Publisher Health

New research has identified the child cancer patients at greatest risk of developing life-threatening infections, in a crucial step towards the development of an early diagnostic test.
There is currently no clinical test to identify which children are likely to develop severe infections during febrile neutropenia (FN) — a condition common in chemotherapy patients — from those who are at low risk.
This landmark study, led by WEHI in Melbourne, could prevent thousands of low-risk cancer patients worldwide from undergoing unnecessary treatment and potentially disrupting their chemotherapy.
At a glance Study identifies first immune profiles in children with cancer that could identify those at risk of serious infection during febrile neutropenia (FN). There was previously no way of determining the patients who will have a benign or severe FN infection. All child cancer patients with FN are currently treated as high-risk and receive intravenous antibiotics, despite less than a quarter of cases requiring it. Milestone discovery could lead to a diagnostic test to identify children at risk of severe FN infections, preventing thousands of patients worldwide from receiving unnecessary and potentially disruptive medical treatment.Children who are given chemotherapy have weakened immune systems, putting them at an elevated risk of contracting potentially life-threatening infections.
Any cancer patient that currently presents to hospital with FN is immediately given intravenous antibiotics to prevent possible infectious complications. While less than a quarter of FN cases will become potentially life-threatening, there is currently no way to determine which patients will fall into this category.

p53 is one of the most important proteins in cancer biology. Often referred to as a “guardian of the genome,” p53 becomes activated in response to various cellular stressors like DNA damage. Its activation induces different processes, such as controlled cell death, that prevent cancer development if a cell becomes abnormal. Because of this, p53 mutations are extremely common in cancers, including hepatocellular carcinoma. However, in a recent article published in Cancer Research, a team of researchers at Osaka University observed that constant activation of p53 in liver cells of patients suffering from chronic liver disease (CLD) could actually promote the development of liver cancer.
CLD can be brought on by different factors including viruses, alcohol use, and fat accumulation, all of which can induce p53 activation. Previous studies have shown that p53 is in a constant state of activation in the liver cells of CLD patients. Yet, it is not clear what role this plays in CLD pathophysiology.
“Clinical data clearly show that p53 is activated in the hepatocytes of individuals with CLD,” says Yuki Makino, lead author of the study. “Because p53 is such a vital part of how the human body prevents tumor formation, its role in CLD became even more intriguing.”
To address their questions, the team generated a mouse model with p53 accumulation in hepatocytes. This was done by deleting Mdm2, the protein responsible for regulating p53 expression by targeting it for degradation. These mice developed liver inflammation with higher amounts of hepatocyte apoptosis and senescence-associated secretory phenotype (SASP), a phenomenon where cells produce signals within the microenvironment that can cause nearby cells to become cancerous. In fact, mice with p53 accumulation did have increased liver tumor development.
“We also observed an expanded population of hepatic progenitor cells (HPCs), which have stem cell-like characteristics,” explains senior author Tetsuo Takehara. “When the HPCs were isolated, grown in culture, and then injected under the skin of lab mice, these animals developed tumors. This suggested that HPCs played a key part in the liver tumor formation seen in the animals with p53 accumulation.”
Interestingly, acceleration of liver tumor development and the other observed phenotypes did not occur when p53 was deleted in addition to Mdm2 in the hepatocytes. These results demonstrated the significance of constant p53 activity in the tumorigenesis.
“We then compared samples from 182 CLD patients with 23 healthy liver samples,” says Dr. Makino. “The CLD liver biopsy samples showed activated p53 was positively correlated with apoptosis levels, SASP, HPC-associated gene expression, and later cancer development.”
The authors concluded that constitutively activated p53 in hepatocytes of CLD patients can create a microenvironment that is supportive of tumor formation from HPCs. Their work proposes a novel and paradoxical mechanism of liver tumorigenesis because p53 is one of the most well-known tumor suppressor genes. These data could highlight p53 as a potential cancer-prevention treatment target for CLD patients.
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Offering intensive, weekly telephone-based cessation counseling along with nicotine replacement for people who smoke and who were undergoing screening for lung cancer resulted in over a two-fold greater cigarette quit rate compared to people who received minimal counseling and nicotine replacement, according to results of a national, randomized trial conducted by investigators at Georgetown Lombardi Comprehensive Cancer Center and colleagues.
The findings appeared July 12, 2022, in JNCI and will be presented at the 2022 World Conference on Lung Cancer in Vienna, Austria, in August 2022.
People with a long-term smoking history are at high risk for lung cancer. Screening with computed tomography (CT) scans can potentially detect lung nodules early so that the disease can be treated in its less advanced stages. When undergoing CT screening, people are routinely offered cessation support, including counseling and nicotine replacement, to help them quit.
“Quitting smoking is very difficult and people who seek medication and support are more successful than those who try to quit on their own,” says Kathryn L. Taylor, Ph.D., professor in the Department of Oncology and a member of the Georgetown Lombardi Comprehensive Cancer Center’s Cancer Prevention and Control Program, and corresponding author of the study. “Importantly, making a quit attempt while undergoing lung screening may provide a boost to one’s motivation to stop smoking.”
The Georgetown Lung Screening, Tobacco, and Health trial randomized 818 people between 50 to 80 years of age with a 20-plus pack year smoking history (e.g., smoking two packs a day for a ten-year period equals 20 pack years). Enrollees at eight lung screening sites nationwide were randomly assigned to either intensive phone counseling of eight, 20-minute sessions along with up to eight weeks of nicotine patches, or three counseling sessions and two weeks of patches, which is similar to what many state tobacco quitlines currently offer people who call seeking assistance with quitting.
During the counseling sessions, tobacco treatment specialists discussed smoking-related goals, nicotine patch use, strategies to address triggers for smoking, readiness to quit, and confidence and motivation to quit.
“Tobacco treatment specialists met participants where they were in their readiness to quit — which ranged from not being ready to make any changes at the moment, but willing to talk about smoking, versus being very ready to quit and wanting specific ideas for making changes to their smoking habits,” notes Randi M. Williams, PhD, MPH, assistant professor in the Department of Oncology at Georgetown and second author of the study.
Self-reported 3-month quit rates were significantly higher in the intensive vs. minimal groups (14.3% vs. 7.9%). Importantly, quit rates that were verified by saliva strips or carbon monoxide tests were lower but with similar relative differences between groups (9.1% vs. 3.9%) of about two-to-one. Compared to the minimal arm, the intensive arm was more effective at spurring cessation among people with greater nicotine dependence (about a 3½ times greater benefit), normal screening results (over a 2½ times greater benefit), high engagement in counseling (a 3 times greater benefit) and patch use (a nearly 3 times greater use). Bolstering the value of intensive counseling for smoking cessation was a companion article appearing concurrently in JNCI Cancer Spectrum and led by researchers at the University of Michigan. The researchers found that even modest cessation rates achieved with intensive telephone counseling and nicotine replacement in the study group of people currently smoking and receiving lung screening led to savings in costs and lives compared to screening alone and would therefore be considered very cost-effective.
“Although the quit rates were modest overall, when comparing 3-month and12-month outcomes, both groups maintained the quit rates over time,” says Taylor. “Our next step is a planned trial with enhanced interventions and strategies to increase enrollment and treatment engagement among people undergoing lung screening in a large healthcare system, including underserved racial and ethnic minority groups, uninsured patients, and people not ready to quit.”
In addition to Taylor and Williams, the other authors from Georgetown include Tengfei Li, George Luta, Laney Smith, Kimberly M. Davis, Tania Lobo, Jeanne Mandelblatt, Jinani Jayasekera and Eric D. Anderson. Cassandra Stanton is at Westat, Rockville, Maryland; Raymond Niaura and David Abrams are at New York University, New York; Rafael Meza, Jihyoun and Jeonand Pianpian Cao are at the University of Michigan, Ann Arbor.
This study was supported by National Cancer Institute (NCI) grants R01CA207228 and R01CA207228-S1 as part of the NCI’s Smoking Cessation at Lung Examination (SCALE) collaboration.

Scientists from the University of Birmingham have shown that a brain-penetrating candidate drug currently in development as a cancer therapy can foster regeneration of damaged nerves after spinal trauma.
The research, published today in Clinical and Translational Medicine, used cell and animal models to demonstrate that when taken orally the candidate drug, known as AZD1390, can block the response to DNA damage in nerve cells and promote regeneration of damaged nerves, so restoring sensory and motor function after spinal injury.
The announcement comes weeks after the same research team showed a different investigational drug (AZD1236) can reduce damage after spinal cord injury, by blocking the inflammatory response. Both studies were supported by AstraZeneca’s Open Innovations Programme, which shares compounds, tools, technologies and expertise with the scientific community to advance drug discovery and development.
AZD1390 is also under investigation by AstraZeneca to block ATM-dependent signalling and repair of DNA double strand breaks (DSBs), an action which sensitizes cancer cells to radiation treatment. The DNA Damage Response system (DDR) is activated by DNA damage, including DSBs in the genome, which occur in several common cancers and also after spinal cord injury.
Professor Zubair Ahmed, from the University’s Institute of Inflammation and Ageing and Dr Richard Tuxworth from the Institute of Cancer and Genomic Sciences hypothesized the persistent activation of this system may prevent recovery from spinal cord injury, and that blocking it would promote nerve repair and restore function after injury.
Their initial studies found that AZD1390 stimulated nerve cell growth in culture, and inhibited the ATM protein kinase pathway — a critical biochemical pathway regulating the response to DNA damage.
The researchers then used animal models to investigate the effect of AZD1390 following spinal cord injury. Here they showed that oral treatment with AZD1390 resulted in significant suppression of the ATM protein kinase pathway, nerve regeneration beyond the site of injury, and the ability of these nerves to carry electrical signals across the site of the injury.
Professor Ahmed commented: “This is an exciting time in spinal cord injury research with several different investigational drugs being identified as potential therapies for spinal cord injury. We are particularly excited about AZD1390 which can be taken orally and reaches the site of injury in sufficient quantities to promote nerve regeneration and restore lost function.
“Our findings show a remarkable recovery of sensory and motor functions, and AZD1390-treated animals being indistinguishable from uninjured animals within 4 weeks of injury.”
Dr Tuxworth added: “This early study shows that AZD1390 could be used as a therapy in life-changing conditions. In addition, repurposing this existing investigational drug potentially means we can reach the clinic significantly faster than developing a new drug from scratch.”
University of Birmingham Enterprise has filed a patent application covering inhibition of the ATM/Chk2 DNA damage response pathway by compounds such as AZD1390, that may represent a potential therapeutic strategy to foster nerve repair.
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An international research group has investigated the mechanisms of cell migration and the impact of tissue rigidity on cell positioning and steering. The research sheds light on e.g. cancer cell migration and opens new possibilities for stopping and directing it.
Have you ever considered why different parts of your body feel hard or soft and what this might mean in terms of your health? Cell biologists from the University of Turku, Finland, together with an international multidisciplinary team of scientist have uncovered for the first time how tissue stiffness determines cell positioning and regulates all types of cell migration ranging from the neuronal growth cone turning to dissemination of malignant cancer cells in brain tumors and breast cancer.
Our bodies are built from billions of cells and each cell has it specific task and carefully determined position within a tissue. Cell positioning is regulated by many factors, including tissue rigidity. Cells are capable of probing and sensing their environment, and different cell types have different preferences for optimal conditions. A little bit like Goldilocks in the story trying out the different beds of the bear family and finding one bed to be too soft, the other one two hard and one to be just right. While this has been well-known for a long time, it has remained a mystery to researchers how cells are able to steer themselves to the optimal environment.
“The prevailing view among scientists was that all cell types prefer high-rigidity environments and migrate towards increasing stiffness. This process has been coined the term ‘durotaxis’ — migration towards hard from Greek and Latin,” says Doctoral Researcher Aleksi Isomursu.
“I was visiting the University of Minnesota for a research project and noticed that brain cancer cells grown on engineered substrates with alternating stiffness show the opposite behavior they turned towards soft,” Isomursu continues.
This observation launched an interdisciplinary research project involving cancer cell biology, computational modelling and engineering and involving researchers from three continents. As the outcome, the researchers uncovered the basic mechanism all cell types use to steer themselves towards their optimal environment.
These results are likely to have medical relevance in the future in stopping and directing cancer cell migration.
“I experimented with different types of drugs and identified ones that could make brain cancer cells stop moving or change direction,” explains Postdoctoral Researcher Mathilde Mathieu.
Identification of the mechanism of cell steering provides explanations for many thus far mysterious steps in cancer dissemination, for example how cancer cells migrate out from the stiff core of a breast tumor.
“These findings have been gaining a lot of interest in researchers and we have even played around with the idea of launching a new term — ‘mollitaxis’, migration towards soft,” says the Principal Investigator of the laboratory at the University of Turku, Professor Johanna Ivaska.
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When infants breastfeed, they receive an immune boost that helps them fight off infectious diseases, according to recent research from Binghamton University Associate Professor of Anthropology Katherine Wander.
She is the lead author of “Tradeoffs in milk immunity affect infant infectious disease risk,” published this June in Evolution, Medicine, and Public Health. Co-authors include Masako Fujita from Michigan State University’s Anthropology Department, Siobhan Mattison from the University of New Mexico’s Anthropology Department and the National Science Foundation; and Frida Mowo, Ireen Kiwelu and Blandina Mmbaga in Tanzania, whose associations include the Kilimanjaro Christian Medical Centre and the Kilimanjaro Clinical Research Institute. Binghamton University graduate students were also part of the research team, with tasks ranging from data collection in Tanzania to data-cleaning and analysis. They include Margaret Duris, Megan Gauck, Tessa Hopt, Katherine Lacy, Angela Foligno, Rebecca Ulloa and Connor Dodge.
For the project, the research team studied almost 100 mother and baby pairs in rural Kilimanjaro. Prolonged breastfeeding is the norm in this population and infectious diseases during infancy are very common, even compared to other areas of East Africa. This makes Kilimanjaro an ideal setting to begin to understand how immune protection from milk might affect infectious disease risk, Wander said.
“You most often hear about the immune system of milk in terms of transferring maternal antibodies to infants via milk — which is probably very important — but it seems there’s much more going on as well. The immune system of milk is a whole system, capable of mounting immune responses,” Wander said. “We’re only beginning to understand the full extent and role of the immune system of milk.”
Milk and immunity
Mother’s milk contains everything needed to mount immune responses, from antibodies to multiple types of immune cells and more. While they originate from the mother’s immune system, these components of milk appear to be curated rather than selected at random from the mother’s blood, although that mechanism remains poorly understood, Wander explained.

“External self-talk,” as it’s clinically known, gets a bad rap. But it can be great for pushing through all sorts of obstacles.Trembling in bed at night, my blankets pulled tight over my head save for an opening I left my face, I would whisper my troubles to my closest confidant: Wall. Wall was the wall nearest my childhood bed and, other than the occasional stray bang or muffled skittering, a nonverbal communicator. That didn’t stop me from hearing and heeding his counsel. Nor did his cheap facade — brownish faux-wood paneling littered with stickers — temper my belief in his tender depths. Wall was a boy like me, but calmer, cooler, more reflective. He listened to me, debated me, grasped the ends of sentences I didn’t finish. Off him I could bounce ideas as well as balls until sleep finally conquered fright.I no longer speak to Wall or to any of his relations: Laces, Ceiling, cantankerous Floor. We seem to have forgotten how to communicate with one another. Besides, we hardly see each other anymore. Instead, I speak aloud to myself. At the museum where I work, I enumerate the day’s tasks and the tools they require: drill, star bit, mag tip, level. In the supermarket, I interrogate my mental shopping list and disparage myself for its illegibility: We need, um … noodles? Eggs? Do we? (Expletive.) I’ve become what I always was: my own Wall.Psychologists call what I do “external self-talk” to differentiate it from regular self-talk, otherwise known as one’s internal monologue or dialogue. Plenty of people do it — just watch a tennis match if you don’t believe me. It’s viewed as normal within certain bounds, even beneficial, though speaker discretion is advised. Like many normal behaviors, it’s also weird if the wrong person observes it, especially when you’re young.I’ve become what I always was: my own Wall.As a kid, I knew that if I talked to myself on school grounds, I risked becoming That Freak Who Talks to Himself, and that the act’s popular associations — acute psychosis, maladjustment — tend toward the negative. Stigma kept me quiet, but its potency diminished as I aged. Also: Look around. People walk the streets talking and gesticulating, tiny white buds in their ears. They pontificate to phone cameras. Determining which unseen audience a pedestrian is addressing has become too difficult a calculation to bother solving; fading self-consciousness and the strange effects of consumer electronics have freed me.Still, I tend to be alone in my apartment or office for my liveliest conversations. They often kick up when I reach an impasse while writing and follow a regular loop. Pressure accumulates until release becomes inevitable. No longer will my internal monologue suffice. The harder reality of spoken language starts to steam out of my mouth. I curse myself. I catch myself. My mutterings invert to a plastic positivity: You’re not the worst person; you needn’t disappear into the ether. Rather, you are good and capable and quite possibly fine. Referring to myself as “you” happens unconsciously, as the voice speaking and the ear hearing edge apart. The gap widens. First person jumps to second. When my assurances fail to assure me, I try a Beckett impression and general advice: You must go on, you’ll go on. As stuck as ever, I gradually transform my pep talk into a kind of psychodynamic session with the self through which I discern the shape of my blockage. I get practical: Break your problem into parts, describe what’s missing, incorporate what impedes you. The distance of “you” finally affords perspective and authority. I make a change. I call it progress. Bubbles of genuine self-belief surge: You can do this; then, I can do this; then, Let’s do this. How could I have doubted myself? Later I’ll sight another impasse, and the process will repeat.Others might prefer to call a friend for help. Why not turn outward? Isn’t this talking to yourself a little antisocial? While I have yet to forswear friendship and its succor entirely — maybe one day! — I have found that vocalized self-analysis, and the willingness to trudge through intellectual and moral quandaries in noisy solitude, is a valuable complement to more traditional conversational outlets, especially when it comes to creative thinking. When I asked friends if they talk to themselves, one described free-associating and playacting to prepare for high-stakes meetings. Another friend, a photographer, refines his intended aesthetic for a job by talking it through, out loud, and anticipates how he’ll deal with hypothetical difficulties come shoot day.Clearly, the twin phenomena of wellness and self-optimization thrum under the hood here. One can imagine the S.E.O.-inspired headlines: “How Talking to Yourself Can Help You Work Smarter, Faster.” Fair enough, but external self-talk is also a means of negotiating who one is and might be. The fear we associate with a person who publicly talks to themselves at length, and without apparent concern for or awareness of the impact their performance has on those around them, is the fear of an eroding self, its supposed constancy and singularity unraveling, its loose threads chatting with each other chaotically. But the act of speaking to myself is a reminder that constancy and singularity are illusory to begin with. That my multiplicity is, in turn, a kind of promise: I needn’t be as I am. You needn’t, either. We might be different than expected in a minor way. Or we might be able to formulate a difficult sentence, which might lead to a paragraph, then a fresh piece, then a new person. Probably not — very probably talking to yourself will not change the world. It may not even radically change you. But the dialogue between current and potential selves is small proof that such change is possible. Or maybe that’s just something I like to tell myself.Paul McAdory is a writer and an editor at Guernica. He has a column forthcoming from Astra Magazine.

Triptans, a commonly prescribed class of migraine drugs, may also be useful in treating obesity, a new study by scientists at UT Southwestern suggests. In studies on obese mice, a daily dose of a triptan led animals to eat less food and lose weight over the course of a month, the team reported in the Journal of Experimental Medicine.
“We’ve shown that there is real potential to repurpose these drugs, which are already known to be safe, for appetite suppression and weight loss,” said study leader Chen Liu, Ph.D., Assistant Professor of Internal Medicine and Neuroscience and an investigator in the Peter O’Donnell Jr. Brain Institute.
Obesity affects more than 41% of all adults in the U.S. and increases the risk of heart disease, stroke, diabetes, and certain types of cancer. Most treatments for obesity focus on eating habits and physical activity.
Scientists have long known that serotonin, a chemical messenger found throughout the brain and body, plays a key role in appetite. However, there are 15 different serotonin receptors — molecules that sense serotonin and signal for cells to change their behavior in response. Researchers have struggled to understand the role of each serotonin receptor in appetite, and previous drugs — including fen-phen and lorcaserin (Belviq) — that targeted certain individual receptors have been withdrawn from the market due to side effects.
Triptans, which are used to treat acute migraines and cluster headaches, work by targeting a different receptor — the serotonin 1B receptor (Htr1b) — that had not previously been well studied in the context of appetite and weight loss, said Dr. Liu.
For the new study, the researchers tested six prescription triptans in obese mice that were fed a high-fat diet for seven weeks. Mice fed two of these drugs ate about the same amount, but mice fed the other four ate less. After 24 days, mice given a daily dose of the drug frovatriptan lost, on average, 3.6% of their body weight, while mice not given a triptan gained an average of 5.1% of their body weight. Dr. Liu and his colleagues saw similar results when they implanted devices into the animals that gave them a steady dose of frovatriptan for 24 days.

It takes a lot of time — and money — to diagnose Alzheimer’s disease. After running lengthy in-person neuropsychological exams, clinicians have to transcribe, review, and analyze every response in detail. But researchers at Boston University have developed a new tool that could automate the process and eventually allow it to move online. Their machine learning-powered computational model can detect cognitive impairment from audio recordings of neuropsychological tests — no in-person appointment needed. Their findings were published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association.
“This approach brings us one step closer to early intervention,” says Ioannis Paschalidis, a coauthor on the paper and a BU College of Engineering Distinguished Professor of Engineering. He says faster and earlier detection of Alzheimer’s could drive larger clinical trials that focus on individuals in early stages of the disease and potentially enable clinical interventions that slow cognitive decline: “It can form the basis of an online tool that could reach everyone and could increase the number of people who get screened early.”
The research team trained their model using audio recordings of neuropsychological interviews from over 1,000 individuals in the Framingham Heart Study, a long-running BU-led project looking at cardiovascular disease and other physiological conditions. Using automated online speech recognition tools — think, “Hey, Google!” — and a machine learning technique called natural language processing that helps computers understand text, they had their program transcribe the interviews, then encode them into numbers. A final model was trained to assess the likelihood and severity of an individual’s cognitive impairment using demographic data, the text encodings, and real diagnoses from neurologists and neuropsychologists.
Paschalidis says the model was not only able to accurately distinguish between healthy individuals and those with dementia, but also detect differences between those with mild cognitive impairment and dementia. And, it turned out, the quality of the recordings and how people spoke — whether their speech breezed along or consistently faltered — were less important than the content of what they were saying.
“It surprised us that speech flow or other audio features are not that critical; you can automatically transcribe interviews reasonably well, and rely on text analysis through AI to assess cognitive impairment,” says Paschalidis, who’s also the new director of BU’s Rafik B. Hariri Institute for Computing and Computational Science & Engineering. Though the team still needs to validate its results against other sources of data, the findings suggest their tool could support clinicians in diagnosing cognitive impairment using audio recordings, including those from virtual or telehealth appointments.
Screening before Symptom Onset
The model also provides insight into what parts of the neuropsychological exam might be more important than others in determining whether an individual has impaired cognition. The researchers’ model splits the exam transcripts into different sections based on the clinical tests performed. They discovered, for instance, that the Boston Naming Test — during which clinicians ask individuals to label a picture using one word — is most informative for an accurate dementia diagnosis. “This might enable clinicians to allocate resources in a way that allows them to do more screening, even before symptom onset,” says Paschalidis.
Early diagnosis of dementia is not only important for patients and their caregivers to be able to create an effective plan for treatment and support, but it’s also crucial for researchers working on therapies to slow and prevent Alzheimer’s disease progression. “Our models can help clinicians assess patients in terms of their chances of cognitive decline,” says Paschalidis, “and then best tailor resources to them by doing further testing on those that have a higher likelihood of dementia.”
Want to Join the Research Effort?
The research team is looking for volunteers to take an online survey and submit an anonymous cognitive test — results will be used to provide personalized cognitive assessments and will also help the team refine their AI model.
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Materials provided by Boston University. Original written by Gina Mantica. Note: Content may be edited for style and length.

Producing biomaterials that match the performance of cartilage and tendons has been an elusive goal for scientists, but a new material created at Cornell demonstrates a promising new approach to mimicking natural tissue.
The results were published July 8 in the Proceedings of the National Academy of Sciences, and provide a new strategy for synthesizing clinical solutions for damaged tissue.
Tissue has to be soft enough to bend and flex, but durable enough to withstand prolonged loading — for example, the weight a knee tendon must support. When tissue wears out or is damaged, collagen hydrogels and synthetic materials have the potential to serve as replacements, but neither alone possesses the right combination of biological and mechanical properties of natural tissue.
Now, Cornell researchers have engineered a biohybrid composite material with the essential characteristics of a natural tissue. The material consists of two main ingredients: collagen — which gives the material its softness and biocompatibility — and a synthetic zwitterionic hydrogel, which contains positively and negatively charged molecular groups.
“These charge groups interact with the negatively and positively charged groups in the collagen, and this interaction is what enables the materials to dissipate energy and achieve high levels of toughness,” said Lawrence Bonassar, the Daljit S. and Elaine Sarkaria Professor in Biomedical Engineering in the College of Engineering and co-lead author of the study.
The biohybrid composite approaches the performance of articular cartilage and other biological tissues, possessing 40% more elasticity and 11 times the fracture energy — a measure of durability — of the zwitterionic material by itself.
Nikolaos Bouklas, assistant professor in the Sibley School of Mechanical and Aerospace Engineering and co-lead author of the study, said the material’s biocompatibility means it can recruit cells and keep them alive.
“Ultimately, we want to create something for regenerative medicine purposes, such as a piece of scaffold that can withstand some initial loads until the tissue fully regenerates,” Bouklas said. “With this material, you could 3D print a porous scaffold with cells that could eventually create the actual tissue around the scaffold.”
In addition, the biohybrid material is self-assembling once the two ingredients are mixed, Bouklas said, creating “the same interconnected network of collagen seen in natural cartilage, which otherwise would be extremely hard to produce.”
The research brought together four research labs from three different departments thanks to a seed grant from the Cornell Center for Materials Research. The collagen used in the biohybrid composite had already been under development in Bonassar’s lab, while the zwitterionic hydrogel was developed by the study’s co-authors Robert Shepherd, associate professor in the Sibley School, and Emmanuel Giannelis, the Walter R. Read Professor of Engineering in the Department of Materials Science and Engineering.
The study’s authors are continuing to research the material and the molecular processes behind its synthesis. Bonassar said the material is well suited for the type of bioprinting pioneered in his lab, and the authors have begun experimenting with using it as a 3D-printing material.
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Materials provided by Cornell University. Original written by Syl Kacapy, College of Engineering, courtesy of the Cornell Chronicle. Note: Content may be edited for style and length.