Publisher Health

Among the populations most significantly affected by COVID-19 are the elderly and patients with preexisting medical conditions including diabetes, hypertension, obesity, metabolic syndrome, cardiovascular disease and chronic lung diseases like COPD and asthma.
In a new study published in the journal JCI Insight, Brown University researchers describe the cellular and molecular events that explain why these groups have a higher risk of infection as well as of severe side effects and death.
“This paper details a major discovery in COVID-19,” said corresponding author Dr. Jack A. Elias, an immunologist and dean of medicine and biological sciences at Brown. “It shows that levels of a protein called chitinase 3-like-1 increase with age as well as co-morbid diseases and infection. What’s more, chitinase 3-like-1 augments SARS CoV-2 infection.”
The findings not only answer important questions about key mechanisms of the complex SARS-CoV-2 virus, Elias said, but also have direct implications for the development of therapeutics to control the viral infection.
Elias is part of a National Institutes of Health-funded laboratory that focuses on the cell and molecular biology of lung injury and repair. Researchers in the lab, including lead study author Suchitra Kamle and co-author Chun Geun Lee, have recently focused on the biology of enzymes and enzyme-like molecules, called chitinases and chitinase-like proteins, respectively. Of particular interest is a chitinase-like protein referred to as chitinase 3-like-1, a molecule naturally found in blood.
“We’ve been studying this gene family here at Brown for a while and we know that it has a large number of biologic effects, as well as tremendously important roles in both health and diseases,” said Lee, a professor (research) of molecular microbiology and immunology.

Stem cells are true multi-talents. They can develop into any cell type of an organism — in humans there are over 200 — and thus perform all vital tasks. Once the stem cells have decided on a task they can no longer be deterred from their goal. The final product, tissues and organs, almost always look the same and consist of defined proportions of different specialised cell types. But how do the cells actually know what they want to become and how many of them are actually allowed to do so?
Is it all just chance?
An important regulator of the distribution of tasks is the control of genes by transcription factors such as NANOG and GATA, which are both initially present in the undifferentiated stem cells. This changes fundamentally, however, in the very early development when the stem cells develop into two new cell types: Cells of the early embryo, in which now only NANOG is present and precursor cells of the fruit bladder which now exclusively carry GATA. Until now, it was thought that the decision of each individual cell was made rather randomly at an early stage, similar to a dice game, except that here only NANOG or GATA can be rolled.
Cells decide collectively
In a previous theoretical paper, Aneta Koseska, co-author of the study and former MPI group leader, was able to establish a new concept with the help of Christian Schröter, showing how stem cells specialize in right proportions in a coordinated manner. In the current publication, Christian Schröter and his team have now succeeded in substantiating the theoretical concept. Using stem cells in a test tube, the researchers were able to show that decision-making does not take place purely randomly at the level of individual cells, as previously assumed, but is communicated within the cell community.
Cheating at the stem cell dice game
In order not to leave the fate of the cells to chance, the researchers manipulated the NANOG-GATA dice in their investigations so that GATA is now rolled more often than NANOG. This was achieved experimentally by artificially increasing the amount of GATA. Even though a six was always rolled — i.e. GATA — the number of fruit bladder precursor cells could not be arbitrarily increased, but similar proportions of the two different cell types continued to emerge. The distribution of tasks during development must therefore be dependent on more than mere chance.
Decisions are communicated in the team
Following their theoretical concept, the scientists investigated the role of cellular communication in embryonic development. As a central means of communication cells use messenger substances such as growth factors, which they produce and secrete themselves. These substances are then received by other cells and control their specialization. If the researchers took away a growth factor that was important for cell development, the cells were no longer able to develop into fruit bladder precursor cells even in the presence of high amounts of GATA. However, the more of the growth factor the cells received, the more fruit bladder precursor cells also developed. Their ability to divide into the right proportions of the two cell types despite disturbances was thus lost. Stem cells must therefore communicate with each other in order to make the right decision.
“Communication in cell development is like working in a team. If the members choose tasks without consulting each other, some things are done twice and others not at all. A team that communicates well, on the other hand, can solve problems that arise and complete even complex projects reliably and efficiently,” Christian Schröter says. “So it’s not just the state of the individual cell that decides on its faith, but the functioning communication with the other cells.”
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The rates of death and health burdens associated with air pollution are borne unequally and inequitably by people of color and those with lower household income and educational attainment in Washington, D.C., according to a new study.
Air pollution is considered the leading environmental risk factor to health, and recent efforts have successfully brought down levels of fine particulate matter, or PM2.5, in the air in the D.C. region.
The new study found that while deaths and health burdens associated with PM2.5 halved between 2000 and 2018 in the D.C. area, disparities and geographical segregations in health effects persist.
Most impacted by PM2.5 air pollution are people living in wards five, seven and eight in the District’s east and southeast regions. Researchers found in southeast wards, baseline disease rates are five times higher for chronic obstructive pulmonary disease, lung cancer and stroke, up to nine times higher for all-cause mortality and coronary heart disease, and over 30 times higher for asthma emergency department visits, compared to northwest neighborhoods.
In these most impacted neighborhoods, residents have 10% lower education and employment rates, 10% more residents are living in poverty, their median household income is $61,000 lower than households in the rest of the city, and residents have about 10 fewer years of life expectancy. The top 10 impacted neighborhoods have a 54% higher proportion of Black residents and a 44% lower proportion of white residents.
This study highlights the importance of detailed health and air quality data, and the researchers hope it can guide future policymaking to address environmental health disparities and serve as a model for addressing air pollution health assessments elsewhere. The research was published in GeoHealth, AGU’s journal investigating the intersection of human and planetary health for a sustainable future.

By watering bean plants (Phaseolus vulgaris) with a solution that contains conjugated oligomers, researchers at the Laboratory of Organic Electronics, Linköping University, have shown that the roots of the plant become electrically conducting and can store energy.
Dr Eleni Stavrinidou, Associate Professor and Principal Investigator in the Electronic Plants Group at the Laboratory of Organic Electronics, showed in 2015 that circuits can be fabricated in the vascular tissue of roses. The conducting polymer PEDOT was absorbed by the plant´s vascular system to form electrical conductors that were used to make transistors. In a later work in 2017, she demonstrated that a conjugated oligomer, ETE-S, could polymerise in the plant and form conductors that can be used to store energy.
“We have previously worked with plants cuttings, which were able to take up and organise conducting polymers or oligomers. However, the plant cuttings can survive for only a few days, and the plant is not growing anymore. In this new study we use intact plants, a common bean plant grown from seed, and we show that the plants become electrically conducting when they are watered with a solution that contains oligomers,” says Eleni Stavrinidou.
The researchers here have used a trimer, ETE-S, which is polymerised by a natural process in the plant. A conducting film of polymer is formed on the roots of the plant, which causes the complete root system to function as a network of readily accessible conductors.
The bean plant roots remained electrically conducting for at least four weeks, with a conductivity in the roots of approximately 10 S/cm (Siemens per centimetre).
The researchers investigated the possibility of using the roots to store energy, and built a root-based supercapacitor in which the roots functioned as electrodes during charging and discharging. “Supercapacitors based on conducting polymers and cellulose are an eco-friendly alternative for energy storage that is both cheap and scalable,” says Eleni Stavrinidou.
The root-based supercapacitor worked well, and could store 100 times more energy than previous experiments with supercapacitors in plants that used the plant stem. The device can also be used over extended periods of time since the bean plants in the experiments continued to live and thrive.
“The plant develops a more complex root system, but is otherwise not affected: it continues to grow and produce beans,” Eleni Stavrinidou assures us.
The results, which have been published in the scientific journal Materials Horizons, are highly significant, not just for the development of sustainable energy storage, but also for the development of new biohybrid systems, such as functional materials and composites. The electronic roots are also a major contribution to the development of seamless communication between electronic and biological systems.
The research group consists of researchers from the Laboratory of Organic Electronics, the Umeå Plant Science Center, the Wallenberg Wood Science Center at Linköping University, and from universities and research institutes in France, Greece and Spain.
Funding bodies for the research have included the EU Horizon Programme FET-OPEN-HyPhOE, the Swedish Research Council, the Wallenberg Wood Science Center, and the Strategic Research Area in Materials Science on Functional Materials (AFM) at Linköping University.
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Materials provided by Linköping University. Original written by Monica Westman Svenselius. Note: Content may be edited for style and length.

As people adhered to stay-at-home orders or self-isolated during the early months of the COVID-19 outbreak, daily commutes turned into shuffles between the bedroom and the living room. Clicking Zoom links erased time spent walking to meeting rooms, and Netflix spilled into time otherwise dedicated to the gym.
In short, a lot of people suddenly became more sedentary during the onset of the pandemic. Recently published research found people who continued to spend a higher amount of time sitting between April and June 2020 were likely to have higher symptoms of depression. A closer investigation into this association could play a role in helping people improve their mental health.
“Sitting is a sneaky behavior,” said Jacob Meyer, assistant professor of kinesiology at Iowa State University and lead author of the paper. “It’s something we do all the time without thinking about it.”
As the director of the Wellbeing and Exercise Laboratory at ISU, Meyer and his team look at how physical activity and sedentary behaviors are related to mental health, and how changes to those influence the way people think, feel and perceive the world.
“In March 2020, we knew COVID was going to affect our behavior and what we could do in lots of weird, funky ways that we couldn’t predict,” Meyer said.
To get a snapshot of those changes, Meyer and a team of researchers received survey responses from more than 3,000 study participants from all 50 states and the District of Colombia. Participants self-reported how much time they spent doing activities, like sitting, looking at screens and exercising, and how those behaviors compared to pre-pandemic times. Using standard clinical scales, they also indicated changes to their mental wellbeing (e.g., depression, anxiety, feeling stressed, lonely).

How ventricular fibrillation will behave in an individual patient can be accurately modelled and predicted using a single mathematical equation, according to Flinders University researchers.
Ventricular fibrillation (VF) is a life-threatening heart rhythm, or arrhythmia, that causes the heart to beat irregularly and is one of the leading causes of sudden death in Australia.
The findings, recently published in the journal Heart Rhythm, could be used to improve patient treatment, including identifying when to intervene or to develop individualised treatment plans that can work more effectively.
Developed by Dr Dhani Dharmaprani from the Flinders Heart Rhythm Research Group in the College of Medicine and Public Health, led by Associate Professor Anand Ganesan, the research team studied the statistical properties of VF, identifying the unique patterns that consistently occurred in human patients, as well as animal and computer models of VF in the heart.
“The issue we have with VF is that because the rhythm is so chaotic it’s been very difficult to fully understand the mechanisms that are responsible for the disorder,” says Dr Dharmaprani, a Biomedical Engineer and Postdoctoral Research Associate in Cardiac Electrophysiology.
“This is further complicated by the fact that everyone’s heart is unique, so how the heart reacts during VF changes from patient to patient.

In “Social Justice Parenting,” Traci Baxley emphasizes the rewards of teaching our children to empathize with and care for others.The holidays will soon be upon us. What is likely to make you feel better — receiving a gift, or giving one to someone in need? Research is clear that, as the proverb goes, it’s better to give than to receive.“Doing kind things makes you feel better,” said Andrew Miles, a sociologist at the University of Toronto. “It fulfills a basic psychological need, like giving our bodies appropriate food. It helps you feel like your life is valuable.”Dr. Miles is currently leading a large, controlled study aiming to quantify the ways in which doing good may help to counter the anxiety and depression that currently undermines the health and well-being of many people in all walks of life.And the need for kindness may have never been greater. The economic, educational and vocational stresses associated with the pandemic continue to take a toll. In addition, the media, the internet, and even neighborhood streets are often filled with physical threats and hateful remarks directed at large segments of the population.Although members of minority groups, be they racial, ethnic, religious or sexual, are increasingly willing to speak out against verbal and physical attacks and discrimination, many targeted individuals continue to suffer in silence. Little wonder that rates of anxiety and depression remain high.Children, who can readily sense the emotional distress of their caregivers, often share the pain. But experts say there’s an antidote that could benefit everyone. They call it “prosocial behavior,” or acting in ways that help other people.In her recently published book, “Social Justice Parenting,” Traci Baxley, an associate professor of education at Florida Atlantic University, emphasizes the rewards of teaching compassion and kindness to a new generation. Her goal in fostering a more just world for all is to raise children “who can ultimately self-advocate, empathize with others, recognize injustice, and become proactive in changing it.”Her book, which I found hard to put down, is replete with excellent examples and advice that can help parents raise children with a healthy self-image and regard for the welfare of others. She wrote, “It is our obligation to teach our children to stand up and be allies for groups that are marginalized and silenced.”Dr. Baxley, the mother of five children, told me that upon returning to school after the pandemic lockdown, many young people experienced an increase in depression and social anxiety that can be counteracted by prosocial behavior. “Just seeing compassion and kindness in action releases chemicals in the brain that helps them calm down,” she said. “It slows the heart rate and releases serotonin that counters symptoms of depression.”Prosocial behavior may come naturally to some. Even children as young as 2 or 3 may spontaneously share a treat or toy with an unhappy playmate. But most children likely need to learn it from the same people who teach them to say “please” and “thank you,” and the earlier in life that happens, the better.For starters, prosocial behavior requires compassion and empathy, the ability to recognize and care about the needs and well-being of others. But compassion without constructive follow-up benefits no one. Step two is kindness, a.k.a., compassion in action. You may be distressed to see an elderly person struggling with heavy packages, but unless you offer to help or at least express a wish to help but explain why you can’t, your compassion goes to waste.One of my proudest moments as a grandmother was learning that a grandson, then in first grade, comforted a classmate who’d become motion sick on a school bus trip. While other children on the bus moved away in disgust, my grandson put his arm on the ill child and asked if he felt better.As my four grandchildren continued to grow, I realized that all of them had too much “stuff” and I’d been remiss by adding to the pile with my holiday gifts of toys and clothes. Henceforth, I told them, I would give them money to donate to any nonprofit group they choose that works to better the lives of others or the world. One boy picked a tutoring program for needy children; one chose an afterschool sports program; another with deep interest in the environment sent his gift to the American Forests; and the youngest, age 10, gave to a local food bank.Dr. Baxley recounts similar episodes in “Social Justice Parenting.” She tells of a son’s excitement at finding a $20 bill, then soon after giving it to an immigrant family holding a sign that read “Can you please help us with our rent?”Too often, Dr. Baxley said, parents place a higher value on getting good grades or winning at sports than on helping people who need it. She said it’s also important to foster a child’s emotional well-being by accepting and nurturing the child you have, not trying to forcefully create the one you want. A child who lacks athletic ability and spurns sports should not be made to participate in one because the parent values it and it could help the child get into college, she said.As a parent of biracial children and an educator, Dr. Baxley recognizes the challenges parents face when dealing with sensitive issues like race, disability, gender nonconformity and homelessness. But she urges parents not to let fear stand in the way of productive conversations. She maintains that even the most difficult topics, like racism, bullying, sexism and death, can be discussed sensitively and sincerely in terms that are age appropriate.Here are some of her suggestions.Listen and be attentive.Instead of trying to find solutions for your children’s concerns, she wrote, “listen with the intent to hear and understand their feelings. Don’t jump in and try to fix the issue or attempt to have the ‘right’ answers to their questions.”It’s not just what you say; it’s how you say it.You won’t always know the right things to say, but it’s important to acknowledge the child’s feelings, avoid being critical, say what you think without judgment and invite feedback. For example, if your young child asks why a homeless person is so dirty, explain that the person has no home and no bathroom and perhaps even suggest making a donation of clothing or food to a homeless shelter.Take action when possible.When dealing with major events and social justice issues, like an environmental catastrophe, the death of a loved one, police killing of Black people, or protests against injustice, strive to clarify misinformation. Perhaps read a book together that helps children deal with painful events, and discuss what action they might consider to mitigate the circumstances.

Researchers at the University of Gothenburg now associate elevated levels of the protein galectin-1 with increased risk of developing type 2 diabetes about 18 years later. At the same time, this protein seems to be a protective factor for the kidneys among type 2 diabetes patients at high risk for diabetic nephropathy.
Findings of the study, a collaboration with researchers at Lund University, have been published in the journal Diabetologia. The researchers point to both negative and positive links between the protein galectin-1 and type 2 diabetes. In a general population, galectin-1 may be associated with an increased risk of diabetes, but in patients with a subtype of diabetes that increases the risk of kidney damage, galectin-1 appears to be beneficial, as patients with high galectin-1 levels in their blood suffer less kidney damage.
“This is probably not as strange as it might sound. My own personal theory is that the actions of galectin-1 found in the kidney are linked to inflammatory processes, whereas the actions of galectin-1 in the adipose tissue appear to be largely linked to metabolic processes. Thus, we can expect to see different mechanisms at work and different outcomes for the same protein,” says Emanuel Fryk, one of the study’s lead authors. Fryk is a resident physician in general medicine and a doctoral student at Sahlgrenska Academy, University of Gothenburg.
Counteracts inflammation
Galectin-1, a protein expressed by fat cells as well as other cells, is involved in both the regulation of inflammation and the function of fat cells in the body. Five years ago, the research team at the University of Gothenburg presented results from a study of individuals with newly diagnosed type 2 diabetes and healthy controls. They proposed that the protein could be involved in pathophysiological mechanisms in the adipose tissue in type 2 diabetes development. Later the team also showed that the protein was linked to higher insulin levels in the blood of one thousand participants in a study known as the Swedish CArdioPulmonary bioImage Study (SCAPIS). The protein was associated with increased insulin levels after adjusting the analysis for known risk factors in type 2 diabetes, such as obesity, age, and gender.
In the Malmö Diet and Cancer Study, the researchers have now been able to confirm that galectin-1 plays a significant role in disease development in type 2 diabetes. In this large population study, participants are also followed over time. The study incorporates analyses of blood samples from more than 4,000 participants, collected between 1991 and 1994. Galectin-1 levels in blood samples was analyzed in order to assess the relation to risk of developing type 2 diabetes, around 18 years after the sample was initially collected. The authors do not propose that galectin-1 should become a new tool in primary care to predict who will develop diabetes, but this is a step forward in better understanding the disease.
“This is an important piece of the puzzle in the research field on why obesity is such a big risk factor for the disease. It is a new clue for scientist trying to find out exactly what happens in the body of individuals with obesity who later develop type 2 diabetes.”
Protection from renal failure
Type 2 diabetes is a complex disease, in which many factors contribute to the development of the disease. One of the most serious complications is chronic kidney disease, which about half of those who have type 2 diabetes develop. The organ damage is permanent and can lead to premature death. For that reason, researchers also looked more closely at those afflicted with kidney disease
and found links to galectin-1 also in this context. By combining genetic analyses and measurements of galectin-1, they could examine the genetic link between galectin-1 and developing diabetes and kidney disease in another Scania based study, but only including individuals with diabetes: the All New Diabetics in Scania (ANDIS) study. The ANDIS study has previously proposed that diabetes can be separated into five subgroups, with one group at significantly higher risk of diabetic renal disease. The subgroup, labeled SIRD (severe insulin-resistant diabetes), is characterized by excess weight and severe insulin resistance.
Based on analysis from the ANDIS study, the researchers now show that elevated levels of galectin-1 may offer protection against kidney damage for this group of patients.
“In two large population-based cohorts in southern Sweden, we demonstrate that galectin-1 is linked to renal function and has potentially prophylactic effects against renal failure among some patients with type 2 diabetes. This puts a new candidate on the table that should be studied as a potential target when developing future pharmaceuticals.”
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Ischemia, which in modern Latin means, “staunching of blood,” is a medical condition in which the blood supply is cut off to different parts of the body. In patients who are bed-ridden, ischemia can manifest as pressure ulcers. Else, it could be the Raynaud’s phenomenon in someone under severe stress. This condition can be rescued by blood reperfusion to the affected areas. However, the latter carries the risk of injuries known medically as ischemia-reperfusion (I/R) injuries.
Skin-based I/R injuries can be exacerbated by inherited immunological mechanisms, for instance in patients who are otherwise showing signs of slow wound healing. To understand the immunological mechanisms underlying the development of this condition better, scientists from Japan, building on previous studies, decided to narrow down their investigation to interleukin-36 receptor antagonist (IL-36Ra), a protein that plays a pivotal immunomodulatory role in wound healing.
Speaking about the motivation behind their research, Mr. Yoshihito Tanaka from Fujita Health University School of Medicine, Japan, who led the team of scientists in the investigation, explains, “We wanted to understand the immunological mechanisms involved in the healing of wounds from cutaneous ischemia-reperfusion injuries, such as pressure ulcers and Raynaud’s phenomenon, to narrow down possible therapeutic targets. Drawing from experience, IL-36Ra appeared to be a promising candidate for kickstarting our investigation.”
Accordingly, Mr. Tanaka worked with his team to understand how deficiency of IL-36Ra affects wound healing in cutaneous I/R injuries. For this, the scientists used mice knocked out for the receptor. Also, they induced cutaneous I/R injuries in knockout and wildtype control mice. Subsequently, they studied corresponding immunological responses in both groups of animals, including the time required for wound healing, infiltration of neutrophils/macrophages (key immune cells) to the site of the wounds, apoptotic skin cells, and activation of other unwanted immunological defense mechanisms. Their findings have been published as a research article in the Journal of The European Academy of Dermatology and Venereology.
The team, comprising Dr. Kazumitsu Sugiura and Dr. Yohei Iwata from Fujita Health University School of Medicine, among others, was able to pinpoint important results. The scientists found that the absence of IL-36Ra, indeed, significantly slows down wound healing in cutaneous I/R injuries, through increased apoptosis, or ‘suicide’ of useful skins cells, excessive recruitment of inflammatory cells, and employment of unnecessary proinflammatory mechanisms. Additionally, they demonstrated the role of Cl-amidine, a protein-arginine deiminase inhibitor as effective in normalizing exacerbated I/R injury in IL-36Ra mice. Based on these observations, the scientists assert their findings are the first conclusive report of the involvement of IL-36Ra in cutaneous I/R injury.
The scientists are positive that they have identified a stalwart therapeutic candidate against cutaneous I/R injuries in IL-36Ra. As Mr. Tanaka optimistically adds, “Our research may lead to the development of therapeutic agents for wound healing of various other refractory skin diseases too.”
The quest for novel therapeutic targets in skin wound healing might just have been empowered by these findings of the team and the future indeed looks brighter for alleviating the painful burden of cutaneous I/R injuries.
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The membranes of cancer cells are more pliant than the membranes of normal cells. A research collaboration has discovered that cancer invasion and migration can be supressed in mice by manipulating the stiffness of the cell membrane. The research group included Lecturer TSUJITA Kazuya and Professor ITOH Toshiki, both of Kobe University’s Biosignal Research Center, and Lecturer SATOW Reiko and Professor Emeritus FUKAMI Kiyoko from Tokyo University of Pharmacy and Life Sciences.
It is hoped that this finding can be applied to the development of novel cancer treatments that exploit the physical characteristics of cells.
These research results were published in Nature Communications on October 11, 2021. Cancer cell membranes are softer compared to those of normal cells. By increasing the membrane tension of cancer cells, the research group succeeded in supressing their migration and invasion in a mouse model. This will contribute towards new treatments that target the physical characteristics of cancer cells.Metastasis is the major cause of cancer-related deaths. As a cancer cell’s malignancy increases, it undergoes amoeba-like structural changes that enable it to migrate more easily. It moves away from the primary lesion, triggering distant metastasis. In recent years, research has revealed that these significant changes to cellular structure and motility are controlled by the physical characteristics of the cell itself. In fact, it has been reported that cancer cells are comparatively ‘soft’ compared to normal cells. The connection between changes in a cell’s physical characteristics and its malignancy has received much attention. However, is not known exactly which physical characteristics are related to a cell’s cancerous nature.
In their research, Tsujita et al. used optical tweezers* to pull the cell surface membrane and analyse it, which enabled them to determine that cancer cells are comparatively softer than normal cells. The firmness of the cell membrane is regulated by the actin cytoskeletal networks that attach to it. This study revealed that in cancer cells, the ERM proteins that maintain this membrane-actin attachment are dissociated from the cell membrane, which makes the membrane soft.
By securely attaching ERM proteins to cancer cell membranes, the researchers were able to restore the membrane-actin attachment so it resembled that of a normal cell. This caused the cancer cell membrane to stiffen and prevented abnormal changes in structure and motility. Furthermore, breast cancer cells with stiffened membranes lost the ability to spread to the lungs in experiments using a mouse model. These results indicate that it could be possible constrain the spread of cancer by manipulating cell membrane tension.
Further Developments
The findings of the current research study could lead to the development of new cancer treatments that exploit the physical characteristics of cancer cells. If the chemical compound that stiffens cell membranes is discovered, then it may also be possible to utilize this in effective medication to prevent cancer invasion and migration.
Glossary
*Optical tweezers: Optical tweezers are concentrated beams of laser light that can be used to trap and move microbeads. Attaching these trapped microbeads to the cell membrane and pulling them forms a membrane tether (a string-like structure) enabling the cell membrane tension to be measured. This functions like a microscopic spring gauge. In 2018, the development of the optical tweezers was awarded the Nobel Prize in Physics.
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