Unlocking Secrets of Dark DNA: Insights from Human-Plant Hybrid Cells

Posted on December 29, 2025 by Igor Mitreski

Groundbreaking Discovery: Plant and Human DNA Interaction

Image Credit: S Saraus/Shutterstock

How crucial is our genome? While some researchers argue that most of our DNA is active and thus essential, others suggest that even random DNA could show high activity levels. Current studies focus on human cells that incorporate substantial segments of plant DNA, shedding light on this topic. According to New Scientist, the largely random plant DNA exhibits nearly equal activity to human DNA.

This research indicates that much genomic activity may lack purpose, further supporting the theory that a significant portion of the human genome is ‘junk DNA.’

“Most activity can be attributed to background noise,” says Brett Aidy, a researcher at the University of Auckland, New Zealand. “This aligns with the concept of junk DNA.”

The primary role of DNA is to encode instructions for protein synthesis, which are essential molecular machines responsible for cellular functions. This genetic blueprint is transcribed into messenger RNA, which transports the instructions to ribosomes, the cellular machinery for protein production.

Previously, it was assumed that nearly all DNA was involved in coding proteins, but now we understand that just 1.2% of the human genome directly encodes proteins. What, then, is the destiny of the remaining DNA?

Since the 1960s, biologists have claimed that much of it is unproductive. While it’s true that some non-coding DNA plays vital roles, ongoing discoveries of functional elements won’t redefine the overarching notion that non-coding DNA is largely inert.

For instance, a 2011 study revealed that: only about 5% of the genome is evolutionarily conserved. Evolution appears indifferent to the rest. Proponents of the junk DNA theory highlight the variability in genome sizes among species. Why, for example, does an onion require five times more DNA than a human? Additionally, why do lungfish possess genomes that are thirty times larger?

In contrast, other scientists explore whether human DNA has functional roles, even if converted RNA lacks known applications. The ENCODE project’s 2012 findings suggest that over 80% of the human genome is active in some form. This raised questions about its classification as junk DNA. Some researchers have coined the term “dark DNA” for non-coding regions whose purpose remains unclear.

In reaction to ENCODE’s claims, in 2013, Sean Eddy from Harvard University proposed a controversial random genome project, hypothesizing that injecting synthetic random DNA into human cells would yield similar activity as noted in ENCODE’s findings.

“If this holds true, the results will call into question the interpretation of activity as indicative of functionality,” he posits. Austin Ganley, also from Auckland University, echoes this sentiment, emphasizing the need for baseline comparisons in the research of functional versus non-functional DNA.

However, synthesizing DNA is resource-intensive. So far, only limited attempts at random genome projects have focused on small DNA segments.

Yet, when Adey and Ganley discovered that Japanese researchers had successfully created human-plant hybrid cells with DNA segments from Thale cress (Arabidopsis), they recognized it as potentially the most extensive random genome experiment to date.

Eddy, though not directly involved, acknowledges the significance. Plants and animals diverged from a common ancestor over 1.6 billion years ago, allowing time for random mutations to accumulate within non-coding DNA segments of Arabidopsis.

Following initial validations that plant DNA behaves as random DNA in human cells, Adey and Ganley assessed DNA-to-RNA conversion rates per 1000 base pairs of non-coding DNA. If DNA to RNA conversion implies functionality, plant DNA should minimal undergo this transformation. Surprisingly, they observed slightly less activity—about 80% of the starting sites per kilobase when compared to human non-coding DNA from Arabidopsis.

This strongly indicates that the genomic activity detected by ENCODE is merely background noise.

“This illustrates the inherent noise in biological systems,” comments Chris Ponting from the University of Edinburgh, UK. “This sequence’s biochemical activity holds no function within human cells.”

“Sophisticated investigations like this were essential,” asserts Dan Graul from the University of Houston, Texas. “This adds experimental evidence confirming the long-held belief that a majority of the human genome is unnecessary. The term ‘dark DNA’ is simply a fantasy created by those envious of physics.”

Although imperfect biological systems produce noise, this noise can lead to beneficial variations that natural selection may target, notes Ganley.

The research team remains puzzled about a 25% increase in human DNA activity. “We still need to investigate the cause behind this finding,” Ganley states.

While some additional RNA generated might serve functional purposes, this does not diminish the overall perspective of junk DNA. Ongoing research is employing machine learning techniques to identify potentially meaningful activities amidst the noise.

The research team intends to publish their outcomes, though they have yet to complete their findings.

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Source: www.newscientist.com

Study Indicates Gray Hair May Result from the Body’s Shutdown of Cancer-Prone Cells.

Posted on November 17, 2025 by

Gray hair might represent the marks left by our bodies in the battle against cancer, according to a new study.

The recently released Natural Cell Biology explores how the cells that provide pigment in our hair and skin “self-destruct” upon damage, as part of the body’s protective measures against cancer.

Researchers have found that when these pigment-producing cells experience certain types of damage, they cease to function on their own instead of continuing to divide.

This selection process helps to prevent the spread of faulty cells that can cause harmful mutations, but it ultimately leads to a decline in pigment-producing cells over time, resulting in gray hair.

While scientists have been examining methods to prevent the self-destruction of pigment cells to combat gray hair, recent findings indicate that gray hair may indicate a significant anti-cancer defensive mechanism.

Damaged DNA can lead to mutations and cause cancer – Credit: Getty

“[This study] indicates that gray hair and melanoma are not unrelated occurrences but are framed as varied outcomes of stem cell stress responses,” stated Professor Emi Nishimura of the University of Tokyo, who spearheaded the research.

The Tokyo team made this revelation while examining mouse melanocyte stem cells, which are responsible for producing hair pigment. They found that these melanocyte cells only sacrificed themselves when their DNA faced a “double-strand break,” or a precise cut on both sides of the DNA helix.

However, when the cells encountered different stressors, like ultraviolet light or carcinogens, they did not undergo self-destruction. Instead, they survived and continued to divide, allowing mutations to accumulate and potentially paving the way for cancer.

These two distinct responses—cells opting for self-sacrifice in some situations but persisting in others—may help clarify why gray hair and skin cancer become increasingly prevalent as we age.

Researchers suggest that gaining a deeper understanding and ultimately controlling this response could lead to innovative methods for eliminating high-risk cells before they turn cancerous.

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Source: www.sciencefocus.com

Can Cells Form in Venus’s Clouds? – Cyworthy

Posted on October 16, 2025 by

Venus, the second planet from the Sun, is often called Earth’s sister planet. If extraterrestrial observers on a remote exoplanet were to analyze our solar system with the same methods used by observers on Earth today, the two planets would appear strikingly similar. Both are rocky, with nearly identical diameters and masses, and both exist within or near the solar system’s habitable zone. However, only one of them is known to support life.

A significant difference between the two planets—and a likely reason for the first—is their atmospheric compositions. Earth’s atmosphere comprises approximately 78% nitrogen and 21% oxygen, whereas Venus’ atmosphere consists of more than 96% carbon dioxide. In the distant past, volcanic activity released this carbon dioxide, triggering an uncontrollable greenhouse effect. This process, coupled with Venus’ proximity to the Sun, has driven its surface temperature to a searing 500°C (900°F).

Harold Morowitz and Carl Sagan first observed in 1967 that although Venus’ barren surfaces may be inhospitable to life as we know it, its clouds present “an entirely different story,” according to Morowitz. The upper atmosphere of Venus contains low levels of water vapor and cloud regions characterized by extreme temperatures and pressures. These conditions could potentially support some types of terrestrial microorganisms and have led scientists to investigate the clouds of Venus. In the 1970s, these clouds were found to be primarily composed of sulfuric acid, which is considered incompatible with life. Nevertheless, a controversial detection of phosphine—gases found in Venus’ clouds that could be produced by microbes on Earth—has prompted some astrobiologists to reevaluate this notion of habitability. This has opened discussions on potential habitability.

Previously, researchers established that biomolecules such as the nucleic acids forming DNA can remain stable for up to one year in sulfuric acid concentrations ranging from 81% to 98%. To advance this research, scientists at the University of Chicago have recently tested whether more complex organic structures can also form in concentrated sulfuric acid.

They began with a set of carbon-based molecules known as lipids. Lipids serve as the foundation of cell membranes, acting as a barrier to the external environment and regulating what enters and exits the cell. The research team contended that cell membranes are essential for life, especially under extreme conditions like those present in Venus’ clouds. Thus, they evaluated whether simple lipids could create membranous structures called vesicles in concentrated sulfuric acid.

Membrane lipids feature one side that is attracted to water, known as the hydrophilic side, and another that repels water, termed the hydrophobic side (Figure below, left). The hydrophilic side consists of long carbon chains, referred to as tails, while the hydrophobic side comprises charged compounds known as polar heads. In cell membranes, lipids are arranged in bilayers, with hydrophilic tails oriented inwards and hydrophobic heads facing outwards (Figure below, right). The research team selected simple, commercially available lipids with tails of 10 or 18 carbon atoms and polar heads of trimethylamine, sulfate, and phosphonate. These tailed lipids were chosen for their solubility and ability to form membrane structures due to their hydrophobic nature.

Illustration of a single simple lipid (left) and stacked lipids forming a cell membrane structure (right). Created by the author.

To assess the lipids’ resilience against sulfuric acid, various concentrations of each 10-carbon lipid were incubated in 1%, 30%, and 70% sulfuric acid for a minimum of 1 hour at room temperature. Utilizing a method that evaluates molecular structures based on their magnetic properties, they examined how increasing acid concentrations affected the lipids. Results indicated that trimethylamine and phosphonate lipids remained stable in up to 70% sulfuric acid, although around 20% of the sulfate head degraded.

The researchers then explored whether the lipids could form vesicles in these sulfuric acid solutions. They prepared lipid mixtures across varying concentrations in 70% to 90% sulfuric acid, measuring the particle size of the lipid-acid mixture using light scattering techniques. They discovered that a 50/50 blend of 10-carbon or 18-carbon lipids produced particles comparable in size to typical vesicles in 70% and 80% sulfuric acid solutions, with these particles maintaining stability even after a week.

Upon examination under a high-powered microscope, the lipid particles formed foam-like vesicles. Lastly, numerical models illustrated that the charged ends of lipid and acid molecules interact at the molecular level to help stabilize the vesicles and prevent the entry of acid.

The researchers concluded that simple lipids can create stable membrane-like structures in sulfuric acid concentrations similar to those found in Venusian clouds. They recommended that future studies conduct laboratory experiments to validate the molecular model and ascertain whether lipid membranes can effectively block sulfuric acid. These scientists are beginning to formulate a clearer picture of the potential types of life that could exist within the cloud layers of Venus, although that picture remains largely incomplete.

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Source: sciworthy.com

Lab-Fertilized Egg Cells Created from Human Skin DNA

Posted on September 30, 2025 by Igor Mitreski

Laboratories enable modification of human egg cell genetic identity

Science Photo Library / Aramie

Human embryos arise from eggs that utilize the DNA from adult skin cells. This was accomplished with mice. This advancement may offer a pathway for same-sex couples or women facing fertility challenges to have biologically related children.

Researchers have successfully replicated animals through cloning techniques. This involves substituting the nucleus of an egg cell with the nuclei from somatic cells such as skin cells. However, in addition to the legal hurdles surrounding human cloning, many couples desire children that carry genes from both partners, necessitating both sperm and eggs. Shoukhrat Mitalipov of Oregon Health and Science University.

This scenario is complicated by the nature of eggs and sperm being haploid, meaning they contain only one set of chromosomes. The challenge lies in halving the complete set of chromosomes found within cells such as skin cells after selecting an optimal combination of the original genes.

Females develop all of their eggs while still in the womb, where the progenitor cells initially containing 46 chromosomes undergo a complicated process of replication, mixing, and division to reduce to 23 chromosomes.

Mitalipov was intrigued by the possibility of employing natural chemical processes that facilitate chromosomal division in mature human eggs both before and after fertilization to replicate this process in his laboratory.

Having achieved this with mice, Mitalipov and his team are now trialing the method with human subjects. They started by extracting the nuclei from hundreds of eggs donated by healthy women, which were left at a specific development stage linked to chromosomal division. Next, the nuclei of skin cells, known as fibroblasts, from healthy female volunteers were inserted into these eggs. Microscopic images displayed the chromosomes aligned on the spindle and the internal structures necessary for chromosomal separation.

The team then injected sperm from a healthy donor to fertilize some of the eggs, utilizing a method akin to that employed in creating babies using third-party mitochondrial DNA, which can also minimize the risk of specific genetic disorders.

This injection typically causes the eggs to undergo chromosome selection and eliminate duplicate DNA, preparing them for additional reception from the sperm. Nonetheless, in the case of the skin-derived eggs, this process was interrupted, with chromosomes aligning but not separating. Consequently, the researchers attempted again with a new batch of fertilized eggs, applying an electrical pulse that allowed calcium to surge into the egg, emulating natural signals triggered when sperm contact the egg’s outer layer, alongside an incubation period with a drug to activate them from their dormant state pre-fertilization.

Through a series of trials, the researchers successfully halved the chromosome counts in the eggs, discarding any excess. By the conclusion of the experiment, 9% of the fertilized eggs had developed into blastocysts — a dense cluster of cells at about 5-6 days post-fertilization, typically moving into the uterus during IVF treatments. However, the team did not pursue the transfer or sustain the blastocyst beyond six days.

Despite the progress made, the mixtures of genes forming the remaining chromosomes appeared particularly susceptible to defects. “I believe this method is still in its early stages and is not presently suitable for clinical applications,” stated MITINORI SAITOU from Kyoto University in Japan.

Lin from Osaka University noted that while the techniques are “very sophisticated and organized,” they remain “inefficient and potentially hazardous for immediate clinical use.” Nevertheless, Hayashi remarked that the team has achieved a “substantial breakthrough in reducing the human genome.” “This advancement will herald new technologies,” he stated.

Mitalipov acknowledged the validity of the criticisms, emphasizing that his team is actively working to address the existing flaws. “At the end of the day, we’re making progress, but we aren’t there yet,” he remarked.

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Source: www.newscientist.com

How Fast Does the DNA Repair Leader in Your Cells Take Control?

Posted on September 26, 2025 by Igor Mitreski

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One factor in our aging process is the buildup of mutations in our cellular DNA.

Mohammed Elamine Aliwi / Alamy

Clusters of proteins seem to significantly influence the rate of DNA repair within our bodies, which in turn determines how quickly mutations accrue in cells throughout one’s life. This dynamic can significantly influence both aging and lifespan.

“It is a very reliable indicator of lifespan across humans and other animals,” states Trey Ideker from the University of California, San Diego. His research team aims to discover treatments that might enhance lifespan by increasing DNA repair mechanisms.

Some researchers assert that the evidence linking this specific protein complex—a collection of two or more proteins that collaborate for a biological function—to mutation rates is compelling. However, more investigation is necessary to concretely establish the relationship between aging and longevity.

Regarding why we age, one proposed theory is that it results from the gradual accumulation of mutations in cellular DNA. As these mutations pile up, the functionality of cellular machinery declines, leading to a cascade of issues.

Cells act like repair teams that address broken DNA, yet their efforts aren’t always adequate. In fact, the efficacy of DNA repair varies, likely influenced by genetic factors.

Ideker’s team has currently compiled evidence indicating that a protein complex known as Dream acts as a master regulator of DNA repair. This complex operates like a supervisor for the repair team. Each complex, potentially existing in numerous identical copies in every cell, is formed by various proteins, and the acronym DREAM reflects the names of its components.

Initially, DREAM was thought to control cell division, but it is now known to repress hundreds of genes tasked with DNA repair, including BRCA2, a gene that heightens breast cancer risk when mutated.

The research group created a metric for DREAM activity by scrutinizing the over 300 genes they initially manage. “This study aims to demonstrate unmistakably that high DREAM activity correlates with increased aging and reduced longevity, while low DREAM activity is favorable for longevity,” he explains.

Using data from studies involving over 100,000 mouse cells across various tissues, the researchers established that cells exhibiting greater DREAM activity harbor more mutations. Subsequently, they examined data from 92 mammalian species and confirmed a strong correlation between reduced DREAM activity and extended maximum lifespans.

In another facet of their experiment, they scrutinized data from a study involving 90 cells, including 80 individuals with Alzheimer’s disease, discovering a connection between DREAM activity and increased risk.

The team also engineered mice to lack the DREAM complex; this was a challenging task since each constituent protein has a unique role, and the entire complex is crucial for cell division early in development. Mice without it would not survive.

To navigate this challenge, they employed a drug-induced genetic strategy to deactivate the DREAM genes when the mice reached 8 weeks of age. The knockout mice exhibited 20% fewer deletion and insertion mutations in brain cells compared to their normal counterparts as they aged, though Ideker notes that the disruption to their lifespan didn’t reflect a significant extension. “The experimental design may not have been suited to uncover that,” he admits. “We now aim to conduct a more conclusive experiment linking it to extended lifespan.”

Despite this, Ideker believes the amassed evidence paints a clear picture. “Our findings indicate that DREAM plays a crucial role in aging and is indeed a significant factor in the accumulation of lifelong mutations,” he asserts.

“These are groundbreaking and significant findings,” remarks Joe ã O Pedro de Magalhães from the University of Birmingham, UK. “The data from their mouse studies indicate a causal connection between DREAM and mutation levels,” he notes; however, the researchers haven’t yet established a direct causal link with aging. “To prove this, we must demonstrate that mice exhibiting low mutation rates also enjoy increased lifespans.”

This illustrates why the theory that mutation accumulation is a key factor in aging remains unproven. Advocates like Ideker reference conditions such as Progeria, wherein individuals age prematurely due to compromised DNA repair mechanisms. Others, including de Magalhães, cite a lack of evidence that simply accumulating mutations is a driver of typical aging, although it does correlate with heightened cancer risk.

Even should DREAM complexes prove instrumental in aging, their multifaceted functions complicate the development of treatments. “Achieving a total loss of DREAM functionality, as we have done, may be too drastic,” advises team member ZANE KOCH from UCSD. “Mildly suppressing DREAM could be the optimal approach for extending lifespans.”

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Source: www.newscientist.com

Cancer Cells Manipulate Immune Proteins to Evade Treatment – Sciworthy

Posted on September 1, 2025 by Igor Mitreski

Cancer arises from the proliferation of abnormal, uncontrolled cells that create dense masses, known as Solid Tumors. These cancer cells possess unique surface markers called antigens that can be identified by immune cells. A crucial component of our immune system, T cells, carry a protective protein known as FASL, which aids in destroying cancer cells. When T cells encounter cancer antigens, they become activated and initiate an attack on the tumor.

One form of immunotherapy, referred to as chimeric antigen receptor T cell therapy or CAR-T therapy, involves reprogramming a patient’s T cells to recognize cancer cell antigens. However, CAR-T therapy often struggles with solid tumors due to the dense, hostile environment within these tumors, which obstructs immune cells from infiltrating and functioning effectively.

Another significant hurdle that clinicians encounter when treating solid tumors is their heterogeneous composition of various cancer cell types. Some of these cells exhibit antigens recognizable by CAR-T cells, while others do not, complicating the design of CAR-T therapies that can target all tumor cells without harming healthy cells. Solid tumors also produce the protein Plasmin, which further impairs the immune system’s ability to break down FASL and eliminate cancer cells.

Researchers from the University of California, Davis investigated whether shielding FASL from plasmin could preserve its cancer-killing capabilities and enhance the efficacy of CAR-T therapy. They found that the human FASL protein contains a unique amino acid compared to other primates, making it more susceptible to degradation by plasmin. Their observations suggested that when FASL was cleaved, it lost its ability to kill tumor cells. However, after injecting an antibody that prevents plasmin from cleaving FASL, it remained intact and preserved its cancer-killing function.

Since directly studying cell behavior in the human body poses challenges, scientists culture tumor cells and cell lines in Petri dishes under controlled laboratory environments. To gain insights into plasmin’s role, the team examined ovarian cancer cell lines obtained from patients, discovering that CAR-T resistant cancer cells exhibited high plasmin activity.

They noted that combining ovarian cancer cells with elevated plasmin levels with normal cells displaying surface FASL diminished FASL levels in the normal cells. When they added FASL-protecting antibodies, CAR-T cells effectively eliminated not only the targeted cancer cells but also nearby cancer cells lacking the specific target antigen. These findings indicated that plasmin can cleave FASL in T cells and undermine CAR-T therapy, suggesting that safeguarding FASL may enhance CAR-T treatment’s effectiveness.

To assess whether tumor-generated plasmin can deactivate human FASL in more natural settings, researchers examined its function in live tumors within an active immune system. They implanted ovarian, mammary, and colorectal tumor cell lines from mice into genetically matched mice to elicit a natural immune response. When human FASL protein was directly injected into mouse tumors, the cancer cells remained intact. In contrast, injecting a drug that inhibits plasmin resulted in cancer cell death. Additionally, administering FASL-protecting antibodies also led to the elimination of cancer cells.

As a final experiment, the team aimed to determine whether activated T cells from the mice’s immune systems could penetrate the tumors and kill cancer cells. They implanted mice with both plasmin-positive and plasmin-negative tumors, treating both with drugs to enhance immune cell activity and boost FASL production.

They discovered that in tumors with low plasmin levels, mouse immune cells expressed high amounts of FASL on their surfaces, while in tumors with elevated plasmin levels, FASL was significantly reduced. Once again, injecting FASL-protected antibodies into these tumors increased FASL levels. The researchers concluded that plasmin can diminish the immune system’s ability to eliminate cancer cells by depleting FASL from immune cells.

In summary, the team found that tumors exploit plasmin to break down the protective protein FASL, evading immune system attacks. Based on their findings, they proposed that plasmin inhibitors or FASL-protected antibodies could augment the effectiveness of immunotherapy in treating cancer.

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Source: sciworthy.com

COVID-19 and Flu Could Reactivate Dormant Lung Cancer Cells

Posted on July 31, 2025 by Igor Mitreski

Lung tissue samples from mice, depicting cells (blue), cancerous cells (green), and proliferation markers (magenta)

Bryan Johnson

Respiratory viruses are capable of triggering the growth of dormant cancer cells that have metastasized to the lungs from other body areas. Infectious diseases, such as influenza, can instigate an inflammatory response that aids the immune system in combating pathogens, yet they may also adversely influence cancer progression.

Cancer fatalities frequently result from tumor cells migrating from their primary sites. These cells may remain dormant in new locations for extended periods—potentially years or decades—before forming detectable tumors.

While it is uncertain if these cells will eventually proliferate, previous studies have suggested that once cancer cells infiltrate the lungs, inflammation induced by respiratory virus infections might play a significant role. “Nevertheless, no comprehensive research has been conducted to establish a clear cause-and-effect relationship,” notes James DeGregori from the University of Colorado.

To address this research gap, DeGregori and his team employed genetically modified mice to develop tumors in their mammary glands. By two months of age, each mouse had developed a mammary tumor and fewer than ten dormant cancer cells in their lungs.

Subsequently, the researchers infected half of the mice with the H1N1 influenza strain, commonly referred to as swine flu, causing illness for approximately two weeks. During the nine days following the infection, the number of lung cancer cells surged by 100-fold, whereas uninfected mice exhibited minimal changes.

In complementary experiments, the team discovered that the SARS-CoV-2 virus, responsible for COVID-19, led to a tenfold increase in cancer cell numbers in the mice’s lungs, again with no significant alterations in uninfected counterparts.

The researchers hypothesized that this expansion occurred due to viral infections elevating the levels of inflammatory molecules known as IL-6.

To investigate this hypothesis, they conducted further experiments with genetically modified mice deficient in IL-6 and found significantly fewer lung cancer cells compared to typical mice with normal IL-6 levels.

Another experiment suggested that IL-6 seemed to rejuvenate dormant cancer cells that had already migrated to the lungs instead of promoting the dissemination of these cells from the breasts.

However, IL-6 levels wane when the infection subsides. At this juncture, the researchers observed that cancer cells in the mouse lungs had ceased to proliferate but had acquired alterations in gene expression typically associated with tumor metastasis, according to DeGregori.

These findings suggest a potential impact on individuals with undetected levels of cancer cells in the lungs who are believed to be in remission, as stated by Anne Zeuner at the National Institutes of Health in Rome, Italy.

To determine the relevance of these findings to humans, researchers analyzed health records from 36,800 women in the U.S. diagnosed with breast cancer before the COVID-19 pandemic, who were thought to be non-metastatic.

Women who tested positive during the initial three years of the outbreak were significantly more likely to receive a diagnosis of secondary lung cancer in that timeframe. However, some women may have avoided testing due to asymptomatic infections, while others might not have sought tests, thereby complicating the validation of this finding, notes DeGregori.

Further research is necessary to corroborate these findings and explore the interactions between various respiratory viruses and cancer types, according to Zeuner. “Individual factors are likely to significantly influence the relationship between respiratory infections and cancer recurrence,” she adds.

The research focused solely on swine flu and SARS-CoV-2, but DeGregori expresses hope that a spectrum of viruses will exhibit similar behaviors, as many are known to elevate IL-6 levels. He also underscores the importance of vaccination, stating, “As a cancer survivor, I would ensure I am protected against common respiratory viruses like influenza and COVID-19,” remarks DeGregori.

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Source: www.newscientist.com

Study: Common Sweetener Erythritol May Impact Brain Cells and Elevate Stroke Risk

Posted on July 17, 2025 by Igor Mitreski

A recent study from the University of Colorado Boulder indicates that erythritol, a widely used non-nutritive sweetener, may be linked to a higher risk of cardiovascular and cerebrovascular events.

Berry et al. Our study demonstrates that erythritol, at concentrations commonly found in standard size sugar-free beverages, negatively impacts cerebral microvascular endothelial cell oxidative stress, ENOS activation, NO production, ET-1 expression, and T-PA release in vitro. Image credit: Tafilah Yusof.

Erythritol is a popular alternative to non-nutritive sugars due to its minimal effects on blood glucose and insulin levels.

This four-carbon sugar has a low-calorie content of 60-80%, being as sweet as sucrose, and commonly replaces sugar in baked goods, confections, and beverages.

Authorized by the FDA in 2001, erythritol is recommended for individuals with obesity, metabolic syndrome, and diabetes, as it aids in regulating calorie consumption, sugar intake, and minimizing hyperglycemia.

Found naturally in small amounts in certain fruits, vegetables, and fermented foods, erythritol is quickly absorbed in the small intestine through passive diffusion.

In humans, erythritol is produced endogenously from glucose and fructose by erythrocytes, liver, and kidneys via the pentose phosphate pathway, making its levels dependent on both endogenous production and external intake.

“Our findings contribute to the growing evidence that non-nutritive sweeteners, often considered safe, could pose health risks,” stated Professor Christopher Desouza from the University of Colorado.

A recent study involving 4,000 participants from the US and Europe revealed that individuals with elevated erythritol levels are at a significantly increased risk of experiencing a heart attack or stroke within three years.

Professor Desouza and his team sought to determine what factors were contributing to this heightened risk.

They exposed human cells lining blood vessels in the brain to erythritol for three hours, using concentrations similar to those found in standard sugar-free beverages.

The treated cells exhibited several alterations.

Notably, they produced significantly less nitric oxide, a molecule critical for dilating blood vessels, while increasing the expression of endothelin-1, which constricts blood vessels.

Furthermore, the challenge of a thrombogenic compound called thrombin significantly slowed the cell’s production of T-PA, a naturally occurring compound that promotes coagulation.

Cells treated with erythritol also generated more reactive oxygen species, or free radicals, which can lead to cellular damage and inflammation.

“We’ve been diligently working to share our findings with the broader community,” noted Auburn Berry, a graduate student at the University of Colorado in Boulder.

“Our research indicates that erythritol may indeed heighten the risk of stroke.”

“Our study solely focused on sugar substitutes,” emphasized Professor Desouza.

“For individuals consuming multiple servings daily, the potential impact could be even more pronounced.”

The researchers caution that their findings are based on lab research conducted on cells, necessitating larger-scale studies involving human subjects.

Nonetheless, they advise consumers to check product labels for erythritol or “sugar alcohol.”

“Considering the epidemiological evidence informing our research, along with our cellular discoveries, monitoring the intake of such non-nutritive sweeteners seems wise,” Professor Desouza remarked.

The study was published today in the Journal of Applied Physiology.

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Auburn R. Berry et al. 2025. The non-nutritive sweetener erythritol negatively affects brain microvascular endothelial cell function. Journal of Applied Physiology 138(6):1571-1577; doi:10.1152/japplphysiol.00276.2025

Source: www.sci.news

Are Adults Capable of Growing New Brain Cells? The Evidence Suggests Yes.

Posted on July 4, 2025 by Igor Mitreski

Generates brain cells from the hippocampus that proliferate in culture

Arthur Chien/Science Photo Library

The ongoing debate about whether adults can produce new brain cells takes a new turn, as evidence increasingly supports that they indeed can. This revelation addresses one of neuroscience’s most disputed questions and raises hopes that this knowledge could be used in treating conditions like depression and Alzheimer’s disease.

Neurons are produced via a process known as neurogenesis, which occurs in both children and adults, as shown in research on mice and macaques. This involves stem cells generating progenitor cells, which multiply and eventually develop into immature neurons that mature over time.

Earlier studies have indicated the presence of stem cells and immature neurons in the hippocampus of adult humans. This brain area, crucial for learning and memory, is a primary site for neurogenesis in younger humans and some adult animals. However, progenitor cells have not yet been detected in adult human brains. “This link was overlooked. It forms a central argument for the emergence of new neurons in the adult human brain,” states Evgenia Salta from the Netherlands Institute of Neuroscience, who was not involved in the latest research.

To establish this link, Jonas Frisen and his team at the Karolinska Institute in Sweden developed a machine learning model capable of accurately identifying progenitor cells. They used hippocampal samples from six young children, donated by their parents for research post-mortem.

The researchers trained an AI model to recognize progenitor cells based on the activity of about 10,000 genes. “In childhood, these cells’ behavior closely resembles that of precursor cells in mice, facilitating their identification,” explains Frisen. “[The idea is] to use molecular fingerprints of childhood progenitor cells to find equivalents in adults.”

To validate the model, the team identified progenitor cells in hippocampal samples from young mice. The model correctly identified 83% of the progenitor cells and misclassified other cell types as progenitor cells in less than 1% of cases. In a further test, the model accurately predicted that progenitor cells were nearly absent in adult human cortical samples, a brain area devoid of evidence supporting neurogenesis in humans.

“They validated their models effectively by transitioning from data on human children to mice and then to adult humans,” says Sandrine Thuret from King’s College London.

With this validation in hand, the researchers can check for neurogenesis in human adults by identifying 14 hippocampal progenitor cells from individuals aged 20 to 78 at the time of their passing.

Crucially, the researchers first introduced a method to enhance the likelihood of detecting progenitor cells. Previous studies have indicated that these cells are extremely rare in adults. The team utilized antibodies to select brain cells that were actively dividing at the time of death, including non-neuronal cells such as immune cells and progenitor cells. This helped filter out common cell types that do not divide, like mature neurons, making rare progenitor cells easier to identify.

Subsequently, they organized the genetic activity data related to these dividing cells into models. “They were enriched due to the selected cells,” remarks Kaoru Song at the University of Pennsylvania. Previous research lacked this approach, he adds.

The team successfully identified progenitor cells in nine donors. “It is well established that environmental and genetic factors in rodents affect how neurogenesis occurs, so I suspect variations in humans may also be attributed to these factors,” Frisen notes.

The findings strongly indicate the presence of adult neurogenesis, according to Thuret, Song, and Salta. “We are adding this missing piece, which significantly advances the field,” Salta states.

“Neurons originate from cell division occurring in adulthood, and that is what this study definitively establishes,” Thuret comments.

Thuret suggests the possibility of examining variations in neurogenesis among adults with brain-affecting conditions such as depression or Alzheimer’s disease. She speculates that medications promoting this process could alleviate symptoms.

However, John Arellano from Yale University cautions that even if adults produce new brain cells, they may be too few in number to be therapeutically beneficial. Thuret, however, believes this is unlikely to create issues. “In mice, a small number of new neurons can significantly impact learning and memory,” she asserts.

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Source: www.newscientist.com

Discovery of Hemifusomes: Biologists Unveil New Organelle Complexes in Human Cells

Posted on June 25, 2025 by Igor Mitreski

A team of biologists from the University of Virginia and the National Institutes of Health has found that half of certain organelles can make up to 10% of vesicle organelles present in cells, yet they do not follow the typical endocytotic pathway.

Cutting-edge Cryo-Electron microscope images of rat-1 cells cultured on Cryo-EM grids. The lamellipodia and filopodia in the upper right corner illustrate the cell boundary, distinguishing the cytoplasm from the extracellular space (ext). Various vesicle organelles are highlighted, including early endosomal-like vesicles (EN, pink), multinuclear bodies (MVB, blue), hemispores (HF, yellow), and inverted hemifusomes (FHF, green). Scale bar – 0.5 µm. Image credit: Tavakoli et al., doi: 10.1038/s41467-025-59887-9.

“It’s like uncovering a new recycling center within a cell,” remarked Dr. Seham Ebrahim, a researcher at the University of Virginia.

“Many believe it plays a role in how cells manage their packaging and processing of materials. If this process fails, it can lead to diseases affecting multiple systems in the body.”

“One such condition is Hermansky-Pudlak syndrome, a rare genetic disorder that may result in albinism, visual impairments, lung issues, and problems with blood clotting.”

“The challenges related to how cells manage their cargo are central to many of these issues.”

“We’re just beginning to grasp how these new organelles fit into the broader context of cellular health and disease.”

“This discovery is thrilling because finding a genuinely new internal cell is rare, and it opens up avenues for exploring entirely new paths.”

Utilizing Cryo-Electron tomography (Cryo-ET), the researchers managed to capture a significant number of images.

They propose that these organelles facilitate the creation of vesicle-based organelles, which function like mixing bowls, small blister-like sacs, and multiple vesicles.

This process plays a critical role in cellular sorting, recycling, and debris management.

Dr. Ebrahim stated, “You can think of vesicles as small delivery trucks within a cell.”

“Part of it functions like a loading dock where cargo is connected and transferred. It’s a step in the process we were unaware of.”

Many of these organelles have gone unnoticed but are surprisingly prevalent in certain areas of the cell.

Researchers aim to enhance their understanding of their significance in proper cell functioning and how issues with them can lead to diseases.

Such findings may contribute to targeted treatments for a range of serious genetic disorders.

“This is only the beginning,” Dr. Ebrahim noted.

“Now that we’ve confirmed the existence of hemifusomes, we can explore their behavior in healthy cells and investigate what occurs when problems arise.”

“It could pave the way for new strategies to address complex genetic disorders.”

The team’s paper was published in the journal Nature Communications.

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A. Cigarette et al. 2025. Proteolipid nanosap interacting with half of hemifusomes mediates polyspore formation. Nat Commun 16, 4609; doi:10.1038/s41467-025-59887-9

Source: www.sci.news

Cancer Cells Hijack Mitochondria from Neurons to Fuel Their Growth

Posted on June 25, 2025 by Igor Mitreski

Neurons Growing Among Cancer Cell Cultures (Stained Green)

Simon Grelet and Gustavo Ayala

Cancer cells are known to hijack energy-generating components from neurons, facilitating their spread to remote locations. This groundbreaking discovery may enhance treatments for the most aggressive tumors.

“This marks the first instance of mitochondrial transfer from nerves to cancer cells,” states Elizabeth Lepasky, who is not directly linked to the study conducted at the Roswell Park Comprehensive Cancer Center in Buffalo, New York. “This signifies a pivotal advancement in cancer neuroscience, a rapidly evolving field.”

Prior knowledge indicated that both intratumor and adjacent tumors produce proteins and electrical impulses that promote cancer growth and dissemination. “A higher density of nerves within tumors correlates with a poorer prognosis,” says Simone Grelet from the University of Southern Alabama.

Earlier investigations have demonstrated that brain tumor cells can absorb mitochondria (the energy-producing organelles) from non-neuronal brain cells. However, the potential for tumor cells to extract mitochondria from neurons remained unclear, according to Grelet.

To explore this, Grelet and his team genetically modified breast cancer cells derived from mice to contain red fluorescent molecules and combined them with mouse neurons that had mitochondria labeled with green pigments in laboratory conditions. Imaging revealed that cancer cells can seize mitochondria from neurons within a matter of hours.

“Cancer cells extend their membranes to absorb mitochondria from neurons,” explains Grelet. “It’s akin to a lineup of mitochondria filtering through a narrow passage, entering the cancer cells sequentially.”

To assess whether this phenomenon occurs in vivo, the researchers injected red breast cancer cells into the mammary glands of female mice to induce tumor growth. They also genetically engineered the surrounding nerves to carry green mitochondria. Approximately one month later, 2% of the cancer cells in these tumors had taken up mitochondria from neurons.

Conversely, 14% of tumor cells that metastasized to the brain exhibited neuronal-derived mitochondria. This suggests that cancer cells acquiring mitochondria from nerves have a significant advantage over other cancer types. Further tests indicate that these mitochondria contribute to greater resilience against the physical and chemical challenges encountered in the bloodstream.

“Cancer cells face numerous hurdles in their migration,” remarks Repasky. “They must escape the primary tumor, navigate barriers to blood vessels, exit the bloodstream, and secure sufficient oxygen and nutrients at secondary sites. By appropriating mitochondria, it appears cancer cells can endure this tumultuous journey,” she adds.

To determine if this process also occurs in humans, researchers examined tumor samples from eight women with metastatic breast cancer. They discovered that tumor cells from distant sites contained, on average, 17% more mitochondria compared to those from breast tumors, suggesting that similar mechanisms are at play in patients, according to Grelet.

Moreover, the team analyzed human prostate tumor samples and observed that cancer cells near nerves contained significantly more mitochondria than those situated further away. “I believe this represents a common mechanism utilized by various tumor types,” asserts team member Gustavo Ayala from the University of Texas Health Science Center in Houston.

The findings indicate that inhibiting mitochondrial transfer could potentially curtail the spread of the deadliest tumors. “We are optimistic that this is achievable, at least for certain tumor types,” Repasky suggests. Ayala mentions that they are working towards developing a drug to facilitate this approach.

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Source: www.newscientist.com

Cells Can Be Divided in Unforeseen Ways

Posted on May 1, 2025 by Igor Mitreski

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                <img class="Image" alt="" width="1350" height="900" src="https://images.newscientist.com/wp-content/uploads/2025/05/01181823/SEI_249575190.jpg" sizes="(min-width: 1288px) 837px, (min-width: 1024px) calc(57.5vw + 55px), (min-width: 415px) calc(100vw - 40px), calc(70vw + 74px)" srcset="https://images.newscientist.com/wp-content/uploads/2025/05/01181823/SEI_249575190.jpg?width=300 300w, https://images.newscientist.com/wp-content/uploads/2025/05/01181823/SEI_249575190.jpg?width=400 400w, https://images.newscientist.com/wp-content/uploads/2025/05/01181823/SEI_249575190.jpg?width=500 500w, https://images.newscientist.com/wp-content/uploads/2025/05/01181823/SEI_249575190.jpg?width=600 600w, https://images.newscientist.com/wp-content/uploads/2025/05/01181823/SEI_249575190.jpg?width=700 700w, https://images.newscientist.com/wp-content/uploads/2025/05/01181823/SEI_249575190.jpg?width=800 800w, https://images.newscientist.com/wp-content/uploads/2025/05/01181823/SEI_249575190.jpg?width=837 837w, https://images.newscientist.com/wp-content/uploads/2025/05/01181823/SEI_249575190.jpg?width=900 900w, https://images.newscientist.com/wp-content/uploads/2025/05/01181823/SEI_249575190.jpg?width=1003 1003w, https://images.newscientist.com/wp-content/uploads/2025/05/01181823/SEI_249575190.jpg?width=1100 1100w, https://images.newscientist.com/wp-content/uploads/2025/05/01181823/SEI_249575190.jpg?width=1200 1200w, https://images.newscientist.com/wp-content/uploads/2025/05/01181823/SEI_249575190.jpg?width=1300 1300w, https://images.newscientist.com/wp-content/uploads/2025/05/01181823/SEI_249575190.jpg?width=1400 1400w, https://images.newscientist.com/wp-content/uploads/2025/05/01181823/SEI_249575190.jpg?width=1500 1500w, https://images.newscientist.com/wp-content/uploads/2025/05/01181823/SEI_249575190.jpg?width=1600 1600w, https://images.newscientist.com/wp-content/uploads/2025/05/01181823/SEI_249575190.jpg?width=1674 1674w, https://images.newscientist.com/wp-content/uploads/2025/05/01181823/SEI_249575190.jpg?width=1700 1700w, https://images.newscientist.com/wp-content/uploads/2025/05/01181823/SEI_249575190.jpg?width=1800 1800w, https://images.newscientist.com/wp-content/uploads/2025/05/01181823/SEI_249575190.jpg?width=1900 1900w, https://images.newscientist.com/wp-content/uploads/2025/05/01181823/SEI_249575190.jpg?width=2006 2006w" loading="eager" fetchpriority="high" data-image-context="Article" data-image-id="2478846" data-caption="The division of human cells may not exactly align with what’s written in textbooks" data-credit="Iokanan VFX Studios/Shutterstock"/>
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                    <p class="ArticleImageCaption__Title">Inaccuracies in Textbook Descriptions of Human Cell Division</p>
                    <p class="ArticleImageCaption__Credit">Iokanan VFX Studios/Shutterstock</p>
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    <p>Researchers have identified a unique type of cell division that enables cells to store information in a way that determines the identity of their offspring. This discovery is key to advancing tissue engineering techniques and deepening our comprehension of cancer progression.</p>
    <p>Traditionally, it was believed that the majority of cells would curl into a spherical shape prior to division, allowing for an even distribution of contents between the "daughter" cells and ensuring they remain of the same type.</p>
    <p>However, stem cells represent an exception, as they can undergo heterogeneous or asymmetric cell division, yielding two distinct types of cells.</p>
    <p>In a surprising find, <a href="https://research.manchester.ac.uk/en/persons/shane.herbert">Schoen Herbert</a> from The University of Manchester, along with his team, observed that non-stem cells in developing zebrafish blood vessels also divide asymmetrically. These endothelial cells migrated to form new vessel branches and divided without adopting a spherical shape, resulting in different cell types.</p>
    <p>By altering the shape of human endothelial cells in laboratory conditions, the team established that a cell's geometry can predict the symmetry of its division. Longer, more slender cells were more likely to divide asymmetrically, indicating that the division process can be influenced by the cell's shape.</p>
    <span class="js-content-prompt-opportunity"/>
    <p>Herbert illustrated that cells do not lose their structural and behavioral information during this process, suggesting they maintain their form, thereby preserving their "memory." "Often, they retain their shape, enabling them to convey this memory," he stated.</p>
    <p>This phenomenon allows for a simultaneous movement, division, and production of various cell types without disrupting the ongoing cellular processes. Such flexibility supports rapid adjustments to developmental needs, like supplying tissues necessary for expanding blood vessels and nerves.</p>
    <p>The implications of this discovery extend to lab-grown tissues, where generating functional blood vessels is a significant hurdle. "Our challenge is to create a specific environment that allows these cells to achieve the shapes and behaviors necessary for forming functional blood vessels," explains team member <a href="https://research.manchester.ac.uk/en/persons/holly.lovegrove">Holly Lovegrove</a> from the University of Manchester. Adjusting cell shapes could pave the way for producing specific cell types, she suggests. Conversely, cancer can spread through the formation of clusters of migrating cells, with these new insights potentially shedding light on that process.</p>
    <p>This research exemplifies how organisms can fine-tune mechanisms like cell rounding to accomplish multiple tasks critical for tissue development. <a href="https://www2.mrc-lmb.cam.ac.uk/group-leaders/a-to-g/buzz-baum/">Buzz Baum</a> from the MRC Institute of Molecular Biology in Cambridge, UK, remarked, "This is a clever method to retain essential information while facilitating network growth by generating more cells."</p>
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Source: www.newscientist.com

Regular blood donations can lead to healthier blood cells

Posted on March 11, 2025 by Igor Mitreski

Blood donation may not be purely altruistic

Serhiihudak/ukrinform/future Publishing by Getty Images

Frequent blood donors may be gaining more than a warm, ambiguous feeling from altruism, as giving blood can increase their ability to produce healthy blood cells and potentially reduce the risk of developing blood cancer.

Hector Huerga Encabo The Francis Crick Institute in London and his colleagues analyzed genetic data extracted from blood cells donated from 217 German men aged 60 to 72 years old. They also looked at samples from 212 men of similar age who donated their blood less than 10 times and found that frequent donors were likely to have blood cells with specific mutations in the genes called. dnmt3a.

To understand this difference, the team added genetically engineered human blood stem cells that produce all blood cells in the body along with these mutations, along with unmodified cells, to the lab dish. To mimic the effects of blood donation, they also added a hormone called EPO. This was the body produced it later and added it to part of the dish.

After 1 month, cells with frequent donor mutations grew 50% faster than cells without mutations, but only in dishes containing EPO. Without this hormone, both cell types would have grown at similar rates.

“It suggests that all blood donation, you have a burst of EPO in your system, and this will support the growth of these cells dnmt3a Mutations,” Encabo says.

To investigate whether it would be beneficial to enable more effectiveness of these mutated blood cells, the team mixed with cells with mutations that cause the risk of leukemia, and again discovered that in the presence of EPO, frequent don cells can effectively lay other blood cells. this is, dnmt3a Mutations are beneficial and may inhibit cancer cell growth, Encabo said.

“It appears that blood donations provide selection pressure to improve stem cell fitness and capacity to fill up.” Ash Toy At the University of Bristol, UK. “It may not only save someone’s life, it may also increase fitness in the blood system.”

I say it needs more work to see if this is really true Markman Soor University College London provides a very simplified picture of what happens in the body of a lab experiment. “This should be examined across much larger cohorts, different ethnicities, women and other age groups,” Mansour says. He also points out that there is no donor. dnmt3a Mutations may not see this benefit.

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Source: www.newscientist.com

CAR T cells achieve an unprecedented 18-year remission in neurocarcinoma

Posted on February 17, 2025 by Igor Mitreski

Microscopic images of neuroblastoma tumors

Simon Belcher/Aramie

Cancer therapy using genetically modified immune cells called CAR T cells has maintained people without potentially fatal neurotumors for a record 18 years.

“This is, to my knowledge, the longest lasting complete remission among patients who have received T-cell therapy in their car,” he says. Karin Stratoff At University College London, where he was not involved in treatment. “This patient will be cured,” she says.

Doctors use CAR T-cell therapy to treat certain blood cancers, such as leukemia. To do this, they collect samples of T cells that form part of the immune system from the patient's blood and genetically manipulate them to target and kill cancer cells. The modified cells are then returned to the body. In 2022, a follow-up study found that this approach was in remission for two people with leukemia for about 11 years.

However, CAR T-cell therapy usually fails against solid tumors such as neuroblastoma. Neuroblastoma occurs when developing neurons in children and usually becomes cancerous before the age of five. Such tumors often resist being attacked by the immune system, reducing the effectiveness of the modified T-cell.

This is the reason Cliona Rooney At Baylor School of Medicine in Houston, Texas, and her colleagues were surprised that people with neuroblastoma in childhood treated with CAR T cell therapy as part of their 2005 trial remained in control of cancer. . 18 years later. “These results were amazing. It's very rare to get a complete response from neuroblastoma with this approach,” says Rooney.

The person was treated at age 4 after several chemotherapy and radiation therapy failed to completely eradicate the cancer. At the time, the team also treated 10 other people who were in the same condition that the cancer had recurred after standard treatment, and they all had virtually no side effects, says Rooney. One of these participants showed no signs of cancer before dropping out of the study nearly nine years later, making follow-up impossible. The remaining nine participants eventually died from cancer. This was mainly killed within a few years of receiving treatment.

It is unclear why some people responded much better than others. “That's a million dollar question. I really don't know why,” Rooney says.

One reason is that each individual's T-cell behaves slightly differently depending on a variety of lifestyle factors, such as their genetics, prior exposure to infections, and diet, Rooney says. In fact, the team found that CAR T cells last longer in the blood among longer surviving participants.

Another explanation is that some participants' tumors were more immunosuppressive and strongly resisted T cells in the car, Rooney says.

The Rooney team is now looking for new ways to design cells so that it can benefit more people. “We have to improve them and make them stronger without increasing toxicity,” she says.

Such efforts are likely to lead to even greater success, Straathof says. “Now we have a glimpse of what is possible.”

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Source: www.newscientist.com

Shared DNA Mutations Impacting the Genome in Cancer Cells

Posted on December 2, 2024 by Igor Mitreski

The human genome consists of approximately 3 billion DNA base pairs. If these base pairs were letters grouped together on a single line, they would fill more than 6,000 novels, too large to fit in a cell. Instead, some proteins organize and reform DNA into a more functional 3D structure called DNA. chromatin. These proteins regulate how different parts of the genome interact, controlling which genes are activated and which remain silent within each cell. One such protein is CCCTC binding factor or CTCF.

For CTCF to work, it must first bind to a specific spot on the DNA called CTCF. binding site. Scientists report that these CTCF binding sites behave differently in each scenario. Some lose their binding ability due to chemical interactions within the DNA, while others remain stable. Scientists call something stable Persistent CTCF binding site.

Scientists have previously reported that mutations in CTCF binding sites are common in cancer cells and disrupt the normal 3D structure of the genome. However, it was unclear whether these mutations were concentrated at persistence sites or what role they played. Australian researchers sought to understand mutations in persistent CTCF binding sites and how they affect different cancers.

To address these questions, the research team developed a computational tool based on machine learning models. CTCF-INSITE. Their tool uses genetic data and the interactions of organic compounds such as methyl in the genome to predict which CTCF binding sites are likely to persist even as CTCF protein levels decline. Researchers will use this tool to determine which persistent CTCF binding sites across the genome may be particularly vulnerable to mutations and whether these mutations are associated with cancer growth. I mapped it.

Using data from several human cell culture samples, including prostate cancer cells, breast cancer cells, and lung cancer cells, researchers developed a tool that allows them to distinguish between stable and unstable CTCF binding sites. trained. They exploited characteristics such as protein binding strength, the relative location of binding sites within the genome, and how distant regions of DNA interact to produce proteins.

The researchers then looked at mutation data from 12 types of cancer. International Cancer Genome Consortium. To avoid imbalance, we filtered out data entries with too few or too many mutations. Next, we applied CTCF-INSITE. A tool to test whether persistent CTCF binding sites are more likely to mutate in cancer cells than other CTCF binding sites.

They found significantly more mutations in persistent CTCF binding sites in all cancer types examined. This means that there were more mutations at these sites than would be expected by random chance. The researchers noted that the mutations were specific to the CTCF binding site, rather than in parts of the DNA close to it. They also reported that these mutations were more prominent in breast and prostate cancer cells than in other types of cancer.

The researchers also sought to understand whether these mutations alter the 3D structure of the genome. Using experimental techniques such as fluorescence imaging, they examined some of these cancer-specific mutations and found that many of them alter the genome structure and reduce the strength and effectiveness of CTCF binding. It turned out that. They explained that this reduction could affect gene expression in a way that promotes cancer growth.

The researchers emphasized that their findings were not limited to one or two types of cancer, as similar results were found for stomach, lung, prostate, breast and skin cancers. Although the exact mutation patterns vary between cancers, persistent CTCF binding sites were reported to have consistently higher mutations overall.

The researchers concluded that their findings may help other cancer researchers understand similarities in the onset and progression of multiple cancer types. They also proposed that their machine learning tools could provide future researchers with CTCF binding site candidates relevant to experiments investigating undocumented causes of cancer.

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Source: sciworthy.com

Breakthrough in cancer treatment: Lab-grown stem cells offer new hope

Posted on September 2, 2024 by Igor Mitreski

Stem cells are produced in the bone marrow and develop into different types of blood cells.

Katerina Conn / SPL/ Alamy

Human blood stem cells have been grown in a laboratory for the first time, which could dramatically improve how certain types of cancer are treated.

The lab-grown cells have so far only been tested in mice, but when injected into the animals, they resulted in functional bone marrow similar to levels seen after umbilical cord blood cell transplants.

Treating cancers such as leukemia and lymphoma with radiation and chemotherapy can destroy blood-forming cells in the bone marrow. A stem cell transplant means new healthy bone marrow and blood cells can grow. The umbilical cord is a particularly rich source of stem cells, but there is a limited amount they can provide, and the transplant may be rejected by the body.

The new method allows researchers to create stem cells from actual patients, eliminating supply issues and reducing the risk that the patient's body will reject the stem cells.

First, they transformed human blood and skin cells into so-called pluripotent stem cells through a process called reprogramming. “This involves temporarily switching on four genes, so that the patient's cells revert to an earlier stage of development that can become any cell in the body,” he said. Andrew Elefanti At the Murdoch Children's Research Institute in Melbourne.

The second step is to turn the pluripotent cells into blood stem cells. “You start by making thousands of tiny, free-floating balls of cells, each containing a few hundred cells, and then you induce them to turn from stem cells to blood vessels to blood cells,” Elefanti says. This process, called differentiation, takes about two weeks and produces millions of blood cells, he says.

When these cells were then injected into mice that lack immune systems, they produced functional bone marrow in up to 50 percent of cases. That means they made the same cells that carry oxygen and fight infection as healthy human bone marrow, Elefanti says. “This unique ability to make all blood cell types over an extended period of time defines them as blood stem cells,” he says.

Abbas Shafi A researcher from the University of Queensland in Brisbane said the work was an “exciting step forward” towards new treatments for blood cancers. “It's never been done before and has great potential for the future.” But even once animal testing is complete, he said a lot of human research still needs to be done before the technique can be used in the clinic.

Simon Cohn Researchers at Flinders University in Adelaide, Australia, say a key advantage of their approach is that it can be scaled up to produce “an essentially limitless supply” of blood stem cells, but they add that the work is based on blood or skin cells, and success rates and blood cell diversity depend on the starting cell type.

“This suggests that treatments are inconsistent even at the preclinical stage in mice, and will need to be addressed before clinical trials in human patients,” he says.

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Source: www.newscientist.com

The discovery of new adrenal cells enhances parenting abilities in mice

Posted on September 2, 2024 by Igor Mitreski

During evolution, new types of cells emerge and perform new functions, resulting in changes in animals. Scientists study the origin and development of these new cell types to understand how they affect the animal’s bodily functions, structure, or behavior.

Scientists previously Mammalian ancestors Mammals live solitary lives, and parental care of young has developed over time in some mammalian groups. A research team led by scientists from Columbia University in New York recently used two closely related mouse species to elucidate how parental care evolved in mammals. The first species, the Asian goshawk, is monogamous and displays strong parenting behaviors, including grooming, herding, and retrieving young that have strayed from their nests. The second species, the deer mouse, is promiscuous and does not display parenting behaviors. The researchers aimed to investigate the genetic drivers of parental care in Asian goshawks.

They performed their experiments on two small clusters of cells located in the top part of each kidney. Adrenal glands These glands produce fat hormones, Steroid hormones Once produced, it immediately affects bodily function. The researchers found that the adrenal glands of monogamous Oldfield mice were six times heavier than those of promiscuous deer mice, an unexpectedly large size difference for such closely related species. When the researchers examined the tissue composition of both glands, they realized that the larger adrenal glands of Oldfield mice were due to larger and more numerous adrenal cells.

To look for molecular differences between the adrenal glands of the two mouse strains, the team studied the RNA molecules in their glands. RNA molecules copy genetic instructions from DNA and carry out the functions of genes. By counting and comparing the types and amounts of RNA molecules in the adrenal glands, the scientists hoped to understand how the adrenal glands functioned differently. They took adrenal tissue from adult mice, broke it down to release the RNA, and counted that RNA. They looked for differences in the amount of RNA, called ribosomal RNA. Akrc18 This level was 3,200 times higher in Oldfield mice than in deer mice, a difference that led the researchers to wonder whether this RNA might be related to the parental behavior seen in Oldfield mice.

The researchers, Akrc18 It produces steroid hormones. Steroid hormones affect parental behavior, so the team tested whether the hormone had an effect on mice. They gave Oldfield mice a single dose of the hormone and measured their parental behavior 20 hours later. They observed that these mice groomed and cuddled their pups longer, brought them back to their nests more frequently, and built stronger nests. In deer mice, which don’t normally show parental behavior, 17% of the injected mice groomed and brought back their pups. From these results, the scientists concluded that the hormone shapes the parental behavior of Oldfield mice.

The researchers also explained that mate bonding is an important aspect of monogamy. To understand partner choice, the researchers measured how long mice huddled with their partners compared to opposite-sex mice of the same species. They found that monogamous Oldfield mice huddled three times longer with their partners than with new individuals, whereas promiscuous deer mice huddled neither with their partners nor with strangers. Injecting the Akrc18 steroid hormone did not change these preferences, suggesting that the hormone only affected parenting behavior and not pair bonding.

The research team found that Oldfield mice had larger adrenal glands and that Akrc18 RNA production was related. To test whether the adrenal glands of the two mouse species had different cell types, the researchers used the RNA from the adrenal glands of both mice that they had previously counted. They used computational methods to search for specific RNAs in the cells and identify what cell types were present. They found that nearly all cell types were shared between the two species, except for one type that was present in Oldfield mice but not in deer mice.

Also, Akrc18 RNA was the most abundant element in these new cells. The researchers examined the structure and composition of the tissue and observed these cells lining the adrenal glands of wolf mice, which are absent in deer mice. The researchers suggested that these cell types may have evolved from existing adrenal cells by increasing production of steroid hormones and related genes. The researchers concluded that the parenting behavior of wolf mice is linked to this new type of cell in the adrenal glands.

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Source: sciworthy.com

Specific brain cells elucidate the maternal soothing influence

Posted on July 26, 2024 by Igor Mitreski

The researchers studied mouse neurons in a part of the brain that is common to all mammals.

Klein & Hubert/naturepl.com

Scientists have identified neurons that become active when mouse pups interact with their mothers, seemingly reducing stress — and the same neurons may also be involved in the mother-child bond in humans.

The zona incerta, located in the center of the mammalian brain, is thought to be involved in integrating sensory information. As we develop, our roles change. In infants, neurons in the zona incerta send information to other brain regions, such as the cortex, promoting neural growth elsewhere.

Its role appears to be changing, Lee Yue Heon Researchers at the Yale School of Medicine and their colleagues suspected that this part of the brain may be involved in establishing a bond between mother and child.

To investigate, the researchers first assessed which neurons in the zona incerta become active when puppies, who are still dependent on milk, interact with their mothers. This involved surgically implanting fiber-optic probes in the brains of some of the puppies, allowing the researchers to detect light emitted when neurons became active.

The researchers found that activated neurons express a hormone called somatostatin, which regulates several bodily functions by inhibiting the release of other hormones, including the stress hormone corticosterone.

Free social interactions between mothers and infants activated these neurons, but contact with toys did not.

The researchers were also interested in how other social interactions might affect this brain region: They found that contact with lactating females who were not the pups' mothers, non-lactating females, siblings, or unrelated males also activated neurons, but not as much as contact with the pups' mothers.

“Our findings suggest that social interaction with the mother elicits the greatest response compared to other social stimuli, with a difference of about 1.5-fold in mean response levels,” the team said. Marcelo de Oliveira Dietrich, Even at Yale University.

In another part of the experiment, the team monitored the infants' brain activity while they were socially isolated: during these periods, which lasted between 10 minutes and 12 hours, no neurons were active, but this changed once the infants were reunited with their mothers.

Reunion also reduced the puppies' stress response, as measured by whether they made crying noises and released corticosterone.

Finally, the team wanted to see whether artificially activating neurons while the puppies were isolated could reduce stress in them: Activating the neurons using chemicals suppressed the puppies' crying and blunted their release of corticosterone.

The researchers believe that the zona incerta may be involved in early social relationships in mammals, as well as the development of other parts of the brain. “The distinct bond between infant and mother” is “a hallmark of mammals,” they write. The bond may be involved in the development of parts of the brain, with the zona incerta acting as “a nodal point that intertwines the elements that define mammalian biology.”

Robert Froemke A researcher from NYU Langone Health in New York says the study demonstrates that certain neurons “essentially serve to soothe infants,” but “it's still a bit unclear how infants sense their mothers — which aspects of smell, touch, or temperature are important,” he says.

“Another open question is how much contact is needed to send a safety signal, and how long that contact lasts? What promotes healthy development, as opposed to neglect?” In humans, “visual and auditory input — the sight and sound of the caregiver — is also likely to be important, or perhaps more important, than olfactory cues,” he says.

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Source: www.newscientist.com

Robotic grin crafted from living human skin cells

Posted on June 25, 2024 by Igor Mitreski

This robot's face can laugh

Takeuchi et al. (CC-BY-ND)

Researchers say smiles made from living human skin could one day be attached to humanoid robots, allowing the machines to emote and communicate in a more lifelike way – and the wrinkles could even be useful for the cosmetics industry.

The living tissue is a mixture of human skin cells grown on a collagen scaffold, then placed on a 3D-printed resin base. Unlike previous similar experiments, this skin also contains the equivalent of ligaments, which are embedded in the layers of tissue beneath the skin of humans and other animals and hold the skin in place, giving it incredible strength and flexibility.

Michio Kawai The Harvard researchers call their ligament equivalents “perforated anchors” because they were made by drilling holes in the robot's plastic base and filling the tiny V-shaped cavities with tissue, which helps the robot's skin stay in place.

The team attached the skin to a smiling robotic face a few centimeters wide, which could be moved by rods attached to a base, and to a similarly sized 3D shape in the shape of a human head (see below), which could not be moved.

“As the roles required of robots expand due to developments in AI technology and other factors, the functions required of robot skin are also starting to change,” Kawai said, adding that having human-like skin could make communication between robots and humans smoother.

3D head shape covered with living skin

Takeuchi et al. (CC-BY-ND)

The research could also have unexpected benefits for the cosmetics industry: In tests, the researchers made the tiny robot's face laugh for a month and found that they could replicate the formation of expression wrinkles on the skin, Kawai says.

“If we can reproduce wrinkle formation on a palm-sized research chip, it could also be used to test new cosmetics and skincare products aimed at preventing, delaying or improving wrinkle formation,” said Kawai, who conducted the research while at the University of Tokyo.

Of course, this skin still lacks some of the functionality and durability of real skin, Kawai says.

“They have no sensing capabilities and no blood vessels to provide them with nutrients and water, so they cannot survive long in air,” he says. “To address these issues, our current challenge is to incorporate neural mechanisms and perfusion pathways into the skin tissue.”

topic:

Source: www.newscientist.com

These plant cells could be used to make your next cup of coffee.

Posted on March 15, 2024 by Igor Mitreski

Coffee is available in a variety of options to suit everyone’s preferences, whether it’s strong and black, iced, or a shot that transcends time and space. But what if there was a completely new type of coffee? Not a different roast, but coffee made from plant cells in a revolutionary way.

While it may sound unconventional, cell-based coffee is a real and burgeoning alternative. The immense popularity of coffee is putting a strain on its sustainability, particularly due to its significant carbon footprint. Producing and exporting 1kg of Arabica coffee to the UK emits greenhouse gases equivalent to an average of 15.33 kg of carbon dioxide.

A cup of coffee requires about 140 liters of water throughout its cultivation, processing, and transportation. Reports suggest that coffee production may be reduced by half by 2050 due to the impacts of climate change.

Despite these challenges, the demand for coffee continues to rise each year, leading to the exploration of cell-based coffee as a solution.

What is cell-based coffee?

Cell-based coffee is produced using cell samples from coffee plants. These cells are cultivated in a controlled environment called a bioreactor, where they receive nutrients and grow. Once they reach the desired amount, they are harvested, dried, and roasted to create a product similar to traditional coffee beans.

How does it compare to real coffee?

While still in the early stages, cell-based coffee shows promise as a potential future of coffee. Researchers are working on refining the process to create a product that mimics the taste, aroma, and flavor profile of traditional coffee. Challenges such as caffeine levels and flavor elements are being addressed to enhance the product.

Credit: Vesa Kippola

Cell-based coffee has shown potential in terms of taste and sensory experience. While it may not be an exact match for traditional coffee yet, improvements are ongoing to create a product that meets consumer expectations.

Why cell-based coffee is better for the environment

Despite the challenges, the environmental benefits of cell-based coffee are significant. It offers a more sustainable alternative to traditional coffee production, with lower water consumption and reduced reliance on large-scale farming. Once perfected, cell-based coffee could offer a flavorful, environmentally friendly option for coffee drinkers.

As technology advances, the availability of cell-based coffee is expected to grow. While initial costs and quantities may be limited, the potential for a more sustainable coffee industry is within reach.

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Source: www.sciencefocus.com

Newly Found Anti-Aging Cells Offer Potential for Prolonged Youthfulness

Posted on January 24, 2024 by Igor Mitreski

The ‘fountain of youth’ isn’t locked away in a philosopher’s stone or a mythical body of water, according to new research. In fact, US scientists say the key to slowing aging is hidden within our bodies.

It was announced in new research that: The secret to anti-aging lies in white blood cells known as T cells. The researchers behind the study discovered that these cells can be reprogrammed into senescent cell-killing machines known as CAR (chimeric antigen receptor) T cells.

When they tested this treatment on mice, they lost weight, improved their metabolism and glucose tolerance, increased physical activity, and led healthier lives. Moreover, there is no tissue damage or toxicity.

“If you give this to old mice, it rejuvenates them. If you give this to young mice, it slows down the aging process. There are currently no other treatments that can do this.” Corina Amor Vegas is an assistant professor at Cold Spring Harbor Laboratory (CSHL) in the United States and one of the authors of the paper.

Researchers call this treatment a “living drug.” That’s because when CAR T cells are genetically modified, they become more aggressive in attacking a group of cells known as senescent cells.

Senescent cells are responsible for many of the conditions and diseases that develop as we age, such as obesity and diabetes. As the years go by, we accumulate more and more of them, and this causes a buildup of harmful inflammation. However, CAR T cells may be able to eliminate them and slow the effects of aging.

This treatment is already approved in the United States to treat blood cancers. But this is the first time scientists have shown that CAR T cells can slow or even reduce the effects of aging.

There are already drugs that can eliminate senescent cells, but these must be taken repeatedly. The effects of CAR T cells, on the other hand, are long-lasting. If he takes one dose when he is young, he will be protected for life.

“With CAR T cells, you could potentially get away with just one treatment. For chronic diseases, this is a big advantage. Think about the patients who need treatment,” said Amor Vegas. If administered intravenously, it will be fine for several years. ”

Scientists will then investigate whether the cells not only make you healthier for the rest of your life, but also help you live longer.

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Source: www.sciencefocus.com

Immune cells exhibit greater independence than previously believed

Posted on December 24, 2023 by Igor Mitreski

New research reveals that immune cells can independently navigate complex environments by actively shaping chemical cues, a discovery with significant implications for understanding immune responses and cancer metastasis. have.

Immune cells exhibit a higher level of self-directed mobility than previously appreciated. InFLAMES researcher Jonah Alanko has shown that these cells are more than just passive reactors to surrounding chemical signals. Instead, they actively modify these signals and skillfully navigate complex environments through self-organization.

Directional cell movement is an essential and fundamental phenomenon of life. This is an important prerequisite for personal development, vascular remodeling, immune response, etc.

The research conducted by postdoctoral researcher Jonah Alanko focused on the migration and navigation of immune cells within the body. Chemokines, a type of signaling protein, play an important role in directing immune cells to specific locations. Chemokines, for example, form in lymph nodes and create chemical cues called chemokine gradients that cells in the body follow. According to Alanko, these chemokine gradients are like scent trails left in the air, getting brighter as you move away from their source.

The traditional idea was that immune cells recognize targets according to pre-existing chemokine gradients. In other words, cells that follow these cues have been viewed as passive actors, when in fact they are not.

Dendritic cells move through a microscopic maze with the help of chemokine gradients they create. In the upper image, the nucleus of the cell is drawn in blue, and the lines in the lower image represent the movement of the cell.Credit: Jonna Alanko, University of Turku

“Contrary to previous notions, we were able to demonstrate for the first time that immune cells do not need pre-existing chemokine gradients to find their way. They can create their own gradients, making complex We can move collectively and efficiently even in difficult environments,” Alanko explains.

cells consume chemokines

Immune cells have receptors that can sense chemokine signals. One of these receptors is called CCR7 and is present on dendritic cells.

Dendritic cells are specialized antigen-presenting cells that have a critical role in activating the overall immune response. We need to find the infection, recognize it, and then move to the lymph nodes with that information. In lymph nodes, dendritic cells interact with other cells of the immune system to mount an immune response against pathogens.

Alanko’s research showed that dendritic cells not only register chemokine signals at the CCR7 receptor, but also actively shape their chemical environment by consuming chemokines. The cells thereby create local gradients that guide their own movement and that of other immune cells. The researchers also discovered that another type of immune cell, her T cells, can benefit from these self-generated gradients to enhance their own directional movement.

“When immune cells are able to create chemokine gradients, they can guide the directional movement of themselves and other immune cells to avoid future obstacles in complex environments,” explains Jonah Alanko. do.

This discovery deepens our understanding of how immune responses are regulated in the body. But it can also reveal how cancer cells direct their movement to cause metastasis.

“The CCR7 receptor has also been found in many types of cancer, and in these cases this receptor has been shown to promote cancer metastasis. Cancer cells use the same mechanisms as immune cells to It may even guide its movement. Our findings therefore have the potential to help design new strategies not only to target specific cancers but also to modify immune responses. ,” said Jonah Alanco.

Reference: “CCR7 acts as both a sensor and a sink for CCL19 to coordinate collective migration of leukocytes” Jonna Alanko, Mehmet Can Uçar, Nikola Canigova, Julian Stopp, Jan Schwarz, Jack Merrin, Edouard Hannezo, Michael Sixt, September 1, 2023; scientific immunology.
DOI: 10.1126/sciimmunol.adc9584

Jonna Alanko is a postdoctoral researcher at the InFLAMES Flagship in the MediCity laboratory at the Faculty of Medicine, University of Turku, Finland. She carried out most of her recently published research in a research group led by Professor Michael Sixt at the Austrian Institute for Science and Technology (ISTA) in Austria.

Source: scitechdaily.com

T cells: the potential secret weapon against the latest coronavirus ‘variants of concern’ amid Pyrrha panic

Posted on December 12, 2023 by Igor Mitreski

A new SARS-CoV-2 variant, Pirora (BA.2.86), has been detected worldwide and is causing concern due to its high mutation rate

Researchers at the La Jolla Institute for Immunology are using immune epitope databases to predict T-cell responses to Pirora, suggesting that past exposure to existing vaccines and variants like Omicron remains important and may have a preventive effect. Although the results are promising, they are still predictive and require further experimental validation. (Credit: SciTechDaily.com)

Utilization of bioinformatics

LJI scientists are using bioinformatics to predict how T cells will adapt to fight the highly mutated Pirora mutant. In August, researchers discovered a new SARS-CoV-2 ‘Variants of concern’ in patients in Israel and Denmark. Since then, this variant has been called BA.2.86 or “Pirola” and has spread all over the world. Pirola’s mutant species is highly mutated, so caution is advised. In fact, Pirora has mutated similarly to the Omicron variant when compared to the earlier SARS-CoV-2 variants that were included in the first vaccinations. As Pyrolla spreads, researchers at La Jolla Immunology Institute (LJI) COVID-19 (new coronavirus infection) Vaccines (or previous SARS-CoV-2 infection) can still protect people from severe disease.

“The concern is that virus With so many mutations, T-cell immunity will ‘escape’,” says LJI Professor Alessandro Sette, Ph.D. in Biological Sciences. New research is currently being conducted Cell hosts and microorganisms This suggests that T cells can accurately detect mutations in pyrola and find their targets.

“Our analysis suggests there is positive news,” says LJI research assistant professor Dr. Alba Grifoni. “It appears that past exposure to Omicron, or vaccination with the new bivalent vaccine, may provide a person with T cells that can ‘catch up’ and generate a specific response to fight Pyrrha. ” LJI Professor Alessandro Sette, Doctor of Biological Sciences
(Credit: La Jolla Institute of Immunology)

Next step

Grifoni emphasizes that these findings are predictive and not observations based on actual pylora infections. Still, she thinks it’s important to see how these “in silico” (in silico) predictions are reflected in recent real-world research. “Although we still need experimental validation, we have established several collaborations around the world and are talking about this issue as we study it,” says Grifoni. Sette added that even with the Pirora variant, many people are still vulnerable to SARS-COV-2 infection. “That’s why people should still get vaccinated, especially the latest vaccines.” The researchers are currently collecting experimental data to learn more about T cell responses to the mutant strains and further strengthen their predictive tools. Griffoni is particularly interested in understanding exactly how people who have received a bivalent vaccine booster or a “breakthrough” infection will mount a T-cell response against future variants.

Reference:

“Existing SARS-2-specific T cells are predicted to cross-recognize BA.2.86,” Alessandro Sette, John Sidney, and Alba Grifoni, December 8, 2023. Cell hosts and microorganisms.DOI: 10.1016/j.chom.2023.11.010 The study, “Existing SARS-2-specific T cells are predicted to mutually recognize BA.2.86,” also includes study author John Sidney. This research was supported by: National Institutes of HealthNational Institute of Allergy and Infectious Diseases (Contract No. 75N93021C00016 and Contract No. 75N93019C00001)

Source: scitechdaily.com

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Tag Archives: cells

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Robotic grin crafted from living human skin cells

These plant cells could be used to make your next cup of coffee.

What is cell-based coffee?

How does it compare to real coffee?

Why cell-based coffee is better for the environment

Newly Found Anti-Aging Cells Offer Potential for Prolonged Youthfulness

Immune cells exhibit greater independence than previously believed

cells consume chemokines

T cells: the potential secret weapon against the latest coronavirus ‘variants of concern’ amid Pyrrha panic

A new SARS-CoV-2 variant, Pirora (BA.2.86), has been detected worldwide and is causing concern due to its high mutation rate

Utilization of bioinformatics

Next step

Reference: