Publisher Health

For more than 30 years, polymerase chain reaction (PCR) has been the gold standard in molecular diagnostic testing, detecting genetic material, such as those from a virus or from human DNA. But PCR, including reverse transcription polymerase chain reaction (RT-PCR), is mostly done at large, centralized laboratories, not in point-of-care (POC) settings, because its instrumentation is bulky, expensive, takes a long time for results, and requires trained technicians to run it. These limitations have led to a shortage of accurate POC diagnostics as well as bottlenecks in test results, particularly during the COVID-19 pandemic.
Researchers at Columbia Engineering and Rover Diagnostics announced today that they have built an RT-PCR platform that gives results in 23 minutes that match the longer laboratory-based tests — faster than other PCR tests on the market. It can be adapted to test for a broad range of infectious diseases including not just COVID-19 but also flu, strep, and other viruses that require fast diagnosis. Its targeted sensitivity is higher than other types of tests such as isothermal, antigen, and CRISPR. And, at just two pounds, the Rover PCR is easy to carry around and can be used by anyone.
“Our aim was to create a platform that can be used in locations where rapid turnaround results are critical, at pharmacies, transportation hubs, public events, and at companies screening employees coming back to work,” said Sam Sia, professor of biomedical engineering and Vice Provost for the Fourth Purpose and Strategic Impact at Columbia.
The system was co-developed with Rover Diagnostics, a biotech start-up co-founded in 2018 bySia and serial tech entrepreneur Mark Fasciano, Rover’s CEO. The platform uses sample preparation techniques developed at Sia’s lab, combined with a new approach to thermal cycling, bypassing the standard approach of Peltier device — which heats the sample from outside the vial. Instead, Rover’s system uses a photothermal process — plasmonic thermocycling — that relies on nanoparticles irradiated by light to rapidly generate heat from inside.
The team successfully performed reverse-transcriptase quantitative PCR (RT-qPCR) in a reaction vessel containing all the PCR reagents. qPCR is the current gold-standard laboratory technique for identifying COVID infection. The technique provides quantitation of infectious units, but it also poses a number of hurdles for point-of-care (POC) miniaturization.
In the study published today in Nature Nanotechnology, the researchers addressed these challenges by leveraging plasmonic nanoparticles — discrete metallic particles that respond to infrared light by releasing heat — to achieve real-time and multiplexed RT-qPCR on clinical specimens.
“This should really move the needle on delivering rapid and accurate molecular clinical diagnostics in decentralized settings,” said Fasciano, a computer scientist turned software and biotech entrepreneur. “Thermal cycling, so critical to DNA and RNA testing, can now be sped up and clinicians and patients alike won’t have to wait so long for results.”
The Rover team is moving forward with a commercial product that can detect COVID-19, its variants, and other infectious diseases.
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Materials provided by Columbia University School of Engineering and Applied Science. Original written by Holly Evarts. Note: Content may be edited for style and length.

Researchers have identified a gene that promotes muscle strength when switched on by physical activity, unlocking the potential for the development of therapeutic treatments to mimic some of the benefits of working out.
Published in Cell Metabolism, the University of Melbourne-led study showedhow different types of exercise change the molecules in our muscles, resulting in the discovery of the new C18ORF25 gene that is activated with all types of exercise and responsible for promoting muscle strength. Animals without C18ORF25 have poor exercise performance and weaker muscles.
Project lead Dr Benjamin Parker said by activating the C18ORF25 gene, the research team could see muscles become much stronger, without them becoming necessarily bigger.
“Identifying this gene may impact how we manage healthy aging, diseases of muscle atrophy, sports science and even livestock and meat production. This is because promoting optimal muscle function is one of the best predictors of overall health,” Dr Parker said.
“We know exercise can prevent and treat chronic diseases including diabetes, cardiovascular disease and many cancers. Now, we hope that by better understanding how different types of exercise elicits these health promoting effects at the molecular level, the field can work towards making new and improved treatment options available.”
In the study, a collaboration between Dr Parker and Professors Erik Richter and Bente Kiens of the University of Copenhagen, Denmark, the team were able to identify the molecular similarities and differences between different types of exercise in human muscle biopsies by analysing proteins and how they change within cells.
“To identify how genes and proteins are activated during and after different exercises, we performed an analysis of human skeletal muscle from a cross-over intervention of endurance, sprint and resistance exercise,” Dr Parker said.
The experimental design allowed researchers to compare signalling responses between the exercise modalities in the same individual, relative to their pre-exercise level. This meant they could monitor how an individual responded to different types of exercise directly in their muscles.
Importantly, it also allowed the study team to identify genes and proteins that consistently change across all individuals and all types of exercise, leading to the discovery of the new gene.
This work was funded by the Australian National Health and Medical Research Council project grant (APP1122376), a Diabetes Australia grant, a University of Melbourne Driving Research Momentum Grant, and a NHMRC Emerging Leader Investigator Grant (APP2009642) to Dr Benjamin Parker.
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Materials provided by University of Melbourne. Note: Content may be edited for style and length.

COVID-19 often leads to neurological symptoms, such as a loss of taste or smell, or cognitive impairments (including memory loss and concentration difficulties), both during the acute phase of the disease and over the long term with “long COVID” syndrome. But the way in which the infection reaches the brain was previously unknown. Scientists from Institut Pasteur and CNRS laboratories have used state-of-the-art electron microscopy approaches to demonstrate that SARS-CoV-2 hijacks nanotubes, tiny bridges that link infected cells with neurons. The virus is therefore able to penetrate neurons despite the fact that they are lacking the ACE2 receptor that the virus usually binds to when infecting cells. The study was published in Science Advances on July 20.
How does SARS-CoV-2 enter brain cells? A study published recently in Science Advances shows that the virus uses nanotubes that form between infected cells and neurons to gain access to neurons. These transient dynamic structures are a result of membrane fusion in distant cells. They enable the exchange of cellular material without the need for membrane receptors, the normal means of entering and exiting the cytoplasm. The Membrane Traffic and Pathogenesis Unit, led by Chiara Zurzolo at the Institut Pasteur, has already found that nanotubes play a role in degenerative diseases such as Alzheimer’s and Parkinson’s by facilitating the transport of proteins responsible for these diseases.
Infecting neurons in the absence of a receptor
Although the human cell receptor ACE2 serves as a gateway for SARS-CoV-2 to enter lung cells — the main target of the virus — and cells in the olfactory epithelium, it is not expressed by neurons. But viral genetic material has been found in the brains of some patients, which explains the neurological symptoms that characterize acute or long COVID. The olfactory mucosa has previously been suggested as a route to the central nervous system, but that does not explain how the virus is able to enter neuronal cells themselves.
According to this new study, SARS-CoV-2 is also thought to be capable of inducing the formation of nanotubes between infected cells and neurons, as well as among neurons, which would explain how the brain is infected from the epithelium. The research team revealed multiple viral particles located both inside and on the surface of nanotubes. Since the virus spreads more rapidly and directly from within nanotubes than by exiting one cell to move to the next via a receptor, this mode of transmission therefore contributes to the infectious capacity of SARS-CoV-2 and its spread to neuronal cells.
But the virus also moves on the external surface of nanotubes, where it can be guided more quickly to cells that express compatible receptors. “Nanotubes can be seen as tunnels with a road on top,” suggests Chiara Zurzolo, Head of the Institut Pasteur’s Membrane Traffic and Pathogenesis Unit, “which enable the infection of nonpermissive cells like neurons but also facilitate the spread of infection between permissive cells.”
State-of-the-art imaging methods with the Titan Krios microscope
This publication combines research on in vitro cultures, showing that healthy neuronal cells are infected if they come into contact with infected cells, with the use of state-of-the-art microscopy tools. The Titan Krios microscope in the Institut Pasteur’s NanoImaging Core Facility offers unprecedented resolution of biological samples and nanomolecules that is closer to real biological conditions. “With this instrument, novel imaging approaches have been developed to evaluate the structure of SARS-CoV-2 and the architecture of nanotubes,” explains Anna Pepe from the Institut Pasteur’s Membrane Traffic and Pathogenesis Unit, first author of the study.
Working in cooperation with the Institut Pasteur’s Ultrastructural BioImaging Core Facility, the research teams used precise investigative methods to detect structures in the nanotubes that were subsequently identified as “virus factories.” The nanotubes between neurons represent a propitious environment for SARS-CoV-2 to develop, since it is invisible to the immune system. Chiara Zurzolo believes that “it may represent a mechanism for immune evasion and viral persistence that could be favorable to the virus.”
This study is an example of how basic interdisciplinary research, involving cellular biologists, virologists and state-of-the-art imaging techniques, can lead to new discoveries. It paves the way for further research on the role of cell-to-cell communication in the spread of SARS-CoV-2. It also encourages exploration of alternative therapeutic approaches to hinder the spread of SARS-CoV-2, alongside current projects that are mainly focused on blocking entry via the ACE2 receptor.
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Materials provided by Institut Pasteur. Note: Content may be edited for style and length.

Heart damage is common among patients hospitalized with COVID-19, leading many to wonder how the virus affects the heart. Now, researchers have found that the spike protein from the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus can lead to heart muscle injury through the inflammatory process, according to preliminary research to be presented at the American Heart Association’s Basic Cardiovascular Sciences Scientific Sessions 2022. The meeting, held in Chicago on July 25-28, offers the latest research on basic and translational cardiovascular science.
The spike protein is found on the surface of SARS-CoV-2, the virus that causes COVID-19. Spike proteins latch onto receptors known as angiotensin-converting enzyme 2 (ACE2) on target cells. The spike protein facilitates virus entry into healthy cells, which is the first step in infection. In addition to infecting the lungs, the virus can also spread to other organs leading to more damage to the body, severe infection and, among some people, death.
“It’s already known from the clinical side that COVID-19 infection can induce heart injury, however, what we don’t know is the mechanistic details of how this occurs. What we suspect is that the spike protein has unknown pathological roles,” said Zhiqiang Lin, Ph.D., lead author of the study and an assistant professor at the Masonic Medical Research Institute in Utica, New York. “Our data show that the spike protein from SARS-CoV-2 causes heart muscle damage. That’s why it’s important to get vaccinated and prevent this disease.”
“Host natural immunity is the first line of defense against pathogen invasion, and heart muscle cells have their own natural immune machinery. Activation of the body’s immune response is essential for fighting against virus infection; however, this may also impair heart muscle cell function and even lead to cell death and heart failure,” Lin said.
The researchers studied whether the SARS-CoV-2 spike protein activates the natural immune response in heart muscle cells. HCoV-NL63 is a coronavirus that infects the respiratory system without causing cardiac injury, although its spike protein also uses ACE2 to mediate virus entry. They studied the potential ability to cause heart disease of both SARS-CoV-2 spike protein and the NL63 spike protein. Their results showed that the SARS-CoV-2 spike protein activated the natural immune response in heart muscle cells and damaged the heart, but the NL63 spike protein did not.
“The fact that the SARS-CoV-2 spike protein is activating the natural immune response may explain the high virulence compared to the other coronaviruses,” Lin said. “The TLR4 signaling is the major pathway that activates the body’s natural immune response, and the SARS-CoV-2 spike protein activates TLR4, not the regular flu spike protein.”
To investigate the impact of the SARS-CoV-2 spike protein on the heart, researchers cloned the SARS-CoV-2 spike protein and the NL63 spike protein into the AAV9 viral vector. The AAV9 viral vector was delivered into lab mice to activate the spike protein in the heart muscle cells. They found that the AAV9-mediated the SARS-CoV-2 spike protein, and not the NL63 spike protein, caused heart dysfunction, hypertrophic remodeling (enlargement) and cardiac inflammation.

A new study from TAU identifies risks in the use of CRISPR therapeutics — an innovative, Nobel-prize-winning method that involves cleaving and editing DNA, already employed for the treatment of conditions like cancer, liver and intestinal diseases, and genetic syndromes. Investigating the impact of this technology on T-cells — white blood cells of the immune system, the researchers detected a loss of genetic material in a significant percentage — up to 10% of the treated cells. They explain that such loss can lead to destabilization of the genome, which might cause cancer.
The study was led by Dr. Adi Barzel from the School of Neurobiology, Biochemistry and Biophysics at TAU’s Wise Faculty of Life Sciences and Dotan Center for Advanced Therapies, a collaboration between the Tel Aviv Sourasky Medical Center (Ichilov) and Tel Aviv University, and by Dr. Asaf Madi and Dr. Uri Ben-David from TAU’s Faculty of Medicine and Edmond J. Safra Center for Bioinformatics. The findings were published in the leading scientific journal Nature Biotechnology.
The researchers explain that CRISPR is a groundbreaking technology for editing DNA — cleaving DNA sequences at certain locations in order to delete unwanted segments, or alternately repair or insert beneficial segments. Developed about a decade ago, the technology has already proved impressively effective in treating a range of diseases — cancer, liver diseases, genetic syndromes, and more. The first approved clinical trial ever to use CRISPR, was conducted in 2020 at the University of Pennsylvania, when researchers applied the method to T-cells — white blood cells of the immune system. Taking T-cells from a donor, they expressed an engineered receptor targeting cancer cells, while using CRISPR to destroy genes coding for the original receptor — which otherwise might have caused the T-cells to attack cells in the recipient’s body.
In the present study, the researchers sought to examine whether the potential benefits of CRISPR therapeutics might be offset by risks resulting from the cleavage itself, assuming that broken DNA is not always able to recover.
Dr. Ben-David and his research associate Eli Reuveni explain: “The genome in our cells often breaks due to natural causes, but usually it is able to repair itself, with no harm done. Still, sometimes a certain chromosome is unable to bounce back, and large sections, or even the entire chromosome, are lost. Such chromosomal disruptions can destabilize the genome, and we often see this in cancer cells. Thus, CRISPR therapeutics, in which DNA is cleaved intentionally as a means for treating cancer, might, in extreme scenarios, actually promote malignancies.”
To examine the extent of potential damage, the researchers repeated the 2020 Pennsylvania experiment, cleaving the T-cells’ genome in exactly the same locations — chromosomes 2, 7, and 14 (of the human genome’s 23 pairs of chromosomes). Using a state-of-the-art technology called single-cell RNA sequencing they analyzed each cell separately and measured the expression levels of each chromosome in every cell.
In this way, a significant loss of genetic material was detected in some of the cells. For example, when Chromosome 14 had been cleaved, about 5% of the cells showed little or no expression of this chromosome. When all chromosomes were cleaved simultaneously, the damage increased, with 9%, 10%, and 3% of the cells unable to repair the break in chromosomes 14, 7, and 2 respectively. The three chromosomes did differ, however, in the extent of the damage they sustained.
Dr. Madi and his student Ella Goldschmidt explain: “Single-cell RNA sequencing and computational analyses enabled us to obtain very precise results. We found that the cause for the difference in damage was the exact place of the cleaving on each of the three chromosomes. Altogether, our findings indicate that over 9% of the T-cells genetically edited with the CRISPR technique had lost a significant amount of genetic material. Such loss can lead to destabilization of the genome, which might promote cancer.”
Based on their findings, the researchers caution that extra care should be taken when using CRISPR therapeutics. They also propose alternative, less risky, methods, for specific medical procedures, and recommend further research into two kinds of potential solutions: reducing the production of damaged cells or identifying damaged cells and removing them before the material is administered to the patient.
Dr. Barzel and his PhD student Alessio Nahmad conclude: “Our intention in this study was to shed light on potential risks in the use of CRISPR therapeutics. We did this even though we are aware of the technology’s substantial advantages. In fact, in other studies we have developed CRISPR-based treatments, including a promising therapy for AIDS. We have even established two companies — one using CRISPR and the other deliberately avoiding this technology. In other words, we advance this highly effective technology, while at the same time cautioning against its potential dangers. This may seem like a contradiction, but as scientists we are quite proud of our approach, because we believe that this is the very essence of science: we don’t ‘choose sides.’ We examine all aspects of an issue, both positive and negative, and look for answers.”
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Materials provided by Tel-Aviv University. Note: Content may be edited for style and length.

An international team of researchers, including those from UNSW’s School of Biotechnology & Biomolecular Sciences, have applied a promising new tool — CLASH — to capture hundreds of undiscovered mechanisms of gene regulation in a strain of multi-drug resistant Staphylococcus aureus (MRSA).
The 500 mechanisms uncovered by the new tool were based on the mRNA of S. aureus. Normally serving merely as instructions for making proteins, these newly revealed mRNAs were controlling other genes in S. aureus through direct interactions — regulating the bacteria’s very own genetic information and antibiotic tolerance.
Among those RNAs found was a mechanism that thickens the bacteria’s cell wall — a change commonly seen in clinical strains of MRSA that are tolerant to last-line antibiotics — potentially identifying new targets for antibiotic treatment. Their work has been published in Nature Communications.
“Before our study, only three other mRNAs had been shown to regulate bacterial RNA,” says co-author Associate Professor Jai Tree. “It’s relatively rare. But looking at our CLASH data was the real surprise. We found that in Staphylococcus aureus, there was evidence for 543 regulatory mRNAs interactions.”
“This is a shift from our current understanding of gene regulation in bacteria.”
This system of adaptation in S. aureus has remained undetected due to a lack of tools for broadly capturing RNA interactions. In other disease-causing bacteria, related techniques rely on the presence of particular proteins, proteins that don’t seem to function in S. aureus.

A key molecule for cancer metastasis has been identified as a molecule already known for its involvement in cardiovascular disease, suggesting a possible treatment approach for both diseases simultaneously.
Cancer is the uncontrolled growth of body cells leading to the formation of tumors, triggered by the accumulation of mutations in a cell’s genome. In order to become malignant, metastasizing cancer, tumor cells go through a series of transformations involving interactions between the body’s immune system and the tumor. However, many mechanistic details in this process are still unclear, making the prevention and treatment of cancer notoriously difficult. However, there is growing evidence that in tumor progression to metastasis, inflammation of blood vessel-lining “endothelial” cells is a key process.
Concerned with the molecular mechanism behind this process in cancer malignancy, a team of researchers led by Professor Kyoko Hida at Hokkaido University have discovered that, in malignant tumors, endothelial cells accumulate a lipid delivery molecule called “low-density lipoprotein” (LDL) and attract immune cells called “neutrophils.” Neutrophils are immune suppressor cells which are known to contribute to tumor progression. The discovery was published in the International Journal of Cancer.
Previous work by the team had revealed that blood vessels in malignant tumors expressed a high level of proteoglycans, and it is known that cancerous tissue is inflamed. These features are similar to what is seen in atherosclerosis, and the team wished to investigate if the similarities went deeper.
The research team showed that metastasizing tumors, in contrast to non-metastasizing ones, accumulate proteoglycan molecules; these, in turn, attach to and accumulate LDL to the walls of blood vessels. The bound LDL becomes oxidized. There are also high levels of its receptor, called “LOX-1,” in the blood vessel-lining endothelial cells of metastasizing tumors. This, they found, causes these cells to produce inflammation signals that attract neutrophils. They then proved that in mice, the suppression of LOX-1 can significantly reduce tumor malignancy, and also that LOX-1 overexpression caused an increase in signaling molecules attracting neutrophils.
As the team hypothesized, this sequence of interactions observed in malignant tumors is not novel: it occurs in atherosclerosis, the hardening of blood vessels. “Atherosclerosis and cancer appear to be completely different diseases, but they share several common pathophysiological features in the blood vessels,” says Kyoko Hida.
Even though some questions remain open, especially on the mechanism of how neutrophils contribute to cancer malignancy, this study is the first to explicitly prove the mechanistic commonalities between cardiovascular disease and cancer progression and trace the mechanism involving LDL accumulation and LOX-1 expression in in-vivo tumor tissue. “Our present study focused on the importance of LOX-1 in endothelial cells as a common factor between cancer and atherosclerosis,” Hida explains. “The presence of neutrophils in tumors is a telltale sign of tumor progression.”
The study also points to a promising approach for treating and preventing malignant cancer — and cardiovascular disease — by targeting neutrophil recruitment to endothelial cells. Hida concludes: “The number of patients with cancer who die not of cancer, but of cardiovascular events, is increasing. Targeting the LOX-1/oxidized LDL axis might be a promising strategy for the treatment of the two diseases concomitantly.”
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Materials provided by Hokkaido University. Note: Content may be edited for style and length.

Many people worldwide suffer from a chronic type of inflammatory bowel disease (IBD) called ulcerative colitis (UC), which is characterized by erosions and ulcers within the mucous membrane of the colon (large intestine). It was understood that UC involves chronic and aggressive inflammation, but more specific details of its pathogenesis were not fully known.
Currently, there is no drug that can completely cure UC. Therefore, clinicians and scientists are aiming to develop a treatment that can target the actual molecular cause. In a recent article published in Scientific Reports, a team led by researchers at Osaka University described the design of an ingestible agent that was able to target the high levels of oxidation associated with UC in a lab mouse model.
Previous studies have shown that there are significant amounts of reactive oxygen species (ROS) in the intestinal mucosa of those with UC. The ROS can lead to oxide accumulation, which stimulates the inflammation that damages the cells, causes the disease’s symptoms, and can even induce colon cancer in some cases.
“Data in the literature pointed to the important role of ROS and oxidative stress in UC,” says lead author Yoshihisa Koyama. “A logical hypothesis from those results is that an efficient antioxidant that can eliminate the ROS may be an effective treatment method for this disease.”
In fact, reports have demonstrated that hydrogen is a strong antioxidant that showed promising results in several diseases, including IBD. The researchers developed a silicon (Si)-based agent ingestible agent that stably generates hydrogen when reacting with water within the gastrointestinal tract. The researchers tested this approach in a mouse model of UC and found that the Si-treated mice had less weight loss, inflammation, and diarrhea compared with the control mice.
The levels of certain proinflammatory cytokines were reduced in the mice given the therapeutic agent. Si-based agent also significantly reduced colon atrophy, the hemorrhage, and injury associated with chronic inflammation. There was also very little infiltration of immune cells, suggesting that the inflammatory response was suppressed.
The team confirmed that the Si-based agent successfully increased the hydrogen levels within the colon.
“Interestingly, we also found that hyperexcitability in the brain area associated with visceral pain was suppressed in Si-based agent treated mice model,” describes Koyama.
Overall, the results of this study suggest that the Si-based agent may be a new therapeutic candidate.
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Materials provided by Osaka University. Note: Content may be edited for style and length.

Emerging evidence suggests that arterial stiffness may be a novel risk factor to be targeted in the prevention and treatment of vascular and metabolic diseases from a young age, a review of studies published in the Journal of Hypertension concludes.
The prevalence of hypertension and obesity has been on the increase globally, despite the targeted effort at promoting weight loss, increasing physical activity, and decreasing sedentary time in the general population. This global challenge informed a recent scientific statement from the American Heart Association on further research into obesity and hypertension in order to mitigate this health burden.
Among middle-aged and older adults, arterial stiffness has been established as a strong predictor of cardiovascular events and all-cause mortality. Hence, a few clinical trials among adults are currently ongoing that examine the likelihood of reversing arterial stiffness. However, among children, adolescents, and young adults, arterial stiffness has been consigned to an intermediate marker of cardiovascular disease and death that occurs in middle age, no thanks to limited longitudinal data and repeated measures of arterial stiffness in a fairly healthy growing young population.
Also, the clinical utility of arterial stiffness as a risk factor for early vascular and metabolic diseases is largely unknown in pediatrics. In this review, recent prospective evidence in a large adolescent population and a middle-aged population that emphasised the value of arterial stiffness as a novel risk factor for hypertension, overweight/obesity, insulin resistance, dyslipidemia, and type 2 diabetes mellitus were summarised. It is often asked what are the risk factors for higher arterial stiffness in adolescents? It is known that maternal smoking habits, early life smoking patterns of adolescents, high salt intake, genetic inheritance, obesity, and elevated blood originating in childhood may contribute to higher arterial stiffening in adolescence.
“Arterial stiffening in adolescence seems to be a subtle, stealthy, but potent risk factor for high blood pressure and metabolic alteration initiating a cascade of biological events finally leading to disease formation such as type 2 diabetes mellitus and premature organ damage. It is therefore expedient for clinicians, pediatricians, public health experts, and policymakers to focus on ways to treat, reduce, and possibly reverse arterial stiffness, particularly from adolescence. An arterial stiffness intervention in adolescence may decrease the incidence of hypertension and metabolic diseases in later life, but further studies are needed,” says Andrew Agbaje, a physician and clinical epidemiologist at the University of Eastern Finland.
This study was supported by research grants from Jenny and Antti Wihuri Foundation, the Finnish Cultural Foundation Central Fund, the Finnish Cultural Foundation North Savo Regional Fund, the Orion Research Foundation sr, the Aarne Koskelo Foundation, the Antti and Tyyne Soininen Foundation, the Paulo Foundation, the Yrjö Jahnsson Foundation, the Paavo Nurmi Foundation, and the Finnish Foundation for Cardiovascular Research.
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Materials provided by University of Eastern Finland. Note: Content may be edited for style and length.

A single chemical is key to controlling when hair follicle cells divide, and when they die. This discovery could not only treat baldness, but ultimately speed wound healing because follicles are a source of stem cells.
Most cells in the human body have a specific form and function determined during embryonic development that does not change. For example, a blood cell cannot turn into a nerve cell, or vice versa. Stem cells, however, are like the blank tiles in a game of Scrabble; they can turn into other types of cells.
Their adaptability makes them useful for repairing damaged tissue or organs.
“In science fiction when characters heal quickly from injuries, the idea is that stem cells allowed it,” said UC Riverside mathematical biologist and study co-author Qixuan Wang.
“In real life, our new research gets us closer to understanding stem cell behavior, so that we can control it and promote wound healing,” Wang said. This research is detailed in a recent Biophysical Journal article.
The liver and stomach regenerate themselves in response to wounds. However, Wang’s team studied hair follicles because they’re the only organ in humans that regenerates automatically and periodically, even without injury.