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Atrandi Raises $25M to Develop New Products Based on Semi-Permeable Capsule Tech

Atrandi Biosciences has raised $25 million in a Series A funding round led by Lux Capital, with participation from Vsquared Ventures, Practica Capital, Metaplanet, and CRIDS Capital. The company plans to use the funds to develop new products based on its semi-permeable capsule (SPC) technology as well as to set up an office in Boston which will allow the company to better serve its U.S. customer base.

Atrandi, which means “you discover” in Lithuanian, was launched in 2016 to address technological challenges associated with single-cell analysis. As Juozas Nainys, PhD, Atrandi’s CEO & co-founder, explained, the company was launched “to bridge a fundamental gap in biological research—the need for high-throughput, scalable technologies to manipulate and analyze single cells with precision.” Furthermore, “our SPC technology is a fundamental breakthrough born from a need to overcome the limitations of existing single-cell analysis tools, giving researchers the possibility to generate rich datasets with an unprecedented combination of throughput, multimodality and data quality.”

Atrandi will use some of the funds from its Series A to extend its offerings for DNA analysis from single cells, Nainys told GEN. The company already has a solution for microbial cells and expects to launch an option that works for eukaryotic cells later this year. They will be able to support whole genome analysis as well as more targeted analysis of single cells. Next year, Atrandi will focus on developing products for multi-omic analysis—specifically DNA and RNA analysis from single cells.

Designed for high-throughput single-cell research, Atrandi’s SPCs are aqueous compartments that are enclosed by a semi-permeable shell. They are designed to isolate single cells and nucleic acids while enabling the exchange of small molecules like enzymes and nutrients. The ability to exchange materials is an important part of SPCs value proposition for single cells and something that sets Atrandi’s technology apart from current droplet microfluidics technologies, according to Nainys. Typically, “once you form a droplet you can add reagents to it … but you can never remove [them],” he explained. “That’s very limiting [because] there are so many different molecular biology reactions that just do not work together or require specific pH [and] buffers.”

Nainys interest in single-cell technologies predates Atrandi’s founding. During his PhD, he worked in a laboratory focused on developing single-cell RNA sequencing technologies. “The single-cell revolution was really brought about by droplet microfluidics,” he said. “The lab that I joined specialized in droplet microfluidics and as experts in that particular technology, we saw that there are … a lot of things that can not be done in droplets.” That led him and Atrandi’s co-founders to launch the company in 2016 with an eye toward developing and commercializing SPCs as well as instruments for generating them.

To date, Atrandi has released three products based on its technology. The first of these is the Flux Microfluidic Device, a user-friendly system designed for high-throughput single-cell isolation into SPCs. The primary goal of this system was to “make the compartmentalization of the sample as seamless as possible so it’s really a push button,” Nainys said. “It’s more for a broader audience that doesn’t want to tinker with the technology.”

The two other products in Atrandi’s portfolio are the Onyx Droplet Generator, a microfluidic platform designed for high-throughput single-cell and single-molecule applications, and the Styx High-Throughput Screening Platform, which is designed for fluorescence-activated droplet sorting. These platforms are designed for users who want more control of their workflows and the ability to adjust different parameters as needed, Nainys said. They are compatible with SPCs as well as droplets. Additionally, “we also worked hard to make sure that the capsules integrate well with any readout method” including sequencing instruments, microscopy, and mass spectrometers.

So far, Atrandi has installed over 150 devices in labs in Europe, North America, and South Korea where they are used for a wide range of applications. About half of its customers are based in U.S. laboratories. People are using the solutions in different ways including studies in oncology, immunology, and microbiology, Nainys said. “It really is all over the map but at the end of the day it’s analyzing single cells as part of a complex biological system.”

News Team by — February 21, 2025 By News Team in Bio Business News
From farmland to construction: Bacteria strains offer sustainable biocement solution

A recent study examines the effectiveness of environmental strains for the production of biocement. The study’s lead author, Dimitrios Terzis, is an EPFL senior scientist and a co-founder of Medusoil, a company that produces organic binders and that opened a production plant in Vaud in 2024.

“For me, it’s essential to keep conducting fundamental research,” says Terzis, a civil engineer at EPFL’s Soil Mechanics Laboratory. His company Medusoil produces organic binders that are similar to biocement.

For the study published recently in Scientific Reports, Terzis worked with scientists from the University of Applied Sciences and Arts of Southern Switzerland to analyze 50 bacteria strains sourced from farmland in Ticino canton. This land is used for grazing dairy cattle and has shown to be particularly well suited for the production of Medusoil’s biocement due to the widely available presence of calcium.

Biocementation relies on stimulating a natural process: The secretion by microorganisms of an enzyme that triggers the formation of carbonate, which then binds with the calcium largely present in the soil to form calcite, a natural cement.

The study identified which naturally occurring strains fabricate the enzyme required for carbonate formation and can be fermented—two factors that make them prime candidates for biocement production. The scientists created a culture of the most promising strain, which was inoculated in a 1.5-meter-high column of sand.

After 24 hours of infiltration, the column was strong enough to sustain its weight and to be used in a variety of geotechnical engineering and geoenvironmental applications, like erosion. The scientists also found that using this strain could cut production costs by 40%.

A paradigm shift

Medusoil, founded seven years ago, supplies organic binders whose carbon impact is at least 55% lower than that of standard cement, which is made by heating an 80% limestone/20% clay mixture to high temperatures. Biocement can be used in a number of geotechnical and building applications, such as to reinforce dams, prevent soil erosion by wind and help protect areas subject to landslides, earthquakes or cyclic loads induced by road and railway traffic.

To test yet another application, the company’s biocement was used in a project in Geneva to recover concrete aggregates from demolished buildings. And because biocement can be employed several times, it supports the circular economy.

In the Scientific Reports study, the authors note that this naturally occurring biocementation process can be applied on a large scale and can help drive a paradigm shift towards greater sustainability in the construction industry.

New production plant

Medusoil reached a new milestone in 2024 with the opening of a production plant in Molondin, near Yverdon-les-Bains. “The plant can generate 400,000 liters of biocement per year, which is enough to stabilize five kilometers of riverbank against erosion,” says Vincent Laurençon, Medusoil’s head of manufacturing.

The company also has a mobile biocementation plant designed to make use of local raw materials. It was recently transported by truck to Romania, for example, where it was employed to reinforce roads. The firm intends to pursue its cutting-edge R&D and has projects lined up this year in France, the Middle East and the Netherlands.

News Team by — February 20, 2025 By News Team in Trending Now

Acting in the right place at the right time is the key to effective medical treatment with minimal side effects. However, this feat remains difficult to achieve.

Biologists and chemists at the University of Geneva (UNIGE) have succeeded in developing a tool that controls the location at which a molecule is activated by a simple pulse of light lasting only a few seconds. Tested on a protein essential for cell division, this system could be applied to other molecules.

The potential applications are vast, both in basic research and in improving existing medical treatments, such as those for skin cancer. These results are published in the journal Nature Communications.

Regardless of how it is administered, a medication does not only act on the affected organ but has a systemic effect on the entire body. This lack of precision carries risks: it may miss its target and not have the desired effect, or it may cause potentially serious side effects. In Switzerland alone, thousands of people suffer from severe drug-related side effects each year.

The solution, simple in theory but highly complex in practice, would be to activate drugs only at the location where they are needed. This challenging research task would, however, make it possible to activate or inactivate a protein in a living organism at a specific location to better understand its functions.

“Everything started from this methodological question,” recalls Monica Gotta, Professor in the Department of Cell Physiology and Metabolism at UNIGE Faculty of Medicine, who initiated and coordinated this research with Nicolas Winssinger, Professor in the Department of Organic Chemistry at UNIGE Faculty of Science.

“We were looking for a way to inhibit a protein involved in cell division, the Plk1 protein, when and where we wanted, to better understand its function in the development of an organism.”

Breaking a biological lock

By combining their expertise in chemistry and biology, the scientists were able to modify a Plk1 inhibitor molecule so that it would be activated by a pulse of light.

“After a complex process, we were able to block the active site of our inhibitor with a coumarin derivative, a compound naturally present in certain plants. This coumarin could then be removed with a simple light pulse,” explains Victoria von Glasenapp, a postdoctoral researcher in the laboratories of Professor Gotta at the Faculty of Medicine and Professor Winssinger at the Faculty of Science, and first author of the study.

The challenge was still to find a way to anchor the inhibitor at the exact point in the body where its action was desired. “We thus modified the inhibitor so that it becomes trapped in the targeted cell by adding a molecular anchor that is released only by light,” explains Nicolas Winssinger.

“This enabled us to activate and anchor the inhibitor with the same light pulse, thereby inactivating Plk1 and stopping cell division at the precise desired location.”

Countless possible applications

The system developed by the UNIGE scientists makes it possible to spatially and temporally control the activity of a molecule in a living organism using light. It can be adapted to numerous molecules to be able to activate a drug only where it is needed.

In the future, a simple laser could therefore activate a treatment exactly where it is needed while sparing the surrounding healthy tissue, thereby limiting undesirable side effects.

“We hope that our tool will be widely used, leading to a better understanding of how living organisms function and, in the long term, to the development of location-specific treatments,” concludes Gotta.

News Team by — February 20, 2025 By News Team in Trending Now
Arc Institute’s AI Model Evo 2 Designs the Genetic Code Across All Domains of Life

“Today, we can for all practical purposes read, write, and edit any sequence of DNA, but we cannot compose it. Maybe we can cut and paste pieces from nature’s compositions, but we don’t know how to write the bars for a single enzymatic passage. However, evolution does.” —Frances Arnold, PhD (Nobel Prize Lecture 2018)

Evo, the genome foundation model developed by the Arc Institute published last November that generalizes across the languages of biology — DNA, RNA, and proteins for both predictive and generative capabilities — has received a major update.

In a new preprint that is not yet peer-reviewed and first published on Arc’s website, Evo 2 moves beyond single-cell genomes of bacteria and archaea to include information from humans, plants, and other more complex single-celled and multi-cellular species in the eukaryotic domain of life.

The model’s resulting research applications span a diverse array of scientific fields including drug discovery, agriculture, industrial biotechnology, and material science. The multimodal and multiscale work is a collaboration with Nvidia along with contributors from Stanford University, UC Berkeley, and UC San Francisco.

“The recipe for life is entirely present in the genetic information contained in our DNA,” said Kimberly Powell, vice president of healthcare at Nvidia. “We’re seeking a deeper understanding of biological complexity. Evolution has solved this problem over millions of years, and Evo 2 aims to learn from this knowledge.”

In healthcare, understanding which gene variants are tied to a disease is an invaluable tool for therapeutics. Early validation of Evo 2’s capabilities showed that the model can identify how genetic mutations affect protein, RNA, and organismal fitness. In tests with variants of BRCA1, a gene associated with breast and ovarian cancer risk, Evo 2 achieved greater than 90% accuracy in predicting which mutations are benign versus disease-causing. 

Patrick Hsu, PhD, Arc Institute co-founder and an assistant professor of bioengineering at UC Berkeley, stated that Evo 2 is the only model that can predict the effects of both coding and noncoding mutations.

“It is the second-best model for coding mutations, but it is state-of-the-art for noncoding mutations, which other variant effect prediction methods, such as AlphaMissense from DeepMind, cannot score,” said Hsu. 

Hsu also described Evo 1 as a “blurry picture of single-cell life” because it was trained on a corpus of 300 billion nucleotides derived from prokaryotic genomes. The team “wanted to be much more ambitious” in this collaboration with Nvidia. 

Evo 2 was built on NVIDIA’s DGX Cloud platform and is trained on more than 9.3 trillion nucleotides from the genomes of more than 128,000 species across the tree of life. The model uses a novel architecture called StripedHyena 2, which enabled training that was “nearly three times faster than optimized transformer models,” according to Dave Burke, PhD, chief technology officer at Arc Institute. The model also has 40 billion parameters and is similar in scale to the current generation of large language models released from Meta, DeepMind, or OpenAI. 

Evo 2 can process DNA sequences of up to 1 million nucleotides at once, allowing it to understand relationships between distant parts of the genome. Hsu stated that this long context length unlocks multiple molecular scales, from short biological molecules, such as tRNA, or clusters of genes (e.g., operons), to entire bacterial genomes or eukaryotic chromosomes. 

Arc Institute and Nvidia describe Evo 2 as the “largest publicly available AI model for biology to date.” Evo 2 is available for public use on the NVIDIA BioNeMo platform and as an interactive user-friendly interface called Evo Designer. In addition, the authors have made its training data, training and inference code, and model weights open source. 
Biology’s app store Understanding biology as a “language” is not a new concept. Advances in genome sequencing have allowed us to “read” the human genome, while the invention of CRISPR technology expanded our toolbox to gene “editing.”  

In 2023, Hsu and Brian Hie, PhD, assistant professor of chemical engineering at Stanford University, began thinking about designing or “writing” biological sequences, including proteins, by starting at the foundational layer of DNA itself. “After all, proteins themselves are encoded directly by the genome,” emphasized Hsu.  

“Machine learning started to revolutionize biology, and models such as AlphaFold or ESMFold enabled protein structure prediction and design. Despite these advances, the complexity of these molecules is dwarfed by the overall complexity of an entire cell,” Hsu continued. 

Given that biological functions are not accomplished by a single protein molecule in isolation, constructing synthetic genomes can provide a valuable research tool to investigate broader biological context, a feat that Evo 2 is tackling head-on. 

“A lot of biological design until now has focused on the molecular level because that’s all that we could control. If we have a powerful model that lets us generate at the scale of complete organisms, then that unlocks a lot of downstream tasks [with a wide array of use cases],” said Hie. 

The Evo 2 preprint described three design tasks that span different levels of genomic complexity: 1) mitochondrial genome 2) prokaryotic genome of Mycoplasma genitalium, a commonly used model of the minimum genome, and 3) yeast chromosome, which represents eukaryotic organisms.

For all three design tasks, the preprint showed evidence supporting genome coherence, such as the construction of genes that code for all the components of the electron transport chain (as predicted by AlphaFold 3) in the case of the mitochondrial genome, and the presence of natural homologs and more complex genomic architecture, such as introns, in the case of the yeast chromosome. 

The preprint also presented a workflow for “generative epigenomics,” which designed DNA sequences with desirable chromatin accessibility profiles to simulate eukaryotic gene regulation.  

When asked about plans for experimental validation, Hie stated that a collaboration with large DNA synthesis and assembly experts from the University of Washington is underway to insert the chromatin accessibility designs into mouse cells for validation studies. 

Looking ahead, the Arc Institute is interested in building on this biological complexity by constructing the virtual cell.  

“The bottleneck to drug discovery is that we don’t know what causes the disease to begin with,” said Hie. “If we have a very capable model of the genome and we couple this with information from the environment through RNA sequencing, gene regulatory networks, and cell signaling networks, then this combined multimodal framework will let us answer these fundamental questions about disease.”

Hie sees Evo 2 as an “operating system”, or a foundational layer, that provides a platform for broad generative functional genomics. While Evo 2 “might not solve all questions in biology,” the model offers a wider breadth of applicability compared to task-specific predecessors, such as AlphaFold for protein structure prediction. 

“We want to empower the research community to build on top of these foundation models. That’s why we put in so much effort with Nvidia to make this fully open source,” weighed in Hsu. “We’re really looking forward to how scientists and engineers build on this ‘app store’ for biology.” 

News Team by — February 20, 2025 By News Team in Biotechnology Daily
Accelerating mRNA Vaccine Production

In principle, mRNA vaccines are ideal for health emergencies as they can be quickly mass produced using a template. The problem is that current cell-based template production methods take too long, says pandemic preparedness organization, CEPI.

And slow template production limits access to vaccines, according to Chaminda Salgado, CMC technology lead, who told GEN about CEPI’s efforts to develop an alternative with French technology firm, DNA script.

“While the process of producing mRNA itself takes only around seven days, the creation of a DNA template can take up to a month, creating a bottleneck in the manufacturing process. That’s because creating a DNA template typically involves living organisms, such as bacteria or yeast, to grow, extract, and purify the required DNA plasmid templates.

“This new project aims to overcome these challenges by generating automated synthetic DNA templates, which don’t need to be grown in living cells and can be rapidly produced within days rather than weeks, without the need for expensive biopharmaceutical facilities or highly trained staff to run the process,” Salgado says.

The plan is to take DNA oligonucleotides made using DNA Script’s enzyme driven synthesis technology—called Syntax—and combine them into longer template sequences using an automated “gene assembler” system.

Manufacturing cost

Replacing cell culture-based template production with synthetic methods could have a significant impact on manufacturing cost and timelines, according to Salgado.

“By streamlining the process, mRNA vaccines could be manufactured and developed even faster and cheaper, meaning vaccines could be given to at-risk populations sooner and potentially help to stop an outbreak in its tracks.

“This technology supports CEPI’s 100 Days Mission—a goal to produce pandemic-busting vaccines within 100 days of a viral threat being identified—and complements a suite of CEPI investments aiming to increase the speed at which vaccines can be manufactured,” he adds.

Another aim of the partnership is to make it easier for people to access vaccines by enabling production in areas without an established manufacturing infrastructure.

Salgado says, “This partnership supports equitable access as it reduces the need for expensive pharmaceutical equipment and infrastructure associated with traditional biologically manufactured DNA templates.

“If successful, the lower costs associated with automated, synthetic DNA template production would remove a potential barrier to the introduction of the technology in Global South countries where resources may be more limited. This could enable the possibility of vaccination closer to the site of an outbreak and avoid delays in vaccine access.”

CEPI and DNA Script are also committed to enabling equitable access to the outputs of the collaboration, Salgado says, adding, “This ultimately includes a commitment to vaccines being available first to populations at risk when and where they are needed at an affordable price should a related vaccine be developed further using CEPI funding.

“Project results, including data generated as part of this project, will be published open access for the benefit of the global scientific community.”

News Team by — February 20, 2025 By News Team in Biotechnology Daily
Cholesterol Metabolite Implicated in Parkinson’s Disease Pathology

Researchers at Wuhan University have discovered a cholesterol metabolite that may play a critical role in the development of Parkinson’s disease (PD). Studies in mice, led by Zhentao Zhang, MD, PhD, indicated that the metabolite, 24-hydroxycholesterol (24-OHC), promotes the spread of Lewy bodies and the death of dopaminergic neurons in the brain, the two major hallmarks of Parkinson’s disease. 24-OHC is produced from cholesterol by the actions of an enzyme, cholesterol 24-hydroxylase (CYP46A1), and the researchers suggest that blocking the activity of 24-OHC or preventing the metabolite from being produced could potentially represent effective strategies for treating Parkinson’s disease.

Zhang and colleagues reported on their findings in PLOS Biology, in a paper titled, “The cholesterol 24-hydroxylase CYP46A1 promotes α-synuclein pathology in Parkinson’s disease.”

PD is the second most common neurodegenerative disease, and leads to slowness of movement, tremor, rigidity, cognitive impairment, and neuropsychiatric symptoms, the authors explained. The disease is characterized by the formation of Lewy bodies composed of aggregates of α-synuclein (α-Syn), and death of dopaminergic neurons in the substantia nigra.

“Converging lines of evidence indicate that α-Syn fibrils can spread in a prion-like manner in the brain, leading to self-propagation and cell-to-cell transmission of protein aggregate,” the investigators stated. “Although it is clear that α-Syn aggregation underlies the pathology of PD, what drives the spread of α-Syn remains unclear.”

Their newly reported study was designed to investigate what causes the spread of pathological α-Syn, with the authors hypothesizing that the culprit is the cholesterol metabolite 24-OHC, which is known to present at high levels in the brains of people with Parkinson’s disease, and which increases with age. “Various types of clinical evidence indicate that the levels of 24-OHC in the cerebral spinal fluid (CSF) are increased in PD patients and are correlated with the duration of the disease,” they wrote, also commenting that “previous studies demonstrate cholesterol 24-hydroxylase (CYP46A1) increases the risk for PD.”

Through their study, the team first confirmed that 24-OHC levels were higher in the blood of patients with Parkinson’s disease as well as in a mouse model of the disease. The results, they wrote, “… suggest that both CYP46A1 and 24-OHC increase in an age-dependent manner and are elevated in PD patients, PD model mice, and aged wild-type mice.”

The researchers then blocked 24-OHC production in the mouse model by knocking out the CYP46A1 enzyme. This reduced both the spread of the harmful α-Syn fibers and damage to the dopamine neurons in the critical part of the brain. “… CYP46A1 knockdown relieves the spread of α-Syn pathology and the loss of dopaminergic neurons,” they commented.

Further experiments with neurons cultured in a dish showed that the addition of 24-OHC caused normal α-Syn to change into harmful α-Syn fibers. Injecting mice with these fibers led to a greater spread of Lewy bodies, more dopaminergic neuron degeneration, and greater motor deficits than did injecting them with α-Syn fibers formed in the absence of 24-OHC. The researchers suggested that drugs that prevent cholesterol from being converted to 24-OHC might therefore be an effective treatment for the disease.

The authors suggest that their findings “… indicate that the cholesterol 24-hydroxylase CYP46A1 plays a pivotal role in the progression of α-synuclein pathology in Parkinson’s disease, highlighting its potential as a therapeutic target for Parkinson’s disease.” In their report, they further stated, “It will be interesting to determine whether CYP46A1 and 24-OHC can serve as theranostic biomarkers for disease-modifying therapies.”

News Team by — February 20, 2025 By News Team in Bio Business News
AI-Guided Receptor Engineering to Improve Performance in Cell Therapies

In a new study published in GEN’s sister peer-review journal, GEN Biotechnology, titled, “Exploring Structure-Function Relationships in Engineered Receptor Performance Using Computational Structure Prediction,” researchers from Northwestern University present a new structure-based analysis to guide the design of synthetic receptors for improved cell therapies.

“A key challenge is that subtle structural changes can have profound functional consequences, and thus cell therapies can benefit from improved methods for tuning receptor functions at the structural level,” said Joshua Leonard, PhD, professor of chemical and biological engineering at Northwestern University and corresponding author of the study, in an interview with GEN.

In cell therapies, engineered receptors need to encompass both safety and efficacy, such as maintaining a resting state until it encounters a disease target. However, the structure of these receptors is generally poorly understood, which can have a substantial impact on therapeutic performance. In the example of CAR T-cell therapies, structurally tuning receptors can avoid tonic signaling, or activation in the absence of the target stimulus, which often drives T-cell exhaustion and diminishes the therapy’s efficacy against targets, such as a tumor. 

The authors generated receptor structural models to investigate the structure-function relationships using a case study that characterized the conversion of natural human cytokine receptors into engineered receptors. They hypothesized that structure prediction might be most feasible on a dataset based on natural receptors, given the reliance of existing tools on sequence alignment with known proteins. 

The study found that specific structural features across the receptor’s ectodomain, which often extends into the extracellular space to trigger signal transduction, and transmembrane domain explained considerable variation in receptor performance, as measured by on-state reporter expression and fold induction of transcription of a reporter gene. 

The authors also extended the analysis to “categorical” variables that describe the identity of specific domain choices and the way in which they are combined, which implicitly captures properties that are unique to the individual chains and not described by structural features directly, such as protein expression, membrane localization, protein stability. Overall, they observed structure-function trends that were largely conserved across structurally diverse receptor sets.

Engineered receptors are a particularly challenging class of proteins to structurally define, as they are relatively large, contain a difficult-to-characterize hydrophobic transmembrane domain, and can adopt multiple conformations. Groundbreaking tools, such as AlphaFold, which solved biology’s hallmark problem of determining a protein’s 3D structure from its sequence and earned DeepMind’s Demis Hassabis, PhD, and John Jumper, PhD, a share of the 2024 Noble Prize in Chemistry, AlphaFold Multimer, and RoseTTAFold (developed by fellow 2024 Nobel Laureate, David Baker, PhD), have been able to construct complete models of natural single-pass transmembrane receptors. However, distilling which structural features impact receptor performance remains an ongoing gap.

“For all the aspects of the receptor we don’t understand, we have to spend more time and effort empirically exploring design choices, and even when good designs are identified, this lack of structural knowledge makes it more difficult to understand why certain choices yield good performance,” said Leonard.

The GEN Biotechnology study proposes potential design rules that are experimentally testable and can guide future engineering across receptor families. Leonard and William Corcoran, lead author of the study and a PhD candidate at Northwestern, expect that these insights will most immediately benefit the design of synthetic receptors that share a similar signaling mechanism, given that the study was based on the conversion of natural receptors (which employ multiple mechanisms) into synthetic receptors (which employ a single mechanism).

Looking ahead, the authors stated that a natural evolution of this workflow is to generate libraries that explore greater design space. In addition, Leonard’s group has several ongoing projects for developing and employing distinct synthetic receptor families and plans to apply the insights from this study to design new synthetic receptors for more applications.

“Ultimately, this study makes us optimistic that protein structure prediction tools, while ever improving, are already useful for making plausible connections between receptor sequence and receptor function, and that fact should accelerate the development of

News Team by — February 20, 2025 By News Team in Bio Business News
Stanford doctor: The breakfast scientifically proven to fend off colon cancer rising in young people

A doctor on the frontlines of America’s colon cancer crisis in young people has revealed the breakfast scientifically proven to stave off the disease.

Dr Suneel Kamath, an oncologist specializing in early-onset colorectal cancers at the world-renowned Cleveland Clinic, told DailyMail.com that mounting research shows how calcium and fiber can protect against the deadly disease.

With this in mind, the colon cancer expert says breakfast is the perfect meal to pack these ingredients into, as there are lots of food options to play with.

A recent study from Harvard University found that people who eat at least two servings of yogurt a week could lower their risk of colon cancers caused by bacteria by 20 per cent.

It followed a study funded by Cancer Research UK in January that found drinking a large glass of milk could be linked to a 17 per cent decrease in the risk of colon cancer.

Meanwhile, many colon cancer experts say that fiber is key in preventing the disease as it feeds ‘good’ bacteria in the gut that shield the colon lining.

Dr Kamath’s first breakfast suggestion is overnight oats with milk, with berries for an extra boost of vitamin C and antioxidants.

The other ingredients comprise non-fat Greek yogurt, honey, and either homemade or store-bought granola.

An 8oz serving provides almost 20 percent (4g) of the recommended daily amount of fiber and 13 percent of your calcium intake.

He says oats, which are wholegrain, are an excellent source of fiber, and which like calcium, has been shown to safeguard against colon cancer.

The oats contain lots of fiber and keep you full, which has the added effect of clearing out the colon and feeding the ‘good’ bacteria.

Fiber is broken down by the body’s gut microbiota – the ecosystem of bacteria, fungi and viruses – through a process called fermentation, which produces beneficial microbes that help protect against colon cancer.

One study suggests that eating three servings (90 grams) of whole grains daily reduces the risk of colorectal cancer by 17 percent.

If you prefer to consume your breakfast on the go, Dr Kamath suggests blending a smoothie with oats, yoghurt and milk.

If neither of the previous options tickle your fancy, his third suggestion is a yoghurt parfait.

When it comes to dairy, a recent study found that an additional 300mg of calcium a day – about the amount in a large glass of milk – could be linked to a 17 per cent decrease in the risk of colon cancer.

Scientists analyzed dietary data from more than 542,000 women to investigate the link between 97 products and nutrients and the chances of someone developing the cancer.

The findings showed that food and drink rich in calcium such as milk and yoghurt were linked to a lower risk of a diagnosis over 16 years.

Calcium was found to have a similar effect from both dairy and non-dairy sources, suggesting it was the main factor responsible for cutting risk.

Along with being packed with calcium thanks to the addition of yogurt and milk, a serving of overnight oats provides up to 20 percent of the recommended daily fiber intake.

Commenting on the importance of carefully selecting your breakfast ingredients, Dr Kamath says: ‘Seems like dairy is beneficial in preventing colorectal cancer, which is an easy thing culturally to add to our diets, especially for breakfast.

‘It seems to mainly driven by calcium intake, so probably adding other foods with calcium would also be beneficial.’

The US has the sixth highest rate of early-onset cancers, with 87 cases per 100,000 people under 50, and colon cancer is among the fastest rising.

Researchers from the University of Missouri-Kansas City recently looked at rates of colorectal cancer in people 10 to 44 years old over the last two decades and found cases had risen in all age groups.

The rate of colorectal cancers grew 500 percent among children ages 10 to 14 and 333 percent among teenagers aged 15 to 19 years.

Rates rose by 71 percent among people 30 to 34 to seven cases per 100,000 people. Among people 35 to 39, rates rose by 58 percent to 12 cases per 100,000 people.

Many young patients have their symptoms dismissed for more benign gastrointestinal conditions, leading to a more aggressive disease.

News Team by — February 19, 2025 By News Team in Trending Now
Macrophages in Newborn, But Not Adult, Mice Help Regenerate Heart Tissue

Newborns with heart complications can rely on their newly developed immune systems to regenerate cardiac tissues, but this isn’t the case in adults. After a heart attack, most adults struggle to regenerate healthy heart tissue, leading to scar tissue buildup and, often, heart failure.

A study in mice by Northwestern Medicine researchers has now identified a critical difference in how immune system macrophages help repair the heart in newborns versus adults after a heart attack. They found that in newborns, macrophages perform a process called efferocytosis, which recognizes and eats dying cells. This process triggers the production of a bioactive lipid called thromboxane, signaling nearby heart muscle cells to divide, and allowing the heart to regenerate damaged heart muscle. In contrast, efferocytosis by adult macrophages ultimately culminates in fibrotic scarring.

The study highlights a fundamental difference in how the immune system drives healing based on age and could point to strategies for improving tissue repair after heart attack in adults.

“Understanding why newborns can regenerate their hearts while adults cannot will open the door to developing treatments that could ‘reprogram’ adult macrophages,” said first and co-corresponding author Connor Lantz, PhD, lead scientist of the bioinformatics core at the Comprehensive Transplant Center at Northwestern University Feinberg School of Medicine.

Lantz, together with co-corresponding author Edward B. Thorp, PhD, professor of experimental pathology at Feinberg, and colleagues, reported on their findings in Immunity, in a paper titled, “Early-age efferocytosis directs macrophage arachidonic acid metabolism for tissue regeneration,” in which they suggest that the pathway identified “… may also be broadly active in other organs after injury.”
The ability to regenerate damaged tissues is “fundamental for survival,” the authors wrote, but this critical function varies across organisms and organ systems. “The diminishment of tissue regeneration often correlates with advancing age,” they continued. The heart is one example of what the team describes as “an age-dependent dichotomy in regenerative potential.” While some vertebrates, including species of salamanders, axolotls, and zebrafish, can naturally regenerate heart tissue throughout adulthood, in mammals, including humans, this cardiac regenerative capacity is lost shortly after birth.

 

“Tissue regeneration is a tightly coordinated process that involves multiple cell types, including cells of the innate immune system,” the researchers further wrote. For their reported study the team examined how the immune system responds to heart injury in mice of different ages, including newborn mice (one day old) and adult mice (eight weeks old).

They found that engulfment of dying cells by newborn macrophages triggered a chemical chain reaction that produced a molecule called thromboxane A2, which unexpectedly stimulated heart muscle cells to multiply and repair the damage. Additionally, the results indicated that nearby muscle heart cells in newborns are primed to respond to thromboxane A2, leading them to change their metabolism to support their growth and healing. This process did not work the same way in adults, however. In contrast, in adults, after an injury, macrophages did not produce enough thromboxane A2, limiting their ability to regenerate heart tissue. “By mimicking the effects of thromboxane, we might one day improve tissue repair after a heart attack in adults,” Lantz said.

“Collectively, our findings … uncover a dichotomy whereby neonatal macrophages recognize injured cells to initiate intercellular signaling and promote tissue regeneration,” the scientists stated. “By contrast, efferocytosis by adult macrophages culminates in persisting fibrotic scarring.”

The researchers found the ability of macrophages to engulf dying cells was enhanced in newborn mice due to increased expression of MerTK, a receptor that recognizes dying cells. When the scientists blocked this key receptor, newborn mice lost their ability to regenerate their hearts, resembling adult hearts after a heart attack. “By genetically inhibiting efferocytosis signaling through genetic ablation of Mertk, the regenerative response in the neonatal heart is altered to resemble that of adult hearts, both in terms of macrophage phenotype and impaired cardiac function,” they further noted.

“Altogether, our findings uncover an age-defined mechanism by which tissue injury reprograms macrophage metabolism to fuel regeneration … Our findings integrate what appears to be a formative immunometabolism signature with recognition of dying cells as well as production of cell mitogens.”

News Team by — February 19, 2025 By News Team in Trending Now
Biomedicine shows the way to future food crops

University of Queensland researchers have for the first time introduced genetic material into plants via their roots, opening a potential pathway for rapid crop improvement.

Professor Bernard Carroll from UQ’s School of Chemistry and Molecular Biosciences said nanoparticle technology could help fine-tune plant genes to increase crop yield and improve food quality.

“Traditional plant breeding and genetic modification take many generations to produce a new crop variety, which is time-consuming and expensive,” Professor Carroll said.

“We have succeeded in having plant roots absorb a benign nanoparticle which was developed by Professor Gordon Xu’s group at UQ for the delivery of vaccines and cancer treatments in animals.

“Plant cell walls are rigid and wood-like, much tougher than human or animal cells so we coated the nanoparticle with a protein that gently loosens the plant cell wall.

“The protein coating helped the nanoparticle break through the cell walls to deliver a synthetic mRNA cargo into plants for the first time.”

mRNAs are natural messenger molecules containing genetic instructions to build and enhance all forms of life.

The research team used the nanoparticles to deliver synthetic mRNA that produces a green fluorescent protein into multiple plant species including Arabidopsis, a miniature member of the canola and cabbage family used extensively in genetic research.

“It was surprising that rather than delivering all of its load in the first cell it entered, the nanoparticle travelled with water through the plant distributing the mRNA as it went,” Professor Carroll said.

“This is exciting because with further improvement, the technology could potentially be used in the future to produce new crop varieties more quickly.

“With further research we could target an issue with a crop such as flavour or quality and have a new variety without the need for a decade of cross breeding or genetic modification.

“Similar to how an mRNA vaccine produces a protein to stimulate the immune system and then degrades away, the mRNA we deliver into plants is expressed transiently and then disappears.”

The nanoparticle technique has been patented by UQ’s commercialisation company UniQuest, which is now seeking partners to further develop the technology.

The research team included Professor Zhi Pin (Gordon) Xu and Dr Jiaxi Yong at UQ’s Australian Institute for Bioengineering and Nanotechnology and Queensland Alliance for Agriculture and Food Innovation.

News Team by — February 19, 2025 By News Team in Biotechnology Daily
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