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A study published in Science Translational Medicine performed at the Latner Thoracic Surgery Research Laboratories and UHN’s Ajmera Transplant Centre has proved that it is possible to convert blood type safely in donor organs intended for transplantation. This finding is an important step towards creating universal type O organs, which would significantly improve fairness in organ allocation and decrease mortality for patients in the waitlist.
“With the current matching system, wait times can be considerably longer for patients who need a transplant depending on their blood type,” explains Dr. Marcelo Cypel, Surgical Director of the Ajmera Transplant Centre and the senior author of the study.
“Having universal organs means we could eliminate the blood-matching barrier and prioritize patients by medical urgency, saving more lives and wasting less organs,” adds Dr. Cypel, who is also a Thoracic Surgeon at UHN’s Sprott Department of Surgery, a Professor in the Department of Surgery at U of T and the Canada Research Chair in Lung Transplantation.
Blood type is determined by the presence of antigens on the surface of red blood cells — type A blood has the A antigen, B has the B antigen, AB blood has both antigens and O has none. Antigens can trigger an immune response if they are foreign to our bodies. That is why for blood transfusions we can only receive blood from donors with the same blood type as ours, or universal type O.
Likewise, antigens A and B are present on the surfaces of blood vessels in the body, including vessels in solid organs. If someone who is type O (meaning they have anti-A and anti-B antibodies in their blood stream) received an organ from a type A donor, for example, the organ in all likelihood would be rejected. Consequently, donor organs are matched to potential recipients in the waitlist based on blood type, among other criteria.
Patients who are type O wait on average twice as long to receive a lung transplant compared to patients who are type A, explains Dr. Aizhou Wang, Scientific Associate at Dr. Cypel’s lab and first author of the study.

Although fractures normally heal, bone will not regenerate under several circumstances. When bone does not regenerate, major clinical problems could result, including amputation.
To enhance the regeneration of bone, the Food and Drug Administration (FDA) approved recombinant human bone morphogenetic protein-2, or BMP-2. However, it is expensive and only moderately effective. It also produces side effects ? some severe.
Researchers at Mayo Clinic, along with colleagues in the Netherlands and Germany, may have a viable, less risky alternative: messenger RNA. This well-known platform for vaccines has already proven to be safe in human use by the FDA.
The findings in a study involving rats are published in Science Advances. These findings show that messenger RNA can be used at low doses to regenerate bone without side effects. Moreover, the quality of the new bone is superior to bone formed by BMP-2. The researchers also say that messenger RNA is a good choice for bone regeneration because it may not need repeat doses. Findings showed the new tissue growth that occurred after applying messenger RNA was biomechanically superior to the alternative method and remained so throughout eight weeks of monitoring.
Human bone develops in one of two ways: direct formation of bone cells from mesenchymal progenitor cells, or through endochondral ossification, in which cartilage forms first and then coverts to bone. The BMP-2 therapy uses the former method, and the messenger RNA approach uses the latter. In general, the researchers say their work proves that this method “can heal large, critical-sized, segmental osseous defects of long bones in a superior fashion to its recombinant protein counterpart.”
The researchers say these findings in rats are limited, and studies are needed in large animals before any translation can be considered for clinical trials.
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Materials provided by Mayo Clinic. Original written by Robert Nellis. Note: Content may be edited for style and length.

Acne is among the most common skin diseases in the United States, according to the American Academy of Dermatology Association, affecting up to 50 million Americans each year. It is also among the least studied.
It’s known that hair follicles assist in the development of a pimple, but new research suggests the skin cells outside of these hair follicles play a larger role. The findings published in the February 16, 2022 issue of Science Translational Medicine.
“These findings may transform the way we treat acne,” said Richard Gallo, MD, PhD, Ima Gigli Distinguished Professor of Dermatology and chair of the Department of Dermatology at UC San Diego School of Medicine. “Previously, it was thought that hair follicles were most important for acne to develop. In this study, we looked at the cells outside of the hair follicle and found they had a major effect on controlling bacteria and the development of acne.”
The cells are called fibroblasts, common in connective tissues throughout the body. In skin, they produce an antimicrobial peptide called cathelicidin, which plays a key role in acne development, said Gallo.
To counter an infection within a hair follicle, the surrounding skin undergoes a process called reactive adipogenesis in which fibroblasts transform into fat cells. Cathelicidin is produced as well to help combat the infection by suppressing bacteria that can cause acne.
The discovery of cathelicidin’s role came as a surprise.

With an alarming rise in the number of prescriptionss filled for non-benzo sleeping/z-drugs and anti-epilepsy gabapentinoids over the last two decades, researchers at Columbia University Mailman School of Public Health aimed to fill in the gap in knowledge in the proportion of overdose deaths involving those medications and learn more about their co-usage with other substances across U.S. demographics categories. They found that the proportion of overdose deaths involving these drugs increased more than three-fold between 2000 and 2018, coinciding with exponential prescription increases since their introduction into the market. Until now there was little data on overdose deaths involving non-benzodiazepines and gabapentinoids. The findings are published in The Lancet Regional Health- Americas.
More than 67 percent of those who died from overdoses with these drugs between 2000 and 2018 had also opioids in their system indicating that using more than one substance is the norm.
“These drug classes were introduced as less dangerous alternatives to opioids and benzodiazepines, creating perceptions among physicians and patients of their supposed increased safety, even without guidelines or data to back up such perceptions and leading to increases in prescribing,” said Silvia Martins, MD, PhD, professor of epidemiology at Columbia Mailman School, and senior author. “Approved for short-term treatment of insomnia, they were touted as safe alternatives to the popular benzodiazepines when introduced to the market as less prone to abuse or dependence. Yet, recent evidence suggests that this alternative may also be as harmful as the product it intended to replace partially. We felt it was critical to further explore and especially determine the dangers of their co-usage.”
Using data from the National Center for Health Statistics, the researchers calculated overdose death rate per 100,000 persons for every year between 2000 and 2018.
Between 2000 and 2018, 788,135 persons died with an overdose code as the underlying cause of death. Of those, 587,884 persons had any T or specific code for the drug involved among their multiple causes of death. In turn, 21,167 among those had a T42.6/T42.7 ICD code, which include gabapentinoids and z-drugs, among their multiple causes of death.
There were more intentional overdoses and a greater proportion of women, a greater share of whites, and those with higher educational background, who died from an overdose between 2000 and 2018 with a T code of T42.6/T42.7 ICD compared to the population of overall overdose casualties.

Proteins are the “workhorses” in every living cell and constitute the chemical basis of life. These little machines are required to turn food into energy, to manage motion and brain activities and to fight off bacteria and viruses. The function of proteins is tightly controlled in response to changing conditions, when for instance an organism encounters stress and needs to adapt. Researchers at the University of Göttingen recently discovered a completely novel group of proteins that functions as a switch to regulate biological activity. Now they have analyzed all known protein structures and it turns out that this group exists in all domains of life, in viruses and bacteria as well as in fungi, plants and animals, including humans. These findings have far-ranging implications for the treatment of many diseases. The results were published in Nature Chemical Biology.
The Göttingen University team initially discovered the new protein switch — known as a “NOS switch” because Nitrogen, Oxygen and Sulphur atoms are connected — in a protein from the human pathogen Neisseria gonorrhoeae. However, the question remained whether this switch was widespread in nature. The researchers have now analyzed the entire database of known protein structures held in a publicly accessible repository for hitherto undetected NOS switches. The computational analysis by first author Dr Fabian Rabe von Pappenheim, University of Göttingen, produced hundreds of hits, which were then all individually analysed in detail. “Investigating these structures was an exciting endeavour. It was like travelling into the unknown for us,” recalls Professor Kai Tittmann, University of Göttingen, who led the study.
The novel NOS switch was found to exist across all domains of life, and often at sites of proteins that are essential for biological function. Remarkably, numerous proteins from some of the most dangerous human pathogens have this switch, including a key enzyme from the SARS-CoV-2 coronavirus. In fact, this switch is a target for the recently approved antiviral drug for patients with mild to modrerate Covid-19 who might be at high risk of developing serious disease. In addition, the researchers discovered several new chemical forms of the NOS switch, which turns out to be a universally used regulation platform in biology. The identified proteins play central roles in almost every aspect of cellular activities, be it the expression of genes, signalling in and between cells, or metabolism.
“We believe that the discovery of these new protein switches will be a springboard for the development of a novel class of drugs that directly targets these switches,” says Tittmann. “Many human proteins with known roles in severe diseases as well as proteins from bacteria and viruses are now known to be controlled by such switches. The newly identified switch is likely to play a central role in regulating their biological function as well.”
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Materials provided by University of Göttingen. Note: Content may be edited for style and length.

In his new book, Johann Hari investigates how our brains have been broken by technology — and what we can do to fight back.The typical American worker focuses on a given task for just three minutes. Each day, we touch or check our phones more than 2,000 times, and spend more than three hours staring at them, on average. So says Johann Hari, an author who has previously written about depression and addiction, in his new book “Stolen Focus.” It is an investigation into how we got ourselves into this distracted state — what Mr. Hari describes as an “attention crisis.”Some factors that Mr. Hari identifies seem straightforward, like the current business model of Big Tech, which makes money in direct proportion to the attention people give it. Other factors he unearths are less commonly discussed, from what we eat (highly processed food, filled with refined carbohydrates) and how we sleep (by some accounts, less than we used to) to the nature of American childhood, with its widespread loss of autonomy. Mr. Hari calls for an “attention rebellion,” a drastic collective action to force major changes, such as instituting a four-day workweek and letting children have much more unsupervised free play.Here, condensed and edited for clarity, is a recent conversation with Mr. Hari about what it will take to reclaim our minds.Do you see a connection between the topics of your three books: depression, addiction and attention?J.H.: There’s always a mystery in my head that I genuinely want to investigate. With this book, I could feel my own attention getting worse. Things that required deep focus, that were core to my sense of self, like reading books and having deep conversations, were getting more and more like running up a down escalator. I could still do them, but they were getting harder. And I could see this happening to most people I knew.I also think there’s a deeper connection. With each of these phenomena — depression, addiction and our attention crisis — we think of them as primarily individual problems and individual flaws. But these are phenomena that are occurring within an environment. As Dr. Joel Nigg, a psychiatry professor who is one of the leading experts on children’s attention problems, put it to me, we need to ask if we are facing what he called an “attentional pathogenic culture,” a culture that is undermining the ability of most of us to focus.What about the pandemic? How have the events of these past two years contributed to our fractured sense of focus?J.H.: It has made us more stressed, and we know that stress triggers a state called vigilance — and vigilance is where you find it harder to focus because your brain is scanning the horizon for danger.The other thing is it’s given us this dystopian vision of the future. Naomi Klein argues that we suddenly got slammed forward to where we would have been in 15 years time with regard to technology. It has shown us a vision of the future that many of us hate. In the last two years, I have not once heard the phrase, “Hooray, another Zoom call!” So it’s given us a vision of the future we are moving toward that we can now consciously choose to abandon and move toward a much better future.On that subject: There are those, like the writer and tech expert Nir Eyal, who say we need to be individually accountable for our own discipline around screen time, rather than blame technology for our distractibility. You call this “cruel optimism,” which you define as a solution that sounds good, but won’t work.J.H.: At the start of the research for the book, I had essentially two stories for what had happened to me. I thought: “One, you’re lacking willpower. And two, someone invented the smartphone.” I decided to exert my willpower, and I went away without my smartphone for three months. I spent three months in Provincetown, Mass., completely offline, in a radical act of will. There were many ups and downs, but I was stunned by how much my attention came back. I could read books for eight hours a day. At the end of my time there, I thought, “I’m never going to go back to how I lived before.” The pleasures of focus are so much greater than the rewards of likes and retweets.Then I got my phone back, and within a few months, I was 80 percent back to where I had been. I only really understood why when I interviewed James Williams, who I would argue is the leading philosopher on attention in the world now, and he said to me, “It’s like you thought the solution to air pollution was for you personally to wear a gas mask.”I’m not against gas masks. Gas masks are great. But they’re not the solution for air pollution.If quitting technology for a sustained period of time isn’t the answer, what were some of the techniques you found effective on an individual level?J.H.: I sleep more, for at least eight hours. I have a time-locking container, which I put my phone in for four hours a day when I write. And I won’t sit down and watch a movie with my boyfriend unless we both lock away our phones.There are people who argue that worrying about the influence of Big Tech on our attention is just the latest moral panic, akin to the outrage that greeted the printing press. How do you respond when you hear that argument?I used to believe that this was the case. But I think the evidence is really overwhelming — and I think most people can see it. It’s also urgent because many of the factors that are invading our attention are poised to hugely accelerate. Think about how much more addictive TikTok is than Facebook. There has to be a movement on the other side, of all of us who say: “No, you don’t get to do this to us. We want to have a life where we can think deeply. We want to have a life where we can read books. We want to have a life where our children can hold conversations.”To that point, the diagnosis of A.D.H.D. has soared since the beginning of this century. Roughly six million American children are now diagnosed with it. But you unearthed ambiguity on this subject — researchers don’t agree on whether A.D.H.D. is a strictly “biological illness.”J.H.: Of all the topics in the book, this was the one where the scientists I interviewed disagreed the most. The evidence is fairly clear that there are some people whose genes make them somewhat more vulnerable to attention problems. However, the extent to which those attention problems are driven by biology has been somewhat overstated. This is the first human society ever that has tried to get kids to sit still for eight hours a day. No one has ever done that before because it’s an absolutely idiotic thing to do.So, I think the diagnosis of A.D.H.D. can be good because it tells children, “This is not your fault.” But I think it’s harmful to give them an exclusively biological story, saying, “This is just a problem in your brain.”Your solution to all of this is to start an “attention rebellion.” What does that look like?J.H.: The first step is consciousness raising. It’s everyone coming together and saying: You think you’re failing because you can’t focus, and actually it’s happening to all of us and it’s happening for big structural reasons.

A future vaccine providing protection against a wide range of coronaviruses that jump from their original animal hosts to humans — including SARS-CoV-2, the cause of COVID-19 — may be possible, say Johns Hopkins Medicine researchers, based on findings from their recent study.
In a paper posted online Jan. 21, 2022, in the Journal of Clinical Investigation, the research team focused on a peptide, or protein fragment, on the SARS-CoV-2 spike protein — the target of the two available messenger RNA (mRNA) vaccines for COVID-19 — called S815-827. Homologs (equivalent peptides) can be found on the spike proteins of MERS-CoV (the virus that causes Middle East Respiratory Syndrome, more commonly known as MERS, and believed to have been passed from camels to humans) and other animal coronaviruses. The researchers were particularly interested in studying the S815-827 homologs seen in coronaviruses hosted by bats because SARS-CoV-2 is believed to have risen from a bat species. Additionally, bat-borne coronaviruses are considered a major threat for producing future zoonotic (animal-to-human) diseases.
Previous research studies looking at a variety of human coronaviruses that cause the common cold have shown that homologs of the S815-827 peptide — also known as an epitope (a protein or portion of a protein that elicits an immune response) — are recognized by infection-fighting cells of the immune system called CD4+ T lymphocytes.
In the first part of their study, the Johns Hopkins Medicine researchers evaluated T cell response to the S815-827 epitope in 38 people who had received two doses of either the Moderna or Pfizer-BioNTech mRNA vaccines against SARS-CoV-2. They found that T cells specific to the peptide were produced by 16 (42%) of the study participants.
“This suggests that a significant portion of the vaccinated population might have T cells that produce an immune response to the epitope,” says study senior author Joel Blankson, M.D., Ph.D., professor of medicine at the Johns Hopkins University School of Medicine. “Since this particular spike protein component is believed to have an important functional role in SARS-CoV-2 infections and is considered less likely to change because of mutations, it’s an appealing target for future vaccines — especially if it also can protect against animal coronaviruses that might migrate to humans.”
CD4+ T lymphocytes are immune system cells, also known as helper T cells, because they assist another type of immune cell, the B lymphocyte (B cell), in responding to surface proteins — antigens — on viruses such as SARS-CoV-2. Activated by the CD4+ T cells, immature B cells become either plasma cells that produce antibodies to mark infected cells for disposal from the body, or memory cells that “remember” the antigen’s biochemical structure for a faster response to future infections. Therefore, a CD4+ T cell response can serve as a measure of how well the immune system responds to a vaccine and yields humoral immunity.

It is becoming increasingly clear that the human microbiome — the collection of bacteria, viruses and fungi that live on and within us — significantly contributes to our health. Indeed, several recent studies have demonstrated the contribution of the microbiome to regulating immune cells that influence bone health.
To find out more, researchers at the Medical University of South Carolina (MUSC) who study osteoimmunology, the interface of the skeletal and immune systems, have examined the impact of the oral microbiome on alveolar bone. The alveolar bone, commonly known as the jaw bone, is a unique bone tissue that houses and supports our teeth. Their results, published online on Jan. 25 in the Journal of Clinical Investigation Insight, showed that healthy microbes in the mouth activated a subset of immune cells within the alveolar bone marrow, which in turn promoted osteoclastic cells that are responsible for breaking down bone. They went on to show that depleting the healthy oral microbiome, using an antiseptic mouthwash, protected against this bone loss in preclinical models, demonstrating a direct link between microbes in the mouth and naturally occuring alveolar bone loss.
“The alveolar bone is different from other bone tissues due to its role in supporting the teeth,” said Chad M. Novince, D.D.S., Ph.D., associate professor in the colleges of Medicine and Dental Medicine, who studies the impact of the microbiome on osteoimmunology and skeletal metabolism. “What is most fascinating to me is that we were able to show that the commensal oral microbiota modulates the communication between immune cells and bone cells, separate from other microbiota communities, that impact alveolar bone health.”
“I think this is really only the start to understanding how the commensal oral microbiome can regulate alveolar bone health and homeostasis,” added Jessica D. Hathaway-Schrader, Ph.D., a postdoctoral scholar in the College of Dental Medicine and first author on this study.
Previously, the Novince lab utilized mouse models with a defined microbiota and showed that specific commensal microbes in the gut could influence normal skeletal development and homeostasis. In the current study, they focused on the oral cavity — a unique space in which the microbes colonizing the mouth are in close proximity to the underlying alveolar bone. Little was known about how interactions between microbes and immune cells in the oral cavity, compared with other anatomic sites, influence alveolar bone health.
In order to understand the interplay between microbes and immune cells within the oral cavity more fully, the Novince lab pioneered two new techniques. The first technique involved innovatively collecting bone marrow from the mandible of mice, which enabled the researchers to perform in-depth studies on immune cells within alveolar bone. The second technique involved developing a novel way to deplete microbes from the oral cavity of mice. The team utilized a unique delivery sponge loaded with chlorhexidine, an antiseptic used to treat gingivitis, to perform oral rinses on the mice.
With these innovations in hand, the team used the chlorohexidine rinse to deplete the commensal oral microbiota. Suppressing the commensal microbial load in the oral cavity, while not altering the commensal microbiota at other sites, dampened the immune response in the alveolar bone marrow. This dampened immune response suppressed bone resorbing osteoclast cells, which had an overall protective effect on alveolar bone loss that naturally occurs due to the burden of commensal microbes.
Analysis of the bone marrow within the mandibles of mice revealed that a subset of immune cells were activated by the presence of commensal oral microbes. One important class of activated immune cells were dendritic cells. These cells act like sentinals of the immune system and alert other immune cells that microbial invaders are present. The other important immune cells that were activated by the presence of commensal oral microbes were CD4+ helper T-cells. These cells help to coordinate the immune response during an infection. Ultimately, these immune cells supported osteoclasts.
Together, these data suggest a tightly coordinated pathway in which commensal oral microbes influence alveolar bone health. Furthermore, reducing the burden of commensal microbes in the mouth through oral antiseptic rinses prevented alveolar bone loss, which could have important clinical implications moving forward.
“We were able to show that the commensal oral microbiota influences alveolar bone homeostasis through osteoimmune mechanisms that are distinct from the systemic microbiome,” said Novince. “If we are able to suppress the healthy oral microbiome to lower levels, it could help protect from alveolar bone loss, even in a state of health.”
This report is the first investigation showing that chlorhexidine reduces naturally occurring alveolar bone loss and suggests that antiseptic oral rinses could support alveolar bone health and homeostasis. To ensure that this potential treatment is safe and effective, future studies aimed at better describing the interaction between the microbiome, immune cells and bone is warranted.
“Although we’re broadly suppressing oral microorganisms with the antiseptic rinse, it will be important to determine which specific microbes are really driving this naturally occurring alveolar bone loss,” said Hathaway-Schrader. “The alveolar bone marrow is a unique environment, and this is the first step in understanding interactions between oral microbes and immune cells important for promoting bone health.”

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system and the most common cause of neurological impairment in young adults. In MS, the patient’s own immune system attacks the brain and spinal cord, resulting in cumulative neurological deficits such as damaged sight, sensory disturbances, motor deficits (e.g. limiting the ability to walk) as well as cognitive impairment. Although the cause of MS is still unclear, a variety of genetic risk factors and environmental influences have already been linked to the disease.
Genetic predisposition alone does not lead to MS
Studies in recent years have clearly shown that genetic risk variants are a necessary condition for developing multiple sclerosis. “Based on our study, we were able to show that about half of the composition of our immune system is determined by genetics,” says Florian Ingelfinger, a PhD candidate at the UZH Institute of Experimental Immunology. The study by the team led by immunologist Burkhard Becher, professor at the Institute of Experimental Immunology at UZH, and the research groups of Lisa Ann Gerdes and Eduardo Beltrán of the Institute of Clinical Neuroimmunology at the LMU Klinikum, shows that these genetic influences, while always present in MS patients, are not on their own sufficient to trigger multiple sclerosis. In the study, 61 pairs of monozygotic twins where one twin is affected by MS whereas the co-twin is healthy were examined. From a genetic point of view, the twins were thus identical. “Although the healthy twins also had the maximum genetic risk for MS, they showed no clinical signs of the disease,” says Lisa Ann Gerdes.
Twin study eliminates genetic influences
Thanks to this globally unique cohort of identical twins, the researchers were able to exclude genetic influences by comparing twins with and without multiple sclerosis. “We are exploring the central question of how the immune system of two genetically identical individuals leads to significant inflammation and massive nerve damage in one case, and no damage at all in the other,” explains Burkhard Becher. Using identical twins enabled the international team of scientists to rule out the genetic influence and specifically track the immune system changes that were ultimately responsible for triggering MS in one twin.
Cutting-edge single-cell technologies and artificial intelligence
The researchers harness state-of-the-art technologies to describe the immune profiles of the twin pairs in rich detail. “We use a combination of mass cytometry and the latest methods in genetics paired with machine learning to not only identify characteristic proteins in the immune cells of the sick twin in each case, but also to decode the totality of all the genes that are switched on in these cells,” Florian Ingelfinger explains. Eduardo Beltrán, an expert in single-cell genomics, adds: “This ensures that we obtain as much information as currently technically possible from these valuable samples.” The team uses a variety of tailored algorithms based on artificial intelligence to extract relevant insights from this immense dataset.

Researchers at Michigan Medicine have found a novel method of measuring growth in the body’s largest artery that may help clinicians to identify potentially fatal heart conditions earlier.
The technique, called vascular deformation mapping, measures changes in the thoracic aorta, which carries blood from the heart to the rest of the body. This new technique uses high-resolution CT imaging to calculate three-dimensional changes in the aortic wall in a manner that significantly outperforms the standard manual rating methods performed by experts, according to results published in Radiology and Medical Physics.
“The technique used in this algorithm has been around for a while, but no one has ever used it to see three-dimensional growth of an aneurysm of the thoracic aorta,” said Nicholas Burris, M.D., corresponding author of the papers, assistant professor of radiology and director of aortic imaging at Michigan Medicine. “This is a promising step towards having technology that pushes the accuracy of measurement past what human raters can achieve, allowing clinicians to have the best possible picture of a patient’s condition.”
Thoracic aortic aneurysm occurs when the largest part of the aorta becomes weakened and grows, or dilates, increasing its risk of a potentially fatal rupture or dissection. For approximately 3% of adult patients over 50 years old with this largely asymptomatic condition, physicians recommend they undergo regular testing, often with CT scans, to measure aortic growth and determine if surgical repair is needed.
Currently, the standard practice to measure growth is done with human “raters” who line up two images and draw a line at two points to find the change. Burris says this process is prone to error, and, in many cases, doctors can’t confidently tell if the thoracic aorta is growing, creating uncertainty regarding the best treatments and follow-up plan.
“The challenge we’re faced with clinically is that a typical aneurysm in the aorta is going to grow only a fraction of a millimeter every year, and the process of manually drawing diameters that precise is very hard to reproduce,” he said. “You have a lot of variability in standard measurements relative to a very small amount of actual aneurysm growth. Basically, you rarely end up getting a confident assessment of growth, which can make it difficult to know what the patient’s actual risk is and how closely they need to be followed with repeat CT scans.”
The vascular deformation mapping technique developed by Burris’ team relies on an image analysis technique known as image registration, which, essentially, aligns the anatomy shown in multiple CT scans by taking any pixel on the first scan and relating its exact position to the pixel on the second scan. When they are all aligned, a three-dimensional color map of the aorta shows how much and where the thoracic aorta has grown.