated, leading to 28 to 55 percent more cells than in the non-autistic controls after six days. In contrast, cells from the other two boys, both with idiopathic autism, grew more slowly and more of those cells died, yielding 40 to 65 percent fewer cells than in controls after six days.

Despite the fact that these individuals are genetically distinct, especially the idiopathic individuals, it is amazing they have a common developmental process dysfunctioncontrol of proliferation, says study co-lead investigator Emanuel DiCicco-Bloom, professor of neuroscience, cell biology and pediatrics at Rutgers University in Piscataway, New Jersey.

This overlap suggests this issue with proliferation control is a common and generalizable mechanism in autism, he adds.

The gene MAPK3, which encodes an enzyme important in brain growth and development, lies within 16p11.2. Exposed to less of the enzymes active form, phosphorylated ERK1 (P-ERK1), neural precursors in the two boys with 16p deletions proliferated more, the scientists found. The opposite held true in boys with more P-ERK1.

Exposing highly prolific precursors to basic fibroblast growth factor (bFGF), which stimulates the ERK pathway, led to a 15 to 30 percent reduction in DNA synthesis in those cells compared with controls; cells with reduced proliferation, however, saw a 15 to 20 percent increase. This discrepancy suggests that atypical proliferation stems from changes in cell signaling.

Stem cells derived from blood cells of the children with idiopathic autisman intermediate step to generating precursor cellsproliferated typically, whereas those from boys with 16p11.2 deletions showed heightened proliferation. The scientists detailed their findings May 26 in Stem Cell Reports.

I am very excited about the idea of convergence between risk variants for psychiatric disordersin this case, idiopathic and 16p11.2, says Kristen Brennand, professor of psychiatry and genetics at Yale University, who did not take part in this research. Even if the direction and magnitude of effects are different, its intriguing that the same pathway is being hit.

The results mirror what is sometimes termed the Goldilocks effect in autism genetics, [in which] either increased or decreased dose or activity of the same gene can lead to risk of autism or another neurodevelopmental disorder, says Jeremy Veenstra-VanderWeele, professor of developmental neuropsychiatry at Columbia University, who was not involved in the study.

These findings suggest that this could be the case for neural precursor cell proliferation generally and perhaps also for response to basic FGF and even ERK signaling in some individuals, he says.

Most of the disruption in brain development in people with autism likely occurs prenatally but manifests during childhood, DiCicco-Bloom says. The results hint at a potential way to diagnose autism earlier in childhoodby taking blood cells, generating neural precursor cells and examining if they proliferate atypically. Then interventions might be employed earlier, DiCicco-Bloom says.

And investigating how autism alters the activity of enzymes such as P-ERK1 could lead to drugs or molecular tools to repair functional abnormalities, which might have an impact, though this is long into the future, DiCicco-Bloom says. Drugs that target P-ERK1 already exist, so clinical trials may one day test such drugs in autistic children who have known problems with this enzyme, he says.

Next, the researchers plan to study more children with idiopathic autism, as well as those with syndromic forms of the condition, such asfragile X syndrome,Rett syndrome andtuberous sclerosis complex, to see if problems with neural proliferation also occur in all these scenarios, DiCicco-Bloom says.

Other future experiments should include following these precursor cells longer to evaluate formation of more mature neurons, or even organoids, Veenstra-VanderWeele says.

Thisarticlewas originally published June 10 onSpectrum, the leading sitefor autism research news.

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Different Forms of Autism Have Opposite Problems with Brain Precursor Cells - The Scientist

Cell Biology

Published Peer Review History at PLOS: Observations from the past three years – The Official PLOS Blog – PLOS

Written by Lindsay Morton

Three years ago PLOS implemented our version of open peer review, which we named with our typical scrupulous precision and total disregard for word count: Published Peer Review History. Since then, the PLOS journals have together published over 18,000 articles with accompanying peer review history. Were pleased to share more preliminary observations based on our first three years of data below. But first, a bit of background

Open peer review can mean many different things. The main unifying feature is an element of openness somewhere in the peer review process, which can range from public comments on all submissions, to an open decision letter after acceptance. PLOS version of open peer review is simple, flexible and modular, dictated by the choices reviewers and authors make during the peer review and publication process.

All PLOS journals default to anonymous peer review. Reviewers have the option to sign their peer reviews if they wish to do so, and are advised of the potential for the review to be published. After an article has been accepted for publication, authors can opt-in to publish the Peer Review History, which includes the key documents from the peer review assessment:

The result is four possible gradations of openness in peer review.

It is very important, we think, to note that the benefits of Published Peer Review History are by no means predicated on reviewers signing their reviews. While reviewers have the opportunity to claim credit if they so choose, the value to the wider scholarly community stems from the availability of their comments. We want to make this absolutely clear because, too often, critique of open peer review can focus on signing, missing the more vital aspect of constructive feedback.

PLOS Peer Review History is organized, time stamped, and machine readable, with the goal of enabling future meta-research. Each element of the history package has a sub-DOI and is tagged and indexed, making it easy to discover and cite, even if youre not reading it on one of the PLOS journal websites. Its also included in AllofPLOS for easier mining and analysis.

You might be thinking so what? When PLOS introduced Peer Review History in 2019, various versions of public review had been available in the scholarly marketplace for a decade or moreat BMJ, EMBO Press, and eLife, just to name a few.

All implementations of open reviewsigned and unsigned, posted as public commentary or published after the factserve to improve transparency and accountability, to demonstrate the quality of peer review and reinforce the validity of the published research, to acknowledge and honor peer reviewers contributions to the literature, and to enrich the scientific record with more expertise.

Our own particular version emphasizes flexibility and author control. After acceptance, PLOS authors must click a check box and opt-in to have their peer reviews published. As a large international publisher with a very broad scope, our goal with Published Peer Review History, as with Open Science in general, has been to bring openness within easy reach for all, while at the same time respecting researchers different values and requirements across disciplines, career stages, and regions. Opt-in works at scale for all the researchers across our portfolio.

The opt-in model is somewhat unusual, as compared to the more established pioneers in Open Peer Review, many of whom mandate openness (e.g. BMJ) or use an opt-out model (e.g. EMBO Press). PLOS opt-in approach results in lower uptake: on average, 40% of PLOS authors opt-in, as compared to the reported greater than 95% of EMBO Press authors who dont opt-out. At the same time, PLOS large publication volume means that, even with a lower rate of uptake, the journals contribute significantly to the total number of articles with public peer reviews available across the published literature. (PLOS journals together published nearly 18,000 articles in 2020. For comparison, the same year eLife published 1,870 articles, BMJ Open published 3,610*, and the five EMBO Press journals published 1,063*.) This absolute scale is helpful with normalizing practices and behaviors.

The opt-in model, in combination with our size and breadth of scope also produces a wealth of data, which we hope can help us to better understand the communities we serve, and inform our future direction with regard to published review.

Since PLOS Published Peer Review History was first introduced, opt-in has remained a remarkably consistent 40%, year after year.**

PLOS two highly selective journals, PLOS Biology and PLOS Medicine, also saw the highest rates of Published Peer Review opt-in among accepted authors, followed by two of the four community journals, PLOS Computational Biology, and PLOS Genetics. PLOS ONE and the remaining two community journals, PLOS Pathogens and PLOS NTDs saw the lowest opt-in rates. PLOS ONEs broad scope and high publication volume accounts for its lower average opt-in rate. Lower adoption among Pathogens and NTDs authors as compared with the other community journals may likewise relate to subject-specific norms and preferences.

When PLOS ONE opt-in rates are broken out by discipline a pattern of subject-area preference becomes apparent. In fields with more than 100 published articles in the time period, opt-ins were strongest in computational biology, public health fields (womens health, public health, mental health), research on caregiving (healthcare, nursing), and specific medical disciplines (emergency medicine, neurology, obstetrics, urology, anesthesiology, pulmonology, clinical trials, etc.). Lower opt-in rates were observed in engineering, math, chemistry, materials science, earth science, geography and various branches of biology (molecular biology, microbiology, cell biology, biotechnology), as well as in fields where medical and bench science intersect, such as basic cancer research.

While clinical in their potential translational applications, PLOS NTDs and PLOS Pathogens frequently publish research on the molecular and cellular aspects of disease, and therefore might expect commensurately lower opt-in rates.

However, PLOS Biology also publishes in the biological fields where PLOS ONE opt-in tends to be weakeryet it has the highest opt-in rate of any journal. Why is that? Perhaps, the journals hands-on, personalized editorial and peer review process influences author opt-in. This would be a fascinating area for investigation.

PLOS has always allowed reviewers to sign their reviews if they choose, but it wasnt until the system updates introduced at the same time as Published Peer Review History (May 22, 2019) that we gained the ability to easily and systematically measure signing. Since then, weve received 49,555 signed reviews (17.81% of all completed reviews). Those signed reviews were performed by 40,276 individuals (about 19.26% of active reviewers) and were linked to 32,869 manuscripts (35.55% of manuscripts considered).

Overall, reviewers decisions to sign reviews are distributed across journals and subject areas in a pattern similar to authors decisions to publish reviews. Signing rates were higher in public health, medicine, and related disciplines and less common in some branches of biology, as well as the physical sciences, earth sciences, engineering and math. Of articles with published peer reviews, 44% also had at least one signed review.

The clearest determinant of signed review was the reviewers recommendation (although reviewer recommendations are visible only to Academic Editors and the journal office). Signing rates were highest among reviewers recommending accept or revise decisions. For that reason, rates of signing on published articles (42.19%) are higher than for manuscripts generally.

At PLOS we have formal and informal conversations with our stakeholders and community members; we gather feedback in person and by email; we conduct surveys and structured interviews; we do meta-research; we observe.

Three years ago, PLOS chose an opt-in over an opt-out model of published review for a number of reasons. Our in-house editorial teams and editorial boards alike were committed to open peer review, and committed to ensuring it was only received positively by giving authors a real choice in the decision. More practically, PLOS serves more than 200 communities of research, each with their own needs and priorities. Open peer review is too important a development to force on those who have concerns and need to see a community embrace it first. Therefore, we chose to make openness easy. By leaving the door open, hopefully we can learn more from those who choose to walk through. And, its our hope that information like this can help inform the next round of discussions, innovations, and policies, leading ultimately to a more efficient, equitable, and trustworthy peer review system.

*Data from Web of Science, May 14, 2022

**All data current through May 9, 2022 unless otherwise noted. To be eligible for inclusion articles must have been submitted after May 22, 2019. Published Peer Review History is available at all PLOS journals, including launched in 2021, however only data from the seven long-established journals is included here.

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Published Peer Review History at PLOS: Observations from the past three years - The Official PLOS Blog - PLOS

Cell Biology

Tessa Therapeutics to Host Scientific Session on CD30 CAR-T targeting of CD30+ Lymphomas at the SDCT-REMEDIS Cell Therapy Conference 2022 – Yahoo…

Tessa Therapeutics Ltd

SINGAPORE, June 13, 2022 (GLOBE NEWSWIRE) -- Tessa Therapeutics Ltd. (Tessa), a clinical-stage cell therapy company developing next-generation cancer treatments for hematological malignancies and solid tumors, today announced that the company will host a scientific session during the SDCT-REMEDIS Cell Therapy Conference 2022 being held virtually from June 23-24, 2022.

Tessas scientific session will focus on CD30 CAR-T targeting of CD30+ lymphomas and will feature a presentation from Dr. Ivan Horak, Chief Medical Officer and Chief Scientific Officer of Tessa Therapeutics. The discussion will be moderated by Dr. Han Chong Toh, Deputy Medical Director, National Cancer Centre Singapore (NCCS), Associate Professor, Cancer & Stem Cell Biology Program and SingHealth-Duke Global Health Institute, Duke-NUS, and Head of Cancer Immunotherapy at the SingHealth Duke-NUS Cell Therapy Centre.

Tessa is currently advancing two clinical programs leveraging distinct CD30 CAR-T technologies for the treatment of CD30+ lymphomas. Tessas lead clinical program TT11 is an autologous CD30 targeting CAR-T therapy currently being investigated as a potential treatment for relapsed or refractory classical Hodgkin lymphoma. Additionally, Tessa is developing an allogenic off-the-shelf CD30-CAR EBVST cell therapy TT11X targeting relapsed or refractory CD30-positive lymphomas. Data demonstrating the safety and efficacy of both programs was previously presented at the 2021 ASH Annual Meeting.

We are very pleased to host a scientific session at the SDCT-REMEDIS Cell Therapy Conference 2022 as it provides an opportunity to educate researchers on opportunities to treat CD30-positive lymphomas via CAR-T and the unique approaches being advanced by Tessa, said Dr. Horak. We look forward to progressing clinical programs investigating our autologous (TT11) and allogenic (TT11X) CAR-T technologies during 2022, with several development milestones expected throughout the year.

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Details on the scientific session are as follows:

Presentation Title:

CD30 CAR-T targeting of CD30+ Lymphomas

Moderator:

Dr. Han Chong Toh, Deputy Medical Director, National Cancer Centre Singapore (NCCS), Associate Professor, Cancer & Stem Cell Biology Program and SingHealth-Duke Global Health Institute, Duke-NUS, and Head of Cancer Immunotherapy at the SingHealth Duke-NUS Cell Therapy Centre

Presenter:

Dr. Ivan Horak, Chief Medical Officer and Chief Scientific Officer of Tessa Therapeutics

Date and Time:

June 23, 2022, 3:25 p.m. (SGT)/3:25 a.m. (EDT)

About Tessa Therapeutics

Tessa Therapeutics is a clinical-stage biotechnology company developing next-generation cell therapies for the treatment of hematological cancers and solid tumors. Tessas lead clinical asset, TT11, is an autologous CD30-CAR-T therapy currently being investigated as a potential treatment for relapsed or refractory classical Hodgkin lymphoma (Phase 2). TT11 has been granted RMAT designation by the FDA and PRIME designation by European Medicine Agency. Tessa is also advancing an allogeneic off-the shelf cell therapy platform targeting a broad range of cancers in which Epstein Barr Virus Specific T Cells (EBVSTs) are augmented with CD30-CAR. A therapy using this platform is currently the subject of a Phase 1 clinical trial in CD30-positive lymphomas. Tessa has its global headquarters in Singapore, where the company has built a state of the art, commercial cell therapy manufacturing facility. For more information on Tessa, visit http://www.tessacell.com.

Cautionary Note on Forward Looking Statements

This press release contains forward-looking statements (within the meaning of the Private Securities Litigation Reform Act of 1995, to the fullest extent applicable) including, without limitation, with respect to various regulatory filings or clinical study developments of the Company. You can identify these statements by the fact that they use words such as anticipate, estimate, expect, project, intend, plan, believe, target, may, assume or similar expressions. Any forward-looking statements in this press release are based on managements current expectations and beliefs and are subject to a number of risks, uncertainties and important factors that may cause actual events or results to differ materially from those expressed or implied by any forward-looking statements contained in this press release, including, without limitation, those related to the Companys financial results, the ability to raise capital, dependence on strategic partnerships and licensees, the applicability of patents and proprietary technology, the timing for completion of the clinical trials of its product candidates, whether and when, if at all, the Companys product candidates will receive marketing approval, and competition from other biopharmaceutical companies. The Company cautions you not to place undue reliance on any forward-looking statements, which speak only as of the date they are made, and disclaims any obligation to publicly update or revise any such statements to reflect any change in expectations or in events, conditions or circumstances on which any such statements may be based, or that may affect the likelihood that actual results will differ from those set forth in the forward-looking statements. Any forward-looking statements contained in this press release represent the Companys views only as of the date hereof and should not be relied upon as representing its views as of any subsequent date. The Companys products are expressly for investigational use pursuant to a relevant investigational device exemption granted by the U.S. Food & Drug Administration, or equivalent competent body.

Tessa Therapeutics Investor Contact

Wilson W. CheungChief Financial Officerwcheung@tessacell.com

Tessa Therapeutics Media Contact

Tiberend Strategic Advisors, Inc.Bill Borden+1-732-910-1620bborden@tiberend.com

Dave Schemelia+1-609-468-9325dschemelia@tiberend.com

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Tessa Therapeutics to Host Scientific Session on CD30 CAR-T targeting of CD30+ Lymphomas at the SDCT-REMEDIS Cell Therapy Conference 2022 - Yahoo...